Dwight Causey

DDT DDE DDD

Chemical Properties DDTDDEDDD Molecular Weight Appearance/ Physical State Colorless Crystals, white powder Crystalline SolidColorless Crystals, white powder Melting Point ( o C) Solubility (at 25 o C) mg/L0.12 mg/L0.090 mg/L Log K ow Log K oc Henry’s Law constant 8.3x10 -6 atm- m 3 /mol 2.5x10 -5 atm- m 3 /mol 4.0x10 -6 atm- m 3 /mol

History  First synthesized in 1874  Insecticidal properties discovered in 1939 by Paul Hermann Müller Won Noble Prize in Physiology and Medicine in 1948  Used to control insect-borne diseases (i.e. malaria and typhus)  Peak of usage in 1962 Registered for use on 334 agricultural commodities 85,000 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  Directly Water 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 time Sequestered 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: hours

DDD Toxicity  96 hour LC 50 : Glass shrimp: 2.4 µg/L Rainbow trout: 70 µg/L Largemouth bass: 42 µg/L Walleye: 14 µg/L  48 hour LC 50 : Daphnid: 4.5 µg/L

DDE Toxicity  96 hour LC 50 : Rainbow trout: 32 µg/L Atlantic Salmon: 96 µg/L Bluegill: 240 µg/L  Egg shell thinning Mallard: 3 µg/g Brown pelican: 3 µg/g

Toxic Effects  Weak estrogenic activities  In the brain: Inhibition of ATP-based reactions Hepatic enzyme induction Disruption 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 known Believed 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- DDE Acted on by phase I CYP2B enzymes Followed by conjugation with glutathione during phase II Then 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  The Comparative Toxicogenomics Database. Mount Desert Island Biological Laboratory  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,  Hazardous Substances Data Bank. National Library of Medicine TOXNET System  Handbook of Acute Toxicity of Chemicals to Fish and Aquatic Invertebrates. U.S. Fish and Wildlife Services  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,  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,  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,  U.S. Department of Health and Human Services. Toxicological Profile for DDT, DDE, and DDD. Agency for Toxic Substances and Disease Registry  World Health Organization. DDT and its Derivatives – Environmental Aspects. Environmental Health Criteria  World Health Organization. DDT and its Derivatives. Environmental Health Criteria