Dwight Causey

DDT

DDE

DDD

Chemical PropertiesDDT DDE DDD

Molecular Weight

354.49 318.03 320.05

Appearance/ Physical State

Colorless Crystals, white powder

Crystalline Solid Colorless Crystals, white powder

Melting Point (oC)

109 89 109-110

Solubility (at 25oC)

0.025 mg/L 0.12 mg/L 0.090 mg/L

Log Kow 6.91 6.51 6.02

Log Koc 5.18 4.7 5.18

Henry’s Law constant

8.3x10-6 atm-m3/mol

2.5x10-5 atm-m3/mol

4.0x10-6 atm-m3/mol

History First synthesized in 1874 Insecticidal properties discovered in 1939 by

Paul Hermann MüllerWon Noble Prize in Physiology and Medicine in 1948

Used to control insect-borne diseases (i.e. malaria and typhus)

Peak of usage in 1962Registered for use on 334 agricultural commodities85,000 tons produced

Cumulative estimated world usage is 2 million tons

History Used in homes for

mothproofing and lice control

Still used today in developing countries to control malaria and lice

Silent Spring by Rachel Carson in 1962, questioned the widespread use of DDT

Mode of Entry into Water Indirectly

Agricultural runoff○ Binds strongly to soil and organic matter

Volatized into the atmosphere○ Redistributed through particulate matter

DirectlyWater pollution plants (sewer pipes to the

ocean)1,000,000 kg (~227 tons) from Montrose

Chemical Company to Palos Verdes shelf

Reactivity Slightly soluble in water Very lipophillic Physical Half-life: 2-15 years

Increases with timeSequestered in micropores

Biological Half-life: 8 years Biodegraded into DDE and DDD under

aerobic and anaerobic conditions, respectively

DDT Derivatives

DDE is the major metabolite Both resist to biodegradation in aerobic

and anaerobic conditions Very long half-lives in water Hydrolysis is a minor process in

degradation Photolysis of DDE is a major process

Half-life: 15-26 hours

DDD Toxicity

96 hour LC50:Glass shrimp: 2.4 µg/LRainbow trout: 70 µg/LLargemouth bass: 42 µg/LWalleye: 14 µg/L

48 hour LC50:Daphnid: 4.5 µg/L

DDE Toxicity

96 hour LC50:Rainbow trout: 32 µg/LAtlantic Salmon: 96 µg/LBluegill: 240 µg/L

Egg shell thinningMallard: 3 µg/gBrown pelican: 3 µg/g

Toxic Effects

Weak estrogenic activities In the brain:

Inhibition of ATP-based reactionsHepatic enzyme inductionDisruption of hormonal mechanisms

Inhibition of Na+/K+ ATPases in the gills Thinning of egg shells in raptors Reduction in cortisol production

Mode of Entry into Organisms Majority enters through food Some enters through absorption from

water through body surfaces (i.e. gills), not believed to be significant when compared to amount entering through food

Very Lipophillic, bioaccumulates Some organisms retain 90%+ of ΣDDT

in their food source

Molecular Mode of Interaction Egg shell thinning in Raptors, 2 possibilities:

DDE inhibits prostaglandin synthesis in the shell gland mucosa, limiting calcium and bicarbonate transport across the mucosa

Embryonic exposure alters shell gland carbonic anhydrase expression, causing eggshell thinning

In fish, no known molecular mechanism is knownBelieved to involve ATPases in the central nervous

system and gills In Insects, causes the irreversible opening of

voltage gated Na+ channels along the axon

Biochemical Metabolism and Breakdown DDT metabolized into DDE and DDD by

microorganisms Mixed-function oxidases may induce the

dechlorination of DDT to DDE in fishes In some mammals, DDE is converted to 2-

methylsulfonyl-DDE and 3-methylsulfonyl-DDEActed on by phase I CYP2B enzymesFollowed by conjugation with glutathione during

phase IIThen through the mercapturic acid pathway, 2-

SH-DDE and 3-SH-DDE are formed

Detoxification Up-regulation of CYP6G1 gene in

Drosophila melanogaster Secretion through urine, feces, semen, and

breast milk Clams shown to dechlorinate DDE to

DDMU under methanogenic or sulfidogenic conditions

Dried and ground seaweed has been shown to increase DDT biodegradation by 80% after 6 weeks, further degradation of DDD also seen

Bibliography Cal/Ecotox Toxicity Data for Brown Pelican (Pelecanus occidentalis) . Office of Environmental Health Hazard

Assessment. 1999. http://www.oehha.ca.gov/cal_ecotox/report/pelectox.pdf The Comparative Toxicogenomics Database. Mount Desert Island Biological Laboratory. 2008.

http://ctd.mdibl.org/ Denholm I, Devine GJ, Williamson MS (2002). Evolutionary genetics. Insecticide resistance on the move.

Science 297 (5590): 2222–3. Evans, D. H. (1987). The Fish Gill: Site of Action and Model for Toxic Effects of Environmental Pollutants.

Environmental Health Perspectives 71, 47-58. Hazardous Substances Data Bank. National Library of Medicine TOXNET System. 2008.

http://toxmap.nlm.nih.gov/toxmap/home/welcome.do Handbook of Acute Toxicity of Chemicals to Fish and Aquatic Invertebrates. U.S. Fish and Wildlife Services.

1980. Kantachote D., Naidu R., Williams B., McClure N., Megharaj M., Singleton I. (2004). Bioremediation of DDT-

contaminated soil: enhancement by seaweed addition. Journal of Chemical Technology & Biotechnology, 79 , 6, 632-638.

Lacroix M., Hontela A. (2003). The organochlorine o,p’-DDD disrupts the adrenal steroidogenic signaling pathway in rainbow trout (Oncorhynchus mykiss). Toxicology and Applied Pharmacology 190, 197-205.

O’Reilly A.O., Khambay B.P.S., Williamson M.S., Field L.M., Wallace B.A., Emyr Davies T.G. (2006). Modelling insecticide-binding sites in the voltage-gated sodium channel. Biochemical Journal, 396, 255-263.

U.S. Department of Health and Human Services. Toxicological Profile for DDT, DDE, and DDD. Agency for Toxic Substances and Disease Registry. 2002.

World Health Organization. DDT and its Derivatives – Environmental Aspects. Environmental Health Criteria 83. 1989. http://www.inchem.org/documents/ehc/ehc/ehc83.htm

World Health Organization. DDT and its Derivatives. Environmental Health Criteria 9. 1979. http://www.inchem.org/documents/ehc/ehc/ehc009.htm