By Curtis C. Tmvis, Holly A. Haftemer-Frey, and Ellen Silbergeld Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzo furans (PCDFs), including the highly toxic 2,3,7,8-tetrachlorodibenzo-pdioxin (TCDD, commonly referred to as “dioxin”), are the subject of much public concern and debate. Because TCDD is the most potent chemical carcinogen ever evaluated by EPA (I), there is widespread fear that exposure to even small amounts of dioxin could lead to serious adverse health effects. EPA has for some years been assessing the nature and extent of the dioxin problem in the United States. We believe that the agency has failed in this task and that the dioxin problem is much broader in scope than the public has been led to believe. Environmental concentrations There is a general perception that dioxin contamination is a localized problem and that control of a few isolated sources, such as municipal solid waste incinerators, will reduce human exposure to acceptable levels. The real-
ity is that dioxin is everywhere and that virtually every man, woman, and child in the United States is being exposed to dioxin daily. PCDDs and PCDFs have been measured in virtually all media, including air, soil, meat, milk, fish, vegetation, h i t s , and human biological samples. Concentrations in urban air are remarkably similar in all industrialized countries, including the United States, West Germany, Sweden, and Japan, ranging from 1.3-9.6 pg/m3, with a geometric mean concentration of 3.4 pg/m3 (2). Background PCDD/ PCDF levels in urban soil have been measured in the United States and Canada. Fifteen urban sites in the United States without a previously known source of contamination had a total PCDDlPCDF concentration ranging from SI to 9100 pglg, with a geometric mean of 1405 pg/g (3). The mean concentration in Canadian urban soil (1819 pglg) is similar (4). Although analysis of PCDDs and PCDFs in commercial milk samples is limited, existing measurements indicate
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global contamination of dairy products. Total PCDD/PCDF levels in whole milk average 0.6 pg/g in Switzerland (5). 0.8 pg/g in West Germany f6), 1.O pglg in Japan (7),and 3.1 pglg in Canada (8). Given that dairy products are a major pathway of human exposure to dioxin (9) and that milk packaging may also be a source (ZO), it is essential that similar measurements be taken in the United States. TCDD levels measured in fish from U S . lakes and rivers confirm that TCDD is bioaccumulated by fish and that low-level contamination of fish is widespread (ZZ). As part of its National Dioxin Study (12). EPA analyzed fish collected from 304 urban sites, none of which had been a known source of TCDD contamination. Concentrations of TCDD in whole fish ranged from nondetectable to 85 pg/g (121, and had a geometric mean concentration of 0.4 pg/g (13).
Sources of environmental input Principal environmental sources of PCDDs and PCDFs are suspected to be industrial sources, including metal reclamation plants, pulp and paper mills, Enviran. Sci. Technol., Vol. 23,NO. 9. 1989 1061
mglkglday (9) times the cancer potency factor for TCDD (1.56 X I@ mglkgl day-')], which could result in more than 300 additional cancer deaths per year (I x lifetimecancer risk X 2.2 X I@ U.S. residents + 70 years). This risk level is about 20 times higher than the level that caused EPA to recommend limiting the use of Alar, a pesticide often sprayed on apples. Although EPA is mandated by law to set standards that protect human health. the agency maintains that existing regulations, such as the Clean Air Act and the Clean Water Act, does not allow it to regulate environmental releases on the basis of food chain exposures. This is a narrow interpretation of the regulatory mandate. It is well established that once pollutants enter the environment, they transfer throughout all media. resulting in wide distribution in the environment and subsequent human e x p sure from multiple media. The reliance on single-medium exposures to regulate toxic pollutants is insufficient, especially because multimedia exposures are the rule and not the exception (32). Given that EPA is charged with setting appropriate standards to ensure that resulting environmental levels do not pose serious risks to human health, we recommend that EPA take the lead in accounting for the food chain in setting standards. The need to set standards that account for all major pathways of human exposure is paramount, given that current food chain risks may already exceed a 1W excess lifetime cancer risk.
and steel mills (14-16); motor vehicles (I7-19); some organic chemical manufacturing processes (20);incinerators, including industrial. hazardous waste, hospital, and municipal solid-waste incinerators (,?&?,?); and forest fires and residential wood burning (21. 23). Despite the concerted acknowledgment by some European countries, Canada, and Japan that dioxin sources are abundant and ubiquitous, EPA continues to function as if control of dioxin emissions from a few localized sources will avert human exposure. The fallacy of that perception is that dioxins are all around us, even in remote areas that do not have any known source of contamination (24, 25). Given the omnipresence of dioxins in the environment, it is imperative that the major sources of PCDDs and PCDFs be determined and controlled, so that background environmental concentrations are not hrrther elevated. Sources, extent of human exposure Evidence of widespread human exposure to PCDDs and PCDFs is p n r vided by the fact that virtually all human adipose tissue samples from individuals in the United States contain PCDDs and PCDFs at levels ranging from 841 to 1460 pglg (2628) with a geometric mean of I178 pglg. Market basket studies conducted recently in West Germany (29). Canada (8). and Japan (30) show that the mean background dietary intake of PCDDs and PCDFs (expressed in toxic equivalents) in industrialized countries is about 98 pg/day, with meat and dairy products accounting for the majority of daily intake (9.29.30).[The toxicity of different PCDD and PCDF isomers is typically expressed in terms of toxic equivalent factors (TEFs), which relate the toxicity of all PCDDlPCDF compounds to the known toxicity of TCDD using one of several weighing schemes (31). Hence, a mixture of PCDDs and PCDFs expressed in TEFs is assumed to have the same toxic effect as TCDD]. In fact, the average individual receives about 12 times more PCDDs and PCDFs from drinking one liter of milk a day [geometric mean concentration of F'CDDs and PCDFs in milk equals 840 pg/L (2)] than from breathing the air [background urban air concentration equals 3.4 pg/m3 (2) x 20 m3 of air inhaled per day yields an inhalation dose of 68 pglday].
EPA's erroneousapproach EPA's regulatory focus has, unfortunately, been on sources rather than on exposures. For example, EPA has yet to directly assess the overall presence of dioxin in U.S. food items. More1W2 Environ. Sci. Technol.. MI. 23. NO.9. lS89
Conclusions and recommendations
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