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Perspectives in Disease Prevention and Health Promotion Health- Risk Estimates for 2,3,7,8-Tetrachlorodibenzodioxin in Soil

At the request of the Environmental Protection Agency and the State of Missouri, CDC undertook a risk assessment study of 2,3,7,8-tetrachlorodibenzodioxin (TCDD) levels in soil. Within the last year, CDC advised Missouri that, in two specific residential areas, soil levels above 1 part per billion (ppb) (ug/kg) of TCDD could result in an unreasonable risk to human health. Later, on June 28, 1983, this assessment was reviewed by a group of outside consultants,* and the assessment was expanded to cover industrial, commercial, farm, and uninhabited areas. The following summarizes these deliberations.

Adequate dose-response data for chronic effects of TCDD are not available from epidemiologic studies of humans. Therefore, extrapolations from animal toxicity experiments (including carcinogenicity and reproduction effects) to possible human health effects have been used to estimate a reasonable level of risk from exposure to this agent. Extrapolations have been derived from a review of published studies; a complex set of assumptions related to human exposure to contaminated soil; and estimates of (1) a dose-response curve, (2) appropriate margins of safety, and/or (3) applicable mechanisms of action.

TCDD is a known carcinogen in animals, and there is considerable discussion about the best way to calculate excess cancer risk in humans exposed to TCDD. General issues of concern include use of appropriate mathematical models for predicting responses at the low end of the dose-response curve, how to use dose-response data from different tissue sites (e.g., liver, lung), and what conversion factors to use in extrapolating from animals to humans to account for species variations (1). Using data from previous toxicologic studies with female rats (2-4), dose-response estimates were derived. The lower boundary of the confidence interval for a dose estimated to increase the risk of developing cancer by one per million was then calculated. For liver cancer (the most sensitive tissue site), a virtually safe dose (VSD) was estimated as 28 femtograms (fg)** per kg body weight (b.w.) per day. For the risk of inducing tumors in less sensitive tissues, a VSD of 1,428 fg/kg b.w./day was estimated. These doses were then extrapolated directly to humans. The model used was linear; therefore, the levels for an increased risk of one excess cancer per 100,000 are 276 fg to 14.3 picograms (pg)**/kg b.w./day.

In addition, using standard toxicologic approaches for assessing reproduction effects of TCDD exposure, a VSD was estimated. Since a "no-observed-effect level" has never been determined, the VSD extrapolated to humans was derived by using a safety factor of 1,000 applied to the lowest level tested in subhuman primates. Using failure to conceive and fetal wasteage as the most sensitive reproduction effects, a VSD of 100 pg/day was derived. However, this VSD is higher than that estimated using carcinogenisis as an end point.

CDC estimated the absorption of TCDD from soil via dermal, gastrointestinal, or respiratory routes for humans having exposure to contaminated soil adjacent to their homes (Figure 1). Estimates of exposure to chemicals in soil are inherently more difficult than estimates of exposure to chemicals in air, water, or food, because soil contamination is less homogeneous, and exposure depends chiefly on individual activities. In this model, the consultants concluded that the greatest contribution of risk came from ingestion of soil, particularly during childhood; the next, from dermal absorption. (Inhalation is a relatively minor contributor in areas with abundant vegetation.) One ppb of TCDD in residential soil was chosen as a level of concern, and at substantially higher levels (e.g., greater than 100 ppb TCDD in soil), calculated risks may increase.

The level of concern for 2,3,7,8-TCDD in soil should not be viewed as a universal standard but rather as an operational starting point to analyze each situation. Characteristics unique to each situation--including locations of the contaminated soil, composition of the population exposed, and the likely frequency and duration of future exposures--factor significantly in assessing each case. These characteristics and the potential for limiting or eliminating future exposure in a timely fashion will influence decisions about appropriate actions at specific sites.

In special situations, e.g., horse-riding arenas, with high dust or soil resuspension, inhalation of TCDD may become a more prominent route of exposure, and this would affect risk estimates. For this level of concern, other routes of exposure that may be indirectly related to soil contamination have not been considered, such as food-chain contamination via grazing cattle or bioconcentration in bottom-feeding fish. Soil levels of TCDD in pastures where cattle graze and pigs root might have to be lower because of the potential for bioaccumulation.

In similar residential areas, 1 ppb of TCDD in soil is a reasonable level at which to consider limiting human exposure. Principal attention should be given to children at play who might ingest such soil.

In assessing the implications of this level of concern for any particular site, one should use additional information and recognize a complex set of underlying assumptions, such as the amount of TCDD people might receive, how often they are exposed, and whether humans have the same response to TCDD as animals. To err on the side of public safety, these assumptions should be conservative and should address factors related to: uniformity of TCDD concentration in soil; uniformity of human access (particularly children's access) to and activity on the soil; intensity, frequency, and duration of exposure; and the bioavailability of TCDD in different soils and through different types of exposure. Furthermore, when soil is measured for TCDD concentration, the adequacy of the sampling plan, the degree of laboratory extraction of TCDD from soil, and the accuracy of its subsequent measurement must be considered. Reported by Office of the Director, Special Studies Br, Chronic Diseases Div, Center for Environmental Health, CDC.

Editorial Note

Editorial Note: For many environmental (and occupational) toxins, adequate dose-response data from epidemiologic studies of humans are not available for predicting risk, particularly at low levels of exposure. Often, toxicologic data on animals are the best available predictors of risk. Cumulative human intake (exposure, dose) can also not be measured directly in many instances (e.g., TCDD, asbestos, formaldehyde); exposure assessments reflect the likely human intake on the basis of chemical levels in the environment and of human activity patterns. Many environmental standards and regulatory decisions--from safe drinking water and air standards to individual decisions at Superfund*** sites or other settings--are based on exposure and risk assessment.

Reference

  1. CDC. Unpublished data.

  2. Kociba RJ, Keyes DG, Beyer JE, et al. Results of a two year chronic toxicity and oncogenicity study of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in rats. Toxicol Appl Pharmacol 1978; 46:279-303.

  3. National Toxicology Program. Carcinogenisis bioassay 2,3,7,8-tetrachlorodibenzo-p-dioxin (CAS #1 174-6-01-6) in Swiss-Webster mice (dermal study). National Toxicology Program Tech Rep Ser 1982; 201:113.

  4. National Toxicology Program. Carcinogenisis bioassay 2,3,7,8-tetrachlorodibenzo-p-dioxin (CAS #1 174-6-01-6) in Osborne-Mendel rats (gavage study). National Toxicology Program Tech Rep Ser 1982; 209:195. *Consultants: Conference on Polyhalogenated Aromatic Compunds--Dr. Donald Barnes, Dr. Judy Bellin, Dr. James Falco, U.S. Environmental Protection Agency; Dr. Frank Cordle, U.S. Food and Drug Administration; Dr. George F. Fries, Pesticide Degradation Laboratory, U.S. Dept of Agriculture; Dr. Donald Grant, Health Protection Br, Health and Welfare, Canada; Dr. Robert Harris, Hazardous Waste and Research Div, Center for Energy and Environmental Studies, Princeton University; Dr. David G. Hoel, National Institute of Environmental Health Sciences; Dr. Nancy Kim, Bureau of Toxic Substances Assessment, New York State Dept of Health; Dr. George Lucier, National Institute of Environmental Health Sciences; Dr. Norton Nelson, New York University Medical Center, Institute of Environmental Medicine; Dr. Henry Pitot, McArdle Cancer Research Institute, University of Wisconsin; Dr. Charles F. Reinhardt, DuPont Company, Haskell Lab; Dr. Robert G. Tardiff, Vienna, Virginia; Dr. John Van Ryzin, Div of Biostatistics, School of Public Health, Columbia University. **Fg = 10((-15))g; pg = 10((-12))g. ***Known officially as the Comprehensive Environmental Response Compensation and Liability Act of 1980. This act provides for liability, compensation, cleanup, and emergency response for hazardous substances released into the environment and the cleanup of inactive hazardous waste disposal sites.



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