Polycyclic Halogenated Hydrocarbons

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Polycyclic halogenated hydrocarbons (PHH) are persistent synthetic or man-made chemicals that are or were heavily used in industry or are by-products of industrial processes. The PHHs of highest concern are halogenated aromatic hydrocarbons, including polychlorinated biphenyls (PCBs) and polychlorinated dibenzo-p-dioxins (dioxins). Both PCBs and dioxins have been shown to be highly toxic to many organ systems in animal studies and are potent fetotoxins (Carpenter 1998; Mukerjee 1998). PCB/dioxin immunotoxicity has been recently reviewed in two studies (Tryphonas 1998; Weisglas-Kuperus 1998). Occupational and transient highlevel exposure from industrial accidents show some immunomodulations in humans, however, only one study has examined endpoints indicative of hypersensitivity, rather than immunosuppression. In 2001, Karmaus and Kruse (Karmaus et al. 2001) conducted an epidemiological study of 340 children that investigated associations between exposures to several persistent environmental contaminants and prevalence of otitis media, respiratory infections, asthma, and elevated IgE levels. Although the authors did not find any associations between PCBs or hexachlorobenzene and asthma symptoms or elevated IgE levels, exposure to the insecticide dichlorodiphe-nyldichloroethene (DDE) was found to be associated with both self-reported asthma symptoms and higher blood levels of IgE. In another study, Reichrtova et al. used placental contamination as a biological marker for exposure of the fetus via placental transfer (Reichrtova et al. 1999). The placental samples were assayed for 21 organochlorine compounds, including dioxin. Specimens of cord blood from neonates were analyzed for levels of total immunoglobulin E. Their results showed higher cord blood IgE levels following in utero dioxin/organochlorine exposure. Increased IgE levels may be associated with allergic sensitization, but it remains to be seen whether these increases can be used as a predictor of subsequent development of atopic asthma.

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