POLYCHLORINATED BIPHENYLS (PCBs)

1. POLYCHLORINATED BIPHENYLS(PCBs) By Jenn Corpuz

2. PHYSICAL & CHEMICAL PROPERTIES • C12H10-xClx • MP: 340-375 C • Thin, lightly colored liquids to yellow or black waxy solids picture from: www.epa.gov

3. PRODUCTION HISTORY • Developed in 1929 • Multiple congeners developed • Used as a coolant for electrical equipment and as a plasticizer in paints, plastics and rubber products • Banned by EPA in 1979 • Products manufactured before 1979 are still releasing PCBs into the environment • Most commonly known as: Aroclor, Phenoclor and Kanechlor

4. MODE OF ENTRY INTO AQUATIC ENVIRONMENT • Run off • Poorly maintained hazardous waste sites containing PCBs • Burning of wastes in municipal or industrial incinerators

5. CHEMICAL REACTIVITY • 209 known congeners (species) • Most common: Aroclor, Phenoclors, Kaneochlors • Most toxic: coplanar mono-orthosubstituted species Figure by Safe et. al.

6. CHEMICAL REACTIVITY (cont’d) • Most species: insoluble in water • Solubility decreases with increasing chlorination • 0.01-0.0001ug/L • Halflives: 3 wks -2 yrs (air) • <6 yrs (aerobic soils/sediments) picture from: www.epa.gov

7. TOXICITY TO AQUATIC LIFE • Sediment bound • Bioaccumulated and magnified through the food chain • Rainbow Trout LC50= 0.32ug/L • Laboratory Rats LD50= 1g/kg by weight • Acute toxicity generally low • Chronic toxicity gave results

8. TOXIC EFFECTS NOTED • PCBs are known carcinogens • Found to be highly associated with cancers in the immune, reproductive and endocrine systems • Iipophilicity allows PCBs to live in animal’s tissues

9. MODE OF ENTRY • Ingestion (most common) • gills

10. MODE OF INTERACTION • Induces AHH and binds to AhR • Binds ARNT • Leads to gene transcription • PCBs have been linked to activation of oncogenes and inactivation of tumor suppressing genes

11. BIOCHEMICAL METABOLISM AND BREAKDOWN • CYP1A and CYP1B are induced • Resulting hydroxylated and methylsulfonyl PCB metabolites bind to DNA • Highly chlorinated biphenyls are metabolized very slowly if at all • Phase II (excretion) is unlikely Figure from Tabb et. al.

12. DEFENSE STRATEGIES FOR DETOXIFICATION • For less chlorinated species: oxygenating chlorine sites excretion through urine • None for highly chlorinated species

13. BIBLIOGRAPHY • www.epa.gov • www.ehponline.org • Hansen, Larry G. “Stepping Backward to Improve Assessment of PCB Congener Toxicities.” Environmental Health Perspectives. Volume 106. Feb 1998. • McConnell, Ernest. “Comparitive Toxicity of PCBs and Related Compounds in Various Species of Animals.” Environmental Health Perspectives. Volume 60. 1985. 29-33. • Neal, Robert A. “Mechanisms of the Biological Effects of PCBs, Polychlorinated Dibenzo-p-dioxins, and Polychlorinated Dibenzofurans in Experimental Animals.” Environmental Health Perspectives. Volume 60. 1985. 41-46. • Safe, Stephen, Stelvin Bandiera, Tom Sawyer, Larry Robertson, Lorna Safe, Andrew Parkinson, Paul E. Thomas, Dene E. Ryan, Linda M. Reik, Wayne Levin, Mary Anne Denomme, and Toshio Fujita. “PCBs: Structure-Function Relationships and Mechanism of Action.” Environmental Health Perspectives. Volume 60. 1985. 47-56. • Tabb, Michelle M., Vladyslav Kholodovych, Feliz Grun, Changcheng Zhou, William J. Welsh, and Bruce Blumberg. “ Highly Chlorinated PCBs inhibit the Human Xenobiotic Response Mediated by Steroid and Xenobiotic Receptor (SXR). Environmental Health Perspectives. Volume 112. 163-169.