Environmental▼News Children’s vulnerability to cancer New, draft risk assessment guidelines for cancer from the U.S. EPA acknowledge for the first time that infants and children are more vulnerable than adults to certain mutagenic chemicals. These early-life exposure guidelines, released in March, call for a dose–response adjustment by as much as 10 times for children up to two years of age, and 3 times for kids aged 3 to 15. The guidelines for children were released as a supplement to broader risk assessment guidance revising how the agency assesses whether a substance could cause cancer in humans. For years, EPA has been struggling with how best to account for differences in children’s responses to chemical exposures. In 1994, the National Research Council recommended that the agency assess risks to infants and kids “whenever it appear[ed] that their risks might be greater than those of adults.” This supplement, if approved by agency review boards, could be expanded to apply to other classes of compounds if evidence supports its use, according to agency officials. For now, its use is restricted to certain compounds that cause gene mutations. There is much that scientists don’t know about how chemicals cause cancer in humans, but the literature indicates that during certain life stages in childhood, small exposures to mutagenic chemicals can seriously impair human devel-
opment. The response adjustment helps address this uncertainty, says Joanne Rodman, acting director of EPA’s Office of Children’s Health Protection. “We think this is a great move for the agency,” Rodman adds. EPA scientists are developing a list of mutgenic chemicals that can be assessed using this approach, staffers say. The broader guidelines update those EPA proposed in 1999 by clarifying agency policy on when it is appropriate to insert a default option into a carcinogenic risk assessment. Default options are conditions staff applies to a risk assessment when critical information is unavailable or limited. For example, if no information exists about a chemical’s ability to cause cancer in humans, EPA regulators have assumed that adverse effects observed in animals have the potential to occur in humans too. The new guidelines ask risk assessors to consider available data, particularly the latest science, before instituting a default assumption. Another difference pertains to the development of a new, so-called weight-of-evidence narrative, which would summarize the full range of available evidence and describe any uncertainties associated with that chemical’s hazard potential and the default options used. For example, a narrative may explain that a chemical could be carcinogenic by some routes of exposure but not others.
Another POP found in foods In addition to dioxins (PCDDs), furans (PCDFs), polychlorinated biphenyls (PCBs), and pesticides, there is another group of persistent organic pollutants (POPs)—polychlorinated napthalenes (PCNs)— harboring in many commonly consumed foods, according to new research in this issue of ES&T (pp 2332–2335). The study is the first to quantitatively examine levels of PCNs in foods and evaluate the dietary intake of PCNs by the general population.
“We are not quite sure about the real contribution of PCNs to total TEQ [toxic equivalency], in which at least PCDD/Fs and PCBs would be included,” says lead author Jose L. Domingo of the Laboratory of Toxicology and Environmental Health at “Rovira i Virgili” University in Spain. Toxic equivalency factors (TEFs), which are commonly used to compare the relative toxicity of an individual congener with 2,3,7,8TCDD—the most toxic dioxin congener—are not available for all PCN
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These two approaches let the data drive the risk assessment, agency officials say, and mark a departure from the 1999 draft guidelines that called for a series of default assumptions to be included in the assessment first, then disproved with data. Officials with the chemical industry group the American Chemistry Council praise EPA’s emphasis on data in these new guidelines but are concerned that the adjustment factor addressing childhood risks may have been developed without supporting evidence. “The agency is responding to the public demand to deal with children more carefully, which is the right goal,” says ACC’s David Clarke. “But have they used the animal and human studies correctly?” “Although the guidance addressing children’s risks is not perfect, we’d like to see it finalized as it is,” says Jennifer Sass of the environmental group Natural Resources Defense Council. But the broader guidelines need to be tightened, as they “would provide too many exceptions to the rule by giving too many opportunities to paralyze the agency with pseudo-scientific arguments,” she adds. Public comments on the proposed cancer risk assessment guidance and draft supplement for early-life exposure to carcinogens are due to EPA in May. The guidelines are available at www.epa.gov/ ncea/raf/cancer2003.htm. —CATHERINE M. COONEY
congeners. Only some of the 75 PCN congeners exhibit dioxin-like toxicity. In general, the more chlorinated PCNs tend to be more toxic than the less chlorinated ones. “There is no reason for concern if we look at the PCNs only—the TEQ values are low, as is the daily intake,” says Simonetta Corsolini of the University of Siena in Italy, who was the first to report finding PCNs in wildlife in Antarctica (Environ. Sci. Technol. 2002, 36, 3490–3496; 340A–341A). “But we must take into account that humans introduce in their body not only PCNs but also
