Dioxin risks revisited

Article Abstract:

Dioxin (tetrachlorodibenzodioxin), a chemical by-product of herbicide manufacturing and component of Agent Orange (a defoliant used in the Viet Nam War), is a potent animal carcinogen (cancer-causing substance), yet precise characterization of its effects in humans has proved difficult. The Environmental Protection Agency (EPA) has set a very conservative cut-off level for acceptable exposure (0.006 picograms per kilogram of body weight) to dioxin, a level as much as 1,700 times lower than in some other countries. The EPA's risk assessment model is a linear one, assuming increasing risk at increasing doses. However, at a recent research meeting at Cold Spring Harbor Laboratory, a point was made that surprised many; to be toxic, dioxin must bind to and activate a receptor. Therefore, there must be some dose level below which no binding can take place, which is safe. An accurate model of dioxin toxicity, according to this view, should be based on an understanding of how molecules actually bind; the approach can be extended to other putative carcinogens, as well. However, dioxin is still controversial substance; debate began immediately at the Cold Spring Harbor meeting over how well any molecular model can predict real-life hazards. The dioxin receptor, called the aromatic hydrocarbon (Ah) receptor, was discovered in the 1970s; it now appears that all effects exerted by dioxin depend on binding to that receptor. Determination of the dose necessary to induce an enzyme system sensitive to dioxin (the cytochrome P450 system) led to an estimate of safe dioxin levels of between 1 and 3 picograms per kilogram per day - similar to levels considered safe in Europe. Several scientists are now at work to develop better estimates of the risk associated with dioxin, based on knowledge of cellular responses. It is unlikely that lowering risk estimates for dioxin, the most potent carcinogen ever tested, will be popular, even if new estimates are more realistic. A strong scientific case for such a step is a prerequisite for its acceptance by other scientists and policy makers. (Consumer Summary produced by Reliance Medical Information, Inc.)

Models, Conferences, meetings and seminars, Safety and security measures, Carcinogenesis

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EPA moves to reassess the risk of dioxin

Article Abstract:

In the aftermath of a proposed new model of the physiologic effects of dioxin (a contaminant in some herbicides), a subject of much debate because of its purported role in causing cancer, data are being reevaluated concerning the possible risks associated with exposure to the chemical. Three scientists recently briefed William K. Reilly, administrator of the Environmental Protection Agency (EPA), with respect to their receptor-based model for determining the health risks posed by dioxin. The model, unlike the currently accepted linear model that assumes a steadily increasing risk as the amount of exposure increases, assumes that binding to a receptor is the first event that must occur before the substance can damage cells. The cell receptor to which dioxin must bind, and which it must activate, is the aryl hydrocarbon (AH) receptor; moreover, not one, but a certain number, of AH receptors must be occupied. Until this threshold has been reached, exposure to dioxin cannot cause physiological effects. Developing the receptor-based model further is now a goal of the EPA; it is hoped that a safe dioxin level, below which no physiologic damage could result, will be developed. Research to better characterize the AH receptor and its functioning is under way. It is likely that dioxin will emerge as less dangerous to health than previously thought, although this is not known with certainty. Another research focus will be to determine the background level of dioxin exposure; if it is high, there is less chance that additional exposure is safe. Reilly wants the model to be developed within one year, at which time the Scientific Advisory Board of the EPA will review the results. (Consumer Summary produced by Reliance Medical Information, Inc.)

United States. Environmental Protection Agency, Reilly, William K.

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High dioxin dose linked to cancer

Article Abstract:

Although one form of dioxin, TCDD, is the most potent carcinogen ever tested, debate has continued for the past 20 years over whether dioxin causes cancer in humans. A recent research report in the January 24, 1991 issue of The New England Journal of Medicine may have gone a long way to resolving the issue. In the study, records from 5,172 chemical workers who were exposed to dioxin on the job between 1942 and 1984 were examined. Workers who had worked longer at their jobs had higher blood levels of TCDD than those who were employed for shorter times. As a group, the subjects had a 15 percent increase in the death rate from all cancers compared with the general population. However, separation of the men into a low-exposure (less than one year) and a high-exposure (one year or more) group revealed major differences in mortality. Those in the high-exposure group had a risk of dying of cancer that was almost 50 percent greater than that of the general population. The increase was primarily in soft-tissue sarcomas, known to be associated with dioxin exposure. This study of a highly-exposed population undoubtedly sets maximum exposure limits. These findings have already been cited by those on both sides of the dioxin-carcinogenicity controversy. (Consumer Summary produced by Reliance Medical Information, Inc.)

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