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Hazardous Waste Conference 1993ATSDR Science Corner: Hazardous Evaluating the Success of Environmental by Ellen K. Silbergeld, Ph.D., University of Maryland, Baltimore.
It is time to make a diagnosis about the health of environmental health. As a nonclinician and an environmental advocate, I suggest the diagnosis is not good. Environmental health suffers from self-inflicted wounds, exhaustion, isolation, and undernourishment. The community of environmental health professionals shares an ambivalence toward the very concept of environmental health. At this meeting, I have heard contradictory goals and priorities expressed. Some participants have stated their allegiance to global issues, such as protection of global climate, habitats, and biodiversity. These seem to be acceptable, politically correct statements. Yet, these same people have raised doubts about important local issues, such as the carcinogenicity of chemicals and the public's concerns about dioxins and pesticides. They have voiced criticisms about how water- and air-quality standards are developed and imposed and have expressed a general disdain for many of the health concerns of the public. These attitudes constitute a serious self-inflicted wound. Consequently, environmental health professionals are now in an antagonistic relationship with the public. This antagonism often comes to a head in their relations with local, regional, and national advocacy groups and with persons concerned about environmental justice. They are in danger of undermining the political support needed by environmental health programs to grow and mature. Environmental health professionals suffer from exhaustion, as do many persons who have dedicated themselves to the public good. They have an enormous number of obligations to which they must respond. To add to their exhaustion, they have lost control over setting priorities and defining missions. Environmental health professionals are increasingly isolated from the public. Their agenda has been captured by other environmental agencies at the federal and local level. Even within some traditional areas of public health, responsibilities have been divided. Achieving optimal efficiency with limited resources is difficult. For instance, the followup of a single case of lead poisoning can involve local and state departments of public health; environmental agencies; occupational safety and health agencies; and other agencies involved in housing, human resources, and sanitation (Anon 1993). Mounting an efficient, coordinated, or timely response under these conditions is extremely difficult. States are also isolated from each other, a factor that separates health professionals from resources or colleagues who might assist in mounting and maintaining critical programs. The symptoms of health professionals' "tired blood" are related to a chronic condition of undernourishment. Although lots of money may be available at the federal level for the environmental agenda, it is not going to public health. This undernourishment does not encourage well-trained, eager, energetic people to enter the field of environmental public health. Training and education have clearly suffered and will not fully recover for another 5-10 years even if we re-infuse new resources now.
Turning now to the issue of evaluating successes in environmental health, I would like to analyze the past and present in terms of what they might tell us about successes in environmental health. From there I will discuss directions and analytic methods that might increase our successes in the future. Talking about failures is easy. Posting signs at rivers and lakes to forbid fishing is a classic example of failure in environmental health. In every such case, we have failed to identify a toxic chemical, to limit its production or disposal, or to notice its presence in an environmental medium until it has reached the top of the food chain where it affects us. The residues of lead in our environment also represent failure. The amount of lead used in household paint and automobile gasoline during the 20th century is equivalent to two mountains, each containing hundreds of thousands of tons of lead (Mushak 1992). The inability of the Public Health Service to obtain the resources needed in 1925 to prevent this second mountain from occurring was one of the most serious environmental health failures (Anon 1992). We will bear the burden of such a failure far into the future. Knowing the distribution of U.S. residences constructed before 1940 allows us to estimate the location and number of homes that probably contain high levels of lead-based paint (ATSDR 1988). As these residences fall into disrepair and become occupied by persons who can afford no better, they become real and immediate hazards of exposure to lead for children and others. Our laxity in recognizing or dealing with hazardous waste has also resulted in visible evidence of failure. The Agency for Toxic Substances and Disease Registry (ATSDR) has mapped the distribution of hazardous waste sites in this country that contain lead (ATSDR 1993). Many states have between 40 and 70 hazardous waste sites that contain lead.
We need some way of measuring success in environmental health programs so that we are talking about the same thing. Epidemiologic and medical measures exist that are commonly applied in public health. Environmental health focuses on remediation or cleanup and on exposure reductions that do not involve site-specific cleanups. Too infrequently do we use such measures as case identification, successful treatment, or the number of cases avoided or prevented. Some notable successes that reduced exposure at the source demonstrate what we can achieve. The remarkable concordance between removing lead from gasoline and removing lead from the blood of Americans is well known to environmental health professionals (ATSDR 1988). This example directs us to prevention at the source, rather than remediation in the environment, which is inefficient and ineffective. We have, however, not looked often enough toward preventing exposures at the source. The important relationship found in the example of leaded gasoline was the correlation between the amount of lead in gasoline and the amount in children's blood. The amount of lead from gasoline in air was not important. The traditional approach would have been to examine the amount of lead in air, which is the medium most proximate to human exposure. We would then attempt to exert controls over lead in air through promulgating and enforcing standards or various activities. The approach of examining the correlation between lead in gasoline and lead in children's blood was a creative leap to a different level of environmental policy, one that was much more effective than regulating lead in air. Contrast the previous example with attempts to limit human exposures to other toxic chemicals. Levels of volatile organic compounds, such as chloroform, benzene, and xylenes, can be found in human tissue. We have dealt with these chemicals by promulgating and attempting to enforce media-specific or source-specific standards. We have never examined how production, use, or disposal of these chemicals affects human exposure. Levels from the National Human Adipose Tissue Survey1 of various dioxins (e.g., 2,3,7,8-tetrachlorodibenzo-dioxin), dibenzofurans, DDT and metabolites, and PCBs indicate considerable body burdens. These levels may now be in a range that raises concern about health endpoints such as neurologic, neuroendocrine, and immunologic effects. We belatedly decided to control the source of production for some of these chemicals. Unfortunately, for many decades to come, we will be dealing with the literal residues of these chemicals in the environment, in such vectors as fish, and in our own tissues (Silbergeld and deFur, in press).
Now for a look at the future. With the exception of lead, we focus mostly on remediation of sources in environmental health. We generally accomplish our goals with various kinds of investigations, data collections, and surveillance systems. We identify point sources and deal with them by emissions permits. We look at environmental media, such as drinking water and air, and we look for consonance with promulgated standards. We can even look at body burdens, as with the NHATS database, as a source-identification tool. We use a variety of tools for remediating identified sources, assuming these permits and other processes of monitoring and oversight have failed. We remediate sources under such authorities as Superfund; we have the Resource Conservation and Recovery Act (RCRA) and other authorities that allow us to look at spills in particular incidents; and other directed areas, usually at the state and local level, concern particular issues in water- and air-quality cleanup and protection. These activities are driven by an underlying set of assumptions about how we set priorities and define our goals. The myriad remediation and abatement tasks, the priority-setting processes, and even the relative risk or unfinished business reports by EPA over the last 3 years have been driven by an imbalance between two fundamental paradigms for examining environmental health. These two fields have different perspectives and definitions. The first has been dominant over the past 15 years in environmental health, regardless of administration, administrators, or agency. It is what I call the toxicologic perspective. It is driven by the finding of a hazard and defined by those processes of risk assessment that we have heard alluded to at this meeting. Another perspective is probably more familiar: the epidemiologic perspective, which is usually case- or disease-driven and seeks to define etiologies.
May I suggest how we might resurrect and empower the epidemiologic perspective and dethrone, just a bit, the toxicologic perspective? I think we are witnessing the death throes of risk assessment, and to continue debate about methodologic problems and scientific issues of the basis of risk assessment misses the point. Neither the endeavor nor the method have been publicly acceptable (Ginsburg 1993), and I predict they will not last much longer. Despite 20 years of arguing about risk assessment and investing enormous amounts of money in the science and public policy aspects of this methodology, we have not solved any of these issues. Risk assessment is still limited in its emphasis on human health. Keep in mind that environmental health, as Peter Galbraith and others noted, has to be, by statute, and should be, by science, holistic in its breadth and compass. In its actual implementation and methodologic development, however, it has focused unduly on one endpoint: cancer. Risk assessment has been unable to give us methods for assessing mixtures of toxic substances, which is how we are exposed to toxic substances in the real world. Risk assessment has methodologic problems that create real problems in public health because it cannot be extrapolated and used in the population, which is the dimension in which epidemiologists and public health people work. Nor does it deal with issues where dose and duration vary. Problems exist in validating the models. Public resistance has not abated, and all these other issues continue to reinforce the public's suspicion. Finally, as this process becomes more abstruse and complex, it becomes less and less acceptable (Silbergeld 1993). What would the epidemiologic perspective give us, and how would we use it? We would start from a different point than the hazard-driven risk assessment model that we use for toxicology. We would ask a fundamental health-based question, which might be this: What are the major types of diseases or disabilities in the U.S. population for which environmental factors could reasonably be proposed as significant or important causes or contributing factors? Another way of asking that question, which we can use to guide our analysis is: What major types of disease and disability are at present poorly explained in terms of other factors? That is, for which diseases do we have a large number of cases or causes for which we cannot find a genetic or other cause in existing knowledge? Out of such questions, we have selected three endpoints that appear to meet the definition of being significant, having a high social cost, and not being well explained by known etiologies. The first is low birthweight, which we can look at as either a continuous or dichotomous variable. It occupies an interesting position in terms of looking at causality and is predictive of later complications in development. That is, a child born with a low birthweight has a very high risk for several later neurodevelopmental and developmental problems (McCormick et al. 1992). Low birthweight can be examined as an outcome for both the status of maternal health and for several adverse conditions of pregnancy. Low birthweight is a sensitive endpoint in experimental studies of reproductive toxicants. Case-control and cohort studies and a few prospective studies suggest strong associations between identified environmental factors and low birthweight. The known factors are maternal exposures to lead, solvents, and polychlorinated biphenyls. The second disease category we explored was the neurodegenerative diseases of aging. We examined Parkinsonism, motor neuron disease, amyotrophic lateral sclerosis, and dementia of the Alzheimers type. In contradistinction to low birthweight, these diseases are chronic and may well be diseases of long latency. That is, they may be the result of earlier events, which then appear in some kind of summated form, perhaps coincident with other events of normal aging, that then permit clinical detection and expression. Subtle, early signs may appear that we could use as biomarkers (NRC 1992). Some environmental factors have been associated with neurodegenerative diseases. Somewhat controversial literature exists on aluminum exposure. Much better (case) literature exists on plant toxins such as lathyrus and the cycads. Good literature is available on manganese exposure, which results in occupational and neurodegenerative diseases resembling Parkinsonism, and interesting literature is forthcoming from Scandinavian studies on an association between the development of neurodegenerative diseases and earlier exposure to solvents. Third, we looked at noncancerous lung disease, with a focus on asthma. Asthma is interesting because it manifests an immediate response to putative provocative agents. Conditions of sensitization or increased response to later exposures are possible. All data suggest striking and alarming increases in the incidence of asthma in the U.S. population (Buist and Vollmer 1990). Asthma may also be an indicator disease related to some socioeconomic factors that are of concern to environmental justice (Marder et al. 1992). We know that environmental and occupational factors are associated with noncancerous lung disease. Dust and air particulates, sulphur dioxide, and other agents have been well correlated in cohort and in case-control studies of asthma and other noncancerous lung diseases.
If we approach the problem of environmental health using epidemiology, we will be involved in the larger context of disease prevention and public health concerns. We will detach ourselves from the sterile controversy over risk assessment and perhaps will equip ourselves with instruments to help answer a question that was posed to me: What are the successes of environmental health? If environmental factors contribute significantly to the incidence of certain diseases or conditions, we would assume that reducing exposures should reduce the incidence or severity of disease. Such thinking will allow us to apply the classic public health epidemiologic model to assess the true success of our activities and investments. If this is the perspective we decide to adopt, we are left with the challenge of how we can set up surveillance systems to detect these changes.
Agency for Toxic Substances and Disease Registry (ATSDR). (1988). Nature and extent of childhood lead exposures in the U.S.: a report to Congress. Atlanta GA: U.S. Department of Health and Human Services, Public Health Service. Agency for Toxic Substances and Disease Registry (ATSDR). (1993). Agency lead initiative. Atlanta: ATSDR Division of Health Assessment and Consultation, U.S. Department of Health and Human Services, Public Health Service. Anonymous. (1992). The hour of lead. Washington DC: Environmental Defense Fund. Anonymous. (1993). A guide for childhood lead poisoning prevention programs and other health care providers. Washington DC: Alliance to End Childhood Lead Poisoning. Buist AS, Vollmer W. (1990). Reflections on the rise in asthma morbidity and mortality. JAMA 264:1719-20. Ginsburg R. (1993). Roundtable on risk assessment. New Solutions. Marder D, Orris P, Addington W. (1992). Effects of racial and socioeconomic factors on asthma morbidity in Chicago. Chest 101:426S-9S. McCormick MC, Brooks-Gunn J, Workman-Daniels K, Turner J, Peckham GJ. (1992). The health and developmental status of very low-birth-weight children at school year. JAMA 267:2204-8. Mushak P. (1992). Lead as the premiere environmental hazard for children in America: criteria and their quantitative application. Environ Res 59:281-309 National Research Council (NRC). (1992). Neurotoxicology. Washington DC: National Academy Press. Silbergeld EK. (1993). Risk assessment: the experience and perspective of U.S. environmentalists. Environ Health Perspect 101: 100-4. Silbergeld EK, deFur P. (In press). Risk assessment of the dioxins. In: Schechter A, ed. The dioxins. New York: Plenum Press. |
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