Harmful effects of industrial chemicals has come from the workplace

Not surprisingly, much evidence of the harmful effects of industrial chemicals has come from the workplace, where exposures tend to be high and sustained relative to those in the ambient environment. For instance, studies of British textile workers alerted researchers to the link between asbestos and lung cancer (131). The reproductive toxicity of the pesticide DBCP (1, 2-dibromo-3-chloropropane) became startlingly clear in the late 1970s and early 1980s when male farm workers in the banana-growing region of Costa Rica were found to be sterile. By the mid-1990s, some 1,500 male workers had been medically diagnosed with sterility from exposure to DBCP (132). While these examples illuminate the risks of high-level exposures, they do not indicate the extent of risk posed by lower levels of exposures that are typically encountered in the environment.

One difficulty in determining the exact magnitude of the potential health risk is that epidemiologic studies, which look at differences between exposed and nonexposed groups, generally show a statistical association between an environmental exposure and adverse effects. They do not attempt to demonstrate cause and effect. In many cases, studies cannot reveal links between an exposure and an adverse effect unless the particular risk is quite high or the effect is unusual (133), as was the case with vinyl chloride and angiosarcoma, a relatively rare form of liver cancer (134). Given these difficulties, some studies will find an association, others will refute it. Thus, proof of a causal relationship often takes years to amass – as with smoking and lung cancer – if it is ever established.

Calculating how much of a specific pollutant a person is exposed to can be daunting. For example, to assess air quality, a city might have only a few monitors dispersed throughout a wide geographic area. The direction of the wind on any given day will do much to determine who is exposed, as will whether that person spent most of the day indoors or out. In addition, air pollution monitors are usually installed on rooftops, so recorded pollutant levels do not describe the exposure of a commuter stuck in traffic, or, say, a small child on a playground. So, although it is widely agreed that ambient air pollution at levels normally encountered in many cities can damage health and even kill, the magnitude of the effect remains controversial. (Estimates range from 200,000 to 570,000 excess deaths per year (135)).

In the absence of definitive human data, investigators often must rely on animal studies and quantitative risk assessment models to estimate the toxicity of a particular substance. In some instances, health effects in wildlife have first alerted researchers to potential dangers of a class of environmental pollutants. For example, reproductive damages in seagulls and other wildlife presented some of the first clues about the adverse effects of DDT (136). More recently, reproductive anomalies in wildlife have sparked concern about the ability of some chemicals to cause ill effects by disrupting the body’s normal hormonal system. Translating effects in wildlife to risks in humans, however, remains difficult. Even laboratory experiments in animals are less than definitive, because it is difficult to extrapolate from effects seen when high doses are given to animals to probable results from the low doses common to human exposure.

Despite widespread public concern over chemical safety, toxicity testing remains inadequate. For the vast majority of chemicals in widespread use, no toxicity testing results are available in the public record (137)(138). Most of the testing for chronic effects that has occurred has focused on cancer. To date, about 74 chemicals or mixtures have been found to cause cancer in humans (139). Hundreds of others, however, cause cancer or mutations in cells or in animals, which raises concerns about their effects in humans.

Of the other potential effects of chemical hazards, such as infertility, birth defects, immune system impairment, or brain damage, even less is known. In the United States, for instance, the chief agency for chemical evaluation spent nearly US$29 million on testing chemicals for cancer in 1991, but just about $6 million for both genetic and reproductive effects (140). Testing for other health concerns, such as immune system effects or endocrine disruption, lags even further behind. Again, the United States provides an apt example: according to a recent study, 86 percent of chemicals in widespread use have not been tested for immunotoxicity, and 67 percent have not been tested for neurotoxicity (141). This focus on cancer means that other important and preventable risks may be overlooked. Standard methods of toxicity testing, for instance, would not have identified lead as a significant hazard – even though the U.S. Centers for Disease Control and Prevention has called lead poisoning the single, most significant preventable disease associated with environmental and occupational exposures (142).

References and Notes

131. John C. Scatarige and Frederick P. Stitik, “Induction of Thoracic Malignancy in Inorganic Dust Pneumoconiosis,” Journal of Thoracic Imagery, Vol. 3, No. 4 (1988), p. 71.

132. Lori Ann Thrupp, “Sterilization of Workers from Pesticide Exposure: The Causes and Consequences of DBCP- Induced Damage in Costa Rica and Beyond,” International Journal of Health Services, Vol. 21, No. 4 (1991), p. 734.

133. National Research Council

, Science and Judgement in Risk Assessment (National Academy Press, Washington, D.C., 1994), p. 2.

134 . L. Tomatis, et al., eds, Cancer: Causes, Occurrence and Control (International Agency for Research on Cancer, Lyon, France, 1990), p. 128.

135. Christopher J. L. Murray and Alan D. Lopez, eds., The Global Burden of Disease: Volume 1 (World Health Organization, Harvard School of Public Health, and The World Bank, Geneva, 1996), p. 311; and World Health Organization (WHO)

, Health and Environment in Sustainable Development: Five Years After the Earth Summit (WHO, Geneva, 1997), p.87.

136. U.S. Environmental Protection Agency (U.S. EPA), Special Report on Environmental Endocrine Disruption: An Effects Assessment and Analysis (U.S. EPA, Washington, D.C., 1997), p. 72.

137. Environmental Defense Fund (EDF), Toxic Ignorance: The Continuing Absence of Basic Health Testing for Top-Selling Chemicals in the United States (EDF, Washington, D.C., 1997), p. 15.

138. Dian Turnheim, “Evaluating Chemical Risks,” OECD Observer, No. 189 (August/September, 1994), pp. 12-15.

139. International Agency for Research on Cancer (IARC), “Overall Evaluations of Carcinogenicity to Humans.”

140. Ellen Silbergeld and Kevin Tonat, “Investing in Prevention: Opportunities to Prevent Disease and Reduce Health Care Costs by Identifying Environmental and Occupational Causes of Noncancer Disease,” Toxicology and Industrial Health: An International Journal

, Vol. 10, No. 6 (1994), p. 676.

141. Ellen Silbergeld and Kevin Tonat, “Investing in Prevention: Opportunities to Prevent Disease and Reduce Health Care Costs by Identifying Environmental and Occupational Causes of Noncancer Disease,” Toxicology andIndustrial Health: An International Journal

, Vol. 10, No. 6 (1994), p. 16.

142. Ellen Silbergeld and Kevin Tonat, “Investing in Prevention: Opportunities to Prevent Disease and Reduce Health Care Costs by Identifying Environmental and Occupational Causes of Noncancer Disease,” Toxicology and Industrial Health: An International Journal

, Vol. 10, No. 6 (1994), pp. 676-677.