2
Establishing a Baseline

The premise of environmental justice is that communities with high concentrations of racial or ethnic minorities or low-income families are disproportionately exposed to a variety of environmental burdens and hazards. Of particular interest for this report is the specific claim that such exposures produce adverse health outcomes that are also borne disproportionately by these populations. An assessment of baseline data is therefore essential to ascertaining the relative role of environmental exposure in determining the health of a population.

This chapter first describes some of the data supporting a general conclusion that there are significant disparities in the health status of the communities of concern. It then examines what is known about disparities in exposures to environmental health hazards. Although the evidence is not as strong or as direct as that establishing disparities in health status, it is sufficient to conclude that in many communities such disparities are real and possibly quite substantial. The chapter then reviews the link between exposures to environmental health hazards and health status, with particular attention to the validity and strength of the inference that disparities in exposure are responsible, at least in part, for the disparities in health status.

Disparities in Health Status in the United States

An extensive body of literature documents the fact that not all segments of the U.S. population have experienced the same advances in health status and gains in life expectancy. Racial and ethnic minority groups, individuals of low socioeconomic status, and medically underserved populations, among others, face lower life expectancies and greater health problems than the middle- and upper-class U.S. white population (Council of Economic Advisors, 1998; National Center for Health Statistics, 1998a,b). Some of the disparities in health



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--> 2 Establishing a Baseline The premise of environmental justice is that communities with high concentrations of racial or ethnic minorities or low-income families are disproportionately exposed to a variety of environmental burdens and hazards. Of particular interest for this report is the specific claim that such exposures produce adverse health outcomes that are also borne disproportionately by these populations. An assessment of baseline data is therefore essential to ascertaining the relative role of environmental exposure in determining the health of a population. This chapter first describes some of the data supporting a general conclusion that there are significant disparities in the health status of the communities of concern. It then examines what is known about disparities in exposures to environmental health hazards. Although the evidence is not as strong or as direct as that establishing disparities in health status, it is sufficient to conclude that in many communities such disparities are real and possibly quite substantial. The chapter then reviews the link between exposures to environmental health hazards and health status, with particular attention to the validity and strength of the inference that disparities in exposure are responsible, at least in part, for the disparities in health status. Disparities in Health Status in the United States An extensive body of literature documents the fact that not all segments of the U.S. population have experienced the same advances in health status and gains in life expectancy. Racial and ethnic minority groups, individuals of low socioeconomic status, and medically underserved populations, among others, face lower life expectancies and greater health problems than the middle- and upper-class U.S. white population (Council of Economic Advisors, 1998; National Center for Health Statistics, 1998a,b). Some of the disparities in health

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--> status are associated with socioeconomic status. For example, at age 45, individuals with family incomes above $25,000 can expect to live from 3 to 7 years longer than those with family incomes below $10,000 (National Center for Health Statistics, 1998b). Also, the death rate from chronic disease for individuals ages 23 to 64 with less than 12 years of education is more than twice as high as that for comparable individuals with more than 12 years of education (National Center for Health Statistics, 1998b). Nonelderly adults living in poverty-stricken areas experience a significantly higher risk of mortality from all causes (Waitzman and Smith, 1998). Although the health status of all U.S. racial and ethnic groups has improved steadily, disparities in major health indicators between white and non-white groups are growing. In general, African Americans, American Indians, and Hispanics are dramatically disadvantaged relative to whites in terms of most health indices, whereas Asian Americans appear to be as healthy, if not healthier, than whites in terms of some indices. These overall group differences, however, mask important differences in the health statuses of subgroups. Americans of Southeast Asian descent, for example, suffer from among the highest rates of cervical and stomach cancers of all U.S. population groups and experience poorer health overall than U.S. whites (Miller et al., 1996). Socioeconomic status appears to operate in complex ways with race and ethnicity to account for the observed differences in health status. In general, white Americans enjoy higher incomes and education attainment levels than any other U.S. racial and ethnic group and therefore are more likely to have health insurance and to be better educated with regard to healthy behaviors and diets, are more likely to seek routine medical care, and are more likely to have better access to preventive medical services. Socioeconomic factors, however, do not completely account for racial and ethnic differences in health status (Williams et al., 1994). Several studies indicate that racial disparities in health status persist even when controlling for socioeconomic status (Advisory Board to the President's Initiative on Race, 1998). Mounting evidence indicates that in addition to resource inequities, other factors, including discrimination in the health care system, racism-related stresses, migration, and differences in levels of acculturation may also lead to poor health among members of racial minority groups (Council of Economic Advisors, 1998; Advisory Board to the President's Initiative on Race, 1998; Williams et al., 1994). As discussed later in this report, disparities in exposure to environmental hazards are also suspected as a factor in the relatively poorer health of individuals in minority and lower-income communities in the United States. The following examples show that significant disparities exist between U.S. racial and ethnic groups in terms of several key health indicators, even when socioeconomic differences are taken into account.

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--> Low Birth Weight During the period from 1989 to 1996, among women with 13 or more years of education, African American women were twice as likely as white women to give birth to low-birth-weight infants (infants weighing less than 2,500 grams [5.5 pounds]) (11.9 versus 5.5 percent). This occurred even though African American women are less likely than white women to smoke during pregnancy, which is considered an important factor in causing low birth weight. Similarly, the percentage of low-birth-weight infants was higher among American Indian women (6.0 percent), Asian or Pacific Islander women (6.8 percent), and Hispanic women (6.0 percent) than white women with similar levels of educational attainment (National Center for Health Statistics, 1998b). Infant Mortality From 1989 to 1991 African American women experienced an infant mortality rate over two and a half times higher than that experienced by white women with the same levels of education (13.7 versus 5.1 per 1,000 births). The infant mortality rates among American Indian women and Hispanic women with similar levels of education were 8.1 and 5.8 per 1,000 births, respectively (National Center for Health Statistics, 1998b). Death Rates African Americans experience higher mortality rates than whites even in areas with equivalent levels of urbanization. In large, core metropolitan areas, the mortality rate among African Americans between 1993 and 1995 was 810.5 deaths per 100,000 population, compared with a rate of 491.9 per 100,000 among the white population. This disparity in mortality is also pronounced in other geographic areas: the mortality rates among African Americans in rural and urban, nonmetropolitan areas were 737.1 and 761.9 per 100,000 population, respectively, compared with rates of 503.9 and 499.4 per 100,000 population, respectively, among whites (National Center for Health Statistics, 1998b). Cancer In general, African American males experience cancer approximately 15 percent more frequently than white males, with incidence rates of 560 and 469 per 100,000 population, respectively. The pattern of cancer incidence rates among males in other racial and ethnic groups is more varied, but disparities are exhibited in specific cancer sites. For example, colon and rectal cancers are more common among Alaskan Native men (79.7 per 100,000 population) and

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--> Japanese American men (64.1 per 100,000 population) than white men (57.6 per 100,000). Racial and ethnic minorities also experience higher rates of mortality from cancer than whites (Parker et al., 1998). Disparities in Exposure to Environmental Hazards Many communities contain environmental hazards that represent potential sources of health risks (for examples, see Table 2-1). Although these can affect all racial, ethnic, and socioeconomic groups, there is evidence that minorities and lower-income groups face higher levels of exposure to these hazards and, therefore, potentially higher rates of adverse health outcomes. It has been shown, for example, that non-whites are disproportionately exposed to ambient air pollutants associated with respiratory symptoms and exacerbation of other ailments (see Table 2-2). One method of determining the potential for increased exposure is to examine the proximity of communities of concern to waste or industrial facilities. Another, more accurate way is to characterize the nature and level of exposures by either direct measurement or estimation. Both of these methods are described below. Examining Proximity to Environmental Health Hazards Numerous studies have shown that race is associated with increased levels of exposure to environmental hazards. The Commission for Racial Justice of the United Church of Christ published a report in 1987 entitled Toxic Wastes and Race in the United States (United Church of Christ Commission for Racial Justice, 1987) and updated it in 1994 (Goldman and Fitton, 1994). The major finding of these studies was that communities that had one or more commercial hazardous-waste facilities had significantly higher proportions of racial minority Table 2-1 Examples of Potential Sources of Environmental Health Hazards Sources Substances Agricultural runoff Allergens Incinerators Heavy metals Industrial facilities Paints and oil wastes Landfills Particulate matter Toxic-waste sites Pesticides and herbicides Waste treatment facilities Radioactive wastes   Solvents   Volatile organic compounds

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--> Table 2-2 Percentage of White, African American, and Hispanic Populations Living in Air Quality Nonattainment Areas, 1992   Percentage     Pollutant White African American Hispanic Particulates 14.7 16.5 34.0 CO 33.6 46.0 57.1 Ozone 52.5 62.2 71.2 SO2 7.0 12.1 5.7 Lead 6.0 9.2 18.5 NOTE: Nonattainment areas refer to those areas that do not meet the National Ambient Air Quality Standards for various pollutants. SOURCE: Wernette and Nieves, 1993. populations than communities with no commercial hazardous-waste facilities. In the United States in 1993, for example, the percentage of people of color (defined as everyone except non-Hispanic whites) was 14.4 percent in zip code areas with no commercial hazardous-waste facilities, 29.5 percent in areas with one facility, and 45.6 percent in areas with three or more facilities, an incinerator, or a large landfill. A similar trend had been evident in 1980. Communities with lower per capita incomes were also more likely to be situated near commercial hazardous-waste sites as well. The original study was one of the important factors in motivating a substantial response to the environmental justice issue from the federal government. Another national study of hazardous-waste sites used census tracts as the unit of analysis as opposed to zip codes (Anderton et al., 1994). Anderton and colleagues examined the differences in race, class, and economic indicators between the populations in census tracts with treatment, storage, and disposal facilities (TSDFs) and those without TSDFs. Although they found no difference in the mean percentage of the population that was African American, that had incomes below the poverty level, or that was on welfare, they did find differences in the percentages of the population that were Hispanic (9.4 percent in census tracts with one or more TSDFs and 7.74 percent in those with none) and that were employed in manufacturing (38.6 and 30.6 percent, respectively). Additionally, Anderton and colleagues (1994) found that the differences became more noticeable in the areas surrounding the census tracts with TSDFs—that is, tracts with TSDFs and ''other tracts that have at least 50 percent of their area within a 4-kilometer (2.5-mile) radius of the center of a tract containing a TSDF" (Brown, 1995, p. 18). Using that level of analysis, Anderton and colleagues found that populations of the areas surrounding TSDFs have higher mean percentages of African Americans (24.7 percent, compared with 13.6 percent in census tracts outside the larger unit of analysis), of Hispanics, (10.7 and

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--> 7.3 percent, respectively), of people with incomes below the poverty level (19.0 and 13.1 percent, respectively), and of people on welfare (13.3 and 8.3 percent, respectively). These results are congruent with those from the United Church of Christ Commission for Racial Justice. American Indians have also been the focus of concerns about exposure to environmental hazards. For example, uranium ore was discarded on Navajo lands in New Mexico during the 1950s (Johnson and Coulberson, 1993). An investigation by the Agency for Toxic Substances and Disease Registry found radiation levels in private residences high enough to cause health concerns, and the discarded ore was removed by the Environmental Protection Agency (EPA) and the Navajo Superfund office. Although it is not currently possible to know the extent to which the environmental concerns faced by American Indians are unique to them, additional site-specific health surveillance studies of this population are under way (Johnson and Coulberson, 1993). The establishment of causal relationships between a health condition and the siting of environmental hazards in proximity to low-income or minority communities is a complicated and debatable exercise. Were waste sites purposely located in these communities because of discriminatory motivations, because of the lack of politically effective opposition, because land was cheap, or because of a combination of these and other factors? Were the communities characterized by the same socioeconomic and racial or ethnic indicators when the waste sites were originally established, or did the composition of the communities evolve later, as a result of economic or other factors? The economics of land values, job opportunities, and transportation undoubtedly assert a strong influence on these outcomes, and the circumstances undoubtedly vary greatly from locale to locale. For the purposes of this report, however, the committee did not believe that it was essential to try to reach conclusions about causality or motivation; no matter how a particular condition came to be, if it represents an environmental health hazard and if the burdens of such a hazard are borne inequitably, then it is appropriate to assess the scope and severity of the health burden and to evaluate potential means of ameliorating it. Characterizing Exposure Proximity to a source is an inexact surrogate of actual contact with toxicants from the source. Quantification of the actual emissions from the source moves the analysis a step closer to measuring actual human exposure to an environmental health hazard. This requires estimating the rate of release and the path of the material into and through the environment. For example, in one community that the committee visited (Tucson, Arizona), a common industrial practice, begun in the 1940s, was dumping organic-solvent waste into earthen ponds. This source released toxicants in two ways: (1) the solvents evaporated from the ponds, creating an airborne means of exposure for workers and the residents in surrounding communities, and (2) the solvents migrated from the ponds into the

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--> ground, where they eventually entered the subsurface water resources that the community used for its domestic water. Measurements of the concentrations in the air and water can help public health practitioners determine the total possible exposure. The characterization of exposure in the community requires an understanding of all of the potential pathways by which pollutant releases may result in exposure. This includes direct pathways such as through the air and drinking water and less obvious pathways such as through uptake by food sources. Studies of this nature need to be sensitive to the ways in which differences in behavior, employment, and lifestyles among subgroups in the population may result in differences in exposure. For example, among the Alutiiq, Yup'ik, and Inupiat Alaskan Native peoples, the yearly intake of wild foods per person is between 171 and 272 kilograms (375 and 600 pounds). Increasing evidence of certain contaminants such as mercury in the wild food supply of these Alaskan Natives has been exhibited by methyl mercury levels that exceed those provisionally established as safe by the World Health Organization. Research that did not account for the variable ingestion of contaminated foodstuffs would fail in determining the relative effects of exposures across populations. As the focus of analysis moves from sources and releases to environmental concentrations, the quality and quantity of the data currently available decrease significantly. Of the more than 60,000 chemicals in commercial use in the United States, data on the concentrations of chemicals in the environment are available for only a small number (National Research Council, 1984; Roe et al., 1997). One systemic gap is measures of indoor concentrations, even though the U.S. population spends much of its time indoors (Environmental Protection Agency, 1993); most monitoring systems focus on the concentrations outdoors or in the workplace. A more accurate description of the amount of toxicants absorbed requires data on actual doses received by humans. Analysis of biological samples (e.g., urine or blood samples) from affected populations can lead to more accurate descriptions of exposure to an environmental health hazard (National Research Council, 1989b), but the samples can be difficult to obtain. Methods for tissue analysis are also limited. The environmental toxicant for which the largest amount of data is available is lead (National Research Council, 1993). It causes a variety of health problems, including neurodevelopmental effects in infants and children and cardiovascular effects in adults. Exposure to lead can be determined by measuring the level of lead in blood. Harmful health effects have been identified for levels of lead in the blood that are greater than or equal to 10 µg/dl. There are multiple sources of lead exposure, with lead-based paint being the most common. Consequently, exposure is high in urban areas, where housing is often old and likely to be coated with lead-based paint. Blood lead levels are consistently higher for poor and minority children and for residents of central cities (Brody et al., 1994; Centers for Disease Control and Prevention, 1991, 1997).

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--> Examining the Link Between Exposure and Health Having concluded that there are clearly disparities in health status and that there are significant disparities in exposure to environmental hazards, the next step in analyzing the issue of environmental justice is to determine whether there are causal relationships between exposure to these hazards and health outcomes and whether the disparities in health status can be attributed to the disparities in exposure. For many of the identified potential environmental hazards, the lack of published research makes it difficult to draw a strong conclusion that disparate exposures result in disparate health outcomes. The difficulties encountered in this type of research are illustrated in the work of Baden and colleagues (1996), who tried to examine both the interactions of multiple environmental hazards and the possible connections of these hazards to adverse health outcomes. They included in their analysis the siting of several possible environmental hazards in the Chicago metropolitan area: the large areas of waste regulated under the Comprehensive Environmental Response, Compensation, and Liability Act of 1980 (the Superfund law), waste-generating sites regulated by the Resource Conservation and Recovery Act, older existing waste disposal sites such as landfills, and emissions from highway exhaust. They conducted regression analyses of census-tract data examining the relationships between proximity to waste disposal sites and poor infant health. The research was unable to account for "causal links between hazardous-waste and ill health effects, … occupational exposure to toxins, parental bioaccumulation of toxins, [or] medically risky behavior such as drinking and use of illegal drugs while pregnant" (Baden et al., 1996, p. 25). The researchers also noted that "use of the census tract for analysis may introduce some aggregation bias" (p. 25). Within these constraints, they concluded that "there was no relationship between the presence of waste sites and low birth weight for children born in Chicago in 1990. … Neither was there one single type of waste site associated with adverse health outcomes, nor did a combination of all of the waste sites (insignificant in themselves) combine to produce adverse infant health outcomes" (p. 26). The researchers' final conclusion was, ''Future research must address these issues" (p. 25). Ecologic studies such as these are subject to a variety of potential biases in addition to the aggregation bias noted by the authors, and are not by themselves adequate for making or excluding causal connections (Greenland and Robins, 1994). In spite of the general lack of published research linking disparate exposures to disparate health outcomes, some well documented links do exist. One such study used field epidemiology methods combined with a prevention intervention trial to document definitively a link between disparate exposure to dimethylformamide and disparate prevalence of toxic liver disease (Friedman-Jiménez and Claudio, 1998; Redlich et al., 1988).

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--> Lack of Health Status Characterization One of the shortcomings in the available literature is that most of the reported studies of environmental justice have characterized disparities only in terms of proximity to potential sources of exposure or, in a few cases, to measured exposures and have not taken the next step of trying to characterize or quantify either exposure or potential differences in health status or disease incidence between these populations and the general population (Bullard, 1990; Glickman et al., 1995; Greenburg, 1993; United Church of Christ Commission for Racial Justice, 1987; U.S. General Accounting Office, 1983; Zimmerman, 1993). Few studies have looked directly at whether local, residential exposure to environmental agents is associated with an increased incidence of disease (Sexton et al., 1993; Wagener et al., 1993). Part of this shortcoming may be due to the fact that, except for some hazards such as lead (see Characterizing Exposure above), little is known about the physiologic or biological mechanisms by which the health hazards cause disease. Although the toxicologies of ozone and other air pollutants have been extensively studied, the mechanisms by which such gases and particles injure the lungs are diverse and not yet fully understood. The goal of fully understanding the effects of any air pollutant has been described as a "daunting task" (Brooks et al., 1995). A large proportion of what is known about disease processes has come from research in the occupational health field. Examples include lung diseases due to dusts (e.g., silica, coal, cotton), the systemic and lung toxicities of metals (e.g., lead, mercury, cadmium, beryllium, and hard metals) and many carcinogens (e.g., asbestos, hexavalent chromates, nickel, vinyl chloride, polycyclic aromatic hydrocarbons, radon, and bischloromethyl ether), and the neurotoxicities of a variety of pesticides and solvents. The lack of knowledge about the specific disease process does not, however, preclude the use of epidemiologic methods to explore possible associations between hazards and disease. The air pollutants listed in Table 2-2 have long been associated with clinically significant adverse health effects, including decreased respiratory function, respiratory infections, the exacerbation of asthma, chronic obstructive pulmonary disease, congestive heart failure, and increased mortality (Brooks et al, 1995). A recent National Research Council report (1998) describes how epidemiologic research has established consistent associations between exposure to outdoor concentrations of small particulate matter (particles smaller than 2.5 micrometers [0.006 inches] in diameter) and the adverse health effects described above. Although the biological basis for such associations is largely unknown and there is limited scientific information about the specific types of particles that cause these health effects, the results of these epidemiologic studies have been relied upon by EPA in setting national ambient air quality standards (National Research Council, 1998). Thus, at least for some air pollutants and lead poisoning, there is strong evidence to support the connection between disproportionate exposure and disproportionate health outcome.

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--> Failure of Differentiation of Populations and Differences in Outcomes A second shortcoming in the literature is the converse of the first, namely, that studies of adverse health effects fail to differentiate the population by race, ethnicity, or socioeconomic class and examine differences in outcomes among them (Frumkin and Walker, 1997). As noted above, occupational health studies are a primary source of knowledge about the health effects of various hazards. However, only a small fraction of the existing occupational health research has provided meaningful information on either the prevalence of occupational diseases in specific racial, ethnic, or socioeconomic population groups or the relation of race, ethnicity, and socioeconomic factors to occupational health. For example, in one systematic review of 116 studies of the epidemiology of occupational cancer published in four journals, only 14 studies (12 percent) provided data on a "non-white" group. The investigators concluded that the published literature contributes little to understanding the complex relationships among occupation, cancer, and race (Kipen et al., 1991). One rationale given for the exclusion of minority subgroups is that the number of subjects would be too small to provide an acceptable statistical power to test the primary study hypotheses with these subgroups. (Appendix A discusses these and other related issues in greater depth.) Other reasons include difficulties in long-term follow-up; inadequate measurement, classification, and reporting of data on race, ethnicity, and relevant socioeconomic variables (Feinleib, 1993; Montgomery and Carter-Pokras, 1993); and difficulties in researcher access to high-risk workplaces that employ low-wage workers. A Case Study: Urban Asthma Many of the challenges posed by an analysis of environmental justice issues are illustrated by the example of urban asthma. A doubling in the rate of asthma in the United States since 1980 and its apparent association with industrialized, urbanized areas has led some investigators to suspect increased levels of exposure to environmental factors as one possible cause (Vogel, 1997). As noted above, Hispanics and African Americans are more likely than whites to live in areas where the levels of particulates, sulfur dioxide, and ozone exceed National Ambient Air Quality Standards—circumstances that may contribute to the prevalence and severity of asthma. The prevalence of asthma appears to be more strongly correlated with lower socioeconomic status than with race and ethnicity (Institute of Medicine, 1993). However, the use of data on numbers of hospitalizations, or emergency room visits or even the rate of morbidity due to asthma as a measure of the relative impact of environmental hazards on those with low socioeconomic status is problematic, because these indicators may be strongly influenced by other factors such as lower rates of health insurance or lower levels of access to high-quality primary health care.

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--> The rates of hospitalization and morality due to asthma are higher in urban, low-income, or minority communities (Weiss and Wagener, 1990; Weitzman et al., 1990). For example, in New York City, African American, Hispanic, and low-income populations were found to have hospitalization and mortality rates from asthma three to five times higher than those for the general New York City population (Carr et al., 1992). African American children are three times more likely than white children to be hospitalized for asthma and asthma-related conditions and four to six times more likely to die from asthma (Mannino et al., 1998; Stapleton, 1998). These data might be viewed as demonstrating that urban asthma is an environmental justice problem. The situation is quite complicated, however, and a conclusive finding of an environmental justice problem is not free of doubt. First, the clinical diagnosis of asthma is not entirely clear-cut, and diagnostic methods and accuracy may vary among different population groups (Gergen, 1996). Second, the etiology of asthma is complex and multidimensional. A variety of toxic, allergenic, dietary, and infectious agents, as well as genetic and acquired susceptibility factors, contribute to the disease. Environmental agents that may induce new-onset asthma or that may aggravate preexisting asthma may come from outdoor or indoor sources at home, work, school, or other locations. Studies have shown that important sources of allergens for asthmatics are household dust mites and cockroaches, which are more likely to be present in urban settings and which are more likely to be encountered by children who spend a great deal of time indoors (Vogel, 1997). Consequently, the attribution of causality to a specific environmental hazard and apportionment of causality among various potential causes are exceedingly difficult if not impossible at this time. Conclusions Not all segments of the U.S. population have benefited to the same extent from advances in health status and gains in life expectancy. Racial and ethnic minority groups, individuals of low socioeconomic status, and medically underserved populations, among others, face lower life expectancies and greater health problems than the U.S. white population (Council of Economic Advisors, 1998; National Center for Health Statistics, 1998b). In addition, many communities contain potential sources of environmental health risks (e.g., industrial facilities, waste treatment sites, or waste disposal sites). These can affect all racial, ethnic, and socioeconomic groups, but there is substantial evidence that minorities and lower-income groups face higher levels of exposure to these hazards in terms of both frequency and magnitude. Although direct links between exposures and health are weak in many instances, the committee believes that allegations of environmental justice problems are frequently well founded and must be taken seriously enough to warrant careful assessment.

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