Organochlorine Pesticides

Chemistry. Organochlorine pesticides were introduced in the 1940s to replace the acutely toxic arsenical pesticides that had been their principal predecessors. They were used extensively in agriculture, in forestry, in the control of insect-borne diseases such as malaria and typhus, and for pest control in homes and neighborhoods. Among the most commonly used organochlorines were 2,2-bis(p-chlorophenyl)-1,1,1-trichloroethane (DDT) and the termiticide chlordane (a mixture of at least fifty different compounds with the majority constituents being cis and trans chlordane; heptachlor; cis and trans nonachlor; alpha, beta, and gamma chlordane). The general mechanism of the organochlorine pesticides' toxicity in insects is central nervous system stimulation and/or depression, depending on the compound and dose. Because the compounds showed little or no acute toxicity in humans, they were initially believed to be safe.

In 1962, with publication of Rachel Carson's Silent Spring, the potential of the organochlorine pesticides for long-term persistence in the environment, for bioaccumulation, and most importantly, for neuroendocrine and reproductive toxi-city became evident. Carson showed that through its ability to disrupt endocrine function, DDT had caused extensive reproductive failure in eagles and ospreys, species high on the food chain that had accumulated large body burdens. In 1972, DDTpro-duction and use were banned in the United States by the newly created EPA.

Environmental distribution. A large number of chlorinated hydrocarbon pesticides and their breakdown products contaminate sediments in the Hudson River basin. The most significant of these contaminants are DDT derivatives, chlordane and its metabolites, and dioxins (Bopp and Simpson, 1989;Bopp etal., 1998). Dieldrin and hex-achlorocyclohexane (HCH, sometimes misnamed benzene hexachloride or BHC), also prototypical organochlorines, are also detectable but less common.

In the lower Hudson River and New York Harbor, residues of organochlorine pesticides are found in various aquatic species (Hauge et al., 1994; Skinner et al., 1996; Kennish and Ruppel, 1996b; Kennish and Ruppel, 1997). For example, DDT levels were found to exceed the regulatory criterion of 5,000 ng/g for human health protection in some samples of American eel. DDT compounds were dominated by their longer half-life degradation products, DDE and DDD. Greatest total DDT concentrations were found in the Newark Bay complex and appear to be associated with the former Diamond Alkali production facility at 80 Lister Avenue (Bopp et al., 1991).

Chlordane, banned since 1988, was used in 24 million United States homes, usually as a termiti-cide, and it has been detected in the home environment as long as thirty-five years after use (Wright, Leidy, and Dupree, 1994). Chlordane concentrations in the Hudson River estuary have been found to exceed regulatory criteria for human health protection for several specimens of American eel, white perch, and the hepatopancreas of blue crab (Skinner et al., 1996). However, only blue crab hepatopancreas showed average concentrations that exceeded the regulatory criterion of 300 ng/g. Greatest concentrations were found in samples taken from the East River and the Newark Bay complex and are possibly due to residential applications for termite control.

Dieldrin concentrations exceeded 50 ng/g only in the hepatopancreas of blue crabs, but even those samples did not exceed the regulatory criterion of 300 ng/g. Hexachlorobenzene, mirex, endrin, and toxaphene were seldom or never detected (Skinner etal., 1996).

Human exposure. Organochlorine pesticides are persistent lipophilic compounds that are highly resistant to biodegradation in the environment (ATSDR, 1994). With the decrease in use of these compounds, body burden levels in United States residents have fallen in recent decades; for example, levels of DDT in the 1960s were about five times higher than current levels (Kutz, Wood, and Bottimore, 1991; Craan and Haines, 1998; Wolff, 1999). Nevertheless, they are ubiquitous in air, soil, water, and sediments, and the primary source of exposure to the general population is through the food chain. Children have an additional route of exposure to organochlorines through breast milk. Meat, dairy products, and fish are the main sources of exposure for adults, and residues have also been measured in fruits, vegetables, and grains (particularly foodstuffs imported from developing countries where DDT is still used). Several studies have examined ethnic differences in environmental exposures to organochlorine pesticides and PCBs. They found that African Americans have higher DDT levels than Caucasians, and the data suggest that this disparity has existed since 1960 (Krieger et al., 1994). In recent studies among 278 women approximately fifty-five years old from New York City who were tested during 1994-96, both African American and Hispanic women had serum levels of DDE almost twice as high as Caucasian women (Wolff etal., 2000a).

The synergistic health effects exerted by complex mixtures of organochlorine pesticides and PCBs are inadequately explored, but are potentially important, since these compounds generally occur together in the environment (Bopp et al., 1998). Recent analyses of body burdens of these pollutants in anglers who eat fish and crabs from the lower Hudson River watershed corroborate that there exists a strong congruence among levels of highly chlorinated PCB congeners and organochlorine pesticides in anglers' blood (A. L. Golden, unpublished data).

Toxicity. Organochlorine pesticides are carcinogenic, they upregulate cytochrome P450 enzymes, and they cause reproductive failure in wildlife (Longnecker et al., 1997). These pollutants are known to modulate hormonal activity, as displayed in various in vitro and in vivo test systems, in wildlife and human populations (ATSDR, 1994). They have both estrogenic and antiestrogenic potential. Workers who are highly exposed to DDT exhibit acute neurological symptoms (Longnecker et al., 1997) and low-dose in utero exposure to DDT during critical periods of development can lead in animal models to irreversible aberrations in adult brain function, including motor, sensory, and cognitive changes (Eriksson and Talts, 2000). However, ambient exposure levels in children, assessed in one study from North Carolina, have not been associated with neurologic or developmental abnormalities in humans (Gladen and Rogan, 1991; Gladen etal., 2000).

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