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NO. B244257
COUBT OF APPEAL OF THE STATE OF CALIFORNIA
FOR THE SECOND APPELLATE DISTRICT
DIVISION 2
FRANCISCO UL4RTF.
Plaintiff and Appellant,
vs.
SCOTT SALES COMPANY.
Defendant and Respondent.
Appeal from the Superior Court of CaliforniaCounty of Los Angeles
Honorable Joseph DiLoretoSuperior Court Case No. BC 452512
APPLICATION FOR LEAVE TO FILE BRIEF OF AMICI CURIAE,COUNCIL FOR EDUCATION AND RESEARCH ON TOXICS
(CERT), ET AL., IN SUPPORT OF APPELLANT
ALEXANDER LAW GROUP, LLPRichard Alexander. Esq. (State Bar No, 48432)
lii \V. Saint John St., Suite 700San Jose. CA 95113
Telephone: (408) 289-1776Telecopier: (408) 287-1776
Anornevs for Arnici CuriaeCOU\UL FOR EDFC\TIO\ \\DRESEARCHO\TO\KSI (ERT J)R
JERROLD ABRAHAM: DR. RICHARD W. CLAPP: DR. RONALD CRYSTAL: DR.D.\\FD . I \SFMO\D DR \RFHLR1 \\j 1 ROBERf I H\RRIO\r J\ fl ‘IEL\iCK DP FE \E\\M \\ PR STEPiFN \1 F\ \PP)( P1
DR. DAVID ROSS: and DR. JANET WEISS
TO THE HONORABLE COURT AND TO THE PRESIDING JUSTICE:
Pursuant to California Rule of Court 8.200(c)(I0), the Council for
Education and Research on Toxics. et al., respectfully request permission to
file the accompanying amici curiae brief in support of Plaintiff and Appellant.
The issue presented by this case - whether the medical and scientific
assumptions underlying last year’s decision by Division 3 in Maxton v. Western
States Metals (2012) 203 CaLApp.4th 81, are erroneous - is ofcritical importance to
workers suffering occupational diseases, to occupational and public health, and to the
administration ofjustice.
The Council for Education and Research on Toxics (CERT) is a public
benefit organization whose charitable purposes are education and research regarding
toxic substances, CERT has funded occupational health conferences and fimded
student attendance at such conferences. CERT has also filed arnicus curiae briefs
regarding toxic hazards of chemicals in the U.S. Supreme Court, the U.S. Court of
Appeals for the First and Second Circuits, the California Supreme Court, the New
York Court of Appeal, and the New York Supreme Court.
The other amici are all physicians. epidemiologists, scientists, and scholars
of science and the history of science and public health.
Accordingly, Amici ask the court to accept the accompanying am ici
curiae brief for filing.
DATED: October J. 2013 ALEXANDER LAW GROUP. LLP
RICHARD ALEXANDER, ESQAttorneys for Amici
NO. B244257
COURT OF \PPEAL OF THE STATE OF CALIFORNL
FOR THE SECOND APPELLATE DISTRICT
DIVISION 2
FRANCISCO URIARTE,
Plaintiff and Appellant,
vs.
SCOTT SALES COMPANY,
Defendant and Respondent.
Appeal from the Superior Court of CaliforniaCounty of Los Angeles
Honorable Joseph DiLoretoSuperior Court Case No. BC 452512
[PROPOSEDI BRIEF OF AMICI CURIAE, COUNCIL FOREDUCATION AND RESEARCH ON TOXICS (CERT), ET AL., IN
SUPPORT OF APPELLANT
ALEXANDER LAW GROUP, LLPRichard Alexander. Esq. (State Bar No, 48432)
Ill W. Saint John St.. Suite 700SanJose. CA 95113
Telephone: 40$) 289-1776Teiecopier: (408 287-1776
Attorneys for Amici CuriaeCOL\UL FoR EDIC \T1O, \M) RLSE\RCHO\ TO\ICS I CERU ) DR
IERR LJ) AI3R \HM DR RICIIRD \\ (LAPP DR ROLL [)C R STL DRDAViD A \SF\1C\D DR ARTHI RI fRA\K DR ROBERI I H\RRISO\DR ROkLDMEL\1CK DR LEE M’AM \“ DR STEPRE\ \I RPP\PORT,
DR DAVID JOSEPH ROSS d DR. JkEEEISS
Frontispiece
Personal protective equipment preventing occupational exposure to Mechiorethamine. a chemicalthat imlike asbestos, is absorbed throuh the skin and is so toxic that it cannot be handled safely.
Source: BD. Naurnann. et al.. Performance-Based Exposure Control Limits for PharmaceuticalActive Ingredients,” Am, Ind Hyg. Assoc. J 57:33.42 (1996).
TABLE OF CONTENTS
I. INTERi..STOFAMICICLTi.UAi.... 1
IL PRELIMINARY STATEMENT
IIL PNEIJMOCONIOSE.S 3
IV. INTERSTITIAL LUNG DISEASE 5
V. LUNG CANCER 7
VI. CHEMICALS THAT CAUSE INTERSTITIAL LUNG DISEASEAND LUNG CANCER 7
VIE ASBESTOS IS NOT THE ONLY MINERAL THAT CAUSESHAR1M BY HANDLING 13
VIII. ASBESTOS IS NOT THE ONLY CAUSE OF OCCUPATIONALLUNG CANCER OR LUNG DISEASE 18
IX. CONCLUSION 20
CERTIFICATION OF WORD COUNT 22
APPENDIX
TABLE OF AUTHORITIES
Cases
Maxton v. Western States Metals(2012) 203 Cal.App.-fth 81 3 R 2
Publications
Agency for Toxic Substances and Disease Registry, “Asbestos Toxicity:
How Are People Exposedhttp ://www.atsdr,cdc ,gov/csem; csem.asp?csem4&po6 ....... 14
Alcgun, M., et al.. “An Epidemic of Silicosis Among Former
Denim Sandblasters,”Fur. Respir. J 32(51:1295-1303 (2008) 10
Apayidin, M.. et at.. “Denim Sandblasters Pneumoconiosis,”
JBR-BRT94(1):36 (2011) 10
Archontogeorgis. K., Ct at.. “Lung Cancer and Interstitial Lung Diseases:
A Systematic Review.”Fuhnonari’ Med. Article 31591$ (2012)
Bakan. N.D,, et al., “Silicosis in Denim Sandblasters,”chest 140(5):1300-1304 (2011) 10
Bans, B.. et al., “Environmental Fibrous Zeolite (Erionite) E.xposure and
Malignant Tumors Other than Mesotheli oma.”I Environ. .Pathoi. Toxicol. O,icol. 15(2-41:183-189 (1996) 11
Carbone, M., et al., “A Mesothelioma Epidemic in Cappadocia: Scientific
Developments and Unexpected Social Outcomes,”Mat, Rev. Cancer 7(2):147-154 (2007) 11
Centers for Disease Control and Prevention. “Sjlicosis in Dental Laboratory
Technicians Five States. 1 994-2000.”Morb. Mortal. Welv. Rep. 53(9):195-197 (2004) 10
Centers for Disease Control and Prevention, “Silicosis Mortality. Prevention,and Control — United States. 1968-2002.”
ho, h hfo 1t 1T7 R 54 1 f) 401 _4u ‘ ifl5 9
Cimrin. A.. et al.. “Sandblasting Jeans Kills Young People.”Fur. Respir. J 28(4):885-886 (2006) 10
Comba. P.. et al.. “Pleural Mesothelioma Cases in Biancavilla Are Relatedto a New Fluoro-edenite Fibrous Amphibole,”
Arch. Environ, Health 58(4):229-32 (2003) ................. 8
Cosgrove. G.P., et aL, “Approach to the Evaluation and Diagnosis ofInterstitial Lung Disease,”
in Schwarz, M., et al,, eds., Interstitial Lung Disease, 5th ed.,Chapter 1 at p. 3 (People’s Medical Publishing House,Shelton, CT, 2011) .,.................................. 5,6
Dam ian, P.. “Development of a Health Risk-Based Surface ContaminationCleanup Standard for Occupational Exposure to Beryllium.”
Toxicol. Mccli. Methods 21(2):97-102 (2011) 16
Day, G.A.. et al.. “Beryllium Exposure: Dermal and ImmunologicalConsiderations.”
Int.Arch. Occup. Environ. Health 79(2):161-164 (2006) 15
Deuhner. D.C.. et al.. ‘Contribution of Incidental Exposure Pathways toTotal Beryllium Exposures,”
Appi. Occup. Environ. Hvg. 16(5):568-578 (2001) 15
Driscoll. T.. et al.. “The Global Burden of Disease Due to OccupationalCarcinogens.”
Am. .1 Jnd. Med. 38:419-431 (2005) 19
Driscoll. I.. et al.. “The Global Burden of Non-Malignant RespiratoryDisease Due to Occupational Airborne Exposures,”
Am. .1. JnI. Med. 48:432-445 (2005) 19
Emond. C.. et al., “Dermal Exposure to Pilot Case Study,”
J Toicol Ernuon Health A 70(6) 529-533 (2(10Th 16
Emri. S.. et al., “Lung Diseases Due to Environmental Exposures toErionite and Asbestos in Turkey,”
Tox:icoLLett, 127(i-3):251-2..57 (2002) ..1i
Fontenot. A.P., “Metal-induced Diffuse Lung Disease,”Scm/n. Respir. Crit. Care Med. 296:662-669 (2008)
Forte. G.. et al.. “Metal Allergens of Growing Significance: Epidemiolocv.lmmunotoxicologv. Strategies for Testing and Prevention.”
In/Jamm.Ailergv Drug Targets 3): 145-162 (2008) 13
Greenberg, M.L, et al.. “Silicosis: A Review,”Dis, Mon. 53:394-416 (2007 8
Hayes. R.B,, “The Carcinogenicity of Metals in Humans,”Cancer C’auses Control 8(3):371-385 (1997) 7
International Agency for Research on Cancer, “A Review of HumanCarcinogens: Arsenic. Metals. Fibres, and Dusts.”
L4RC Monographs on the Evaluation of(arcinogenic Risksto Humans. Monograph 100C (IARC. 2012)
International Agency for Research on Cancer, “A Review of HumanCarcinogens: Arsenic, Metals, Fibres, and Dusts,”
IARC Monographs on the Evaluation ofC’arcinogenic Risksto Humans, Monograph 100C (IARC, 2012) 11
International Agency for Research on Cancer. “Beryllium. Cadmium.Mercury and Exposures in the Glass Manufacturing Industry,”
JARC Monographs on the Evaluation of€arcinogenic Risksto Humans, Monograph 5$ (IARC. 1993) ii
J.K. Wagoner, et al,, “Beryllium: an Etiologic Agent in the Induction ofLung Cancer, Nonneoplastic Respiratory Disease, and Heart Disease amongIndustrially Exposed Workers,”
Environ, Res, 21( ):15-34 (1980) 10
Jasani. B.. et aL, “Mesothelioma Not Associated with Asbestos Exposure.”Arch. Pathol. Lab. Mea 136( ):262-267 (2012 8
Kelleher, P., “Inorganic Dust Pneumonias: the Metal-related ParenchvmalDisorders,”
Environ. HLJli/i Perspect. 1 08( Suppi 4 ):685-696 (2000)
Langer. A.M.. “Mineraloav.”U.S. Department of Health and Human Services. PublicHealth Service. Centers for Disease Control. NationalInstitute for Occupational Safety and Health. OccuvarionalResvirarorv Diseases at p. 3 (September 1986) [DHHS Pub.86-102] 4
Maxwell, R,, et al.. “Surveillance for Silicosis. 1993 — Illinois, Michigan,New Jersey, North Carolina, Ohio, Texas, and Wisconsin,”
Morb, Mortal. Wklv. Rep. C’DC Surveill. Summ. 46(1): 13-28 (1997)9
Meiklejohn, A., “History of Lung Diseases of Coal Miners in Great Britain:Part II,”
Br. J Med. 9:93-98 (1951) 3
Muetterties. M.. et ci.. “Sandlbasters.”in M. Greenberg. ed.. Occupational, Industrial, andEnvironmental Toxicoiogt’, 2nd ed. (Mosbv, Philadelphia. PA,2003) 9
Naumann, B.D.. et aT.. “Performance-Based Exposure Control Limits for
Pharmaceutical Active ingredients,”Am. md. Hig. Assoc. J 57:33-42 (1996) 16, 17
Nemery, B., “Metal Toxicity and the Respiratory Tract,”Eur, Respir. I 3(2):202-219 (1990) 8
OSHA News Release 13-1767-NAT, “US Department of Labo?s OSHAAnnounces Proposed Rule to Protect Workers Exposed to CrystallineSilica.”
(August 23. 2013) available online atwww.oshaJ2Joshawebowadisp.show
documeni2ptable=NEWSRELEASES&pidr-r’)362I 10
Parks, et aL, “Occupational Exposure to Crystalline Silica andAutoimmune Disease,”
.Eflviron. Health Perpect. 107(Suppi. 5):793-802 (1999) 8
Ramazzn.i, B , De Morbis Artificum Diatriba (Liseases of Workers)(Modena, 1700)
Ryan, et aL, “Erionite in Road Gravel Associated with Interstitialand Pleural Changes: An Occupational Hazard in Western United States,”
J Occup. Environ. Med. 53(8):892-898 (2011) 11
Shay, U, et al., “Considerations for the Development of Health-BasedSurface Dust Cleanup Criteria for Beryllium,”
crit. Rev. Toxicol, 43(3):220-243 (2013) 16
Steenland, K., et aL, “Review of Occupational Lung Carcinogens,”Am. J md. Med. 29:474-490 (1996) 8
Thomas, CA., et al., “Long-Term Efficacy of a Program to PreventBeryllium Disease,”
Am. J hid. Med. 56(7):733-74l (2013) 16
Travis, W.D., et aL, World Health Organization International HistologicalClassification ofTumours: Histological Typing ofLung and PleuralTumours,
3d ed. (Springer-Verlag, 1999) ........... 7
U.S. Department of Health and Human Services, Public Health Service,Centers for Disease Control, National Institute for Occupational Safetyand Health, Occupational Respiratory Diseases at p. 3
(September 1986) [DHHS Pub. 86-102] ..... 6
Valiante, DJ., et aL, “Highway Repair: A New Silicosis Threat,”Am. I Public Health 94(5):876-880 (2004) ........ 9
Wild, P., et aL, “Lung Cancer and Exposure to Metals: the EpidemiologicalEvidence
Methods Mol. Biol, 472:139-167 (2009) ..................... 7
Wilt, LL, et aL, “The Diagnosis of Pneumoconiosis and Novel Therapies,.”in B anks, et aL, eds., OccupationalLung Disease: AnInternational Perspective at p. 119 Chap...man & FlaIlMedicaL London 1998 3
‘t Mannetje, A. et aL, “Occupational Exposure to Metal Compounds andLung Cancer: Results from a Multi-Center Case-Control Study in Central/Eastern Europe and UK,”
Cancer causes C’ontroi 22(12): 1669-80 (2011) 7
I.
INTEREST OF AMICI CURIAE
Arnicus. the Council for Education and Research on Toxics (CERT). is
a public benefit corporation. whose charitable purposes are education and
research regarding toxic substances. CERT has funded occupational health
conferences and funded student attendance at such conferences. CERT has
also filed amicus curiae briefs regarding toxic hazards ofchemicals in the US.
Supreme Court, the U.S. Court of Appeals for the First and Second Circuits,
the California Supreme Court, the New York Court of Appeal, and the New
York Supreme Court.
Amici Dr. Jerrold Abraham, Dr. Richard W. Clapp, Dr. Ronald Crystal,
Dr. David A. Eastmond. Dr. Arthur L. Frank. Dr. Robert J. Harrison. Dr.
Ronald Melnick. Dr. Lee Newman. Dr. Stephen M. Rappaport. Dr. David
Joseph Ross. and Dr. Janet Weiss are physicians. epidemiologists, scientists,
and scholars of science and the history of science and public health. Brief
biographies of Amici are included in the Appendix to this Brief.
None of the amid has any financial or other similar imerest in the
outcome ofthis lawsuit. Amici appear on their own behalfto inform this Court
that asbestos is not the only chemical that causes lung cancer or lung disease,
and is not the only “inherently dangerous” chemical to which workers are
exposed.
IL
PRELIMINARY STATEMENT
Amici submit this brief to inform the Court that asbestos is not the OnlY
substance that can cause lung cancer or fibrotic lung disease and that asbestos
is not the only “inherently dangerous” substance known to mankind, Indeed,
as Amici will show, there are many minerals, metals, and other substances that
are known to cause fibrotic lung disease andior lung cancer. Amici also wish
to explain that it is scientifically incorrect to classi’ substances as “inherently
dangerous” based on handling, rather than based on their innate toxicity. This
issue is pertinent to the “inherently dangerous” exception to the component
parts doctrine.
In Maxton v. Western States Metals (2012) 203 Cal.App.4th 81.
Division 3 of the Second Appellate District held that raw asbestos is
“inherently dangerous.” hut that metals (and presumably other substances) that
cause pulmonary fibrosis are not “inherently dangerous” and “are not
analogous to raw asbestos,” The Court further determined that “[a]sbestos
itself is dangerous when handled in any form even if it is unchanged by the
manufacturer” and that “asbestos is dangerous when it leaves the supplier’s
control,” but that metals “only became dangerous because of
manufacturing process[es].” This brief will explain that the assumptions of
the Maxton court are scientifically incorrect.
Respondents rely on Maxton. hut the premise that chemicals are only
“inherently dangerous” if they cause harm “when handled in any form” is
scientifically incorrect. The inherent danger of a chemical is exclusively a
function of its toxicity. i.e.. the severity of the toxic effects it causes and its
poienci in mducing such effects I h. i sZ. that a chemical x ill Laue tO\IL
injury is a function of toxicity and exposure. which does relate to how the
chemical is handled. For example. \vater is not inherently dangerous because
it is not toxic to the human body (it is essential to life, even though water can
cause death by drowning. On the other hand, cyanide is inherently dangerous
because it causes death by in estion. although it can be “handled” without
injury. The Maxton court erred when it concluded that a chemical is inherently
dangerous only if it causes harm “when handled in any form.” Indeed, it is a
principle of occupational health that any chemical can be handled safely
provided that adequate protective measures are implemented and rigorously
followed,
IlL
PNEU1’IOCONIOSES
“Pneumoconioses are lung diseases which result from mineral dust
deposition in the lung and the subsequent host response. This term is derived
from the Greek language (pneurno, the Greek root for lung and konis, the root
for dust) and has been applied in clinical medicine since the 1 9 century
(Meiklejohn, 1951). These are illnesses rooted in antiquity, which have had
their highest human toll during the industrial age, yet it remains a tragedy of
our time that these preventable diseases have not disappeared.” A book
published by the U.S. Department of Health and Human Services more than
Wilt. J.L.. et al.. “The Diagnosis of Pneumoconiosis and \ovelfherapies m Banks I) E Lt al eds Oc ;ipanonal Lung Dn& ace inInternational Perspective at p. ii 9 (Chapman & Hall Medical, London 1998).Liting Meikleinhn Histor or Lung Diseases ot Coal Miners in Great BritimPart II,” Br, J MeL 9:93-98 (1951).
25 years ago contains the following introductory passage in. a chapter titled
Natural Agents of Disease
Exploitation of metal ores and fossil fliels, and thequarrying and mining of nonmetallic rocks and minerals, arecarried out primarily on and within the earth’s continental crustwhich extends from the tidal zones along the ocean margins ofland masses to the mountainous highlands and interior “shields”of continents. The lithological units constituting the earth’ssurface may range from unconsolidated beach sands to dense,crystalline rock massifs which often form the “spines” of manyof the great mountain ranges of the world,
Those who work in these environments may be exposedby inhalation to powders arising from fragmented orcomminuted rocks, minerals, and ores. Miners, millers, stonemasons, quarry men, tunnel drivers, to name but a few, maydevelop pneumoconiosis and, in some instances, malignantneoplasms as the result of such exposures. These diseases arealso evident among working populations which process orhandle such materials in secondary capacities. 2
Thus, there is a class of occupational lung diseases called
“pneumoconioses” caused by inhalation of mineral and metal dusts, As will
be shown, asbestos is not the only mineral that causes these diseases. Indeed,
as will be explained, historically, minerals other than asbestos are responsible
for most of the morbidity and mortality among workers exposed to inorganic
dusts,
2 Langer, AJ•.t, “Mineral..ogy,” in US. Department of Health andHuman. Services, Public Health Service, Centers fcr Disease Control, Nationalinstitute for Occupational Safety and Health, Occupational Respiratory Diseasesat p. 3 (Septemfer 1986) [DHHS Pub. 8& 1 02j,
Iv,
INTERSTITIAL LUNG DISE:ASE•.
“The intersti.tiai lung diseases (ILDs), also referred to a.s diffuse
parenchymal lung diseases, are a diverse group ofpulmonary disorders that are
classified together because of similar clinical, radiographic, physiologic, or
pathologic manifestations,... In general, the major abnormality in interstitial
lung disorders is disruption of the distal lung parenchyma.... When the lung
is injured, epithelial cell basement membranes lose their integrity, heralding
the appearance, depending on the injury, of a variety of inflammatory cells,
regenerating type II epithelial cells and fibroblasts, resulting in the
accumulation of extracellular matrix components. . . . Continuation of this
process can be fueled by persistent injury (bloodbome or inhaled) or by
profibrotic cytokines released from the regenerating alveolar epithelium,
inflammatory cells, and the proliferating fibroblasts themselves. . . . This is
reflected pathologically as either inflammation and/or fibrosis.”
A leading textbook on interstitial lung diseases identifies more than a
hundred such diseases, classifying them clinically in five tables: (1) Collagen
Vascular Disease Associated, (2) Drug- and Treatment-Induced, (3) Primary
or Unclassified Disease Related, (4) Occupational and Environmental
Exposure Related, and (5) Idiopathic Interstitial Pneumonias and Autoimmune
Diseases. The fourth table classifies occupational and environmental
Cosgove, G.P., et aL, “Approach to the Evaluation and Diagnosisof interstitial Lung Disease,“ in S.chwarz, lvi., et aL, eds., Interstiti.i LungDisease, 5” ed., Chapter 1 at p. 3 (People’s Medical Publishing House , Shelton,CT, 2011).
M atpp. 35, Tables Li through L5.
exposure related interstitial lung diseases in two main groups: diseases caused
b.y inhalation of inorganic, matter and disease caused by inhalation of organic
matter. The. former are the pneumoconioses and the lat.ter compri.se a class of
other occupationally-related lung diseases, most of whic.h are generally
referred to as hypersensitivity pneumonitis.
In the first part of Table 1-4 (Clinical Classification of ILD:
Occupational and Environmental Exposure Related) from this textbook,
regarding pneumoconioses, the following fibrotic lung diseases are listed:
Silicosis, Asbestosis, Talc pneumoconiosis, Kaolin pneumoconiosis,
Diatomaceous earth pneumoconiosis, Aluminum oxide fibrosis, Berylliosis.
Indium compounds, Hard metal fibrosis, Coal workers’ pneumoconiosis,
Baritosis (barium), Antimony pneurnoconiosis, Polyvinylchloride
pneumoconiosis, Shale pneumoconiosis, Siderosis (arc welder’s lung),
Stannosis (tin), Silicone pneumonitis, Wood burning interstitial fibrosis,
Textile worker’s pneumoconiosis, and Flock lung (nylon).
Although generally useful and informative, this list is incomplete. It
does not include several pneumoconioses that have long been recognized in the
medical literature, such as silicate pneumoconiosis, cobalt pneumoconiosis,
silver pneumoconiosis, fibrous glass pneumoconiosis, zirconium
pneumoconiosis, rare earths pneumoconiosis, and mixed dust
pneumoconiosis6 Thus, it is readily apparent that asbestos is not the only
mineral that can cause fibrotic lung disease,
Id at p. 5, Table 1-4, Clinical Classification of ILD: Occupationalar.d Environmental Exposure Related.
6 See, generally, U.S. Department of H.eaIth and Human. Services,Public Health Service, Centers for .Disease Control, National Institute forOccupational Safety and H.ealth, Occupational Respiratory Diseases at p. 3(September 1986) [DHHS Pub 86-102]
V.,
LUNG CANCER
Lung cancer is a collection ofvarious. malig.nances of]ung tissue,7 The
interstitial lung diseases are not lung cancers, although a link between
interstitial lung disease and lung cancer has long been suspected and current
evidence does suggest an association between interstitial lung diseases and the
development of lung cancer,
VI
CHEMICALS THAT CAUSE INTERSTITIAL LUNG DISEASE
AND LUNG CANCER
Several minerals and metals that cause interstitial lung disease can also
cause lung cancer,9 Asbestos is a mineral that causes pleural plaques (fibrosis
W,D. Travis, et al,, World Health Organization InternationalHistological Classification of Tumours: Histological Typing ofLung and PleuralTumours, 3d ed (Springer-Verlag, 1999).
8
K. Archontogeorgis, et al,, “Lung Cancer and Interstitial LungDiseases: A Systematic Review,” Pulmonary Med Article 315918 (2012).
A. t Mannetje, et al, “Occupational Exposure to Metal Compoundsand Lung Cancer: Results from a Multi-Center Case-Control Study inCentra].!Eastem Europe and UE,” C’ancer causes con.troi 22(12):1669-80 (2011);P. Wild, et al,, “Lung Cancer and Exposure to Metals: the EpidemiologicalEvidence,” Methods Mol, Bioi, 472:139167(20:09); AP. Fontenot, “Metal-inducedDiffuse Lung Disease,” SCmin. Respir. (‘Cit. Care Med 29(6):662-669 (2008); P.Kelleher, “Inorganic Dust Pneumonias: the Metal-related Parenc.hyniai Disorders,”Em iron Health Perspect I 08(Suppl 4) 685-696 (2000) R B Hayes, “TheCarcinogenicit’ ofMetals in Humans (‘ancer Causes Control 8(3) 371-385 (1 997
of the parietal pleura) and an interstitial lung disease called “asbestosis,” but
also causes lung cancer and mesothelioma, Although mesothelioma has been
referred to as a “signature disease,” i.e.. a disease caused only by exposure to
asbestos, there are, in fact, other causes of mesothelioma, including the
nonashestos fiber erionite and fluoroedenite.
Silica, which Lriarte alleges was contained in the sands sppIied by
Respondents. is a metalloid that causes an interstitial lung disease called
“silicosis.” It can also cause lung cancer and immune-mediated diseases such
as nephritis (kidney disease). rheumatoid arthritis. scieroderma. systemic lupus
ervthematosus. Wegener’ s granulomatosis and vasculitis. The International
Agency for Research on Cancer recently determined that “[t]here is sufficient
evidence in humans for the carcinogenicit\ of crystalline silica in the form of
quartz or cristohalite” and concluded that “[cjrvstailine silica in the form of
quartz or cristohalite dust causes cancer of the lung.”2 Respiratory disease
associated with occupational exposure to crystalline silica has been described
K. Steenland, et al., “Review of Occupational Lung Carcinogens,” Am. J md. Med29:474-490 (1996); B. Nemerv. “Metal Toxicity and the Respirato Tract,” Eur.Respir. J 3(2):202-219 (1990).
B. Jasani, et al., “Mesothelioma Not Associated with AsbestosExposure,”Arch. Pathol, Lab, Med l36(3):262-267 (2012); P Comba, et al., “PleuralMesothelioma Cases in Biancavilla Are Related to a New Fluoro-edenite FibrousAmphibole,” Arch. Environ. health 58( ):229-32 (2003).
M.L Greenberg. et al.. “Silicosis: A Review,” Dis. Mon. 53:394-416(2007); C.G. Parks. et al.. “Occupational Exposure to Crystalline Silica andAutoimmune Disease,” Environ. Health Perspect. l07(Suppl. 5):793-802 (1 999).
international :\encv tbr Research on Cancer, “A Review of Humancrcinoe’s -.r.n1L Metals Fibres and Dusts DRC lIo;’ae’ aphs m ih
I t1 ‘(w2L.1 1? 0. i Ui mai \Fino..,,ranh 1 1 K I \R( () I
throughout histoiy. Hippocrates d.escribed a conditicn of “breath.lessness.” in
miners, and in 1690, Lohneiss noted that when “the dust and stones fall upon
the lungs, th.e men h.ave lung disease, breathe with difficulty.”’3 Ii. 1700,
Bernardino Ramazzini described so-called “miners’ phthisis,” and other trades
of the day in which workers inhaled substantial quantities of dusts.’4 These
dust-related afflictions have been known by various names, including “miners’
phthisis,” “dust consumption,” “mason’s disease,” “grinders’ asthma,”
“potters’ rot,” and “stonecutters’ Peacock and Greenhow reported
finding silica dust in the lungs of miners in the 1 860s, and 10 years later,
Visconti coined the term “silicosis” to describe the age-old
Although mining has been recognized as a cause of silicosis for centuries, the
advent of the pneumatic jackhammer and occupations such as sandblasting,’7
4. Muetterties, et el,, “Sandlbasters,” in M. Greenberg, ed.,Occupational Industrial, and Environmental Toxicology, 2nd ed. (Mosby,Philadelphia, PA, 2003).
B. Ramazzini, Dc Morbis Artificum Diatriba (Diseases of Workers)(Modena, 1700).
Id
Id
Centers for Lise.ase Control and Prevent.ion, “Silicosis Mort.aiity,Prevention., and Control United Ste te.s., 1968-2002,” Mdrb. Mdrtal, Wkiv. Rep.54(16):4.0i-405 (2005); R, Maxwell, et al., “Surve.ii.iance for Si.licosis, 1993 —
illinois, Michigan., New Jersey, North Carolina, Ohio, Texas, and Wisconsin,” Morb.MOrtal. Wkiy. R.ep. CDC Shrveill. Summ. 46(1).: 1 328 (1997).
9
highway repair: dental laboratory work and even the production of frded
denim jeans- have unfortunately resulted in modem cases ofsilicosis. Despite
efforts to prevent silicosis. the Occupational Safe and Health Administration
has concluded that such efforts were inadequate to protect American workers
and recently proposed a new rule to protect workers exposed to crystalline
silica, estimating it would save nearly 700 lives and prevent 1.600 new cases
of silicosis annuailv.
Beryllium is a metal that causes an interstitial lung disease called
Chronic Beryllium Disease (CBD): beryllium also causes lung cancer and
diseases of other organs, including heart disease,22 The International Agency
D.J. Valiante. et al ..“Highwav Repair: A New Silicosis Threat,” Am.I Public Health 94( ):876-880 (2004).
Centers for Disease Control and Prevention, “Silicosis in DentalLaboratory Technicians — Five States, 1994-2000,” Morb. Mortal. Wkly. Rep.53(9):195-197 (2004).
See. e.g.. A. Cimrin. et al.. “Sandblasting Jeans Kills Young People:’Eu, Rcspir J 28(4) 885 886 (2006) NI Akgun et al \n Epidemic of SiliosisAmong Former Denim Sandblasters.” Eur. Respir. I 32(5):1295-1303 (2008); NI.Apayidin, et al .. “Denim Sandblasters’ Pneumoconiosis,” JBR-BRT94(l):36 (2011);N.D. Bakan, et al., “Silicosis in Denim Sandblasters,” Chest l40(5):1300-l304(2011).
OSHA News Release 13-1767-NAT. iJS Department of Labor’sOSILA Announces Proposed Rule to Protect Workers Exposed to Crystalline Silica,”
\ugust 23 20laailahle online at
_____ox\adI%p
sho\\ -
docurnent?ptab1eNEWSRELESES&pid=24621
J.K. Wagoner, et aI., “Beryllium: an Etiologic Agent in the Inductionof Lung Cancer, Nonneoplastic Respiratory Disease. and Heart Disease amongIndustrially Exposed Workers,” Ehviron. Rev 21(1): 15-34 (1980).
for Research on Cancer has classified. be.r ilium as a known human carcinog.en
si.nce 1993 bas.ed or. its abi.lit’ to caus.e lung. cancer.23
Erionite is a naturally occurring fibrous mineral of the zeolite family
that causes calcified plural plaques24and may cause interstitial lung disease,25
Erionite has been found to cause an extraordinarily high incidence of pleural
mesothelioma in Turkey26 and also causes lung cancer,27 According to its
recent review, the International Agency for Research on Cancer found that
“[tjhere is sufficient evidence in humans for the carcinogenicity of erionite,”
and concluded that “[ejrionite causes mesothelioma,” 28
Talc is a mineral that is widely used in the ceramic, paper, plastics,
rubber, paint, and cosmetic industries, Four distinct forms of pulmonary
International Agency for Research on Cancer, “Beryllium, Cadmium,Mercury and Exposures in the Glass anufacturing Industry,” L4RC Monographs onthe Evaluation ofCarcinogenic Risks to Humans, Monograph 58 (IARC, 1993).
S. Emri, et al., “Lung Diseases Due to Environmental Exposures toErionite and Asbestos in Turkey,” Toxicol, Leti. l27(1-3):251-257 (2002).
P.H. Ryan, et al., “Erionite in Road Gravel Associated with Interstitialand Pleural Changes: An Occupational Hazard in Western United States,” I Occup.Environ, Med 53(8):892-898 (2011).
M. Carbone, et al., “A Mesothelioma Epidemic in Cappadocia:Scientific Developments and Unexpected Social Outcomes,” Nat. Rev, Cancer7(2):i47154 (2007).
B. Bans, et al., “Environmental Fibrous Zeolite (Erionite) Exposureand Malignant Tumors Other than Mesothelioma,” I Environ. Pathol. Toxicol.Oncol. l5(24):l83-189 (1996:>.
international Agency for ]Res•earch on “A Review of HumanCarcinogens: Arsenic , Metals, Fibres, and Dusts,” L4RC Monographs on theEaluatzon of&vurogenic Risks to Humans Monograph 100C (IARC 2012)
disease caused by talc have been defined. Three of them (talcosilicosis.
talcoasbestosis, and pure talcosis) are associated with inhalation and differ in
the composition of the inhaled substance, The fourth form, a result of
intravenous administration oftaic. is seen in drug users who inject medications
intended for oral use. The disease most commonly affects men. with a mean
age in the fourth decade of life. Presentation of patients with talc
granulomatosis can range from asvmptomatic to fulminant disease.
Symptomatic patients typically present with nonspecific complaints, including
procressive exertional dvspnea. and cough. Late complications include chronic
respiratory failure. pulmonary arterial hypertension, and cor pulmonale.
Histoi of occupational exposure or of drug addiction is the major clue to the
diagnosis. The high-resolution computed tornoaphy (HRCT) finding ofsmall
centrilohular nodules associated with heterogeneous conglomerate masses
containing high-density amorphous areas, with or without panlobular
emphysema in the lower lobes, is highly suggestive ofpulmonary talcosis. The
characteristic histopathologic feature in talc pneumoconiosis is the striking
appearance of birefringent. needle-shaped particles of talc seen within the
giant cells and in the areas of pulmonary fibrosis with the use of polarized
light. In conclusion, computed tomography can play an important role in the
diagnosis of pulmonary talcosis, since suggestive patterns may be observed.
The presence of these patterns in drug abusers or in patients with an
occupational history of exposure to talc is highly suggestive of pulmonary
talcosis.
VII.
ASBESTOS IS NOT THE ONLY MINERAL
THAT CAUSES H4RM BY HANDLING
Without citation to any medical, toxicolocical. or other scientific
authority, the Mixton court asserted that asbestos is the only substance that “is
dangerous when handled in any form even if it is unchanged by the
manufacturer,” In making this assertion, the Maxton court erred on two
counts, First, the Maxton court erred, because it may be possible for asbestos
to be used without causing harm, provided that all recommended respiratory
protective measures and cleanup procedures are rigorously followed at all
times and in all industries,29 Second, there are numerous other substances,
including certain metals, chemicals, and physical and biologic agents, that are
as dangerous as asbestos, some of which may be considered to he even more
dangerous than asbestos because oftheir greater toxic potency and their ability
to cause injury acutely or through multiple routes of entry. For such
substances, even greater personal protective and safe use requirements than
those required for asbestos are necessary.
l-listoricaliv. industries have not rigorously followed safety protectionsnecessary to avoid harm from asbestos. resulting in the epidemic of asbestos-related disease filling court dockets. The failure of industries to rigorously followall necessary precautions to prevent asbestos-related disease have promptedseveral international health agencies, including the World Health Organization(WHO. to recommend a global ban on asbestos to protect worker health.
e neialh G Forte et al Metal AilerLLns ot (TIo’.1nL
S1gnlticnLL Fpiderniolog Immurotoxicolog’ Strnitegies br I esting andPrecntion Inliarnin 1lkig Drug Targtrc “( l4-l62 21ioS [ Metal-inducedalleric contact dermatitis (ACD) is expressed in a wide range of cutaneousreactions following dermal and systemic exposure to products such as cosmetics
and tattoos, detergents, jewellery and piercing, leather tanning. articular
The toxicirv of asbestos derives from the inhalation of asbestos fibers.
which lodge in lung tissue and cause disease over time. As the U.S. Aency
for Toxic Substances Disease Reaistrv states on its website: “The air pathway
(inhalation ofcontaminated air or dust) is the most important route ofexposure
to asbestos, the route that most commonly leads to illness.”3’ Although
asbestos is toxic when inhaled, asbestos is not systemically absorbed through
human skin and therefore can be “handled,” provided proper respiratory
protection is worn, asbestos fibers are thoroughly washed from hands and
other exposed skin surfaces, and residual asbestos fibers are properly disposed
of, so they will not become entrained into workplace air from which they could
subsequently be inhaled by workers or any other persons.3 As the Agency for
Toxic Substances and Disease Registry states: “Today, with the advent of
personal protective equipment, dermal contact is rarely a significant exposure
pathway. In the past. handling asbestos could result in heavy dermal contact
and exposure. Asbestos fibers could become lodged in the skin, producing a
callus or corn, but not more serious health effects.”
prostheses and dental implants. Apart from the well known significance of nickelin developing ACD. other metals such as aluminium. beryllium, chromium.cobalt. copper, gold. iridium. mercury. palladium, rhodium and titaniumrepresented emeruing causes of skin hvpersensitivitv.”j
Agency for Toxic Substances and Disease Registry. “Asbestos Toxicity:How Are People Exposed to at hrtp: 7www.atsdr.cdc.gov csem!csem.asp?csem=4&po6.
In so stating. Amici are not suggestine that asbestos should he handledwithout proper dermal protection: Amici believe that all regulatory requirementsfor handling asbestos. including but not limited to respiratory and dermalprotections. be implemented and rigorously followed.
Agency fbr Toxic Substances and Disease Registrv.”Asbestos Toxicity:How Are People Exposed to Asbestos?” at http:/vww.atsdr.cdc . gov/csemIcsem.asp?csenv4&po6.
Whereas asbestos is not dermally absorbed, recent research indicates
that beryllium can inducesensitization through dermal exposure. For this
reason, greater dermal protection is required to protect workers from the toxic
hazards of beryllium than those of asbestos. Like asbestos fibers. beryllium
particles can he inhaled and cause Chronic Beryllium Disease and lung
cancer:” However, unlike asbestos, the sensitization from beryllium results
from an immunologic reaction. The immunologic reaction induced by
beryllium is called beryllium sensitization and is tpical1v ascertained using a
blood test called the Beryllium Lymphocyte Proliferation Test (BLPT). For
decades, the beryllium industry attempted to prevent workers from developing
CBD and sensitization through engineering controls and personal protective
equipment designed to prevent inhalation of beryllium dusts. While these
efforts effected a reduction in the incidence of CBD. they were not successful
in preventing the occurrence of either CBD or beryllium sensitization. It was
only within the past decade, after more than 50 years of unsuccessful efthrts
to prevent beryllium-related disease, that scientists realized that beryllium
sensitization and disease may result from seemingly insignificant dermal
exposures.
The fibrotic lung disease caused by beryllium was formerly calledBerylliosis and is now called Chronic Beryllium Disease (CBD).
See, D.C. Deuhner. et aL, “Contribution of Incidental ExposurePathways to Total Beryllium Exposures,” Appi. Occup. Environ. Hyg. 16(5):568-578 (2001) [“Recent workplace epidemiologic studies have been relativelyunsuccessful in correlating disease with workplace air concentrations ofberyllium, thereby failing to support the hypothesis that dose by the respiratoryroute determines the risk of disease, This has led to consideration of thehypotheses that dermal or oral exposures to beryllium can influence disease risk,either as a cause of sensitization or to induced tolerance to bervlliurn.”j: (l.A.Dax et al Buxllnun I ‘pouie Dermal and Immunological Considrmon111
- C 1).. i 1 ‘1 i2 if1 16..t 21)of F IThe puip’. ‘1 t1’ls
Another example of a chemical to which workers are exposed that
requires extrem.e protective measures to prevent di.sease is Mechiorethamine,
‘LIt an antineoplastic agent (niogen mustard) that acts as a biological
ailcylating aent and is effective against a number of lymphatic cancers.
Normal rapidly dividing cells are also susceptible to the cytotoxic effects of
mechiroethamine, It has a high order of acute toxicity, is corrosive to soft
tissue, and causes bone marrow suppression, toxic effects on the GI tract,
developmental toxicity, and an increased incidence of malignant tumors in
animals at relatively low dosages. In clinical use serious toxicities associated
with therapy include nausea, vomiting, bone marrow suppression, infertility,
and an increased incidence of secondary malignancies.” 36 The chemical is so
short communication is to present information regarding the potential importanceof skin exposure to beryllium, an exposure and alternate immune responsepathway to the respiratory tract, which has been largely overlooked inepidemiologic and exposure assessment studies.”]; C. Emond, et aL, “DermalExposure to Beryllium: A Pilot Case Study,” J Toxicol, Environ. Health A70(6):529-533 (2007) [“Although daily dermal exposure may be small, because ofuncertainties, a precautionary principle should be applied in an active sense.”]; P.Damian, “Development of a Health Risk-Based Surface Contamination CleanupStandard for Occupational Exposure to Beryllium,” Toxicot Mccli. Methods21(2):97-102 (2011) [devising a Surface Contamination Cleanup Standard (SCS)for non-malignant beryllium disease and commenting that “[t]he non-cancer SCSwas determined virtually entirely by the dermal absorption exposure pathway,with negligible contributions from the incidental ingestion and inhalationpathways”]; E. Shay, et al,, “Considerations for the Development of Health-BasedSurface Dust Cleanup Criteria for Beryllium,” crit, Rev, Toxicol, 43(3):220-243(2013) [“Recent studies have suggested dermal exposure as a pathway for BeS[beryllium sensitization].”; C.A. Thomas, et aL, “Long-Term Efficacy of aProgram to Prevent Beryllium Disease,” Am, I hid Med. 56(7):733-74 1 (2013)[“The combination of increased respiratory and dermal protection, enclosure andimproved ventilation of high-risk processes, dust migration control, improvedhousekeeping, and worker and management education should utility in reducingsensitization in the program’s first 9 years,”].
36 B.D. Naumann . et al., “PerfOrmance-Based Exposure. Control Lim.itsfor Pharm.aeeutica...l Ac.tive Ingredients,” Am lad. Hg. Assoc. 1 57:33-42 (1996).
toxic th,at scientists empioye.d by Merck, the manufacturer of
MechIoi.etham.ine, devis.ed a special Ferforman.ce-Ba.sed Exosure Control
Limit (PB-.ECL)” syste.m for preventing, exposures to it and other lil<e
extremely t.oxic chemicals37 As the Merck scientists explained it, “{tjhe
evolution ofthe performance-based concept began with the realization that the
increased level of contaimnent required to control dusts ofpotent compounds
was analogous to the Biosafety level (BSL 1-4) practices and techniques,
safety equipment and facilities used by research facilities that handle
microorganisms of increasing pathogenicity. The engineering approaches
developed to create physical barriers to preclude the escape of even a single
highly pathogenic organism (which might theoretically result in fatal
consequences) were very similar conceptually to the control strategies being
implemented within the industry for potent drugs.” The Merck scientists
determined that Mechlorethamine should be classified as a PB-ECL Category
4 substance, a category of “compounds ... that can produce life-threatening
effects, with symptoms that may be incapacitating and may require immediate
medical intervention, They may also have short-term or long-term effects that
are not reversible and could have disabling consequences. Exposure limits are
expected to be below 1 tg/m3, if they can be established at all, and a total
containment approach is used to control exposures.”38 Regarding
“containment,” the Merck scientists specified: “Open handling is not permitted
under any circumstances. All operations require the use of an appropriate
containment technology designed to prevent leakage to the workplace. In
general, glove boxes, totally enclosed processes, and materials transport
Id.
38 Id
systems would be expected.” Regarding personal protective equipment. the
Merck scientists specified: “Only powered air puriing respirators or air
supplied respirators are permitted. For dusts. only J:-1FPA filters are permitted.
Double gloves are encouraed for all personnel entering the area.... Tvvek or
an equivalent outer protective garment is required. Double Tvvek is
recommended. Garment must be impervious to the chemicals involved.”
Thus, Mechiorethamine is an example of a chemical that is so toxic it cannot
be “handled” without extreme protective measures, “total containment” being
required to prevent all occupational exposure.
VIII.
ASBESTOS IS NOT THE ONLY CAUSE OF OCCUPATIONAL
LUNG CANCER OR LUNG DISEASE
Although asbestos has generated more litigation than any other lung
toxicant. asbestos is not the only cause of occupational lung cancer or
nonmalignant occupational lung disease.4
While exposure to asbestos accounts for almost all malignant
mesotheliomas among workers exposed to eight selected occupational
Id.
Id
In addition to asbestos, silica dust and beryllium, the InternationalAgency for Research on Cancer classifies arsenic. cadmium, chromium VI.and nickel as known human carcinogens based on sufficient evidence of
causal relationships between exposure to these agents and the development
of lung cancer in workers. It is also well established that metallic dusts
deposited in the lung can cause pulmonary fibrosis and functional
jmparmcut,
carcinogens, asbestos exposures were associated with only about 22% of
occupational lung cancers worldwide in 2000. Based on Weighted Relative
Risk calculations. seventv-eieht percent of occupational lung cancers
approximately 80.000 lung cancer deaths) were caused h exposures to silica.
cadmium. nickel, arsenic. chromium. diesel fumes. and beryllium.
Asbestos is also not the only cause of occupational nomalignant lung
disease, In the year 2000. there were an estimated 3 1 8.000 deaths and
3,733,000 DALYs from occupational Chronic Obstructive Pulmonary Disease
(COPD)43 and 386.000 deaths and 1.62 1,000 Disability-Adjusted Life Years
(DALYs) from asthma,44 compared to 30,000 deaths and 1,288,000 DALYs
from all pneumoconioses.45The three major causes ofmortality and morbidity
from pneumoconiosis are asbestosis, silicosis and coal workers’
pneumoconiosis. [T]he estimates for pneumoconioses as a result of
exposure to silica. asbestos, and coal mind dust indicate that there may have
been approximately 9000 deaths and 490.000 DALYs from silicosis. 7000
deaths and 3 80.000 DALYs from asbestosis. and 14.000 deaths and 370.000
J)ALYs from coal workers’ pneumoconiosis in the year 2000.
1’. Driscoll, et al., “The Global Burden of Disease Due to OccupationalCarcinogens,” Am. I bid. Med. 48:419-43 1 2005).
° The primary causes of Chronic Obstructive Pulmonary Disease aresmoking and environmental exposures.
The major cause of asthma is environmental exposures.
I. Driscofl, et al,, “The Global Burden of Non-Malignant RespiratoiDisease Due to Occupational Airborne Exposures.’ Am. I hid Med 48:432-445(2005).
Id.
Ix,
CONCLUSION
Contrary to the assumptions of the Maxton court, asbestos is not the
only substance that can cause lung cancer or fibrotic lung disease and asbestos
is not the only “inherently dangerous” substance known to humankind.
Indeed, there are many minerals, metals, and other substances that are known
to cause fibrotic lung disease and or lung cancer. Asbestos is not the only
mineral that causes pneurnoconiosis or interstitial lung disease. Indeed.
historically, minerals other than asbestos were responsible for most of the
morbidity and mortality among workers exposed to inorganic dusts. Nor is
asbestos the only cause of occupational lung cancer.
It is scientifically incorrect to classi substances as inherentlv
dangerous” based on handling, rather than on innate toxicity, as did the
Maxton court, In fact, if all necessary precautions were taken and followed at
all times and in all industries, it is possible that asbestos could be used without
causing harm to workers, although some metals such as beryllium, and some
chemicals such as Mechiorethamine, require even greater protective measures
than do asbestos to prevent occupational injury and disease,
Although literature linked asbestos to lung disease as early as the 1 890s,
it took decades for American public health agencies to recognize the harmful
effects of asbestos, It was not until 1972 that the federal government adopted
a standard that protected workers from the harmful effects of asbestos. While
strong measures to prevent harmful exposure to asbestos have been
implemented in most industries, such has not occurred with regard to other
inhaled toxicants that can be just as harmful and as deadly, Industrial hygiene
protections and legal protections for fibrogenic dusts lag far behind those
which ha.ve big been ir..piemented for asbestos, It is ti.me fOr regulators and
the courts to re.ognize the. hazards of fibrogenic metals and in.organic
ni.aterials and not to. assume that... asbestos is th.e only harmful i.nhaied substance
to which American workers are occupationally exposed. Arnici hope that thi.s
Court will not make the same erroneous medical and scientific assumptions as
Division 3 did in analyzing the “inherently dangerous” exception to the
component parts doctrine.
Respectflully submitted,
ALEXAWDER LAW GROUP, LLP
RICHARD ALEXANDER. ESQAttorneys for Amici
CERTIFICATION OF WORD COUNT
(California Rule of Court, Rule 14(b)(I))
The text of this Brief consists of 5335 :vords • as counted by the Corel
WordPerfect Version X4 word processing program used to generate this
Petition, Cal. Rule of Court, Rule 14(b)(l).
Respectfully submitted,
DATED: October i0, 2013 ALEXANDER LAW GROUP, LLP
RICHARD ALEXAND R, ESQAttorneys for Amici
Dr. Jerroid Abraham has, for more than 20 years, served as Professorof Patholony at the State Lniversitv of New York in Syracuse. For almost 30years, Dr. Abraham served as Director of Environmental and OccupationalPathology in the Department ofPatholo v at the SUNY Health Science Center.Dr. Abraham is recognized for developing analytical techniques for examininglung tissue using scanning electron microscopy to identify inorganic particlesin lung tissue and quantiI their burden in lungs, especially for diagnosis ofinterstitial lung diseases.
Dr. Richard XV. Clapp is an epidemiologist with an MPH from theHarvard School of Public Health and a DSc in Epidemiology from BostonUniversity School of Public Flealth. He has worked in state and local healthdepartments. as director of a community health center, a statewide childhoodlead poisoning prevention program. and the Massachusetts Cancer Registry.Dr. Clapp’s research has focused on cancer in military veterans and in workersand communities with toxic hazards.
Dr. Ronald Crystal has, for the past 20 years, served as Chief of theDivision of Pulmonarv and Critical Care Medicine at the New York WeillCornell Medical Center. For the last decade he has also served as Chairmanof the Department of Genetic Medicine at Weill Medical College of CornellUniversity. From 1975 to 1993. Dr. Crystal was the Chief of the PulmonaryBranch of the Heart, Lung and Blood Institute of the National Institutes ofHealth. During that time. Dr. Crystal led the NIH’s research programregarding interstitial lung disease and published many articles regarding thepathogenesis of interstitial and other lung diseases.
Dr. David A. Eastmond is presently the Chair, Cell Biology &Neuroscience and Professor of Cell Biology & Toxicologist at the Universityof California, Riverside. Dr. Eastmonds research focuses on the mechanismsinvolved in the toxicity and carcinogenesis of environmental agents. Oneimportant goal of this research is to allow adverse health effects associatedwith chemical exposure in human populations to be more accurately estimated.He graduated from Brigham Young University with a B.S. in Zoology and anM.S. in Entomology, and from UC Berkeley with a Ph.D. in EnvironmentalHealth Sciences. His postdoctoral work was at the Lawrence LivermoreNational Lab in Livermore. CA. Dr. Eastmond served as President of theFn ironmenti1 \lurigen SOC 1c,.t from Ma\ 2003 to October 20113 a the Chair
of the Environmental Toxicology Program at the University of California,Riverside from 1999 to 2004, and is cur.entiy a Council Membe.r on th.eNational Council on Radiation Protection and Measurements,
Dr. Arthur U Frank received his M.D. degree from the Mount SinaiSchool of Medicine and his PhD. in biomedical sciences from the CityUniversi of New York. He is board certified in internal medicine andoccupational medicine, As a commissioned officer in the Public HealthService, he conducted research at the National Cancer Institute. His majorresearch activities have included the study of occupational lung diseases andoccupational cancers, especially those related to asbestos exposure. He hasalso worked in the area of agricultural safety and health. He currently servesas Professor ofPublic Health at the Drexel University School ofPublic Healthin Philadelphia, Pennsylvania.
Dr. Robert J. Harrison is Clinical Professor of Medicine at theUniversity ofCalifornia at San Francisco and Visiting Professor in the SchoolofPublic Health at the University of California at Berkeley. Dr. Harrison alsoserves as Chief of the Occupational Health Surveillance and EvaluationProgram of the California Department of Public Health.
Dr. Ronald L. Melnick served as a Senior Toxicologist and Director ofSpecial Programs in the Environmental Toxicology Program at the NationalInstitute of Environmental Health Sciences (NIEHS) and as Group Leader ofthe Toxicokinetic and Biochemical Modeling Group in the Laboratory ofComputational Biology and Risk Analysis at NIEHS. At NIEHS he designed,monitored and interpreted National Toxicology Program (NTP) toxicity andcarcinogenesis studies, as well as mechanistic studies to characterize thebehavior of environmental carcinogens. He also served as the agencyrepresentative to the White House Office of Science and Technology Policyand on numerous scientific review and advisory panels. Dr. Melnick receivedthe 2007 David P. RaIl Award for Advocacy in Public Health from theAmerican Public Health Association,
Dr. Lee Newman serves as Professor of the Colorado School ofPublicHealth and School of Medicine and Director of the Center for Worker Healthand Environment and the Mountain and Plains Education and Research Centerat the University of Colorado.
Dr. Stephen M. Rappaport received his Ph.D. in EnviromnentalSciences and Engineering from the University of North Carolina. where heserved as Professor from 1990 to 2006. He currently is Professor ofEnvironmental Health at the Ijriiversitv of California. Berkeley. where hedirects the J3erkelev Center for Exposure Biology, a multidisciplinary programthat brings together Berkeley researchers from Public Health. Chemistry, andElectrical Engineering to develop a new generation of biomarkers andhiosensors for environmental epidemiology.
Dr. David Joseph Ross is the Medical Director of the Lung &Heart-Lung Transplant Program and Director of the Pulmonary ArterialHypertension & Thromboendarterectomy Programs at Ronald Reagan -
UCLA Medical Center. Under Dr. Ros& leadership. the lung transplantprogram at UCLA has saved the lives ofhundreds, even thousands, ofpatientswho would otherwise have died from terminal lung disease. Dr. Ross isboard-certified in internal medicine and pulmonary and critical care medicine,Dr. Ross has managed pre- and post-transplant care for several workers whodeveloped interstitial lung disease and other pulmonary disorders fromoccupational exposure to inhaled metals and other inorganic, as well asorganic. iulmonai’ toxicants.
Dr. Janet \Veiss is a physician who is board-certified in Pathology,Toxicology. Medical Toxicology, and Preventive Medicine (OccupationalMedicine). Dr. Weiss has consulted for OSHA. EPA. the Califlrnia PoisonControl Center. NIOSH. and the American Industrial Hgienc i-\ssociation.
PROOF OF SERVICE
I am employed in the County of Santa Clara, State of California. I am over the ageof 18 years and am not a party to the within action. Mv business address is 111 W. SaintJohn St.. Suite 700, San Jose, CA 95113.
On October 11, 2013. I served the foregoing document, described as:APPLICATION FOR LEAVE TO FILE BRIEF OF AMICI CURIAE, COUNCIL FOREDUCATION AND RESEARCH ON TOXICS (CERT), ET AL., iN SUPPORT OFAPPELLANT AND [PROPOSEDJ AMICI BRIEF OF COUNCIL FOR EDUCATIONAND RESEARCH ON TOXICS (CERT). ET AL., IN SUPPORT OF APPELLANT onthe parties to this action as follows:
X (BY MAIL) I caused copies of such document, enclosed in sealed envelopes, tobe deposited in the mail at San Jose, California with postage thereon fully prepaid to thepersons and addresses indicated on the attached list. I am “readily familiar” with the firrnspractice of collecting and processing correspondence for mailing. It is deposited with U.S.Postal Service on that same day in the ordinary course of business, I am aware that onmotion of any party served, service is presumed invalid if the postal cancellation date orpostage meter date is more than one day after the date of deposit for mailing set forth in thisaffidavit.
— (BY FACSIMILE) I served the foregoing document by faxing true copies thereoffrom facsimile number (562) 436-1561. to the facsimile numbers indicated on the attachedlist. Said document was transmitted by facsimile transmission, which was reported completeand without error.
— (BY E-MAIL) I delivered such document by electronic mail to the firms listed onthe attached list.
— (BY OVERNIGHT MAIL) I caused such document to be delivered to the firmsindicated on the attached list by Express Mail or by another express service carrier, byplacing the document in an envelope designated by the carrier and addressed as indicated onthe attached list, with the delivery fees provided for, and depositing same in a box or facilityregularly maintained by that carrier or by delivering same to an authorized courier or driverauthorized by the carrier to receive documents.
I declare under penalty of perjury under the laws of the State of California that theabove is true and correct.
Executed on October Vl, 2013. at San Jose, Califo
Ann Mostek. Declarant
SERVICE LIST(Lriarte v. Scott Sales Company. Case No. BC244257:
Raphel Metzger, Esq. Atornevs for Appel lam.
Metzger Law Group FRANCISCO URIARTE
401 F. Ocean Blvd.. Suite 800Long Beach, CA 90802
Brian P. Barrow. Esq. Attorneys for Appellant,
Simon Greenstone Panatier Bartlett PC FRANCISCO URIARTE
301 E, Ocean Blvd.. Suite 1950Long Beach, CA 90802
Craig Rasmussen, Esq. Attorneys for Respondent.
Stephen C. Snider, Esq. J.R. SIMPLOT COMPANY
Snider. Diehi & Rasmussen1111W. Tokav StreetP.O. Box 560Lodi. CA 95241
Jill A. Franklin, Esq. Attorneys for Respondent,
Schaffer. Lax. McNaughton & Chen SCOTT SALES CO.
515 S. Figueroa St.. Suite 1400
Los Angeles, CA 90071
Jonathan S. Vick. Esq. Attorneys for Respondent.
Atkinson, Andelson, Loya. Ruud & Romo SCOTT SALES CO.
1 2800 Center Court Dr.. Suite 300
Cerritos, CA 90703
The Hon. Joseph E. DiLoretoThe Hon. Ross Ii. Kleinc/o Clerk of the CourtLos Angeles County Superior Court
South District415 \V, Ocean BoulevardLong Beach, CA 90802459 1
California 5 CourtOffice of the Clerk - First Floor
350 McAllister StreetSan Francisco. CA 94012-7303[4 copie.s per CRC &.44(b)(.i)]
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