Teratogen update: polychlorinated biphenyls.

Polychlorinated biphenyls, synthetic hydrocarbon compounds once used as hydraulic fluids and lubricants in electrical transformers and capacitors, are among the most ubiquitous and persistent environmental contaminants. Although banned in most Western nations since the 1970s, substantial residues of these compounds persist in air, water, soil, and sediment world wide (Swain, ’83) and can be detected in biological tissue in most residents of industrialized countries (Jensen, ’87). Because they are hydrophobic and lipophilic, PCBs become increasingly concentrated as they are transferred through the aquatic food chain. Consumption of fatty sports fish from contaminated bodies of water, such as Lake Michigan, provides a major source of human exposure. Transplacental passage has been documented in humans (Kodama and Ota, ’77; J. Jacobson et al., ’84a), although relatively small quantities reach the fetus. Much larger quantities are transferred postnatally via maternal milk due to its high lipid content (Masuda et al., ’78; J. Jacobson et al., ’89). Polychlorinated dibenzofurans (PCDFs) and dibenzo-pdioxins (PCDDs) are highly toxic by-products in the manufacture and combustion of PCBs that accumulate in biological tissue and the environment in a manner similar to the parent compounds, albeit at considerably lower levels (Kubiak et al., ’89). The PCBs used for industrial purposes were complex mixtures of various congeners, eachwith its own unique molecular structure and potentially different toxicological effects. The non-ortho coplanar PCB congeners, which are structural analogs of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; ‘‘dioxin’’), are known to be highly toxic in several organ systems (Safe, ’90), but little is known about the relative neurotoxicity of the PCB congeners. Two dioxin-like congeners (Nos. 77 and 126) have been shown to be neurotoxic in experiments with laboratory animals (Tilson et al., ’79; Eriksson et al., ’91; Holene et al., ’95). However, certain di-orthosubstituted congeners, such as No. 17, lead to reduced dopamine levels in the caudate nucleus, hypothalamus, and substantia nigra in laboratory monkeys (Seegal et al., ’90), suggesting that neurodevelopmental disruption may also be caused by nondioxin-like congeners.