Overview of exposure, toxicity, and risks to children from current levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compounds in the USA

Abstract

Studies of children indicate that exposure of the general population to low levels of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) does not result in any clinical evidence of disease, although accidental exposure to high levels either before or after birth have led to a number of developmental deficits. Breast-fed infants have higher exposures than formula-fed infants, but studies consistently find that breast-fed infants perform better on developmental neurologic tests than their formula-fed counterparts, supporting the well-recognized benefits of breast feeding. Children receive higher exposures to PCDD/Fs from food than adults on a body-weight basis but those exposures are below the World Health Organization’s tolerable daily intake. Laboratory rodents appear to be at least an order of magnitude more sensitive than humans to the aryl hydrocarbon receptor-mediated effects of these substances, which makes them poor surrogates for predicting quantitative risks but makes them good models for establishing safe levels of human exposure by organizations mandated to protect public health. Any exposure limit for PCDD/Fs based on developmental toxicity in sensitive laboratory animals can be expected to be especially protective of human health, including the health of infants and children. Because body burdens and environmental levels continue to decline, it is unlikely that children alive today in the USA will experience exposures to PCDD/Fs that are injurious to their health.

Introduction

Since risk management aimed at reducing emissions of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds was initiated in the 1970s, substantial decreases in environmental levels and in body burdens have been observed. Although somewhat uncertain due to changes in analytical methodologies over time, available data on emissions, environmental and food levels, and tissue levels indicate a several-fold reduction in exposures and body burdens since 1970 (Hays and Aylward, 2003). The US Environmental Protection Agency (EPA) reported that emissions from quantified sources—such as waste incineration, pesticide manufacture, and chlorine bleaching of pulp and paper—decreased from more than 14,000 g TEQ¹/year in 1987 to about 1500 g TEQ/year in 2000—a 90% decrease—and are expected to continue to decline (EPA, 2005a). Human body burdens of TCDD in the US decreased 10-fold and dioxin TEQ decreased 4–5-fold between 1972 and 1999 which, due to the long elimination half-lives of dioxins and dioxin-like compounds—polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs)—implies a decrease in exposure of more than 95% (Hays and Aylward, 2003). EPA has estimated that more than 90% of the remaining human exposures to PCDD/Fs occur through food consumption, primarily from animal fat (EPA, 2004). PCDD/Fs are not deliberately added to food or created during food processing. Natural sources of PCDD/Fs, such as forest fires, contribute to a background level of exposure from food (EPA, 2004), as may unregulated anthropogenic sources such as uncontrolled burning of household waste in barrels (Lemieux et al., 2003). The EPA has been debating the extent to which PCDD/Fs pose risks to health since 1990; no risk estimate or exposure limit is agreed upon.

Risk management of PCDD/F emissions was initiated because of concerns about its potential carcinogenicity, but concerns have broadened to include other potential human health effects, such as developmental toxicity. Children receive higher doses of PCDD/Fs from food than adults on a body-weight basis (FDA, 2004, Charnley and Doull, 2005) but eliminate PCDD/Fs more rapidly than adults (Kreuzer et al., 1997). Both fat and serum levels of PCDD/Fs have been found to increase with age (Falk et al., 1999, Luotamo et al., 1991) although they are decreasing with time. Nonetheless, children may be subject to higher potential risks from PCDD/Fs than adults because they are still developing.

This paper examines the available evidence relevant to evaluating health risks to children during childhood from PCDD/F exposure and toxicity and draws conclusions about the extent to which current risk management practices account for age-related differences in risk.