Source: Adapted from Skinner et al., 1996. Samples were taken from six areas in the New York-New Jersey Harbor estuary: the New York Bight apex; lower bay; upper bay; Arthur Kill, Kill van Kull, and Newark Bay; Jamaica Bay; and East and Harlem Rivers.

reduction, they are thermally stable, and they are nonflammable. Because of their stability, PCB mixtures of thirty to seventy congeners ranging from clear oils to viscous waxy compounds were used extensively in the United States from the 1930s until the 1970s. Their widest application was in the manufacture of dielectric fluids used for insulation in electrical generators and transformers. PCBs were also used in carbonless copy papers, lubricants, printing inks, and as "inert" ingredients in pesticides. Heating or incomplete combustion of PCBs can give rise to dioxins and furans.

Environmental distribution. The chemical stability that made PCBs so useful in industrial applications makes them extremely persistent in the environment. Although manufacture of PCBs was halted in the United States in 1978 because of concern for their potential to cause adverse health effects, PCBs continue to be found widely. Across the United States, PCBs have been detected in 432 Super-fundhazardouswastedisposal sites (ATSDR, 1998).

PCBs are present in high concentrations in upper Hudson River sediments and in fish from Hudson Falls, New York (the site of a former General Electric transformer manufacturing facility) to at least the southern tip of Manhattan (Bopp et al., 1981; Bopp et al., 1982; Kennish et al., 1992; Kennish and Ruppel, 1996a; Skinner et al., 1996).

PCBs are lipid-soluble and bioaccumulative, and they can reach very high concentrations in fish. As seen in Table 28.1, samples taken from throughout the New York Harbor estuary by the New York State Department of Environmental Conservation show especially high levels occur in predator species high on the aquatic food chain, such as striped bass and bluefish, as well as in predatory, bottom-feeding species, such as eels, crabs, and lobsters (Skinner et al., 1996). In recent years, levels of PCBs in Hudson River fish have declined appreciably. With this decline, there has been a change in the mix of PCB congeners, with a relative decline in abundance of the less highly chlorinated species and persistence of the more heavily chlorinated moieties (Bopp etal., 1998).

Human exposure. Virtually the entire United States population has been exposed to at least low levels of PCBs through their diet (Robinson et al., 1990). The United States Food and Drug Administration (USFDA) regards PCBs as "unavoidable environmental contaminants" of foods; nevertheless, they have set tolerance limits for PCBs of 3 ppm in poultry, 2 ppm in fish and shellfish, 1.5 ppm in cow's milk and manufactured dairy products, and 0.2 ppm in infant and junior foods (USFDA, 2000). Consumption of contaminated fish and shellfish is considered the most significant route of human exposure to PCBs outside of the workplace (ATSDR, 1998; Laden et al., 1999).

While pregnant women and women of childbear-ing age comprise only a small fraction of the fish-eating population, they are the groups at greatest risk within that population. PCBs and other persistent pollutants that enter the bodies of childbear-ing women can result in transplacental and lac-tational exposures of human fetuses and nursing infants (Longnecker et al., 1997). These contaminants have been shown to cross the placenta without hindrance, and because they are lipid-soluble, they tend to concentrate in human breast milk (Craan and Haines, 1998). In a study of pregnant African American and Hispanic women in New York City, the levels of PCBs were similar for the two groups, but the two highest levels (10 parts per billion (ppb) and 18 ppb) were in African American women (Berkowitz, Lapinski, and Wolff, 1996). Other recent studies of older women by the same authors revealedhigher serum PCB levels inAfrican Americans as compared to Hispanics (median 56 ppb versus 3 ppb) in New York City. Comparable body burdens of PCBs were measured in women residing in the Northeast and Midwest regions of the United States (mean 5.6 ppb), which were significantlyhigherthanlevelsinwomenfrom the South or West (mean 4.5 ppb) (Laden et al., 1999).

Toxicity. Neurodevelopmental toxicity in infants and children is the health effect of greatest current concern from PCB exposure (Longnecker et al., 1997). A growing body of evidence indicates that PCBs have negative neurodevelopmental effects even at the relatively low levels found in the general population of the United States (Gladen and Rogan, 1991; Patandin et al., 1999). Primarily because of the potential for PCBs in fish to cause developmental neurotoxicity, the state health departments of New York and New Jersey currently advise women of childbearing age to consume no fish from the Hudson River and associated waters (NYSDOH, 2000; NJDEP, 1995).

Public health concern about the neurodevelopmental effects of PCBs was triggered initially by reports of toxicity in the children of women who were exposed to high levels of PCBs and dioxin analogues in two incidents in Asia. In the Yusho and Yu-Cheng oil disease episodes in Japan and Taiwan respectively, cooking oil was contaminated by PCBs and other related compounds, especially fu-rans (Chen et al., 1992; Guo, Lai, and Chen, 1995). Children exposed prenatally exhibited a variety of toxic effects including low birth weight, abnormal skin pigmentation, delayed developmental milestones, and lower intelligence quotients (IQs) as compared to unexposed siblings.

Of most relevance in the United States today are data suggesting that even low levels of exposure to PCBs may have effects on the developing nervous system (Gladen and Rogan, 1991; Jacobson and Jacobson, 1996b; Patandin et al., 1999). Gladen and Rogan examined a general population cohort of children in North Carolina to study the effects of PCB exposure in the top fifth percentile of exposure (PCB levels above 3.5 ppm in fat of maternal breast milk). They found lower scores in these children at eighteen and twenty-four months than in peers on several scales of psychomotor development (Gladen and Rogan, 1991). Antenatal exposures appeared more hazardous than postnatal breast milk exposures. Furthermore, preliminary analyses show associations between antenatal exposure to PCBs in these children and early onset of puberty (Gladen, Ragan, and Rogan, 2000).

Jacobson has followed a cohort of Michigan children with above-average intrauterine exposure to PCBs via maternal consumption of contaminated Lake Michigan fish (Jacobson and Jacobson, 1996b and 1997). They observed adverse effects on McCarthy Verbal and Memory Scale scores at age four years that appeared to be dose-dependent across a range of cord serum PCB levels (Jacobson and Jacobson, 1996a). When PCB exposures were expressed in terms of maternal breast milk PCB levels, effects were limited to children in the highest exposure category, defined as a breast milk fat PCB level >1.25 ppm (Jacobson and Jacobson, 1996a). In a subsequent follow-up of the Michigan cohort at age eleven (Jacobson and Jacobson, 1996b), full scale IQ was inversely associated with prenatal exposure to PCBs rather than postnatal exposure via breast milk. Experimental animal studies of the neurode-velopmental toxicity of PCBs are generally consistent with the human data in terms of the relative importance of pre- versus postnatal exposure and in the general functional domains affected (Lilienthal and Winneke, 1991; Schantz et al., 1995; Herr, Goldey, and Crofton, 1996; Mundy et al., 1998).

The carcinogenicity of PCBs has been established in animal species as well as in humans. PCBs have been declared probable human carcinogens by EPA, the Occupational Safety and Health Administration (OSHA), the National Institute for Occupational Safety and Health (NIOSH), and the World Health Organization (WHO). In animal studies, chronic dietary exposure to PCBs results in the development of liver toxicity and liver cancers (Kimbrough, 1995, Mayes et al., 1998). In epidemiologic studies of PCB-exposed workers, the most notable finding has been an increased death rate from cancer of the liver, cancer of the kidney, and melanoma (Brown, 1987; Brown and Jones, 1981; Longnecker et al., 1997; Sinks et al., 1992). A recent epidemiologic study of the mortality experience of General Electric workers in upstate New York reported no excess cancer mortality (Kimbrough, Doemland, and LeVois, 1999). Several serious flaws and limitations were noted, however, in the methodology ofthat study; of most importance, the majority of workers had no opportunity for occupational exposure to PCBs, resulting in probable dilution of any excess risk of cancer mortality (Bove, Slade, andCanady, 1999; Frumkin and Orris, 1999).

Concern about a possible role of PCBs in the etiology of hormonally-related diseases such as breast cancer has prompted several investigations of the effects of environmental (that is, dietary) PCB exposure in women. Overall, these epidemiologic data on PCB exposure and breast cancer suggest no substantial increase in risk (Krieger et al., 1994; Longnecker et al., 1997; Helzlsouer et al., 1999; Wolff et al., 2000b; Zheng et al., 2000), although the importance of prenatal exposures to hormonally active chemicals in cancer development is a new and intriguing area of research that has only begun to be explored (Wolff and Toniolo, 1995).

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