Polybrominated biphenyls (PBB) were used as a fire retardant. In common with other halogenated hydrocarbons, PBBs are lipophilic and resistant to chemical and metabolic degradation. Cattle on about 25 Michigan farms were exposed to as much as 250 g per head of PBB when it was accidentally mixed in cattle feed in 1973 to 1974. Livestock exposures several orders of magnitude lower occurred on several hundred other farms because of carryover and equipment contamination in feed mills. Approximately 85% of the Michigan population received some exposure to PBB because dairy product marketing involves mixing milk from many farms. A few cases of high human exposure, which may have been as great as 10 g, occurred when residents of the more highly exposed farms consumed their own products. Although numerous clinical signs and pathological changes were reported in exposed cattle, only anorexia, lacrimation, emaciation, hyperkeratosis, and kidney damage were confirmed in controlled studies. The acute toxicity of PBB in laboratory animals is low, but a variety of subacute effects have been reported. Induction of microsomal enzymes, enlargement and histopathological changes of the liver, fetotoxicity, and immunosuppression are among the more significant. Epidemiological studies of exposed humans have revealed no pattern of clinical signs or symptoms that were related to PBB exposure. A complete evaluation of the human consequences of exposure to PBB await the conclusion of long-term epidemiological studies.

Extrapolations from animal toxicity experiments (including carcinogenicity and reproductive effects) to possible human heath effects can be used to estimate a reasonable level of risk for 2,3,7,8-tetrachlorodibenzodioxin (2,3,7,8-TCDD). Extrapolations are derived from: (1) review of published studies, (2) a complex set of assumptions related to human exposure to contaminated soil, and (3) estimates of (a) a dose response curve, (b) appropriate margins of safety, and/or (c) applicable mechanisms of action. One ppb of 2,3,7,8-TCDD in soil is a reasonable level at which to begin consideration of action to limit human exposure for contaminated soil.

The polychlorinated dibenzo-p-dioxins and dibenzofurans (dioxins) are groups of compounds with similar chemical and toxicological properties. Carcinogenicity was considered the most serious toxic end point when setting previous regulatory policies, but recent concerns have focused on the possible endocrine-disrupting activities of the dioxins. Toxicity is related to the 2,3,7,8 pattern of chlorine substitution, a pattern that also leads to chemical and metabolic stability. Dioxins are practically insoluble in water and concentrate in lipids of biological systems, leading to low background concentrations in fat of the general human population. Major environmental sources of dioxins are emissions from industrial chlorination processes and combustion of materials containing chlorine. Inhalation and water have been ruled out as significant exposure pathways, which suggests that food is the primary source. Pathways of entry into food chains are atmospheric transport of emissions and their subsequent deposition on plants, soils, and water. The major food sources seem to be fat-containing animal products and some seafoods. This conclusion is based on evaluations of potential environmental pathways involving dioxins and related compounds. Generally, dioxins and other lipophilic compounds are not taken up and translocated by plants, so residues in foods and feeds derived from seeds should be negligible. Animals on high-roughage diets, or those that ingest contaminated soil, are the most likely to accumulate dioxin residues from the environment. The conclusion that animal products are a major source of human exposure requires verification by appropriate food sampling programs and animal metabolism studies. If it is desirable to reduce human exposure to dioxins via the food supply, reduction of sources would be a more effective strategy than changing agricultural practices and food consumption patterns.

When rats and birds were treated with o, p-DDT, their reproductive tissues exhibited the same response as when they were treated with estrogen. Weight, water content, glycogen, and RNA increased in uteri and oviducts of rats, chickens, and quail receiving o, p-DDT; p, p-DDT produced little if any response. The o, p-DDT did not accumulate in the reproductive or adipose tissues to a greater extent than p, p-DDT.

Pentachlorophenol (PCP) treated wood has been hypothesized as an important source of dioxins in milk and beef. This phase of studies to evaluate the hypothesis involved the administration of PCP-treated wood to cows and measurement of the transfer of polychlorinated dibenzo-pdioxins (PCDD) and dibenzofurans (PCDF) to milk. The 3 g/day dose of ground wood was administered to four cows for 56 days. This dose provided a PCP intake of 4.8 mg/ day and PCDD/F intakes in the range of 0.3 µg/day for 2,3,7,8-TCDD to 17 000 µg/day for 1,2,3,4,6,7,8,9-OCDD. Steady state with respect to excretion in milk was reached because concentrations of PCDD/Fs in milk fat were reasonably constant from day 28 through day 56. The PCDFs without chlorine in the 4 and 6 positions were metabolized and not transported to milk. The other PCDFs and all PCDDs had intake adjusted concentrations in milk that were inverse to the number of chlorines. Variations among cows in concentrations of specific congeners were small and were not related to body weight, dry matter intake, or production of milk and milk fat. The transfer coefficients calculated for the PCDD/Fs in this study provide tools for reducing uncertainty in risk assessments.