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Sociodemographic aspects of human susceptibility to toxic chemicals:
Environmental Toxicology and Pharmacology 4 (1997) 261 – 269
Sociodemographic aspects of human susceptibility to toxic chemicals: Do class and race matter for realistic risk assessment? Ken Sexton School of Public Health, Uni6ersity of Minnesota, P.O. Box 807 UMHC, 420 Delaware Street, S.E., Minneapolis, MN 55455, USA
Abstract Susceptibility is well-recognized as a potentially important aspect of health risk assessment, particularly for groups such as pregnant women and their fetuses, infants, children, the elderly, and the infirm, that are known or suspected to be more vulnerable to environmental insults. More recently, it has become apparent that economically disadvantaged groups are likely to be systematically both more exposed and more susceptible to environmental pollution. This article reviews the reasons why low-income communities and many racial minorities are at an increased risk because they are more susceptible to the adverse health effects of toxic chemicals. The scientific challenges of quantifying the magnitude of environmental health risks for these groups are discussed, emphasizing ramifications for risk assessment and risk management decisions. Problems incorporating susceptibility into risk-based decision making are identified, and specific actions are recommended to address these deficiencies. © 1997 Elsevier Science B.V. Keywords: Susceptibility; Risk assessment; Risk management; Susceptibility factors; Environmental justice; Socioeconomic status; Racial groups
1. Introduction A fundamental goal of pollution control strategies, including federal statutes such as the Clean Air Act (CAA), the Safe Drinking Water Act (SDWA), and the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA), is to protect people from the adverse health effects of environmental pollutants. To be successful, these strategies depend on accurate identification of those individuals, groups, and populations who are at highest comparative risk so that, if warranted, appropriate prevention or intervention actions can be taken. Conceptually, individuals and subpopulations are deemed to be at potentially greater risk when they are either exposed above a health-related benchmark (e.g. exposures above National Ambient Air Quality Standards) or more susceptible to the effects of exposures (e.g. predisposed to develop bladder cancer after exposure to N-substituted aryl compounds because of acetylation phenotype). Those who are both more exposed and more susceptible are considered to be at highest risk of adverse health effects. 1382-6689/97/$17.00 © 1997 Elsevier Science B.V. All rights reserved. PII S 1 3 8 2 - 6 6 8 9 ( 9 7 ) 1 0 0 2 0 - 5
Susceptibility differences, both between individuals and between populations, are recognized as potentially important for realistic risk assessment (EPA, 1995). But in reality, appropriate and sufficient data are rarely available to characterize real-world distributions of susceptibility adequately. Consequently, quantitative risk assessments typically have difficulty accounting for differences between the general population and groups traditionally assumed to be more susceptible to the effects of pollution, such as pregnant women and their fetuses, infants, children, the elderly, and the infirm. Even more difficult to evaluate and quantify is the degree to which poor, disadvantaged people (i.e. those in lower socioeconomic strata) and people of color (e.g. African Americans, Native Americans, Hispanics, and Asian Americans) are more susceptible to environmentally induced dysfunction, disability, disease, and death. This article provides a brief overview and survey of the reasons for concern about higher susceptibility among those in our society who are poor, have limited formal education, are unemployed or work under haz-
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Table 1 Poverty rates by ethnicity, race, and age (adapted from Montgomery and Carter-Pokras, 1993) Age (years)
White (%)
Black (%)
Total Hispanic (%)
Mexican-American (%)
Puerto Rican (%) Asian/Pacific Islander (%)
Total US (%)
B18 18–64 ]65
16.9 9.6 10.9
46.6 25.7 33.3
39.9 23.9 22.0
39.9 24.7 22.0
52.2 28.1 18.8
21.9 11.7 12.9
16.3 11.0 10.5
Source: Current Population Survey, March 1993.
ardous conditions, or are members of certain ethnic and racial minorities. The focus is on susceptibility factors related to social class and/or racial group that are acquired as a consequence of people’s quality of life and lifestyle. The discussion is divided into six major sections: (1) effects of class and race on health status; (2) effects of class and race on environmental health risk; (3) susceptibility factors related to class or race; (4) incorporating susceptibility into health risk assessments; (5) an environmental justice critique of risk assessment; and (6) confronting the dilemma of what to do.
2. Effects of class and race on health status It is well established that rates of disease and death in the United States vary significantly by social class and ethnicity/race (Polednak, 1989; Navarro, 1990; Graham et al., 1992; Coultas et al., 1993; Montgomery and Carter-Pokras, 1993; Hahn and Eberhardt, 1995). Both are predictors of health status, and both are associated with acquired susceptibility factors, such as access to health-promoting and health-protecting resources (e.g. healthy diet and sanitation) and preventative medical practices (e.g. prenatal care and childhood immunization), as well as lifestyle choices about alcohol and tobacco use, sexual behavior, and occupation (Kerner et al., 1993). Nevertheless, the relative roles of social class and ethnicity/race in affecting health status, as well as the exact nature of their interactions are a matter of debate (Denton and Massey, 1988; House et al., 1990; McCord and Freeman, 1990; Williams, 1990; Baquet et al., 1991; Freeman, 1991; Kipen et al., 1991; CDC, 1993; Pappas et al., 1993; Corcoran, 1995; Hahn and Eberhardt, 1995; Williams and Collins, 1995). There is general consensus that, regardless of its relationship to ethnicity/race, socioeconomic status is a critical factor affecting morbidity and mortality. Yet despite its apparent importance, the mechanisms by which socioeconomic status (SES) exerts its influence are largely a matter of conjecture. Because income, education, and occupation are not likely to influence health directly, they are obviously proxies for other variables. But insufficient evidence is available linking
other variables to a direct impact on health. Most studies attempt to control for such obvious confounders as cigarette smoking and heavy alcohol consumption, both of which are more frequent among the disadvantaged. Although a host of other potential factors, such as stress, exposure to environmental agents, and diet, which are related to socioeconomic status can be postulated, ‘‘there is very little evidence to point to any of them as the major cause of the health difference between the advantaged and the disadvantaged’’ (Angell, 1993). The influence of ethnicity/race on health status is also well known and, as with socioeconomic status, the causal relationships are poorly understood (McGinnis and Foege, 1993). While some researchers maintain that ethnicity/race exerts an influence separate from social class (Denton and Massey, 1988; Wagener and Williams, 1993; Brown, 1995), others believe that the apparent effects of this variable are due primarily to differences in socioeconomic status (Navarro, 1990; Baquet et al., 1991; Freeman, 1991; Graham et al., 1992). Although disparities in health status by ethnicity/race are substantial, the causes, which certainly include differences in quality-of-life variables and lifestyle choices, are not well elucidated. The situation is further complicated by the fact that ethnicity/race is associated with both absolute and relative poverty. Although the largest number and highest percentage of poor Americans are white, as shown in Table 1, a disproportionate percentage of African Americans, Hispanics, Mexican Americans, and Puerto Rican Americans, particularly children, live in poverty (Montgomery and Carter-Pokras, 1993; Kerner et al., 1993; Corcoran, 1995; Williams and Collins, 1995). Consequently, it is often difficult to distinguish the separate effects of class and race on health status. Health status is clearly a product of multiple variables, many of which are poorly understood (McGinnis and Foege, 1993). There is substantial evidence suggesting that large-scale societal factors are the primary determinants of health; determining not only individuals’ social class but also their access to resources and exposure to risk factors. What is not well-understood is how position in social structure constrains and shapes daily life in ways that adversely affect health (Williams and Collins, 1995).
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Today, there is mounting evidence that disparities in health status between higher and lower SES strata are increasing, and that the health of some racial groups is steadily deteriorating (Kerner et al., 1993; Williams and Collins, 1995). These realities recently moved Williams and Collins (1995) to observe that ‘‘Racial and socioeconomic inequality in health is arguably the single most important public health issue in the United States’’.
3. Effects of class and race on environmental health risk For regulatory officials charged with protecting environmental health, observed disparities in health status by social class and racial group raise concerns about the possible role of environmental agents (Sexton et al., 1993a,b; Zimmerman, 1993; Ringquist, 1997). To address these concerns from a risk-based perspective we need answers to three questions: (1) do environmental health risks vary by class and race? (2) if so, to what extent do differential environmental health risks contribute to higher rates of morbidity and mortality among disadvantaged groups? and (3) how can we intervene effectively and efficiently to prevent or mitigate those environmental health risks deemed to be unacceptable? In most instances, there is a shortage of scientific evidence to answer these and other relevant questions with an acceptable degree of certainty (Sexton et al., 1993a,b; Zimmerman, 1993, 1997). A major problem in this regard is the difficulty of demonstrating the existence of a causal relationship between exposures to environmental agents and subsequent disease or injury unless the link is strong (e.g. radon-induced lung cancer in uranium miners). The challenges that can complicate attempts to verify causality are abundant, as summarized in Table 2. Therefore, attempts to answer the three risk-related questions posed above are hampered not only by complexity and uncertainty surrounding the major determinants of health, and by variations in these determinants according to class and race, but also by difficulties inherent in establishing a causal link between environmental agents and subsequent adverse health effects. One way to think about hypothesized, though as yet largely unexplored inter-relationships among class and race, exposure- and susceptibility-related attributes, and environment health risks is depicted in Fig. 1. This conceptual model allows us to postulate how social class or racial group might be causally related to higher exposures or to increased susceptibility, and therefore to higher-than-average health risks. It highlights a series of three scientific questions that are important for risk assessment and risk management. (1) How do important exposure- and susceptibility-related at-
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tributes affect environmental health risk? (2) How do class and race affect important exposure- and susceptibility-related attributes? (3) How do class and race differentially affect environmental health risks? Resolution of the first question allows for realistic and quantitative assessment of environmental health risks encountered by those at potentially greater risk. Answers to the second question provide an indication of whether certain sociodemographic groups are disproportionately represented in at-risk categories. And answers to the third question elucidate some of the interrelationships among class and race, affording an opportunity to distinguish the relative influence of each on environmental health risks. These three questions are not independent of one another. Answers to the first question allow us to raise the second, and, taken together, answers to the first two questions let us draw some tentative conclusions about the third. Developing scientifically credible answers to these and related questions will provide a sound scientific basis for realistic assessment of the differential effects of class and race on environmental health risks, thereby making it easier to develop effective and efficient strategies for prevention, mitigation, and remediation. But it will take time to get definitive answers, and it is debatable whether we have the luxury of waiting for conclusive scientific evidence before taking action to safeguard vulnerable segments of our society. For example, although the scientific evidence is fragmented, uneven, and sparse, there is good reason to suspect that low-income groups tend to be more susceptible because of factors related to their quality of life and lifestyle (Navarro, 1990; Wildavsky, 1990; Kipen et al., 1991; Kerner et al., 1993; Rios et al., 1993; Sexton et al., 1993a,b; Grassman, 1996a,b). The available eviTable 2 Common problems that complicate attempts to establish causality between exposure to environmental agents and adverse health effects 1. 2. 3. 4.
5. 6. 7. 8. 9.
Incomplete understanding of disease etiology Wide range of non-environmental causes for most diseases to which environmental agents contribute Environmental agents often enhance or exacerbate, rather than cause disease or dysfunction Lack of methods, measurements, and models to (a) estimate exposure, dose, and effects accurately, and (b) characterize variability over individuals, time, and space accurately Lack of surveillance and reporting systems for exposure and environmentally related health outcomes Long latency period from exposure to adverse health effects for many environmentally induced diseases (e.g. cancer) Multiple exposures, both simultaneously and sequentially, to a diversity of environmental agents Observed health endpoint (e.g. lung damage) may not be the primary target system (e.g. immune system) Inherent variability among individuals in biological susceptibility to environmentally induced illness and injury
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Fig. 1. Conceptual model of the causal relationships between sociodemographic variables (i.e. socioecononic status and ethnicity/race) and environmenal health risks.
dence suggests that low-income groups, which contain a disproportionate percentage of many ethnic and racial minorities, are more likely to lack knowledge about environmental health issues, to have a substandard diet, to lack access to adequate health care, to smoke cigarettes and drink alcohol, and, in general, to live more stressful and less healthful lives (Denton and Massey, 1988; McCord and Freeman, 1990; Williams, 1990; Graham et al., 1992; Kerner et al., 1993; Montgomery and Carter-Pokras, 1993; Corcoran, 1995; Hahn and Eberhardt, 1995; Williams and Collins, 1995). Many observational studies conducted over the past several years have found that poor people, and especially poor blacks and Hispanics, are more likely than affluent whites to live near sources of environmental pollution, such as waste sites, reside in urban areas where ambient levels of certain pollutants, such as lead, ozone, carbon monoxide, and particulate matter are elevated, eat significantly greater amounts of contaminated fish, and be employed in potentially dangerous occupations, such as migrant farm work (Sexton et al., 1993a,b). Moreover, it is well-documented that these same groups have higher rates of morbidity and mortality than the general population (Navarro, 1990; Wildavsky, 1990; Williams, 1990, Kerner et al., 1993; Montgomery and Carter-Pokras, 1993; Hahn and Eberhardt, 1995; Williams and Collins, 1995).
4. Susceptibility factors related to class or race Although the term susceptibility is used frequently by exposure analysts, epidemiologists, and toxicologists, in the context of risk assessment it has no standard, cross-disciplinary definition (Grassman, 1996b). For the purposes of this discussion, susceptibility is defined as the combination of intrinsic and acquired characteristics of an individual or a population of individuals that alters biological response to environmental insults. Susceptibility is meant to refer to the totality of susceptibility factors and their interactions that make some people ‘more sensitive’ or ‘more vulnerable’ to the adverse health effects of pollution than others. From a practical standpoint, the most susceptible individuals in the population are those who respond biologically at the lowest levels of environmental insult. Because the total variability in susceptibility to a given health effect is difficult, if not impossible, to measure, Grassman (1996a,b) has suggested the use of ‘susceptibility factors’, which are analogous to epidemiologic risk factors. A susceptibility factor is defined to mean a risk factor related to susceptibility, such as genetic predisposition, smoking, obesity, or poor nutrition, which increases the likelihood of illness or injury from environmental exposures. Susceptibility factors
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can influence the magnitude of response (e.g. level of enzyme activity), the type of response (e.g. reproductive versus developmental effects), or both (Grassman, 1996a). As summarized in Table 3, there are two general types of susceptibility factors: intrinsic and acquired (Grassman, 1996a,b). Intrinsic susceptibility factors are inherent, fixed characteristics in an individual or population at a point in time, as for example, gender, age, genetics, and ethnicity/race. Acquired susceptibility factors are variable characteristics of individuals or populations caused by the realities of life (e.g. access to health care, preexisting disease, exposure to environmental agents, and stress) or choices about lifestyle (e.g. use of alcohol and tobacco, nutrition, fitness, sexual behavior, and illicit drug use).
4.1. Intrinsic susceptibility factors Intrinsic susceptibility factors have received the most attention from environmental health scientists, and there is substantial evidence showing that age and gender are important determinants of susceptibility to specific environmental agents. It is well recognized, for example, that the very young and the elderly are more vulnerable to the effects of some air pollutants, including aeroallergens (e.g. pollens), microorganisms (e.g. bacteria and viruses), and pesticides (e.g. organophosphates). Pregnant women, and particularly their fetuses, are an especially sensitive group due to physiologic changes during pregnancy, and may be more susceptible to pollutants such as carbon monoxide and pesticides that are cholinesterase inhibitors (Sexton et al., 1993a,b). Differences in genetic make-up may increase the likelihood that some individuals will respond biologiTable 3 Types of susceptibility factors Intrinsic Genetics Gender Age Ethnicity/race Acquired Quality of life (realities) Access to health care Pre-existing disease/injury Psychosocial factors (e.g. stress) Exposure to environmental agents Lifestyle (choices) Nutrition Fitness Tobacco use Alcohol use Illicit drug use Sexual behavior
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cally to a particular environmental insult. This enhanced susceptibility might be caused by the presence of one or more genetic alleles that promote adverse effects from exposures or by the absence of alleles that provide protection (e.g. resistance) from environmentally induced disease. In specific instances, there are data suggesting that genetic factors affect susceptibility to particular chemicals, as for example, debrisoquine hydroxylation phenotype and lung cancer from cigarette smoke, aryl hydrocarbon hydroxylase (AHH) inducibility and lung cancer from polycyclic aromatic hydrocarbons, and acetylation phenotype and bladder cancer from N-substituted aryl compounds (Vine and McFarland, 1990). There is a substantial body of evidence showing differences in genetically determined traits among certain ethnic and racial groups, including differences in anthropometric, physiologic, and biochemical characteristics between blacks and whites (Polednak, 1989), and differences in response to cardiovascular agents and central nervous system agents among a variety of groups (Levy, 1993). There is also data suggesting that genetic factors may give rise to differences between ethnic/racial groups in susceptibility to pollution exposures, as for example, deficiency of the enzyme glucose6-phosphate dehydrogenase (G-6-PD) in people from Africa, Asia, and the Mediterranean (i.e. possible increased vulnerability from the effects of ozone and nitrogen dioxide), sickle cell anemia in African Americans (i.e. may increase risks from carbon monoxide exposures), and slow rate of acetylation in the liver (i.e. risk factor for bladder cancer from exposure to aromatic amines) (Sexton et al., 1993b). In general, however, the extent to which genetic factors contribute to increased susceptibility and to related increases in environmental risks for ethnic and racial minorities is not well understood. With the exception of effects conferred by different frequencies of genetic polymorphisms, intrinsic susceptibility associated with ethnicity and race appears to be relatively rare. In most cases, it is likely that the variability within a particular ethnic or racial group is greater than the variability between any two groups. When discussing these kinds of issues, it is important to acknowledge explicitly the sensitivity of data that purport to show differences in people by culture and race, especially when based on genetic factors. Ethical considerations must always be taken into account in the differentiation of individuals and groups by cultural and racial attributes (NRC, 1989).
4.2. Acquired susceptibility factors Susceptibilities that appear to be ethnic or racial in origin are often acquired factors related to socioeconomic status (Navarro, 1990; Baquet et al., 1991; Free-
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Table 4 Examples of how acquired susceptibility factors might affect human responses to environmental agents 1. 2. 3. 4.
5. 6.
Pre-existing disease, such as asthma or diabetes, increases susceptibility to the adverse effects of exposure Inadequate diet, such as vitamin or mineral deficiency, or low protein, impairs host defense mechanisms and systems Use of alcohol, tobacco, or illicit drugs damage respiratory and cardiovascular systems, making them more susceptible to effects of pollution Cumulative exposure to multiple environmental hazards, at work and at home, causes increased susceptibility (e.g. exposure to both aflatoxin-contaminated food and hepatitis B infection increases the risk of hepatocellular carcinoma) or results in more than additive health effects (e.g. tobacco smoke and asbestos or radon exposure) Inadequate access to health care delays recognition, diagnosis and treatment of environmentally induced disease Psychosocial stress, as might be caused by unemployment, underemployment, poverty, inadequate living and working conditions, and language problems, reduces host resistance to adverse health effects
man, 1991; Grassman, 1996a,b). Acquired susceptibility factors are vulnerabilities resulting from the circumstances of life and may modify intrinsic factors. They can be divided into two subgroups: quality-of-life and lifestyle factors. Quality-of-life factors, such as access to health care, preexisting disease, pyschosocial stress, and exposure to environmental agents, develop from the realities of being poor and disadvantaged, and are factors over which those in the lower socioeconomic strata have little or no control. Lifestyle factors, such as nutrition, fitness, alcohol and tobacco use, illicit drug use, and sexual behavior, are the result of decisions made by individuals. These are factors over which people nominally exercise control; however, personal decisions about lifestyle are strongly influenced by SES (Williams, 1990; Kerner et al., 1993; Montgomery and Carter-Pokras, 1993; Williams and Collins, 1995). Although data are scarce, there is little doubt that acquired susceptibility factors can have a profound impact on both exposures to environmental pollutants and vulnerability to related adverse health effects (Sexton et al., 1993a,b; Grassman, 1996a,b). Examples of how acquired susceptibility factors might affect human responses to environmental agents are summarized in Table 4. It is likely that these and other acquired traits are probably the most important, as well as the least understood factors affecting human susceptibility to toxic chemicals (Grassman, 1996b).
5. Incorporating susceptibility into risk assessments Despite the potential importance of intrinsic and acquired susceptibility factors, they have not been routinely addressed in EPA risk assessments due to a paucity of appropriate information. Nevertheless, the need to take account of the potential for differing susceptibilities among population subgroups is recognized explicitly in EPA’s Guidance for Risk Characterization (EPA, 1995). The Guidance document states that agency risk assessors are expected to address and provide descriptions of risk to important subgroups of the population, such as highly exposed or highly sus-
ceptible groups. Although recognizing that, in most cases, the state of the science is not yet adequate to define population distributions of susceptibility, the EPA recommends that ‘‘If a full description of the range of susceptibility in the population cannot be presented, an effort should be made to identify subgroups that, for various reasons, may be particularly susceptible’’. The Guidance document emphasizes the importance of identifying highly susceptible subgroups, and, if possible, characterizing and quantifying their risk. As noted in the document, ‘‘Generally, selection of the population segments is a matter of either a priori interest in the subgroup (e.g. environmental justice considerations), in which case the risk assessor and risk manager can jointly agree on which subgroups to highlight, or a matter of discovery of a sensitive or highly exposed subgroup during the assessment process. In either case, once identified, the subgroup can be treated as a population in itself, and characterized in the same way as the larger population…’’ But, despite EPA’s official guidance to agency risk assessors directing them to take account of susceptible subgroups, there is no formal EPA guidance or policy on how to do it. In general, there are three ways to incorporate susceptibility into health risk assessments (Grassman, 1996b): (1) risk can be measured or estimated in the subpopulation with the identified susceptibility factors; (2) risk can be measured or estimated in the general population and then divided by a scaled uncertainty factor; or (3) risk can be measured or estimated in the general population and then divided by a default uncertainty factor. Selection of a particular approach depends on variables such as the type of susceptibility factor, the nature of the relationship between exposure, susceptibility, and outcome, the adequacy of available scientific information, the purpose of the assessment, and institutional constraints (e.g. resources). As a practical matter, data deficiencies usually prevent risk assessors from using the first approach, forcing them, if they consider susceptible populations at all, to use uncertainty factors.
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As Grassman (1996a) has pointed out, epidemiologic studies have not historically provided the kind of doseresponse information needed to calculate risk to susceptible populations. Several reasons for this deficiency were listed: failure to evaluate potential susceptibility factors; incorrect identification of susceptibility factors; inclusion of susceptibility factors with questionable environmental etiology; inadequate documentation of exposures; incomplete documentation of adverse health outcomes; and failure to take account of multiple susceptibility factors. To be able to incorporate susceptibility into quantitative risk assessments, assessors need rigorous epidemiologic studies, in combination with clinical and animal toxicology studies, that document the exposure–response (or dose – response) relationship for important susceptibility factors. Until such studies are available, however, quantitative assessment of risks to susceptible groups are not feasible in most cases. Due to the fact that risk-based decision making is integral to implementation of pollution control strategies, the problems of assessing risks to susceptible populations have potentially consequential implications for safeguarding environmental health. Of particular concern is the possibility that current risk assessment and risk management approaches do not provide adequate protection for disadvantaged groups.
6. An environmental justice critique of risk assessment Much of the current EPA focus on incorporating susceptibility into risk assessments stems from concerns about ‘environmental justice’ (Sexton et al., 1993a; Cotton, 1994; Kraft and Scheberle, 1995; Perlin et al., 1995; Ringquist, 1997; Zimmerman, 1993, 1997). A growing body of evidence indicates that low-income groups, a disproportionate percentage of whom are people of color, tend to be both more exposed to environmental chemicals and more susceptible to related health effects than the general population. This situation has spurred calls for environmental justice, which can be broadly defined as adequate protection from the health effects of pollution for everyone in our society, regardless of age, culture, ethnicity, gender, race, or socioeconomic status. Some scientists, legal scholars, and environmental justice advocates assert that the existing risk assessment methodology/process is a major cause of inequity and injustice (Israel, 1995; Kuehn, 1996). The proponents of this view allege that EPA’s risk assessments systematically undervalue environmental health risks for poor communities and people of color, thereby creating an excessive burden of pollution and environmental hazards for low-income groups and racial minorities. A central theme in these ‘environmental justice’ critiques is the failure of tradition methods, practices, and pro-
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cesses to incorporate susceptibility adequately into health risk assessments. Israel (1995) lists four major objections to the risk assessment process that are commonly raised by environmental justice advocates: (1) health studies and risk assessments are used to justify government inaction in the face of real risks; (2) risk management decision making is politically motivated, ignoring risks experienced in poor and minority communities; (3) scientific risk assessments fail to account for community perceptions of risk; and (4) the risk assessment methodology is itself discriminatory. It has been suggested that this last criticism is based on informational biases that occur within the process, which keep regulatory agencies from adequately considering unusual exposure patterns and unusual susceptibilities. As a consequence, Israel argues that risk assessments distort the true nature of environmental health risks and lead to less-than-adequate protection for disadvantaged groups (Israel, 1995). To correct these informational bias problems and create a more equitable risk assessment process, Israel recommends the following changes to the process: (1) more effective and exhaustive gathering of relevant demographic data; (2) reduction of generalized exposure and susceptibility estimates; (3) public participation in the various stages of risk assessment decision making; (4) implementation of various mechanisms to impose the burden of demonstrating safety on the private sector; and (5) abandonment of generalized risk assessments in determining clean-up standards at specific sites. Similarly, Kuehn (1996) believes that because risk assessment fails to address issues like multiple and cumulative exposures, synergistic effects, increased susceptibilities, and qualitative aspects of risk, it seriously underestimates the magnitude of many risks, particularly for highly exposed and highly susceptible racial and ethnic subpopulations. Kuehn (1996) says that ‘‘as currently structured and as proposed for more widespread use, the process does not offer a safe haven from distributional inequities or from the dominating influences of resources and political power on environmental decision making. The hazards faced by people of color and lower incomes are likely to be given insufficient attention by quantitative risk assessment, and important non-quantitative aspects of risk will be left out of the decision-making process’’. As a remedy, Kuehn (1996) suggests the following changes: (1) to revise the methodology of quantitative risk assessment to address differences in the distribution of risk; (2) if critical risk-related information is missing, assume a reasonable worst case as an incentive for the private sector to fill important data gaps; (3) include more qualitative analyses in risk characterization; (4) provide a full, comprehensive, and understandable exposition of the uncertainties; (5) institute an open,
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accessible, and fair process for assessing and managing risks; and (6) change the current focus on management of risk to a more holistic approach that considers alternative processes and products that might prevent or avoid risk in the first place. According to Israel (1995), Kuehn (1996) and others concerned about environmental justice, the difficulty encountered by risk assessors in dealing with susceptibility issues has contributed directly to greater (and unacceptable) environmental health risks for low-income communities and people of color.
7. Confronting the dilemma of what to do The decision makers are confronted with a dilemma; how should potentially susceptible groups be accounted for in risk assessment and risk management decisions when the relationship between exposure and adverse health effects for the important susceptibility factors is unknown? In considering this conundrum, it is important to keep in mind that the most important risk-related question is not ‘are low-income, disadvantaged populations more susceptible to the adverse health effects of pollution?’, because most observers tend to agree that they probably are. The more consequential question is ‘how much more susceptible are they?’ If, for example, the variability in susceptibility within the general population is consistently less than 10-fold, then it is conceivable that risk assessors and managers do not necessarily have to take any extraordinary precautions to protect susceptible groups. If, on the other hand, susceptibility for highly sensitive groups is often an order of magnitude or more greater than that for the general population, then special risk assessment and risk management procedures may be required. The challenge, of course, is to know when and under what circumstances the latter situation prevails. An even more momentous question for many is whether risk assessment is part of the solution or part of the problem? As noted by Kuehn (1996), quantitative risk assessment typically squeezes out factors that cannot be quantified, lending support to Gresham’s Law —quantitative information of any kind tends to retard the circulation of qualitative information. He points out that EPA risk assessments are often criticized for giving more credence and weight to tangible factors that can be measured, at the expense of less tangible, less-easily-measured, though not necessarily less important, non-quantifiable variables. The result is that risk-based decisions are likely to be biased in favor of hard, quantifiable evidence and against soft, non-quantifiable aspects of risk. Consequently, there is a built-in, systematic bias, which hinders recogni-
tion that economically disadvantaged groups bear a disproportionate burden of risk. The title of this article asks whether class and race matter for realistic risk assessment. Despite the absence of systematically collected data, the weight of the evidence suggests the answer is an unequivocal ‘yes’. Environmental health risks are routinely higher for economically disadvantaged populations because they are both more exposed and more susceptible than the general population. To what extent elevated environmental health risks contribute to higher rates of morbidity and mortality for these groups is uncertain. Nevertheless, the fact that the current state of the science prevents us from quantifying the nature, magnitude, and scope of the effect should not be used as an excuse for doing nothing. To address susceptibility concerns, four complementary actions are warranted and should be undertaken now. First, develop formal procedures for implementing EPA’s Guidance for Risk Characterization, thereby providing mechanisms for considering susceptible populations, both quantitatively and qualitatively, as an integral part of risk assessment. Second, establish clear-cut procedures whereby decision makers must explicitly consider susceptible populations as part of risk management. Third, begin a comprehensive research program aimed at conducting well-designed scientific studies to characterize the relationship between exposure and health effects for important susceptibility factors, and fourth, implement a surveillance system that provides for the systematic, ongoing collection of exposure-related, health-related, and susceptibility-related information in economically disadvantage populations. These actions will go a long way toward achieving the vision espoused by Alexander Hamilton at the Constitutional Convention in 1787. There can be no truer principle than this…that every individual of the community at large has an equal right to the protection of government.
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K. Sexton / En6ironmental Toxicology and Pharmacology 4 (1997) 261–269 Cotton, P., 1994. Pollution and poverty overlap becomes issue, administration promises action. J. Am. Med. Assoc. 271, 967 – 970. Coultas, D.B., Gong, H., Grand, R., Handler, A., McCurdy, S., Player, R., Rhoades, E.R., Samet, J.M., Thomas, A., Westley, M., 1993. Respiratory diseases in minorities of the United States. Am. J. Crit. Care Med. 149, S93–S131. Denton, N.A., Massey, D.S., 1988. Residential segregation of blacks, hispanics, and asians by socioeconomic status and generation. Soc. Sci. Q. 69, 797 –817. EPA (Environmental Protection Agency), 1995. Guidance for Risk Characterization. Science Policy Council, Washington, DC. Freeman, H., 1991. Race, poverty, and cancer. J. Natl. Cancer Inst. 83, 51 – 52. Graham, J.D., Chang, B., Evans, J.S., 1992. Poorer is riskier. Risk Anal. 12, 333 – 337. Grassman, J.A., 1996a. Obtaining information about susceptibility from the epidemiologic literature. Toxicology 111, 253–270. Grassman, J.A., 1996b. Incorporation of Information on Susceptible Populations into Risk Assessments. Unpublished Report based on work as a 1994 Fellow in the American Association for the Advancement of Science/US Environmental Protection Agency Fellowship Program, National Institute of Environmental Health Sciences, Research Trangle Park, NC. Hahn, R.A., Eberhardt, S., 1995. Life expectancy in four US racial/ ethnic populations: 1990. Epidemiology 6, 350–355. House, J.S., Kessler, R.C., Herzog, A.R., 1990. Age, socioeconomic status, and health. Milbank Q. 68, 383–411. Israel, B.D., 1995. An environmental justice critique of risk assessment. N. Y. Univ. Environ. Law J. 3, 469–522. Kerner, J.F., Dusenbury, L., Mandelblatt, J.S., 1993. Poverty and cultural diversity: challenges for health promotion among the medically underserved. Annu. Rev. Publ. Health 14, 355– 377. Kipen, H.M., Wartenberg, D., Scully, P.F., Greenberg, M., 1991. Are non-whites at greater risk for occupational cancer?. Am. J. Ind. Med. 19, 67 – 74. Kraft, M.E., Scheberle, D., 1995. Environmental justice and the allocation of risk: the case of lead and public health. Policy Stud. J. 23, 113 – 122. Kuehn, R.R., 1996. The environmental justice implications of quantitative risk assessment. Univ. Ill. Law Rev. 1996, 103–172. Levy, R.A., 1993. Ethnic and Racial Differences in Response to Medicines. National Pharmaceutical Council, Reston. McCord, C., Freeman, H.P., 1990. Excess mortality in Harlem. N. Engl. J. Med. 322, 173–177. McGinnis, J.M., Foege, W.H., 1993. Actual causes of death in the United States. J. Am. Med. Assoc. 270, 2207–2212.
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Montgomery, L.E., Carter-Pokras, O., 1993. Health status by social class and/or minority status: implications for environmental equity research. Toxicol. Ind. Hyg. 9, 729 – 773. Navarro, V., 1990. Race or class versus race and class: mortality differentials in the United States. Lancet 336, 1238 – 1240. NRC, National Research Council, 1989. Biological Markers in Reproductive Toxicology. National Academy Press, Washington, DC. Pappas, G., Queen, S., Hadden, W., Fisher, G., 1993. The increasing disparity in mortality between socioeconomic groups in the United States, 1960 and 1986. N. Engl. J. Med. 329, 103–109. Perlin, S.A., Setzer, R.W., Creason, J., Sexton, K., 1995. Distribution of industrial air emissions by income and race in the United States: an approach using the toxic release inventory. Environ. Sci. Technol. 29, 69 – 80. Polednak, A.P., 1989. Racial and Ethnic Differences in Disease. Oxford University Press, New York. Ringquist, E.J., 1997. Environmental justice: normative concerns and empirical evidence. In: Vig, N.J., Kraft, M.E. (Eds.), Environmental Policy in the 1990s: Reform or Reaction? 3rd ed. Congressional Quarterly Press, Washington, DC. Rios, R., Poje, G.V., Detels, R., 1993. Susceptibility to environmental pollutants among minorities. Toxicol. Ind. Hyg. 9, 797 –820. Sexton, K., Olden, K., Johnson, B.L., 1993a. Environmental justice: the central role of research in establishing a credible scientific foundation for informed decision making. Toxicol. Ind. Health 9, 685 – 727. Sexton, K., Gong, H., Bailar, J.C., Ford, J.G., Gold, D.R., Lambert, W.E., Utell, M.J., 1993b. Air pollution health risks: do class and race matter?. Toxicol. Ind. Health 9, 843 – 878. Vine, M.F., McFarland, L.T., 1990. Markers of susceptibility. In: Hulka, B.S., Wilcosky, T.C., Griffith, J.D. (Eds.), Biologic Markers in Epidemiology. Oxford University Press, New York. Wildavsky, A., 1990. Richer is safer. Public Interest 60, 23 –39. Williams, D.R., 1990. Socioeconomic differentials in health: a review and redirection. Soc. Psych. Q. 53, 81 – 99. Wagener, D.K., Williams, D.R., 1993. Equity in environmental health: data collection and interpretation issues. Toxicol. Ind. Health 9, 775 – 795. Williams, D.R., Collins, C., 1995. US socioeconomic and racial differences in health: patterns and explanations. Annu. Rev. Sociol. 21, 349 – 386. Zimmerman, R., 1993. Social equity and environmental risk. Risk Anal. 13, 649 – 666. Zimmerman, R., 1997. Environmental justice. In: Molak, V. (Ed.), Fundamentals of Risk Analysis and Risk Management. Lewis, Boca Raton.
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Sociodemographic aspects of human susceptibility to toxic chemicals: Do class and race matter for realistic risk assessment? Ken Sexton School of Public Health, Uni6ersity of Minnesota, P.O. Box 807 UMHC, 420 Delaware Street, S.E., Minneapolis, MN 55455, USA
Abstract Susceptibility is well-recognized as a potentially important aspect of health risk assessment, particularly for groups such as pregnant women and their fetuses, infants, children, the elderly, and the infirm, that are known or suspected to be more vulnerable to environmental insults. More recently, it has become apparent that economically disadvantaged groups are likely to be systematically both more exposed and more susceptible to environmental pollution. This article reviews the reasons why low-income communities and many racial minorities are at an increased risk because they are more susceptible to the adverse health effects of toxic chemicals. The scientific challenges of quantifying the magnitude of environmental health risks for these groups are discussed, emphasizing ramifications for risk assessment and risk management decisions. Problems incorporating susceptibility into risk-based decision making are identified, and specific actions are recommended to address these deficiencies. © 1997 Elsevier Science B.V. Keywords: Susceptibility; Risk assessment; Risk management; Susceptibility factors; Environmental justice; Socioeconomic status; Racial groups
1. Introduction A fundamental goal of pollution control strategies, including federal statutes such as the Clean Air Act (CAA), the Safe Drinking Water Act (SDWA), and the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA), is to protect people from the adverse health effects of environmental pollutants. To be successful, these strategies depend on accurate identification of those individuals, groups, and populations who are at highest comparative risk so that, if warranted, appropriate prevention or intervention actions can be taken. Conceptually, individuals and subpopulations are deemed to be at potentially greater risk when they are either exposed above a health-related benchmark (e.g. exposures above National Ambient Air Quality Standards) or more susceptible to the effects of exposures (e.g. predisposed to develop bladder cancer after exposure to N-substituted aryl compounds because of acetylation phenotype). Those who are both more exposed and more susceptible are considered to be at highest risk of adverse health effects. 1382-6689/97/$17.00 © 1997 Elsevier Science B.V. All rights reserved. PII S 1 3 8 2 - 6 6 8 9 ( 9 7 ) 1 0 0 2 0 - 5
Susceptibility differences, both between individuals and between populations, are recognized as potentially important for realistic risk assessment (EPA, 1995). But in reality, appropriate and sufficient data are rarely available to characterize real-world distributions of susceptibility adequately. Consequently, quantitative risk assessments typically have difficulty accounting for differences between the general population and groups traditionally assumed to be more susceptible to the effects of pollution, such as pregnant women and their fetuses, infants, children, the elderly, and the infirm. Even more difficult to evaluate and quantify is the degree to which poor, disadvantaged people (i.e. those in lower socioeconomic strata) and people of color (e.g. African Americans, Native Americans, Hispanics, and Asian Americans) are more susceptible to environmentally induced dysfunction, disability, disease, and death. This article provides a brief overview and survey of the reasons for concern about higher susceptibility among those in our society who are poor, have limited formal education, are unemployed or work under haz-
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Table 1 Poverty rates by ethnicity, race, and age (adapted from Montgomery and Carter-Pokras, 1993) Age (years)
White (%)
Black (%)
Total Hispanic (%)
Mexican-American (%)
Puerto Rican (%) Asian/Pacific Islander (%)
Total US (%)
B18 18–64 ]65
16.9 9.6 10.9
46.6 25.7 33.3
39.9 23.9 22.0
39.9 24.7 22.0
52.2 28.1 18.8
21.9 11.7 12.9
16.3 11.0 10.5
Source: Current Population Survey, March 1993.
ardous conditions, or are members of certain ethnic and racial minorities. The focus is on susceptibility factors related to social class and/or racial group that are acquired as a consequence of people’s quality of life and lifestyle. The discussion is divided into six major sections: (1) effects of class and race on health status; (2) effects of class and race on environmental health risk; (3) susceptibility factors related to class or race; (4) incorporating susceptibility into health risk assessments; (5) an environmental justice critique of risk assessment; and (6) confronting the dilemma of what to do.
2. Effects of class and race on health status It is well established that rates of disease and death in the United States vary significantly by social class and ethnicity/race (Polednak, 1989; Navarro, 1990; Graham et al., 1992; Coultas et al., 1993; Montgomery and Carter-Pokras, 1993; Hahn and Eberhardt, 1995). Both are predictors of health status, and both are associated with acquired susceptibility factors, such as access to health-promoting and health-protecting resources (e.g. healthy diet and sanitation) and preventative medical practices (e.g. prenatal care and childhood immunization), as well as lifestyle choices about alcohol and tobacco use, sexual behavior, and occupation (Kerner et al., 1993). Nevertheless, the relative roles of social class and ethnicity/race in affecting health status, as well as the exact nature of their interactions are a matter of debate (Denton and Massey, 1988; House et al., 1990; McCord and Freeman, 1990; Williams, 1990; Baquet et al., 1991; Freeman, 1991; Kipen et al., 1991; CDC, 1993; Pappas et al., 1993; Corcoran, 1995; Hahn and Eberhardt, 1995; Williams and Collins, 1995). There is general consensus that, regardless of its relationship to ethnicity/race, socioeconomic status is a critical factor affecting morbidity and mortality. Yet despite its apparent importance, the mechanisms by which socioeconomic status (SES) exerts its influence are largely a matter of conjecture. Because income, education, and occupation are not likely to influence health directly, they are obviously proxies for other variables. But insufficient evidence is available linking
other variables to a direct impact on health. Most studies attempt to control for such obvious confounders as cigarette smoking and heavy alcohol consumption, both of which are more frequent among the disadvantaged. Although a host of other potential factors, such as stress, exposure to environmental agents, and diet, which are related to socioeconomic status can be postulated, ‘‘there is very little evidence to point to any of them as the major cause of the health difference between the advantaged and the disadvantaged’’ (Angell, 1993). The influence of ethnicity/race on health status is also well known and, as with socioeconomic status, the causal relationships are poorly understood (McGinnis and Foege, 1993). While some researchers maintain that ethnicity/race exerts an influence separate from social class (Denton and Massey, 1988; Wagener and Williams, 1993; Brown, 1995), others believe that the apparent effects of this variable are due primarily to differences in socioeconomic status (Navarro, 1990; Baquet et al., 1991; Freeman, 1991; Graham et al., 1992). Although disparities in health status by ethnicity/race are substantial, the causes, which certainly include differences in quality-of-life variables and lifestyle choices, are not well elucidated. The situation is further complicated by the fact that ethnicity/race is associated with both absolute and relative poverty. Although the largest number and highest percentage of poor Americans are white, as shown in Table 1, a disproportionate percentage of African Americans, Hispanics, Mexican Americans, and Puerto Rican Americans, particularly children, live in poverty (Montgomery and Carter-Pokras, 1993; Kerner et al., 1993; Corcoran, 1995; Williams and Collins, 1995). Consequently, it is often difficult to distinguish the separate effects of class and race on health status. Health status is clearly a product of multiple variables, many of which are poorly understood (McGinnis and Foege, 1993). There is substantial evidence suggesting that large-scale societal factors are the primary determinants of health; determining not only individuals’ social class but also their access to resources and exposure to risk factors. What is not well-understood is how position in social structure constrains and shapes daily life in ways that adversely affect health (Williams and Collins, 1995).
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Today, there is mounting evidence that disparities in health status between higher and lower SES strata are increasing, and that the health of some racial groups is steadily deteriorating (Kerner et al., 1993; Williams and Collins, 1995). These realities recently moved Williams and Collins (1995) to observe that ‘‘Racial and socioeconomic inequality in health is arguably the single most important public health issue in the United States’’.
3. Effects of class and race on environmental health risk For regulatory officials charged with protecting environmental health, observed disparities in health status by social class and racial group raise concerns about the possible role of environmental agents (Sexton et al., 1993a,b; Zimmerman, 1993; Ringquist, 1997). To address these concerns from a risk-based perspective we need answers to three questions: (1) do environmental health risks vary by class and race? (2) if so, to what extent do differential environmental health risks contribute to higher rates of morbidity and mortality among disadvantaged groups? and (3) how can we intervene effectively and efficiently to prevent or mitigate those environmental health risks deemed to be unacceptable? In most instances, there is a shortage of scientific evidence to answer these and other relevant questions with an acceptable degree of certainty (Sexton et al., 1993a,b; Zimmerman, 1993, 1997). A major problem in this regard is the difficulty of demonstrating the existence of a causal relationship between exposures to environmental agents and subsequent disease or injury unless the link is strong (e.g. radon-induced lung cancer in uranium miners). The challenges that can complicate attempts to verify causality are abundant, as summarized in Table 2. Therefore, attempts to answer the three risk-related questions posed above are hampered not only by complexity and uncertainty surrounding the major determinants of health, and by variations in these determinants according to class and race, but also by difficulties inherent in establishing a causal link between environmental agents and subsequent adverse health effects. One way to think about hypothesized, though as yet largely unexplored inter-relationships among class and race, exposure- and susceptibility-related attributes, and environment health risks is depicted in Fig. 1. This conceptual model allows us to postulate how social class or racial group might be causally related to higher exposures or to increased susceptibility, and therefore to higher-than-average health risks. It highlights a series of three scientific questions that are important for risk assessment and risk management. (1) How do important exposure- and susceptibility-related at-
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tributes affect environmental health risk? (2) How do class and race affect important exposure- and susceptibility-related attributes? (3) How do class and race differentially affect environmental health risks? Resolution of the first question allows for realistic and quantitative assessment of environmental health risks encountered by those at potentially greater risk. Answers to the second question provide an indication of whether certain sociodemographic groups are disproportionately represented in at-risk categories. And answers to the third question elucidate some of the interrelationships among class and race, affording an opportunity to distinguish the relative influence of each on environmental health risks. These three questions are not independent of one another. Answers to the first question allow us to raise the second, and, taken together, answers to the first two questions let us draw some tentative conclusions about the third. Developing scientifically credible answers to these and related questions will provide a sound scientific basis for realistic assessment of the differential effects of class and race on environmental health risks, thereby making it easier to develop effective and efficient strategies for prevention, mitigation, and remediation. But it will take time to get definitive answers, and it is debatable whether we have the luxury of waiting for conclusive scientific evidence before taking action to safeguard vulnerable segments of our society. For example, although the scientific evidence is fragmented, uneven, and sparse, there is good reason to suspect that low-income groups tend to be more susceptible because of factors related to their quality of life and lifestyle (Navarro, 1990; Wildavsky, 1990; Kipen et al., 1991; Kerner et al., 1993; Rios et al., 1993; Sexton et al., 1993a,b; Grassman, 1996a,b). The available eviTable 2 Common problems that complicate attempts to establish causality between exposure to environmental agents and adverse health effects 1. 2. 3. 4.
5. 6. 7. 8. 9.
Incomplete understanding of disease etiology Wide range of non-environmental causes for most diseases to which environmental agents contribute Environmental agents often enhance or exacerbate, rather than cause disease or dysfunction Lack of methods, measurements, and models to (a) estimate exposure, dose, and effects accurately, and (b) characterize variability over individuals, time, and space accurately Lack of surveillance and reporting systems for exposure and environmentally related health outcomes Long latency period from exposure to adverse health effects for many environmentally induced diseases (e.g. cancer) Multiple exposures, both simultaneously and sequentially, to a diversity of environmental agents Observed health endpoint (e.g. lung damage) may not be the primary target system (e.g. immune system) Inherent variability among individuals in biological susceptibility to environmentally induced illness and injury
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Fig. 1. Conceptual model of the causal relationships between sociodemographic variables (i.e. socioecononic status and ethnicity/race) and environmenal health risks.
dence suggests that low-income groups, which contain a disproportionate percentage of many ethnic and racial minorities, are more likely to lack knowledge about environmental health issues, to have a substandard diet, to lack access to adequate health care, to smoke cigarettes and drink alcohol, and, in general, to live more stressful and less healthful lives (Denton and Massey, 1988; McCord and Freeman, 1990; Williams, 1990; Graham et al., 1992; Kerner et al., 1993; Montgomery and Carter-Pokras, 1993; Corcoran, 1995; Hahn and Eberhardt, 1995; Williams and Collins, 1995). Many observational studies conducted over the past several years have found that poor people, and especially poor blacks and Hispanics, are more likely than affluent whites to live near sources of environmental pollution, such as waste sites, reside in urban areas where ambient levels of certain pollutants, such as lead, ozone, carbon monoxide, and particulate matter are elevated, eat significantly greater amounts of contaminated fish, and be employed in potentially dangerous occupations, such as migrant farm work (Sexton et al., 1993a,b). Moreover, it is well-documented that these same groups have higher rates of morbidity and mortality than the general population (Navarro, 1990; Wildavsky, 1990; Williams, 1990, Kerner et al., 1993; Montgomery and Carter-Pokras, 1993; Hahn and Eberhardt, 1995; Williams and Collins, 1995).
4. Susceptibility factors related to class or race Although the term susceptibility is used frequently by exposure analysts, epidemiologists, and toxicologists, in the context of risk assessment it has no standard, cross-disciplinary definition (Grassman, 1996b). For the purposes of this discussion, susceptibility is defined as the combination of intrinsic and acquired characteristics of an individual or a population of individuals that alters biological response to environmental insults. Susceptibility is meant to refer to the totality of susceptibility factors and their interactions that make some people ‘more sensitive’ or ‘more vulnerable’ to the adverse health effects of pollution than others. From a practical standpoint, the most susceptible individuals in the population are those who respond biologically at the lowest levels of environmental insult. Because the total variability in susceptibility to a given health effect is difficult, if not impossible, to measure, Grassman (1996a,b) has suggested the use of ‘susceptibility factors’, which are analogous to epidemiologic risk factors. A susceptibility factor is defined to mean a risk factor related to susceptibility, such as genetic predisposition, smoking, obesity, or poor nutrition, which increases the likelihood of illness or injury from environmental exposures. Susceptibility factors
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can influence the magnitude of response (e.g. level of enzyme activity), the type of response (e.g. reproductive versus developmental effects), or both (Grassman, 1996a). As summarized in Table 3, there are two general types of susceptibility factors: intrinsic and acquired (Grassman, 1996a,b). Intrinsic susceptibility factors are inherent, fixed characteristics in an individual or population at a point in time, as for example, gender, age, genetics, and ethnicity/race. Acquired susceptibility factors are variable characteristics of individuals or populations caused by the realities of life (e.g. access to health care, preexisting disease, exposure to environmental agents, and stress) or choices about lifestyle (e.g. use of alcohol and tobacco, nutrition, fitness, sexual behavior, and illicit drug use).
4.1. Intrinsic susceptibility factors Intrinsic susceptibility factors have received the most attention from environmental health scientists, and there is substantial evidence showing that age and gender are important determinants of susceptibility to specific environmental agents. It is well recognized, for example, that the very young and the elderly are more vulnerable to the effects of some air pollutants, including aeroallergens (e.g. pollens), microorganisms (e.g. bacteria and viruses), and pesticides (e.g. organophosphates). Pregnant women, and particularly their fetuses, are an especially sensitive group due to physiologic changes during pregnancy, and may be more susceptible to pollutants such as carbon monoxide and pesticides that are cholinesterase inhibitors (Sexton et al., 1993a,b). Differences in genetic make-up may increase the likelihood that some individuals will respond biologiTable 3 Types of susceptibility factors Intrinsic Genetics Gender Age Ethnicity/race Acquired Quality of life (realities) Access to health care Pre-existing disease/injury Psychosocial factors (e.g. stress) Exposure to environmental agents Lifestyle (choices) Nutrition Fitness Tobacco use Alcohol use Illicit drug use Sexual behavior
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cally to a particular environmental insult. This enhanced susceptibility might be caused by the presence of one or more genetic alleles that promote adverse effects from exposures or by the absence of alleles that provide protection (e.g. resistance) from environmentally induced disease. In specific instances, there are data suggesting that genetic factors affect susceptibility to particular chemicals, as for example, debrisoquine hydroxylation phenotype and lung cancer from cigarette smoke, aryl hydrocarbon hydroxylase (AHH) inducibility and lung cancer from polycyclic aromatic hydrocarbons, and acetylation phenotype and bladder cancer from N-substituted aryl compounds (Vine and McFarland, 1990). There is a substantial body of evidence showing differences in genetically determined traits among certain ethnic and racial groups, including differences in anthropometric, physiologic, and biochemical characteristics between blacks and whites (Polednak, 1989), and differences in response to cardiovascular agents and central nervous system agents among a variety of groups (Levy, 1993). There is also data suggesting that genetic factors may give rise to differences between ethnic/racial groups in susceptibility to pollution exposures, as for example, deficiency of the enzyme glucose6-phosphate dehydrogenase (G-6-PD) in people from Africa, Asia, and the Mediterranean (i.e. possible increased vulnerability from the effects of ozone and nitrogen dioxide), sickle cell anemia in African Americans (i.e. may increase risks from carbon monoxide exposures), and slow rate of acetylation in the liver (i.e. risk factor for bladder cancer from exposure to aromatic amines) (Sexton et al., 1993b). In general, however, the extent to which genetic factors contribute to increased susceptibility and to related increases in environmental risks for ethnic and racial minorities is not well understood. With the exception of effects conferred by different frequencies of genetic polymorphisms, intrinsic susceptibility associated with ethnicity and race appears to be relatively rare. In most cases, it is likely that the variability within a particular ethnic or racial group is greater than the variability between any two groups. When discussing these kinds of issues, it is important to acknowledge explicitly the sensitivity of data that purport to show differences in people by culture and race, especially when based on genetic factors. Ethical considerations must always be taken into account in the differentiation of individuals and groups by cultural and racial attributes (NRC, 1989).
4.2. Acquired susceptibility factors Susceptibilities that appear to be ethnic or racial in origin are often acquired factors related to socioeconomic status (Navarro, 1990; Baquet et al., 1991; Free-
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Table 4 Examples of how acquired susceptibility factors might affect human responses to environmental agents 1. 2. 3. 4.
5. 6.
Pre-existing disease, such as asthma or diabetes, increases susceptibility to the adverse effects of exposure Inadequate diet, such as vitamin or mineral deficiency, or low protein, impairs host defense mechanisms and systems Use of alcohol, tobacco, or illicit drugs damage respiratory and cardiovascular systems, making them more susceptible to effects of pollution Cumulative exposure to multiple environmental hazards, at work and at home, causes increased susceptibility (e.g. exposure to both aflatoxin-contaminated food and hepatitis B infection increases the risk of hepatocellular carcinoma) or results in more than additive health effects (e.g. tobacco smoke and asbestos or radon exposure) Inadequate access to health care delays recognition, diagnosis and treatment of environmentally induced disease Psychosocial stress, as might be caused by unemployment, underemployment, poverty, inadequate living and working conditions, and language problems, reduces host resistance to adverse health effects
man, 1991; Grassman, 1996a,b). Acquired susceptibility factors are vulnerabilities resulting from the circumstances of life and may modify intrinsic factors. They can be divided into two subgroups: quality-of-life and lifestyle factors. Quality-of-life factors, such as access to health care, preexisting disease, pyschosocial stress, and exposure to environmental agents, develop from the realities of being poor and disadvantaged, and are factors over which those in the lower socioeconomic strata have little or no control. Lifestyle factors, such as nutrition, fitness, alcohol and tobacco use, illicit drug use, and sexual behavior, are the result of decisions made by individuals. These are factors over which people nominally exercise control; however, personal decisions about lifestyle are strongly influenced by SES (Williams, 1990; Kerner et al., 1993; Montgomery and Carter-Pokras, 1993; Williams and Collins, 1995). Although data are scarce, there is little doubt that acquired susceptibility factors can have a profound impact on both exposures to environmental pollutants and vulnerability to related adverse health effects (Sexton et al., 1993a,b; Grassman, 1996a,b). Examples of how acquired susceptibility factors might affect human responses to environmental agents are summarized in Table 4. It is likely that these and other acquired traits are probably the most important, as well as the least understood factors affecting human susceptibility to toxic chemicals (Grassman, 1996b).
5. Incorporating susceptibility into risk assessments Despite the potential importance of intrinsic and acquired susceptibility factors, they have not been routinely addressed in EPA risk assessments due to a paucity of appropriate information. Nevertheless, the need to take account of the potential for differing susceptibilities among population subgroups is recognized explicitly in EPA’s Guidance for Risk Characterization (EPA, 1995). The Guidance document states that agency risk assessors are expected to address and provide descriptions of risk to important subgroups of the population, such as highly exposed or highly sus-
ceptible groups. Although recognizing that, in most cases, the state of the science is not yet adequate to define population distributions of susceptibility, the EPA recommends that ‘‘If a full description of the range of susceptibility in the population cannot be presented, an effort should be made to identify subgroups that, for various reasons, may be particularly susceptible’’. The Guidance document emphasizes the importance of identifying highly susceptible subgroups, and, if possible, characterizing and quantifying their risk. As noted in the document, ‘‘Generally, selection of the population segments is a matter of either a priori interest in the subgroup (e.g. environmental justice considerations), in which case the risk assessor and risk manager can jointly agree on which subgroups to highlight, or a matter of discovery of a sensitive or highly exposed subgroup during the assessment process. In either case, once identified, the subgroup can be treated as a population in itself, and characterized in the same way as the larger population…’’ But, despite EPA’s official guidance to agency risk assessors directing them to take account of susceptible subgroups, there is no formal EPA guidance or policy on how to do it. In general, there are three ways to incorporate susceptibility into health risk assessments (Grassman, 1996b): (1) risk can be measured or estimated in the subpopulation with the identified susceptibility factors; (2) risk can be measured or estimated in the general population and then divided by a scaled uncertainty factor; or (3) risk can be measured or estimated in the general population and then divided by a default uncertainty factor. Selection of a particular approach depends on variables such as the type of susceptibility factor, the nature of the relationship between exposure, susceptibility, and outcome, the adequacy of available scientific information, the purpose of the assessment, and institutional constraints (e.g. resources). As a practical matter, data deficiencies usually prevent risk assessors from using the first approach, forcing them, if they consider susceptible populations at all, to use uncertainty factors.
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As Grassman (1996a) has pointed out, epidemiologic studies have not historically provided the kind of doseresponse information needed to calculate risk to susceptible populations. Several reasons for this deficiency were listed: failure to evaluate potential susceptibility factors; incorrect identification of susceptibility factors; inclusion of susceptibility factors with questionable environmental etiology; inadequate documentation of exposures; incomplete documentation of adverse health outcomes; and failure to take account of multiple susceptibility factors. To be able to incorporate susceptibility into quantitative risk assessments, assessors need rigorous epidemiologic studies, in combination with clinical and animal toxicology studies, that document the exposure–response (or dose – response) relationship for important susceptibility factors. Until such studies are available, however, quantitative assessment of risks to susceptible groups are not feasible in most cases. Due to the fact that risk-based decision making is integral to implementation of pollution control strategies, the problems of assessing risks to susceptible populations have potentially consequential implications for safeguarding environmental health. Of particular concern is the possibility that current risk assessment and risk management approaches do not provide adequate protection for disadvantaged groups.
6. An environmental justice critique of risk assessment Much of the current EPA focus on incorporating susceptibility into risk assessments stems from concerns about ‘environmental justice’ (Sexton et al., 1993a; Cotton, 1994; Kraft and Scheberle, 1995; Perlin et al., 1995; Ringquist, 1997; Zimmerman, 1993, 1997). A growing body of evidence indicates that low-income groups, a disproportionate percentage of whom are people of color, tend to be both more exposed to environmental chemicals and more susceptible to related health effects than the general population. This situation has spurred calls for environmental justice, which can be broadly defined as adequate protection from the health effects of pollution for everyone in our society, regardless of age, culture, ethnicity, gender, race, or socioeconomic status. Some scientists, legal scholars, and environmental justice advocates assert that the existing risk assessment methodology/process is a major cause of inequity and injustice (Israel, 1995; Kuehn, 1996). The proponents of this view allege that EPA’s risk assessments systematically undervalue environmental health risks for poor communities and people of color, thereby creating an excessive burden of pollution and environmental hazards for low-income groups and racial minorities. A central theme in these ‘environmental justice’ critiques is the failure of tradition methods, practices, and pro-
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cesses to incorporate susceptibility adequately into health risk assessments. Israel (1995) lists four major objections to the risk assessment process that are commonly raised by environmental justice advocates: (1) health studies and risk assessments are used to justify government inaction in the face of real risks; (2) risk management decision making is politically motivated, ignoring risks experienced in poor and minority communities; (3) scientific risk assessments fail to account for community perceptions of risk; and (4) the risk assessment methodology is itself discriminatory. It has been suggested that this last criticism is based on informational biases that occur within the process, which keep regulatory agencies from adequately considering unusual exposure patterns and unusual susceptibilities. As a consequence, Israel argues that risk assessments distort the true nature of environmental health risks and lead to less-than-adequate protection for disadvantaged groups (Israel, 1995). To correct these informational bias problems and create a more equitable risk assessment process, Israel recommends the following changes to the process: (1) more effective and exhaustive gathering of relevant demographic data; (2) reduction of generalized exposure and susceptibility estimates; (3) public participation in the various stages of risk assessment decision making; (4) implementation of various mechanisms to impose the burden of demonstrating safety on the private sector; and (5) abandonment of generalized risk assessments in determining clean-up standards at specific sites. Similarly, Kuehn (1996) believes that because risk assessment fails to address issues like multiple and cumulative exposures, synergistic effects, increased susceptibilities, and qualitative aspects of risk, it seriously underestimates the magnitude of many risks, particularly for highly exposed and highly susceptible racial and ethnic subpopulations. Kuehn (1996) says that ‘‘as currently structured and as proposed for more widespread use, the process does not offer a safe haven from distributional inequities or from the dominating influences of resources and political power on environmental decision making. The hazards faced by people of color and lower incomes are likely to be given insufficient attention by quantitative risk assessment, and important non-quantitative aspects of risk will be left out of the decision-making process’’. As a remedy, Kuehn (1996) suggests the following changes: (1) to revise the methodology of quantitative risk assessment to address differences in the distribution of risk; (2) if critical risk-related information is missing, assume a reasonable worst case as an incentive for the private sector to fill important data gaps; (3) include more qualitative analyses in risk characterization; (4) provide a full, comprehensive, and understandable exposition of the uncertainties; (5) institute an open,
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accessible, and fair process for assessing and managing risks; and (6) change the current focus on management of risk to a more holistic approach that considers alternative processes and products that might prevent or avoid risk in the first place. According to Israel (1995), Kuehn (1996) and others concerned about environmental justice, the difficulty encountered by risk assessors in dealing with susceptibility issues has contributed directly to greater (and unacceptable) environmental health risks for low-income communities and people of color.
7. Confronting the dilemma of what to do The decision makers are confronted with a dilemma; how should potentially susceptible groups be accounted for in risk assessment and risk management decisions when the relationship between exposure and adverse health effects for the important susceptibility factors is unknown? In considering this conundrum, it is important to keep in mind that the most important risk-related question is not ‘are low-income, disadvantaged populations more susceptible to the adverse health effects of pollution?’, because most observers tend to agree that they probably are. The more consequential question is ‘how much more susceptible are they?’ If, for example, the variability in susceptibility within the general population is consistently less than 10-fold, then it is conceivable that risk assessors and managers do not necessarily have to take any extraordinary precautions to protect susceptible groups. If, on the other hand, susceptibility for highly sensitive groups is often an order of magnitude or more greater than that for the general population, then special risk assessment and risk management procedures may be required. The challenge, of course, is to know when and under what circumstances the latter situation prevails. An even more momentous question for many is whether risk assessment is part of the solution or part of the problem? As noted by Kuehn (1996), quantitative risk assessment typically squeezes out factors that cannot be quantified, lending support to Gresham’s Law —quantitative information of any kind tends to retard the circulation of qualitative information. He points out that EPA risk assessments are often criticized for giving more credence and weight to tangible factors that can be measured, at the expense of less tangible, less-easily-measured, though not necessarily less important, non-quantifiable variables. The result is that risk-based decisions are likely to be biased in favor of hard, quantifiable evidence and against soft, non-quantifiable aspects of risk. Consequently, there is a built-in, systematic bias, which hinders recogni-
tion that economically disadvantaged groups bear a disproportionate burden of risk. The title of this article asks whether class and race matter for realistic risk assessment. Despite the absence of systematically collected data, the weight of the evidence suggests the answer is an unequivocal ‘yes’. Environmental health risks are routinely higher for economically disadvantaged populations because they are both more exposed and more susceptible than the general population. To what extent elevated environmental health risks contribute to higher rates of morbidity and mortality for these groups is uncertain. Nevertheless, the fact that the current state of the science prevents us from quantifying the nature, magnitude, and scope of the effect should not be used as an excuse for doing nothing. To address susceptibility concerns, four complementary actions are warranted and should be undertaken now. First, develop formal procedures for implementing EPA’s Guidance for Risk Characterization, thereby providing mechanisms for considering susceptible populations, both quantitatively and qualitatively, as an integral part of risk assessment. Second, establish clear-cut procedures whereby decision makers must explicitly consider susceptible populations as part of risk management. Third, begin a comprehensive research program aimed at conducting well-designed scientific studies to characterize the relationship between exposure and health effects for important susceptibility factors, and fourth, implement a surveillance system that provides for the systematic, ongoing collection of exposure-related, health-related, and susceptibility-related information in economically disadvantage populations. These actions will go a long way toward achieving the vision espoused by Alexander Hamilton at the Constitutional Convention in 1787. There can be no truer principle than this…that every individual of the community at large has an equal right to the protection of government.
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