Genetic and environmental interactions determine cancer risks but some cancer incidence is primarily a result of inherited genetic deficits alone. Most cancers have an occupational, viral, nutritional, behavioral or iatrogenic etiology. Cancer can sometimes be controlled through broad public health interventions including industrial hygiene and engineering controls. Chromium and nickel are two human carcinogens associated with industrial exposures where public health measures apparently work. Carcinogenic mechanisms of these metals are examined by electron-spin-resonance-spectroscopy and somatic-mutation-and-recombination in Drosophila melanogaster in this report. Both metals primarily affect initiation processes in cancer development suggesting important theoretical approaches to prevention and followup.

Long range atmospheric and stream transport and oceanic currents drive the ecologic process of PCB deposition in the abiotic environment. In contrast short range transport via bioaccumulation-biomagnification up the food chain determines PCB congener profiles and concentrations and their adverse effects in biological organisms. Two research approaches to congeners, with potential to associate specific adverse human health effects with PCB concentrations in indigenous small populations, are summarized in this study. The field epidemiological approach includes giving questionnaires to target population groups in conjunction with sampling for PCBs (and selected persistent organic pollutants and metals), in foods purchased or hunted and collected by Inuit peoples. Direct determination of contaminant levels in food sources and among individuals in selected comparative subpopulations is also presented.

Lung cancers are significantly increased among workers exposed to chromate (Cr6+, Cr3+), chromium pigments (Cr6+) and chromium plating (Cr6+). Chromium lung burdens and cancer risk increase proportionately with duration of employment at long latencies. However, this epidemiologic information alone is insufficient in determining whether Cr6+ or Cr3+ are equally important in causing cancer. We have attempted to combine epidemiologic data with data from the Drosophila melanogaster somatic-mutation-recombination-test and from the in vitro electron-spin-resonance spectroscopy study to demonstrate that following somatic recombination plays a more important role than somatic mutation in chromium carcinogenesis. Cr4+ is more important than Cr5+ or Cr6+ in inducing somatic recombination while Cr6+ produces more and bigger clones than Cr4+ in somatic mutation. Cr3+ produces negative results in this fruit-fly wing-spot-assay. When the larvae and flies exposed to Cr6+ and Cr4+ are examined by ESR, only Cr5+ and Cr3+ are found. Thermodynamic parameters deltaE, deltaH, and deltaS are also estimated from these latter experiments to explain the relative importance of Cr6+, Cr4+, Cr3+ in chromium carcinogenesis among exposed industrial workers.

Contents: I. Abstract. II. Is PCB an "endocrine disrupter" in the environment? III. Is PCB responsible for other adverse health effects in this index species? IV. Seals are relevant in human health risk assessment: a comparison of hyperaldosteronism between seal and canine. V. Museum specimens of seal jaw osteoporosis indicate historical PCB contamination. VI. Are specific PCB congeners found in seal populations? VII. Does the array of PCB congeners differ between seal and fish? VIII. PCBs near a Tennessee superfund site. IX. Can PCB inhibit fish cytochrome P450? X. PCB biomagnification patterns along the fish-seal-polar bear food web. XI. Geographic variation of the xenobiotic methylsulfonyl metabolite of PCB (MeSO 2 -PCB) in polar bears. XII. Which chlorinated hydrocarbons bioaccumulate in arctic marine mammals? XIII. Experimental evidence for PCBs as endocrine disruptors. XIV. Conclusion. I. Abstract.Wildlife populations are adversely affected in polluted environments. Nevertheless, a cause-and-effect relationship between excessive exposure to chlorinated hydrocarbons and Disclaimer. The opinions and conclusions expressed in this paper are those of the authors and do not necessarily reflect those of the U.128 CHIU ET AL. induction of pathologic disorders in animals, is difficult to demonstrate without verification from experiments following the rationale of Koch's postulates. Deleterious effects of chlorinated chemicals such as DDT on songbird reproduction, as demonstrated by the clutch size of eggs in a nest, however, is an example, where exposure and causation are apparent. With amelioration of DDT pollution, clutch size increases, and the cause-and-effect relationship is established. Similar examples of exposure to DDT and PCBs inducing reproductive disorders and endocrine disruption among marine mammals have been documented in industrialized nations of northern Europe and in the upper latitudes of the Northern Hemisphere. Population declines in ringed, grey and harbor seals are apparently due to a rapid decrease in their rates of reproduction 1 . These latter observations are best interpreted in light of experiments conducted by Reijnders 2 . Reijnders exposed harbor seals to relatively high dietary levels of PCBs and induced PCB-blood-lipids among seals to an average of 25 mg/kg compared to 10 mg/kg among controls. The treated seals had a significantly reduced reproductive rate. A relationship between increased PCB-bloodlevels in vivo and the decrease in reproductive rates in this experiment is highly instructive for interpreting the decline of fertility in seal populations in polluted Baltic Sea waters. These linked observations are dependent upon demonstration of pathologic mechanisms associated with occlusion and stenosis of the uterine lumen among affected females in seal populations.PCB congeners apparently disrupt endocrine-system-functions leading to, or associated with, increases in endometriosis, fetal abortion, glomerulonephropathies and osteoporosis. This observation is further highlighted by R...