David H. Cleverly

Interim procedures for estimating risks associated with exposures to mixtures of chlorinated dibenzodioxins and -dibenzofurans (CDDs and CDFs)

Abstract A set of weighting factors is proposed for expressing the toxicity of mixtures of CDDs/CDFs in terms of an equivalent amount of 2,3,7,8-TCDD. The factors are applied to a variety of environmental samples and the results compared to those obtained using a number of alternative factors which have been proposed.

Development and validation of an air-to-beef food chain model for dioxin-like compounds

A model for predicting concentrations of dioxin-like compounds in beef is developed and tested. The key premise of the model is that concentrations of these compounds in air are the source term, or starting point, for estimating beef concentrations. Vapor-phase concentrations transfer to vegetations that cattle consume, and particle-bound concentrations deposit onto soils and these vegetations as well. Congener-specific bioconcentration parameters, coupled with assumptions on cattle diet, transform soil and vegetative concentrations into beef fat concentrations. The premise of the validation exercise is that a profile of typical air concentrations of dioxin-like compounds in a United States rural environment is an appropriate observed independent data set, and that a representative profile of United States beef concentrations of dioxin-like compounds is an appropriate observed dependent result. These data were developed for the validation exercise. An observed concentration of dioxin toxic equivalents in whole beef of 0.48 ng/kg is compared with a predicted 0.36 ng/kg. Principal uncertainties in the approach are identified and discussed. A major finding of this exercise was that vapor phase transfers of dioxin-like compounds to vegetations that cattle consume dominate the estimation of final beef concentrations: over 80% of the modeled beef concentration was attributed to such transfers.

A statistical survey of dioxin-like compounds in United States beef : A progress report

The USEPA and the USDA have completed the first statistically designed survey of the occurrence and concentration of CDDs and CDFs in the fat of beef animals raised for human consumption in the United States. Back fat was sampled from 63 carcasses at federally inspected slaughter establishments nationwide. The sample design called for sampling beef animal classes in proportion to national annual slaughter statistics. All samples were analyzed using a modification of EPA method 1613, using isotope dilution, High Resolution GC/MS to determine the rate of occurrence of 2,3,7,8-substituted CDDs/CDFS. The whole weight method detection limits ranged from 0.05 ng kg-1 for TCDD to 3 ng kg-1 for OCDD. The results of this survey showed a mean concentration (reported as I-TEQ, lipid adjusted) in U.S. beef animals of 0.35 ng kg-1 and 0.89 ng kg-1 when either non-detects are treated as 0 value or assigned a value of 1/2 the detection limit, respectively.

Regulatory analysis of pollutant emissions, including polychlorinated dibenzo-p-dioxins (CDDs) and dibenzofurans (CDFs), from the stacks of municipal waste combustors

Abstract Municipal waste combustors (MWCs) are known to emit into the air quantities of CDDs, CDFs and other carcinogenic and toxic organic and inorganic compounds from the stack. In support of a regulatory determination, an impact analysis, including a quantitative risk assessment of 13 pollutants in the air emissions, was conducted to evaluate the impacts of further controls on emissions. This paper describes the Environmental Protection Agencys (EPA) regulatory analysis of dioxins and other pollutant emissions from MWCs, and discusses the Agencys findings.

RISK FROM EXPOSURE TO POLYCHLORINATED DIBENZO-p-DIOXINS AND DIBENZOFURANS EMITTED FROM MUNICIPAL INCINERATORS

Abstract Incineration of wastes seems to be one of the major sources of PCDFs and PCDFs (dioxins). Their prevalence and extreme stability in the environment, bioavailability and bioaccumulation in the biota and human adipose tissues and breast milk are of much concern. 2,3,7,8-TCDD is one of the most toxic chemicals known and has been found to have teratogenic and carcinogenic activities in animals. Exposure to TCDD can result in chloracne, general weakness, drastic weight loss, hyperpigmentation of skin, hirsutism, porphyria cutanea tarda, liver damage, changes in activities of various liver enzymatic levels, abnormal lipid metabolism, abnormalities of the endocrine and immune systems, and possible teratogenic effects in humans. Moreover, chronic bioassay data indicate that TCDD is one of the most potent carcinogens known. It promotes liver and skin carcinogeneses, and is an initiator for various target organs in rodent test systems. There is only a limited number human epi-studies on carcinogenic outcome as a result of exposure to TCDD in isolated population. According to the classification system of the International Agency for Research on Cancer (IARC), the qualitative evidence for carcinogenicity of TCDD is considered to be “sufficient” in animals and “nadequate” in humans. Consequently, this chemical has been placed in IARCs 2B category. A modification of the multistage model is utilized for extrapolating high-dose, two-year animal cancer bioassay data to estimate human cancer risk for long-term, low-dose human exposure. The upper limit of incremental cancer risk is 3.3 × 10 −5 for a continuous lifetime exposure to 1 pg m −3 of TCDD in ambient air. With the exception of 2,3,7,8-TCDD and a mixture of 1,2,3,6,7,8- and 1,2,3,7,8,9-HxCDDs, the chronic toxicity data on the rest of the 75 PCDD and 135 PCDF congeners are badly deficient. In the a absence of chronic bioassay data on other PCDFs and PCDFs, several TCDD equivalent approaches have been proposed for risk assessment on other congeners or mixtures. This paper compares the various approaches.

Residential proximity to industrial combustion facilities and risk of non-Hodgkin lymphoma: A case-control study

BackgroundResidence near municipal solid waste incinerators, a major historical source of dioxin emissions, has been associated with increased risk of non-Hodgkin lymphoma (NHL) in European studies. The aim of our study was to evaluate residence near industrial combustion facilities and estimates of dioxin emissions in relation to NHL risk in the United States.MethodsWe conducted a population-based case–control study of NHL (1998–2000) in four National Cancer Institute-Surveillance Epidemiology and End Results centers (Detroit, Iowa, Los Angeles, Seattle). Residential histories 15 years before diagnosis (similar date for controls) were linked to an Environmental Protection Agency database of dioxin-emitting facilities for 969 cases and 749 controls. We evaluated proximity (3 and 5 km) to 10 facility types that accounted for >85% of U.S. emissions and a distance-weighted average emission index (AEI [ng toxic equivalency quotient (TEQ)/year]).ResultsProximity to any dioxin-emitting facility was not associated with NHL risk (3 km OR = 1.0, 95% CI 0.8-1.3). Risk was elevated for residence near cement kilns (5 km OR = 1.7, 95% CI 0.8-3.3; 3 km OR = 3.8, 95% CI 1.1-14.0) and reduced for residence near municipal solid waste incinerators (5 km OR = 0.5, 95% CI 0.3-0.9; 3 km OR = 0.3, 95% CI 0.1-1.4). The AEI was not associated with risk of NHL overall. Risk for marginal zone lymphoma was increased for the highest versus lowest quartile (5 km OR = 2.6, 95% CI 1.0-6.8; 3 km OR = 3.0, 95% CI 1.1-8.3).ConclusionsOverall, we found no association with residential exposure to dioxins and NHL risk. However, findings for high emissions and marginal zone lymphoma and for specific facility types and all NHL provide some evidence of an association and deserve future study.

RISK FROM EXPOSURE TO POLYCHLORINATED DIBENZO-p-DIOXINS AND DIBENZOFURANS EMITTED FROM MUNICIPAL INCINERATORS *

Incineration of wastes seems to be one of the major sources of PCDDs and PCDFs (dioxins). Their prevalence and extreme stability in the environment, bioavailability and bioaccumulation in the biota and human adipose tissues and breast milk are of much concern. 2,3,7,8-TCDD is one of the most toxic chemicals known and has been found to have teratogenic and carcinogenic activities in animals. Exposure to TCDD can result in chloracne, general weakness, drastic weight loss, hyperpigmentation of skin, hirsutism, porphyria cutanea tarda, liver damage, changes in activities of various liver enzymatic levels, abnormal lipid metabolism, abnormalities of the endocrine and immune systems, and possible teratogenic effects in humans. Moreover, chronic bioassay data indicate that TCDD is one of the most potent carcinogens known. It promotes liver and skin carcinogeneses, and is an initiator for various target organs in rodent test systems. There is only a limited number of human epi-studies on carcinogenic outcome as a result of exposure to TCDD in isolated population. According to the classification system of the International Agency for Research on Cancer (IARC), the qualitative evidence for carcinogenicity of TCDD is considered to be “sufficient” in animals and “inadequate” in humans. Consequently, this chemical has been placed in IARCs 2B category. A modification of the multistage model is utilized for extrapolating high-dose, two-year animal cancer bioassay data to estimate human cancer risk for long-term, low-dose human exposure. The upper limit of incremental cancer risk is 3.3 × 10-5 for a continuous lifetime exposure to 1 pg m-3 of TCDD in ambient air. With the exception of 2,3,7,8-TCDD and a mixture of 1,2,3,6,7,8- and 1,2,3,7,8,9-HxCDDs, the chronic toxicity data on the rest of the 75 PCDD and 135 PCDF congeners are badly deficient. In the absence of chronic bioassay data on other PCDDs and PCDFs, several TCDD equivalent approaches have been proposed for risk assessment on other congeners or mixtures. This paper compares the various approaches.