request to strike and expunge chemtura …that you remove my claim no. 14317 from chemtura...

Honorable Robert E. GerberUnited States Bankruptcy JudgeUnited States Bankruptcy CourtSouthern District of New YorkOne Bowling GreenNew York, NY 10004

July 22, 2010

Re: REQUEST TO STRIKE AND EXPUNGE CHEMTURA CORPORATION'S DOCKET #3197, AND TO REMOVE MY CLAIM FROM CHEMTURA CORPORATION'S BANKRUPTCY PROCEEDINGS WITHOUT PREJUDICE

Dear Judge Gerber:

I respectfully request that you strike and expunge Chemtura Corporation's Docket #3197, and that you remove my Claim No. 14317 from Chemtura Corporation's Bankruptcy proceedings without prejudice.

I have in my possession and/or access to evidence that would convince a Grand Jury that there is a need for criminal trials. This evidence would prove in criminal trials that Mikey Hazelwood and other people who worked for Great Lakes Chemical Corporation (currently called Chemtura Corporation) defrauded the United States in ways that resulted in the death of my father, and caused physical harm to the Kids of the Pathfinders Camp. Chemtura Corporation has profited, and plans to continue profiting, from these criminal offenses.

In December 2009, after seven and a half years of searching for the right person in our Government, it became clear to me that U.S. Attorney Deborah Groom was the one person who has the authority to prosecute the people who defrauded the United States in ways that resulted in the death of my father and physical harm to the Kids of the Pathfinders Camp. In the week of December 10, 2009, U.S. Attorney Deborah Groom received a copy of the attached Summary of Proof of Claim. She has been looking at it with my request for her to let me know if there is any part of it that she has any doubt – so that I may provide to her evidence to clear up any doubt that she may have. She has assured me that she will respond to my request.

Statutes of limitations are overridden when fraud causes injury or death in Arkansas, and there are no statutes of limitations for murder. U.S. Attorney Deborah Groom has not presented to me anything that would indicate that she has any doubt about any part of the attached Summary of Proof of Claim. This gives me hope that the United States Government could eventually enforce the law, and that the perpetrators who worked for Great Lakes Chemical Corporation (currently called Chemtura Corporation) may be held accountable for what they did to my family and the Kids of the Pathfinders Camp.

Please review the information in the attached correspondence, entitled “REQUEST TO REMOVE CLAIMS NOS. 11875; 14263; 14270; AND 14317 FROM CHEMTURA CORPORATION'S CHAPTER 11 BANKRUPTCY PROCEEDINGS,” dated April 5, 2010, and take notice of the fact that I clearly stated that “I do not have the financial resources that it would take to

of 3 of Request to Strike & Expunge Docket #3197

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0911233100726000000000003

Docket #3380 Date Filed: 7/26/2010

present the voluminous amount of evidence that supports every word of my Summary of Proof of Claim, unless I have the help of the United States Department of Justice.” I would like to add, here and now, that I know that if U.S. Attorney Deborah Groom puts forth bona fide effort into receiving my evidence, and into conducting her own investigation, she will have good reason to initiate and/or implement the granting of Crime Victims' Rights described in 18 U.S.C. § 3771 to my family and the Kids of the Pathfinders Camp.

I am requesting that my Claim be removed from Chemtura Corporation's chapter 11 Bankruptcy proceedings without prejudice, because the United States Bankruptcy Court for the Southern District of New York is not the proper venue for the Claim that I have against Chemtura Corporation.

The United States Constitution Article III Section 2 Paragraph 3 says: “The trial of all crimes, except in cases of impeachment, shall be by jury, and such trial shall be held in the state where the said crimes shall have been committed;...,” and the crimes, which were committed by people who worked for Great Lakes Chemical Corporation (currently called Chemtura Corporation) were committed against the United States, against my family, and against the Kids of the Pathfinders Camp in the state of Arkansas. Wherefore, the trials for these crimes should be by jury in the state of Arkansas.

I do not have the money that it would cost for me to travel all the way to New York. On the other hand, I can afford to travel to Arkansas, and I can afford to stay in Arkansas for as long as it takes for me to present my evidence to U.S. Attorney Deborah Groom, and to see that justice is served. However, if the Order in Chemtura Corporation's Docket #3197 is not expunged, and if my Claim is not removed from Chemtura Corporation's Bankruptcy proceedings without prejudice, justice - for the crimes that have been committed against the United States, against my family, and against the Kids of the Pathfinders Camp - will be extremely impaired. I would appreciate it if you would strike and expunge Chemtura Corporation's Docket #3197, and remove my Claim No. 14317 from Chemtura Corporation's Bankruptcy proceedings without prejudice, so that justice may be served.

My understanding of Bankruptcy law is limited to what little bit I have studied during the past few months. I would like to believe that it is not legal to use the Bankruptcy Court to be permitted to profit from defrauding the United States in ways that result in death and physical harm. If it is legal to use the United States Bankruptcy Court to be allowed to profit from defrauding the United States, to profit from murder, and to profit from poisoning children, then it should be published and made known to everyone that it is legal. But if it is not legal, please do not set a precedent by allowing Chemtura Corporation to get away with it.

I have attached an electronic copy of my Summary of Proof of Claim, because the color pictures of maps and aerial photos must be seen clearly to completely understand it. I am assuming that, if you have looked at my Summary of Proof of Claim, what you have seen is like the copy that Chemtura Corporation's lawyers sent to me with the pictures too dark and distorted to understand what the color pictures show. The attached pdf file which contains my Summary of Proof of Claim is identified as“Electronic_Version_of_Amended_Summary.pdf.”

Before reading my Summary of Proof of Claim, please read the Note to Reader, which is attached pdf file identified as Note to Reader of Summary of Proof of Claim.pdf .

I have attached a copy of my April 5, 2010 “REQUEST TO REMOVE CLAIMS NOS. 11875;


14263; 14270; AND 14317 FROM CHEMTURA CORPORATION'S CHAPTER 11 BANKRUPTCY PROCEEDINGS,” because the information it contains could also be helpful in understanding how important it is to strike and expunge Chemtura Corporation's Docket #3197, and to remove my Claim from Chemtura Corporation's Bankruptcy proceedings without prejudice. The attached pdf file which contains this document is identified as “2010_04_06_11_40_59.pdf.”

You may also find attached a copy of Chemtura Corporation's Docket #3197. It has been included to make it possible for all recipients of this correspondence to see it. The pdf file which contains this document is identified as “0911233100713000000000017.pdf.”

Again, I respectfully request that you strike and expunge Chemtura Corporation's Docket #3197, and that you remove my Claim from Chemtura Corporation's Bankruptcy proceedings without prejudice. Sincerely,

_________________________________ Frank McKinnon, on behalf of Joe S. McKinnon and the Kids of the Pathfinders Camp 903 N. Missouri Ave. Roswell, New Mexico 88201 Office Phone (575) 627-3391 Cell Phone (575) 420-8199

Cc: U.S. Attorney Deborah Groom [email protected]; U.S. Attorney Susan Golden [email protected]; Charles Moulton, Sr. Assistant Attorney General for Arkansas [email protected]; Attorney General Eric Holder via U.S. Postal Service; FBI Director Robert Mueller [email protected]; U.S. Attorney Marie O'Rourke marie.o'[email protected]; Rick Ehrhart [email protected]; Patrick Young [email protected]; Mark Potts [email protected]; Glenn Fine [email protected]; Kathleen Kohl [email protected];Ignacia Moreno [email protected]; John Cruden [email protected]; Scott Fulton [email protected]; Lisa Jackson [email protected]; Sam Coleman [email protected];Alfredo “Al” Armendariz [email protected]; David Hartely [email protected]; Gerald Delavan [email protected]; Teresa Marks [email protected]; Kids of the Pathfinders Camp via www.frankmckinnon.com , Facebook and email; Thomas Browne [email protected]


mailto:[email protected]


http://www.frankmckinnon.com/















mailto:marie.o'[email protected]





K&E 17320229.1

UNITED STATES BANKRUPTCY COURT SOUTHERN DISTRICT OF NEW YORK

) In re: ) Chapter 11 ) CHEMTURA CORPORATION, et al.,1 ) Case No. 09-11233 (REG) ) Debtors. ) Jointly Administered )

ORDER GRANTING DEBTORS’ OBJECTION TO

FRANK MCKINNON’S PROOF OF CLAIM NO. 14317 Upon the Debtors’ Objection to Frank McKinnon’s Proof of Claim No. 14317

(the “Objection”)2 filed by Chemtura Corporation and its affiliated debtors and debtors in

possession in the above-captioned chapter 11 cases (collectively, the “Debtors”), requesting

entry of an order disallowing and expunging proof of claim number 14317, filed on November

17, 2009 by Frank McKinnon (the “Disputed Claim”), pursuant to sections 105(a) and 502(b) of

title 11 of the United States Code (the “Bankruptcy Code”) and Rule 3007 of the Federal Rules

of Bankruptcy Procedure (the “Bankruptcy Rules”); and consideration of the Objection and the

relief requested therein being a core proceeding pursuant to 28 U.S.C. §§ 157 and 1334; and

venue being proper before this court pursuant to 28 U.S.C. §§ 1408 and 1409; and due and

proper notice of the Objection having been provided; and it appearing that no other or further

notice need be provided; and the Court having determined that there exists just cause for the

1 The Debtors in these chapter 11 cases, along with the last four digits of each Debtor’s federal

taxpayer-identification number, are: Chemtura Corporation (3153); A&M Cleaning Products, LLC (4712); Aqua Clear Industries, LLC (1394); ASCK, Inc. (4489); ASEPSIS, Inc. (6270); BioLab Company Store, LLC (0131); BioLab Franchise Company, LLC (6709); Bio-Lab, Inc. (8754); BioLab Textile Additives, LLC (4348); CNK Chemical Realty Corporation (5340); Crompton Colors Incorporated (3341); Crompton Holding Corporation (3342); Crompton Monochem, Inc. (3574); GLCC Laurel, LLC (5687); Great Lakes Chemical Corporation (5035); Great Lakes Chemical Global, Inc. (4486); GT Seed Treatment, Inc. (5292); HomeCare Labs, Inc. (5038); ISCI, Inc. (7696); Kem Manufacturing Corporation (0603); Laurel Industries Holdings, Inc. (3635); Monochem, Inc. (5612); Naugatuck Treatment Company (2035); Recreational Water Products, Inc. (8754); Uniroyal Chemical Company Limited (Delaware) (9910); Weber City Road LLC (4381); and WRL of Indiana, Inc. (9136).

2 Capitalized terms not otherwise defined herein shall have the meaning ascribed to them in the Objection.

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0911233100713000000000017

Docket #3197 Date Filed: 7/13/2010

2 K&E 17320229.1

relief granted herein and that such relief is in the best interest of the Debtors, their estates and

creditors and all other parties in interest; and upon the arguments and testimony presented at the

Hearing before the Court, and any responses to the Objection having been withdrawn, resolved,

or overruled on the merits; and after due deliberation and sufficient cause appearing therefore, it

is hereby ORDERED that:

1. The Objection is granted.

2. The Disputed Claim is hereby disallowed and expunged pursuant to

section 502(b) of the Bankruptcy Code.

3. The terms and conditions of this Order shall be immediately effective and

enforceable upon entry of the Order.

4. This Court retains jurisdiction with respect to all matters arising from or

related to the implementation of this Order.

New York, New York s/ Robert E. Gerber Dated: July 13, 2010 Honorable Robert E. Gerber

United States Bankruptcy Judge

NOTE TO READER OFSUMMARY OF PROOF CLAIM

Kurtzman Carson Consultants received and filed my Proof of Claim Form and Summary of Proofof Claim No. 11875, on the Bar Date October 30, 2009;

Kurtzman Carson Consultants received and filed my Proof of Claim Form and Summary ofProof of Claim No. 14263, on November 6, 2009. It was filed to amend and replace my Proof of Claimand Summary of Proof of Claim No. 11875.

Kurtzman Carson Consultants received and filed my Proof of Claim Form and Summary of Proofof Claim No. 14270 , on November 18, 2009. It was filed to amend and replace my Proof of ClaimForm and Summary of Proof of Claim No. 14263. I noticed that the Summary of Proof of Claim forClaim No. 14270 did not have my signature on page 121 where it says "I declare, under penalty ofperjury that the foregoing Summary of Proof of Claim is true and correct.," so I mailed thesame Summary of Proof, again, with my signature. Kurtzman Carson Consultants received it and filedit as Claim No. 14317, on November 20, 2009; thereby amending and replacing all of my previousProof of Claim Forms and Summaries of Proof of Claim.

The following pages are a copy of an electronic version of the text and pictures of the Summaryof Proof of Claim for Claim No. 14317, except for one date correction on page 2 in paragraph 3.1,changing 2002 to 200[9], which was made on January 7, 2010 as noted in this version.

Understanding this Summary of Proof of Claim is impossible without seeing the pictures clearly. The best way to see the pictures clearly is to view them on the electronic version, which may be found at www.frankmckinnon.com/files/Electronic_Version_of_Amended_Summary.pdf

UNITED STATES BANKRUPTCY COURTSOUTHERN DISTRICT OF NEW YORK _________________________________________ )In re: ) Chapter 11 ) Frank McKinnon, ) Case No. 09 - 11233 (REG) on behalf of Joe S. McKinnon's Family ) and Kids of the Pathfinders Camp ) Jointly Administered ) Claimant for KCC Claim #: 11875 and 14263 ) For Case No. 09 - 11247 and _________________________________________) Case No. 09 - 11233 Consolidated

Re: Corrected: 2nd Edition of AMENDED SUMMARY OF PROOF OF CLAIM AND PROOF OF CLAIM FORM TO REPLACE ALL PREVIOUS VERSIONS OF SUMMARY OF PROOF OF CLAIM AND PROOF OF CLAIM FORM (Correction made on 1/7/2010)

TO: CHEMTURA CORPORATION; THE UNITED STATES (U.S.) BANKRUPTCY COURT SOUTHERN DISTRICT OF NEW YORK; U.S. ATTORNEY GENERAL ERIC HOLDER; MARY PATRICE BROWN, ACTING COUNSEL FOR U.S. DEPARTMENT OF JUSTICE (DOJ) OFFICE OF PROFESSIONAL RESONSILITY; JOHN C. CRUDEN, ACTING ASSISTANT ATTORNEY GENERAL FOR THE DOJ ENVIRONMENTAL AND NATURAL RESOURCES DIVISION; DEBORAH J. GROOM, U.S. ATTORNEY FOR WESTERN DISTRICT OF ARKANSAS; GREGORY J. FOURATT, U.S. ATTORNEY FOR DISTRICT OF NEW MEXICO; ROBERT S. MUELLER, III., DIRECTOR OF THE FEDERAL BUREAU OF INVESTIGATION (FBI); LISA P. JACKSON, ADMINISTRATOR OF THE U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA); MARIE A. O'ROURKE, VICTIM'S RIGHTS OMBUDSMAN; AND SOME OTHER GOVERNMENT OFFICIALS.

I, Frank McKinnon, son of Joe S. McKinnon, respectfully submit this 2nd Edition of Amended Summary of Proof of Claim and Proof of Claim Form to replace all previous versions of my Summary of Proof of Claim and Proof of Claim Form that have been received from me and filed by Chemtura Corporation's Debtors' Agent of Kurtzman Carson Consultants LCC - in response to a document, entitled: "NOTICE OF BAR DATE FOR FILING PROOFS OF CLAIM ON OCTOBER 30, 2009"(Notice of Bar Date), on behalf of Joe S. McKinnon's Family and the Kids of the Pathfinders Camp.

I respectfully move Chemtura Corporation's Debtors' Agent and the Court to consolidate Debtors who hold liability for this Claim. Attached to the last page of this 2nd Edition of Amended Summary of Proof of Claim is a Proof of Claim Form, which consolidates Debtors who hold liability for this Claim as: Great Lakes Chemical Corporation/Chemtura Corporation with Case Numbers: 09-11247 and 09-11233 with Court Claim Number: 11875 filed on 10/30/2009 and Court Claim Number: 14263 filed on 11/6/2009. This 2nd Edition of Amended Summary of Proof of Claim and Proof of Claim Form has been amended to correct some typographical errors and to provide information to make the facts easier for the rest of the recipients to understand. The dollar amounts are the same. The purpose of amending it is to provide all recipients with the same information. It is the first version of my Summary of Proof of Claim and Proof of Claim Form to be received by all identified recipients.

2nd Edition of Amended Summary of Proof of Claim for Joe S. Mckinnon's Family and Kids of Pathfinders Camp Page 1 of 154

SUMMARY OF PROOF OF CLAIM

In the United States, profiting from committing murder and causing physical harm to children, while defrauding the United States, the ways that Perpetrators at GLCC have done, are criminal offenses. The ways that Perpetrators at GLCC successfully executed their conspiracy to defraud the United States, which caused the death of Joe S. McKinnon and physical harm to approximately 507 Kids of the Pathfinders Camp, are criminal offenses. These criminal offenses and/or effects of these criminal offenses are under the jurisdiction and areas of stewardship held by all government officials who have received this Summary of Proof of Claim. Arkansas is part of the United States. In Arkansas, when fraud causes injury or death, statutes of limitations are overridden. There are no statutes of limitations for murder.

PLEASE TAKE NOTICE that you have received this Summary of Proof of Claim for at least one of the reasons, which follow:

(1) Chemtura Corporation is receiving this Summary of Proof of Claim, because this Summary of Proof of Claim is a response to the Notice of Bar Date that I received from Chemtura Corporation, and because Chemtura Corporation holds criminal and civil liability for the injuries and death of Joe S. McKinnon, for the injuries of the Kids of the Pathfinders Camp, and for ruining the Pathfinders Camp.

(2) The U.S. Bankruptcy Court Southern District of New York is receiving this Summary of Proof of Claim, because the Notice of Bar Date says that "IF THE DEADLINE APPLIES TO YOU AND YOU FAIL TO FILE A PROOF OF CLAIM BY THE BAR DATE, YOUR CLAIM WILL BE FOREVER BARRED...," and because I do not know whether or not the October 30, 2009 Bar Date applies to the restitution and compensation that Chemtura owes to Joe S. McKinnon's Family and the Kids of the Pathfinders Camp.

(3) Attorney General Eric Holder: You are receiving this Summary of Proof of Claim, because I am respectfully seeking your help in determining whether or not it is legal for Chemtura Corporation to use chapter 11 Bankruptcy protection to avoid criminal and civil liability for the murder of Joe S. McKinnon and the poisoning of the Kids of the Pathfinders Camp.

(3.1) Your office received my Petition for WOHCAS of Environmental Law 2009, on March 2, 200[9], and received my 2nd Attempt with Amended Petition for WOHCAS of Environmental Law 2009, on March 17, 2009. Then, on October 14, 2009, I became aware of a policy on your DOJ web page that makes me believe that you may not have received your copies of these documents, yet. However, I can verify that other people in the DOJ did receive these documents on March 2 and March 17, 2009. Because it would have been treasonous for people in the DOJ, who received either or both versions of my Petition for WOHCAS of Environmental Law 2009, to have done anything other than to make sure that you did receive copies of both versions, I am fairly sure that you did receive copies. Because there is a small possibility that you haven't received your copies, yet, I have made copies available on my web site. See References 1 and 2 for web page addresses.

(3.2) Both versions of my Petition for WOHCAS of Environmental Law 2009 contain criminal complaints regarding the crimes that Perpetrators at GLCC (otherwise called Chemtura Corporation) committed against Joe S. McKinnon and the Kids of the Pathfinders Camp. Both versions, also, contain Notices of Constitutional Challenges with Requests for Opinions, Rulings and Intervention,


regarding statutory laws and policies that guide behavior of people who work for federal health, environmental, and law enforcement, agencies, which have been derived from subversive, corrupt, abusive, and unconstitutional acts of Congress, executive orders, and judicial rulings, and which have been used by GLCC/Chemtura to get a way with the murder of Joe S. McKinnon and the poisoning of the Kids of the Pathfinders Camp.

(3.3) I am respectfully requesting your help. I believe that Joe S. McKinnon's Family and the Kids of the Pathfinders Camp deserve your help.

(4) Mary Patrice Brown: You are receiving this Summary of Proof of Claim, because a web page that is published by the DOJ Office of the Inspector General says that "...misconduct by a Department attorney or law enforcement personnel that relate to the exercise of the attorney's authority to investigate, litigate, or provide legal advice are the responsibility of the Department's Office of Professional Responsibility," and because your office appears to be the only part of the DOJ that has acknowledged having any potential stewardship over this matter. The information that your office has already received regarding the misconduct and corruption in the US Attorneys Office of New Mexico is only one of many similar situations involved in this matter. I am respectfully requesting your help. I believe that Joe S. McKinnon's Family and the Kids of the Pathfinders Camp deserve your help.

(5) John Cruden: You are receiving this Summary of Proof of Claim, because the insidious crimes that have been committed by Perpetrators at GLCC look very much like the more severe cases that the DOJ Environmental and Natural Recourse Divisions (ENRD) has pursued in the past, according to the web pages published by the ENRD; and because 2 of the Kids of the Pathfinders Camp who came with me to the Pathfinders Camp in 1988 from Chinle, Arizona are members of the Navajo, otherwise called Dine, tribe. I am respectfully requesting your help. I believe that Joe S. McKinnon's Family and the Kids of the Pathfinders Camp deserve your help.

(6) Deborah J. Groom: You are receiving this Summary of Proof of Claim, because the Pathfinders Camp was located in the Western District of Arkansas. I am respectfully requesting your help. I believe that Joe S. McKinnon's Family and the Kids of the Pathfinders Camp deserve your help.

(7) Gregory J. Fouratt: You are receiving this Summary of Proof of Claim, because a man who served New Mexico as an educator for many years was murdered, and approximately 493 children from New Mexico played, swam, and slept in GLCC's Poison at the Pathfinders Camp in Arkansas, while Perpetrators at GLCC knew that this was happening, and while these Perpetrators at GLCC were defrauding the United States. I am respectfully requesting your help. I believe that Joe S. McKinnon's Family and the Kids of the Pathfinders Camp deserve your help.

(8) Robert S. Mueller, III: You are receiving this Summary of Proof of Claim, because Perpetrators at GLCC caused GLCC to make excessively high amounts of revenue and profit by defrauding the United States. Their successful conspiracy to defraud the United States, and their flagrant defiance and violations of federal laws, caused the death of Joe S. McKinnon, and caused physical harm to approximately 507 misinformed and unsuspecting victims from New Mexico, Arizona, and Arkansas, at the Pathfinders Camp, while the Perpetrators at GLCC knew that we were in danger of death and/or physical harm. Public officials - at county, state, and federal levels of government - have, also, participated in GLCC's conspiracy to defraud the United States. Chemtura Corporation was created by merging GLCC with Crompton Corporation in 2005. I am respectfully


requesting your help. I believe that Joe S. McKinnon's Family and the Kids of the Pathfinders Camp deserve your help.

(9) Lisa P. Jackson: You are receiving this Summary of Proof of Claim, because the FBI says: "Dude ! Let the EPA do their job, and get on with your life." I would like to be able to follow these instructions as soon as possible. But this matter involves the USEPA in many ways that need to be rectified before I will be able to follow the FBI's instructions. I am respectfully requesting your help. I believe that Joe S. McKinnon's Family and the Kids of the Pathfinders Camp deserve your help.

(10) Marie A. O'Rourke: You are receiving this Summary of Proof of Claim, because victim's rights are being violated. I am respectfully requesting your help. I believe that Joe S. McKinnon's Family and the Kids of the Pathfinders Camp deserve your help.

(11) Some Other Government Officials: You are receiving this Summary of Proof of Claim, because you are in a position where I believe you can help, and you have either taught me something and/or your behavior gives me reasons to trust you. I am respectfully requesting your help. I believe that Joe S. McKinnon's Family and the Kids of the Pathfinders Camp deserve your help.

On about September 3, 2009, I received a Notice of Bar Date with a deadline of October 30, 2009 for filing a Proof of Claim Form to show how much Chemtura Corporation may owe the estate of Joe S. McKinnon. It requires a dollar amount. My understanding is that it is not my job, but it is the job of U.S. Attorneys and the U.S Courts to place a dollar amount for what is owed in restitution and compensation for the crimes that have been committed by Perpetrators at GLCC (Crimes of GLCC). But I can read well enough to understand what is reasonable and legal. With an understanding that Joe S. McKinnon's Family and the Kids of the Pathfinders Camp could be forever barred from receiving any restitution and compensation for the Crimes of GLCC if I did not place a dollar amount on the Proof of Claim Form before the October 30, 2009 Bar Date, I placed a range of reasonable and legal dollar amounts on the Proof of Claim Form and made sure that it was received by Chemtura's Debtors' Agent before the deadline. Throughout this Summary of Proof of Claim are reasons that make the range of dollar amounts that I have placed on the Proof of Claim Form reasonable and legal. I have provided a reasonable and legal dollar amount for the maximum, which is not the maximum that could be considered reasonable and legal for Chemtura Corporation to be required to pay Joe S. McKinnon's Family and the Kids of the Pathfinders Camp, but is an amount that I believe would be as fair and just as can be expected for restitution and compensation. I have also provided less dollar amounts that could be acceptable under certain conditions.

Now that I have met the October 30, 2009 Bar Date deadline with Chemtura Corporation's Debtors' Agent of Kurtzman Carson Consultants LCC, I am submitting this Amended Summary of Proof of Claim and Proof of Claim Form for the purpose of correcting some typographical errors, and for clarifying facts to make them easier to understand for the rest of the recipients.

I have, recently, been communicating with people in the USEPA in an effort to encourage them to find some environmental sampling data from a study that the USEPA conducted of the sediment in the Camp Pond and of the air in the Pathfinders Camp between 1976 and 1978, which may give me reason to submit another Amended Summary of Proof of Claim, if they find this data in the near future. Otherwise, obtaining and using this environmental sampling data will be up to the U.S Attorneys who represent Joe S. McKinnon's Family and the Kids of the Pathfinders Camp.


Because it is apparently necessary, I am respectfully demanding Crime Victims' Rights, here and now, as described in 18 U.S.C. § 3771. See Exhibit A. I am also respectfully demanding rights described in the 5th Amendment of the U.S. Constitution where it says that no person shall be "deprived of life...or property, without due process of law...nor...without just compensation." Due process of law, in this case, includes: (1) U.S. Attorneys representing Joe S. McKinnon's Family and the Kids of the Pathfinders Camp; (2) an opportunity to meet with U.S. Attorneys for the purpose of giving to them my information and evidence with them putting forth a bona fide effort in receiving and understanding it; and (3) the same U.S. Attorneys putting forth a bona fide effort in presenting it to a Grand Jury, and so on...in accordance to a Grand Jury's decision.

In 1972, the above photographs of Joe S. McKinnon and the Kids of the Pathfinders Camp were published in an article about the Pathfinders Camp in the El Dorado News Times. The first large group


of kids camped here in 1956. The last large group of kids stayed in the Camp Lodge in 1988. Joe S. McKinnon lived here 3/4 of the time, year round, between 1986 and 1995. Smaller groups of kids spent time here until 2001. I came with ADEQ and USEPA people, a small group of other concerned people, and by myself, for environmental sampling in 2003 and 2004. Approximately 507 Kids of the Pathfinders Camp that I have counted for my Claim stayed here between 1970 and 2001.

PATHINDERS CAMP

Highway Department Areal Photograph of Pathfinders Camp 1975

The USEPA started studying the sediment of the Camp Pond, and the air of the Pathfinders Camp in 1976, and completed this study in 1978. I will elaborate on the topic of the USEPA's Camp Pond sediment samples later in this Summary of Proof of Claim. The USEPA air samples from the Pathfinders Camp contained many of GLCC's chemical compounds. I have listed these chemical compounds. This list of GLCC's chemical compounds that the USEPA identified in the air of the Pathfinders Camp is, as follows:


(1) ethylene dibromide

(2) 1-chloro-2-bromoethane

(3) dibromopropane (4) Allyl bromide

(5) butane + dichlorodifluoromethane

(6) acetaldehyde

(7) isopentane

(8) trichlorofluoromethane

(9) propanal + C5H10 isomer

(10) n-pentane

(11) acetone

(12) C5H10 isomer

(13) dichloromethane + fluorotrichloromethane

(14) isopropanol

(15) C6H12 isomer

(16) 2-methylpentaneCamp Pond in Late 1980s or Early 1990s

(17) 3-methylpentane

(18) hexafluorobenzene

(19) chloroform

(20) methyl cyclopentane

(21) 2,3-dimethylpentane

(22) methyl isopropyl ketone

(23) methylhexane isomer + trichloroethylene

(24) C6C12 isomer

(25) n-hexane

(26) perfluorotoluene

(27) 1,1,1-trichloroethane

(28) 3-methylhexane


(29) C7H14 isomer

(30) n-heptane

(31) butanal isomer

(32) carbon tetrachloride

(33) C7H14 isomer

(34) 2,4-dimethylhexane

(35) C8H16 isomer

(36) trimethylpentane isomer

(37) 2,3-dimethylbenzene

(38) 4-methylheptane

(39) 1,trans-2-dimethylcyclohexane

(40) C9H20 isomer

(41) C8H16 isomer

(42) tetrachloroethylene

(43) 2,4-dimethylheptane

(44) ethylcyclohexane

(45) ethylbenzene

(46) 4-methyloctane

(47) m-xylene

(48) styrene + C9H18 isomer

(49) o-xylene

(50) methyl ethylcyclohexane isomer

(51) n-nonane

(52) isopropylbenzene

(53) dimethylcyclopentane isomer + pentanal (54) methylcyclohexane (55) C7H14 isomer

(56) C8H16 isomer

(57) C6H10

(58) benzene

(59) cyclohexane

(60) 2-methylhexane

(61) 1,2,3-trimethylcyclopentane

(62) toluene



(65) 1,cis-2-dimethylcyclohexane

(66) hexanal

(67) n-octane

(68) silane compound (BKG)

(69) 2-methyloctane or 2,4- dimethylheptane

(70) trimethylcyclohexane isomer

(71) trimethylcyclohexane isomer

(72) p-xylene

(73) 3-methyloctane


(74) dimethylpentanol (tent.) isomer

(75) tetramethylhexane isomer

(76) propylcyclohexane

(77) p-ethyltoluene

(78) C11H24 isomer

(79) dimethyloctane isomer

(80) C11H22 isomer

(81) C4-alkyl benzene isomer

(82) C12H26 isomer

(83) n-butylbenzene + propyltoluene isomer

(84) n-undecane

(85) n-dodecane (tent.)

(86) C10H22 isomer

(87) dimethyloctane isomer

(88) n-heptanal

(89) C9H18 isomer

(90) C10H20 isomer

(91) n-propylcyclohexane

(92) m-ethyltoluene

(93) 3-methylnonane

(94) 0-ethyltoluene

(95) n-decane

(96) C11H24 + C4-alkyl benzene isomer

(97) butylcyclohexane

(98) nonanal

(99) C13H28 isomer

(100) C15H32 isomer

There are studies that show how some of these chemical compounds that the USEPA identified in the air of the Pathfinders Camp decompose to become other toxic substances. Such studies, which have been easy to find on http://toxnet.nlm.nih.gov, show that the air of the Pathfinders Camp had more forms of GLCC's toxic substances, which include the following:

(1) Toxic gases & vapors (such as hydrogen bromide, bromine, & carbon monoxide) may be released when ethylene dibromide decomposes. (Reference 406) This apparently means that Joe S. McKinnon and the Kids of the Pathfinders Camp were also likely exposed to:

(1.1) hydrogen bromide

(1.2) bromine

(1.3) carbon monoxide

(2) Under certain conditions, fluorocarbon vapors may decompose on contact with flames or hot surfaces, creating the potential hazard of inhalation of toxic decomposition products of trichlorofluoromethane. (Reference 407) This apparently means that Joe S. McKinnon and the Kids of the Pathfinders Camp may have been exposed to fluorocarbon vapors.


(3) Chloroform "has been shown to produce phosgene, hydrogen chloride, water, carbon dioxide and chlorine." (Reference 408) Chloroform decomposes at ordinary temperature in sunlight in the absence of air, and in the dark in the presence of air..." (Reference 409) This apparently means that Joe S. McKinnon and the Kids of the Pathfinders Camp were also exposed to:

(3.1) phosgene

(3.2) hydrogen chloride

(3.3) chlorine

(4) "[Trichloroethylene] TCE should be packaged in steel drums. These drums should be stored in a cool, dry, well-ventilated area because TCE will slowly decompose to corrosive HCL when exposed to light & moisture. (Reference 403) [Trichloroethylene] SLOWLY DECOMPOSED WITH FORMATION OF HYDROCHLORIC ACID BY LIGHT IN PRESENCE OF MOISTURE (Reference 404) This apparently means that Joe S. McKinnon and the Kids of the Pathfinders Camp were also exposed to hydrochloric acid.

(5) "Pentanal does contain chromophores that absorb at wavelengths >290 nm(4) and will undergo photodegradation to form propene, vinyl alcohol and ethanal." (Reference 410). Ethanal is a synonym for acetaldehyde. Acetaldehyde is already listed in the USEPA study. This apparently means that Joe S. McKinnon and the Kids of the Pathfinders Camp were also likely exposed to:

(5.1) propene, which is a synonym for propylene

(5.2) vinyl alcohol, which is a synonym for vinyl acetate

(6) "...A typical experiment in the presence of active species such as NOx and SO2 showed that benzene photodegradation was considerably accelerated above that in air alone(2). Its half-life in the presence of active species was 4-6 hr with 50% mineralization to CO2 in approximately 2 days(3). Products of degradation include phenol, 2-nitrophenol, 4-nitrophenol, 2,4-dinitrophenol, 2,6-dinitrophenol, nitrobenzene, formic acid, and peroxyacetyl nitrate..." (Reference 411) This apparently means that Joe S. McKinnon and the Kids of the Pathfinders Camp were also exposed to

(6.1) phenol

(6.1) 2-nitrophenol

(6.2) 4-nitrophenol

(6.3) 2,4-dinitrophenol

(6.4) 2,6-dinitrophenol

(6.5) nitrobenzene

(6.6) formic acid

(6.7) peroxyacetyl nitrate


In June of 2002, during my first attempt to report the murder of Joe S. McKinnon and the poisoning of the Kids of the Pathfinders Camp to the Federal Bureau of Investigation (FBI), an employee of the FBI said, "Dude! Let the EPA do their job, and get on with your life."

A few weeks later, while a group of Arkansas Department of Environmental Quality (ADEQ) employees was shown the location of the Camp Pond on a map, an employee of the ADEQ said, "Those kids got fried."

In June of 2004, while discussing this situation with an employee of the U.S. Public Health Services Agency for Toxic Substance and Disease Registry (ATSDR), the employee of the ATSDR said that, if they did what needs to be done with my situation, it would open the gate for a thousand more just like it.

Also in June of 2004, while I was asking an employee of the U.S. Environmental Protection Agency (USEPA) why he was unable to analyze the 2004 USEPA Camp Pond sediment samples for toxic substances that were unique to Great Lakes Chemical Corporation (GLCC), the employee of the USEPA said that he could only do what was allowed by people who ranked higher than him.

Two of many excuses for not investigating the murder of my father and the poisoning of the Kids of the Pathfinders Camp that have been used by people in official positions of authority to investigate have been: (1) because my father had diabetes, (2) and because his death certificate said that the cause of death was "myocardial infarction," and did not say that the cause of death was exposure to toxic or hazardous substances. It did not matter to them that the reason his death certificate didn't say that the cause of his death was exposure to toxic or hazardous substances was because nobody knew that his death could have been caused by exposure to toxic or hazardous substances (Poison) from GLCC at the the Pathfinders Camp, except for the Perpetrators at GLCC, until nearly 2 years after he died. It did not matter to them that I have reams of his medical records that look like toxicological studies of GLCC's chemical compounds (Poisons) that the USEPA has identified in the air of the 40 acres of my grandparents' land that we used for the Pathfinders Camp.

I have checked, and have only been able to find 2 of my relatives who have had diabetes. My father and my grandmother lived the later years with diabetes. My grandmother was diagnosed with it first. She spent a lot of time in the garden next to the "Parker's Chapel Water Tower." I am fairly sure that she didn't have it until after GLCC became our next-door-neighbor and started putting Poison into the air that we were breathing. My father was diagnosed with it after he had spent a summer with chronic exposure to GLCC's Poisons as he worked on the Camp Lodge and Camp Pond. His bedroom, with nothing but screens between him and the outside air of the Camp Lodge, was about 100 meters north of the "Parker's Chapel Water Tower." USEPA air samples from the top of the "Parker's Chapel Water Tower," indicate that my father and my grandparents spent a lot of time being exposed to GLCC's Poisons. GLCC is a manufacturer of brominated chemicals. Studies of exposure to brominated chemicals have shown links to cancer, heart disease, diabetes, and a wide variety of other diseases. GLCC's operations have also involved emissions of a variety of solvents, including toluene, benzene, trichloroethylene, and carbon tetrachloride which have also been linked to cancer, heart disease, diabetes, symptoms similar to Parkinson's disease, and a wide variety of other diseases.

My grandparents unsuspectingly lived for decades with chronic exposure to GLCC's Poisons. It is very likely that my grandmother's diabetes and cancer were caused by her chronic exposure to GLCC's Poisons. It is possible that my grandfather's Parkinson's disease and hallucinations were, also,


caused by his chronic exposure to GLCC's Poisons.

My father's medical records look very much like the information from toxicological studies of GLCC's Poisons that the USEPA found in the air of the Pathfinders Camp. His medical records also show that his physicians could not figure out the reasons for many of his diseases, which became increasingly worse the more he stayed at he Pathfinders Camp, while he was unsuspectingly living with chronic exposure to GLCC's Poisons. If his physicians would have known where he was spending most of his time between 1986 and 1995, I am sure that they would not have been so lost for answers.

Most of the Kids of the Pathfinders Camp stayed at the Camp 24 hours per day for between one week and four weeks at a time. Some of us spent longer time spans at the Camp; as much as ten weeks for some. My stays at the Camp ranged from three days to five months at a time, with most of my stays being two or three weeks at a time. I have noticed that OSHA has standards for many of GLCC's Poisons, which place time limits that a person can be exposed to them. For example benzene, which is one of GLCC's Poisons that we were exposed to, has OSHA standards, which follow (quotation marks omitted):

(1) The employer shall assure that no employee is exposed to an airborne concentration of benzene in excess of one part of benzene per million parts of air (1 ppm) as an 8 hr TWA. The employer shall assure that no employee is exposed to an airborne concentration of benzene in excess of 5 ppm as averaged over any 15 min period. (Reference 435)

(2) Permissible Exposure Limit: Table Z-2 8-hr Time Weighted Avg: 10 ppm. (Note: This standard applies to the industry segments exempt from the 1 ppm 8 hr TWA and 5 ppm STEL of the benzene standard at 1910.1028) (Reference 436)

(3) Permissible Exposure Limit: Table Z-2 Acceptable Ceiling Concentration: 25 ppm. (Note: This standard applies to the industry segments exempt from the 1 ppm 8 hr TWA and 5 ppm STEL of the benzene standard at 1910.1028). (Reference 436)

(4) Permissible Exposure Limit: Table Z-2 Acceptable maximum peak above the acceptable ceiling concentration for an 8-hour shift. Concentration: 50 ppm. Maximum Duration: 10 minutes. (Note: This standard applies to the industry segments exempt from the 1 ppm 8 hr TWA and 5 ppm STEL of the benzene standard at 1910.1028.) (Reference 436)

Many Kids of the Pathfinders Camp, and some of our children, have physicians who have, also, been lost for answers regarding our diseases.

I spent several months trying to get my father's biological samples analyzed by the Arkansas Department of Health, the Criminal Investigations Division (CID) of the USEPA, the Forensics Lab of the USEPA, the lab at the ADEQ, and the ATSDR, but none of them would analyze his biological samples. I checked with some private labs, and found that the prices that they charged for such services made it impossible for me to have his biological samples analyzed by a private lab. I learned, from the Arkansas Attorney General's Office, that a way that I could get Joe S. McKinnon's biological samples analyzed by the government would be if I could convince the Union County Prosecuting Attorney to initiate a criminal investigation.

I visited with the Union County Prosecuting Attorney, Joe Wray, for the purpose of convincing


him that it would be appropriate for him to initiate a criminal investigation, and showed him documents with information that made evident that anyone who spent time at the Pathfinders Camp was in an area where it would have been impossible to avoid exposure to high levels of GLCC's Poisons. Joe Wray told me that he would initiate a criminal investigation, if I could convince the Union County Coroner to tell him that he should. (While standing in front of Joe Wrey's desk, I looked out the window behind him and noticed that the most prevalent object that I could see was the ENSCO incinerator stack. A few years later, I learned that Joe Wrey was no longer working for Union County.)

While I was visiting the Union County Coroner, Curtis Butterfield, in an effort to convince him that - in light of newly found evidence, which shows how it would have been impossible for my father to have avoided many years of chronic exposure to high levels of toxic substances from GLCC at the Pathfinders Camp - it would be appropriate for him to reevaluate the cause of my father's death, and for him to tell Prosecuting Attorney Wray to initiate a criminal investigation, regarding the murder of my father, regarding poisoning of the Kids of the Pathfinders Camp, and regarding poisoning the people who lived in Parkers Chapel, Mr. Butterfield said: "Frankie, I know you are right...I loved your Granny, your Granddaddy, and your Daddy...went church with them...I know, from working at the South Plant, that it isn't so much what you can see and smell, but it is what you can't see and smell that'll kill you...But Great Lakes owns this town...and I can't..."

Between 2002 and 2009, I wasted a lot of time, money, and energy, trying to figure out how to get help from the government in dealing with the murder of Joe S. McKinnon and the poisoning of the Kids of the Pathfinders Camp. My findings make apparent that GLCC/Chemtura owns a bit more than the "town" of El Dorado, in Union County, Arkansas.

Then, in January 2009, I found what looked like it could be another opportunity to try getting help from the government, when I discovered that Department of Energy radioactive materials were poured into GLCC's Tailbrine Pond, which leaked into the aquifer that provided water for the spring fed Camp Pond, and that the DOE radioactive materials were, also, poured into GLCC's leaking injection wells, which, obviously, also, contributed to the contamination of the groundwater in GLCC's plume. I found out about the radioactive materials in GLCC's Tailbrine Pond, in GLCC's injection wells, and in the aquifer that provided water for the Camp Pond, while I was dealing with the corruption and abuse of power that were used by Pete V. Domenici and George W. Bush in their efforts to promote the nuclear industry in a way that posed a threat of placing my family in harms way, much like the harm that was caused by Perpetrators at GLCC. I submitted a document entitled: "Petition for Writ of Habeas Corpus Ad Subjiciendum (WOHCAS of Environmental Law 2009)," on March 2, 2009, in the U.S. District Court of New Mexico. Part of my Petition for WOHCAS of Environmental Law 2009 is a criminal complaint, which mentions crimes that were committed by Mikey Hazelwood, John Talpas, Greg Withrow, Nick T. Macchiarolo, and others associated with GLCC, (Perpetrators at GLCC) against Joe S. McKinnon and the Kids of the Pathfinders Camp.

The U.S. District Court Administrator filed my criminal complaint as a civil case. I explained to the Court Administrator that an FBI agent told me that the FBI "can't touch it if it is a civil case." I asked the Court Administrator to get my Petition for WOHCAS of Environmental Law 2009 out of civil court, because the only reason it was submitted to the District Court was to give my Oath of Affirmation before a Magistrate Judge to fulfill one of the requirements for making a criminal complaint, because it had already been in front of the Magistrate Judge long enough to fulfill this requirement, and because, as long as it was in civil court, the crime victims were being deprived of


Crime Victim's Rights. Then, the Court Administrator told me that the only way it could be a criminal case was if the U.S. Attorney filed the criminal complaint. Then, she told me that, if I sent her an email requesting that it be taken out of civil court, she would forward it to the Judge. I sent her an email requesting that it be taken out of civil court on March 16, 2009.

As of November 9, 2009, all information that I have received indicates that the case of my Petition for WOHCAS of Environmental Law 2009, - which contains a criminal complaint with information regarding crimes that were committed by Perpetrators at GLCC, otherwise called Chemtura, - filed on March 2, 2009, has not been removed, dismissed, or closed by the U.S. District Court of New Mexico.

Between 2002 and 2009, I tried several times, with no success, to receive help from the FBI and the U.S. Attorneys Office. My last attempt at seeking help from the FBI and the U.S. Attorneys Office was during the first 2 weeks of March 2009. During this attempt, an agent of the FBI told me that the FBI could not investigate unless the U.S. Attorneys Office instructed them to. Paul Spiers, an Assistant U.S. Attorney in New Mexico, explained that the only way the U.S. Attorneys Office would look at my evidence was if the FBI asked them to. He also told me that (while acting as the U.S. Attorney in Charge) he would not authorize an FBI investigation. At this point, I had nearly 7 years of experience at having my rights violated by government employees as they aided and abetted in the crimes that Perpetrators at GLCC committed against Joe S. McKinnon and the Kids of the Pathfinders Camp. With this in mind, copies of emails between the FBI agent and me, along with a transcript of a recorded conversation that I had with U.S. Attorney Paul Spiers, are included in my 2nd Attempt with Amended Petition for WOHCAS of Environmental Law 2009, which also includes my criminal complaint that mentions the crimes of Perpetrators at GLCC.

I submitted my 2nd Attempt with Amended Petition for WOHCAS of Environmental Law 2009 to the Office of U.S. Attorney General Eric Holder with email (electronic mail), on March 17, 2009, and received verbal confirmation that it had been receive by the Investigations Division of the DOJ Office of the Inspector General, early in the morning of March 18, 2009. Then, a few hours later, Chemtura Corporation filed for chapter 11 Bankruptcy protection.

This Summary of Proof of Claim is supported by a voluminous amount of evidence in official documents held by the Arkansas Department of Health, the ADEQ, the ATSDR, the USEPA, the U.S. Geological Survey Office (USGS), the U.S. Court of Appeals for the District of Columbia (D.C. Cir.), digitally recorded and cassette taped audio recordings, photographs, VHS video and 8 mm film movie recordings, many credible witnesses, correspondences, credible logs of information and data, environmental sampling data, biological samples of Joe S. McKinnon (Last time I asked, his biological samples were still safely being stored by a legitimate entity, and waiting to be analyzed by the Government of the United States), Joe S. McKinnon's medical records, and, potentially, medical records of the Kids of the Pathfinders Camp. I do not have the medical records for the Kids of the Pathfinders Camp, except for my immediate family. But I have talked to many of the Kids of the Pathfinders Camp, and have found that many of us, and some of our children, have suffered diseases that have very likely been caused by the fact that we slept, played, and swam in GLCC's Poison at the Pathfinders Camp.

On May 30, 2002, I started becoming aware of the fact that the death of my father (Joe S. McKinnon) had been caused by chronic exposure to GLCC's Poison, and that approximately 493 kids


from New Mexico, 2 kids from Arizona, and about 12 kids who lived near the Pathfinders Camp (Kids of the Pathfinders Camp) - swam, slept, and played in GLCC's Poison at the Pathfinders Camp in what we thought was a pristine wilderness summer camp that my father and I built on my grandparents' land, where I lived when I was born and where I spent most of my summers and holidays, in a community called Parkers Chapel, about 3 miles southwest of El Dorado, Arkansas. The Perpetrators, in the poisoning of Joe S. McKinnon and the Kids of the Pathfinders Camp, worked for GLCC.

PLEASE TAKE NOTICE that, because the USEPA was studying GLCC when these air samples were taken from the Pathfinders Camp, because I have seen evidence that indicates that the source of these chemical compounds was GLCC's chemical plant next to the Pathfinders Camp, and because I have seen no evidence to indicate that most of these chemical compounds could have come from any source other than GLCC, I am assuming that most, if not all, of the chemical compounds that the USEPA has identified as being in the air of the Pathfinders Camp are related to GLCC. I am willing to exclude any of these chemical compounds from this list of GLCC's chemical compounds in the air of the Pathfinders Camp, if I receive information presenting evidence that provides a reason to doubt GLCC didn't own them. GLCC's chemical compounds in the air of the Pathfinders Camp with relevant information about health effects is, as follows:

ETHYLENE DIBROMIDE:

(1) The USEPA identified ethylene dibromide in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA published information, which shows the following:

(1.1) Air sample taken between 1425 hour on 3/5/77 and 1625 hour on 3/6/77 shows detection of Ethylene dibromide at 700 ng/m3.

(1.2) Air sample taken between 1850 hour on 3/30/77 and 1353 hour on 3/31/77 shows detection of Ethylene dibromide at 1,260 ng/m3.

(1.3) Air sample taken sometime between 1976 and 1978 shows detection of 1,2-Ethylene dibromide at 7.2 ng/m3

(2) This information, related to the relevant health effects of Ethylene dibromide, is from the ATSDR, which is, as follows (quotation marks omitted): (2.1) Synonyms include 1,2-dibromoethane, glycoldibromide, and bromofume.

(2.2) Persons whose clothing or skin is contaminated with liquid ethylene dibromide (above 50ºF) can secondarily contaminate others by direct contact or through offgassing vapor.

(2.3 A liquid at room temperature, ethylene dibromide readily penetrates skin, cloth, and other protective materials such as rubber and leather. It is nonflammable.

(2.4) Ethylene dibromide is a colorless, heavy liquid with a sweet chloroform-like odor. It's odor is not detectable at a low enough concentration to be considered a warning of excessive exposure.


(2.5) Absorption can occur by the inhalation, oral, and dermal routes. It is toxic by these three routes of exposure. Toxicity is thought to be due to metabolic products of ethylene dibromide.

(2.6) Ethylene dibromide is a nonflammable colorless liquid with a sweet chloroform-like odor at room temperature above 50ºF (10ºC). It is slightly soluble in water and soluble in most organic solvents. It is heavier than water. When heated to decomposition, it may release gases and vapors such as hydrogen bromide, bromine, and carbon monoxide. Ethylene dibromide should be stored in a dry place at ambient temperature.

(2.7) Inhalation is an important route of exposure. Ethylene dibromide's odor is not detectable at a low enough concentration to be considered a good warning of excessive exposure. Ethylene dibromide vapors are heavier than air and can accumulate in poorly ventilated or low-lying areas.

(2.8) Fatalities have occurred among workers cleaning a tank containing residues of ethylene dibromide. The dermal route also contributed to the exposure.

(2.9) Children exposed to the same levels of ethylene dibromide as adults may receive larger doses because they have greater lung surface area:body weight ratios and higher minute volume:weight ratios. In addition, they may be exposed to higher levels than adults in the same location because of their short stature and the higher levels of ethylene dibromide vapors found nearer to the ground.

(2.10) Ethylene dibromide can penetrate ordinary rubber gloves and leather. Prolonged skin contact with the liquid may cause erythema, blistering, and skin ulcers. Skin absorption may contribute to systemic toxicity.

(2.11) Because of their relatively larger surface area: weight ratio, children are more vulnerable to toxicants absorbed through the skin.

(2.12) Acute toxic effects, including fatal systemic poisoning, can result from ingestion. Rapid effects following ingestion can include abdominal pain, diarrhea, nausea, vomiting, and drowsiness.(Reference 19)

(3) The U.S. Public Health Services Center for Disease Control (CDC) provides some relevant information, as follows: "...The half life of ethylene dibromide in water at 20 C and at a pH of 7 is about 14 years..." (See Reference 24)

(4) This information related to the relevant health effects for ethylene dibromide is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(4.1) LIQ ON SKIN CAUSES BLISTERS IF EVAPORATION IS DELAYED. INHALATION CAUSES DELAYED PULMONARY LESIONS. DROWSINESS OCCURS ... DEATH APPEARS TO BE DUE TO RESP OR CIRCULATORY FAILURE, COMPLICATED BY PULMONARY EDEMA... (Reference 356)

(4.2) ... PROLONGED CONTACT WITH SKIN LEADS TO REDNESS, EDEMA &


BLISTERING WITH EVENTUAL SLOUGHING ULCERATION. (Reference 357)

(4.3) ...RESULTS INDICATED THAT ETHYLENE DIBROMIDE WAS A DNA DAMAGING AGENT....(Reference 358)

(4.4) Symptoms /include/: dermatologic /lesions/, stomach ache, jaundice, & hematuria. (Reference 359)

(4.5) ... Retrospective mortality survey of 161 workers ... exposed to ethylene dibromide at two ethylene dibromide manufacturing plants ... results indicated an observed increase in deaths due to malignant neoplasms and nonmalignant respiratory disease ... among the workers in one plant. (Reference 360)

(4.6) Damage to the eyes; /with a/ potential for reproductive abnormalities. (Reference 361)

(4.7) In human beings, /ethylene dibromide produces/ moderate depression of the CNS & pulmonary congestion after exposure by inhalation, & /it causes/ acute GI distress & pulmonary edema after ingestion. (Reference 362)

(4.8) Acute dermal exposure produces painful local inflammation, swelling, & blistering. (Reference 363)

(4.9) Toxic gases & vapors (such as hydrogen bromide, bromine, & carbon monoxide) may be released when ethylene dibromide decomposes. (Reference 355)

(4.10) ...Persistence can vary greatly from soil to soil. In one laboratory screening study using 100 soils, half-lives ranging from 1.5 to 18 weeks were determined...In one field, ethylene dibromide was detected in soil 19 years after its last known application...(Reference 364)

PLEASE TAKE NOTICE that the ATSDR says that "...higher levels of ethylene dibromide vapors [are] found nearer to the ground." I am pointing out, here and now, that this would have made the concentration levels higher in the air that Joe S. McKinnon and the Kids of the Pathfinders Camp were exposed to near the ground of the Pathfinders Camp than the levels detected on top of the "Parker's Chapel Water Tower." This would also be true for many other GLCC's chemical compounds in the air of the Pathfinders Camp.

HYDROGEN BROMIDE:

This information related to the relevant health effects for hydrogen bromide is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) HBr, hydrogen bromide, the gas, and HBr, the aqueous acid (hydrobromic acid), have the same CAS Registry number. Since the gas becomes the acid in aqueous systems and volatilization of the gas can occur from aqueous systems, it is often difficult to determine which is being considered in a specific item in the literature. In those cases where the distinction can be made, it will be noted in the


occurrence.

(2) /SIGNS AND SYMPTOMS/ ... Highly toxic /gas/ ... Being severely irritating to upper resp tract. The ... /acid/ formed neutralizes the alkali of tissues and can cause death as a result of edema or spasm of larynx and inflammation of upper resp system. Concn of 0.13-0.2% are lethal ... In exposures lasting a few min. (Reference 365)

(3) /SIGNS AND SYMPTOMS/ /GAS/ ... Also corrosive to skin and mucous membranes and can cause severe burns. Exposure to high concn may ... Result in dermatitis. Contact with eyes rapidly causes severe irritation of eyes and eyelids. (Reference 366)

(4) /SIGNS AND SYMPTOMS/ Inhalation of hydrogen bromide causes irritation of the upper respiratory tract, and a concentration of about 35 ppm causes irritation of the throat after short exposure. More severe exposures result in pulmonary edema, and often in laryngeal spasm. (Reference 367)

(5) /SIGNS AND SYMPTOMS/ Inhalation causes severe irritation of nose and upper respiratory tract, lung injury. Ingestion causes burns of mouth and stomach. Contact with eyes causes severe irritation and burns. Contact with skin causes irritation and burns. (Reference 368)

(6) /SIGNS AND SYMPTOMS/ Skin contact with the vapor or liquid causes severe tissue irritation and necrosis. (Reference 369)

(7) /SIGNS AND SYMPTOMS/ Contact of solutions of hydrobromic acid with the eyes, skin, or mucous membranes may cause burns. (Reference 370)

(8) /CASE REPORTS/ ...The clinical course of two patients who developed acute pneumonitis followed by reactive airways dysfunction syndrome after bathing in a hot tub /is described/. Additional findings were present and suggested that exposure to a corrosive agent was responsible. Bromine and hydrobromic acid generated from a widely used water disinfectant were implicated as the underlying cause. Physicians should be alert to the possibility that such exposures may initiate or exacerbate inflammatory pulmonary disease. (Reference 371)

(9) ...MAY BE HIGHLY IRRITATING TO EYES, SKIN, MUCOUS MEMBRANES, RESPIRATORY TRACT. /GAS/ (Reference 372)

(10) Skin contact with the vapor or liquid causes severe tissue irritation. ... (Reference 373)

(11) The vapors of hydrogen bromide are severely irritating to the mucous membranes of the eyes and nose. (Reference 374)

BROMINE:

This information related to the relevant health effects for bromine is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):


(1) /SIGNS AND SYMPTOMS/ Dermal: There is a rare cutaneous manifestation of bromide accumulation known as bromoderma tuberosum, which progresses from red papules to pustules that enlarge and develop into indurated lesions with a central ulcer. This effect is related to the ingestion of bromides formerly used in medications and, in theory, to chronic inhalation of low-level concentrations of bromine. (Reference 375)

(2) /SIGNS AND SYMPTOMS/ Dermal: Pure bromine (liquid or vapor) is extremely irritating to the skin. Unlike most other chemical agents, there is no immediate visible skin reaction after contact. The delay before initial signs of injury become apparent often results in more extensive damage. The most common local effects are blister formation, brownish discoloration of the skin and slow-healing ulcers. (Reference 376)

(3) /SIGNS AND SYMPTOMS/ Skin burns can occur from liquid bromine spills. Bromine initially causes a cooling effect on the skin and after a delay will produce a burning sensation that can progress to deep chemical burns as well as a brown discoloration of the skin. (Reference 377)

(4) /SIGNS AND SYMPTOMS/ Upper and lower respiratory tract: Initial irritant symptoms of bromine vapor inhalation include: dyspnea, coughing, choking, and wheezing. In addition, immediate or delayed bronchoconstriction and the development of laryngeal spasm, glottal edema, asthma and cheobronchitis. With increased parenchymal penetration, there may be associated peribronchiolar abscesses, pulmonary infiltrates consistent with chemical pneumonitis, bronchiolitis obliterans and pulmonary edema. Acute obstructive ventilatory impairment may lead to severe hypoxemia, metabolic acidosis, measles-like rash and subsequent death. It should be noted that more severe respiratory symptoms may be delayed for several hours after the exposure. (Reference 378)

(5) /SIGNS AND SYMPTOMS/ Mucous Membranes: Exposure to low concentrations produces lacrimation, rhinorrhea, eye irritation with mucous secretions from the oropharyngeal and upper airways, coughing, dyspnea, choking, wheezing, epistaxis, and headache. A brownish discoloration of the tongue and buccal mucosa may occur and be accompanied by a characteristic breath odor. Inflammatory lesions of the upper airway, photophobia and blepharospasm are seen with higher concentrations. (Reference 379)

(6) /SIGNS AND SYMPTOMS/ SYMPTOMS ... FOLLOWING INHALATION OF ... SMALL AMT INCLUDE COUGHING, NOSEBLEED, FEELING OF OPPRESSION, DIZZINESS, & HEADACHE, FOLLOWED AFTER SOME HOURS BY ABDOMINAL PAIN & DIARRHEA, & SOMETIMES BY MEASLESLIKE ERUPTIONS ON TRUNK & EXTREMITIES. ... PUSTULES & FURUNCLES APPEAR IN EXPOSED AREAS OF SKIN OF THOSE WHO HANDLE BROMINE ... BRIEF CONTACT OF LIQ WITH SKIN LEADS TO ... VESICLES & PUSTULES. IF NOT REMOVED AT ONCE, IT INDUCES DEEP, PAINFUL ULCERS. (Reference 380)

(7) /SIGNS AND SYMPTOMS/ INHALATION OF HIGH ... CONCN CAUSES INFLAMMATORY LESIONS TO THE MUCOUS MEMBRANES ... THE TONGUE AND PALATE LOOK INFLAMED AND BECOME EDEMATOUS AND SPASM OF THE GLOTTIS OCCURS; THERE IS ASTHMATIC BRONCHITIS ... PHOTOPHOBIA & BLEPHAROSPASM OCCUR ... CAN PRODUCE FATAL CHEM BURNS OF LUNGS. PERSONS EXPOSED REGULARLY TO CONCN 3-6 TIMES HIGHER THAN THE EXPOSURE LIMIT FOR 1 YR COMPLAIN OF HEADACHE, PAIN IN THE REGION OF THE HEART, INCREASING IRRITABILITY, LOSS OF


APPETITE, JOINT PAINS, AND DYSPEPSIA. DURING THE 5TH OR 6TH YR OF WORK THERE MAY BE LOSS OF CORNEAL REFLEXES, PHARYNGITIS, VEGETATIVE DISORDERS, AND THYROID HYPERPLASIA ACCOMPANIED BY THYROID DYSFUNCTION. CARDIOVASCULAR DISORDERS ALSO OCCUR IN THE FORM OF MYOCARDIAL DEGENERATION AND HYPOTENSION; FUNCTIONAL AND SECRETORY DISORDERS OF THE DIGESTIVE TRACT MAY ALSO OCCUR. SIGNS OF INHIBITION OF LEUCOPOIESIS AND LEUCOCYTOSIS ARE SEEN IN BLOOD. THE BLOOD CONCENTRATION OF BROMINE VARIES BETWEEN 0.15 MG/100 CC TO 1.5 MG/100 CC INDEPENDENTLY OF DEGREE OF INTOXICATION. (Reference 381)

(8) /SIGNS AND SYMPTOMS/ CONCN OF 11-23 MG/CU M PRODUCES SEVERE CHOKING ... 30-60 MG/CU M IS EXTREMELY DANGEROUS ... 200 MG/CU M WOULD PROVE FATAL IN VERY SHORT TIME ... VAPORS CAN CAUSE ACUTE AS WELL AS CHRONIC POISONING ... IT HAS CUMULATIVE PROPERTIES ... . (Reference 382)

(9) /SIGNS AND SYMPTOMS/ May be harmful if inhaled. Liquid and vapor cause severe eye and skin burns even in short single exposure. Respiratory damage occurs at low vapor concentrations. (Reference 383)

(10) /SIGNS AND SYMPTOMS/ Ten ppm bromine gas is a severe irritant and cannot be tolerated. (Reference 384)

(11) /SIGNS AND SYMPTOMS/ Bromine is a lacrimator at concentrations below 6.5 mg/ cu m. (Reference 385)

(12) /SIGNS AND SYMPTOMS/ Clinical description: The majority of exposures to bromine occur by inhalation and typically lead to symptoms of ocular, nasal, and respiratory irritation. Signs and symptoms of poisoning include eye redness and lacrimation, nose and throat irritation, cough, and dyspnea. Ingestion of liquid bromine can cause abdominal pain and hemorrhagic gastroenteritis with secondary shock. Signs and symptoms might also include brown discoloration of mucous membranes and the tongue. (Reference 386)

(13) /CASE REPORTS/ A maintenance technician in a chemical company developed a cough with severe bronchospasm and spontaneous pneumomediastinum following an accidental exposure to bromine. The chest radiograph on admission was normal and only a surveillance chest x-ray taken a few hours later demonstrated the presence of eumomediastinum. ... (Reference 387)

(14) /CASE REPORTS/ A 21-year-old male had a chemical burn on the right forearm when he inadvertently spilled bromine during an experiment. Since he inhaled vaporized bromine and had dyspnea and pharyngalgia, he arrived at ... /the/ hospital in an ambulance as an emergency patient. On arrival, he kept a clear consciousness with a pulse rate of 98, body temperature of 36.8 degrees C, blood pressure of 132/80 mmHg, respiratory rate of 25, and oxygen saturation of 100%. (10 L/min of oxygen were administered.) He had marked dry coughs. His clothes had a foreign odor with mucosal irritation. Arterial blood gas analysis and blood biochemistry were normal. Based on these findings, he was diagnosed with chemical airway damage and bulbar conjunctiva from the exposure to bromine and a chemical burn on the right forearm. His respiratory condition became worse after admission, resulting in pulmonary edema. He was endotracheally intubated and controlled with an artificial ventilator on


Day 3 after his injury. He was continuously treated with steroids and sivelestat sodium hydrate, which gradually improved his respiration. He was released from the artificial ventilator and extubated on Day 7. Although dyspnea associated with body movement and hoarseness persisted after extubation, the symptoms decreased and he was discharged on Day 41. ... (Reference 388)

(15) Liquid /bromine/ penetrates the tissue rapidly and produces eruptions, irritations, and painful injuries which heal slowly. (Reference 389)

CARBON MONOXIDE:

This information related to the relevant health effects for carbon monoxide is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) SYMPTOMATOLOGY: 1. NO SYMPTOMS OR SHORTNESS OF BREATH DURING VIGOROUS MUSCULAR EXERCISE (0 TO 10% COHB (CARBOXYHEMOGLOBIN). 2. A MILD HEADACHE ...AND BREATHLESSNESS ON MODERATE EXERCISE (10-20% COHB). 3. THROBBING HEADACHE, IRRITABILITY, EMOTIONAL INSTABILITY, IMPAIRED JUDGEMENT, DEFECTIVE MEMORY, AND RAPID FATIGUE (20-30% COHB). (Reference 390)

(2) SYMPTOMATOLOGY: 4. SEVERE HEADACHE, WEAKNESS, NAUSEA & VOMITING, DIZZINESS, DIMNESS OF VISION, CONFUSION (30-40% COHB). 5. INCREASING CONFUSION, SOMETIMES HALLUCINATIONS, SEVERE ATAXIA, ACCELERATED RESPIRATIONS...(40-50% COHB). 6. SYNCOPE OR COMA WITH INTERMITTENT CONVULSIONS, TACHYCARDIA WITH A WEAK PULSE...(50-60% COHB)... PALLOR OR CYANOSIS.7. INCREASING DEPTH OF COMA WITH INCONTINENCE OF URINE & FECES (60-70% COHB). 8. PROFOUND COMA WITH DEPRESSED OR ABSENT REFLEXES, A WEAK THREADY PULSE, SHALLOW AND IRREGULAR RESPIRATIONS AND COMPLETE QUIESCENCE (70-80% COHB). 9. RAPID DEATH FROM RESPIRATORY ARREST (ABOVE 80% COHB). 10. MISCELLANEOUS & ATYPICAL REACTIONS INCLUDE VARIOUS SKIN LESIONS, SWEATING, HEPATOMEGALY, HYPERPYREXIA, ALBUMINURIA, OLIGURIA, ANGINAL PAIN, & CONGESTIVE HEART FAILURE... (Reference 391)

(3) SYMPTOMATOLOGY: 11. DURING CONVALESCENCE A BRONCHOPNEUMONIA MAY DEVELOP BECAUSE OF THE ASPIRATION OF SALIVA OR VOMITUS... 12. MYOCARDIAL INFARCTION, WITH OR WITHOUT CORONARY THROMBOSIS, MAY APPEAR AT ANY TIME UP TO ONE WEEK FOLLOWING AN ACUTE POISONING. 13. AFTER AN UNEVENTFUL CONVALESCENCE, SIGNS OF NERVE OR BRAIN INJURY MAY APPEAR AT ANY TIME WITHIN THREE WEEKS FOLLOWING AN ACUTE EXPOSURE. AMONG PERMANENT SEQUELAE ARE NEUROPATHIES, VARIOUS MOTOR AND MENTAL DEFECTS, SOME OF WHICH MIMIC MULTIPLE SCLEROSIS OR PARKINSONISM, AND DEATH. (Reference 392)

(4) Rapidly fatal cases of carbon monoxide poisoning are characterized by congestion and hemorrhages in all organs. In longer-term, eventually fatal cases, the hypoxic lesions observed are related to the duration of posthypoxic unconsciousness. ... The maximal period of carbon monoxide


induced posthypoxic unconsciousness compatible with complete neurological recovery is 21 hr in patients under 48 years of age and 11 hours in older patients. Complete recovery of mental functon was not observed when the carbon monoxide induced unconsciousness exceeded 15 hours in the older or 64 hours in the younger group. (Reference 393)

(5) THE FETUS MAY BE EXTREMELY SUSCEPTIBLE TO EFFECTS OF CARBON MONOXIDE, AND THE GAS READILY CROSSES THE PLACENTA. INFANTS BORN TO WOMEN WHO HAVE SURVIVED SHORT TERM EXPOSURE TO A HIGH CONCENTRATION OF THE GAS WHILE PREGNANT OFTEN DISPLAY NEUROLOGICAL SEQUELAE, AND THERE MAY BE GROSS DAMAGE TO THE BRAIN. (Reference 393)

(6) A CARBON MONOXIDE-INTOXICATED PATIENT DEVELOPED INCR PERMEABILITY-TYPE PULMONARY EDEMA DEMONSTRATED BY A NORMAL CAPILLARY WEDGE PRESSURE AND PRODUCTION OF PROTEIN-RICH EDEMA FLUID. (Reference 394)

(7) PATIENT WITH POSSIBLE RESIDUAL NEUROLOGIC EFFECTS FROM CARBON MONOXIDE AND RETROSPECTIVE STUDY OF PEDIATRIC PATIENTS WITH ACUTE DIAGNOSIS OF CARBON MONOXIDE POISONING ARE PRESENTED. EVIDENCE FOR CONCLUSION THAT CARBON MONOXIDE CAN PRODUCE RESIDUAL NEUROLOGICAL INJURY IS INCLUDED. (Reference 395)

(8) The tissues most affected are those most sensitive to oxygen deprivation, such as the brain and the heart, and the lesions are predominantly hemorrhagic. The severe headache following exposure to carbon monoxide is believed to be caused by cerebral edema and increased intracranial pressure resulting from excessive transudation across hypoxic capillaries. (Reference 396)

(9) Acute carbon monoxide poisoning can cause myocardial injury or aggravate underlying vascular disease. High level chronic exposures (carboxyhemoglobin 20-30%) have been reported to produce a severalfold increase in the incidence of coronary artery disease in tatami may makers in Northern Japan. These workers heated their buildings with charcoal braziers while tightly sealing windows and doors to conserve heat during cold winter weather. (Reference 397) (10) Severe carbon monoxide poisoning produces anatomic changes (eg, cerebral edema, hemorrhagic focal necrosis, venodilation, petechiae, perivascular infarct). Bilateral necrosis of the globus pallidus is the characteristic lesion of carbon monoxide toxicity. Other vulnerable areas of the cerebral gray matter include the substantia nigra, hippocampus, cerebral cortex, and cerebellum. These histopathological changes are indistinguishable from other causes such as hypoxia, cardiorespiratory arrest, hypoglycemia, and cyanide poisoning. Rarely, a postanoxic demyelination occurs that follows an initial recovery and progresses to irritability, confusion, coma and death. A 'moth-eaten' appearance characterizes this anoxic leukoencephalopathy in which most of the damage appears in the gray matter of the cerebral cortex, pallidum, thalamus, and cerebellar cortex. (Reference 398)

(11) Neurologic sequelae include visual loss, dementia, retardation, constructional apraxia, temporospacial disorientation, memory loss, dysphasia, personality changes, concentration deficits, and frank psychosis. Parkinson's disease does occur after acute carbon monoxide exposures but is very rare. After initial recovery from carbon monoxide exposure patients may develop neurologic symptoms (apathy, mutism, amnesia, urinary incontinence, headache, irritability, personality changes, confusion,


memory loss, visual changes) within 2 to 4 weeks of exposure. (Reference 399)

(12) Retinal venous engorgement and peripupillary hemorrhage occur occasionally in both acute and subacute carbon monoxide exposures. Their presence should alert the physician to the possibility of carbon monoxide poisoning. In one series of 12 poisonings, all patients exposed to carbon monoxide over 12 hours had hemorrhages in the nerve fiber layer of the retina. Carbon monoxide decreases light sensitivity and dark adaptation. Cochlear and brain stem hypoxia leads to a central hearing loss and vestibular dysfunction (nausea, vomiting, vertigo), with vestibular symptoms usually more prominent than auditory loss. (400)

(13) Several cases of hemolytic anemia have been reported after severe carbon monoxide poisoning. Thrombocytopenic purpura with respiratory dysfunction occurred in a patient who had a 20% carboxyhemoglobin level 12 hours post-exposure. (401)

(14) Rhabdomyolysis, acute renal failure, and peripheral neuropathies (eg, ulnar palsy) occur rarely. Myonecrosis may be massive, leading to edema, compartment syndrome, and acute renal failure. (Reference 401)

(15) Severe visual disturbances occur as a consequence of acute poisoning in which there has been a period of unconsciousness. ... The types of visual disturbance which have been reported may be grouped symptomatically as follows: (a) amaurosis or hemianopsia, (b) constriction of visual fields, and (c) visual abnormalities associated with optic nerve disturbances. (Reference 402)

1-CHLORO-2-BROMOETHANE:

(1) The USEPA identified 1-choro-2-bromoethane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA published information, which shows the following:

(1.1) Air sample taken between 1650 hour on 3/5/77 and 1700 hour on 3/6/77 shows detection of 1-chloro-2-bromoethane at 2,520 ng/m3.

(1.2) Air sample taken between 1700 hour on 3/6/77 and 1840 hour on 3/7/77 shows detection of 1-chloro-2-bromoethane at 4,200 ng/m3.

(1.3) Air sample taken between 1855 hour on 3/16/77 and 1630 hour on 3/17/77 shows detection of 1-chloro-2-bromoethane at 700 ng/m3.

(2) This information related to the relevant health effects for 1-chloro-2-bomoethane is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) Headache, gastric discomfort, pallor, mucous membranes irritation, lowering of blood pressure & body temperature, & ultimately coma have been described as signs of acute ethylene chlorobromide intoxication. (Reference 20)


(2.2) In chronic exposure injury to the liver, kidneys & eyes may occur. (Reference 21)

(2.3) HAZARDOUS BY ALL ROUTES, INCLUDING PERCUTANEOUS ABSORPTION. MAY PRODUCE ANESTHESIA & LIVER AND KIDNEY INJURIES. (Reference 22)

(2.4) Skin, Eye and Respiratory Irritations: An irritant to skin, eyes, & mucous membranes. (Reference 23)

(2.5) If released to air, a vapor pressure of 33.1 mm Hg at 25 deg C indicates 1-bromo-2-chloroethane will exist solely as a vapor in the ambient atmosphere. Vapor-phase 1-bromo-2-chloroethane will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 42 days. If released to soil, 1-bromo-2-chloroethane is expected to have very high mobility based upon an estimated Koc of 34. Volatilization from moist soil surfaces is expected to be an important fate process based upon a Henry's Law constant of 9.1X10-4 atm-cu m/mole. 1-Bromo-2-chloroethane may volatilize from dry soil surfaces based upon its vapor pressure. If released into water, 1-bromo-2-chloroethane is not expected to adsorb to suspended solids and sediment based upon the estimated Koc. Volatilization from water surfaces is expected to be an important fate process based upon this compound's Henry's Law constant. Estimated volatilization half-lives for a model river and model lake are 2 and 122 hours, respectively. An estimated BCF of 4 suggests the potential for bioconcentration in aquatic organisms is low. Estimated hydrolysis half-lives of 3 and 32 years at pHs 8 and 7, respectively... (Reference 281) DIBROMOPROPANE:

(1) The USEPA identified dibromopropane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA published information, which shows that air sample taken between 1802 hour on 3/9/77 and 1620 hour on 3/10/77 shows detection of dibromopropane at 560 ng/m3. (2) The Colorado Department of Public Health and Environment published information regarding relevant health effects of dibromopropane, as follows (quotation marks omitted):

(2.1) Dibromochloropropane (DBCP) must be created by chemical synthesis. It is used as a soil fumigant and nematocide. It has been banned from production or application in the United States since 1977, except for restricted use in pineapple horticulture in Hawaii. It is still used in other parts of the world....

(2.2) ACUTE HEALTH EFFECTS

(2.2.1) High levels of exposure produce CNS depression (rats) which implies that sufficient exposure in man would produce dizziness, confusion and eventually coma and death. CNS depression from DBCP was not observed in humans.

(2.2.2) DBCP is a mild irritant of mucous membranes. Ingestion of DBCP may result in pulmonary edema.

(2.2.3) DBCP is mildly irritating to skin, especially in repeated contact. DBCP is mildly


irritating to the eye. It is not caustic to skin or eye.

(2.2.4) Acute ingestion of DBCP may create GI distress.

(2.2.5) DBCP causes significant liver damage (cloudy swelling) in animal tests, but this was not seen in man.

(2.2.6) DBCP causes kidney damage (nephritis) in animal testing and loss of sperm production with sterility in human male workers. This was not reversible in the most severely affected men.

(2.3) CHRONIC HEALTH EFFECTS

(2.3.1) Chronic exposure to DBCP (by any route) may be expected to produce damage to liver, kidney, bone marrow (pancytopenia or loss of red and white blood cells and platelets) and testicles.

(2.3.2) Work exposure has resulted in testicular toxicity with sterility. Similar levels of exposure apparently do not affect ovarian function. Among those males who recovered fertility and fathered offspring, follow up studies did not detect any excess of birth defects associated with prior DBCP exposure.

(2.3.3) DBCP damages chromosomes in a variety of test systems and causes cancer in some animal studies.

(Reference 25)

(3) This information, related to the relevant health effects for dibromopropane, is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(3.1) The present study examines how variations in position, number, and type of halogen substituents affect renal and testicular necrosis, renal and testicular DNA damage, and the tissue distribution of the halogenated propanes. Groups of five male MOL:WIST rats were given single ip injections, ranging from 85 to 3000 um/kg of 1,2-dibromo-3-chloropropane (DBCP), 1,2,3-tribromopropane (TBP), 1,3-dichloro-2-bromopropane (DB2CP), or 1-bromo-2,3-dichloropropane (B2,3DCP), 1,3-dibromopropane, 1,2-dibromopropane, 1,2,3-trichloropropane or 1-bromo-3-chloropropane. The most potent in causing organ damage in both kidney and testes were DBCP and TBP. DB2CP was less organ toxic than DBCP or TBP, but induced more organ damage than B2,3DCP and DC2BP. The ability of the halogenated propanes to induce DNA damage in vivo correlated well with their ability to induce organ damage. However, DNA damage occurred at lower doses and after a shorter period of exposure. DNA damage may be an initial event in the development of organ necrosis by halogenated propanes in general. Testicular DNA damage induced by the halogenated propanes in vivo correlated well with the DNA damage observed in isolated testicular cells in vitro, showing that toxicity was due to in situ activation. The findings established a good relationship between in vivo organ necrogenic effects and DNA damage for a series of halogenated propanes. Both the type, the number, and the position of the halogens affected the toxic potential. The most toxic of the halogenated propanes contained three halogens with at least two vicinal bromines.


(3.3) Mortality rates in workers exposed to brominated chemicals in manufacturing research facilities from 1935 to 1976 were investigated epidemiologically. These workers were potentially exposed to 1,2-dibromo-3-chloropropane, polybrominated biphenyls, tris(2,3-dibromopropyl)phosphate, trimethylene chlorobromide, and DDT as well as various organic and inorganic bromides. Data was collected from personnel records and death certificates. Standardized mortality ratios were calculated for comparison against rates for American white males. In all, 2,806 male workers were identified as living, 578 workers were identified as deceased. Almost half of the cohort had worked less than 6 mo. The average term of employment was 3 yr 9 mo. Overall, the standardized mortality ratio for workers was lower than that of American white males. Deaths from diabetes mellitus occurred more frequently in these workers, with rates more than twice the number expected...(Reference 283)

(3.4) A historical prospective mortality study was conducted for 3579 white male workers employed between 1935 and 1976 at four Vesicol Chemical Corporation facilities. The members of the study cohort were potentially exposed to brominated compounds including 1,2-dibromo-3-chloropropane (DBCP), tris(2,3-dibromopropyl)phosphate, trimethylene chlorobromide. Some were exposed to DDT, polybrominated biphenyls (PBB) and others to radiation from rare earths process. Overall mortality was lower than expected, particularly in diseases of the circulatory system, nonmalignant respiratory diseases and diseases of the digestive system...Mortality from diabetes mellitus was significantly elevated among the maintenance workers hired in the early 1940's. A significant mortality excess due to diseases of the circulatory system was observed among workers potentially exposed to DBCP and or rare earth process. Mortality from testicular cancer was significantly higher in those exposed to organic bromides. The common potential exposure of the testicular cancer decedents was methyl bromide. A number of other cause specific mortality excesses were also noted. (Reference 284)

ALLYL BROMIDE:

(1) The USEPA identified allyl bromide in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA published information, which shows that air sample taken between 1976 and 1978 detected allyl bromide at 24.8 ng/m3.

(2) This information related to relevant health effects for allyl bromide is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) Causes severe eye and skin burns. Serious health hazard. May be harmful if absorbed through skin or inhaled. Irritating to eyes, skin, and respiratory system. (Reference 26)

(2.2) Skin, Eye and Respiratory Irritations: Irritation of eyes and respiratory tract. (Reference 27)

(3) Safety data for 3-bromo, published by Safety Officer in Physical Chemistry at Oxford University (Reference 28), says the following (quotation marks omitted):


(3.1) Synonyms: allyl bromide, bromoallylene, 3-bromo-1-

(3.2) Harmful if swallowed or inhaled. May be harmful in contact with the skin. Liquid may burn skin or eyes.

ACETALDEHYDE:

(1) The USEPA identified acetaldehyde in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that acetalehyde was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for acetaldehyde is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) Acetaldehyde: reasonably anticipated to be a human carcinogen. (Reference 44)

(2.2) CLASSIFICATION: B2; probable human carcinogen. BASIS FOR CLASSIFICATION: Based on increased incidence of nasal tumors in male and female rats and laryngeal tumors in male and female hamsters after inhalation exposure. HUMAN CARCINOGENICITY DATA: Inadequate. ANIMAL CARCINOGENICITY DATA: Sufficient. /Based on former classification system/ (Reference 45)

(2.3) /HUMAN EXPOSURE STUDIES/ A majority of ... unacclimated subjects ... experienced eye irritation at 50 ppm after 15 minutes; however, eye irritation in sensitive persons occurred after exposure at concentations as low a 25 ppm for 15 minutes. This study also reported that at 200 ppm all subjects had red eyes and transient conjunctivitis, and a majority of the subjects suffered from nose and throat irritation. (Reference 46)

(2.4) /SIGNS AND SYMPTOMS/ Acetaldehyde vapor irritation of the human eye is detectable at 50 ppm in air and becomes excessive for chronic industrial exposure above 200 ppm. Higher concn and extended exposure may injure the corneal epithelium, causing persistent lacrimation, photophobia and foreign body sensation. A splash of liquid acetaldehyde can be expected to cause painful but superficial injury of the cornea, with rapid healing; the liquid evaporates so rapidly at body temperature that contact is brief and self limited. (Reference 47)

(2.5) /SIGNS AND SYMPTOMS/ Clinical effects of exposure to acetaldehyde vapors include concentration-dependent erythema, coughing, pulmonary edema, and narcosis. At high concentrations, paralysis leading to death can occur. (Reference 48)

(2.6) /SIGNS AND SYMPTOMS/ Repeated exposure to vapors causes dermatitis and conjunctivitis. (Reference 49)


(2.7) /SIGNS AND SYMPTOMS/ A splash of liquid acetaldehyde was reported to cause a burning sensation, lachrymation and blurred vision. Prolonged periods of contact with the skin result in erythema and burns; repeated contact may result in dermatitis, due either to primary irritation or to sensitization. (Reference 50)

(2.8) /GENOTOXICITY/ Human lymphocytes (from known alcoholics) were exposed to acetaldehyde concn of 0.02 mg/mL and 0.04 mg/mL. Results indicate that chromosomal aberrations occurred at both concentrations. (Referemce 51)

(2.9) /GENOTOXICITY/ Human leukocytes were incubated in the presence of vinyl acetate or acetaldehyde (10-20 mM) for 4 hr at 37 deg C in vitro. DNA damage was analysed by alkaline elution. None of the compounds induced a detectable increase in the frequency of DNA strand breaks. Cells exposed to 5 Gy of X-ray immediately after treatment and before alkaline elution showed a clear, dose-dependent retardation of the elution rate in comparison with X-irradiated control cells. These results demonstrate that both vinyl acetate and acetaldehyde induce DNA cross-links in human cells. (Reference 52)

(2.10) /GENOTOXICITY/ Acetaldehyde induces chromosomal aberration and sister chromatid exchange in a variety of test systems... (Reference 53) (2.11) /GENOTOXICITY/ The conditions under which acetaldehyde induces sister chromatid exchange and DNA damage in human lymphocytes in vitro were investigated... (See Reference 54)

(2.12) /GENOTOXICITY/ The effects of DNA damage induced by the typical environmental pollutant acetaldehyde were studied with single cell gel electrophoresis (SCGE) and high performance liquid chromatography with electrochemical detection (HPLC-EC). The results showed that acetaldehyde not only could cause DNA strand breakage but also DNA-DNA, DNA-protein crosslinks of lymphocytes of human peripheral blood. The reaction of acetaldehyde with DNA in vitro was weak, but the oxidative ability was enhanced and the reaction could produce a number of 8-OHdG adducts mediated by the Fe2+... (Reference 55)

(2.13) /GENOTOXICITY/ Freshly isolated human lymphocytes from two healthy donors were incubated with 0, 1.56, 6.25, 25, and 100 mM of ... acetaldehyde in complete medium for 1 hr. ... Acetaldehyde induced both single-strand (even at the lowest concentration of 1.56 mM) and double-strand breaks (only at the highest concentration of 100 mM). Following exposure to acetaldehyde, cells were incubated in complete medium for 30, 60, and 120 min. During this incubation period, most cells were unable to repair DNA single- and double-strand breaks caused by acetaldehyde. ... A significant cell loss /was also observed/ after exposure to acetaldehyde... (Reference 56)

ISOPENTANE:

(1) The USEPA identified isopentane in air samples taken from the top of the "Parker's Chapel Water Tower," which is on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that isopentane was detected in the air of the Pathfinders Camp.


(2) This information related to relevant health effects for isopentane is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) /SIGNS AND SYMPTOMS/ ACUTE ... SYMPTOMS: Inhalation--Cough. Dizziness. Drowsiness. Headache. Shortness of breath. Sore throat. Irregular heartbeat; Skin--Dry skin. Redness; Eyes--Redness. Pain; Ingestion--Abdominal pain. Nausea. Vomiting. (Reference 57)

(2.2) /SIGNS AND SYMPTOMS/ EFFECTS OF SHORT-TERM EXPOSURE: ... /Isopentane/ is irritating to the eyes, the skin and the respiratory tract. Swallowing the liquid may cause aspiration into the lungs with the risk of chemical pneumonitis. The substance may cause effects on the central nervous system and heart, resulting in impaired functions. EFFECTS OF LONG-TERM OR REPEATED EXPOSURE: The liquid defats the skin. (Reference 57)

(2.3) /SIGNS AND SYMPTOMS/ Repeated or prolonged skin contact will dry and defat skin, resulting in irritation and dermatitis. Direct contact of liq hydrocarbons with lung tissue (aspiration) will result in chem pneumonitis, pulmonary edema, and hemorrhage. /Aliphatic hydrocarbons/ (Reference 58)

(2.4) /SIGNS AND SYMPTOMS/ ... /SRP: CNS depressant/ effects may be accompanied by exhilaration, dizziness, and headache. ... Loss of appetite, nausea, a persisting taste of gasoline, confusion, inability to do fine work and loss of consciousness in extreme cases. /Saturated aliphatic hydrocarbons/ (Reference 60)

(2.5) Isopentane ... is a weak cardiac sensitizer. (Reference 61)

(2.6) Irritating to the nose and throat. (Reference 62)

(2.7) The substance is irritating to the eyes, the skin and the respiratory tract. (Reference 63)

TRICHLOROFLUOROMETHANE:

(1) The USEPA identified trichlorofluoromethane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that trichlorofluoromethane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for trichlorofluoromethane is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) BY INHALATION, LARGE, ACUTE DOSES HAVE RESULTED IN CARDIAC SENSITIZATION (ARRHYTHMIA) OR BRONCHIAL CONSTRICTION LEADING TO


DEATH ... . (Reference 64)

(2.2) ... BRADYCARDIA IS THE USUAL RESPONSE IN HUMAN SUBJECTS INHALING 10% OF CFC 11. ... IT IS REASONABLE TO SUGGEST THAT BRADYCARDIA IN MAN ORIGINATES FROM IRRITATION OF THE UPPER RESPIRATORY TRACT, & THAT CARDIAC EFFECTS CAN BE INITIATED PRIOR TO ABSORPTION OF CFC 11 IN THE LUNGS. (Reference 65)

(2.3) MAY BE /CENTRAL NERVOUS SYSTEM DEPRESSANT/ ... IN HIGH CONCN. (Reference 66)

(2.4) Workers ... /involved in a spill of/ large volume of CFC-11 were exposed to high concentrations and developed /CNS depressant/ effects. In one case, unconsciousness occurred, and in another, potentiation of the endogenous adrenaline effect and tachycardia. (Reference 67)

(2.5) /In a patient/ gastric perforation ... occurred one-half hour after accidental ingestion of refrigerated Freon 11; transient jaundice and liver enzyme elevation postoperatively was /also/ reported in this patient. (Reference 68)

(2.6) Deaths resulting from cardiovascular collapse after arrhythmias have been reported after inhalation of Freons 11 and 12. (Reference 69)

(2.7) Trichlorofluoromethane ... a liquid used mainly as a refrigerant, has no known systemic toxic effect on the eye. (Reference 70)

(2.8) Ten subjects /were exposed/ to CFC-11, CFC-12, CFC-114, two mixtures of CFC-11 and CFC-12, and a mixture of CFC-12 and CFC-114 (breathing concentrations between 16 and 150 g/cu m) for 15, 45, or 60 seconds, and found significant acute reduction of ventilatory lung capacity (FEV50, FEF25) on exposure to each chlorofluorocarbon, as well as bradycardia and increased variability in heart rate in seven subjects, negative T-waves in two subjects (one was exposed to CFC-11 and CFC-12), and atrioventricular block in 1 subject (CFC-114). Mixtures exerted stronger respiratory effects than individual chlorofluorocarbon at the same level of exposure. (Reference 71)

(2.9) Trichlorofluoromethane can affect the body if it is inhaled or if it comes in contact with the eye or skin. It can also affect the body if it is swallowed. (Reference 72)

(2.10) Freon 11, inhaled at 5% concentration, sensitizes the myocardium to epinephrine. A 6% concentration results in apnea and areflexia. A 10% concentration produces cardiac arrhythmias. Deaths resulting from cardiovascular collapse after arrhythmias have been reported after inhalation of /Freon 11/ ... . (Reference 73)

(2.11) EXCESSIVE SKIN CONTACT WITH LIQ FLUOROCARBONS SHOULD BE MINIMIZED TO PREVENT DEFATTING OF SKIN ... /FLUOROCARBONS/ (Reference 74)

(2.12) Fluorocarbon vapors are 4 to 5 times heavier than air. Thus high concn tend to accumulate in low-lying areas, resulting in hazard of inhalation of concentrated vapors, which may be fatal. /Fluorocarbons/ (Reference 75)


(2.13) Under certain condition, fluorocarbon vapors may decompose on contact with flames or hot surfaces, creating potential hazard of inhalation of toxic decomposition products. /Fluorocarbons/ (Reference 76)

(2.14) Freons are toxic to humans by several mechanisms. Inhaled fluorocarbons sensitized the myocardium to catecholamines, frequently resulting in lethal ventricular arrhythmias. Because they are gases heavier than air, fluorocarbons can displace atmospheric oxygen, thus resulting in asphyxiation. These compounds also have a central nervous system (CNS) anesthetic effect analogous to a structurally similar general anesthetic, halothane. Pressurized refrigerant or liquid fluorocarbons with a low boiling point have a cyrogenic effect on exposed tissues, causing frostbite, laryngeal or pulmonary edema, and gastrointestinal perforation. Certain fluorocarbons degrade at high temperatures into toxic products of chlorine, hydrofluoric acid, or phosgene gases. /Freons/ (Reference 77)

(2.15) ... HIGH VAPOR CONCN (EG, 20%) MAY CAUSE CONFUSION, PULMONARY IRRITATION, TREMORS & RARELY COMA ... BUT ... THESE EFFECTS WERE GENERALLY TRANSIENT & WITHOUT LATE SEQUELAE. /FLUOROCARBON REFRIGERANTS & PROPELLANTS/ (Reference 78)

(2.16) Intentional inhalation of aerosols containing extremely high concentrations of mixtures of CFC-11 & CFC-12 has caused instantaneous death. The /Intentions Program on Chemical Safety/ considered the deaths associated with these exposures to be caused by cardiac arrhythmia, aggravated by elevated levels of catecholamines due to stress or by moderate hypercapnia. (Reference 79)

FLUOROCARBON VAPORS:

Inhaled fluorocarbons sensitized the myocardium to catecholamines, frequently resulting in lethal ventricular arrhythmias. Because they are gases heavier than air, fluorocarbons can displace atmospheric oxygen, thus resulting in asphyxiation. These compounds also have a central nervous system (CNS) anesthetic effect analogous to a structurally similar general anesthetic, halothane. Pressurized refrigerant or liquid fluorocarbons with a low boiling point have a cyrogenic effect on exposed tissues, causing frostbite, laryngeal or pulmonary edema, and gastrointestinal perforation. Certain fluorocarbons degrade at high temperatures into toxic products of chlorine, hydrofluoric acid, or phosgene gases (http://toxnet.nlm.nih.gov). (Reference 437)

N-PENTANE:

(1) The USEPA identified n-pentane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that n-pentane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for n-pentane is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):


(2.1) The HSDB says PENTANE Synonym: n-pentane 109-66-0

(2.2) /HUMAN EXPOSURE STUDIES/ Pentane is a CNS depressant, but is not as effective as the C1-C4 gases. The intensity of CNS depression appears generally to decr with increasing molecular weight, but increases for the highly symmetrical cmpds. Only a small increment in dose separates CNS depression and lethality. The aspiration hazard of pentane is considerably less than that of kerosene, octane, nonane, or decane. (Reference 89)

(2.3) /HUMAN EXPOSURE STUDIES/ Dermal effects of pentane vapors applied to the skin of 5 volunteers were studied. Erythema, hyperemia, swelling, and pigmentation were observed after dermal exposure. The volunteers complained of a constant burning sensation accompanied by itching, and blisters after 5 hr of exposure. There was no evidence of anesthetic effects on the skin. When pentane was removed after 5 hr, pain continued for 15 min. (Reference 90)

(2.4) /HUMAN EXPOSURE STUDIES/ Low toxicity. Very high vapor concns produce narcosis. Aspiration into lungs can produce chemical pneumonitis or pulmonary edema. (Reference 91)

(2.5) /HUMAN EXPOSURE STUDIES/ Volunteers suffered from painful burning sensations, accompanied by itching, after topical application of pentane; after 5 hours, blisters formed on the treated areas. (Reference 93)

(2.6) /HUMAN EXPOSURE STUDIES/ Chronic exposure to pentane has resulted in anoxia. (Reference 94)

(2.7) /HUMAN EXPOSURE STUDIES/ Moderately toxic by inhalation and intravenous routes. Narcotic in high concentration. The liquid can cause blisters on contact. (Reference 95)

(2.8) Skin, Eye and Respiratory Irritations: ... Irritation of eyes, skin, nose. Direct contact may cause dermatitis; aspiration of liquid may cause chemical pneumonia. (Reference 96)

ACETONE:

(1) The USEPA identified acetone in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that acetone was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for acetone is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) /HUMAN EXPOSURE STUDIES/ In human volunteers, topical application of acetone for 30 or 90 minutes produced considerable damage to the skin, with a high degree of restoration after


72 hr ... (Reference 97) (2.2) /HUMAN EXPOSURE STUDIES/ Hematological effects have been observed in humans after inhalation exposure to acetone in controlled laboratory studies of volunteers. Statistically significant increased white blood cell counts and decreased phagocytic activity of neutrophils, compared with controls, were observed in the volunteers after a 6-hr exposure or repeated 6-hr exposures for 6 days to 500 ppm.... (Reference 98)

(2.3) /SIGNS AND SYMPTOMS/ Effects similar to ethyl alcohol... but anesthetic potency is greater. 10-20 mL taken by mouth without ill effect. In acute cases a latent period may be followed by restlessness and vomiting leading to hematemesis and progressive collapse with stupor. (Reference 99)

(2.4) /SIGNS AND SYMPTOMS/ Workers having been exposed to 1000 ppm, 3 hr/day for 7-15 years, also complained of chronic inflammation of airways, stomach and duodenum; some of them complained of dizziness and asthenia. Similar complaints were reported after exposure... to 700 ppm. (Reference 100)

(2.5) /SIGNS AND SYMPTOMS/ Prolonged or repeated skin contact may defat the skin and produce dermatitis. (Reference 101) (2.6) /SIGNS AND SYMPTOMS/ Repeated exposure to 25-920 ppm: chronic conjunctivitis, pharyngitis, bronchitis, gastritis, and gastroduodenitis. /Route not specified/ (Reference 102) (2.7) /SIGNS AND SYMPTOMS/ Severe toxic effects: 4,000 ppm= 9,650 mg/cu m, 60 minutes; symptoms of illness: 800 ppm= 1,930 mg/cu m, 60 minutes. (Reference 103)

(2.8) /SIGNS AND SYMPTOMS/ Symptoms following acute acetone ingestion include nausea, vomiting, gastric hemorrhage, sedation, respiratory depression, ataxia, and paresthesia. Depression resembles alcoholic stupor, but its onset is quicker than that with ethanol. Coughing and bronchial irritation may be the only clues to ingestion of quantities that are too small to produce sedation. Hyperglycemia and ketonemia with acidosis that resembles acute diabetic coma may be present. (Reference 104)

(2.9) /SIGNS AND SYMPTOMS/ Exposure for 15 minutes to 1660 ppm causes irritation of eyes and nose... (Reference 105)

(2.10) /CASE REPORTS/ ...Onset of hepatorenal lesions in 2 men and 2 women acutely exposed to acetone /is described/. One person had inhaled acetone vapors whereas the others had ingested acetone. Clinical manifestation of liver injury was observed in all four workers and renal lesions were detected in two. (Reference 106)

(2.11) /CASE REPORTS/ Acute acetone intoxication was reported in a 10-year old boy who wore a hip cast set with a mixture of 90% acetone, 9% pentane and 1% methyl salicylate. The following symptoms were described: restlessness, headache, vomiting (positive benzidine for blood), stupor, blood pressure 80/60, rapid and irregular respiration rate. (Reference 107)

(2.12) /CASE REPORTS/ ...A 17 month-old girl was given approximately 4.88 mL/kg (3,850


mg/kg bolus dose) of acetone through her gastronomy tube. The child was found gagging, unresponsive, and diaphoretic with dilated sluggish pupils, right arm tonic-clonic activity, and left eye deviation, and she was unresponsive to verbal or painful stimuli. ... (Reference 108)

(2.13) /CASE REPORTS/ ...A 53-year-old woman /was/ admitted to the hospital after ingestion of nail polish remover. Vital signs were generally normal, but neurological examination showed that even though she was oriented, the patient was lethargic but arousable and had a shortened attention span. ... (Reference 109) (2.14) /CASE REPORTS/ A 55-year-old woman presented with Guillain-Barre syndrome, nephrotic syndrome and multiple tubular dysfunction under occupational exposure to an organic solvent, which contained acetone as the principal solvent. In this case, the onset of the nephrotic syndrome and tubular dysfunction coincided with the development of the neurological manifestation. Renal biopsy demonstrated minimal change glomerulopathy with moderate tubulointerstitial nephritis. Several clearance tests that evaluated tubular transport functions revealed multiple tubular defects (including the Na(+)-K(+)-Cl(-) cotransporter of thick ascending limb and distal proton pump). ... (Reference 110)

DICLOROMETHANE:

(1) The USEPA identified dichloromethane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that dichloromethane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for dichloromethane is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) Dichloromethane: reasonably anticipated to be a human carcinogen. (Reference 320)

(2.2) ... TWO CASES OF /SRP: DICHLOROMETHANE/ POISONING IN PAINTERS WHO SUFFERED FROM HEADACHE, GIDDINESS, STUPOR, IRRITABILITY, NUMBNESS AND TINGLING IN THE LIMBS /ARE REPORTED/.

(2.3) METHYLENE CHLORIDE IS MILDLY IRRITATING TO SKIN ON REPEATED CONTACT. PROBLEM MAY BE ACCENTUATED BY CHEMICAL BEING SEALED TO SKIN BY SHOES OR TIGHT CLOTHING. SITUATION IS MOST SEVERE WITH PAINT REMOVER FORMULATIONS THAT FORM A "SKIN" OR FILM. (Reference 321)

(2.4) ... A CHEMIST DEVELOPED TOXIC ENCEPHALOSIS WITH ACOUSTICAL AND OPTICAL DELUSIONS AND HALLUCINATIONS AFTER BEING EXPOSED TO METHYLENE CHLORIDE FOR 1 YR. (Reference 322)


(2.5) FOUR NIGHT-SHIFT WORKERS WERE FOUND UNCONSCIOUS ... /AFTER EXPOSURE TO METHYLENE CHLORIDE/ 3 RECOVERED ... 4TH WAS DEAD WHEN AMBULANCE ARRIVED. OF 3 WHO RECOVERED, 1 SHOWED SIGNS OF ACUTE BRONCHITIS, 1 OF IRRITATION OF UPPER RESP TRACT & 1 CONJUNCTIVITIS & LACRIMATION. ALL SHOWED SOME ANEMIA & POLYMORPHONUCLEAR LEUCOCYTOSIS. (Reference 323)

(2.6) SEVERAL DEATHS HAVE BEEN REPORTED FROM ... /SRP: DICHLOROMETHANE/ USE AS ANESTHETIC ... (Reference 324)

(2.7) 3-YR OCCUPATIONAL EXPOSURE TO 300-1000 PPM DICHLOROMETHANE CAUSED MEMORY LOSS WITH INTELLECTUAL IMPAIRMENT & BALANCE DISTURBANCES IN 58-YR-OLD MAN. BILATERAL TEMPORAL LOBE DEGENERATION OCCURRED. PERSISTENT HIGH LEVEL OF ENDOGENOUS BLOOD CARBON MONOXIDE FORMED FROM DICHLOROMETHANE WAS THE REASON FOR TOXICITY. (Reference 325) (2.8) ... A 13 year-old boy who was ... using a paint remover that contained dichloromethane (DCM) ... was discovered dead no more than 9 hr after exposure. ... DCM was the primary agent responsible for death. (Reference 326)

(2.9) A case control study was carried out in 44 women who had a spontaneous abortion during employment in the pharmaceutical industry. Three age matched female pharmaceutical factory workers who had given birth to a child were chosen as controls for every case. Information about occupational exposures was obtained from questionnaires completed by the occupational physician or nurse at the factory. Exposure to chemicals was more common among the cases than the controls. For chloride (dichloromethane) the increase in odds ratio (OR) was of significance (OR= 2.3, p= 0.06). (Reference 327)

(2.10) All solvent-exposed female workers in a factory producing loudspeakers were examined in order to assess neurotoxic signs and symptoms possibly related to organic solvent exposure. ... Symptoms of neurasthenia and paraesthesia were significantly more frequent in the exposed group. Five of the exposed workers, whose neurasthenic symptoms could not be related to alternative causes, underwent neuropsychological testing. One of these workers had test results compatible with toxic encephalopathy caused by solvents. In another worker cerebral dysfunction was suspected. (Reference 328)

(2.11) THE HOME USE OF PAINT REMOVERS CONTAINING METHYLENE CHLORIDE CAN RESULT IN ELEVATION OF CARBOXYHEMOGLOBIN THAT CONTINUES FOLLOWING EXPOSURE TO LEVELS THAT STRESS CARDIOVASCULAR SYSTEM. PATIENTS WITH DISEASED CNS MAY NOT BE ABLE TO TOLERATE THIS UNEXPECTED STRESS. (Reference 329)

(2.12) Phosgene poisoning has been reported to occur in several cases where methylene chloride was used in the presence of an open fire. (Reference 330)

(2.13) /Produces/ skin inflammation and skin burns. (Reference 331)


(2.14) Skin, Eye and Respiratory Irritations: Irritation of eyes and respiratory tract. (Reference 332)

(2.15) ... Acute exposure ... may cause myocardial infarction in individuals with atherosclerotic heart disease... (Reference 333)

TRICHLOROETHYLENE:

(1) The USEPA identified trichloroethylene in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents'' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that trichloroethylene was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for trichloroethylene is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) Trichloroethylene: reasonably anticipated to be a human carcinogen. (Reference 336) (2.2) IN ACUTE INHALATION EXPOSURES RAPID COMA MAY ENSUE WITH EVENTUAL DEATH FROM HEPATIC OR RENAL FAILURE. AN OCCASIONAL SUDDEN DEATH SUGGESTS VENTRICULAR FIBRILLATION. SEQUELAE, WHICH MAY BE MORE COMMON AFTER INHALATION THAN AFTER INGESTION, INCLUDE LIVER AND KIDNEY LESIONS, REVERSIBLE TRIGEMINAL (OR OTHER NERVE) DEGENERATION AND PSYCHIC DISTURBANCES. (Reference 337)

(2.3) Trichloroethylene is only mildly irritating to the skin if allowed to evaporate. From continued use of the material in contact with the skin, defatting can take place. (Reference 338)

(2.4) Prolonged occupational exposure to trichloroethylene has been associated with impairment of peripheral nervous system function, persistent neuritis and temporary loss of tactile sense and paralysis of the fingers after direct contact with the solvent. (Reference 339)

(2.5) A case of severe liver necrosis following a prolonged (4-1/2 hour) use of trichloroethylene as an anesthetic has been reported. (Reference 340)

(2.6) Following chronic and acute overexposure to trichloroethylene during operation of a dry cleaning unit, symptoms included symmetrical bilateral VIIIth cranial nerve deafness as well as cerebral cortical dysrhythmia and alterations in the electroencephalogram. The patient recovered after the exposure stopped. (Reference 341)

(2.7) Acute overexposure to trichloroethylene resulted in chronic involvement of the bulbar cranial nerves and esophageal and pharyngeal motility impairment. (Reference 342)


(2.8) Autopsy findings in a 16 yr old boy who died while sniffing plastic cement containing TCE indicated severe heart failure. ... Liver failure is not the usual cause of death among solvent sniffers, but liver biopsies often reveal toxic centrilobular necrosis. (Reference 343)

(2.9) Chromosome analyses of cultured lymphocytes from 28 workers aged 23-67 who had been employed on degreasing unit using trichloroethylene for 1-21 years showed high rates of hypodiploid cells (9 of 28). (Reference 344)

(2.10) ...an abnormal trigeminal somatosensory evoked potential was observed in subjects who had the longest and most intense exposure periods. (Reference 345)

(2.11) 77 of 104 trichloroethylene workers showed abnormal electrocardiographic tracings, which may precede permanent heart damage. (Reference 346)

(2.12) Adverse psychological and behavioral abnormalities have been reported in industrial overexposures and include symptoms of headache, fatigue, lightheadedness, depression, insomnia, irritability, and confusion. Cranial and peripheral neuropathies have been associated with industrial and medical use. Selective trigeminal neuralgia has been diagnosed in one study in 20% of trichloroethylene workers by demonstrating electrophysiological abnormalities. (Reference 347)

(2.13) Skin: defatting action /of trichloroethylene/ can cause dermatitis. (Reference 348)

(2.14) Human subjects with high repeated, but non-occupational, exposure may exhibit toxic effects on the liver (e.g., elevated aspartate & alanine aminotransferase), renal insufficiency, & abnormal EEG patterns. (Reference 349)

(2.15) Acute effects on the CNS are characterized by two sequential phases (i.e., excitation & depression), & are usually reversible. ... In the early phase of excitation, euphoria & inebriation are present. The subsequent phase of CNS depression is characterized by various degrees of narcosis culminating in coma. Muscular hypotomy, muscular spasms, reduced tendon reflexes, & loss of coordination may occur. (Reference 350)

(2.16) Childhood leukemia in a community in Massachusetts, USA, where water from two wells was contaminated with trichloroethylene /was studied/. Measurements made in 1979 showed a concentration of 267 ppb (ug/l) trichloroethylene in the well water. Twenty cases of childhood leukemia were diagnosed in the community in 1964-83, and these were associated with a significantly higher estimated cumulative exposure to water from the two contaminated wells than a random sample of children from the community (observed cumulative exposure, 21.1; expected cumulative exposure, 10.6; p= 0.03). (Reference 351)

(2.17) A study conducted in New Jersey, USA, during 1979-87 included 75 towns, of which 27 were included in a /previous/ study. Trichloroethylene concentrations were measured during 1984-85, and an average level was assigned to each town. The highest level assigned was 67 ug/l. The water supply of six towns contained > 5 ug/l trichloroethylene (average, 23.4 ug/l). Women in these towns had a significantly higher total incidence of leukemia than the inhabitants of towns were the concentration of trichloroethylene in drinking water was < 0.1 ug/l (relative risk, 1.4; 95% CI, 1.1-1.9); no such effect was seen for men (1.1, 0.84-1.4). The risk among women was particularly elevated for


acute lymphocytic leukemia, chronic lymphocytic leukemia in childhood was also significantly increased, in girls but not in boys. Increased risks for non-Hodgkin's lymphoma were apparent in towns in the highest category of trichloroethylene contamination (0.2; 0.94-1.5 for men and 1.4; 1.1-1.7 for women) and was particularly elevated for high-grade lymphomas. (Reference 352)

(2.18) Exposure to trichloroethylene vapor may cause irritation of the eyes, nose, and throat. (Reference 253)

(2.19) [Trichloroethylene] TCE should be packaged in steel drums. These drums should be stored in a cool, dry, well-ventilated area because TCE will slowly decompose to corrosive HCL when exposed to light & moisture. (Reference 403)

(2.20) SLOWLY DECOMPOSED WITH FORMATION OF HYDROCHLORIC ACID BY LIGHT IN PRESENCE OF MOISTURE (Reference 404)

(2.21) Autoxidation products, such as phosgene and dichloroacetylene, added stabilizers, such as epichlorohydrin, and decomp products, such as chlorine and hydrochloric acid, may be responsible for some of the toxic and carcinogenic effects reported for trichloroethylene.

(2.22) Trichloroethylene slowly decomposes to corrosive HCL when exposed to light & moisture (Reference 403). In other words SLOWLY DECOMPOSED WITH FORMATION OF HYDROCHLORIC ACID BY LIGHT IN PRESENCE OF MOISTURE (Reference 404).

(2.23) Chlorine is also a product of decomposing trichloroethelyene (Reference 405).

(3) An article, entitled: "Trichloroethylene (TCE) Is A Risk Factor For Parkinsonism, Study Shows," provides relevant information, which is, as follows: "ScienceDaily (Jan. 9, 2008) — Parkinson's disease, the most common neurodegenerative movement disorder caused by aging, can also be caused by pesticides and other neurotoxins. A new study found strong evidence that trichloroethylene (TCE) is a risk factor for parkinsonism, a group of nervous disorders with symptoms similar to Parkinson's disease." (Reference 335)

HYDROCHLORIC ACID:

This information related to relevant health effects for hydrochloric acid is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) HYDROGEN CHLORIDE Synonym: hydrochloric acid 7647-01-0

(2) HCl, hydrogen chloride, the gas, and HCl, the aqueous acid (hydrochloric acid), have the same CAS Registry number. Since the gas becomes the acid in aqueous systems and volatilization of the gas can occur from aqueous systems, it is often difficult to determine which is being considered in a specific item in the literature. In those cases where the distinction can be made, it will be noted in the occurrence.


(3) /SIGNS AND SYMPTOMS/ Fatal if swallowed. Corrosive. Causes irreversible eye damage or skin burns. Harmful if absorbed through skin or inhaled. /Emulso Germicidal Bowl Cleaner Disinfectant/ (Reference 412)

(4) /SIGNS AND SYMPTOMS/ Burns on the face may produce serious and disfiguring scars. Digestive diseases are frequent and are characterized by dental molecular necrosis in which the teeth lose their shine, turn yellow, become soft, pointed, and then break off. (Reference 413)

(5) /SIGNS AND SYMPTOMS/ Mists of heated metal pickling soln may cause bleeding of nose & gums, as well as ulceration of nasal and oral mucosa. ...(Reference 414) (6) /SIGNS AND SYMPTOMS/ SYMPTOMATOLOGY (after ingestion or skin contact): 1) Corrosion of mucous membranes of mouth, throat, and esophagus, with immediate pain and dysphagia. The necrotic areas are at first grayish white but soon acquire a blackish discoloration and sometimes a shrunken or wrinkled texture; the process is described as a "coagulation necrosis." 2) Epigastric pain, which may be associated with nausea and the vomiting of mucoid and "coffee-ground" material. At times, gastric hemorrhage may be intense, and the vomitus then contains fresh blood. Profound thirst /SRP: may be present/. 3) Ulceration of all membranes and tissues with which the acid comes in contact ... . /Acids/ (Reference 415)

(7) SIGNS AND SYMPTOMS/ SYMPTOMATOLOGY (after ingestion or skin contact): 4) Circulatory collapse with clammy skin, weak and rapid pulse, shallow respirations, and scanty urine. Circulatory shock is often the immediate cause of death. 5) Asphyxial death due to glottic edema. 6) Late esophageal, gastric and pyloric strictures and stenoses, which may require major surgical repair, should be anticipated. Signs of obstruction commonly appear within a few weeks but may be delayed for months and even years. Permanent scars may also appear in the cornea, skin and oropharynx. 7) Uncorrected circulatory collapse of several hours' duration may lead to renal failure and ischemic lesions in the liver and heart. /Acids/ (Reference 416)

(8) /SIGNS AND SYMPTOMS/ Hydrogen chloride (HCl) in the lung can cause /SRP: delayed/ pulmonary edema. In order for hydrogen chloride in air to reach the lung, it must be transported either as an aerosol or as a deposit on soot particles of less than 3 um in diameter. Particulates in smoke from incineration of chlorinated polymers can transport HCl gas to the lung.(Reference 417)

(9) /SIGNS AND SYMPTOMS/ Ingestion of hydrochloric acid causes edema of the glottis. (Reference 418)

(10) /SIGNS AND SYMPTOMS/ CONTACT WITH CONCENTRATED SOLUTIONS OF HYDROCHLORIC ACID IN CLEANING METAL GIVES RISE TO SMALL BURNS AND ULCERATIONS OF THE HANDS. (Reference 419)

(11) /SIGNS AND SYMPTOMS/ Caution: Corrosive burns may result from the inhalation of acid fumes and from skin contact with or the ingestion of strong acid. Symptoms after ingestion or skin contact include immediate pain and ulceration of all membranes and tissues which come in contact with the acid. Ingestion may be assoc with nausea, vomiting and intense thirst; corrosion of the stomach may lead within a few hours or a few days to gastric perforation and peritonitis. Late


esophageal, gastric and pyloric strictures and stenoses should be anticipated. Contact of conc acid with the eye can cause extensive necrosis of the conjunctiva and corneal epithelium, resulting in perforation or opaque scarring. Chemical pneumonitis can be expected after respiratory exposure to acid vapors or after tracheobronchial aspiration of ingested acid. Death may occur due to complications such as circulatory shock, asphyxia due to glottic or laryngeal edema, perforation of the stomach with peritonitis, gastric hemorrhage, infection or anition due to stricture formation. (Reference 420)

(12) /SIGNS AND SYMPTOMS/ Sharp, pungent irritating odor; recognition odor in air 10 ppm; TLV = 5 ppm; 35 ppm causes irritation of throat; 50-100 ppm can be tolerated for 1 hr. Longer exposure may result in pulmonary edema and laryngeal spasm. Concn of 1,000-2,000 ppm are dangerous even for brief exposure. Anhydrous fumes are more harmful than mists. Can damage vision. Symptoms include vomiting, diarrhea, intense thirst, and circulatory collapse. (Reference 421) (13) /SIGNS AND SYMPTOMS/ Inhalation of hydrochloric acid at irritating concentrations causes coughing, pain, inflammation, and edema of the upper respiratory tract. At high concn, the gas causes necrosis of the bronchial epithelium, constriction of the larynx and bronchi, and closure of the glottis. Concentrations of the 1000 to 2000 ppm and higher are immediately dangerous. One fatal case of overexposure has been reported; postmortem examination showed severe pulmonary hemorrhage, edema, and pneumonitis. (Reference 422)

(14) /SIGNS AND SYMPTOMS/ Short term exposures have been reported to induce transitory obstruction in the respiratory tract, which diminishes with repeated exposure, suggesting adaption. Acclimatized workers can work undisturbed with a hydrogen chloride level of 15 mg/cu m (10 ppm), but long-term exposure can affect the teeth, resulting in erosion of the inciso-labial surfaces. (Reference 423)

(15) /SIGNS AND SYMPTOMS/ Small quantities are reportedly more easily detected by taste than by smell ... 52 mg/cu m (approx 35 ppm), a level below the threshold for taste or eye irritation, can induce sneezing, laryngitis, chest pain, hoarseness, and a feeling of suffocation. (Reference 424)

(16) /SIGNS AND SYMPTOMS/ Exposure to hydrochloric acid can produce burns on the skin and mucous membranes, the severity of which is related to the concentration of the solution. Subsequently, ulceration may occur, followed by keloid and retractile scarring. Contact with the eyes may produce reduced vision or blindness. frequent contact with aqueous solutions of hydrochloric acid may lead to dermatitis. ... Dental decay, with changes in tooth structure, yellowing, softening and breaking of teeth, and related digestive diseases are frequent after exposures to hydrochloric acid. (Reference 425)

(17) /SIGNS AND SYMPTOMS/ Dysphagia and transient ulceration of the esophagus with luminal narrowing are usually observed following ingestion of hydrochloric acid. (Reference 426)

(18) /SIGNS AND SYMPTOMS/ Acid aspiration leads to an inflammatory response characterized by the activation and pulmonary entrapment of platelets and white blood cells. (Reference 427)

(19) /SIGNS AND SYMPTOMS/ Splash contact of concentrated strong acids, such as hydrochloric acid can prove as severely and devastatingly injurious to the eye as splashes of strong


alkalies. (Reference 428)

(20) /SIGNS AND SYMPTOMS/ Respiratory: Hydrogen chloride gas is intensely irritating to the mucous membranes of the nose, throat, and respiratory tract. Brief exposure to 35 ppm causes throat irritation, and levels of 50 to 100 ppm are barely tolerable for 1 hour. The greatest impact is on the upper respiratory tract; exposure to high concentrations can rapidly lead to swelling and spasm of the throat and suffocation. Most seriously exposed persons have immediate onset of rapid breathing, blue coloring of the skin, and narrowing of the bronchioles. Patients who have massive exposures may develop an accumulation of fluid in the lungs. Exposure to hydrogen chloride can lead to Reactive Airway Dysfunction Syndrome (RADS), a chemically- or irritantinduced type of asthma. Children may be more vulnerable to corrosive agents than adults because of the relatively smaller diameter of their airways. Children may also be more vulnerable to gas exposure because of increased minute ventilation per kg and failure to evacuate an area promptly when exposed. (Reference 429)

(21) /SIGNS AND SYMPTOMS/ Ocular: Exposure of the eyes to concentrated hydrogen chloride vapor or hydrochloric acid can cause corneal cell death, cataracts, and glaucoma. Exposure to dilute solutions can cause stinging pain and injuries such as ulcers of the eye surface. (Reference 430)

(22) /SIGNS AND SYMPTOMS/ Cardiovascular: Ingestion of concentrated hydrochloric acid or massive skin exposure to either hydrochloric acid or hydrogen chloride gas may cause low blood pressure as a result of gastrointestinal bleeding or fluid displacement. After acute exposure, pulmonary function generally returns to baseline in 7 to 14 days. (Reference 431) (23) /SIGNS AND SYMPTOMS/ A rare and unusual complication of ingestion of high levels of hydrogen chloride is an increase in the concentration of chloride ions in the blood, causing an acid-base imbalance. Because of their higher metabolic rates, children may be more vulnerable to toxicants interfering with basic metabolism. (Reference 432) (24) /CASE REPORTS/ Stenosis of the distal trachea has been reported after aspiration of 35% hydrochloric acid. The signs of obstructive pulmonary disease (dyspnea, wheezing) developed approximately 6 weeks after exposure and were initially mistaken for reactive airway dysfunction syndrome. A computerized tomography scan of the chest revealed the tracheal stenosis. The patient was treated with tracheal stenting. (Reference 433)

(25) /CASE REPORTS/ After ingestion of muriatic acid (27% HCL), findings in 24 patients consisted of mucosal edema, submucosal edema or hemorrhage, ulcerations, sloughing of mucosa, atony, & dilatation. Strictures of esophagus were present in chronic phase. (Reference 434)

(26) /CASE REPORTS/ ... A report by soviet investigators that workers exposed to hydrochloric acid suffered from gastritis. A number of cases of chronic bronchitis were also observed. (Reference 439)

(27) /CASE REPORTS/ Dental erosion of the incisors was observed in 90% of picklers in a zinc galvanizing plant in the Netherlands, who spent 27% of their time in air containing concentrations of hydrogen chloride above the exposure limit (7 mg/cu m). (Reference 440)

(28) /CASE REPORTS/ /The authors/ report a case of acute ST segment elevated myocardial


infarction associated with hydrochloric acid ingestion. Severe systemic acidosis developed shortly after massive hydrochloric acid ingestion; it was complicated by the presence of acute myocardial infarction. (Reference 441)

(29) /CASE REPORTS/ ... /The authors/ report the case of a 53-year-old female who received a fatal chemical burn due to extravasation from a subclavian central venous catheter of hydrochloric acid infused to correct severe metabolic alkalosis. (Reference 442)

(30) /CASE REPORTS/ A 29-year-old man with schizophrenia presented to the emergency department with abdominal pain immediately after ingesting approximately 200 mL of cleaning solution containing 36% hydrochloric acid. Initial unenhanced CT of the chest, abdomen, and pelvis showed an intact stomach and a small amount of free intraperitoneal fluid. Direct endoscopy showed mucosal injury in the oropharynx, hypopharynx, and supraglottic region, and diffuse caustic injury to the esophageal mucosa. Because of worsening clinical status, a contrast-enhanced CT of the abdomen was performed 2 days later, showing gastric necrosis and perforation. The patient died shortly thereafter. (Reference 443)

(31) /EPIDEMIOLOGY STUDIES/ The objective of this study is to assess the incidence and long-term results of a rarely discussed medical problem -- aspiration pneumonia resulting from the intentional ingestion of acid. The medical records of 370 patients treated at one tertiary care institution for corrosive acid injury during a 12-year period were reviewed retrospectively. The study subjects included any patients who were found to have acid ingestion related aspiration pneumonia confirmed by chest film within 24 hr of injury. All available data of these patients with or without aspiration pneumonia were analyzed. Of the 370 patients with corrosive acid injury, 15 (4.2%) had acid-aspiration pneumonia which was related to their intentional ingestion of a strong acid, hydrochloric acid (pH<1). The data for 14 patients with aspiration pneumonia and 268 without aspiration pneumonia was complete and available for analysis. Patients with aspiration pneumonia were found to be significantly older (52.2+/-6.2 to 41.7+/-0.9 years old, P=0.017), had a higher incidence of nasogastric tube irrigation (35.7-6.0%, P=0.000), had more conscious disturbance (50.0-17.5%, P=0.016), and required more endotracheal tube intubation (50.0-3.0%, P=0.000). Aspiration pneumonia was found to significantly increase the mortality rate in acid injured patients who required emergency abdominal surgery (87.5-32.0%, P=0.000) and in those who did not (28.5-5.1%, P=0.05). Two of the six survivors of aspiration pneumonia later developed laryngeal sequelae. (Reference 444)

(32) /OTHER TOXICITY INFORMATION/ Upper limit of safety for man ... about 45 mg/cu m (30 ppm) ... even this might be harmful if daily exposures were continued over periods longer than 1 month. (Reference 445)

CHLORINE:

This information related to relevant health effects for chlorine is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) /SIGNS AND SYMPTOMS/ Chlorine reacts with water in human tissues to form certain harmful acids. The severity of injury depends on the concentration of the gas, duration of contact, water


content of the tissue involved and the presence of existing lung disease. ... Chlorine can be absorbed into the body by all routes. Gas irritates the eyes and causes tears. The extent of the injury depends on the concentration of the gas. This can range from mild mucous membrane irritation (after 1 hour) to toxic lung disease and water-logged lungs or death within a few minutes. Inhalation: Initially, irritation of the eyes, nose and throat, followed by coughing and wheezing, shortage of breath, sputum production and chest pain. Larger exposures may lead to heart and lung failure. Those surviving exposure may have persistent cough for up to 14 days or even several months. Symptoms may include chest pains, vomiting and coughing. Skin contact: Irritation, pain, redness, blister and burns. Liquid chlorine may cause burns on contact. Eye contact: Irritation and inflammation. Liquid chlorine may cause burns on contact. (Reference 446)

(2) /SIGNS AND SYMPTOMS/ After inhalation of chlorine patients are suffering from lacrimation, conjunctival irritation, rhinorrhea, cough, headache, sore throat, chest burning, dyspnea, nausea, vomiting, and heightening of anxiety especially in those prone to "neurosis"; severe exposure can lead to severe tracheobronchitis, pulmonary edema, and acute hypoxemic respiratory failure; short-term high level exposures can also aggravate pre-existing heart diseases, producing electrocardiographic changes and congestive heart failure; at sufficiently high doses (i.e. war-time conditions) the exposure to chlorine can cause shock, coma, respiratory arrest, and death; people exposed during physical exertion appear especially vulnerable; controlled human exposure data suggest some people to be more responsive to the effects of chlorine gas; epidemiologic data also indicate that certain subpopulations (e.g. smokers) may have a greater risk of adverse effects due to chlorine inhalation. (Reference 447)

(3) /SIGNS AND SYMPTOMS/ EXPOSURE SYMPTOMS: 1 to 3 ppm, mild mucous membrane irritation after 1 hour; 5 to 15 ppm, moderate irritation of upper respiratory tract; 30 ppm, immediate chest pain, vomiting, and coughing; 40 to 60 ppm, toxic pneumonitis and pulmonary edema; 430 ppm, lethal after 30 minutes; 1,000 ppm, fatal within a few minutes. INHALATION: Initially: irritation of the eyes, nose and throat, followed by coughing and wheezing, dyspnea, sputum production and chest pain. Larger exposures may lead to hyperchloremic acidosis; anoxia may lead to cardiac and/or respiratory arrest and pulmonary edema. Following chemical pneumonitis respiratory distress and chest pain generally subsides within 72 hours; cough may persist for up to 14 days, however in one case reduced airway flow and mild hypoxemia persisted for 14 months. DERMAL: Irritation, pain, erythema, blister and burns. Liquid chlorine may cause burns on contact. EYES: Irritation and conjunctivitis. Liquid chlorine may cause burns on contact. (Reference 448)

(4) /SIGNS AND SYMPTOMS/ HAZARDS TO HUMANS AND DOMESTIC ANIMALS: DANGER. Fatal if inhaled or absorbed through skin. Corrosive. Causes irreversible eye damage and skin burns. (Reference 449)

(5) /SIGNS AND SYMPTOMS/ Acute exposure... vomiting. ...Anxiety ...chronic exposure. ...Concentrations of 0.8-1 ppm cause permanent, although moderate, reduction in pulmonary function. (Reference 450)

(6) /SIGNS AND SYMPTOMS/ Caution: Potential symptoms of overexposure are burning of eyes, nose and mouth; lacrimation, rhinorrhea; coughing, choking and substernal pain; nausea, vomiting; headache, dizziness; syncope; pulmonary edema; pneumonia; hypoxemia; dermatitis; eye and skin burns. (Reference 451)


(7) /SIGNS AND SYMPTOMS/ Prolonged or frequently repeated skin contact may cause allergic reactions in some individuals. (Reference 452)

(8) /SIGNS AND SYMPTOMS/ Corrosive effect and pulmonary effect: Complete destruction of skin or mucous membrane. (Reference 453)

(9) /SIGNS AND SYMPTOMS/ In human poisoning incidents involving accidental ingestion of household bleach, chlorine has caused a burning sensation in the mouth and throat, irritation to the digestive tract and stomach, and vomiting. Exposure to chlorine gas causes effects ranging from bronchitis, asthma and swelling of the lungs, to headaches, heart disease and meningitis. Acute exposure causes more severe respiratory and lung effects, and can result in fatalities. (Reference 454)

(10) /SIGNS AND SYMPTOMS/ ... Discussed briefly the drying effects on the skin and hair of chlorinated water. Swimmers have reported a bleaching effect of chlorine on their hair, some have developed "green hair", and many a chemical conjunctivitis. There have also been occasional reports of asthma precipitated by exposure to chlorinated water ... (Reference 455)

(11) /SIGNS AND SYMPTOMS/ ... Men exposed in bleaching rooms to concentration of the order of (5 ppm)... suffer from disease of the bronchi, and become predisposed to tuberculosis. ...Irritates skin causing sensations of burning or prickling, inflammation or even blister formation. (Reference 456)

(12) /CASE REPORTS/ ... Twenty-two patients exposed briefly to undiluted chlorine at home or work, were evaluated with a battery of neurobehavioral and visual tests. Their test scores, expressed as percentage predicted, were compared with those of unexposed subjects. Chlorine-exposed subjects had impaired balance (with eyes open and eyes closed), delayed simple and choice reaction times, impaired color discrimination, impaired visual field performance, decreased hearing, and decreased grip strength. Blink reflex latency was delayed on the right. Cognitive performance (i.e., digit symbol and vocabulary), peg placement, trail making A and B, and verbal recall were significantly below predicted levels. Well-learned memory functions were not impaired. Adverse mood states scores were elevated as were the frequencies of 28 of 35 common symptoms. Forced vital capacities were reduced. The duration of chlorine exposures was from a breath or two to several hours, and exposures were associated with impaired neurophysiologic and neuropsychologic functions. Impairments appeared insidiously, were noted 1 to 48 mo after exposure, and persisted. ... (Reference 457) (13) /CASE REPORTS/ /The authors/ present a patient with accidental chlorine gas poisoning who died from pulmonary thrombosis due to a marked increase in hemostatic factors such as von Willebrand factor after recovering from the acute poisoning. (Reference 448)

(14) /CASE REPORTS/ ... /The authors/ report the case of a 14-y-old boy with a history of asthma who was exposed to chlorine gas as a result of an ill-advised science experiment. His clinical condition deteriorated over the course of several hours, and he required intubation and ventilatory support. During his hospitalization, he developed the acute respiratory distress syndrome. He was treated with positive pressure ventilation, beta-adrenergic agonists, and corticosteroids. After 19 d, he was extubated and subsequently made an excellent recovery. ... (Reference 449)

(15) /CASE REPORTS/ A previously healthy 23-year-old man with nonproductive cough and


sore throat presented to the hospital a few hours after chlorine gas exposure at a fitness center swimming pool. Initial physical examination and chest radiograph were normal. Thirty-six hours later he developed worsening dyspnea and cough, with development of blood-tinged sputum. Arterial blood gas analysis showed mild hypoxemia and a subsequent chest radiograph demonstrated diffuse tiny nodular opacities. Findings on a thin-section computed tomogram of the chest were consistent with diffuse bronchiolitis. Pulmonary function tests showed a mild obstructive abnormality and he demonstrated substantial bronchodilator response. The patient was treated with oral corticosteroids and an inhaled beta(2) agonist, to which he responded well, with full clinical recovery occurring over 5 months. (Reference 450)

(16) /CASE REPORTS/ /The authors/ report the case of a 9-year-old girl who developed dyspnea, hypoxemia, and pneumonitis approximately 12 hrs after exposure to chlorine released from aerosolized swimming pool purification tablets. Her course was characterized by improvement with supplemental oxygen and bronchodilator therapy. Follow-up pulmonary testing at 4 months after the episode revealed the presence of mild obstructive reactivity of the airways, but she was able to perform normal activities without requiring medications. (Reference 451)

(17) /CASE REPORTS/ Patient had myasthenia gravis manifested by laryngeal stridor after accidental exposure to chlorine gas. Diagnosis was established by correction of abnormal pulmonary function after injection of edrophonium chloride, Patient subsequently had generalized myasthenia gravis. (Reference 452)

ISOPROPANOL: (1) The USEPA identified isopropanol in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that isopropanol was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for isopropanol is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) SYMPTOMATOLOGY: 1. DIZZINESS, INCOORDINATION, HEADACHE, CONFUSION, STUPOR & COMA. 2. GASTROENTERITIS WITH VOMITING, HEMATEMESIS, & DIARRHEA. 3. HYPOTENSION, WITH OR WITHOUT BRADYCARDIA, & SOMETIMES ... CIRCULATORY COLLAPSE. 4. PERSISTENT COMA WITH HYPOTHERMIA. 5. DEATH BY RESP ARREST. 6. LATE MANIFESTATIONS: ASPIRATION PNEUMONIA; KIDNEY & LIVER DYSFUNCTIONS, WHICH ARE USUALLY MILD & TRANSIENT, BUT THE RENAL IMPAIRMENT MAY BE SERIOUS. (Reference 127)

(2.2) ISOPROPYL ALCOHOL IS NOT A DERMAL IRRITANT ... ALTHOUGH SEVERE CASES /PRIMARY/ OF ALLERGIC CONTACT DERMATITIS HAVE BEEN REPORTED ... . [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World


(Reference 128)

(2.3) An incr incidence of cancer of the paranasal sinuses was observed in workers at factories where isopropyl alcohol was manufactured by the strong acid process. The risk for larynegeal cancer may also have been elevated in these workers. It is unclear whether the cancer risk is due to the presence of diisopropyl sulfate, which is an intermediate in the process, to isopropyl oils, which are formed as by-products, or to other factors, such as sulfuric acid. /Isopropyl alcohol manufacture/ (Reference 129)

(2.4) ... /Isopropyl and n-propyl/ alcohols are about twice as toxic as ethanol; the fatal dose by ingestion is 250 ml. ... The principal manifestation of acute isopropyl or n-propyl poison is CNS depression. Symptoms and signs: (From inhalation, ingestion, or skin absorption) ... persistent nausea, vomiting, abdominal pain, hematemesis, refractory ... /CNS depression/, areflexia, depressed respirations, and oliguria followed by diuresis. Deep coma has resulted from sponging with isopropyl alcohol. Generalized tenderness, induration, and edema of muscles may occur. ... Prolonged contact with the skin can cause corrosion. (Reference 130)

(2.5) Isopropanol intoxication has a rapid onset of action (30-60 min), with peak effects within several hr. ... Severe poisoning presents early with deep coma, resp depression, and hypotension. Central nervous system: Dizziness, poor coordination, headache, and confusion progress to stupor, coma, and loss of deep tendon reflexes in serious cases. Serious nervous system depression often persists for 24 hr. ... Pupils often are miotic, and nystagmus usually is present. Gastrointestinal tract: Gastric irritation appears early, with abdominal pain and vomiting being prominent. Hematemesis may occur. Cardiovascular system: The hypotension associated with large overdoses probably results from peripheral vasodilation. ... Tachycardia was the most common finding ... Organ dysfunction: Cases of acute tubular necrosis, hepatic dysfunction, hemolytic anemia, and myoglobinuria have been reported. ... Mild hypothermia may occur ... .(Reference 131)

(2.6) Acute inhalation exposure to isopropanol can produce central nervous system depression that may be prolonged by acetone, a metabolite of isopropanol. lethalities have occurred in very young and newborn children. Ingestion of isopropanol has been implicated in the deaths of a number of adults, particularly among alcoholics. Pulmonary congestion was the most frequent postmortem finding and is typical, although not diagnostic or specific, of deaths involving drug-induced central nervous system depression. (Reference 132)

(2.7) It can be an irritant of the eyes, mucous membranes, & respiratory tract. (Reference 133)

2-METHYLPENTANE:

(1) The USEPA identified 2-methylpentane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that 2-methylpentane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for 2-methylpentane is from the


"Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says that it is "a human eye irritant." (Reference 134)

3-METHYLPENTANE:

(1) The USEPA identified 3-methylpentane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that 3-methylpentane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for 3-methylpentane is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says that "A high risk of spontaneous abortion was observed in women exposed to organic solvents during pregnancy." (Reference 135)

HEXAFLUOROBENZENE:

(1) The USEPA identified hexafluorobenzene in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that hexafluorobenzene was detected in the air of the Pathfinders Camp.

(2) There is a relevant journal article published by the International Anesthesia Research Society, entitled: "ANESTHETIC PHARMACOLOGY Hexafluorobenzene Acts in the Spinal Cord, Whereas O-Difluorobenzene Acts in Both Brain and Spinal Cord, to Produce Immobility." (Reference 136)

CHLOROFORM:

(1) The USEPA identified chloroform in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that chloroform was detected chloroform in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for chloroform is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):


(2.1) Reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity in animals. (Reference 137)

(2.2) /HUMAN EXPOSURE STUDIES/ Most data on the controlled exposure of /humans/ to chloroform have resulted from its clinical use as an anesthetic. This use of chloroform was described as early as 1847 ... Induction of anesthesia may result from inhalation of chloroform vapors at a concentration of 24 to 73 g/cu m air. For maintenance of anesthesia, concentrations in the range of 12 to 48 g/cu m are required. As with animals, chloroform anesthesia may result in death in humans due to respiratory and cardiac arrhythmias and failure. Because of the relatively high frequency of "late chloroform poisoning" (liver toxicity), its use as anesthetic has been abandoned. Other effects related to chloroform inhalation are: increase in the rate and depth of respiration during induction and light anesthesia, minute volume decrease in deep anesthesia, hypothermia, depletion of adrenal adrenaline content, hypotension, depression of gastrointestinal tract motility, respiratory acidosis, hyperglycemia, ketosis, constriction of the spleen, increase in the number of leucocytes (especially polymorphonuclear cells), a decrease in clotting time and an increase in prothrombin time. The characteristics and severity of the effects depend on depth and duration of anesthesia ... (Reference 138)

(2.3) Chloroform "has been shown to produce phosgene, hydrogen chloride, water, carbon dioxide and chlorine." (Reference 408) Chloroform decomposes at ordinary temperature in sunlight in the absence of air, and in the dark in the presence of air..." (Reference 409)

PHOSGENE:

This information related to relevant health effects for phosgene is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) SIGNS AND SYMPTOMS/... Phosgene decomposes to form hydrochloric acid and carbon monoxide. This occurs in the bronchioles and alveoli of the lungs, resulting in pulmonary edema followed by bronchopneumonia and occasionally lung abscess. (Reference 453)

(2) /SIGNS AND SYMPTOMS/ A casualty who complains of shortness of breath should be questioned extensively about exposure ... .. The most important things to do for such a casualty are to ensure he is free from contamination (he is out of the smoke or wearing his mask) and is kept completely at rest. Complete rest is extremely important. There were instances in World War I in which phosgene casualties who were breathing comfortably at rest collapsed and died after walking a few yards. Even a little exertion can greatly intensify the effects of these agents. A casualty who is short of breath requires assisted ventilation with oxygen, or oxygen alone. A dyspneic casualty must be evacuated as quickly as possible to a medical facility that can provide intensive pulmonary care. A casualty who becomes dyspneic within the first few hours after exposure will probably not survive, even with intensive care. (Reference 454)

(3) /SIGNS AND SYMPTOMS/ During or immediately after exposure to dangerous concentrations of phosgene, the following signs and symptoms may develop: Coughing; Burning sensation in the throat and eyes; Watery eyes; Blurred vision; Difficulty breathing or shortness of breath; Nausea and vomiting. Skin contact can result in lesions similar to those from frostbite or burns.


Following exposure to high concentrations of phosgene, a person may develop fluid in the lungs (pulmonary edema) within 2 to 6 hours. Exposure to phosgene may cause delayed effects that may not be apparent for up to 48 hours after exposure, even if the person feels better or appears well following removal from exposure. Therefore, people who have been exposed to phosgene should be monitored for 48 hours afterward. Delayed effects that can appear for up to 48 hours include the following: Difficulty breathing; Coughing up white to pink-tinged fluid (a sign of pulmonary edema); Low blood pressure; Heart failure. (Reference 455)

(4) /SIGNS AND SYMPTOMS/ Inhalation is the most important route of exposure for phosgene. Because of phosgene?s mild upper respiratory, eye, and skin irritancy and mildly pleasant odor, an exposed victim may not actively seek an avenue of escape before lower respiratory damage has occurred. Pulmonary edema is the cause of death after a clinical latency period of </=24 hrs. (Reference 456)

(5) /SIGNS AND SYMPTOMS/ Numerous cases of severe acute phosgene poisoning at the workplace have been reported. In most cases workers accidentally inhaled phosgene gas, in some cases additional dermal exposure occurred... . Initial symptoms were coughing, eye and upper airway irritation, chest tightness, nausea, and emesis. These symptoms usually subsided upon removal from phosgene. The following latent period, where the patient experienced relative well-being and sometimes even returned to work, lasted for 1 to 24 hr. During the subsequent edema phase the patient experienced progressive respiratory distress, sometimes symptoms like coughing, burning sensation of the upper airways, thoracic pain, chest tightness, emesis and nausea returned. Lung auscultation revealed initially crepitation and later coarse rhonch and rales. Chest roentgenogram showed peribronchial infiltration or varying degrees of lung edema. Pulmonary function tests showed a decreased diffusion capacity of the blood-air barrier and arterial hypoxemia. Respiratory insufficiency was indicated by tachypnea, dyspnea, tachycardia, cyanosis and decreased pO2. As lung edema formation increaseed large amounts of frothy sputum were expectorated and hematocrit and hemoglobin concentration increased showing hemoconcentration. Sometimes partial lung atelectasis or emphysema were seen. Some patients had elevated body temperature, metabolic acidosis, impaired hepatic and renal funciton or reduced leucocyte count. Recovery normally was achieved within 1 to 3 weeks. (Reference 457)

(6) /SIGNS AND SYMPTOMS/ Acute Poisoning: Inhalation. Moderate exposure results in mild cough, mucous membrane irritation and ocular irritation. The patient is generally asymptomatic for 30 minutes to 24 hours after exposure. Delayed symptoms then occur including: chest pain, discomfort, thirst, headache, nausea, increased cough with hemoptysis, cyanosis, a feeling of suffocation and dyspnea. Clinical diagnosis by chest x-ray shows diffuse interstitial infiltrates and chest sounds reveal bilateral crackles. The patient develops signs and symptoms secondary to hypoxia and pulmonary edema. Death would result from anoxia. Massive exposures can result in pulmonary intravascular hemolysis, thrombus formation and immediate death due to pulmonary circulation occlusion. (Reference 458)

(7) /SIGNS AND SYMPTOMS/ Acute Poisoning. Skin exposure: Possibility of dermal burning with massive exposures, some dermal irritation with lower exposures. ... Eye contact: Ocular irritation and severe burning. A case of severe exposure to liquid phosgene resulted in corneal opacification. (Reference 459)


(8) /SIGNS AND SYMPTOMS/ Chronic poisoning. ... Inhalation: Symptoms of cough and shortness of breath are occasionally persistent. Documented cases show return to normal limits of lung function within a period of weeks, however complete recovery may take a period of years The inhalation of phosgene may increase the severity of subsequent viral influenza. (Reference 460)

(9) /SIGNS AND SYMPTOMS/ RESPIRATORY: Inhaling low concentrations of phosgene may cause no signs or symptoms initially, or symptoms may be due only to mild irritation of the airways; these symptoms (dryness and burning of the throat and cough) may cease when the patient is removed from exposure. However, after an asymptomatic interval of 30 minutes to 48 hours, in those developing severe pulmonary damage, progressive pulmonary edema develops rapidly with shallow rapid respiration, cyanosis, and a painful paroxysmal cough producing large amounts of frothy white or yellowish liquid. Inadequate, labored respiration, during which abnormal chest sounds are evident, may be accompanied by increased distress and apprehension. Insufficient oxygenation of arterial blood, and massive accumulation of fluid in the lungs may be accompanied by cardiovascular and hematological signs. Exposure to phosgene has been reported to result in Reactive Airway Dysfunction Syndrome (RADS), a chemically- or irritantinduced type of asthma. (Reference 461) (10) /SIGNS AND SYMPTOMS/ CARDIOVASCULAR: Cardiovascular collapse may occur if the patient is severely hypovolemic and hypoxemic from accumulation of fluid in the lungs. Destruction of red blood cells in the pulmonary circulation can cause capillary plugging that leads to strain on the right side of the heart and death. (Reference 462)

(11) /SIGNS AND SYMPTOMS/ DERMAL: If the skin is wet or moist, contact with phosgene vapor can cause irritation and redness of the skin. Contact with liquid phosgene under pressure can result in frostbite. Because of their relatively larger surface area:body weight ratio, children are more vulnerable to toxicants affecting the skin. (Reference 463)

(12) /SIGNS AND SYMPTOMS/ OCULAR: High vapor concentrations cause tearing and increased presence of blood in the eye. Contact with liquid phosgene may result in clouding of the cornea and delayed perforation. (Reference 464)

(13) /SIGNS AND SYMPTOMS/ ... Exposure to gas may cause conjunctival hyperemia, but at irritating concentrations there is automatic protection through blepharospasm, and by far the greatest danger is to the lung. (Reference 465)

(14) /SIGNS AND SYMPTOMS/ The most serious effect of phosgene is lung irritation. Only a relatively small portion of the inhaled gas hydrolyzes in the respiratory passages, but in the moist atmosphere of the terminal spaces of the lungs complete hydrolysis occurs with irritant effects upon the alveolar walls and blood capillaries. The result of this action is a gradually increasing edema, until as much as 30 to 50% of total blood plasma has accumulated in the lung, causing "dry land drowning." the air spaces grow less and less; the blood is thickened by loss of plasma, which results in slowed circulation; oxygen exchange is slowed; and the overworked heart, with insufficient oxygen, weakens. The end result may be either asphyxiation or heart failure and this may be delayed. High concentrations of phosgene are immediately corrosive to lung tissue and result in sudden death by suffocation. (Reference 466)

(15) /SIGNS AND SYMPTOMS/ The danger period usually is 6 to 24 hours after exposure


with the development of peribronchial edema, pulmonary congestion, and alveolar edema, all leading to death from anoxia. The delay is ascribed to slow intrapulmonary hydrolysis of phosgene to hydrogen chloride and chloride. (467) (16) /SIGNS AND SYMPTOMS/ In massive exposures immediate death sometimes results from occlusion of the pulmonary circulation secondary to intravascular hemolysis and thrombus formation. (Reference 468)

(17) /SIGNS AND SYMPTOMS/ Recovery from acute phosgene intoxication is usually complete, however, most victims of severe poisonings complain of chronic symptoms such as shortness of breath on exertion or reduced physical fitness for several months to several years after the accident. In patients where phosgene poisoning has led to chronic disability, the effects are more closely related to smoking habits, psychological disorders, or existing pulmonary abnormalities than to the severity of exposure. Pathological effects to organs other than the lung are rare and are considered to be caused by anoxia, not by a direct action of phosgene. (Reference 469) (18) /SIGNS AND SYMPTOMS/ ... 20 ppm by volume cause lung injuries in 2 min, 25 ppm for as little as 30 minutes is very dangerous, and 90 ppm is rapidly fatal for exposures of 30 minutes or less. (Reference 470)

(19) /SIGNS AND SYMPTOMS/ Exposures exceeding approximately 3 ppm produce acute upper respiratory tract irritation affecting the eyes, nose, throat, and upper portion of the tracheobronchial tree. Progressively increasing phosgene exposures produce tracheitis, bronchitis, and pulmonary edema. (Reference 471) (20) /SIGNS AND SYMPTOMS/ Direct contact with liquid phosgene ... can cause severe burns. (Reference 472)

(21) /SIGNS AND SYMPTOMS/ The irritant properties of phosgene are not sufficient to give warning of hazardous concn. A trained observer can recognize 0.5 ppm as being "sweet" & at about 1 ppm, the odor becomes typical of the "musty or newmown-hay" smell usually ascribed to phosgene. Workers exposed to phosgene can lose their ability to detect low concn through olfactory fatigue. (Reference 473)

(22) /SIGNS AND SYMPTOMS/ In industrial poisoning, 52/82 workers affected. Symptoms: respiratory tract irritation-94%; malaise, nausea and vomiting-54%; headache-40%; burning and lacrimation of eyes and other-30%. Pulmonary edema in 3 persons. (Reference 474)

(23) /SIGNS AND SYMPTOMS/ In November 1966, phosgene was accidentally released from a factory in Japan; 382 people were poisoned and 12 were hospitalized. Signs & symptoms observed in the 12 patients on admission were headache (9), nausea (9), cough (8), dyspnea (7), fatigue (7), pharyngeal pain (5), chest tightness (5), chest pain (5), & fever (3). Lacrimation & redness of the eyes were only observed in one patient. Seven patients showed evidence of pulmonary edema as revealed by chest X-rays 48 hours after the exposure. These findings indicate that pulmonary edema may develop even 48 hours after exposure without initial symptoms of eye or nose irritation. (Reference 475)


(24) /SIGNS AND SYMPTOMS/ Levels of 2 to 5 ppm will induce mild respiratory symptoms, with prolonged exposure to such levels considered dangerous. Exposure to levels greater than 50 ppm are considered massive and will likely be rapidly fatal. At doses of 200 ppm phosgene has been shown to pass through the blood-air barrier and react with the blood constituents to cause clotting. (Reference 476)

(25) CASE REPORTS/ Liquid phosgene splashed in the eyes caused complete opacification of both corneas in one patient, leading ultimately to perforation and formation of symblepharon. (Reference 477)

(26) /CASE REPORTS/ A 30-yr-old male, working in an industrial factory, had accidentally inhaled some phosgene. The exposure evoked intense coughing, sense of suffocating and burning of eyes. He was hospitalized approximately 8 hr later showing respiratory distress, tachypnea, tachycardia, hypotension, and cyanosis. The chest roentgenogram showed pulmonary edema, with patches of bronchopneumonia. Respiratory distress and cyanosis increased and the patient died approximately 41 hr after the phosgene inhalation. The autopsy revealed pulmonary edema and bronchiolar necrosis. The changes were more marked in the lower lobes than in the upper lobes. (Reference 478)

(27) /CASE REPORTS/ A 25-year-old male was exposed to liquid phosgene when a valve ruptured and was admitted 4.5 hr after exposure, with lung edema already apparent. The patient developed a progressive metabolic acidosis and died several h ours after hospitalization. (Reference 479)

(28) /CASE REPORTS/ A male, age 31, was exposed to phosgene when a pipe conducting the gas accidentally ruptured. That evening, he reported to the hospital with signs of acute progressive pulmonary edema and extreme hemoconcentration and leukocytosis. Despite aggressive therapy, the patient died 3.5 hours after admission. (Reference 480)

(29) /SURVEILLANCE/ Six patients /were examined/ 3 to 14 months after phosgene intoxication and ...imparied pulmonary function /was observed/ in all cases, although these decrements varied in type and severity and showed no correlation with the original degree of intoxication. Ten patients were re-examined 3 to 9 years after occupational phosgene poisoning, 5 of them stated that for 1 to 3 years after the intoxication they had experienced symptoms of exertional dyspnea, palpitation, chest oppression, increased perspiration, cough and expectoration. It was concluded that complete recovery after phosgene poisoning may require up to several years. (Reference 481) (30) When inhaled, phosgene travels to the very end of the smallest airways, the bronchioles, and causes damage to these airways. Additionally, it causes damage to the thin membrane that separates the smallest blood vessels (the capillaries) and the air sacs (the alveoli). Phosgene reacts with the proteins and enzymes in these alveolar-capillary membranes to cause damage to the membranes. These membranes usually function to separate the blood the capillaries from the air in the alveoli, but when the membranes are damaged, they cannot do this. Blood, or at least the liquid part of the blood, the plasma, can leak through the damaged membrane into the alveoli. When the plasma leaks into the alveoli, the air sacs become full of fluid, and air cannot enter them. Therefore, exchange of oxygen from the air into the blood is hindered, and the casualty suffers oxygen deprivation. The extent of the lack of oxygen depends on the extent of the phosgene exposure and the number of alveoli filled with


plasma. This is similar to what happens with drowning, in that the alveoli fill up with fluid. However, in this instance, it is fluid from the blood, not from an external source. For this reason, phosgene poisoning is sometimes referred to as dry land drowning. (Reference 482)

(31) ...A severe eye, skin, and mucous membrane irritant. (Reference 483) (32) Because of phosgene's mild upper respiratory, eye, and skin irritancy and mildly pleasant odor, an exposed victim may not actively seek an avenue of escape before lower respiratory damage has occurred. (484)

METHYL CYCLOPENTANE:

(1) The USEPA identified methyl cyclopentane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that chloroform was detected chloroform in the air of the Pathfinders Camp.

(2) New Jersey Department of Health and Senior Services published a web page, entitled:"HAZARDOUS SUBSTANCE FACT SHEET," which provides relevant information regarding the health effects of Methyl Cyclopentane, as follows:

(2.1) The following acute (short-term) health effects may occur immediately or shortly after exposure to Methyl Cyclopentane:

(2.1.1) Contact can irritate the skin and eyes.

(2.1.2) Breathing Methyl Cyclopentane can irritate the nose and throat.

(2.1.3) Exposure can cause you to feel dizzy, lightheaded, and to pass out. Higher levels can cause seizures, unconsciousness, and death.

(2.2) ...Other Long-Term Effects * Methyl Cyclopentane may damage the nervous system.

(Reference 139)

2,3-DIMETHYLPENTANE:

(1) The USEPA identified 2,3-dimethylpentane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that 2.3-dimethylpentane was detected in the air of the Pathfinders Camp.

(2) According to a web page that is published by the government of New Jersey, entitled:


"Right to Know Hazardous Substance Fact Sheet," 2,3-dimethylpentane has health effects of irritation to eyes and skin. If it is inhaled, its health effects include: nose and throat irritation, headache, dizziness, lack of coordination, nausea and vomiting. (Reference 140)

METHYL ISOPROPYL KETONE:

(1) The USEPA identified methyl isopropyl ketone in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that methyl isopropyl ketone was detected in the air of the Pathfinders Camp.

(2) There is a web site provided by the Canadian Centre for Occupational Health and Safety (CCOHS), with relevant information about methyl isopropyl ketone from "The International Programme on Chemical Safety (IPCS)," which says that "Acute Hazards / Symptoms," include the following (quotation marks omitted):

(2.1) Inhalation: Cough. Dizziness. Drowsiness. Dullness. Headache. Sore throat.

(2.2) Skin: Dry skin. Redness.

(2.3) Eyes: Redness. Pain.

(2.4) Ingestion: Abdominal pain. Nausea. (See Inhalation).

(Reference 141)

N-HEPTANE:

(1) The USEPA identified n-heptane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that n-heptane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for n-heptane is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) HEPTANE Synonym: n-heptane 142-82-5

(2.2) /SIGNS AND SYMPTOMS/ Potential symptoms of overexposure are lightheadedness, giddiness, stupor, vertigo, incoordination; loss of appetite, nausea; unconsciousness. Direct contact may cause dermatitis; aspiration of liquid may cause chemical pneumonia. (Reference 142)


(2.3) /SIGNS AND SYMPTOMS/ Concentrations of 4.8% heptane caused respiratory arrest within 3 minutes. Survivors showed marked vertigo and incoordination requiring 30 min for recovery; they also exhibited mucous membrane irritation, slight nausea, and lassitude. A narrow margin exists between the onset of CNS depression or convulsions and cardiac sensitization and recovery or death. (Reference 143)

(2.4) /SIGNS AND SYMPTOMS/ Numerous cases of polyneuritis have been reported, following prolonged exposure to a petroleum fraction containing various isomers of heptane as major ingredients. /Fractionated petroleum/ (Reference 144)

(2.5) /SIGNS AND SYMPTOMS/ In workers exposed to solvent mixtures containing pentane, hexane, and heptane, polyneuropathy was observed, including signs of anorexia, asthenia, paresthesia, fatigue, and bilateral symmetrical muscle paralysis in the legs. /SRP: Polyneuropathy may be due to other components of petroleum distillate./ (Reference 145)

(2.6) /SIGNS AND SYMPTOMS/ Direct skin contact with heptane may cause pain, burning, and itching. (Reference 146)

(2.7) /CASE REPORTS/ Hematological effects in workers exposed to heptane in a rubber tire factory have been reported. These include slight anemia, slight leukopenia, and slight neutropenia. (Reference 147)

N-HEXANE:

(1) The USEPA identified n-hexane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that n-hexane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for n-hexane is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) /HUMAN EXPOSURE STUDIES/ Inhalation of 5000 ppm for 10 minutes produces marked vertigo; 2500-1000 ppm for 12 hours produces drowsiness, fatigue, loss of appetite, paresthesia in distal extremities; 2500-500 ppm produces muscle weakness, cold pulsation in extremities, blurred vision, headache, anorexia, and onset of polyneuropathy. (Reference 148)

(2.2) /HUMAN EXPOSURE STUDIES/ Slightly toxic by ingestion and inhalation. Human systemic effects include: hallucinations, structural change in nerve or sheath... may be irritating to respiratory tract and narcotic in high concentrations. (Reference 149)

(2.3) /HUMAN EXPOSURE STUDIES/ Nerve conduction blocks, defined by a significant reduction in amplitude or area of the compound muscle action potential at proximal compared with


distal sites of stimulation, have been described in glue-sniffers and in workers with industrial exposure at an early stage of n-hexane neuropathy. The frequency with which this focal conduction anomaly appears is described and discussed in the case of a very homogeneous group of 10 young workers diagnosed with n-hexane polyneuropathy. Partial conduction blocks occurred in only two workers and may have been related to the intensity and duration of toxic exposure. (Reference 150)

(2.4) /HUMAN EXPOSURE STUDIES/ ... The study involved 26 workers diagnosed as having polyneuropathy following n-hexane exposure. The FM-100 Hue test was used to determine color discrimination in study volunteers. Their results were compared with a control group of 50 people who had not been exposed to n-hexane. The mean total error score for the exposed group was 168.3 (SD = 70.5) for the right eye and 181.5 (SD = 103.0) for the left eye. The mean total error scores for the control group for the right and left eyes were 36.0 (SD = 19.8) and 35.6 (SD = 18.2), respectively. Differences between total and partial error scores for exposed and control groups were statistically significant (P < 0.001). These results may indicate a relationship between n-hexane exposure and development of defects in color vision, and would support a recommendation for periodic assessment of workers exposed to n-hexane and chemically related solvents. (Reference 151)

(2.5) /HUMAN EXPOSURE STUDIES/ In an offset printing factory with 56 workers, 20 (36%) developed symptomatic peripheral neuropathy due to exposure to n-hexane. Another 26 workers (46%) were found to have subclinical neuropathy. The initial change in the nerve conduction study was reduced amplitude of the sensory action potentials, followed by reduced amplitude of the motor action potentials, reduction in motor conduction velocities and increase in distal latencies. These changes indicate primary axonal degeneration with secondary demyelination. Sural nerve biopsy in a severe case showed giant axonal swellings due to accumulation of 10nm neurofilaments, myelin sheath attenuation and widening of nodal gaps. The development of neuropathy bore no direct relationship to the duration of exposure, hence factors such as individual susceptibility may be important. Optic neuropathy and CNS involvement were uncommon and autonomic neuropathy was not encountered. (Reference 152)

(2.6) /HUMAN EXPOSURE STUDIES/ ... n-Hexane could cause overt polyneuropathy in workers exposed to more than 100 ppm time-weighted average concentrations (TWA). (Reference 153)

(2.7) /HUMAN EXPOSURE STUDIES/ To estimate the quantitative relation between exposure to airborne n-hexane and various markers of immune function, 35 male workers were examined and compared with unexposed controls. Urinary 2,5-hexanedione concentrations were significantly higher in the exposed group than in the unexposed. A significant suppression was observed in the serum immunoglobulin (IgG, IgM and IgA) levels between two populations. Also, a significant correlation was found between urinary 2,5-hexanedione concentrations and serum Ig level of the exposed group. 4. No significant difference between white blood cell counts was found in the two groups. (Reference 154)

(2.8) /HUMAN EXPOSURE STUDIES/... Hexane neuropathy is associated with giant axonal swellings containing accumulations of neurofilaments along the course of the nerve fibers. Nerve fibers degenerate distal to the site of the swelling and myelin loss may occur, producing secondary demyelination. (Reference 155)

(2.9) /HUMAN EXPOSURE STUDIES/ Chronic hexane intoxication has been decribed by


several investigators. The clinical course includes a slow-developing bilateral, symmetrical, sensimotor, and peripheral neuropathy. (Reference 156)

(2.10) /HUMAN EXPOSURE STUDIES/ A ...mild central nervous depressant in acute exposures. ...Vapor causes anesthesia of short duration without sequelae. ...It tends to vaporize when swallowed or aspirated into the tracheobronchial tree. The result can be a rapid dilution of alveolar air and a marked fall in its oxygen content, with asphyxia and consequent brain damage or cardiac arrest. The irritative pulmonary lesions occurring after the aspiration of higher homologues (e.g. octane, nonane, decane, etc) and of mixtures thereof (e.g. kerosene) do not appear to be a problem with... hexane. ...Toxic neuropathies including quadraplegia have occurred among juvenile glue sniffers. (Reference 157)

(2.11) /HUMAN EXPOSURE STUDIES/ ...Solvents such as ...hexane ...may contact the eye in industrial or lab accidents. These substances... dissolve fats. ...They cause pain on contacting the eye, and exam after generous splash of solvent shows dulling of the cornea. ...Damage appears to be scattered loss of epithelial cells due to solution of some of the fats that occur in these cells. (Reference 158)

(2.12) /HUMAN EXPOSURE STUDIES/ 93 of 1662 workers exposed to organic solvents, which consisted mainly of n-hexane and a small amount of toluene, were found to have sensory polyneuropathy (53), sensorimotor polyneuropathy (32), or sensorimotor polyneuropathy with amyotrophy (8). Cranial nerve involvements such as visual disorders and facial numbness were observed. About 50% showed denervation and reinnervation of the nerves. (Reference 159)

(2.13) /HUMAN EXPOSURE STUDIES/ Among 93 cases of n-hexane polyneuropathy during a large outbreak in 1968, 44 were studied. Over a few yr most of the cases completely recovered, except for a few with mild sensory impairment, after providing for 100 ppm as the maximal allowable concn of n-hexane and well equipped ventilation systems in individual houses. During the rescreening in 1981, before which there occurred only 2 pt, 21 cases with mild n-hexane polyneuropathy were observed, revealing mostly the same features as in the previous outbreak in 1968. From these data it may be suggested that, in spite of less than 50 ppm of n-hexane concn in a room, the sandal workers have suffered from neurotoxicity from this organic solvent. (Reference 160)

(2.14) /HUMAN EXPOSURE STUDIES/ Hexane may be the most highly toxic member of the alkanes. ... When ingested, it causes nausea, vertigo, bronchial and general intestinal irritation, and CNS depression. Concns of about 50 g may be fatal to humans. ... In studies in human volunteers, ... exposure to 5,000 ppm for 10 min caused marked vertigo and nausea. (Reference 161)

(2.15) /HUMAN EXPOSURE STUDIES/ ... The more important manifestations, which develop insidiously, are those of chronic peripheral neuropathy. Both sensory and motor symptoms have been reported as the initial manifestation of peripheral nervous system damage. Touch perception seems to be somewhat more impaired than vibratory or position sense. Distal symmetric motor weakness is common in the majority of cases and may progress to involve pelvic and thigh muscles in severely affected persons. ... As with other toxic solvents, deterioration of nerve function may persist for several weeks after removal from exposure to the chemical. (Reference 162)

(2.16) /HUMAN EXPOSURE STUDIES/ Inhalation causes irritation of respiratory tract,


cough, mild depression, cardiac arrhythmias. Aspiration causes severe lung irritation, coughing, pulmonary edema; excitement followed by depression. Ingestion causes nausea, vomiting, swelling of abdomen, headache, depression. (Reference 163)

(2.17) /HUMAN EXPOSURE STUDIES/ Acute inhalation effects of hexane are euphoria, dizziness, and numbness of limbs. (Reference 164)

(2.18) /HUMAN EXPOSURE STUDIES/ Occupational exposures to hexane concns of 1,000-25,500 for 30-60 min caused drowsiness. Two workers at an hexane extraction facility reported transient paraesthesia following excessive acute exposure to hexane. (Reference 165)

(2.19) /HUMAN EXPOSURE STUDIES/ A "stocking and glove" anesthesia that results in sensory impairment and muscular weakness in the feet and hands usually develops. Nerve biopsies show morphological changes of neurofilament-filled axonal swellings and degeneration of the distal axon. There is a marked reduction in conduction velocity in sensory and motor nerves. (Reference 166) (2.20) /HUMAN EXPOSURE STUDIES/ Hexane caused eye lesions in the macula of 11 of 15 workers exposed for 5-21 yr in an adhesive bandage factory. (Reference 167)

(2.21) /CASE REPORTS/ /The case of/ a 55-year-old male parkinsonian patient with chronic exposure to n-hexane for 17 years /is described/. The results of neurophysiological (electromyography, evoked potentials), neuroradiological (MRI) and neuropsychological tests performed on the patient suggest a role of this solvent at the level of the central nervous system. Biological susceptibility to neurotoxic compounds is discussed briefly. (Reference 168)

(2.22) /CASE REPORTS/ This report describes our second case of parkinsonism in a subject exposed to n-hexane. Positron emission tomography studies demonstrated regional striatal abnormalities of the nigrostriatal dopaminergic system and of glucose metabolism that were different from those found in idiopathic Parkinson's disease. (Reference 169)

(2.23) /CASE REPORTS/ ... This report describes the case of a worker who developed peripheral neuropathy, with a histologic pattern characteristic of n-hexane toxicity, after chronic on-the-job exposure to n-hexane at concentrations less than 450 ppm... (Reference 170)

(2.24) /CASE REPORTS/ Three women developed a predominantly motor polyneuropathy following industrial exposure to an adhesive agent containing 80.4% of n-hexane as a volatile substance. Histological and electron-microscopic studies were carried out on sural nerve and on soleus muscle. In the nerve, there were polymorphous changes in both myelin sheaths and axons of large diameter fibres. Irregular and swollen myelin sheaths and segmental swelling of axons with dissolution of neurotubules and evident increase of neurofilaments were frequently observed. Polymorphous inclusion bodies were often present in Schwann cell cytoplasm. The small myelinated and unmyelinated fibres did not show significant changes. The muscles showed denervation atrophy and focal degenerative myopathic changes, with presence of lymphocytic infiltrates and phagocytosis. This study confirms the noxious effect of n-hexane on the peripheral nerve, with development, in our cases, of a toxic polyneuropathy and denervation muscular atrophy with consistent myopathic changes. (Reference 171)


(2.25) /CASE REPORTS/ Electroneurographic (ENeG) and evoked potential (EP) studies were regularly performed on 11 printing workers with n-hexane polyneuropathy after cessation of exposure. At the initial examination, the ENeG studies simulated a demyelinative process. Further slowing of nerve conduction velocity, or further decreasing of action potential amplitude, or both in the follow up ENeG study were found in about half the patients. The motor distal latency did not worsen. Nerve conduction returned to normal earlier in the sensory than in the motor nerves. After the patients had regained full motor capability, conduction velocities in motor nerves were still significantly slowed. These ENeG characteristics correlate with the pathological and pathophysiological changes in experimental hexa-carbon neuropathies. The initial findings from the EP studies indicated a conduction abnormality in the central nervous system (CNS). Delayed worsening occurred in the amplitude of visual EPs in three patients. On serial follow up, the interpeak latency and interpeak amplitude of visual EPs improved little. Residual abnormalities were also found in the interpeak latency of auditory EPs in the brainstem and in the absolute latency of scalp somatosensory EPs from the peroneal nerve. Astroglial proliferation in the CNS probably impedes recovery of the abnormalities in EP. (Reference 172)

(2.26) /CASE REPORTS/ Somatosensory, brainstem auditory and pattern-reversal visual evoked potentials (SEP, BAEP and PVEP) were studied in 5 patients with n-hexane polyneuropathy to determine if the CNS was affected. In SEPs, the median central conduction (N13-to-N20) was normal but the tibial central conduction (N22-to-P40) was delayed. The central conduction time (I-to-V interval) of the BAEP was also prolonged. However, the P100 latency of the PVEP was normal. The present data indicate that the spinal cord and the brainstem are primarily affected in chronic n-hexane intoxication. (Reference 173)

(2.27) /CASE REPORTS/ 3 CASES OF N-HEXANE NEUROPATHY IN SHOE INDUSTRY WERE REPORTED. IN MOST SEVERE CASES SYMPTOMS CONSISTED OF DYSARTHRIA, DISPROPORTIONATE ATAXIA OF GAIT, BLURRED VISION, AND SOMETIMES AFTER RECOVERY OF PERIPHERAL NEUROPATHY, APPEARANCE OF LEG SPASTICITY. (Reference 174)

(2.28) Skin, Eye and Respiratory Irritations: ... Irritation of eyes and nose; dermatitis; aspiration of liquid may cause chemical pneumonia. (Reference 175)

(2.29) Hexane is an irritant to the skin. (Reference 176)

1,1,1-TRICHLOROETHANE:

(1) The USEPA identified 1,1,1-trichloroethane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that 1,1,1-trichloroethane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for 1,1,1-trichloroethane is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site


http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) /SIGNS AND SYMPTOMS/ Inhalation of very high 1,1,1-trichloroethane concentrations for a short period can produce severe cardiac arrhythmias and death in humans. Arrhythmias are thought to be produced indirectly by 1,1,1-trichloroethane by sensitization of the heart to epinephrine. ... In addition, reduced blood pressure, occasionally severe, has been reported in humans following brief exposure to high concentrations of 1,1,1-trichloroethane. Acute exposure to lower concentrations (<1,000 ppm) did not affect clinical cardiovascular parameters such as blood pressure, pulse, heart rate, or electrocardiogram in the humans tested. (Reference 177)

(2.2) /SIGNS AND SYMPTOMS/ Impairment of central nervous system functions is the most characteristic feature of TCE. The earliest symptoms are usually slight impairment of equilibrium and coordination, followed by lassitude and headache. (Reference 178)

(2.3) /SIGNS AND SYMPTOMS/ Some individual variation in susceptibility appears likely at least at lower exposure levels. Early symptoms may include mild eye and nasal discomfort and impairment of equilibrium and coordination. Increased lassitude and headache occur with heavier exposures and in severe poisoning progressive CNS depression occurs. Hepatotoxicity may not become manifest until near-anesthetic levels are reached. Nausea is apparently not common. Several deaths have occurred following industrial exposure in confined spaces and also in the context of solvent abuse ... (Reference 179)

(2.4) /SIGNS AND SYMPTOMS/ Systemic effects: most symptoms and signs reflect the depressant effect on the central nervous system, which include disturbances in equilibrium and coordination, followed by headache and general lassitude. With increasing concentrations there may be progressive drowsiness and disorientation, progressing finally to coma and respiratory arrest. With heavy exposures myocardial depression and hypotension can occur. Cardiac arrhythmia and deaths have occurred. Serious hepatotoxicity is uncommon even with moderately high levels. Following inhalation, mild mucous membrane and upper respiratory tract irritation can occur. Severe irritant effects on the gastrointestinal tract mucosa have been observed following ingestion. Contact dermatitis has been described. (Reference 180)

(2.5) /CASE REPORTS/ Two patients showed evidence of chronic cardiac toxicity after repeated exposure to 1,1,1-trichloroethane. In both cases there was circumstantial evidence of a deterioration after routine anaesthetic use of the related compound halothane. An adolescent boy who sniffed trichloroethane presented with multiple ventricular arrhythmias during tonsillectomy. Follow up showed mild chronic left ventricular impairment. A 54 year old man had repeated industrial exposure to trichloroethane and deteriorated from mild stable cardiac failure to end stage cardiac failure after halothane anaesthesia for herniorrhaphy. Chronic cardiac toxicity is a previously unreported feature of this type of solvent exposure ... (Reference 181)

(2.6) /CASE REPORTS/ A 13-year-old male was found dead in the woods subsequent to 1,1,1-trichloroethane (TCE) inhalation. Autopsy findings included tissue congestion of lung, liver and kidney. ... (Reference 182)

(2.7) CASE REPORTS/ A fatal case of 1,1,1-trichloroethane (methyl chloroform) poisoning, in which the patient survived, without recovering consciousness, for more than 3 years, is described.


The brain showed symmetrical infarction of the lenticular nuclei and of the occipital cortex, changes which may have been the cause of neurological manifestations during life. The pattern of cerebral hypoxia was similar to, but not identical with that found in carbon monoxide poisoning, and might be specific for 1,1,1-trichloroethane poisoning. (Reference 183)

(2.8) CASE REPORTS/ THIS REPORT DESCRIBES A CASE OF NEAR-FATAL INTOXICATION FOLLOWING ACCIDENTAL EXPOSURE OF A CHILD TO 1,1,1-TRICHLOROETHANE. EXPOSURE TO HIGH LEVELS OF THIS SOLVENT WHICH IS WIDELY USED IN INDUST & DOMESTIC PREPN CAN RESULT IN RESP DEPRESSION &/OR DYSRHYTHMIAS. (Reference 184)

(2.9) CASE REPORTS/ Three women developed peripheral neuropathy after frequent, prolonged dermal contact with formulations of 1,1,1-trichloroethane and other chemicals at their workplace. The women initially complained of numbness in their limbs, and subsequent nerve conduction studies showed alterations in peripheral nerve activity. The effect was diagnosed as primarily a distal sensory peripheral neuropathy. These cases were unusual because the effect was greater in the hands than in the feet, the reverse of most peripheral neuropathies. Sural nerve biopsies in two of the women performed 3-4 years after diagnosis revealed chronic neuropathy. (Reference 185)

(2.10) Skin, Eye and Respiratory Irritations: Vapors cause a slight smarting of the eyes or respiratory system if present in high concn. Vapors: Irritating to nose and throat. Liquid: irritating to eyes. (Reference 186)

(2.11) It is an irritant of the skin, eyes, mucous membranes, and upper respiratory tract?It may also cause slight lacrimation. (Reference 187)

3-METHYLHEXANE:

(1) The USEPA identified 3-methylhexane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that 3-methylhexane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for 3-methylhexane is from a Material Safety Data Sheet for 3 methylhexane, published by Scott Specialty Gasses. (Reference 188)

(2.1) ACUTE EFFECTS: Vapor or mist is irritating to the eyes, skin, mucous membranes, and upper respiratory tract. Ingestion of the liquid causes gastrointestinal irritation. Central nervous system (CNS) depression and pulmonary edema may occur. It is an aspiration hazard. Symptoms include burning sensation, coughing, wheezing, shortness of breath, headache, nausea, and vomiting. Loss of consciousness and death due to respiratory failure.

(2.2) CHRONIC EFFECTS: None known


METHYLCYCLOHEXANE:

(1) The USEPA identified methylcyclohexane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that methylcyclohexane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for methylcyclohexane is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) Nervous system disturbances - /CNS depression/. (Reference 189) (2.2) Lightheadedness, drowsiness; ... . (Reference 190)

(2.3) ... IRRITANT & DEFATTING ACTION ON THE SKIN. /CYCLOPARAFFINS/ (Reference 191)

(2.4) Skin, Eye and Respiratory Irritations: Skin irritation; irritation of nose and throat. (Reference 192)

CARBON TETRACHLORIDE:

(1) The USEPA identified carbon tetrachloride in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that carbon tetrachloride was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for carbon tetrachloride is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) Carbon Tetrachloride: reasonably anticipated to be a human carcinogen. (Reference 193)

(2.2) In individuals who have experienced short-term overexposure, delayed effects may include damage to the heart, liver, and kidneys. Symptoms of liver damage may result in jaundice and dark urine. (Reference 194)

(2.3) Acute symptoms: irritation of eyes, nose, throat; headache, dizziness; nausea, vomiting, hematemesis; abdominal cramps, diarrhea; nervousness; dyspnea, cyanosis; oliguria, proteinuria, hematuria; jaundice, hepatomegaly; optic neuritis; unconsciousness, coma; ventricular fibrillation.


Chronic symptoms: dermatitis' anorexia, nausea, vomiting, abdominal pain; apathy, mental confusion; headache, dizziness; fatigue; restriction of visual fields, diminished visual acuity; loss of weight; jaundice; evidence of renal damage. (Reference 195)

(2.4) Carbon tetrachloride vapor is a /CNS depressant/ and causes severe damage to the liver and kidneys. ... In humans the majority of fatalities have been the result of renal injury with secondary cardiac failure. ... Liver damage occurs more often after ingestion of the liquid than after inhalation of the vapor. Human fatalities from acute renal damage have occurred after exposure for at 1/2 to 1 hr to concn of 1000 to 2000 ppm. Cardiac arrhythmias have been reported. (Reference 196)

(2.5) ... A moderate exposure to carbon tetrachloride vapor resulted in a severe acute renal and hepatic failure. The unusual severity of carbon tetrachloride toxicity is best explained by the induction of carbon tetrachloride microsomal activation due to phenobarbital therapy for epilepsy. ... (Reference 197)

(2.6) Greatest number of acute poisonings follow its use in poorly ventilated rooms and are due to inhalation. (Reference 198)

(2.7) Carbon tetrachloride is a CNS depressant. (Reference 199)

(2.8) Carbon tetrachloride in the environment may pose a long-term danger because of its possible carcinogenic potential. In urban and industrial areas where higher concentrations of carbon tetrachloride in the air occur, other toxic effects such as liver and renal damage may result. (Reference 200)

(2.9) THE ODOR IS ONE TO WHICH AVG INDIVIDUAL BECOMES READILY ADAPTED. ... WOULD CERTAINLY NOT BE CONSIDERED A SATISFACTORY WARNING OF EXCESSIVE EXPOSURE. (Reference 201)

(2.10) Three case reports describe the occurrence of liver tumors associated with cirrhosis in people who had been exposed to carbon tetrachloride. A mortality study of laundry and dry-cleaning workers exposed to a variety of solvents suggest excesses of respiratory cancers (17 observed, 10.0 expected), cervical cancers (10 observed, 4.8 expected); liver tumors (4 observed, 1.7 expected) and leukemia (5 observed, 2.2 expected). (Reference 203)

(2.11) Skin, Eye and Respiratory Irritations: ... Prolonged exposure causing irritation of the mucous membrane ... (Reference 204)

(2.12) Eye contact with liquid carbon tetrachloride causes burning and intense irritation. (Reference 205)

TETRACHLOROETHYLENE:

(1) The USEPA identified tetrachloroethylene in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time


obtaining this sampling data then I have had. However, the USEPA publication shows that tetrachloroethylene was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for tetrachloroethylene is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) Tetrachloroethylene: reasonably anticipated to be a human carcinogen. (Reference 206)

(2.2) ... acute hepatic necrosis and oliguric uremia have followed human exposure. (Reference 207)

(2.3) /CNS depressant/ ... in high concentrations. Defatting action on skin can lead to dermatitis. (Reference 208)

(2.4) Excessive exposure ... has resulted in effects on the central nervous system, mucous membranes, eyes, & skin, & to a lesser extent the lungs, liver, kidneys. The effects most frequently noted have been on the nervous system. Unconsciousness, dizziness, headache, vertigo or light ... /CNS depression/ have occurred in many instances after occupational exposures. (Reference 209)

(2.5) Perchloroethylene has been reported to produce effects on the liver in humans. The concn ... generally appeared to be in excess of 100 ppm. (Reference 210)

(2.6) A CASE OF CNS DEPRESSION & 2 CASES OF ACUTE OLIGURIC UREMIA AFTER INHALATION OF PERCHLORETHYLENE VAPORS FROM NEWLY CLEANED CLOTHES IN A SELF-SERVICE DRY-CLEANING MACHINE ARE REPORTED. (Reference 212)

(2.7) A PT IS REPORTED WHO HAD A CONNECTIVE TISSUE TYPE OF DISEASE CLINICALLY SIMILAR TO VINYL CHLORIDE DISEASE, POSSIBLY CAUSED BY ABNORMAL SENSITIVITY TO PERCHLORETHYLENE TO WHICH HE WAS EXPOSED IN HIS OCCUPATION. (Reference 213) (2.8) CHANGES IN NEUROLOGICAL NATURE OF WORKERS EXPOSED TO TETRACHLOROETHYLENE AT GREATER THAN MAC (MAXIMUM PERMISSIBLE CONCENTRATION) WERE RELATED TO DEFECTIVE ACTION OF LIVER & SUPRARENAL GLAND CORTEX. INCR IN AMINOTRANSFERASE IN BLOOD SERUM & SLIGHT SHIFTS IN PROTEINOGRAMS OBSERVED. (Reference 214)

(2.9) SIX WK OLD BREAST-FED INFANT HAD OBSTRUCTIVE JAUNDICE & HEPATOMEGALY. TETRACHLOROETHYLENE WAS DETECTED IN MILK & BLOOD. AFTER DISCONTINUANCE OF BREAST-FEEDING RAPID CLINICAL & BIOCHEM IMPROVEMENT WERE NOTED. (Reference 215)

(2.10) Pulmonary edema occurred in a laundry worker who was found unconscious after exposure to tetrachloroethylene vapor. ... Multiple premature ventricular contractions in otherwise healthy workers have been reported in occupational tetrachloroethylene exposures, but no direct link


with sudden death has been made. Chronic exposure has not produced cardiovascular toxicity. (Reference 217)

(2.11) A 68 year old launderette worker was anesthetised & suffered erythema & 30% superficial burns after spilling a container of tetrachloroethylene over his clothes. The defatting property of tetrachloroethylene would lead to cracking of damaged skin. (Reference 218)

(2.12) A 21 year old man who had been exposed to fumes of tetrachloroethylene developed acute pulmonary edema & became comatose. He received isoprenaline 800 ug in 1 l of dextrose injection iv, furosemide 40 mg, aminophylline 250 mg, & dexamethasone 10 mg iv. Oxygen was admin. After 6 hr, improvement was noted. No evidence of liver or kidney damage was seen. (Reference 219)

(2.13) Acute exposure to tetrachloroethylene by inhalation results in central nervous system depression. Liver & kidney toxicity have been reported as effects of acute exposures to very high doses. In dry cleaners chronically exposed to tetrachloroethylene, incr levels of markers of early renal damage &/or dysfunction were attributed to the exposure. (Reference 220)

(2.14) Skin, Eye and Respiratory Irritations: Eye exposure can lead to conjunctivitis; Skin exposure can lead to inflamation; Inhalation can lead to respiratory tract irritation. (Reference 221)

(2.15) Tetrachloroethylene vapor is a mucous membrane & upper resp irritant at levels above 75 to 100 ppm. (Reference 222)

ETHYLCYCLOHEXANE:

(1) The USEPA identified ethyclyclohexane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that ethyclyclohexane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for ethyclyclohexane is from a web page published by an organization call Environmental Working Group (EWG), which says: "Health Effects related to ethylcyclohexane: Birth or developmental effects, Cancer, Organ system toxicity." (Reference 223)

ETHYLBENZENE:

(1) The USEPA identified ethylbenzene in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that ethylbenzene was detected in the air of the Pathfinders Camp.


(2) This information related to relevant health effects for ethylebenzene is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) PROLONGED EXPOSURE TO ... VAPORS MAY RESULT IN FUNCTIONAL DISORDERS, INCREASE IN DEEP REFLEXES, IRRITATION OF UPPER RESPIRATORY TRACT, HEMATOLOGICAL DISORDERS (LEUKOPENIA AND LYMPHOCYTOSIS, IN PARTICULAR) AND ... HEPATOBILIARY COMPLAINTS. (Reference 224)

(2.2) ... ASPIRATION OF EVEN A SMALL AMT OF ETHYLBENZENE MAY CAUSE SEVERE INJURY, SINCE ITS LOW VISCOSITY AND SURFACE TENSION WILL CAUSE IT TO SPREAD OVER A LARGE SURFACE OF PULMONARY TISSUE. ... (Reference 225)

(2.3) Produces an irritant effect from chronic inhalation at 100 ppm (0.492 mg/L)/8 hr. /From table/ (Reference 226)

(2.4) ... /IT HAS BEEN/ SHOWN THAT CONCN OF 1 MG/L & EVEN 0.1 MG/L MAY BE DANGEROUS & MAY PRODUCE FUNCTIONAL & ORGANIC DISTURBANCES (NERVOUS SYSTEM DISORDERS, TOXIC HEPATITIS & UPPER RESP TRACT COMPLAINTS). CONCN AS LOW AS 0.01 MG/L MAY LEAD TO ... INFLAMMATION OF UPPER RESP TRACT MUCOSA. (Reference 227)

(2.5) Ethyl benzene vapor has a transient irritant effect on human eyes at 200 ppm in air. At 1000 ppm on the first exposure it is very irritating and causes tearing, but tolerance rapidly develops. At 2000 ppm eye irritation and lacrimation are immediate and severe; 5000 ppm causes intolerable irritation of the eyes and nose. (Reference 228) (2.6) ETHYLBENZENE IS MORE VOLATILE THAN STYRENE AND ITS MANUFACTURE IS ACCOMPANIED BY A GREATER HAZARD OF ACUTE POISONING. ... (Reference 229)

(2.7) Skin, Eye and Respiratory Irritations: ... CHARACTERIZED ... AS MOST SEVERE IRRITANT OF THE BENZENE SERIES. (Reference 230)

(2.8) A concn of 200 ppm causes eye irritation. A concn of 100 ppm for 8 hr caused irritative effects in a human. (Reference 231) (2.9) EXPOSURE TO CONCN OF 5000 PPM /24.6 MG/L/ ... CAUSES INTOLERABLE IRRITATION OF EYES, MUCOUS MEMBRANES & NOSE. (Reference 232)

M - XYLENE:

(1) The USEPA identified m-xylene in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data


then I have had. However, the USEPA publication shows that m-xylene was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for m-xylene is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) 3-XYLENE Synonym: m-xylene 108-38-3.

(2.2) /SIGNS AND SYMPTOMS/ Inflammation of the skin and mucous membranes; irritation of respiratory tract; hard to breath, lack of appetite, nausea, vomiting, fatigue, headache, dizziness, incoordination, irritability, CNS depression, anemia; partial paralysis of hands and feet. /m-xylene/ (Reference 233)

(2.3) /SIGNS AND SYMPTOMS/ At high concentrations, xylene vapor may cause severe breathing difficulties which may be delayed in onset. Repeated or prolonged exposure ... may cause a skin rash. /Xylenes/ (Reference 234)

(2.4) Skin, Eye and Respiratory Irritations: Xylene vapor may cause irritation of the eyes, nose, and throat. At high concentrations, xylene vapor may cause severe breathing difficulties which may be delayed in onset. Repeated or prolonged exposure ... may cause a skin rash. /Xylenes/ (Reference 235)

(2.5) Vapor irritates eyes and mucous membranes ... Liquid irritates eyes and mucous membranes. /Xylenes/ (Reference 236)

BENZENE:

(1) The USEPA identified benzene in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that benzene was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for benzene is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) Benzene is classified as a "known" human carcinogen (Category A) under the Risk Assessment Guidelines of 1986. Under the proposed revised Carcinogen Risk Asessment Guidelines (USEPA, 1996), benzene is characterized as a known human carcinogen for all routes of exposure based upon convincing human evidence as well as supporting evidence from animal studies. Epidemiologic studies and case studies provide clear evidence of a causal association between exposure to benzene and acute nonlymphocytic leukemia and also suggest evidence for chronic


nonlymphocytic leukemia and chronic lymphocytic leukemia. Other neoplastic conditions that are associated with an increased risk in humans are hematologic neoplasms, blood disorders such as preleukemia and aplastic anemia, Hodgkin's lymphoma, and myelodysplastic syndrome. These human data are supported by animal studies. The experimental animal data add to the argument that exposure to benzene increases the risk of cancer in multiple species at multiple organ sites (hematopoietic, oral and nasal, liver, forestomach, preputial gland, lung, ovary, and mammary gland). It is likely that these responses are due to interactions of the metabolites of benzene with DNA ... Recent evidence supports the viewpoint that there are likely multiple mechanistic pathways leading ... to leukemogenesis from exposure to benzene. HUMAN CARCINOGENICITY DATA: Benzene is a known human carcinogen based upon evidence presented in numerous occupational epidemiological studies. Significantly increased risks of leukemia, chiefly acute myelogenous leukemia, have been reported in benzene-exposed workers in the chemical industry, shoemaking and oil refineries. ANIMAL CARCINOGENICITY DATA:... many experimental animal studies, both inhalation and oral, also support the evidence that exposure to benzene increases the risk of cancer in multiple organ systems, including the hematopoietic system, oral and nasal cavities, liver, forestomach, preputial gland, lung, ovary, and mammary gland .... (Reference 237)

(2.2) Benzene is irritant to skin, & by defatting the keratin layer may cause erythema, vesiculation, & dry & scaly dermatitis. (Reference 238)

(2.3) AFTER A SHORT EXPOSURE TO A LARGE AMT OF BENZENE, BY INGESTION OR BY BREATHING CONCENTRATED VAPORS, THE MAJOR TOXIC EFFECT IS ON THE CNS. SYMPTOMS FROM MILD EXPOSURE INCL DIZZINESS, WEAKNESS, EUPHORIA, HEADACHE, NAUSEA, VOMITING, TIGHTNESS IN CHEST, & STAGGERING. IF EXPOSURE IS MORE SEVERE, SYMPTOMS PROGRESS TO BLURRED VISION, TREMORS, SHALLOW & RAPID RESP, VENTRICULAR IRREGULARITIES, PARALYSIS, & UNCONSCIOUSNESS. (Reference 239)

(2.4) Long-term exposure to benzene usually is due to the inhalation of vapor or to contact with the skin. Signs and symptoms of long-term exposure to benzene incl effects on the CNS & the GI tract (headache, loss of appetite, drowsiness, nervousness, & pallor), but the major manifestation of toxicity is aplastic anemia. Bone marrow cells in early stages of development are most the sensitive ... & arrest of maturation leads to gradual depletion of circulating cells. (Reference 240)

(2.5) BENZENE (BENZOL) ... HAS SPECIFIC TOXIC EFFECT ON BLOOD FORMATION, CAUSING APLASTIC ANEMIA & TENDENCY TO HEMORRHAGE. OCCASIONALLY HEMORRHAGES IN RETINA & IN CONJUNCTIVA ARE FOUND IN SYSTEMIC POISONING BY BENZENE. IN RARE INSTANCES NEURORETINAL EDEMA & PAPILLEDEMA HAVE BEEN DESCRIBED ACCOMPANYING RETINAL HEMORRHAGES. IT HAS NOT BEEN ESTABLISHED THAT BENZENE CAN INDUCE RETROBULBAR NEURITIS OR OPTIC NEURITIS ... (Reference 241)

(2.6) PATHOLOGICAL FINDINGS FROM ... INHALATION INCL ACUTE GRANULAR TRACHEITIS, LARYNGITIS & BRONCHITIS, MASSIVE HEMORRHAGE OF LUNG, CONGESTIVE GASTRITIS, INFARCT OF SPLEEN, ACUTE CONGESTION OF KIDNEYS, & MARKED CEREBRAL EDEMA. (Reference 242)


(2.7) CHRONIC BENZENE TOXICITY IS EXPRESSED AS BONE MARROW DEPRESSION RESULTING IN LEUCOPENIA, ANEMIA, OR THROMBOCYTOPENIA (LEUKEMOGENIC ACTION). WITH CONTINUED EXPOSURE THE DISEASE PROGRESSES TO PANCYTOPENIA RESULTING FROM BONE MARROW APLASIA. EVIDENCE HAS ACCUM IMPLICATING BENZENE IN THE ETIOLOGY OF LEUKEMIAS IN WORKERS IN INDUSTRIES WHERE BENZENE WAS HEAVILY USED. IT HAS BEEN SUGGESTED THAT LEUKEMIA IS AS FREQUENT A CAUSE OF DEATH FROM CHRONIC BENZENE EXPOSURE AS IS APLASTIC ANEMIA. (Reference 243)

(2.8) MANY CASES OF ACUTE LEUKEMIA DEVELOPING AS TERMINAL STAGE OF APLASTIC ANEMIA RESULTING FROM EXPOSURE TO BENZENE MAY HAVE BEEN MISSED BECAUSE BONE MARROW PUNCTURE WAS NOT PERFORMED. BENZENE LEUKEMIA IS ACUTE STEM CELL OR MYELOBLASTIC LEUKEMIA, SOMETIMES ALEUKEMIA. THERE MAY BE A LATENT PERIOD EXTENDING OVER SEVERAL YEARS BETWEEN CESSATION OF EXPOSURE WITH MORE OR LESS PRONOUNCED ANEMIA, & THE ONSET OF LEUKEMIA. (Reference 244)

(2.9) Diabetes has been linked to benzene exposure. (Reference 281)

(2.10) "...A typical experiment in the presence of active species such as NOx and SO2 showed that benzene photodegradation was considerably accelerated above that in air alone(2). Its half-life in the presence of active species was 4-6 hr with 50% mineralization to CO2 in approximately 2 days(3). Products of degradation include phenol, 2-nitrophenol, 4-nitrophenol, 2,4-dinitrophenol, 2,6-dinitrophenol, nitrobenzene, formic acid, and peroxyacetyl nitrate..." (Reference 411) This apparently means that Joe S. McKinnon and the Kids of the Pathfinders Camp were also exposed to

(2.10.1) 2-nitrophenol

(2.10.2) 4-nitrophenol

(2.10.3) 2,4-dinitrophenol

(2.10.4) 2,6-dinitrophenol

(2.10.5) nitrobenzene

(2.10.6) formic acid

(2.10.7) peroxyacetyl nitrate

2-NITROPHENOL:

This information related to relevant health effects for 2-nitrophenol is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) Symptomatology: 1. Burning pain in mouth & throat. White necrotic lesions in mouth,


esophagus & stomach. Abdominal pain, vomiting ... & bloody diarrhea. 2. Sweating, weakness, headache, dizziness, tinnitus. 3. Shock: Weak irregular pulse, hypotension, shallow respiration, cyanosis, & profound fall in body temp. 4. Possibly fleeting excitement (delirium), followed by unconsciousness. Convulsions are rarely seen except in children. 5. Stertorous breathing, mucous rales, rhonchi, frothing at nose & mouth ... pulmonary edema are sometimes seen. Characteristic odor of phenol on breath. 6. Scanty, dark-colored or "smokey" urine. If death does not occur promptly, moderately severe renal insufficiency may appear. 7. Methemoglobinemia, Heinz bodies, hemolytic anemia and hyperbilirubinemia have been reported occasionally. 8. Death from resp, circulatory or cardiac failure. 9. If spilled on skin, pain is followed promptly by numbness. Skin becomes blanched, & a dry opaque eschar forms over the burn. When eschar sloughs off, a brown stain remains. /Phenol/ (Reference 485)

(2) Inhalation or ingestion causes headaches, drowsiness, nausea, and blue color in lips, ears, and fingernails (cyanosis). ... Contact with eyes causes irritation. ... Can be absorbed through intact skin to give same symptoms as for inhalation. (Reference 486)

(3) ...Dust: irritating to eyes, nose & throat; ... solid: irritating to skin & eyes (Reference 487)

4-NITROPHENOL:

This information related to relevant health effects for 4-nitrophenol is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) Symptomatology: 1. Burning pain in mouth & throat. White necrotic lesions in mouth, esophagus & stomach. Abdominal pain, vomiting ... & bloody diarrhea. 2. Sweating, weakness, headache, dizziness, tinnitus. 3. Shock: Weak irregular pulse, hypotension, shallow respiration, cyanosis, & profound fall in body temp. 4. Possibly fleeting excitement (delirium), followed by unconsciousness. Convulsions are rarely seen except in children. 5. Stertorous breathing, mucous rales, rhonchi, frothing at nose & mouth ... pulmonary edema are sometimes seen. Characteristic odor of phenol on breath. 6. Scanty, dark-colored or "smokey" urine. If death does not occur promptly, moderately severe renal insufficiency may appear. 7. Methemoglobinemia, Heinz bodies, hemolytic anemia and hyperbilirubinemia have been reported occasionally. 8. Death from resp, circulatory or cardiac failure. 9. If spilled on skin, pain is followed promptly by numbness. Skin becomes blanched, & a dry opaque eschar forms over the burn. When eschar sloughs off, a brown stain remains. /Phenol/ (Reference 488)

(2) IN STUDY OF N-ACETOXY-2-ACETYLAMINOFLUORENE-INDUCED REPAIR SYNTHESIS IN HYDROXYUREA-TREATED HUMAN DIPLOID FIBROBLASTS (WI-38), A TUMOR PROMOTER, PHENOL, INHIBITED DNA REPAIR SYNTHESIS ONLY @ HIGH CONCN; THE ANALOG 4-NITROPHENOL DID SO @ MUCH LOWER CONCN. (Reference 489)

(3) POISONINGS ARE ASSUMED TO RESEMBLE BOTH PHENOL & ANILINE. (Reference 490)


(4) Inhalation or ingestion causes headaches, drowsiness, nausea, and blue color in lips, ears, and fingernails (cyanosis). ... Contact with eyes causes irritation. ... Can be absorbed through intact skin to give same symptoms as for inhalation. (Reference 491)

(5) ...Dust: irritating to eyes, nose & throat; ... solid: irritating to skin & eyes (Reference 492)

(6) Irritating to skin, eyes, and respiratory system. (Reference 493)

2,4-DINITROPHENOL:

This information related to relevant health effects for 2,4-dinitrophenol is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) 2,4-DINITROPHENOL Synonym: 2 4 dinitrophenol 51-28-5

(2) SYMPTOMATOLOGY: 1. MARKED FATIGUE, TREMENDOUS THIRST, PROFUSE SWEATING, FLUSHING OF FACE. 2. NAUSEA, VOMITING, ABDOMINAL PAIN AND OCCASIONALLY DIARRHEA. 3. RESTLESSNESS, ANXIETY, EXCITEMENT, OCCASIONALLY LEADING TO CONVULSIONS. 4. A RISE IN BODY TEMPERATURE, WHICH IS ROUGHLY PROPORTIONAL TO THE TOXIC DOSE, MAY CULMINATE IN SEVERE HYPERPYREXIA. 5. TACHYCARDIA, HYPERPNEA, DYSPNEA, CYANOSIS AND SOMETIMES MUSCLE CRAMPS. 6. LOSS OF CONSCIOUSNESS, CESSATION OF BREATHING AND DEATH. 7. LATE COMPLICATIONS: A. DECR URINE OUTPUT WITH ALBUMINURIA, CASTS, PIGMENT, SOMETIMES BLOOD CELLS, DUE TO TOXIC NEPHRITIS. B. JAUNDICE & TENDERNESS IN LIVER REGION DUE TO TOXIC HEPATITIS. 8. OCCASIONAL HYPERSENSITIVITY REACTIONS AFTER REPEATED EXPOSURES (OR IN CHRONIC POISONING) INCLUDE AGRANULOCYTIC ANGINA, SKIN RASHES, PERIPHERAL /NEUROPATHY/ ... AND CATARACT FORMATION. /DINITROPHENOL/ (Reference 494)

(3) IN ACUTE INDUSTRIAL POISONING, NYSTAGMUS /INVOLUNTARY RAPID MOVEMENT OF THE EYE/ ... SAID TO BE PRESENT IN CASES OF MODERATE POISONING, & DILATED PUPILS WERE NOTED IN SEVERE CASES WITH POOR PROGNOSIS. (Reference 495)

(4) In a poisoned person, the result is an almost immediate incr in oxygen consumption, body temp, breathing rate, and heart rate. Because circulation and resp do not accelerate in proportion to the metabolic demand, anoxia and acidosis develop. ... It is a milder corrosive to skin and mucous membranes than phenol, but concentrated soln have produced corrosion of the oropharyngeal, esophageal and gastric mucous membranes. It exerts direct actions on the cerebrum and lower brain centers, consisting of stimulation followed by depression. In the kidney, it may produce necrotizing tubular injury. If the acute phase of poisoning is survived, the patient usually tolerates later complications, which may include renal insufficiency and toxic hepatitis. The fulminating type of poisoning is characterized by sudden onset, severe symptoms, and prompt death (within 24 hours). Death is due to resp or circulatory collapse, especially the former. Many factors undoubtedly contribute to this collapse, notably hyperpyrexia, ... dehydration, muscle rigor (due to heat and/or lactic acid), and


occasionally pulmonary edema. ... In subacute poisoning due to repeated daily exposures, some individuals complain of lassitude, headache, and malaise, while others experience a disarming sense of well-being, energy, and drive. /Dinitrophenol/ (Reference 496)

(5) ESTIMATES OF INCIDENCE OF CATARACTS AMONG PEOPLE TAKING DINITROPHENOL FOR REDUCING /WEIGHT/ VARIED FROM 0.1% TO 1%. ONSET OF CATARACT OCCURRED SEVERAL MO AFTER DRUG HAD BEEN USED. CATARACTS WERE OF UNIFORM SORT OCCURRING IN BOTH EYES, APPEARING FIRST IN ANTERIOR CORTEX AS FINE GRAY CLOUDY OPACITIES ASSOCIATED WITH A SPOTTY LUSTERLESS APPEARANCE OF THE ANTERIOR LENS CAPSULE. IN POSTERIOR CORTEX, GOLDEN GRANULAR OPACITIES APPEARED, WITH POLYCHROMATIC SPECULAR REFLECTIONS. WITH RAPID PROGRESS OF THE CATARACT, THE LENSES BECAME SWOLLEN & EMBRYONIC SUTURE LINES WERE SEPARATED BY DARK CLEFTS. SOON THE WHOLE LENS BECAME OPAQUE WITH MATURE CATARACT. /SRP: NO LONGER USED AS A MEDICINE IN THE USA./ (Reference 497)

(6) /IN ACUTE POISONING FROM INGESTION/ SKIN BECOMES HOT & FLUSHED, & PROFUSE PERSPIRATION, INTENSE THIRST, SEVERE HEADACHE, NAUSEA, VOMITING, ABDOMINAL PAIN, RESTLESSNESS, ANXIETY, DELIRIUM, & GENERALIZED WEAKNESS OCCUR. EXCESSIVE HYPERPYREXIA, ACIDOSIS, & DEHYDRATION MAY BE FOLLOWED BY CIRCULATORY OR RESP COLLAPSE & DEATH. (Reference 498) (7) /FORMER/ TYPICAL TREATMENT REGIMEN FOR WT CONTROL CONSISTED OF 1 CAPSULE CONTAINING 75 MG OF 2,4-DINITROPHENOL OR 100 MG OF THE SODIUM SALT TAKEN 3 TIMES DAILY AFTER MEALS (2-5 MG/KG/DAY). ... NINE DEATHS /REPORTED AS/ RESULTING FROM USE OF DINITROPHENOL AS WT REDUCING AGENT. /SRP: NOT IN CURRENT USE IN THE USA./ (Reference 499)

(8) Hematologic alterations in humans resulting from 2,4-dinitrophenol exposure include hemolytic anemia, neutropenia, and eosinophilia. (500) (9) ... 27 REPORTED CASES OF FATAL OCCUPATIONAL DINITROPHENOL POISONING IN UNITED STATES BETWEEN 1914 & 1916. ... TWO CASES OF DINITROPHENOL POISONING DURING MFR OF PICRIC ACID, WHEN 2,4-DINITROPHENOL WAS PRODUCED AS INTERMEDIATE. (Reference 501)

(10) DUST: POISONOUS IF INHALED OR IF SKIN IS EXPOSED. SOLID: POISONOUS IF SWALLOWED. LIQ OR SOLID IRRITANT CHARACTERISTICS: CAUSES SMARTING OF SKIN & FIRST-DEGREE BURNS ON SHORT EXPOSURE; MAY CAUSE SECOND-DEGREE BURNS ON LONG EXPOSURE. (Reference 502)

(11) DUST & VAPOR OF DINITROPHENOL ... REPORTED TO BE IRRITATING TO MUCOUS MEMBRANE IN INDUSTRIAL EXPOSURE, BUT NO CONTACT INJURIES ... REPORTED. (Reference 503)

(12) 2,4-Dinitrophenol causes maculopapular dermatitis. (Reference 504)


(13) FIRST-DEGREE BURNS ON SHORT EXPOSURE; MAY CAUSE SECOND-DEGREE BURNS ON LONG EXPOSURE. (Reference 505)

(14) Dermatitis may be due to either primary irritation or allergic sensitivity. (Reference 506)

(15) 2,4-Dinitrophenol signs and symptoms are fever/hyperthemia (increased metabolic rate), skin discoloration (pseudojaundice), acidosis (metabolic, delayed), hypotension, cataract (subcapsular), hearing impairment (delayed). (Reference 507) 2,6-DINITROPHENOL:

This information related to relevant health effects for 2,6-dinitrophenol is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) 2,6-DINITROPHENOL Synonym: 2 6 dinitrophenol 573-56-8

(2) Dermatitis results from skin contact. Cataracts may be produced. A fatal dose in adults is 1 to 3 g by mouth. Symptoms incl headache, loss of appetite, vomiting, abdominal pain, diarrhea, fever, chest pains, dizziness, fatigue, jaundice, leg cramps, cyanosis, anxiety, pulmonary edema, convulsions. (Reference 508)

(3) Miscellaneous hazards in the use of dinitrophenol include neutropenia, agranulocytosis, and cataract formation. (Reference 509)

(4) Highly toxic; absorbed by skin. Dust inhalation may be fatal. /Dinitrophenol/ (Reference 510)

(5) 2,4-dinitrophenol does not produce methemoglobin, but the 2,3-, 2,5-, 2,6-, and 3,4-isomers do produce it. (Reference 511)

(6) ...Dust and vapor of dinitrophenol have been reported to be irritating to mucous membrane in industrial exposure ... . /Dinitrophenol/ (Reference 512)

FORMIC ACID:

This information related to relevant health effects for formic acid is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) Signs and symptoms from accidental or intentional overdoses (50 g or more) are salivation, vomiting, a burning sensation in the mouth and pharynx, and severe pain. Circulatory collapse may follow, causing death. Ingestion of; or skin contact with, smaller quantities of formic acid may produce ulceration of membranes. Contact with eyes may cause permanent scarring of the cornea. Dilute solutions (eg, 10%) appear to be noncorrosive. (Reference 513)


(2) SIGNS AND SYMPTOMS/ Chronic absorption has been reported to cause albuminuria, hematuria. (Reference 514)

(3) /SIGNS AND SYMPTOMS/ Principal hazard is that of severe primary damage to skin, eye or mucosal surface. Sensitization is rare, but may occur in person previously sensitized to formaldehyde. (Reference 515)

(4) /SIGNS AND SYMPTOMS/ Lacrimation, increased nasal discharge, cough, throat discomfort, erythema, and blistering may occur depending upon solution concentrations. (Reference 516)

(5) /SIGNS AND SYMPTOMS/ Extensive exposure can result in depressive effects to the central nervous system (CNS), like visual and mental disturbances. After oral intake... severe acidosis... and nephropathy may occur. (Reference 517)

(6) /SIGNS AND SYMPTOMS/ Accidental or intentional overdoses (50 g or more) are reported to produce salivation, vomiting, a burning sensation in the mouth and pharynx, diarrhea, and severe pain. Circulatory collapse may follow, causing death. (Reference 518)

(7) /CASE REPORTS/ A worker who had suffered splashes of hot formic acid to his face developed marked dyspnea with difficulty in swallowing, inability to speak, and died 6 hours later. (Reference 519)

(8) /CASE REPORTS/ 45 cases of ingestion of formic acid were described. Abdominal pain, vomiting, hematemesis, dysphagia, dyspnea, burns in the gastrointestinal tract with subsequent strictures, coagulation disorders, pneumonia, acute kidney failure and hepatic dysfunction occurred. After ingestion of 45-200 g formic acid, 9 of 16 patients died after perforations in the gastrointestinal tract and 5 died of acute kidney failure. (Reference 520)

(9) /CASE REPORTS/ A case in which a patient sustained an inhalation injury as a result of aerosolized formic acid is reported. The patient sustained a partial thickness burn to the face from a chemical spray; however, as a result of aerosolization, he also inhaled formic acid. This resulted in a reversible pulmonary chemical injury. Inhalation of formic acid results in a reactive airway dysfunction syndrome, a common response to inhalation of an occupational irritant. (Reference 521)

(10) A skin and severe eye irritant. (Reference 522) PEROXYACETYL NITRATE:

This information related to relevant health effects for formic acid is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) /SIGNS AND SYMPTOMS/ In humans, the lowest level causing eye irritation was 0.64 mg/cu m for 2 hr. (Reference 523)


(2) /SIGNS AND SYMPTOMS/ Peroxyacetyl nitrate (PAN) is a ubiquitous air pollutant formed from NO(2) reacting with acetoxy radicals generated from ambient aldehydes in the presence of sunlight and ozone. It contributes to eye irritation associated with photochemical smog and is present in most urban air. (Reference 524)

PHENOL:

This information related to relevant health effects for cyclohexane is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) Toxicity Summary: HUMAN TOXICITY: Phenol is toxic with a probable oral lethal dose to humans of 50-500 mg/kg. Some individuals may be hypersensitive with lethality or serious effects at very low exposures. Rapid absorption and severe systemic toxicity can occur after any route of exposure including skin. Death and severe toxicity are usually due to effects on the CNS, heart, blood vessels, lung, and kidneys. However, toxic manifestations may vary somewhat with the route. Observed effects from acute exposure may include: shock, delirium, coma, pulmonary distress, phenolic breath, scanty/dark urine, and death. Protracted or chronic exposure usually results in major damage to the liver, kidneys and eyes. Pigmentary changes of the skin have been noted. Consumption of water contaminated with phenol resulted in diarrhea, mouth sores, burning of the mouth, and dark urine. Phenol is highly caustic to tissues. Skin exposure results in pain, then numbness, blanching, severe burns, and eschar formation. Ingestion leads to burning of throat and severe gastrointestinal inflammation. Inhalation can result in pulmonary irritation and edema. ANIMAL TOXICITY: Toxicity in animals is similar to that of humans, although additional effects have been observed. LD50's in animals range from 250-500 mg/kg, differing very little with route of exposure or species, except for the cat which is unusually susceptible with an oral lethal dose of 80 mg/kg. Additional reported toxic effects include irritation and corrosivity of skin and eyes in rabbits, induction of skin tumors in mice, reproductive effects in rats, and mutagenicity with Salmonella, E coli and Drosophila. Phenol is also highly toxic to aquatic life and frogs. METABOLISM: Phenol is metabolized and excreted principally by the kidneys as the sulfate or glucuronide, although some phenol may be excreted unchanged, especially at high doses. Other reported metabolites include hydroquinone, other quinones and catechols. (Reference 552)

(2) /SIGNS AND SYMPTOMS/ SYMPTOMATOLOGY: Burning pain in mouth and throat. White necrotic lesions in mouth, esophagus and stomach. Abdominal pain, vomiting ... and bloody diarrhea. Pallor, sweating, weakness, headache, dizziness, tinnitus. Shock: Weak irregular pulse, hypotension, shallow respirations, cyanosis, pallor, and a profound fall in body temperature. Possibly fleeting excitement and confusion, followed by unconsciousness ... Stentorous breathing, mucous rales, rhonchi, frothing at nose and mouth and other signs of pulmonary edema are sometimes seen. Characteristic odor of phenol on the breath. Scanty, dark-colored ... urine ... moderately severe renal insufficiency may appear. Methemoglobinemia, Heinz body hemolytic anemia and hyperbilirubinemia have been reported ... Death from respiratory, circulatory or cardiac failure. If spilled on skin, pain is followed promptly by numbness. The skin becomes blanched, and a dry opaque eschar forms over the burn. When the eschar sloughs off, a brown stain remains. (Reference 553)

(3) /CASE REPORTS/ Several cases of sudden death or intra- or postoperative complications


have been reported after phenol face peels ... . (Reference 554)

(4) /CASE REPORTS/ Major cardiac arrhythmias were noted ... in 10 out of 43 patients during phenol face peels. (Reference 555)

(5) /CASE REPORTS/ 14 mg/kg resulted in GI effects, and ingestion of 140 mg/kg caused death. (Reference 556)

(6) /CASE REPORTS/ ... 1 ounce of 89% phenol was mistakenly given in a measured container to an outpatient. ... The patient immediately ... collapsed. Within 30 min she had an unrecordable blood pressure and sustained respiratory arrest. ... The patient experienced ventricular tachycardia 1 hr post-ingestion, and resuscitation was effected ... over first 24 hr ... ventricular arrhythmias, seizures, and metabolic acidosis. ... Subsequent esophagitis and gastrointestinal bleeding occurred. The patient survived. ... (Reference 557)

(7) /CASE REPORTS/ ... A 32 yr old male ... spilled a solution of phenol over his scalp, face, neck, shoulders and back. The victim died 10 min later. There was coagulation necrosis of the skin and left eye and acute dermatitis veneta with acute passive congestion of the lungs, liver, spleen, and kidneys. (Reference 558)

(8) /CASE REPORTS/ An employee accidentally spilled 4-5 liters of 78% aq phenol on himself. Following immediate irrigation with alcohol, he exhibited superficial skin burns, became comatose and died shortly thereafter. (Reference 559)

(9) /CASE REPORTS/ A 19 yr old female ingested 15 ml of phenol and complained of severe nausea, burning in the throat, and epigastrium. Laryngoscopic exam revealed superficial burns and slight edema of the hypopharynx. Despite gastric lavage with olive oil and iv saline admin, she continued to be nauseated. One hr later she began to vomit blood and to have diarrhea, passing copious amounts of blood with clots. She gradually became cyanotic and stuporous. Her blood pressure decreased markedly and her extremities became cold. She experienced periods of relapse and recovery during treatment but died 17.5 hr after ingestion. (Reference 560)

(10) /CASE REPORTS/ Chronic systemic absorption of phenol has caused gray coloration of the sclera with brown spots near the insertion of rectus muscle tendons, associated with blue or brown discoloration of the tendons over the knuckles of the hands. This is a form of ochronosis, known as carbolochronosis, of which 20 cases ... /were reported/ up to 1942... . (Reference 561)

CYCLOHEXANE:

(1) The USEPA identified cyclohexane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that cyclohexane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for cyclohexane is from the "Hazardous


Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) HIGH CONCENTRATIONS MAY ACT AS A ... /CNS DEPRESSANT/, SKIN IRRITANT. (Reference 245)

(2.2) VAPOR CAUSES WEAK ANESTHESIA OF BRIEF DURATION BUT MORE POTENT THAN HEXANE. (Reference 246) (2.3) Skin, Eye and Respiratory Irritations: The vapor is irritating to the skin, eyes, and respiratory tract. (Reference 247)

TOLUENE:

(1) The USEPA identified toluene in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that toluene was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for toluene is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) ... TOLUENE CAUSES DEFATTING OF SKIN WITH SUBSEQUENT DANGER OF DRYNESS, FISSURING AND SECONDARY INFECTION. (Reference 248)

(2.2) ... SUDDEN DEATH AMONG "SNIFFERS" MAY BE ATTRIBUTED TO LETHAL CARDIAC ARRHYTHMIAS FOLLOWING SENSITIZATION OF THE MYOCARDIUM. (Reference 249)

(2.3) VAPORS OF TOLUENE CAUSE NOTICEABLE SENSATION OF IRRITATION TO HUMAN EYES AT 300-400 PPM IN AIR, BUT EVEN AT 800 PPM IRRITATION IS SLIGHT. ... IN HUMAN VOLUNTEERS EXPOSED TO CONCN AS HIGH AS 800 PPM ... DILATION OF PUPILS & IMPAIRMENT OF REACTION IN ASSOCIATION WITH FATIGUE AT END OF 8 HR, ALSO SLIGHT PALLOR OF FUNDI. (Reference 250)

(2.4) WORKERS IN PHARMACEUTICAL PLANT IN FRANCE EXPOSED TO TOLUENE DEVELOPED LEUKOPENIA, & NEUTROPENIA. WITHIN 6 MO, THOSE AFFECTED SHOWED INCR IN CLOTTING TIME & DECR IN PROTHROMBIN LEVEL ... (Reference 251) (2.5) PERIPHERAL BLOOD LYMPHOCYTES FROM 32 MALE ROTOGRAVURE WORKERS SHOWED NO SIGNIFICANT DIFFERENCE FROM CONTROLS IN FREQUENCY OF CHROMOSOME ABERRATIONS & SISTER CHROMATID EXCHANGES. (252)


(2.6) Patients (3) with history of recurrent toluene abuse were hospitalized and severe metabolic acidosis, electrolyte abnormalities, hypoalkemia, and muscular weakness were present. Distal renal tubular acidosis was believed to be present in 2/3 patients. (Reference 253)

(2.7) Child of a mother with a 14 year history of solvent abuse showed symptoms of fetal alcohol syndrome. (Reference 254) (2.8) A 27-year-old male developed cerebral and cerebellar atrophy over a period of five years of extensive glue sniffing. He also developed bilateral optic atrophy with blindness and severe sensorineural hearing loss. (Reference 255)

(2.9) Vapors irritate eyes and upper respiratory tract; Cause dizziness, headache, anesthesia, and respiratory arrest. Liquid irritates eyes. If aspirated, causes coughing, gagging, distress, and rapidly developing pulmonary edema. If ingested causes vomiting, griping, diarrhea, and depressed respiration. Kidney and liver damage may follow ingestion. (Reference 256)

(2.10) General health effects include lethality, growth, morbidity, liver and kidney damage and miscellaneous effects. Neurobehavioral effects include epidemiological and clinical findings, activity and sleep, performance and learning, electrophysiological effects. Evaluation and synthesis of data is included. It was concluded that low level exposure to toluene has its primary effect on the CNS. From a systematic or general point of view it is not clear what this effect is. Both depressant and excitatory effects (possibly concentration dependent) were reported as well as other kinds of results. Other health effects were not life threatening at any exposure level short of that producing lethality. Effects were reversible even at extremely high exposure levels for very long durations. (Reference 257)

(2.11) Toluene embryopathy is characterized by microcephaly, central nervous system dysfunction, attentional deficits and hyperactivity, developmental delay with greater language deficits, minor craniofacial and limb anomalies, and variable growth deficiency. Previously, three affected children, born to women who inhaled toluene regularly throughout pregnancy, have been reported. Two more cases are described emphasizing the importance of toluene as a potential human teratogen. (Reference 258)

(2.12) Toxicities associated with toluene: CNS depression, syncope, coma, cardiac arrhythmias and sudden death, ataxia, convulsions, rhabdomyolysis, increased creatine phosphokinase, abdominal pain, nausea, vomiting, hematemesis, peripheral neuropathy, paresthesias, encephalopathy, optic neuropathy, cerebella ataxia, distal renal tubular acidosis, hyperchloremia, hypokalemia, azotemia, hypophosphatemia, hematuria, proteinuria, pyruria, normalities, decreased cognitive function, fatal overdose. /From table/ (Reference 259) (2.13) Children with microcephaly, minor craniofacial and limb anomalies, central nervous system defects, attention disorders, developmental delay, learning disorders, and language deficits were born to mothers who abuse toluene by inhalation during pregnancy. (Reference 260)

(3) A web page, published by an organization called "Oxford Journals," has some relevant information in what appears to be a summary of an article, which says: "Hypothalamic Syndrome and Central Sleep Apnoea Associated with Toluene Exposure...From the University Department of Medicine, Western General Hospital Crewe Road South, Edinburgh EH4 2XU *Paediatric Department,


Victoria Hospital Hayfield Road, Kirkcaldy, Edinburgh EH52 5SB Department of Respiratory Medicine, City Hospital 51 Greenbank Drive, Edinburgh EH52 5SB Accepted for publication 13 September 1990. We describe a young man who developed extensive hypothalamic dysfunction including diabetes insipidus, adipsia, hyperprolactinaemia, and poikiliothermia together with central sleep apnoea following exposure to toluene.

(4) Nathanael J McKeown, DO, Assistant Professor, Oregon Health and Science University; Medical Toxicologist, Oregon Poison Center; Attending Physician, Emergency Medicine, Portland Veteran Affairs Medical Center, Oregon Health and Science University is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, and Wilderness Medical Society. (Reference 319) He provides relevant information about the toxicity of toluene, which is, as follows (quotation marks omitted):

(4.1) ...Occupational asthma has occurred in some workers exposed to toluene levels considered safe in the workplace...

(4.2) Central nervous system

(4.2.1) Acute intoxication from inhalation is characterized by rapid onset of CNS symptoms including euphoria, hallucinations, delusions, tinnitus, dizziness, confusion, headache, vertigo, seizures, ataxia, stupor, and coma.

(4.2.2) Chronic CNS sequelae include neuropsychosis, cerebral and cerebellar degeneration with ataxia, seizures, choreoathetosis, optic and peripheral neuropathies, decreased cognitive ability, anosmia, optic atrophy, blindness, ototoxicity, and deafness.

(4.3) ...Toluene has direct negative effects on cardiac automaticity and conduction and can sensitize the myocardium to circulating catecholamines. "Sudden sniffing death" secondary to cardiac arrhythmias has been reported. Pulmonary effects include bronchospasm, asphyxia, acute lung injury (ALI), and aspiration pneumonitis.

(4.4) Gastrointestinal[:] GI symptoms from inhalation and ingestion may result in abdominal pain, nausea, vomiting, and hematemesis. Hepatotoxicity manifests with ascites, jaundice, hepatomegaly, and liver failure...

(4.5) ...Reported renal toxicity from toluene exposure includes renal tubular acidosis (RTA), hypokalemia, hypophosphatemia, hyperchloremia, azotemia, sterile pyuria, hematuria, and proteinuria.

(4.6) Hematologic consequences of exposure may include lymphocytosis, macrocytosis, eosinophilia, hypochromia, and basophilic stippling, and in severe cases, aplastic anemia.

(4.7) ...contact with skin may range in severity from dermatitis to extensive chemical burns with coagulation necrosis.

(4.8) Toluene can affect skeletal muscles directly, resulting in rhabdomyolysis and myoglobinemia. Profound hypokalemia due to RTA can produce severe muscle weakness mimicking


Guillain-Barré syndrome. In animal studies, chronic inhalational exposure to toluene was found to affect bone metabolism, contributing to bone resorption and inhibition of bone formation.6

(4.9) Prolonged exposure to toluene by inhalation is associated with CNS, heart, liver, kidney, and lung damage. Other sequelae include muscle weakness, nasal ulcerations, recurrent epistaxis, chronic rhinitis, neuropsychiatric abnormalities, GI symptoms, and peripheral neuropathies

HEXANAL:

(1) The USEPA identified hexanal in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that hexanal was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for hexanal is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) ...The increased concentrations of lower molecular weight aldehydes, including hexanal, may interfere with cholesterol transport and gap junctional intercellular communication. (Reference 261)

(2.2) Skin, Eye and Respiratory Irritations: Vapor: irritating to eyes, nose & throat...Liquid: irritating to skin & eyes. (Reference 262)

P-XYLENE:

(1) The USEPA identified p-xylene in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that p-xylene was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for p-xylene is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) 4-XYLENE Synonym: p-xylene 106-42-3

(2.2) /SIGNS AND SYMPTOMS/ Conjunctivitis, dermatitis, irritation to respiratory tract, dyspnea, anorexia, nausea, vomiting, fatigue, headache, vertigo (dizziness), incoordination, irritation, gangrene, anemia. (Reference 263)


(2.3) /SIGNS AND SYMPTOMS/ Inflammation of the skin and mucous membranes; irritation of respiratory tract; /difficulty breathing/, lack of appetite, nausea, vomiting, fatigue, headache, dizziness, incoordination, irritability, CNS depression, anemia; partial paralysis of hands and feet. /m-xylene/ (Reference 264)

(2.4) /SIGNS AND SYMPTOMS/ Vapor irritates eyes and mucous membranes and may cause dizziness, headache, nausea, and mental confusion. Liquid irritates eyes and mucous membranes. Swallowing or absorption through skin would cause poisoning. Prolonged exposure to skin contact may result in dermatitis. /xylenes/ (Reference 265)

(2.5) /SIGNS AND SYMPTOMS/ Human data indicate that acute inhalation exposures to 460 ppm mixed xylene and 100 ppm p-xylene vapors produce mild and transient eye irritation ... . This effect is probably the result of direct contact of the xylene vapor with the eye. (Reference 266)

(2.6) /SIGNS AND SYMPTOMS/ At high concentrations, xylene vapor may cause severe breathing difficulties which may be delayed in onset. Repeated or prolonged exposure ... may cause a skin rash. /Xylenes/ (Reference 267) (2.7) Skin, Eye and Respiratory Irritations: Xylene vapor may cause irritation of the eyes, nose, and throat. /Xylenes/ (Reference 268)

(2.8) Vapor irritates eyes and mucous membranes ... Liquid irritates eyes and mucous membranes. /Xylenes/ (Reference 269)

(2.9) Human data indicate that acute inhalation exposures to 460 ppm mixed xylene and 100 ppm p-xylene vapors produce mild and transient eye irritation ... . This effect is probably the result of direct contact of the xylene vapor with the eye. (Reference 270)

N-HEPTANAL:

(1) The USEPA identified n-heptanal in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that n-heptanal was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for n-heptanal is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) /SIGNS AND SYMPTOMS/ ... The halogenated aliphatic aldehydes, and the unsaturated aldehydes are particularly irritating. The mucus membranes of the nasal and oral passages and the upper respiratory tract are affected, producing a burning sensation, an increased ventilation rate, bronchial constriction, choking, and coughing. The eyes tear, and a burning sensation is noted on the skin of the face. During low exposures, the initial discomfort may abate after 5 to 10 minutes but will


recur if exposure is resumed after an interruption. /Aldehydes/ (Reference 271)

(2.2) Skin, Eye and Respiratory Irritations: ... The halogenated aliphatic aldehydes, and the unsaturated aldehydes are particularly irritating. The mucus membranes of the nasal and oral passages and the upper respiratory tract are affected, ... . /Aldehydes/ (Reference 271)

N-UNDECANE:

(1) The USEPA identified n-undecane in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that n-undecane was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for n-undecane is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) /HUMAN EXPOSURE STUDIES/ Direct aspiration into the lungs of paraffins with carbon numbers C6 to C16 may cause chemical pneumonitis, pulmonary edema, and hemorrhaging. /C6-C16 Aliphatic hydrocarbons/ (Reference 272)

(2.2) /HUMAN EXPOSURE STUDIES/ Exposure to undecane during industrial use causes eye and skin irritation. It is irritating to mucous membranes and the upper respiratory tract. (Reference 273)

PROPANAL:

(1) The USEPA identified propanal in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that propanal was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for propanal is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) PROPIONALDEHYDE Synonym: propanal 123-38-6

(2.2) /HUMAN EXPOSURE STUDIES/ In an experimental study with humans, irritation of the eyes and upper respiratory tract commenced at 14 to 16 mg/cu m. (525)


(2.3) /HUMAN EXPOSURE STUDIES/ Twelve Asian volunteers were patch-tested with propionaldehyde applied to the forearm for 5 minutes. The skin reaction was observed for 60 minutes; all 12 volunteers developed erythema with 5 exhibiting strong erythema and 7 exhibiting weak erythema. (Reference 526)

(2.4) /HUMAN EXPOSURE STUDIES/ Three Asian subjects who reported experiencing severe facial flushing in response to ethanol ingestion were subjects of patch testing to aliphatic alcohols and aldehydes. An aqueous suspension of 75% (v/v) of each alcohol and aldehyde was prepared and 25 uL was used to saturate ashless grade filter paper squares which were then placed on the forearm of each subject. Patches were covered with Parafilm and left in place for 5 minutes when the patches were removed and the area gently blotted. Sites showing erythema during the next 60 minutes were considered positive. All three subjects displayed positive responses to ethyl, propyl, butyl, and pentyl alcohols. Intense positive reactions, with variable amounts of edema, were observed for all the aldehydes tested (valeraldehyde as well as acetaldehyde, propionaldehyde, and butyraldehyde). (Reference 527)

(2.5) /SIGNS AND SYMPTOMS/ The vapor may cause respiratory irritation but is not a strong enough irritant of eyes or respiratory tract to be considered significant factor in smog. (Reference 528)

(2.6) /SIGNS AND SYMPTOMS/ Aldehydes increase airflow at concentrations below those that decrease respiratory frequency. /Aldehydes/ (Reference 529)

(2.7) /SIGNS AND SYMPTOMS/ Irritates the skin causing a burning sensation and rash on contact. Inhalation can irritate the respiratory tract and may cause nosebleeds, sore throat, cough and phlegm. Higher exposures can cause pulmonary edema, a medical emergency that can be delayed for several hours. This can cause death. Long term exposure: Can irritate the lungs; bronchitis may develop. (Reference 530)

(2.8) /GENOTOXICITY/ There was one report of a weak positive increase in the incidence of sister-chromatid exchange (SCE) in an in vitro human lymphocyte assay that failed to meet the criteria of either a three-point monotonic dose-response or a doubling of the SCE frequency above its appropriate negative control. (Reference 531)

(2.9) Irritating to skin, eyes, and respiratory system. (Reference 532)

PENTANAL:

(1) The USEPA identified pentanal in air samples taken from the top of the "Parker's Chapel Water Tower," which was on my grandparents' 40 acres of land that we used for the Pathfinders Camp. The USEPA owns the sampling data that would show the amount detected, but appears to have lost it. I believe that the FBI and U.S. Attorneys Office would have an easier time obtaining this sampling data then I have had. However, the USEPA publication shows that pentanal was detected in the air of the Pathfinders Camp.

(2) This information related to relevant health effects for pentanal is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000


chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(2.1) /HUMAN EXPOSURE STUDIES/ Three Asian subjects who reported experiencing severe facial flushing in response to ethanol ingestion were subjects of patch testing to aliphatic alcohols and aldehydes. An aqueous suspension of 75% (v/v) of each alcohol and aldehyde was prepared and 25 uL was used to saturate ashless grade filter paper squares which were then placed on the forearm of each subject. Patches were covered with Parafilm and left in place for 5 minutes when the patches were removed and the area gently blotted. Sites showing erythema during the next 60 minutes were considered positive. All three subjects displayed positive responses to ethyl, propyl, butyl, and pentyl alcohols. Intense positive reactions, with variable amounts of edema, were observed for all the aldehydes tested (valeraldehyde as well as acetaldehyde, propionaldehyde, and butyraldehyde). (Reference 533) (2.2) /SIGNS AND SYMPTOMS/ /CNS depressant/ and irritation common to aldehydes, but they are mild. (Reference 534)

(2.3) /SIGNS AND SYMPTOMS/ Exposure at high levels can cause you to feel dizzy and lightheaded. Poisonous if swallowed. (Reference 535)

(2.4) Vapor may irritate eyes. (Reference 536)

(2.5) "Pentanal does contain chromophores that absorb at wavelengths >290 nm(4) and will undergo photodegradation to form propene, vinyl alcohol and ethanal." (Reference 410). Ethanal is a synonym for acetaldehyde. Acetaldehyde is already listed in the USEPA study. This apparently means that Joe S. McKinnon and the Kids of the Pathfinders Camp were also likely exposed to:

(5.1) propene, which is a synonym for propylene

(5.2) vinyl alcohol, which is a synonym for vinyl acetate

PROPYLENE:

/HUMAN EXPOSURE STUDIES/ At a concentration of 6.4% for 2.25 min, mild intoxication, paresthesias, and inability to concentrate /have been/ noted. However, memory was not impaired. At 12.8% in 1 min, the same symptoms were markedly accentuated and at 24 and 33% unconsciousness followed in 3 min. Human exposure to 23% propylene for 3 to 4 min however did not produce unconsciousness (http://toxnet.nlm.nih.gov). (Reference 438) VINYL ACETATE:

This information related to relevant health effects for vinyl acetate is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):


(1) SIGNS AND SYMPTOMS/ Factory workers exposed to vinyl acetate showed gradual deterioration of heart muscles, arrhythmias, amplitude decrease in electrocardiogram, and recognized myocardium dystrophies, fainting spells, pain around the heart area, and a sensation of dying. (Reference 537)

(2) /SIGNS AND SYMPTOMS/ Industrial experience has revealed severe irritation of skin with blister formation. (Reference 538)

(3) /CASE REPORTS/ One case of burn of a human cornea has been listed as returned to normal in less than forty-eight hours. (Reference 539)

(4) /EPIDEMIOLOGY STUDIES/ A nested case-control study was undertaken in a cohort of 29139 men employed in two chemical manufacturing facilities and a research and development center, who had died in 1940-1978 with non-Hodgkin`s lymphoma, multiple myeloma, lymphocytic or nonlymphocytic leukemia. Exposure odds ratios (OR) were examined in relation to 111 work areas, 21 specific chemicals (OR based on an ever/never basis), and 52 chemical activity groups. Exposure to vinyl acetate was associated with non-Hodgkin's lymphoma in seven of 52 men (OR 1.2), multiple myeloma in three of 20 men (OR 1.6), non-lymphocytic leukemia in two of 39 men (OR 0.5), and with lymphocytic leukemia in two of 18 men (OR 1.8). Examination of OR related to the exposure duration was not done because of the OR /less than/ 1.3 or number of cases /less than/ 4. (Reference 540)

(5) /EPIDEMIOLOGY STUDIES/ A cross-sectional epidemiologic study of vinyl acetate operators in a chemical plant revealed that the workers were exposed to an average concentration of 5 to 10 ppm vinyl acetate with potential acute exposures at 300 ppm. Irritation of the eyes and throat was reported by those employees exposed at 21 ppm, but no complaints of eye irritation were recorded when exposures were maintained below 10 ppm. The authors concluded that concentrations up to 10 ppm were unlikely to produce respiratory or ocular irritation in most workers; however, concentrations above 20 ppm appeared to produce irritation in the majority of the exposed workers. (Reference 541) (6) /SURVEILLANCE/ In a vinyl resin plant 456 workers (313 men and 143 women) were examined for the presence of chronic nonspecific diseases of the respiratory tract (CNDRT). The % of chronic bronchitis was higher in vinyl chloride and vinyl acetate department. (Reference 542) (7) /SURVEILLANCE/ Abnormal pregnancies were related to chemical pollutants present in working atmosphere in the production of acetylene and vinyl acetate. (Reference 543)

(8) /GENOTOXICITY/ ...Vinyl acetate /was/ tested for ... ability to induce chromosome aberrations in cultured human lymphocytes. The effects of a 24-hr treatment (48 hr after culture initiation) were studied both in whole-blood cultures (with 2 X 10+8 erythrocytes/mL) and in isolated lymphocytes (with 4000 erythrocytes/mL). ... Vinyl acetate (0.125-2 mM) ... induced a distinct dose-dependent increase in chromatid-type aberrations and a slight elevation in chromosome-type breaks in both culture types. The lowest concentration giving a positive result was 0.25 mM. The clastogenic effects of vinyl acetate were somewhat more pronounced in isolated lymphocytes than in whole blood. Vinyl acetate is known to be rapidly hydrolyzed in vitro to acetaldehyde, which probably explains the positive result. (Reference 544)

(9) /GENOTOXICITY/ Human leukocytes were incubated in the presence of vinyl acetate ...


(10-20 mM) for 4 hr at 37 degrees C in vitro. DNA damage was analyzed by alkaline elution. /Vinyl acetate did not induce/ a detectable increase in the frequency of DNA strand breaks. (Reference 545)

(10) /GENOTOXICITY/ A 48-hr treatment with vinyl acetate (0.05-1 mM) induced a drastic increase in sister chromatid exchanges (SCEs) and (in first division cells) structural chromosome aberrations in cultured human lymphocytes. The effects were more pronounced in cultures of isolated lymphocytes than in whole-blood cultures. (Reference 546) (11) /GENOTOXICITY/ The frequency of sister chromatid exchange (SCE) was studied in cultures of human lymphocytes exposed to vinyl acetate or acetaldehyde for various time periods and in different phases of the cell cycle. Equimolar concn (0.1-2.4 mM) of vinyl acetate and acetaldehyde induced very similar, dose-dependent increases of sister-chromatid exchange. The sister-chromatid exchange frequency in cells treated with vinyl acetate increased linearly with exposure times up to 24 hr. Cells exposed to vinyl acetate or acetaldehyde in the late G1-phase of the cell cycle showed a two-fold higher sister-chromatid exchange frequency than cells exposed in early G1. Cultures treated with vinyl acetate in the first G1-phase showed a significant increase of sister-chromatid exchange during 3 subsequent cell cycles. Thus, (1) acetaldehyde is likely to be responsible for the sister-chromatid exchange induction /noted/ in vinyl acetate treated cells, (2) the sister-chromatid exchange inducing activity of acetaldehyde persists for several cell cycles in vitro, and (3) removal of sister-chromatid exchange inducing acetaldehyde damage occurs during G1. Taken together, the data suggest that acetaldehyde has slow turn-over in human lymphocytes in vitro, and may accumulate in the cells, possibly by forming reversible Schiff bases, and when release gives rise to sister-chromatid exchange inducing DNA cross-links. ( Reference 547)

(12) ...CHANGES IN VITAL FUNCTION CAPACITY & MAX VENTILATION CAPACITY WERE FOUND IN PERSONS EMPLOYED IN PRODUCTION OF VINYL ACETATE. DISTURBANCES OF PULMONARY FUNCTIONS DEPEND ON THE INTENSITY & DURATION OF THE EFFECT OF THE CHEM CMPD. (Reference 548)

(13) Vinyl acetate vapor at concn below 250 mg/cu m is a primary irritant to the upper respiratory tract & eyes & the liquid may irritate the skin ... .(Reference 549)

In 2005, I submitted a FOIA to the USEPA request for the rest of the lab results the from 1976-1978 core sediment samples of the Camp Pond, and air samples of the Pathfinders Camp, and I spent a lot of time writing emails and talking on the telephone with employees of the USEPA in an effort to find the rest of these lab results, but nothing has come from these efforts, yet. As previously mentioned, I have, recently, been communicating with USEPA employees about this environmental sampling data. The last USEPA employee who talked with me about this, is checking a few more possible locations where it may be, on October 9, 2009.

On about May 30, 2002, I made a verbal Claim that was related to this Claim, on behalf of Joe S. McKinnon's Family and the Kids of the Pathfinders Camp, against and/or to GLCC, and published the same Claim on my web site (www.frankmckinnon.com), with related information, starting in June 2002.

In response to my May 30, 2002 Claim, GLCC hired a law firm in Albuquerque. A lawyer, from the Albuquerque law firm, contacted me, and made it appear as if I would be sued if I didn't stop


publishing information related to my Claim on my web site. I ignored this threat of being sued, and continued adding to the information related to my Claim, because I believed that I held an ethical, moral, and legal, responsibility to inform all of the Kids of the Pathfinders Camp about what we were exposed to at the Pathfinders Camp. Then, the Albuquerque lawyer made an offer, on behalf of GLCC, to pay me $10,500.00 (Ten Thousand Five Hundred Dollars), in July 2002, for 2.4 acres of "Land" that I inherited [where the Pathfinders Camp Lodge was].

I responded to GLCC's offer by letting them know that we would talk about my father (Joe S. McKinnon), the Kids of the Pathfinders Camp, and the Pathfinders Camp, before we could talk about any "Land." Along with the Albuquerque lawyer, two more persons associated with GLCC that I communicated this to were Jeff Lipshaw, who was GLCC's "Head Legal Counsel," and a chemical plant manager that Jeff Lipshaw assigned to be my contact person at GLCC, named Greg Withrow. I tried again, and again, but it didn't matter how much I tried to get them to talk about Joe S. McKinnon, the Kids of the Pathfinders Camp, and the Pathfinders Camp, they would only talk about the "Land" and what they called its "current market value."

So that it is clear that my Claim and Summary of Proof of Claim has nothing to do with the potential of Chemtura paying for "Land," I sold my 2.4 acres of land to my father's younger brother, Robert McKinnon, in about 2005 or 2006.

The Perpetrators at GLCC committed fraud, deception, flagrant defiance and violations of state and federal laws, and repetitive assaults by poison inflicted on Joe S. McKinnon and the Kids the Pathfinders Camp (Crimes of GLCC). These Crimes of GLCC were committed with malice aforethought, which resulted in many years of suffering toxic and /or hazardous exposure injuries and premature death for Joe S. McKinnon, and resulted in toxic and/or hazardous exposure injuries suffered by Kids of the Pathfinders Camp. These Crimes of GLCC brought excessively high amounts of revenue and profit to employees, managers, corporate officials, board directors, and investors of GLCC, and made it possible for Chemtura Corporation to continue making excessively high amounts of revenue and profit at the expense of Joe S. McKinnon's Family and the Kids of the Pathfinders Camp. Therefore, the debtors for this Claim are Great Lakes Chemical Corporation (Case No. 09-11247) and Chemtura Corporation (Case No. 09-11233).

Perpetrators at GLCC knew that GLCC's Poison was in the Pathfinders Camp Pond, and in the air of the Pathfinders Camp, as far back as the 1976 - 1978 USEPA study. They successfully committed a conspiracy to defraud the Arkansas Department of Health, the ADEQ, the ATSDR, the USEPA, the D.C. Cir., Joe S. McKinnon, and the Kids of the Pathfinders Camp. This resulted in the toxic and/or hazardous exposure injuries and death of Joe S. McKinnon, and resulted in toxic and/or hazardous exposure injuries suffered by Kids of the Pathfinders Camp. The last toxic and/or hazardous exposure injury suffered by a misinformed and unsuspecting Kid of the Pathfinders Camp was in 2001.

The Perpetrators' conspiracy to defraud the Arkansas Department of Health, the ADEQ, the ATSDR, the USEPA, the D.C. Cir., Joe S. McKinnon, and the Kids of the Pathfinders Camp, involved submissions of: false and misleading maps, false and misleading environmental sampling data, false and misleading land use surveys in risks assessments, distorted and tampered areal photographs, false and misleading documents that were suppose to show the potential direction of contaminated groundwater flow (groundwater isopleths), false and misleading pleadings in the D.C. Cir., and other false and misleading documents, which were submitted with the intent and purpose of concealing the


fact that the Perpetrators at GLCC knew that the air, water, and soil, of the 40 acres of my grandparents' land, which we used for the Pathfinders Camp, were contaminated with Poison from GLCC. The Perpetrators' false and misleading information has been held and deemed to be true and factual by the Arkansas Department of Health, the ADEQ, the ATSDR, the USEPA, and the D.C. Cir., and has caused physical harm, or bodily injuries, and death of Joe S. McKinnon, and caused physical harm, or bodily injuries, of Kids of the Pathfinders Camp, because we were misinformed and unsuspecting.

The phrase "Kids of the Pathfinders Camp" is used to describe approximately 507 misinformed and unsuspecting people who stayed at the Pathfinders Camp between 1970 and 2001, including members of Joe S. McKinnon's family.

The Perpetrators at GLCC knew that Joe S. McKinnon and the Kids of the Pathfinders Camp were in danger of physical harm, or bodily injury, and death from exposure to GLCC's Poison at the Pathfinders Camp. But they never told us about it. If the Perpetrators at GLCC would have told us about GLCC's Poison at the Pathfinders Camp, and/or if they would have not defrauded the Arkansas Department of Health, the ADEQ, the ATSDR, the USEPA, the D.C. Cir., Joe S. McKinnon, and the Kids of the Pathfinders Camp, we would have been informed, and we would have known better than to sleep, play, and swim in GLCC's Poison at the Pathfinders Camp.

The Arkansas Department of Health, the ADEQ, the ATSDR, the USEPA, and the D.C. Cir., have made decisions that had an impact on whether or not Joe S. McKinnon and the Kids of the Pathfinders Camp would be informed about GLCC's Poison at the Pathfinders Camp. The decisions, which these state and federal agencies, and the D.C. Cir., made, were based on false and misleading information that was given to them by Perpetrators at GLCC. Customarily, these state and federal government agencies, and the D.C. Cir., render services that produce information, guidelines, permits, prohibited behavior, law enforcement, etc..., which are used as instruments to help people mitigate property damage, bodily injury, disease, and premature death.

18 U.S.C § 1365(h) and 21 U.S.C.§ 321(h)(2) cause these government services to fit the definition of "consumer product" for reasons, which follow:

(1) 18 U.S.C § 1365(h) says the following: "...the term “consumer product” means... any... “device”..., as...defined in section 201 of the Federal Food, Drug, and Cosmetic Act (21 U.S.C. § 321); or...any...product..., which is customarily produced or distributed for consumption by individuals, or use by individuals for purposes of personal care..."

(2) 18 U.S.C.§ 321(h)(2) says the following: "The term “device”... means an instrument..., or other similar or related article, including any component, part, or accessory, which is...intended for use in the diagnosis of disease or other conditions, or in the cure, mitigation, treatment, or prevention of disease, in man or other animals...,"

Because18 U.S.C § 1365(h) says that the term “consumer product” means any “device," as defined in section 201 of the Federal Food, Drug, and Cosmetic Act (21 U.S.C. § 321); or any product, which is customarily produced or distributed for consumption by individuals, or use by individuals for purposes of personal care...", and because 21 U.S.C. § 321 says that a device is an instrument intended for use in mitigation or prevention of disease in man or animals, the services provided by the Arkansas Department of Health, the ADEQ, the ATSDR, the USEPA, and the D.C. Cir., in this case, are


"consumer products." Defrauding the Arkansas Department of Health, the ADEQ, the ATSDR, the USEPA, and the D.C. Cir., caused the effect of tampering with these "consumer products" in ways that caused the toxic and/or exposure injuries and death of Joe S. McKinnon, and caused toxic and/or hazardous exposure injuries for the Kids of the Pathfinders Camp.

The Perpetrators' behavior of defrauding the Arkansas Department of Health, the ADEQ, the ATSDR, the USEPA, and the D.C. Cir. also completely ruined the Pathfinders Camp. If my father and I had known that the air, water, and soil, on my grandparents' land, where we built the Pathfinders Camp Pond and Lodge, were contaminated with GLCC's Poison, we would have built the Pathfinders Camp somewhere else. My father and I spent a great deal of time, energy, and money, between 1969 and 1995, building and maintaining the Pathfinders Camp. We would have continued working on building and maintaining the Pathfinders Camp, because we had plans of taking many more large groups of kids to stay there. But, in 1995, GLCC's Poison had caused my father become blind and too sick and crippled to work on anything anymore. During the next five years, he spent most of his time in bed, and died in September 2000, while he was still unsuspecting and misinformed.

My son was 2 years old, in July 2001, when I took him to the Pathfinders Camp. We were planning to live year round in the Camp Lodge, like my father had done between 1986 and 1995. Within a few hours, I had to carry my son into the medical clinic in El Dorado with him limp and his lips turning blue. He was diagnosed and - apparently, successfully, - treated for croup and conjunctivitis. I had not yet found out about GLCC's Poison at the Pathfinders Camp at this point. Then, while studying the Crimes of GLCC, in 2004, I found out that the horn that was sounding at GLCC's chemical plant, while my son was at the Pathfinders Camp, was a warning for employees at GLCC's chemical plant to evacuate. The video that I learned this from gave directions to evacuating employees to go to a destination that was about a half a mile further from the chemical plant than the Pathfinders Camp Lodge was located.

18 U.S.C § 1365 describes behavior that has been demonstrated by the Perpetrators at GLCC, and gives guidelines of punishments for these crimes, where it says the following: "... (a) Whoever, with reckless disregard for the risk that another person will be placed in danger of death or bodily injury and under circumstances manifesting extreme indifference to such risk, tampers with any consumer product that affects interstate...commerce, or the labeling of, or container for, any such product, or attempts to do so, shall — (1) in the case of an attempt, be fined under this title or imprisoned not more than ten years, or both; (2) if death of an individual results, be fined under this title or imprisoned for any term of years or for life, or both; (3) if serious bodily injury to any individual results, be fined under this title or imprisoned not more than twenty years, or both; and (4) in any other case, be fined under this title or imprisoned not more than ten years, or both." (Reference 6)

18 U.S.C § 1365 continues to describe behavior that has been demonstrated by Perpetrators at GLCC, where it says the following: "....the term “communicates false information” means communicates information that is false and that the communicator knows is false, under circumstances in which the information may reasonably be expected to be believed... (Reference 6)

18 U.S.C § 1365 describes behavior of conspiracy like the behavior that has been demonstrated by the Perpetrators at GLCC, and gives guidelines of punishment for these crimes, where it says the following: "...(e) Whoever is a party to a conspiracy of two or more persons to commit an offense under subsection (a) of this section, if any of the parties intentionally engages in any conduct in


furtherance of such offense, shall be fined under this title or imprisoned not more than ten years, or both..." (Reference 6)

18 U.S.C § 287 describes behavior like the behavior of Perpetrators at GLCC, and gives guidelines of punishment for these crimes, where it says: "Whoever makes or presents to any person or officer in the civil, military, or naval service of the United States, or to any department or agency thereof, any claim upon or against the United States, or any department or agency thereof, knowing such claim to be false, fictitious, or fraudulent, shall be imprisoned not more than five years and shall be subject to a fine in the amount provided in this title. (Reference 550)

18 U.S.C § 1001 describes behavior like the behavior of Perpetrators at GLCC, and gives guidelines of punishment for these crimes, where it says: "(a)...whoever, in any matter within the jurisdiction of the executive, legislative, or judicial branch of the Government of the United States, knowingly and willfully— (1) falsifies, conceals, or covers up by any trick, scheme, or device a material fact; (2) makes any materially false, fictitious, or fraudulent statement or representation; or (3) makes or uses any false writing or document knowing the same to contain any materially false, fictitious, or fraudulent statement or entry; shall be fined under this title,...imprisoned not more than 8 years, or both." (Reference 551)

31 U.S.C. § 3729 provides guidelines for dealing with behavior that has been demonstrated by Perpetrators at GLCC as they have knowingly and recklessly provided false and misleading information to the USEPA and the D.C. Cir., including information that was used by the ATSDR, with the intent and purpose of concealing the potential physical harm that GLCC's Poison at the Pathfinders Camp was causing for Joe S. McKinnon and the Kids of the Pathfinders Camp. I will share this information with the U.S. Attorneys who represent Joe S. McKinnon's Family and the Kids of the Pathfinders Camp. (Reference 562) Joe S. McKinnon's Family and the Kids of the Pathfinders Camp have rights described in 18 U.S.C § 3771, 18 U.S.C. § 3663A, Mandatory Restitution Act of 1996, and the 5th Amendment of the U.S. Constitution, just like, and no different than, what every other victim of crimes - like these that have been committed by Perpetrators at GLCC - deserve, in any part of the United States, regardless of age, ethnicity, socioeconomic circumstances, or where in the United State we have lived or currently live. Furthermore, if anyone in the United States has the fundamental human right of prosecution and compensation for human rights abuses, the level of harm and cruelty in the human rights abuses that have been committed by Perpetrators at GLCC, along with the aiding and abetting in these human rights abuses that have been caused by and/or committed by some corrupt government officials, against Joe S. McKinnon's Family and the Kids of the Pathfinders Camp, certainly give us justification for expecting and deserving these fundamental human rights.

The Proof of Claim Form requires a dollar amount for my Claim. Recent events have made evident that the U.S. Government, currently, recognizes the damage that corruption of the past few decades has done. Even though there is still corruption and a lot of damage to repair, progress in cleaning up the corruption and repairing the damage that it has done gives me hope that there could, eventually, be fair and Constitutional circumstances surrounding my Claim, where the U.S. Constitution, and federal statutes that have been created to assure fair treatment of crime victims, are respected and followed. Under such fair and Constitutional circumstances, Joe S. McKinnon's Family and the Kids of the Pathfinders Camp would be represented by U.S. Attorneys, who would be pursuing


criminal charges with the necessary budget and cognitive skills to apply laws and arguments to determine the most appropriate and reasonable dollar amount to demand for restitution and compensation that Chemtura Corporation owes to Joe S. McKinnon's Family and the Kids of the Pathfinders Camp.

My Claim is submitted to be filed for the purpose of reserving, asserting, and/or demanding, rights that are described in 18 U.S.C § 3771, 5th Amendment of the U.S. Constitution, and 18 U.S.C. § 3663A, and, potentially, described in other laws that U. S. Attorneys and U.S. Courts can determine to be applicable, regarding the restitution and compensation that Chemtura owes to Joe S. McKinnon's Family and the Kids of the Pathfinders Camp.

There is an Internet article, which has an introduction that I believe is true for the people of the United States. But my experiences of the past 7 years of dealing with the Crimes of GLCC/Chemtura have given me an understanding that believing this statement about human rights is true is much easier than proving it is true. This article is entitled: "THE FUNDAMENTAL HUMAN RIGHT TO PROSECUTION AND COMPENSATION." The Introduction is as follows: "...The right to obtain financial compensation for a human rights abuse and to have the perpetrator of such an abuse prosecuted and punished is itself a fundamental human right that cannot be taken from a victim or waived by a government. Although it is sometimes tempting to enact a general amnesty in order to heal a nation's wounds, promote harmony, and "let bygones be bygones," such efforts rarely achieve their goals because the wounds fester and the victims need a just resolution to their suffering. The only way to bring true healing to a divided society is to face up to the wrongs that were committed, to prosecute those who violated the fundamental human rights of others, and provide compensation to the victims." (Reference 9).

If the people of the United States do have the fundamental human right to prosecution and compensation for human rights abuses, my submission of my Claim and Summary of Proof of Claim is, also, for the purpose of asserting, or demanding, and/or reserving, the human right to prosecution and compensation for the human rights abuses that have been committed by Perpetrators at GLCC against Joe S. McKinnon and the Kids of the Pathfinders Camp.

As far as I have been able to determine, the DOJ is not, currently, operating in a way that makes rights described in: 18 U.S.C § 3771, 5th Amendment of the U. S. Constitution, 18 U.S.C. § 3663A, and the fundamental human right of prosecution and compensation, accessible to Joe S. McKinnon's Family and the Kids of the Pathfinders Camp. If I would be given a bona fide opportunity to give my supporting evidence to an Agent of the Federal Bureau of Investigation (FBI), a U.S. Attorney, or an Agent of the Criminal Investigations Division (CID) of the USEPA, with a reasonable amount of time and budget to explain my supporting evidence and have it validated, I have no doubt that U.S. Attorneys would have good reason and the ability to successfully prosecute the Perpetrators of the Crimes of GLCC to the fullest extent of the law. But, at this point, I have put an enormous amount of time and effort into giving my supporting evidence to Agents of the FBI, U.S. Attorneys, and Agents of the CID of the USEPA, in a way that I could, at least, explain the insidious details, and have been denied permission to meet with anyone from the FBI, the U. S. Attorneys Office, and the CID USEPA, especially for the purpose of giving them my supporting evidence and explaining the insidious details. This has resulted in Joe S. McKinnon's Family and the Kids of the Pathfinders Camp being denied rights described in: 18 U.S.C § 3771, 5th Amendment of the United States Constitution, 18 U.S.C. § 3663A, and the fundamental human right of prosecution and compensation.


The Executive Office of United States Attorneys has a web page entitled: "Office of the Victims' Rights Ombudsman," which displays a copy of 18 U.S.C. § 3771. (See Exhibit A for copy of 18 U.S.C. § 3771). 18 U.S.C. § 3771(a)(4-8) says "A crime victim has the following rights:" "...(4) The right to be reasonably heard at any public proceeding in the district court involving release, plea, sentencing, or any parole proceeding. (5) The reasonable right to confer with the attorney for the Government in the case. (6) The right to full and timely restitution as provided in law. (7) The right to proceedings free from unreasonable delay. (8) The right to be treated with fairness and with respect for the victim's dignity and privacy.

The Federal Bureau of Investigation has a web page entitled: "Victim Assistance," which has a heading of: "Victim Assistance Home." This web page lists 18 U.S.C. § 3771(a)(1-8), and follows it with the following:

"For purposes of these rights and services, victims are defined in specific ways in the law. A crime victim means a person who has been directly and proximately harmed (physically, emotionally, or financially) as a result of the commission of a federal offense or an offense in the District of Columbia. In the case of a crime victim who is under 18 years of age, incompetent, incapacitated, or deceased, the legal guardians of the crime victim or the representatives of the crime victim's estate, family members, or any other persons appointed as suitable by the court may assume the crime victim's rights, as long as that person is not a defendant in the crime being investigated or prosecuted. Foreign citizens may be victims in some cases. Businesses, corporations, and nonprofit organizations can be eligible victims, and an authorized representative of the entity should be designated for purposes of notification. A government agency or entity is not considered a victim for purposes of these rights."

"Most of these rights apply after charges have been filed by a U.S. Attorney's Office. The FBI's responsibility for assisting victims is continuous until the investigation is closed or until it is turned over to a U.S. Attorney’s Office for prosecution."

(Reference 8)

The 5th Amendment of the U.S. Constitution says that No person shall be...deprived of life,...or property, without due process of law... nor without just compensation. (Reference 10)

Joe S. McKinnon has been deprived of life, and Joe S. McKinnon's Family has been deprived of the life of Joe S. McKinnon, because the Perpetrators at GLCC defrauded the United States with malice aforethought. The lives of the Kids of the Pathfinders Camp have been wrongfully altered in ways that may never be rectified, because the Perpetrators at GLCC defrauded the United States with malice aforethought. The Pathfinders Camp has been completely ruined by GLCC's Poison, because Perpetrators at GLCC defrauded the United States with malice aforethought. The lives that Joe S. McKinnon's family and the Kids of the Pathfinders Camp would have had - if we had not played, swam, and slept in GLCC's Poison at the Pathfinders Camp - have been taken without without due process of law and without just compensation. The Pathfinders Camp has been ruined without due process and without just compensation.

18 U.S.C. § 3663A(a) says the following: "(1) Notwithstanding any other provision of law,


when sentencing a defendant convicted of an offense described in subsection (c), the court shall order, in addition to, or in the case of a misdemeanor, in addition to or in lieu of, any other penalty authorized by law, that the defendant make restitution to the victim of the offense or, if the victim is deceased, to the victim’s estate. (2) For the purposes of this section, the term “victim” means a person directly and proximately harmed as a result of the commission of an offense for which restitution may be ordered including, in the case of an offense that involves as an element a scheme, conspiracy, or pattern of criminal activity, any person directly harmed by the defendant’s criminal conduct in the course of the scheme, conspiracy, or pattern. In the case of a victim who is under 18 years of age, incompetent, incapacitated, or deceased, the legal guardian of the victim or representative of the victim’s estate, another family member, or any other person appointed as suitable by the court, may assume the victim’s rights under this section, but in no event shall the defendant be named as such representative or guardian. (3) The court shall also order, if agreed to by the parties in a plea agreement, restitution to persons other than the victim of the offense." (Reference 6)

18 U.S.C. § 3663A(c) says the following: "(1) This section shall apply in all sentencing proceedings for convictions of, or plea agreements relating to charges for, any offense— (A) that is...(iii) an offense described in section 1365 (relating to tampering with consumer products); and (B) in which an identifiable victim or victims has suffered a physical injury or pecuniary loss." (Reference 6)

On July 13, 2007, I started using my experiences with GLCC as part of my justification for a Petition for Emergency Order of Protection or Injunction, in state court, seeking injunctive relief from the threats of property damage, injuries, and death that Pete Domenici, George W. Bush, and their followers were posing on people who live in southeastern New Mexico by talking about making southeastern New Mexico the location for the Global Nuclear Energy Partnership nuclear fuel reprocessing plant and nuclear waste burner reactor. My petition for injunctive relief was moved to federal court where it was assigned to a judge who had been nominated by Pete Domenici and appointed by George W. Bush. My dealing with the corruption in the United States District Court and United States Attorneys Office of New Mexico resulted in me filing a criminal complaint in the United States District Court of New Mexico on March 2, 2009. Part of my criminal complaint describes crimes that Perpetrators at GLCC committed (Crimes of GLCC) against Joe S. McKinnon and the Kids of the Pathfinders Camp. My criminal complaint was submitted, again, with more detail, on March 17, 2009, in a way that is described, as follows:

(1) On March 2, 2009, Debbie Wheeler, who identified herself as being a Court Administrator for the United States District Court for the District of New Mexico, filed a document for me, which she received from me through electronic mail. That document is entitled: "PETITION FOR WRIT OF HABEUS CORPUS AD SUJICIENDUM OF ENVIRONMENTAL LAW (WOHCAS of Environmental Law 2009)." Part of this petition is a criminal complaint, which reports the Crimes of GLCC. It was filed in the Court of a Magistrate Judge for the purpose of fulfilling the requirement of giving my Oath of Affirmation for a criminal complaint to a Magistrate Judge. It was also submitted with electronic mail to the following:

(1.1) United States Attorney General Eric H. Holder Jr.;

(1.2) President Barak Obama

(1.3) Sr. Assistant Attorney General of Arkansas Charles Moulton;


(1.4) Assistant Attorney General of New Mexico Steve Farris;

(1.5) Many Affected State and Federal Employees;

(1.6) Many Affected Persons Who Hold the Rank of Common People.

(2) Debbie Wheeler, the Court Administrator, filed my PETITION FOR WOHCAS of Environmental Law 2009 as a civil case 1:2009cv00216 on March 2, 2009. I pointed out to her that it was not a civil case, but it was a criminal complaint. She was unable to explain or cite the official guidelines she was following, but told me that the only way she could file it was as a civil case. The only reason it was filed in the United States District Court was to give my Oath of Affirmation to a Magistrate Judge, as I was following guidelines in the United States Code of Law for making a criminal complaint. The rest of it was intended for the United States Attorney General and President of the United States. As far as I can tell, this case has not been dismissed or closed. This petition may either be viewed through PACER or by going to my web site (See Reference 1 for web page address).

(3) On March 17, 2009, I submitted a document, entitled: "2nd Attempt with AMENDED PETITION FOR WRIT OF HABEAS CORPUS AD SUBJICIENDUM (WOHCAS) of Environmental Law 2009." See Reference 2 for web address. It contains the same facts with more details about the Crimes of GLCC. I submitted it through electronic mail to the people who are listed, as follows:

(3.1) Adrian Scott in the [DOJ] Office of the Inspector General

(3.2) U.S. Attorney General Eric H. Holder Jr.;

(3.3) President Barak Obama

(3.4) Sr. Assistant Attorney General of Arkansas Charles Moulton;

(3.5) Assistant Attorney General of New Mexico Steve Farris;

(3.6) Many Affected State and Federal Employees;

(3.7) Many Affected Persons Who Hold the Rank of Common People.


When I was 12 years old, in 1974, instead of going back to Roswell for the winter, I stayed with my grandparents for first 10 weeks of that school year. I took daily walks to the part of my grandparents' land that was north of the railroad track. GLCC did not have a fence along the southern border of the GLCC's chemical plant.

Even though my grandparents owned land on both sides of the railroad track, my grandparents had a fence to keep the cows and ponies off of the railroad track. While standing on the south side of this fence, I observed people using bulldozers to bury rusty barrels (drums). On one of my daily walks to the railroad track, while I was observing the people burying drums, I saw them use the bulldozers to push some of these drums through my grandparents' fence. On the following day, my grandfather and I


had $90.00 worth of barbed wire that GLCC paid for, and we were fixing the fence. Before we could fix the fence, I had to roll the drums back across our fence line. While rolling the drums, I noticed that they were almost full of fluid that was leaking out of them. I found out, 28 years later, that those rusty barrels, or drums, they were burying at GLCC, and pushing through my grandparents' fence contained poison.

GLCC's leaking Tailbrine Pond, spills and leaks from train-tanker cars, and thousands of buried leaking drums and cylinders, caused GLCC's Poison to be in the aquifer that provided groundwater for the spring fed Camp Pond. This aquifer has been reported to have an elevation of about 297 feet above sea level near the Tailbrine Pond, and an elevation of about 240 feet above sea level near the Camp Pond. Gravity causes water to flow downward.

1975 Highway Department Areal Photograph

PLEASE TAKE NOTICE that GLCC's chemical plant is north of: (1) the Camp Lodge where we slept, (2) the Camp Pond where we swam, and (3) the air and the soil of trail to the railroad track and the rest of my grandparents' 40 acres of land, which we used for the Pathfinders Camp, that was contaminated with GLCC's Poisons. Perpetrators at GLCC knew that we were there, and never said a word about GLCC's Poisons at the Pathfinders Camp.

PLEASE TAKE NOTICE that we spent large amount of time playing in the field that is on the north side of the "Parker's Chapel Water Tower." Many of us walked on the road that is on the west side of the "Parker's Chapel Water Tower a few times each day. Many of us spent a lot of time in the garden on the east side of the "Parker's Chapel Water Tower." I spent a lot of time directly under the "Parker's Chapel Water Tower" during the 1970s and 1980s. And nobody said a word about GLCC's Poison in the air.

Just in case it has not been made clear, PLEASE ALSO TAKE NOTICE that some of us spent a lot of time walking along the railroad track near the Tailbrine Pond.

The USEPA took some core samples from the Camp Pond Sediment in July 1977. Analysis of these core samples shows a detection of a GLCC product called Tetrabromobisphenol A at 300 ug/kg. And nobody said a word about GLCC's Poison in the Camp Pond. The USEPA likely found a lot more of GLCC's Chemicals (Poisons) in these sediment samples. I have been trying to get the USEPA to letme have a copy of the lab results for the sampling data of these core samples from the Camp Pond. I believe the FBI and U.S. Attorneys would have a much easier time getting copies of these lab results than I have had. These core sediment samples are identified as being from the pond 200 meters northof the "Parker's Chapel Water Tower."


This information related to relevant health effects for Tetrabromobisphenol A is from the "Hazardous Substances Data Bank (HSDB) - Comprehensive, peer-reviewed toxicology data for about 5,000 chemicals," which is made available by the United States National Library of Medicine's web site http://toxnet.nlm.nih.gov, says the following (quotation marks omitted):

(1) 2,2',6,6'-TETRABROMOBISPHENOL A Synonym: tetrabromobisphenol a 79-94-7.


(2) NIOSH (NOES Survey 1981-1983) has statistically estimated that 224 workers are potentially exposed to 2,2',6,6'-tetrabromobisphenol A in the US(1). Occupational exposure to 2,2',6,6'-tetrabromobisphenol A may occur through inhalation of dusts and dermal contact with this compound at workplaces where 2,2',6,6'-tetrabromobisphenol A is produced or used(SRC). Monitoring data indicate that the general population may be exposed to 2,2',6,6'-tetrabromobisphenol A via inhalation of ambient air and dermal contact with this compound(SRC). (Reference 274)

(3) ...Composite samples of human hair collected from barber shops in El Dorado and Magnolia, Arkansas contained 2,2',6,6'-tetrabromobisphenol A at concentrations of up to 2 to 5 ug/kg(1). (Reference 275)

(4) Synonyms:

(4.1) 2,2-BIS(3,5-DIBROMO-4-HYDROXYPHENYL)PROPANE (4.2) 2,2-BIS(4-HYDROXY-3,5-DIBROMOPHENYL)PROPANE

(4.3) BROMDIAN

(4.4) FG 2000

(4.5) FIRE GUARD 2000

(4.6) FIREMASTER BP4A (4.7) 4,4'-ISOPROPYLIDENEBIS(2,6-DIBROMOPHENOL)

(4.8) 4,4'-ISOPROPYLYLIDENEBIS(2,6-DIBROMOPHENOL)

(4.9) PHENOL, 4,4'-ISOPROPYLIDENEBIS(2,6-DIBROMO-

(4.10) PHENOL, 4,4'-(1-METHYLETHYLIDENE)BIS(2,6-DIBROMO-

(4.11) TETRABROMOBISPHENOL A

(4.12) 3,5,3',5'-TETRABROMOBISPHENOL A (5) Other sources of information about tetrabromobishenol A, say the following:

(5.1) Long after they were banned, PCBs and DDT are still found in Arctic mammals, as is the still widely used flame retardant tetrabromobisphenol A, according to the Canadian Arctic Contaminants Assessment Report II, published by the government of Canada. Some of these chemicals are known to be hormone-system or metabolism disrupters and carcinogens. If they turn out to have transgenerational effects, humans may be as much at risk as other species. This particular “if” is a big one; most of these substances have not been tested for inheritability. (Reference 276)

(5.2) According to Wikipedia www.wikipedia.org, bisphenol-A (BPA) is an organic compound


used in an important monomer in the production of polycarbonate. It has an annual production of 2-3 million tons, suspected of being hazardous to humans since the 1930s, and is found in the following common products: baby and water bottles, sports equipment, medical and dental devices, dental composite (white) fillings and sealants, lenses, and household electronics, all CDs and DVDs, and Epoxy resin coatings on the inside of almost all food and beverage cans. BPA is also a precursor to the flame retardant, tetrabromobisphenol A, and was formerly used as a fungicide.

(5.3) West Palm Beach, FL (JusticeNewsFlash.com)–The U.S. Food and Drug Administration (FDA) www.fda.gov has finally decided to reconsider bisphenol-A (BPA) toxicity. The FDA has been accused by its own advisory board of failing to adequately consider research about the dangers of BPA. This toxic chemical is found in many plastic baby bottles, plastic food containers and metal can food linings. The National Toxicology Program, developed by the U.S. Department of Health and Human Services www.hhs.gov, claims there are many reason to be concerned about BPA. This toxic chemical has a high possibility of causing serious harm to fetuses, infants and children.

(5.4) The Journal of the American Medical Association published a study, in September 2009. The study stated adults, with high levels of BPA in their urine, were more prone to heart and liver disease and diabetes. More than 200 animal studies have linked ingesting minute amounts of the toxic substance to a long list of serious medical conditions:

(5.4.1) -reproductive problems

(5.4.2) -brain damage

(5.4.3) -immune deficiencies

(5.4.4) -metabolic abnormalities

(5.4.4) -behavioral oddities (hyperactivity/learning deficits/reduced maternal willingness to nurse offspring)

(Reference 277)

(5.5) There is a web page, entitled: "Environmental Factor [ ] Your Online Source for NIEHS News," dated October 2009, says the following:

(5.5.1) "...NIEHS and National Toxicology Program (NTP) Director Linda Birnbaum, Ph.D., D.A.B.T., A.T.S., presented the first seminar of the 2009 – 2010 NIEHS Distinguished Lecture Series on September 8 titled “Halogenated Flame Retardants: Does the Benefit Justify the Risk?...”

(5.5.2) "...According to Birnbaum, One of these brominated molecules, tetrabromobisphenol A (TBBPA), doesn’t escape into the environment easily because it chemically binds with the product matrix, but when the matrix does break down, it could have devastating consequences.“TBBPA can eventually generate bisphenol A (BPA), and we all know about BPA and its endocrinedisrupting properties,” Birnbaum said..."

(5.5.3) "...She also discussed another concern regarding TBBPA. “When TBBPA burns, it


generates brominated dioxins. TBBPA also disturbs the homeostasis of the thyroid system,” she explained. “It does so by binding with a higher affinity to transthyretin, a major thyroid transport protein in mammals, than to the natural ligand T4. This process could interrupt a key step during development in rodents and humans.”..."

(Reference 278)

(5.6) There is a web page headed with "PubMed.Gov U.S. National Library of Medicine National Institute of Health, which says the following: "Tetrabromobisphenol A (TBBPA) is a commonly used brominated flame retardant (BFR) utilized to reduce the flammability of a variety of products. Studies have indicated that a number of BFRs are becoming widely distributed within the environment and are bio-accumulating within organisms. There has been much speculation that a variety of phenolic pollutants (including compounds chemically related to TBBPA, such as bisphenol A) may cause endocrine disruption and Ca2+ dysregulation in cells involved in spermatogenesis. In this study we therefore investigate the effects of TBBPA on mouse TM4 Sertoli cells (essential for sperm development). Results show that TBBPA increases Ca2+ within these cells in the 5-60 microM concentration range (EC50, 21 microM). TBBPA also causes cell death (LC50, 18 microM) partly via apoptosis, involving Ca2+-dependent mitochondrial depolarisation. Studies on intracellular Ca2+ transporters shows that TBBPA can inhibit sarcoplasmic/endoplasmic reticulum Ca2+-ATPases (SERCA) at low concentrations (IC50, 0.4 to 1.2 microM) and also activate the Ryanodine receptor Ca2+ channel within the 0.4-4 microM concentration range. Therefore these studies suggest that the cytotoxic effects of TBBPA on cells is partly due to dysregulation of Ca2+ signalling, by directly affecting Ca2+ transport proteins."

(Reference 279)

Although I suspect that there are more reasons for nobody telling us about GLCC's Poison in the soil, air, and water of the Pathfinders Camp, I can prove one major reason, which is the fact that Perpetrators at GLCC defrauded the Arkansas Department of Health, the ADEQ, the ATSDR, the USEPA, and the D.C. Cir.

One of many examples of fraud and deception committed by Perpetrators at GLCC is the way they played with the terms "on-site" and "off-site." If the USEPA and ATSDR and/or ADEQ and the Arkansas Department of Health were planning to conduct a study "off-site," Perpetrators at GLCC provided maps with boundaries that made it look like parts of my grandparents' land where Perpetrators at GLCC knew that Kids of the Pathfinders Camp played, swam, and slept, in GLCC's Poisons appeared to be "on-site," and owned by GLCC.

An example of "on-site" "off-site" fraud and deception used by Perpetrators at GLCC to defraud the United States with false and misleading maps happened in 1978. Richard D. Karkkainen, an Environmental Engineer for GLCC, submitted a map, as part of a landfill permit application. This map has about 17.5 acres, of the 40 acres of my grandparents' land that we were using for the Pathfinders Camp, inside the boundaries of GLCC's chemical plant site, which gave it the appearance of being on-site and being owned by GLCC.


1978 Map for Landfill Permit Application

Above is a copy of a map that Richard Karkkainen submitted with a landfill permit application in 1978. This map includes about 17.5 acres of my grandparents' land that we used for the Pathfinders Camp, including the Camp Pond. According to Richard Karkkainen, he drew this map while using information that he received from GLCC's Land Manager, Mikey Hazelwood.


A copy of GLCC's 1978 landfill permit application map is below. It has the boundaries of the 40 acres of my grandparents' land that we used for the Pathfinders Camp superimposed on it. While drawing this superimposed boundaries of the Pathfinders Camp, my wife, Robin McKinnon, identified the Camp Pond as the "SUMMER CAMP'S SPRING FED SWIMMING HOLE," and drew a line pointing to the she outlined the Camp Pond. While following my instructions, Robin drew arrows to show that we used the entire 40 acres of my grandparents' land for the Pathfinders Camp, and wrote "KIDS PLAYED OVER THE WHOLE 40 ACRES."

I called Richard (Dick) Karkkainen, on October 2, 2002. He told me that, while he worked for GLCC, that he ran into resistance as he tried to clean up the big mess that had been made. He also agreed that GLCC had "just let things fly and land where they may back there."

Regarding our conversation about the above map, I sent a letter, dated October 2, 2002, in which I wrote: "Dear Mr. Karkkainen, I would like thank you for talking with me today. Enclosed you will find the material you requested. I hope this helps you. Feel free to call or write me anytime. Best wishes, Frank L. McKinnon"

In response to my October 2, 2002 letter to Mr. Karkkainen, he sent me an email, dated October 5, 2002, in which he wrote: "I received your information. Thanks. The map in question was hand prepared by me; that is my printing on the map. The 1978 application for landfill was replaced by an application with much more detail as required by the subsequent passage of RCRA...The map prepared by IT Corporation is apparently correct; I was in charge of the IT Office that prepared that map and did


substantial investigation and remediation of the site. GLCC was responsible in carrying out corrective action on that site....I regret not knowing about the Pathfinder Group..."

The IT Corporation map that Richard Karkkainen mentioned, in his October 5, 2002 email, was made from an areal photograph that was taken in 1981 (3 years after the false and misleading 1978 Landfill Permit Application Map), and was submitted with a Monitoring Assessment for the North and South Landfills in 1987 (9 years after the false and misleading 1978 Landfill Permit Application Map). I have found other maps that have correct boundaries as early as 1982. But, I have seen no evidence showing that the ADEQ and the USEPA believed that anyone other than GLCC used any part of the area that GLCC falsely claimed ownership of in the 1978 Landfill Permit Application Map until I brought the Camp Pond to the attention of the ADEQ and the USEPA in 2002 (24 years later). There is lot more regarding the ways that this and other false and misleading information impaired services that should have been provided by the ADEQ and the USEPA in 2004 that should be addressed by U.S. Attorneys.

1987 IT Corporation Corrected Map


Richard Karkkainen apparently believed it would be a good idea to make very clear that GLCC really didn't own any part of the Pathfinders Camp for this 1987 "on-site" study. Mr. Karkkainen, or somebody working for him at IT Corporation, made a clear correction for this "on-site" study, which makes very clear that all of the 40 acres of my grandparents' land, which we used for the Pathfinders Camp, is "off-site" and does not belong to GLCC, by placing a label on this area and printing the phrase: "PROPERTY BOUNDARY," which is easier to see in a enlarged view of the of Richard Karkkainen's 1987 IT Corporation Corrected Map next to his 1978 GLCC map, in the pictures below.

1987 IT Corporation Corrected Map 1978 GLCC Landfill Permit Application Map

False boundaries on maps and playing with the terms "on-site" and "off-site" was only one effective method that Perpetrators at GLCC used to defraud the United States. They also used false and misleading land use surveys in risks assessments, distorted and tampered areal photographs, and other false and misleading information in a way that impaired services that should have been provided by Supefund and Enforcement Divisions of the USEPA.

I have reviewed enough documents to understand that, while Richard Karkkainen worked for GLCC, he was the person who communicated with government agencies when it involved environmental monitoring and remediation. He says he was in charge of IT Corporation's activities at this chemical plant after he left GLCC. This placed Richard Karkkainen in a position of continuing to be a person for government agencies depended on for understanding environmental monitoring, direction of groundwater flow, "on-site" and "off-site" boundaries, and other necessary knowledge for remediation. Keep in mind that he says that he received his information about GLCC's boundaries from Mikey Hazelwood. His October 5, 2002 email also says that he didn't know about the "Pathfinder Group." Mikey Hazelwood's manipulation of information regarding boundaries is a long, insidious, story of a successful conspiracy to defraud the United States that I should describe to FBI and/or U.S. Attorneys under fair and Constitutional Circumstances. Until then, for the sake of providing enough information for heed to be taken to this Summary of Proof of Claim, I am declaring


that a pattern of deception on maps, areal photographs, and other information impaired services that would have been provided by state and federal: health, environmental, and law enforcement agencies.

1980 Highway Department Photograph of Pathfinders Camp

The 1980 Highway Department Areal Photograph provides a clear view of the Camp Pond that Mikey Hazelwood's information on Richard Karkkainen's false and misleading 1978 Permit Application Map says is "on-site" and clearly owned by GLCC. There were no labels on it when I received it. I labeled significant parts of this areal photographs. I labeled the Vance's worm farm. The Vance's had a worm farm where they raised worms to sell for fish bait. Their worms died in 1981. Mr. Vance talked to a manager at GLCC, who told him that it couldn't have been anything from GLCC. From then on, Mr. Vance says that his worms had growth and reproductive problems.


PLEASE TAKE NOTICE that contaminated groundwater flowed southward from GLCC's tailbrine pond in the aquifer that provided water for Mr. Vance's pond that he used for his worms, and provided water for the Camp Pond. An extensive study of groundwater isopleth maps submitted to the ADEQ and USEPA by Perpetrators at GLCC is another example of Perpetrators at GLCC defrauding the United States that I will provide to the U.S. Attorneys who represent Joe S. McKinnon's Family and the Kids of the Pathfinders Camp.

1985 Superfund Photograph of Pathfinders Camp

I received the above 1985 areal photograph from USEPA Region 6 Superfund in 2003 or 2004, which also shows the Camp Pond. I put no labels on it, but reduced the size to fit this page and serve the purpose of showing that USEPA Superfund was looking at this area. The Camp Pond is visible, if you know what you are seeing. Perpetrators at GLCC defrauded the EPA in ways that impaired the services that should have been provided by the Superfund and Enforcement Branches of the USEPA.


I have seen a consistent pattern of deceptive behavior demonstrated by Perpetrators at GLCC where they provided to the ADEQ and the USEPA information that made the the wooded areas of my grandparents' land, which we used as the Pathfinders Camp, appear to be either "on-site" and owned by GLCC, or "off-site," undeveloped and not being used by the general population, depending on whether or not the study was being conducted "on-site" or off-site."

Just as Perpetrators played with the terms: "on-site" and "off-site," to defraud the United States, and keep Joe S. McKinnon and the Kids of the Pathfinders Camp misinformed and unsuspecting, the term "fence line' was also played with by the Perpetrators at GLCC for the same purpose. GLCC did not own a fence between southern border of GLCC's chemical plant and the 40 acres of my grandparents' land that we used for the Pathfinders Camp. The only fence that was between the GLCC's chemical plant and my grandparents' 40 acres of land that we used for the Pathfinders Camp was the fence that my grandparents used to keep a few cows and ponies from going past the railroad tracks. When GLCC was required to conduct "fence line" air monitoring, they were not required to monitor the air leaving the chemical plant site across the southern border of GLCC's chemical plant site onto Joe S. McKinnon and the Kids of the Pathfinders Camp.


Below is a copy of a letter that Richard Karkkainen wrote, in 1976, which makes his malice aforethought evident in playing with the term "fence line" to impair the services of the USEPA and the A.D.P.C.E. (now called the ADEQ) in their efforts to monitor the air that was leaving GLCC's chemical plant, by directing them away from monitoring the air that was leaving GLCC's chemical plant across the southern border onto Joe S. McKinnon and the Kids of the Pathfinders Camp.

There is a lot more that I should share with the FBI and U.S. Attorneys Office regarding this long and insidious story that involves incidents in which Perpetrators at GLCC defrauded the United States in ways that impaired services of the Arkansas Department of Health, the ADEQ, the USEPA, the ATSDR, and the D.C. Cir. that should have been provided to Joe S. McKinnon and the Kids of the


Pathfinders Camp to mitigate diseases and death for Joe S. McKinnon, and diseases of the Kids of the Pathfinders Camp thereby causing the effect of tampering with services or "consumer products."

To go along with false and misleading maps and playing with the terms "on-site," "off-site," and "fence line," Perpetrators at GLCC submitted false and misleading environmental sampling data, false and misleading land use surveys in risks assessments, distorted and tampered areal photographs, false and misleading documents that were suppose to show the potential direction of groundwater flow (groundwater isopleths), and other false and misleading documents. They also submitted false and misleading pleadings in the D.C. Cir.

Perpetrators at GLCC defrauding the ADEQ and Arkansas Department of Health in Little Rock, Arkansas; the USEPA Superfund and Enforcement Divisions at the Region 6 offices in Dallas, Texas and Headquarters in Washington, D.C., and the ATSDR offices in Dallas, between 1978 and 2000 in ways that impaired services and caused the effect of tampering with services or "consumer products" that should have been provided by the Arkansas Department of Health, the ADEQ, and the USEPA Superfund and Enforcement Divisions to Joe S. McKinnon and the Kids of the Pathfinders Camp.

Perpetrators at GLCC defrauding the Arkansas Department of Health and ADEQ in Little Rock, Arkansas; the D.C. Cir. in Washington D.C., and the USEPA in Dallas, Texas; Arlington, Virginia; and Washington D.C., between 1994 and 1999 in ways that impaired services and caused the effect of tampering with services or "consumer products" that should have been provided by the Arkansas Department of Health, the ADEQ, the D.C. Cir., and the USEPA to Joe S. McKinnon and the Kids of the Pathfinders Camp.

There was a situation that involved Perpetrators at GLCC, the Arkansas Department of Health, and the USGS that impaired services and caused the effect of tampering with services or "consumer products" that should have been provided by the the Arkansas Department of Health, the ADEQ, the USEPA, the ATSDR, and the D.C. Cir. to Joe S. McKinnon and the Kids of the Pathfinders Camp.

To go along with a voluminous amount of GLCC's false and misleading information that I have found, which has been held and deemed to be true and factual by Arkansas Department of Health, the ADEQ and the USEPA, the USGS, and the D.C. Cir., I have recorded interviews of former GLCC employees that described their knowledge and/or involvement in the following:

(1) Routinely pouring GLCC's Poison into the creek at an outfall where it leaves the chemical plant site;

(2) Routinely tampering with environmental samples before sending them to the ADEQ;

(3) Routinely following a "procedure" of decreasing the workload of machinery by "90 percent" whenever they were being inspected by the ADEQ or USEPA, especially during stack emissions testing;

(4) Illegal burial of thousands of drums and cylinders containing GLCC's Poisons;

(5) Routinely emptying cylinders of methyl bromide with chloropicrin into the wind that blew onto the Pathfinders Camp (See copy of 2nd Attempt of Amended Petition for WOHCAS Environmental Law 2009 for information about the "Popping Field.");


(6) One former GLCC employee described how waste Ethylene dibromide was routinely boiled off into the air, heated by a steam-line, in an old railoard tank-car, with cases of Folgers coffee added to it to hide the smell;

(7) One former GLCC employee described how he, routinely, poured wastes from his work, which contained Potassium cyanide and/or other toxic chemicals onto the floor of the fine chemicals area, and used a hose with water to wash toxic waste into a concrete ditch. Rainwater caused the contents of this concrete ditch to empty into the ditch by the railroad track east of the Tailbrine Pond, which you can see in the aerial photographs that I am using for this Summary of Proof of Claim;

(9) Many more similar stories.

I have learned about many activities at GLCC that very likely contributed to causing GLCC's Poison to be in the Camp Pond, in the soil that we played on, and in the air that we breathed at the Pathfinders Camp.

Regardless of which crime, incident of neglect, accident, faulty engineering, incident of recklessness, unforeseen conditions, or uncontrolled conditions, caused GLCC's Poison to be at the Pathfinders Camp, it was impossible for a person to sleep in the Camp Lodge, or swim in the Camp Pond, or to hike through the woods of the Pathfinders Camp, without being exposed to harmful levels of GLCC's Poison. Perpetrators at GLCC submitted to the Arkansas Department of Health, ATSDR, the ADEQ, and the USEPA: false and misleading maps, false and misleading environmental sampling data, false and misleading land use surveys in risks assessments, distorted and tampered areal photographs, false and misleading groundwater isopleths that were supposed to show the potential direction of groundwater flow, and other false and misleading documents. They also submitted false and misleading pleadings in the D.C. Cir. Perpetrators at GLCC successfully defrauded the ATSDR, the USEPA, and the D.C. Cir. with the intent and purpose of concealing the fact that they knew that the Camp Pond, and other parts of 40 acres of my grandparents' land, which we used for the Pathfinders Camp, were contaminated with Poison from GLCC, and to conceal the fact that they knew Joe S. McKinnon and the Kids of the Pathfinders Camp were there and being exposed harmful levels to GLCC's Poison.

Defrauding the ATSDR, the USEPA, and the D.C. Cir. has been the same as defrauding the United States. Perpetrators at GLCC successfully executed an insidious conspiracy to defraud the United States in ways that disrupted the intended functions of the ATSDR, the USEPA, and the D.C. Cir., which caused Joe S. McKinnon to suffer and die of diseases that were caused by chronic exposure to GLCC's Poison at the Pathfinders Camp. The Perpetrators' conspiracy to defraud the United States also caused approximately 507 Kids of the Pathfinders Camp to swim, play, and sleep, in GLCC's Poison at the Pathfinders Camp. Many of the Kids of the Pathfinders Camp, and some our children, have suffered diseases, which can only be explained by the fact that we swam, played, and slept, in GLCC's Poison at the Pathfinders Camp. Some of GLCC's toxic substances (Poisons), which have been detected in the air, surface water, soil, and groundwater of the my grandparents 40 acres of land that we used for the Pathfinders Camp, cause diseases that may go undetected for for 20 to 30 years, or longer. It was like the Pathfinders Camp was a drain for GLCC's Poison. Finding out that we were poisoned has been an extremely traumatic experience for Joe S. McKinnon's Family and the Kids of the Pathfinders Camp.


I will provide all supporting evidence to the US Attorneys who represent Joe S. McKinnon's Family and the Kids of the Pathfinders Camp. After U.S. Attorneys have received my supporting evidence, after they have put forth bona fide effort to understand and validate my supporting evidence, and after they have used my supporting evidence to put forth a bona fide effort to represent Joe McKinnon's Family and the Kids of the Pathfinders Camp in pursuing criminal charges against the Perpetrators at GLCC, unless they run into government corruption, I have no doubt that their next step would be to assert rights described in 18 U.S.C § 3771(a)(6), 18 U.S.C. § 3663A, Mandatory Restitution Act of 1996, the 5th Amendment of the U.S. Constitution. and, potentially, other laws that the U.S. Attorneys and U.S. Courts can find to be applicable to restitution and compensation to be paid by Chemtura to Joe S. McKinnon's Family and the Kids of the Pathfinders Camp.

The only way that Joe S. McKinnon's Family and the Kids of the Pathfinders Camp could be treated fairly, in this case, would be under the fair and Constitutional circumstances that are described in above paragraph. But, because the Notice of Bar Date says: "IF THE DEADLINE APPLIES TO YOU AND YOU FAIL TO FILE A PROOF OF CLAIM BY THE BAR DATE, YOUR CLAIM WILL BE FOREVER BARRED...," because I do not know whether or not the October 30, 2009 Bar Date applies to the restitution and compensation that Chemtura owes to Joe S. McKinnon's Family and the Kids of the Pathfinders Camp, and because the only response that I have received from the United States Department of Justice regarding my efforts of seeking representation from United States Attorneys, in this case, is a letter, from the Operations Section of the DOJ Office of the Inspector General, which tells me that my information has been referred to the United States Department of Justice Office of Professional Responsibility, and verbal assurance from people in that office that tells me that my information is being reviewed, along with their verbal assurance that I will be receiving a written response from them, I am apparently placed in the position of being required to determine a dollar amount for the value of the life that Joe S. McKinnon would have had if he had not been misinformed and unsuspecting, if he had not suffered for about 30 years from toxic and/or hazardous exposure injuries from being repetitively assaulted with GLCC's Poison, and if he had not died from diseases that were caused by exposure to GLCC's Poison at the Pathfinders Camp. I am apparently, also, placed in the position of being required to determine a dollar amount for the value of the lives that the Kids of the Pathfinders Camp (including Joe S. McKinnon's Family) would have had if we would not have been misinformed and unsuspecting as we played, slept, and swam in GLCC's Poison at the Pathfinders Camp, which was caused by the Perpetrators at GLCC successfully executing a conspiracy to defraud the United States.

Perpetrators at GLCC made free will choices to defraud the United States. They made free will choices with malice aforethought to murder Joe S. McKinnon and poison the Kids of the Pathfinders Camp. Until this matter is rectified, every penny made by Chemtura Corporation, with any part of Chemtura Corporation that has been derived from GLCC, will continue to be at the expense of Joe S. McKinnon's Family and the Kids of the Pathfinders Camp. Because Chemtura Corporation was formed, in 2005, by merging GLCC and Crompton Corporation, the entire company called Chemtura Corporation has been derived from Great Lakes Chemical Corporation. This means that every penny that Chemtura Corporation has made and will make in revenue has been and continues to be at the expense of Joe S. McKinnon's Family and the Kids of the Pathfinders Camp. The same goes for any company by any name that has been or will be derived from Great Lakes Chemical Corporation.

Proper and/or legal methods of: manufacturing and storage of toxic substances, and disposition and/or recycling of toxic and/or hazardous wastes, like GLCC's Poisons, is expensive. GLCC made


excessive revenue and/or profits by using improper and/or illegal methods of manufacturing and storage of toxic chemicals, by using improper and/or illegal methods of disposition of toxic and/or hazardous waste, and by defrauding the United States, which caused the Pathfinders Camp to be like a drain for GLCC's Poison, and caused physical harm to Joe S. McKinnon and the Kids of the Pathfinders Camp. Considering the fact that, if it were not for GLCC's Perpetrators' success in their conspiracy to defraud the United States by concealing GLCC's culpability in the physical harm that their conspiracy inflicted on Joe S. McKinnon and the Kids of the Pathfinders Camp, the infrastructure that was necessary for Chemtura Corporation to be created and exist would not have existed, and Chemtura Corporation would not exist. Thus, Chemtura Corporation would not have been able to make any revenue and/or profits since it was created in 2005, and would not have the potential to continue making any revenue and/or profit, unless it has been or will be derived from GLCC's Perpetrators' success in their conspiracy to defraud the United States, and unless it has been derived from their success in concealing their culpability in the physical harm that their conspiracy inflicted on Joe S. McKinnon and the Kids of the Pathfinders Camp. There is a web page that provides guidelines for dealing with situations like this matter, under fair and Constitutional circumstances, regarding 18 U.S.C § 3681. These guidelines are, as follow (quotation marks omitted):

18 U.S.C § 3681 says the following (quotation marks omitted):

(a) Upon the motion of the United States attorney made at any time after conviction of a defendant for...an offense against the United States resulting in physical harm to an individual, and after notice to any interested party, the court shall, if the court determines that the interest of justice or an order of restitution under this title so requires, order such defendant to forfeit all or any part of proceeds received or to be received by that defendant, or a transferee of that defendant, from a contract relating to...or emotions regarding such crime.

(b) An order issued under subsection (a) of this section shall require that the person with whom the defendant contracts pay to the Attorney General any proceeds due the defendant under such /contract.

(c) (1) Proceeds paid to the Attorney General under this section shall be retained in escrow in the Crime Victims Fund in the Treasury by the Attorney General for five years after the date of an order under this section, but during that five year period may -

(A) be levied upon to satisfy -

(i) a money judgment rendered by a United States district court in favor of a victim of an offense for which such defendant has been convicted, or a legal representative of such victim; and

(ii) a fine imposed by a court of the United States; and

(B) if ordered by the court in the interest of justice, be used to -

(i) satisfy a money judgment rendered in any court in favor of a victim of any offense for which such defendant has been convicted, or a legal representative of such victim; and

(ii) pay for legal representation of the defendant in matters arising from the offense for which such defendant has been convicted, but no more than 20 percent of the total proceeds may be so used.


(2) The court shall direct the disposition of all such proceeds in the possession of the Attorney General at the end of such five years and may require that all or any part of such proceeds be released from escrow and paid into the Crime Victims Fund in the Treasury.

(d) As used in this section, the term "interested party" includes the defendant and any transferee of proceeds due the defendant under the contract, the person with whom the defendant has contracted, and any person physically harmed as a result of the offense for which the defendant has been convicted.

EFFECTIVE DATE [ ] Chapter effective 30 days after Oct. 12, 1984, see section 1409(a) of Pub. L. 98-473, set out as a note under section 10601 of Title 42, The Public Health and Welfare.(Reference 11)

The DOJ has a web page that gives information about dealing people like the Perpetrators at GLCC who have defrauded the United States. Relevant information from this web page is, as follows (quotation marks omitted):

The general conspiracy statute, 18 U.S.C. § 371, creates an offense "[i]f two or more persons conspire either to commit any offense against the United States, or to defraud the United States, or any agency thereof in any manner or for any purpose. (emphasis added). See Project, Tenth Annual Survey of White Collar Crime, 32 Am. Crim. L. Rev. 137, 379-406 (1995)(generally discussing § 371).

The operative language is the so-called "defraud clause," that prohibits conspiracies to defraud the United States. This clause creates a separate offense from the "offense clause" in Section 371. Both offenses require the traditional elements of Section 371 conspiracy, including an illegal agreement, criminal intent, and proof of an overt act

Although this language is very broad, cases rely heavily on the definition of "defraud" provided by the Supreme Court in two early cases, Hass v. Henkel, 216 U.S. 462 (1910), and Hammerschmidt v. United States, 265 U.S. 182 (1924). In Hass the Court stated: The statute is broad enough in its terms to include any conspiracy for the purpose of impairing, obstructing or defeating the lawful function of any department of government . . . [A]ny conspiracy which is calculated to obstruct or impair its efficiency and destroy the value of its operation and reports as fair, impartial and reasonably accurate, would be to defraud the United States by depriving it of its lawful right and duty of promulgating or diffusing the information so officially acquired in the way and at the time required by law or departmental regulation. Hass, 216 U.S. at 479-480. In Hammerschmidt, Chief Justice Taft, defined "defraud" as follows:

To conspire to defraud the United States means primarily to cheat the Government out of property or money, but it also means to interfere with or obstruct one of its lawful governmental functions by deceit, craft or trickery, or at least by means that are dishonest. It is not necessary that the Government shall be subjected to property or pecuniary loss by the fraud, but only that its legitimate official action and purpose shall be defeated by misrepresentation, chicane or the overreaching of those charged with carrying out the governmental intention. Hammerschmidt, 265 U.S. at 188.

The general purpose of this part of the statute is to protect governmental functions from frustration and distortion through deceptive practices. Section 371 reaches "any conspiracy for the purpose of impairing, obstructing or defeating the lawful function of any department of Government."


Tanner v. United States, 483 U.S. 107, 128 (1987); see Dennis v. United States, 384 U.S. 855 (1966). The "defraud part of section 371 criminalizes any willful impairment of a legitimate function of government, whether or not the improper acts or objective are criminal under another statute." United States v. Tuohey, 867 F.2d 534, 537 (9th Cir. 1989).

The word "defraud" in Section 371 not only reaches financial or property loss through use of a scheme or artifice to defraud but also is designed and intended to protect the integrity of the United States and its agencies, programs and policies. United States v. Burgin, 621 F.2d 1352, 1356 (5th Cir.), cert. denied, 449 U.S. 1015 (1980); see United States v. Herron, 825 F.2d 50, 57-58 (5th Cir.); United States v. Winkle, 587 F.2d 705, 708 (5th Cir. 1979), cert. denied, 444 U.S. 827 (1979). Thus, proof that the United States has been defrauded under this statute does not require any showing of monetary or proprietary loss. United States v. Conover, 772 F.2d 765 (11th Cir. 1985), aff'd, sub. nom. Tanner v. United States, 483 U.S. 107 (1987); United States v. Del Toro, 513 F.2d 656 (2d Cir.), cert. denied, 423 U.S. 826 (1975); United States v. Jacobs, 475 F.2d 270 (2d Cir.), cert. denied, 414 U.S. 821 (1973).

Thus, if the defendant and others have engaged in dishonest practices in connection with a program administered by an agency of the Government, it constitutes a fraud on the United States under Section 371. United States v. Gallup, 812 F.2d 1271, 1276 (10th Cir. 1987); Conover, 772 F.2d at 771. In United States v. Hopkins, 916 F.2d 207 (5th Cir. 1990), the defendants' actions in disguising contributions were designed to evade the Federal Election Commission's reporting requirements and constituted fraud on the agency under Section 371.

The intent required for a conspiracy to defraud the government is that the defendant possessed the intent (a) to defraud, (b) to make false statements or representations to the government or its agencies in order to obtain property of the government, or that the defendant performed acts or made statements that he/she knew to be false, fraudulent or deceitful to a government agency, which disrupted the functions of the agency or of the government. It is sufficient for the government to prove that the defendant knew the statements were false or fraudulent when made. The government is not required to prove the statements ultimately resulted in any actual loss to the government of any property or funds, only that the defendant's activities impeded or interfered with legitimate governmental functions. See United States v. Puerto, 730 F.2d 627 (11th Cir.), cert. denied, 469 U.S. 847 (1984); United States v. Tuohey, 867 F.2d 534 (9th Cir. 1989); United States v. Sprecher, 783 F. Supp. 133, 156 (S.D.N.Y. 1992)(þit is sufficient that the defendant engaged in acts that interfered with or obstructed a lawful governmental function by deceit, craft, trickery or by means that were dishonest"), modified on other grounds, 988 F.2d 318 (2d Cir. 1993).

In United States v. Madeoy, 912 F.2d 1486 (D.C. Cir. 1990), cert. denied, 498 U.S. 1105 (1991), the defendants were convicted of conspiracy to defraud the government and other offenses in connection with a scheme to fraudulently obtain loan commitments from the Federal Housing Administration (FHA) or Veterans Administration (VA). The court held that the district court had properly instructed the jury that: the Government must prove beyond a reasonable doubt the existence of a scheme or artifice to defraud, with the objective either of defrauding the FHA or the VA of their lawful right to conduct their business and affairs free from deceit, fraud or misrepresentation, or of obtaining money and property from the FHA by means of false and fraudulent representations and promises which the defendant knew to be false. Madeoy, 912 F.2d at 1492.

Prosecutors considering charges under the defraud prong of Section 371, and the offense prong


of Section 371 should be aware of United States v. Minarik, 875 F.2d 1186 (6th Cir. 1989) holding limited, 985 F.2d 962 (1993), and related cases. See United States v. Arch Trading Company, 987 F.2d 1087 (4th Cir. 1993). In Minarik, the prosecution was found to have "used the defraud clause in a way that created great confusion about the conduct claimed to be illegal," and the conviction was reversed. 875 F.2d at 1196. After Minarik, defendants have frequently challenged indictments charging violations of both clauses, although many United States Courts of Appeals have found it permissible to invoke both clauses of Section 371. Arch Trading Company, 987 F.2d at 1092 (collecting cases); see also United States v. Licciardi, 30 F.3d 1127, 1132-33 (9th Cir. 1994)(even though the defendant may have impaired a government agency's functions, as part of a scheme to defraud another party, the government offered no evidence that the defendant intended to defraud the United States and a conspiracy to violate an agency regulatory scheme could not lie on such facts).

In summary, those activities which courts have held defraud the United States under 18 U.S.C. § 371 affect the government in at least one of three ways:

They cheat the government out of money or property; They interfere or obstruct legitimate Government activity; or They make wrongful use of a governmental instrumentality.

[cited in USAM 9-42.001] (Reference 12)

People in corporate offices of Chemtura Corporation were aware of my Claim, except for the dollar amount, prior to March 18, 2009; the day that Chemtura Corporation filed for chapter 11 Bankruptcy protection. Considering the success that Perpetrators at GLCC have had in executing their conspiracy to defraud the United States in ways that have frustrated, disrupted, and impaired, the functions of the Arkansas Department of Health, the ADEQ, the USEPA, the ATSDR, and the D.C. Cir., people in the corporate offices of Chemtura Corporation might believe that it would be okay to ignore and forget my Claim.

GLCC's Perpetrators' successful conspiracy to defraud the Arkansas Department of Health, the ADEQ, and the USEPA, and the D.C. Cir., has had the effect of tampering with the services, or "consumer products," that should have been provided to Joe S. McKinnon and the Kids of the Pathfinders Camp, between 1970 and 2009. If the Perpetrators at GLCC had not been so successful at their conspiracy to defraud these government entities, Joe S. McKinnon and the Kids of the Pathfinders Camp would not have been in need of the services, or "consumer products," that should have been provided by: the FBI to Joe S. McKinnon's Family and the Kids of the Pathfinders Camp, since June of 2002; and we would not be in need of the services, or "consumer products," that should have been and/or should be provided by the rest government employees and entities to whom this Summary of Proof of Claim is addressed.

I would like to be able to ignore the fact that Perpetrators at GLCC successfully executed a conspiracy to defraud the United States, which caused my father to suffer and die from diseases that were caused by GLCC's Poisons at the Pathfinders Camp. I would like to be able to ignore the fact that Perpetrators at GLCC successfully executed a conspiracy to defraud the United States, which is causing


Kids of the Pathfinders Camp to suffer diseases that are results of exposure to GLCC's Poisons at the Pathfinders Camp. But I hold a legal, moral, and ethical responsibility to file this Summary of Proof of Claim and Proof of Claim Form on their behalf. And I cannot ignore these facts. It would be wrong for anyone who holds culpability, liability, or stewardship, for this matter to ignore these facts.

I believe that there are good people at Chemtura Corporation, and believe that they are capable of transforming their company - from a company that has profited by operating with insidious, reckless, criminal, behavior - to become a company that will be prosperous and law abiding. This transformation can only happen after the Crimes of GLCC and the effects of GLCC's Poisons have had on Joe McKinnon's Family, the Kids of the Pathfinders Camp, and the Pathfinders Camp, have been properly addressed.

It is possible that United States Attorney General Eric Holder and/or President Barak Obama will address my 2nd Attempt with Amended Petition for WOHCAS of Environmental Law 2009, or the information in this Summary of Proof of Claim, in a way that opens access to rights described in 18 U.S.C § 3771, 5th Amendment of the United States Constitution, 18 U.S.C. § 3663A, and the fundamental human right of prosecution and compensation for human rights abuses that Perpetrators at GLCC have committed against Joe S. McKinnon's Family and the Kids of the Pathfinders Camp. It is, also, possible that it will be the next United States Attorney General and President, or the next, or it could be those that follow them, who address Constitutional Challenges that my 2nd Attempt with Petition for WOHCAS of Environmental Law 2009 presents along with the information in this Summary of Proof of Claim. Regardless of how long it takes for this matter to be resolved, every penny that Chemtura Corporation makes in revenue and/or profit will be at the expense of Joe S. McKinnon's Family and the Kids of the Pathfinders Camp, until we have access to the above mentioned rights, or until Chemtura Corporation voluntarily makes a bona fide effort to rectify the harm and damages that the Crimes of GLCC and GLCC's Poison have done.

I talked on the telephone with the Investigations Division of the Department of Justice Office of the Inspector General long enough to make sure my 2nd Attempt with Amended Petition for WOHCAS of Environmental Law 2009 had been received and read by at least one person in that office had read some of it, on March 17, 2009.

I received a letter, dated April 22, 2009, from the Operations Section of the Department of Justice Office of the Inspector General, which indicates that the information that the Investigations Division received from me had been referred to the the United States Department of Justice Office of Professional Responsibility. I have talked with people in the Office of Professional Responsibility a few times, since April 22, 2009. Every time that I have talked with them, the conversations ended with them assuring me that their office was reviewing my information, and that I would be receiving a written response from them. Unless their written response, or a written response from United States Attorney General Eric Holder, tells me that they have decided that Joe S. McKinnon's Family and the Kids of the Pathfinders Camp do not have rights that are described in 18 U.S.C § 3771, 5th Amendment of the United States Constitution, 18 U.S.C. § 3663A, and the fundamental human right of prosecution and compensation for human rights abuses, I will continue to hope that we may, eventually, be represented by United States Attorneys - who will let me give them my supporting evidence in a way that I can explain the insidious details, so they can validate my evidence, prosecute the Perpetrators at GLCC to the fullest extent of the law, and cause the Court to order Chemtura Corporation to pay a reasonable amount in restitution and compensation.


The Notice of Bar Date says: "...the Bankruptcy Court entered an order establishing October 30, 2009...as the deadline (the "Bar Date") for any person or entity (including individuals, corporations, partnerships, trusts and governmental units) to file a proof of claim ( a "Proof of Claim"). The Bar Date and the procedures for filing a Proof of Claim apply to all Claims (as defined in section 101(5) of the Bankruptcy Code) against a Debtor that arose prior to March 18, 2009, except as specifically excluded below." Then, below that it says: "YOU ARE RECEIVING THIS NOTICE because you may have a Claim against one or more of the Debtors. However, not everyone who receives this notice will have a Claim against a Debtor."

11 U.S.C. § 101(5) says: "(A) says: "The term “claim” means— right to payment, whether or not such right is reduced to judgment, liquidated, unliquidated, fixed, contingent, matured, unmatured, disputed, undisputed, legal, equitable, secured, or unsecured; or (B) right to an equitable remedy for breach of performance if such breach gives rise to a right to payment, whether or not such right to an equitable remedy is reduced to judgment, fixed, contingent, matured, unmatured, disputed, undisputed, secured, or unsecured."

The Notice of Bar Date says: "IF THE DEADLINE APPLIES TO YOU AND YOU FAIL TO FILE A PROOF OF CLAIM BY THE BAR DATE, YOUR CLAIM WILL BE FOREVER BARRED. THIS MEANS THAT YOU WILL NOT BE ELIGIBLE TO VOTE ON ANY CHAPTER 11 PLAN AND YOU WILL NOT BE ELIGIBLE TO RECEIVE ANY DISTRIBUTION FROM THE DEBTORS ON ACCOUNT OF YOUR CLAIM."

The Notice of Bar Date says: "You MUST file a Proof of Claim if you have a Claim against any of the Debtors that arose before March 18, 2009, except for the types of Claims listed below. Acts or omissions that occurred before March 18, 2009 may give rise to Claims that are subject to the Bar Date, even if the Claims may not have become known or fixed or liquidated until after March 18, 2009."

The Notice of Bar Date says: "...In addition, you must attach to your Proof of Claim any documents on which your Claim is based (if the documents are voluminous, you may instead attach a summary)..." PLEASE TAKE NOTICE that the documents and other forms of evidence, which support my Claim, are extremely voluminous.

The Notice of Bar Date says: "...You also must specifically identify the Debtor against which you assert a Claim by name and case number..."

PLEASE TAKE NOTICE that people in the corporate offices of Chemtura Corporation knew about the Crimes of GLCC and GLCC's Poison at the Pathfinders Camp prior for a few years prior to filing for chapter 11 Bankruptcy protection on March 18, 2009. They have, also, been aware of the effects that the Crimes of GLCC and GLCC's Poison at the Pathfinders Camp may have had on Joe S. McKinnon, the Kids of the Pathfinders Camp, and the Pathfinders Camp, for a few years prior to March 18, 2009. I haven't seen Chemtura Corporation's list of liabilities for these chapter 11 Bankruptcy proceedings, but it is reasonable to expect Chemtura Corporation's legal team to already have the Crimes of GLCC and the effects that GLCC's Poison at the Pathfinders Camp may have had on Joe S. McKinnon, the Kids of the Pathfinders Camp, and the Pathfinders Camp, somewhere on Chemtura Corporation's list of liabilities.


The Notice of the Bar Date says that "For your Proof of Claim to be valid, it must...be denominated in United States dollars..."

To determine the dollar amount for the life of Joe S. McKinnon, whose way of life and genetic heritage would have very likely made him excessively healthy, and would have very likely caused him to live 20 to 30 years longer than he did, if he had not been, chronically, exposed to GLCC's Poison at the Pathfinders Camp, which was a result of the Crimes of GLCC, is not as simple as calculating lost income and expenses. He was not just an ordinary man, not just an ordinary father, and not just an ordinary teacher and coach, because he kept the achievements, comfort, and general wellbeing, of the kids he served, and of his own children, as higher priorities than his own comfort, wellbeing, and potential achievements, and because his dedication to helping hundreds of teenagers grow up to be the kind of adults that make the world a better place for everyone went far above and beyond what would be expected of anyone.

Determining the dollar amount for the debt that Chemtura owes Joe S. McKinnon's Family for harmful effects that the Crimes of GLCC and GLCC's Poison at the Pathfinders Camp had on the life that Joe S. McKinnon could have had if he had not died prematurely is not all there is to consider, because it also involves considering how his life was injuriously affected by the Crimes of GLCC and GLCC's Poison for about 30 years prior to his death.

Measuring the harmful and injurious effects that the Crimes of GLCC and GLCC's Poison have caused for Joe S. McKinnon's Family and the Kids of the Pathfinders Camp, involves more than just calculating Chemtura's debt by considering the costs and/or expenses for injuries of approximately 507 people, because some of GLCC's Poisons at the Pathfinders Camp cause epigenetic changes (damage to DNA), which makes it likely that the posterity of Joe S. McKinnon's Family and the Kids of the Pathfinders Camp will suffer injurious and/or harmful effects of GLCC's Crimes and Poison for infinite, future, generations.

Because the Notice of Bar Date requires me to place a dollar amount on my Claim, and because I am only seeking what is considered by the United States Courts to be reasonable, fair, in line with statutory law and the United States Constitution, I am providing information about some cases that I have found on the Internet, which have some characteristics like my Claim, to give us examples of what is a reasonable and legal dollar amount for restitution and compensation. These examples are, as follow (quotation marks omitted):

EXAMPLE 1:

"U.S. Seeks Nearly $4 Million in Restitution from Family Secret Mobsters [] UNITED STATES DISTRICT COURT NORTHERN DISTRICT OF ILLINOIS EASTERN DIVISION UNITED STATES OF AMERICA ) ) No. 02 CR 1050 v. )) Judge James B. Zagel [] FRANK CALABRESE SR., et al. ) MOTION FOR IMPOSITION OF RESTITUTION [ ] This cause comes before the Court on motion of the United States for imposition of restitution, pursuant to the Mandatory Victims Restitution Act (“MVRA”), in the above-captioned matter against defendants Frank Calabrese Sr., James Marcello, Joseph Lombardo, Paul Schiro, and Anthony Doyle.1 For the reasons discussed below, these defendants are jointly and severally liable for a total restitution amount of $3,909,166.30.2... The charged conspiracy involved, among other categories of criminal conduct, the murders of 18 individuals. See Doc. #397 at 9-10. There is little dispute that these murders were part of the


conspiracy, and were committed to advance the criminal objectives of the Chicago Outfit..."(Reference 13)

EXAMPLE 2:

"FOR IMMEDIATE RELEASE [ ] ENRD [ ] SATURDAY, APRIL 29, 2000 [ ] ...WWW.USDOJ.GOV...WASHINGTON, D.C. -- In the longest sentence ever imposed for an environmental crime, a federal judge has ordered an Idaho man to serve 17 years in prison for his crimes that left a 20-year-old employee with permanent brain damage from cyanide poisoning, the Department of Justice announced. Allan Elias also was ordered to pay $6 million in restitution to the victim and his family. (Reference 14)

EXAMPLE 3:

FOR IMMEDIATE RELEASE [ ] MONDAY, MAY 13, 2002 [ ] WWW.USDOJ.GOV [ ] ASHLAND, INC. PLEADS GUILTY TO ENDANGERING EMPLOYEES UNDER THE CLEAN AIR ACT (Reference 15)

MINNEAPOLIS, MN.- Ashland, Inc. pleaded guilty today in United States District Court to criminal charges related to a May 16, 1997 fire and explosion at its former Minnesota refinery, the Department of Justice announced today. As part of the plea, Ashland agreed to pay more than $7 million in fines and restitution.

Ashland pled guilty to two criminal counts that charged it with negligent endangerment under the Clean Air Act and submitting a false certification to environmental regulators. Ashland also agreed to a deferred prosecution for a violation of the New Source Performance Standards (NSPS) of the Clean Air Act.

Under the terms of the plea agreement, Ashland has agreed to pay restitution to the victims. The primary victim, a former Ashland employee and member of the Emergency Response Team (ERT), will receive $3.5 million and medical coverage for him and his family, and each of the other four Ashland employees injured in the fire will also receive $10,000.

"This case embodies the Justice Department's commitment to holding accountable environmental offenders for their criminal deeds that harm both people and the environment," said Tom Sansonetti, Assistant Attorney General of the Department of Justice's Environment and Natural Resources Division.

Ashland will also pay a criminal fine of $3.5 million; sponsor a workshop at a national petroleum conference dealing with the Clean Air Act's New Source Performance Standards for petroleum wastewater systems; take out full-page notices in the two major Twin Cities newspapers acknowledging their guilt and how the case was resolved; pay $50,000 to each of the three local fire departments that responded to the fire; and add another $50,000 to their own ERT budget.

Ashland has also agreed to upgrade all of its process sewers, junction boxes and drains at the St. Paul Park refinery (now owned by Marathon Ashland Petroleum LLC, a joint-venture between Ashland and Marathon Oil Company) to help ensure this type of incident never again occurs. This project is


estimated to cost $3.7 million.

EXAMPLE 4:

Also in 2005, Motiva Enterprises, a joint venture of Shell Oil Company and a subsidiary of the Saudi government's national oil company, pleaded guilty to negligently endangering workers at an explosion in Delaware City, Del., facilities in July 2001. The blast killed one worker, Jeffrey Davis, and injured eight others. The company also pleaded guilty to allowing some 99,000 gallons of sulfuric acid to drain into the Delaware River after the explosion and negligently releasing sulfuric acid into the air.The company was fined $10 million for a criminal violation of the Clean Air Act, paid a $12 million civil penalty for violations of other federal and state environmental laws, and more than $35 million to settle with Davis' family. (Reference 16)

EXAMPLE 5:

In October 2007, a subsidiary of British Petroleum (BP) pleaded guilty to a one-count felony violation of the Clean Air Act for a March 2005 explosion at a Texas oil refinery that killed 15 workers and injured more than 170 others. The company agreed to pay a record fine of $50 million under the Clean Air Act. According to a BP spokesman, the company has also paid more than a $1.6 billion dollars in civil settlements to families of the victims thus far, with hundreds of claims outstanding. (Reference 16)

EXAMPLE 6:

Worker Safety: The Longest Sentence Ever for an Environmental Crime. A Wharton-educated businessman and attorney was convicted of knowingly endangering the health and safety of his employees during illegal hazardous waste storage and disposal activities that left a 20-year-old employee with severe permanent brain damage from cyanide poisoning. In addition to the knowing endangerment charges, Elias was convicted on two counts of illegal disposal of hazardous waste, and making false statements to OSHA inspectors in an effort to conceal the knowing endangerment of his employees. On April 28, 2000, a federal district court in Idaho handed down the longest sentence ever for an environmental crime -- 17 years in prison. Elias was also ordered to pay approximately $6 million in restitution to the family of the injured employee, and $400,000 in cleanup costs. (Reference 17)

DOLLAR AMOUNT FOR THIS CLAIM:

Keeping in mind that the only way Joe S. McKinnon's Family and the Kids of the Patfinders Camp will be treated fairly in this case will be after FBI agents and U.S. Attorneys have met with me for the bona fide purpose of receiving information and other evidence that I have collected, with them having a reasonable amount of time, budget, and willingness to understand the insidious details of the Crimes of the Perpetrators at GLCC and GLCC's Poison at the Pathfinders Camp, and for U.S. Attorneys to put forth a bona fide effort to use this information and other evidence to prosecute the Perpetrators at GLCC to the fullest extent of the law, and keeping in mind that, under such fair and Constitutional circumstances, my understanding is that the amount of restitution and compensation will depend on decisions made by the U.S. Attorneys and U.S. Courts, I can only place a dollar amount on this Claim as being what appears to be reasonable and legal for the debt that Chemtura owes to Joe S.


McKinnon's Family and the Kids of the Pathfinders Camp. After looking at the listed examples of cases, and many other similar cases, it does appear to be reasonable and legal to Claim that restitution and compensation could be as much as $8,000,000,00 (EIGHT MILLION DOLLARS) for the death of Joe S. McKinnon, $3,000,000.00 (THREE MILLION DOLLARS) for the harmful damage that has been done by Perpetrators at GLCC to each Kid of the Pathfinders Camp, and $384,000.00 to cover the financial damage that dealing with the Crimes of GLCC has already caused for me. This would be a total of $1,529.384,000 (ONE BILLION FIVE HUNDRED TWENTY-NINE THOUSAND THREE HUNDRED EITHTY-FOUR THOUSAND DOLLARS).

It would be reasonable and legal to place a dollar amount for this Claim at $509,384,000.00 (FIVE HUNDRED NINE MILLION THREE HUNDRED EIGHTY-FOUR THOUSAND DOLLARS) with potential for more, and potential for less, but no less than $59,384,000.00 (FIFTY-NINE MILLION THREE HUNDRED EIGHTY-FOUR THOUSAND DOLLARS).

PLEASE TAKE NOTICE of this necessary modification in the part of my Proof of Claim Form for Creditor's Name and Address:

It was: Joe S. McKinnon Estate It is changed to: Joe S. McKinnon's Family C/O Frank McKinnon and Kids of Pathfinders Camp 903 N. Missouri C/O Frank McKinnon Roswell, NM 88201 903 N. Missouri Ave. Roswell, NM 88201

I declare, under penalty of perjury that the foregoing Summary of Proof of Claim is true and correct.

Respectfully submitted

__________________________________ (Signature)

Date: ____11/12/2009____

Frank L. McKinnon, on behalf of: Joe S. McKinnon's Family and the Kids of the Pathfinders Camp 903 N. Missouri Ave Roswell, NM 88201 telephone: (575) 420-8199 email: [email protected]


REFERENCES

(1) http://www.frankmckinnon.com/files/WOHCASO_Environmental_Law_2009_corrected_.pdf

(2) http://www.frankmckinnon.com/files/2nd_Attempt_WOHCAS_of_Environmental_Law_2009.pdf

(3) http://www.usdoj.gov/usao/eousa/vr/cvra/18_USC_3771.html

(4) http://www.law.cornell.edu/uscode/18/usc_sec_18_00003663---A000-.html

(5) "Williams, Glanville (1983), Textbook of Criminal Law (2 ed.), London: Stevens & Sons,"http://en.wikipedia.org/wiki/Malice_aforethought#cite_ref-0

(6) Cornell Law Library at http://www.law.cornell.edu/uscode/...

(7) http://www.usdoj.gov/usao/eousa/vr/cvra/18_USC_3771.html

(8) http://www.fbi.gov/hq/cid/victimassist/crimevictims.htm

(9) "THE FUNDAMENTAL HUMAN RIGHT TO PROSECUTION AND COMPENSATION" by Jon M. Van Dyke1, William S. Richardson School of Law, University of Hawai`i at Manoa, Myres McDougal Lecture, Regional Conference of the American Society of International Law "Military Intervention on Humanitarian Grounds after Rwanda, Kosovo, Sierra Leone and East Timor" University of Denver College of Law March 25, 2000 http://www.ipunlimited.org/Media_Center/Shift_Happens/Fundamental_Right_to_Prosecuti /fundamental_right_to_prosecuti.html

(10) http://constitutioncenter.org/633876696043236250.pdf

(11) http://law.onecle.com/uscode/18/3681.html

(12) http://www.usdoj.gov/usao/eousa/foia_reading_room/usam/title9/crm00923.htm

(13) http://www.thechicagosyndicate.com/2008/10/us-seeks-nearly-4-million-in.html#

(14) http://www.usdoj.gov/opa/pr/2000/April/239enrd.htm

(15) http://justice.gov/opa/pr/2002/May/02_enrd_286.htm

(16) http://www.pbs.org/wgbh/pages/frontline/mcwane/penalty/initiative.html

(17) http://www.usdoj.gov/enrd/ENRD_2000_Lit_Accomplishments.html

(18) EPA-560-6-78-002 or http://nepis.epa.gov/Exe/ZyNET.exe/40001GYV.txt?ZyActionD=ZyDocument&Client=EPA&Index=1976%20Thru%201980&Docs=&Query=%28parker%27s%20chapel%29%20OR%20FNAME%3D%2240001GYV.txt%22%20AND%20FNAME%3D%2240001GYV.txt%22&Time=&EndTime=&SearchMethod=1&TocRestrict=n&Toc=&TocEntry=&QField=&QFieldYear=&QFieldMonth=&QFieldDay=&UseQField=&IntQFieldOp=1&ExtQFieldOp=1&XmlQuery=&File=D%3A%5CZYFILES%5CINDEX%20DATA%5C76THRU80%5CTXT%5C00000010%5C40001GYV.txt&User=ANONYMOUS&Password=anonymous&SortMethod=h%7C-&MaximumDocuments=10&FuzzyDegree=0&ImageQuality=r75g8/r75g8/x150y150g16/i425&Display=p%7Cf&DefSeekPage=x&SearchBack=ZyActionL&Back=ZyActionS&BackDesc=Results%20page

(19) http://www.atsdr.cdc.gov/Mhmi/mmg37.html


(20) [International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 1083] **PEER REVIEWED**


(22) [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-162] **PEER REVIEWED**

(23) [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 735] **PEER REVIEWED**

(24) http://cdc.gov/niosh/pdfs/77-221b.pdf

(25) http://www.cdphe.state.co.us/rma/resourcenotebook/Chemicals/dibromo.pdf

(26) [Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 49-15] **PEER REVIEWED**

(27) [ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988., p. 22] **PEER REVIEWED**

(28) http://msds.chem.ox.ac.uk/BR/3-bromo.html

(29) [Rohrig TP; Am J Forensic Med Pathol 18 (3): 299-302 (1997)] **PEER REVIEWED**

(30) [Williams DR, Cole S; Resuscitation 37 (1): 43-45 (1998)] **PEER REVIEWED**

(31) [Doring G, Baumeister FA; Klin Padiatr 214 (5): 295-298 (2002)] **PEER REVIEWED**

(32) [Mathew B et al; Br J Addict 84 (5): 563-4 (1989)] **PEER REVIEWED**

(33) [Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988., p. 967] **PEER REVIEWED**

(34) [Fernandez F et al; Dev Med Child Neurol 28 (3): 361-3 (1986)] **PEER REVIEWED**

(35) [Fuke C, Miyazaki T; Legal Medicine 4 (2): 134-138 (2002)] **PEER REVIEWED**

(36) [Cartwright TR, Brown ED; Arch Intern Med 143(10): 2007-2008 (1983)] **PEER REVIEWED**

(37) [USEPA; Ambient Water Quality Criteria Doc: Halomethanes p.C-47-8 (1980) EPA 440/5-80-051] **PEER REVIEWED**


(39) http://toxnet.nlm.nih.gov/

(40) [Haddad, L.M., Clinical Management of Poisoning and Drug Overdose. 2nd ed. Philadelphia, PA: W.B. Saunders Co., 1990., p. 1281] **PEER REVIEWED**

(41) [WHO; Environmental Health Criteria 113: Fully Halogenated


Chlorofluorocarbons p.90 (1990)] **PEER REVIEWED**

(42) [WHO; Environmental Health Criteria 113: Fully Halogenated Chlorofluorocarbons p.90 (1990)] **PEER REVIEWED**

(43) [Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 1195] **PEER REVIEWED**

(44) [DHHS/National Toxicology Program; Eleventh Report on Carcinogens: Acetaldehyde (75-07-0) (January 2005). Available from, as of July 31, 2009: http://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s001acet.pdf ] **PEER REVIEWED**

(45) [U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on Acetaldehyde (75-07-0) Available from: http://www.epa.gov/ngispgm3/iris on the Substance File List as of March 15, 2000] **PEER REVIEWED**

(46) [American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED**

(47) [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 32] **PEER REVIEWED**

(48) American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED**

(49) [Dreisbach, R.H. Handbook of Poisoning. 12th ed. Norwalk, CT: Appleton and Lange, 1987., p. 186] *PEER REVIEWED** (50) [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V71 324 (1985)] **PEER REVIEWED**

(51) [Badr FM, Hussain F; Genetics 86: S2-3 (1977) as cited in USEPA; Chemical Hazard Information Profile: Acetaldehyde (Draft) p.29 (1983)] **PEER REVIEWED**

(52) [Lambert BO et al; Mutat Res 146: 301-3 (1985)] **PEER REVIEWED**

(53) [He SM, Lambert B; Environ Mol Mutagen 16 (2): 57-63 (1990)] **PEER REVIEWED**

(54) [Lambert B, He SM; Annals of the New York Academy of Sciences 534: 369-76 (1988)] **PEER REVIEWED**

(55) [Xi, Z-G et al; Bian Ji, Zhongguo Ke Xue Yuan Huan Jing Ke Xue Wei Yuan Hui 25 (3): 102-5 (2004)] **PEER REVIEWED** PubMed Abstract

(56) [Singh NP et al; Mutat Res 337 (1): 9-17 (1995)] **PEER REVIEWED** PubMed Abstract

(57) [IPCS, CEC; International Chemical Safety Card on Isopentane. (April 1994). Available from, as of October 11, 2006: http://www.inchem.org/documents/icsc/icsc/eics1153.htm ] **PEER REVIEWED**

(58) [IPCS, CEC; International Chemical Safety Card on Isopentane. (April 1994). Available from, as of October


11, 2006: http://www.inchem.org/documents/icsc/icsc/eics1153.htm ] **PEER REVIEWED**

(59) [International Labour Office. Encyclopedia of Occupational Health and Safety. Volumes I and II. New York: McGraw-Hill Book Co., 1971., p. 687] **PEER REVIEWED**

(60) [Hamilton, A., and H. L. Hardy. Industrial Toxicology. 3rd ed. Acton, Mass.: Publishing Sciences Group, Inc., 1974., p. 264] **PEER REVIEWED**

(61) [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 4:26] **PEER REVIEWED**

(62) [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] **PEER REVIEWED** (63) [IPCS, CEC; International Chemical Safety Card on Isopentane. (April 1994). Available from, as of October 11, 2006: http://www.inchem.org/documents/icsc/icsc/eics1153.htm ] **PEER REVIEWED**

(64) [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 782] **PEER REVIEWED**


(66) [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989., p. 1517] **PEER REVIEWED**






(72) [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. 1] **PEER REVIEWED**








(79) [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1621] **PEER REVIEWED**




(83) [Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 2002. 4th ed.Vol 1 A-H Norwich, NY: Noyes Publications, 2002., p. 1954] **PEER REVIEWED**




(87) [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 2633] **PEER REVIEWED**

(88) [European Chemicals Bureau; IUCLID Dataset, 3-Methylbutanal (590-86-3). Available from, as of January 14, 2009: http://ecb.jrc.ec.europa.eu/esis/index.php?GENRE=CASNO&ENTREE=590-86-3 ] **PEER REVIEWED**

(89) [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V4 23] **PEER REVIEWED**


(91) [Prager, J.C. Environmental Contaminant Reference Databook Volume 2. New York, NY: Van Nostrand Reinhold, 1996., p. 685] **PEER REVIEWED**

(92) [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New


York, N.Y. (2001)., p. V4 23] **PEER REVIEWED**

(93) [American Conference of Governmental Industrial Hygienists. Documentation of Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices for 2001. Cincinnati, OH. 2001., p. 2] **PEER REVIEWED**



(96) [O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1277] **PEER REVIEWED**

(97) [European Chemicals Bureau; IUCLID Dataset, ACETONE (67-64-1). Available from, as of January 22, 2007: http://ecb.jrc.it/esis/esis.php ] **PEER REVIEWED**

(98) [DHHS/ATSDR; Toxicological Profile for Acetone p.13 (1994)] **PEER REVIEWED**

(99) [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-168] **PEER REVIEWED**



(102) [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983., p. 150] **PEER REVIEWED**

(103) [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983., p. 150] **PEER REVIEWED**

(104) [Gossel, T.A., J.D. Bricker. Principles of Clinical Toxicology. 3rd ed. New York, NY: Raven Press, Ltd., 1994., p. 89] **PEER REVIEWED**

(105) [Thienes, C., and T.J. Haley. Clinical Toxicology. 5th ed. Philadelphia: Lea and Febiger, 1972., p. 137] **PEER REVIEWED**



(108) [U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on ACETONE (CAS# 67-64-1) Available from: http://www.epa.gov/iris/index.html on the Substance File List as of January 22, 2007.] **PEER REVIEWED**

(109) [U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on ACETONE (CAS#


67-64-1) Available from: http://www.epa.gov/iris/index.html on the Substance File List as of January 22, 2007.] **PEER REVIEWED**

(110) [Chen JK et al; Am J Nephrol 22 (5-6): 560-5 (2002)] **PEER REVIEWED** PubMed Abstract

(111) [DHHS/ATSDR; Toxicological Profile for Acetone p.13 (1994)] **PEER REVIEWED**

(112) [Kerr MA et al; Cancer Causes Control 11 (7): 635-43 (2000)] **PEER REVIEWED** PubMed Abstract

(113) [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V71 299 (1999)] **QC REVIEWED**



(116) [Browning, E. Toxicity and Metabolism of Industrial Solvents. New York: American Elsevier, 1965., p. 246] **PEER REVIEWED**


(118) [BARROWCLIFF DF, KNELL AJ; J SOC OCCUP MED 29 (1): 12-4 (1979)] **PEER REVIEWED**

(119) [WINNEKE G; NEUROBEHAV TOXICOL TERATOL 3 (4): 391-5 (1981)] **PEER REVIEWED**

(120) [USEPA; Health Assessment Document: Dichloromethane (Methylene chloride) (Draft) p.5-9 (1982) EPA-600/8-82-004] **PEER REVIEWED**

(121) [Winek, C.L. Drug and Chemical Blood-Level Data 1985. Pittsburgh, PA: Allied Fischer Scientific, 1985.] **PEER REVIEWED**

(122) [STEWART RD, HAKE CL; JAMA 235 (4): 398-401 (1976)] **PEER REVIEWED**

(123) [PUTZ VR ET AL; J ENVIRON PATHOL TOXICOL 2 (5): 97-112 (1979)] **PEER REVIEWED**

(124) [ITII. Toxic and Hazarous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1982., p. 335] **PEER REVIEWED**


(126) [Sullivan, J.B. Jr., G.R. Krieger (eds.). Hazardous Materials Toxicology-Clinical Principles of Environmental Health. Baltimore, MD: Williams and Wilkins, 1992., p. 693] **PEER REVIEWED**



(128) Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V15 235 (1977)] **PEER REVIEWED**

(129) [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. S7 229 (1987)] **PEER REVIEWED**

(130) [Dreisbach, R.H. Handbook of Poisoning. 12th ed. Norwalk, CT: Appleton and Lange, 1987., p. 178] **PEER REVIEWED**


(132) [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V71 1031 (1999)] **PEER REVIEWED** (133) [Sullivan, J.B. Jr., G.R. Krieger (eds.). Hazardous Materials Toxicology-Clinical Principles of Environmental Health. Baltimore, MD: Williams and Wilkins, 1992., p. 1107] **PEER REVIEWED**

(134) [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984., p. 1901] **PEER REVIEWED**

(135) [Agnesi R et al; Intl Arch Occup Environ Health 69 (5): 311-316 (1997)] **PEER REVIEWED** PubMed Abstract

(136) http://www.anesthesia-analgesia.org/cgi/content/abstract/104/4/822

(137) [NTP; Eleventh Report on Carcinogens - Chloroform (January 31, 2005) Available from, as of October 17, 2008: http://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s038chlo.pdf ] **PEER REVIEWED**

(138) [Fodor GG, Roscovanu A; Zentrialbl Bakteriol (Orig B) 162: 34 (1976) as cited in USEPA; Ambient Water Quality Criteria Doc: Halomethanes p.C-40 (1980) EPA 440/5-80-051] **PEER REVIEWED**

(139) http://nj.gov/health/eoh/rtkweb/documents/fs/1245.pdf

(140) http://nj.gov/health/eoh/rtkweb/documents/fs/qr/4147qr.pdf

(141) http://www.inchem.org/documents/icsc/icsc/eics0816.htm


(143) [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V4 p.47] **PEER REVIEWED**





York, N.Y. (2001)., p. V4 p.48] **PEER REVIEWED**




(150) [Pastore C et al; Muscle Nerve 26 (1): 132-5 (2002)] **PEER REVIEWED**(151) [Issever H et al; Occup Med (Lond) 52 (4): 183-6 (2002)] **PEER REVIEWED**

(152) [Chang CM et al; J Neurol Neurosurg Psychiatry 56 (5): 538-42 (1993)] **PEER REVIEWED**

(153) [Takeuchi Y; Environ Res 62 (1): 76-80 (1993)] **PEER REVIEWED**

(154) [Karakaya A et al; Hum Exp Toxicol 15 (1): 56-8 (1996)] **PEER REVIEWED**

(155) [Rom, W.N. (ed.). Environmental and Occupational Medicine. 2nd ed. Boston, MA: Little, Brown and Company, 1992., p. 566] **PEER REVIEWED**



(158) [Doull, J., C.D.Klassen, and M.D. Amdur (eds.). Casarett and Doull's Toxicology. 3rd ed., New York: Macmillan Co., Inc., 1986., p. 481] **PEER REVIEWED**

(159) [Sobue I et al; Int J Neurol 11 (4): 317-30 (1978)] **PEER REVIEWED**

(160) [Iida M; Electroencephalogr Clin Neurophysiol (Suppl) 36: 671-81 (1982)] **PEER REVIEWED**


(163) [Rom, W.N. (ed.). Environmental and Occupational Medicine. 2nd ed. Boston, MA: Little, Brown and Company, 1992., p. 566] **PEER REVIEWED**






York, N.Y. (2001)., p. V4 37] **PEER REVIEWED**

(168) [Vanacore N et al; Neurol Sci 21 (1): 49-52 (2000)] **PEER REVIEWED**

(169) [Pezzoli G et al; Mov Disord 10 (3): 279-82 (1995)] **PEER REVIEWED**

(170) [Ruff RL et al; Clin Toxicol 18 (5): 515-9 (1981)] **PEER REVIEWED**

(171) [Scelsi R et al; J Neurol Sci 47 (1): 7-19 (1980)] **PEER REVIEWED**

(172) [Chang YC; Br J Ind Med 48 (1): 12-7 (1991)] **PEER REVIEWED**

(173) [Huang CC, Chu NS; Clin Electroencephalogr 20 (3): 162-8 (1989)] **PEER REVIEWED**

(174) [RIZZUTO N ET AL; EUR NEUROL 19 (5): 308-15 (1980)] **PEER REVIEWED**



(177) [U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for 1,1,1-Trichloroethane p.59 (2006) PB/95/264396. Available from, as of December 24, 2007: http://www.atsdr.cdc.gov/toxpro2.html#bookmark05 ] **PEER REVIEWED**

(178) [IPCS; Poisons Information Monograph 540: 1,1,1-Trichloroethane. (April 1991). Available from, as of December 18, 2007: http://www.inchem.org/documents/pims/chemical/trichlor.htm ] **PEER REVIEWED**



(181) [McLeod AA et al; Br Med J (Clin Res Ed) 294 (6574): 727-9 (1987)] **PEER REVIEWED** PubMed Abstract

(182) [Winek CL et al; Forensic Sci Int 87 (2): 161-5 (1997)] **PEER REVIEWED** PubMed Abstract

(183) [Gresham GA, Treip CS; Forensic Sci Int 23 (2-3): 249-53 (1983)] **PEER REVIEWED** PubMed Abstract

(184) [GERACE RV; ANN EMERG MED 10 (10): 533-4 (1981)] **PEER REVIEWED**

(185) [U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for 1,1,1-Trichloroethane p.111 (2006) PB/95/264396. Available from, as of December 24, 2007: http://www.atsdr.cdc.gov/toxpro2.html#bookmark05 ] **PEER REVIEWED**

(186) [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] **PEER REVIEWED**



York, N.Y. (2001)., p. 122] **PEER REVIEWED**

(188) http://www.scottecatalog.com/msds.nsf/MSDSNo/589-34-4?OpenDocument

(189) [Cralley, L.J., L.V. Cralley (eds.). Patty's Industrial Hygiene and Toxicology. Volume III: Theory and Rationale of Industrial Hygiene Practice. 2nd ed., 3A: The Work Environment. New York, NY: John Wiley Sons, 1985., p. 174] **PEER REVIEWED**

(190) [Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985., p. 592] **PEER REVIEWED**



(193) [DHHS/National Toxicology Program; Eleventh Report on Carcinogens: Carbon Tetrachloride (56-23-5) (January 2005). Available from, as of July 31, 2009: http://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s029carb.pdf ] **QC REVIEWED**

(194) [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. 1] **PEER REVIEWED



(197) [Mahieu P et al; Acta Clin Belg 41 (4): 241-247 (1986)] **PEER REVIEWED**

(198) [NIOSH; Criteria Document: Carbon Tetrachloride p.18 (1975) DHEW Pub. NIOSH 76-133] **PEER REVIEWED**

(199) [USEPA, Office of Drinking Water; Criteria Document (Final Draft): Carbon Tetrachloride (1982) p.II-2 Contract No 2-813-03-644-09] **PEER REVIEWED**

(200) [USEPA; Health Assessment Document: Carbon Tetrachloride p.2-7 (1984) EPA-600/8-82- 001F] **PEER REVIEWED**



(203) [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. S4 74 (1982)] **PEER REVIEWED**


(204) [Worthing, C.R., S.B. Walker (eds.). The Pesticide Manual - A World Compendium. 7th ed. Lavenham, Suffolk, Great Britain: The Lavenham Press Limited, 1983., p. 93] **PEER REVIEWED** (205) [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. 1] **PEER REVIEWED**

(206) [DHHS/National Toxicology Program; Eleventh Report on Carcinogens: Tetrachloroethylene (127-18-4) (January 2005). Available from, as of July 31, 2009: http://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s169tetr.pdf ] **QC REVIEWED**


(208) [The Merck Index. 10th ed. Rahway, New Jersey: Merck Co., Inc., 1983., p. 1315] **PEER REVIEWED**

(209) [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 464] **PEER REVIEWED**

(210) [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values, 4th ed., 1980. Cincinnati, Ohio: American Conference of Governmmental Industrial Hygienists, Inc., 1980., p. 325] **PEER REVIEWED**


(212) [LARSEN NA ET AL; UGESKR LAEG 139 (5): 270-5 (1977)] **PEER REVIEWED**

(213) [SPARROW GP; CLIN EXP DERMATOL 2 (1): 17-22 (1977)] **PEER REVIEWED**

(214) [CHMIELEWSKI J ET AL; BULL INST MARIT TROP MED GDYNIA 27 (2): 197-205 (1976)] **PEER REVIEWED**

(215) [BAGNELL PC, ELLENBERGER HA; CAN MED ASSOC J 117 (9): 1047-8 (1977)] **PEER REVIEWED**

(216) [IKEDA M ET AL; TOXICOLOGY LETTERS 5: 251 (1980)] **PEER REVIEWED**

(217) [Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988., p. 986-7] **PEER REVIEWED**

(218) [Reynolds, J.E.F., Prasad, A.B. (eds.) Martindale-The Extra Pharmacopoeia. 28th ed. London: The Pharmaceutical Press, 1982., p. 107] **PEER REVIEWED**

(219) [Reynolds, J.E.F., Prasad, A.B. (eds.) Martindale-The Extra Pharmacopoeia. 28th ed. London: The Pharmaceutical Press, 1982., p. 107] **PEER REVIEWED**

(220) [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V63 191 (1995)] **PEER REVIEWED**

(221) [ITII. Toxic and Hazarous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical


Information Institute, 1982., p. 507] **PEER REVIEWED**


(223) http://www.ewg.org/chemindex/chemicals/22924








(231) [Cleland, J.G., G.L. Kingsbury. Multimedia Environmental Goals for Environmental Assessment. Volume 1. EPA-600/7-77-136a. Research Triangle Park, NC: EPA, Nov. 1977., p. E-148] **PEER REVIEWED**

(232) [Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 1232] **PEER REVIEWED**



(237) [U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on Benzene (71-43-2). Available from: http://www.epa.gov/ngispgm3/iris on the Substance File List as of March 15, 2000] **PEER REVIEWED**


(239) [Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1683] **PEER REVIEWED**


(240) [Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1683] **PEER REVIEWED**


(242) [Goodman, L.S., and A. Gilman. (eds.) The Pharmacological Basis of Therapeutics. 5th ed. New York: Macmillan Publishing Co., Inc., 1975., p. 906] **PEER REVIEWED**

(243) [SNYDER R ET AL; LIFE SCIENCES 21 (12): 1709-22 (1977)] **PEER REVIEWED**

(244) [VIGLIANI EC, FORNI A; ENVIRON RES 11 (1): 122-7 (1976)] **PEER REVIEWED**




(248) [International Labour Office. Encyclopedia of Occupational Health and Safety. Volumes I and II. New York: McGraw-Hill Book Co., 1971., p. 1414] **PEER REVIEWED**

(249) [Hamilton, A., and H. L. Hardy. Industrial Toxicology. 3rd ed. Acton, Mass.: Publishing Sciences Group, Inc., 1974., p. 276] **PEER REVIEWED**



(252) [MAKI-PAAKKANEN J ET AL; J TOXICOL ENVIRON HEALTH 6: 775 (1980)] **PEER REVIEWED**

(253) [Fiscman CM, Oster JR; Am Med Assoc 241 (16): 1713-15 (1979) as cited in NRC; Alkyl Benzenes p.284 (1981)] **PEER REVIEWED**

(254) [Toutant C, Lippman S; Lancet 1 (8130): 1356 (1979)] **PEER REVIEWED**

(255) [Ehyai A, Freemon FR; J Neural Neurosurg Psychiatry 46 (4): 349-51 (1983)] **PEER REVIEWED**


(257) [Benignus VA; Neurotoxicol 2 (3): 567-88 (1981)] **PEER REVIEWED**

(258) [Hersh JH; J Med Genet 26 (5): 333-7 (1989)] **PEER REVIEWED**

(259) [Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 1494] **PEER REVIEWED**



(261) [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V5:991] **PEER REVIEWED**

(262) [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Manual Two. Washington, DC: U.S. Government Printing Office, Oct., 1978.] **PEER REVIEWED**



(265) [Armour, M.A. Hazardous Laboratory Chemicals Disposal Guide. Boca Raton, FL: CRC Press Inc., 1991., p. 461] **PEER REVIEWED**

(266) [DHHS ATSDR; Toxicological Profile for Xylenes (Update) (PB2008-100008) p.71 (August 2007) Available from, as of August 29, 2008: http://www.atsdr.cdc.gov/toxprofiles/tp71.pdf ] **PEER REVIEWED**



(269) [Armour, M.A. Hazardous Laboratory Chemicals Disposal Guide. Boca Raton, FL: CRC Press Inc., 1991., p. 461] **PEER REVIEWED**

(270) [DHHS ATSDR; Toxicological Profile for Xylenes (Update) (PB2008-100008) p.71 (August 2007) Available from, as of August 29, 2008: http://www.atsdr.cdc.gov/toxprofiles/tp71.pdf ] **PEER REVIEWED**




(274) [(1) NIOSH; National Occupational Exposure Survey (NOES) (1983)] **PEER REVIEWED**

(275) [(1) DeCarlo V; Ann NY Acad Sci 320: 678-81 (1979)] **PEER REVIEWED**

(276) http://www.miller-mccune.com/science_environment/environment-becomes-heredity-489.print

(277) http://www.justicenewsflash.com/2009/01/07/fda-fails-babies-at-risk_20090107535.html


(278) http://www.niehs.nih.gov/news/newsletter/2009/october/docs/efactor.pdf

(279) http://www.ncbi.nlm.nih.gov/pubmed/18329244?dopt=Abstract

(280)[Wong O; Quant Occupat Cancer as cited in: Branbury Report No. 9, Peto R, Schneiderman M (eds.) pp. 359-78 (1981)] **PEER REVIEWED**

(281) http://toxnet.nlm.nih.gov/

(282) [Lag M et al; Chem Res Toxicol 4 (5): 528-34 (1991)] **PEER REVIEWED**

(283) [Wong O; Quant Occupat Cancer as cited in: Branbury Report No. 9, Peto R, Schneiderman M (eds.) pp. 359-78 (1981)] **PEER REVIEWED**

(284) [Anon; An Historical Prospective Mortality Study of Vesicol Workers Potentially Exposed to Brominated Chemicals. Tabershaw Occupational Med Associates, Rockville, MD 121 pp. (1981)] **PEER REVIEWED**

(285) [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. 60 297 (1994)] **PEER REVIEWED**



(288) [Snyder, R. (ed.) Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume 1: Hydrocarbons. Amsterdam - New York - Oxford: Elsevier, 1987., p. 205] **PEER REVIEWED**


(300) [USEPA; Health Assessment Document: Styrene (Draft) p.3-23 (1985)] **PEER REVIEWED**

(301) [NTP; Executive Summary: Styrene (Draft) p.13 (1985)] **PEER REVIEWED**

(302) [NAS/NRC; The Alkyl Benzenes p.323 (1981)] **PEER REVIEWED**

(303) [NIOSH; Criteria Document: Styrene p.15 (1983) DHEW Pub. NIOSH 83-119] **PEER REVIEWED**


(305) [Environment Canada; Tech Info for Problem Spills: Styrene (Draft) p.71 (1981)] **PEER REVIEWED**

(306) [Commission of the European Communities. Legislation on Dangerous Substances - Classification and Labelling in the European Communities. Vol. II. London and Trotman Ltd., 1989., p. 224] **PEER REVIEWED**

(307) [International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 2115] **PEER REVIEWED** (308) [NORPPA H; CARCINOGENESIS (LOND) 2 (3): 237-42 (1981)] **PEER REVIEWED**



(310) [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981.] **PEER REVIEWED**



(313) [Snyder, R. (ed.) Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume 1: Hydrocarbons. Amsterdam - New York - Oxford: Elsevier, 1987., p. 220] **PEER REVIEWED**

(314) [Gosselin, R.E., H.C. Hodge, R.P. Smith, and M.N. Gleason. Clinical Toxicology of Commercial Products. 4th ed. Baltimore: Williams and Wilkins, 1976., p. II-114] **PEER REVIEWED**

(315) [The Chemical Society. Foreign Compound Metabolism in Mammals Volume 3. London: The Chemical Society, 1975., p. 530] **PEER REVIEWED**


(317) http://www.ewg.org/tapwater/contaminants/contaminant.php?contamcode=2993

(318) S TEELUCKSINGH, CR STEER*, CJ THOMPSON, SECKL, JR, NJ DOUGLAS and CRW EDWARDS http://qjmed.oxfordjournals.org/cgi/content/abstract/78/2/185

(319) http://emedicine.medscape.com/article/818939-overview

(320) [DHHS/National Toxicology Program; Eleventh Report on Carcinogens: Dichloromethane (75-09-2) (January 2005). Available from, as of July 31, 2009: http://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s066dich.pdf ] **QC REVIEWED**





(325) [Browning, E. Toxicity and Metabolism of Industrial Solvents. New York: American Elsevier, 1965., p. 245]


**PEER REVIEWED**

(326) [BARROWCLIFF DF, KNELL AJ; J SOC OCCUP MED 29 (1): 12-4 (1979)] **PEER REVIEWED**

(327) [USEPA; Health Assessment Document: Dichloromethane (Methylene chloride) (Draft) p.5-9 (1982) EPA-600/8-82-004] **PEER REVIEWED**

(328) [Taskinen H et al; Br J Ind Med 43: 199-205 (1986)] **PEER REVIEWED**

(329) [Storstein J, Stabell K; Tidsskr Nor Laegeforen 106 (3): 1132-35 (1986)] **PEER REVIEWED**

(330) [STEWART RD, HAKE CL; JAMA 235 (4): 398-401 (1976)] **PEER REVIEWED**





(335) http://www.sciencedaily.com/releases/2008/01/080107181340.htm

(336) [DHHS/National Toxicology Program; Eleventh Report on Carcinogens: Trichloroethylene (79-01-6) (January 2005). Available from, as of July 31, 2009: http://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s180tce.pdf ] **QC REVIEWED**



(339) [Bardodej Z, Vyskocil J; AMA Arch Ind Health 13: 581 (1956) as cited in USEPA; Ambient Water Quality Criteria Document: Trichloroethylene p.C-17 (1980) EPA 440/5/80-007] **PEER REVIEWED**

(340) [Herdman KN; Br Med J (3): 689-90 (1945) as cited in Health and Safety Executive Monograph: Trichloroethylene #6 p.14 (1982)] **PEER REVIEWED**

(341) [Tomasini M, Sartorelli E; Med Lav 62: 277-80 (1971) as cited in USEPA; Health Assessment Document: Trichloroethylene (Draft) p.5-2 (1983) EPA-600/8-82-006B] **PEER REVIEWED**

(342) [Lawrence WH, Partyka EK; Ann Int Med 95 (6): 710 (1981) as cited in USEPA; Health Assessment Document: Trichloroethylene (Draft) p.5-2 (1983) EPA-600/8-82-006B] **PEER REVIEWED**



(344) [Konietzko H et al; Arch Toxicol 40 (3): 201-6 (1978)] **PEER REVIEWED**

(345) [Barret L et al; Arch Environ Health 42 (5): 297-302 (1987)] **PEER REVIEWED**

(346) [Zenz, C., O.B. Dickerson, E.P. Horvath. Occupational Medicine. 3rd ed. St. Louis, MO., 1994, p. 721] **PEER REVIEWED**



(349) [WHO; Environ Health Criteria 50: Trichloroethylene p.82 (1985)] **PEER REVIEWED**

(350) [WHO; Environ Health Criteria 50: Trichloroethylene p.82 (1985)] **PEER REVIEWED**


(352) [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V63 104 1995] **PEER REVIEWED**


(354) (Szymańska and Piotrowski, 2000; Szymańska, 1998; Casini et al., 1986; Forkert, 1985; Kluwe et al., 1984; Rush et al., 1984; Roth, 1981; Reid et al., 1973; Patrick and Kennedy, 1964).




(358) [PEROCCO P, PRODI G; CANCER LETT 13 (3): 213-18 (1981)] **PEER REVIEWED**


(360) [NIOSH; Current Intelligence Bulletin Ethylene Dibromide #37 p.5 (1981)] **PEER REVIEWED**

(361) [Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V13 267 (1981)] **PEER REVIEWED**

(362) [Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1689] **PEER


REVIEWED**


(364) [(1) Swann RL et al; Res Rev 85: 17-28 (1983) (2) Rathbun RE; U.S. Geological Survey Professional Paper 1589: 1-151 (1998) (3) Call F; J Sci Food Agric 8: 81-5 (1957) (4) Pignatello JJ, Cohen SZ; Rev Environ Contam Toxicol 112: 2-46 (1990) (5) Cohen SZ et al; ACS Symp Ser 259: 297-325 (1984) (6) Steinberg SM et al; Environ Sci Technol 21: 1201-8 (1987)] **PEER REVIEWED**

(365) [National Research Council. Prudent Practices for Handling Hazardous Chemicals in Laboratories. Washington, DC: National Academy Press, 1981., p. 98] **PEER REVIEWED**

(366) [National Research Council. Prudent Practices for Handling Hazardous Chemicals in Laboratories. Washington, DC: National Academy Press, 1981., p. 98] **PEER REVIEWED**

(367) [Burns MJ, Linden CH; Chest 111: 816-9 (1997)] **PEER REVIEWED**


(369) [Braker W, Mossman A; Matheson Gas Data Book 6th Ed p.373 (1980)] **PEER REVIEWED**


(371) [Burns MJ, Linden CH; Chest 111: 816-9 (1997)] **PEER REVIEWED**




(375) [IPCS INCHEM; Poisons Information Monographs, Bromine (PIM 080). Available from, as of June 25, 2007: http://www.inchem.org/pages/pims.html ] **PEER REVIEWED**







York, N.Y. (2001)., p. 3:802] **PEER REVIEWED**




(385) [European Chemicals Bureau; IUCLID Dataset, Bromine (CAS # 7726-95-6) p.37 Available from, as of June 19, 2007: http://ecb.jrc.it/esis/esis.php ] **PEER REVIEWED**

(386) [CDC: Chemical Emergencies. Case Definition. Bromine. (March 4, 2005). Available from, as of June 12, 2007: http://www.bt.cdc.gov/agent/bromine/pdf/casedef.pdf ] **PEER REVIEWED** (387) [IPCS INCHEM; Poisons Information Monographs, Bromine (PIM 080). Available from, as of June 25, 2007: http://www.inchem.org/pages/pims.html ] **PEER REVIEWED**

(388) [Inagaki N et al; Chudoku Kenkyu 18 (2): 141-7 (2005)] **PEER REVIEWED** PubMed Abstract

(289) [Seiler, H.G., H. Sigel and A. Sigel (eds.). Handbook on the Toxicity of Inorganic Compounds. New York, NY: Marcel Dekker, Inc. 1988., p. 145] **PEER REVIEWED**




(393) [Gilman, A.G., T.W. Rall, A.S. Nies and P. Taylor (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 8th ed. New York, NY. Pergamon Press, 1990., p. 1620] **PEER REVIEWED**

(394) [FEIN A ET AL; CHEST 78 (5): 726 (1980)] **PEER REVIEWED**

(395) [BINDER JW, ROBERTS RJ; CLIN TOXICOL 16 (3): 287 (1980)] **PEER REVIEWED**









(403) http://toxnet.nlm.nih.gov,**PEER REVIEWED**

(404) [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989., p. 1516] **PEER REVIEWED**




(408) Holbrook MT; Kirk-Othmer Encycl Cheml Technol. 4th ed. NY, NY: John Wiley and Sons 5: 1051-62 (1993)

(409) Prager JC; Environ Contamin Ref Databook. NY, NY: Van Nostrand Reinhold 1: 453 (1995) (9) Jensen S, Rosenberg R; Water Res 9: 659-61 (1975)] **PEER REVIEWED**

(410) Tadic J et al; J Photochem Photobiol A:Chem 143: 169-79 (2001)] **PEER REVIEWED**

(411) ...(2) Yanagihara S et al; Proc Int Clean Air Cong 4th, pp. 472-7 (1977) (3) Korte F, Klein W; Ecotox Environ Saftey 6: 311-27 (1982) (4) Nojima K et al; Chemosphere 4: 77-82 (1975) (5) Hoshino M et al; Kokuritsu Kogai Kekyusho Kenkyu Hokoku 5: 43-59 (1978) (6) Kopczynski SL; Int J Air Water Pollut 8: 107-20 (1964)...

(412) [EPA; Pesticide Product Label System (PPLS) - Search Results for Emulso Germicidal Bowl Cleaner Disinfectant. Company no. 9367, product 5. Label approved on April 5, 2002. Available from, as of July 30, 2007: http://oaspub.epa.gov ] **PEER REVIEWED**





(417) [Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. 12(80) 1006] **PEER REVIEWED**


(418) [Environment Canada; Tech Info for Problem Spills: Hydrochloric Acid (Draft) p.99 (1981)] **PEER REVIEWED**

(419) [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 2961] **PEER REVIEWED** (420) [O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006.., p. 826] **PEER REVIEWED**



(423) [WHO; Environ Health Criteria 21: Chlorine and Hydrogen Chloride p.19 (1982)] **PEER REVIEWED**




(427) [Huval WV et al; Surgery 94 (2): 259-66 (1983)] **PEER REVIEWED**


(429) [U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Medical Management Guidelines for Hydrogen Chloride p.5 (2007). Available from, as of July 19, 2007: http://www.atsdr.cdc.gov/MHMI/mmg.html ] **PEER REVIEWED**




(433) [Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1296] **PEER REVIEWED**

(434) [MUHLETALER CA ET AL; AM J ROENTGENOL 134 (6): 1137-40 (1980)] **PEER REVIEWED**


(435) [29 CFR 1910.1028(c) (7/1/99)] **PEER REVIEWED**

(436) [29 CFR 1910.1000 (7/1/99)] **PEER REVIEWED**





(441) [Yanturali S et al; Mt Sinai J Med 72 (6): 409-12 (2005)] **PEER REVIEWED** PubMed Abstract

(442) [Buchanan IB et al; South Med J 98 (8): 822-4 (2005)] **PEER REVIEWED** PubMed Abstract

(443) [Kanne JP et al; AJR Am J Roentgenol 185 (3): 682-683 (2005)] **PEER REVIEWED**

(444) [Tseng YL et al; Eur J Cardiothorac Surg 21 (4): 638-43 (2002)] **PEER REVIEWED** PubMed Abstract


(446) [WHO/Eastern Mediterranean Regional Office; Public Information on Biological & Chemical Threats. Chlorine. p. 17 (2003)] **PEER REVIEWED**

(447) [European Chemicals Bureau; IUCLID Dataset, Chlorine (CAS # 7782-50-5) p.98 Available from, as of June 19, 2007: http://ecb.jrc.it/esis/esis.php ] **PEER REVIEWED**

(448) [IPCS INCHEM; Poisons Information Monographs, Chlorine (PIM 947). Available from, as of June 20, 2007: http://www.inchem.org/pages/pims.html ] **PEER REVIEWED**

(449) [USEPA/Office of Pesticide Programs; Reregistration Eligibility Decision Document - Chlorine Gas p.38-50. EPA738-R-99-001 (February 1999) Available from, as of June 7, 2007: http://cfpub.epa.gov/oppref/rereg/status.cfm?show=rereg ] **PEER REVIEWED**


(451) [O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006.., p. 347] **PEER REVIEWED** (452) [USEPA/Office of Pesticide Programs; Reregistration Eligibility Decision Document - Chlorine Gas p.38-50. EPA738-R-99-001 (February 1999) Available from, as of June 7, 2007: http://cfpub.epa.gov/oppref/rereg/status.cfm?show=rereg ] **PEER REVIEWED**

(453) [Dreisbach, R.H. Handbook of Poisoning. 12th ed. Norwalk, CT: Appleton and Lange, 1987., p. 199] **PEER REVIEWED**


(454) [USEPA/Office of Pesticide Programs; Reregistration Eligibility Decision Facts Document - Chlorine Gas p.2 EPA738-R-99-001 (February 1999) Available from, as of June 7, 2007: http://cfpub.epa.gov/oppref/rereg/status.cfm?show=rereg ] **PEER REVIEWED**


(456) [Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 848] **PEER REVIEWED**

(457) [Kilbrun KH et al; Arch Environ Health 55 (1): 31-7 (2000)] **PEER REVIEWED** PubMed Abstract

(448) [Suzuki S et al; Clin Appl Thromb Hemost 7 (4): 356-8 (2001)] **PEER REVIEWED** PubMed Abstract

(449) [Traub SJ et al; Vet Hum Toxicol 44 (4): 235-9 (2002)] **PEER REVIEWED** PubMed Abstract

(450) [Parimon T et al; Respir Care 49 (3): 291-4 (2004)] **PEER REVIEWED** PubMed Abstract

(451) [Vohra R, Clark RF; Pediatr Emerg Care 22 (4):254-7 (2006)] **PEER REVIEWED** PubMed Abstract

(452) [Foulks CJ; South Med J 74 (11): 1423-24 (1981)] **PEER REVIEWED**


(454) [Chemical Casualty Care Division/USAMRICD; Field Management of Chemical Casualties Handbook, 2nd ed. (July 2000). Available at https://www.rke.vaems.org/wvems/Libraryfiles/Dis/E_04.pdf as of July 17, 2007] **PEER REVIEWED**

(455) [CDC; Emergency Preparedness & Response. Facts About Phosgene. Available from, as of July 17, 2007: http://www.bt.cdc.gov/agent/phosgene/basics/facts.asp ] **PEER REVIEWED**

(456) [NAS/NRC Board on Environmental Studies and Toxicology; Acute Exposure Guideline Levels for Selected Airborne Chemicals: Volume 2, p. 16-7. National Academies Press, Washington, DC (2002)] **PEER REVIEWED**

(457) [European Chemicals Bureau; IUCLID Dataset, Phosgene (75-55-5) p. 38 (2000 CD-ROM edition). Available from, as of July 16, 2007: http://ecb.jrc.it/esis/esis.php ] **PEER REVIEWED**

(458) [IPCS; Poisons Information Monograph 419. Phosgene. (October 1997). Available from, as of July 16, 2007: http://www.inchem.org/documents/pims/chemical/pim419.htm ] **PEER REVIEWED**



(461) [ATSDR; Medical Management for Phosgene (COCl2 ) CAS 75-44-5; UN 1076. p. 5-6. Available from, as of July 17, 2007: http://www.atsdr.cdc.gov/MHMI/mmg176.pdf ] **PEER REVIEWED**

(462) [ATSDR; Medical Management for Phosgene (COCl2 ) CAS 75-44-5; UN 1076. p. 6. Available from, as of July 17, 2007: http://www.atsdr.cdc.gov/MHMI/mmg176.pdf ] **PEER REVIEWED**

(463) [ATSDR; Medical Management for Phosgene (COCl2 ) CAS 75-44-5; UN 1076. p. 6. Available from, as of


July 17, 2007: http://www.atsdr.cdc.gov/MHMI/mmg176.pdf ] **PEER REVIEWED**

(464) [ATSDR; Medical Management for Phosgene (COCl2 ) CAS 75-44-5; UN 1076. p. 6. Available from, as of July 17, 2007: http://www.atsdr.cdc.gov/MHMI/mmg176.pdf ] **PEER REVIEWED**

(465) [Grant, W. M. Toxicology of the Eye. 2nd ed. Springfield, Illinois: Charles C. Thomas, 1974., p. 826] **PEER REVIEWED**




(469) [USEPA; Health Assessment Document: Phosgene p.4-42 (1986) EPA-600/8-86-022A] **PEER REVIEWED**





(474) [Kuzelova M et al; Prac Lek 27 (4): 115-7 (1975)] **PEER REVIEWED**

(475) [WHO; Environ Health Criteria 193: Phosgene p.39 (1997)] **PEER REVIEWED**



(478) [European Chemicals Bureau; IUCLID Dataset, Phosgene (75-55-5) p. 37 (2000 CD-ROM edition). Available from, as of July 16, 2007: http://ecb.jrc.it/esis/esis.php ] **PEER REVIEWED** (479) [European Chemicals Bureau; IUCLID Dataset, Phosgene (75-55-5) p. 37 (2000 CD-ROM edition). Available from, as of July 16, 2007: http://ecb.jrc.it/esis/esis.php ] **PEER REVIEWED**

(480) [USEPA; Health Assessment Document: Phosgene p.4-27 (1986) EPA-600/8-86-022A] **PEER REVIEWED**



(482) [Chemical Casualty Care Division/USAMRICD; Field Management of Chemical Casualties Handbook, 2nd ed. (July 2000). Available at https://www.rke.vaems.org/wvems/Libraryfiles/Dis/E_04.pdf as of July 17, 2007] **PEER REVIEWED**


(484) [NAS/NRC Board on Environmental Studies and Toxicology; Acute Exposure Guideline Levels for Selected Airborne Chemicals: Volume 2, p. 16. National Academies Press, Washington, DC (2002)] **PEER REVIEWED**

(485) [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-197] **QC REVIEWED**

(486) [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] **QC REVIEWED**



(489) [POIRIER MC; DISS ABSTR INT B 37: 5493 (1977)] **PEER REVIEWED**





(494) [Osol, A. (ed.). Remington's Pharmaceutical Sciences. 16th ed. Easton, Pennsylvania: Mack Publishing Co., 1980., p. III-157] **PEER REVIEWED**

(495) [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 358] **PEER REVIEWED** (496) [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-157] **PEER REVIEWED**



(499) [National Research Council. Drinking Water & Health, Volume 4. Washington, DC: National Academy Press, 1981., p. 237] **PEER REVIEWED**


(500) [USEPA; Chemical Hazard Information Profile: 2,4-Dinitrophenol p.5 (1981) EPA-560/2-76-010] **PEER REVIEWED**

(501) [National Research Council. Drinking Water & Health, Volume 4. Washington, DC: National Academy Press, 1981., p. 237] **PEER REVIEWED**





(506) [Sittig, M. Handbook of Toxic And Hazardous Chemicals. Park Ridge, NJ: Noyes Data Corporation, 1981., p. 185] **PEER REVIEWED**

(507) [Kimbrough, R.D., P. Grandjean, D.D. Rutstein. Clinical Effects of Environmental Chemicals. New York, NY: Hemisphere Publishing Corp., 1989., p. 20] **PEER REVIEWED**



(510) [Hawley, G.G. The Condensed Chemical Dictionary. 10th ed. New York: Van Nostrand Reinhold Co., 1981., p. 375] **QC REVIEWED**

(511) [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 463] **PEER REVIEWED**






(517) [Seiler, H.G., H. Sigel and A. Sigel (eds.). Handbook on the Toxicity of Inorganic Compounds. New York, NY: Marcel Dekker, Inc. 1988., p. 200] **PEER REVIEWED**




(520) [EPA/Office of Pollution Prevention and Toxics; High Production Volume (HPV) Challenge Program's Robust Summaries and Test Plans. Available from: http://www.epa.gov/chemrtk/viewsrch.htm on Formates (December 2001) as of July 12, 2005.] **PEER REVIEWED** (521) [EPA/Office of Pollution Prevention and Toxics; High Production Volume (HPV) Challenge Program's Robust Summaries and Test Plans. Available from: http://www.epa.gov/chemrtk/viewsrch.htm on Formates (December 2001) as of July 12, 2005.] **PEER REVIEWED**


(523) [Vyskocil A et al; Hum Exp Toxicol 17 (4): 212-20 (1998)] **PEER REVIEWED** PubMed Abstract

(524) [DeMarini DM et al; Mutat Res 457 (1-2): 41-55 (2000)] **PEER REVIEWED** PubMed Abstract



(527) [United Nations Environment Programme: Screening Information Data Sheets on n-Valeraldehyde (110-62-3) (October 2005) Available from, as of January 15, 2009: http://www.chem.unep.ch/irptc/sids/OECDSIDS/sidspub.html ] **PEER REVIEWED**






(533) [United Nations Environment Programme: Screening Information Data Sheets on n-Valeraldehyde (110-62-3) (October 2005) Available from, as of January 15, 2009:


http://www.chem.unep.ch/irptc/sids/OECDSIDS/sidspub.html ] **PEER REVIEWED**




(537) [AGARONYAN ZP, AMATUNI VA; KROVOOBRASHCHENIE 13 (4): 31-6 (1980)] **PEER REVIEWED**



(540) [European Chemicals Bureau; European Union Risk Assessment Report Draft, Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED**


(542) [JEDRYCHOWSKI W ET AL; PRZEGL LEK 36 (9): 679-82 (1979)] **PEER REVIEWED**

(543) [TALAKINA EI ET AL; GIG TR PROF ZABOL (3): 46-7 (1977)] **PEER REVIEWED**

(544) [Jantunen K et al; Mutat Res 159 (1-2): 109-16 (1986)] **PEER REVIEWED** PubMed Abstract

(545) [Lambert B et al; Mutat Res 146 (3): 301-3 (1985)] **PEER REVIEWED** PubMed Abstract

(546) [Norppa H et al; Cancer Res 45 (10): 4816-21 (1985)] **PEER REVIEWED** PubMed Abstract

(547) [He SM, Lambert B; Mutat Res 158 (3): 201-8 (1985)] **PEER REVIEWED**

(548) [AMATUNI VG, AGARONYAN ZP; ZH EKSP KLIN MED 19 (4): 72-8 (1979)] **PEER REVIEWED**


(550) http://www.law.cornell.edu/uscode/18/usc_sec_18_00000287----000-.html


(552) http://toxnet.nlm.nih.gov **PEER REVIEWED**



(554) [Marzulli, F.N., H.I. Maibach. Dermatotoxicology 4th ed. New York, NY: Hemisphere Publishing Corp., 1991., p. 857] **PEER REVIEWED**

(555) [Marzulli, F.N., H.I. Maibach. Dermatotoxicology 4th ed. New York, NY: Hemisphere Publishing Corp., 1991., p. 858] **PEER REVIEWED**

(556) [Cleland, J.G., G.L. Kingsbury. Multimedia Environmental Goals for Environmental Assessment. Volume 1. EPA-600/7-77-136a. Research Triangle Park, NC: EPA, Nov. 1977., p. E-182] **PEER REVIEWED**

(557) [Haddad, L.M. and Winchester, J.F. Clinical Management of Poisoning and Drug Overdosage. Philadelphia, PA: W.B. Saunders Co., 1983., p. 810] **PEER REVIEWED**


(559) [NIOSH; Criteria Document: Phenol p.41 (1976) DHEW Pub NIOSH 76-196] **PEER REVIEWED**

(560) [Bennett IL; Ann Intern Med 32: 324-7 (1950)] **PEER REVIEWED**



EXHIBIT A

18 U.S.C. § 3771. Crime victims' rights (a) RIGHTS OF CRIME VICTIMS.--A crime victim has the following rights: (1) The right to be reasonably protected from the accused.(2) The right to reasonable, accurate, and timely notice of any public court proceeding, or any parole proceeding, involving the crime or of any release or escape of the accused.(3) The right not to be excluded from any such public court proceeding, unless the court, after receiving clear and convincing evidence, determines that testimony by the victim would be materially altered if the victim heard other testimony at that proceeding.(4) The right to be reasonably heard at any public proceeding in the district court involving release, plea, sentencing, or any parole proceeding.(5) The reasonable right to confer with the attorney for the Government in the case.(6) The right to full and timely restitution as provided in law.(7) The right to proceedings free from unreasonable delay.(8) The right to be treated with fairness and with respect for the victim's dignity and privacy.

(b) RIGHTS AFFORDED.--In any court proceeding involving an offense against a crime victim, the court shall ensure that the crime victim is afforded the rights described in subsection (a). Before making a determination described in subsection (a)(3), the court shall make every effort to permit the fullest attendance possible by the victim and shall consider reasonable alternatives to the exclusion of the victim from the criminal proceeding. The reasons for any decision denying relief under this chapter shall be clearly stated on the record.


(c) BEST EFFORTS TO ACCORD RIGHTS.--

(1) GOVERNMENT.--Officers and employees of the Department of Justice and other departments and agencies of the United States engaged in the detection, investigation, or prosecution of crime shall make their best efforts to see that crime victims are notified of, and accorded, the rights described in subsection (a).

(2) ADVICE OF ATTORNEY.--The prosecutor shall advise the crime victim that the crime victim can seek the advice of an attorney with respect to the rights described in subsection (a).

(3) NOTICE.--Notice of release otherwise required pursuant to this chapter shall not be given if such notice may endanger the safety of any person.

(d) ENFORCEMENT AND LIMITATIONS.--

(1) RIGHTS.--The crime victim or the crime victim's lawful representative, and the attorney for the Government may assert the rights described in subsection (a). A person accused of the crime may not obtain any form of relief under this chapter.

(2) MULTIPLE CRIME VICTIMS.--In a case where the court finds that the number of crime victims makes it impracticable to accord all of the crime victims the rights described in subsection (a), the court shall fashion a reasonable procedure to give effect to this chapter that does not unduly complicate or prolong the proceedings.

(3) MOTION FOR RELIEF AND WRIT OF MANDAMUS.--The rights described in subsection (a) shall be asserted in the district court in which a defendant is being prosecuted for the crime or, if no prosecution is underway, in the district court in the district in which the crime occurred. The district court shall take up and decide any motion asserting a victim's right forthwith. If the district court denies the relief sought, the movant may petition the court of appeals for a writ of mandamus. The court of appeals may issue the writ on the order of a single judge pursuant to circuit rule or the Federal Rules of Appellate Procedure. The court of appeals shall take up and decide such application forthwith within 72 hours after the petition has been filed. In no event shall proceedings be stayed or subject to a continuance of more than five days for purposes of enforcing this chapter. If the court of appeals denies the relief sought, the reasons for the denial shall be clearly stated on the record in a written opinion.

(4) ERROR.--In any appeal in a criminal case, the Government may assert as error the district court's denial of any crime victim's right in the proceeding to which the appeal relates.

(5) LIMITATION ON RELIEF.--In no case shall a failure to afford a right under this chapter provide grounds for a 2263 new trial. A victim may make a motion to re-open a plea or sentence only if--

(A) the victim has asserted the right to be heard before or during the proceeding at issue and such right was denied;

(B) the victim petitions the court of appeals for a writ of mandamus within 10 days; and

(C) in the case of a plea, the accused has not pled to the highest offense charged. This paragraph does


not affect the victim's right to restitution as provided in title 18, United States Code.

(6) NO CAUSE OF ACTION.--Nothing in this chapter shall be construed to authorize a cause of action for damages or to create, to enlarge, or to imply any duty or obligation to any victim or other person for the breach of which the United States or any of its officers or employees could be held liable in damages. Nothing in this chapter shall be construed to impair the prosecutorial discretion of the Attorney General or any officer under his direction.

(e) DEFINITIONS.--For the purposes of this chapter, the term 'crime victim' means a person directly and proximately harmed as a result of the commission of a Federal offense or an offense in the District of Columbia. In the case of a crime victim who is under 18 years of age, incompetent, incapacitated, or deceased, the legal guardians of the crime victim or the representatives of the crime victim's estate, family members, or any other persons appointed as suitable by the court, may assume the crime victim's rights under this chapter, but in no event shall the defendant be named as such guardian or representative.

(f) PROCEDURES TO PROMOTE COMPLIANCE.--

(1) REGULATIONS.--Not later than 1 year after the date of enactment of this chapter, the Attorney General of the United States shall promulgate regulations to enforce the rights of crime victims and to ensure compliance by responsible officials with the obligations described in law respecting crime victims.

(2) CONTENTS.--The regulations promulgated under paragraph (1) shall--

(A) designate an administrative authority within the Department of Justice to receive and investigate complaints relating to the provision or violation of the rights of a crime victim;

(B) require a course of training for employees and offices of the Department of Justice that fail to comply with provisions of Federal law pertaining to the treatment of crime victims, and otherwise assist such employees and offices in responding more effectively to the needs of crime victims;

(C) contain disciplinary sanctions, including suspension or termination from employment, for employees of the Department of Justice who willfully or wantonly fail to comply with provisions of Federal law pertaining to the treatment of crime victims; and

(D) provide that the Attorney General, or the designee of the Attorney General, shall be the final arbiter of the complaint, and that there shall be no judicial review of the final decision of the Attorney General by a complainant."

(Reference 7)

Note: This electronic version of my Summary of Proof of Claim does not have a copy of the Proof of Claim Form attached to the last page yet. But all information on the Proof of Claim Form may be found on previous pages.
