The stress–exposure disease framework () provides a conceptual framework from which to understand the relationships among race, environmental conditions, and health. It extends the framework of Sexton et al. (1993)
) explicitly hypothesizing that residential segregation is a major reason why “race” is important; b
) incorporating an ecological or multilevel perspective; and c
) arguing that racial variation in stressors may account for differences in vulnerability to health risks.
Exposure–disease–stress model for environmental health disparities.
Reflecting the multilevel approach, emphasizes both community processes (top) and individual mechanisms (bottom). The shading reflects the exposure–disease paradigm. To simplify our presentation, we have separated individual and community processes. However, many processes are interrelated. For example, community wealth is partly a function of individual wealth (e.g., when individuals contribute to the tax base), and individual wealth is also partly determined by community wealth (e.g., when rising property values benefit individual homeowners).
The framework shows that ethnicity is highly correlated with residential location, with minorities and whites often living segregated from one another. Differential residential location comes with differential exposure to health risks. In particular, neighborhood stressors and pollution sources create adverse health conditions, which are counterbalanced by neighborhood resources. Structural factors help determine the boundaries from which health promotion is possible and partially determine the contemporary state of stressors, resources, and pollution in a community. When community stressors and pollution sources outweigh neighborhood resources, levels of community stress manifest or increase. Community stress is a state of ecological vulnerability that may translate into individual stressors, which in turn may lead to individual stress. Individual stress may then make individuals more vulnerable to illness when they are exposed to environmental hazards. Further, compromises in individual and community health may further weaken community resources, leading to a vicious cycle. Hence, we include in our framework a return loop from health back to stress.
As an example, zoning policies and tax incentives (structural factors) may encourage the entry of new pollutant industries. The increase in pollutants may lead to economic and social uncertainty (stressors) by driving down local property values, increasing the flight of jobs and fostering a climate of uncertainty and fear. Neighborhood organizations (resources) may not be able to counterbalance these effects, leading to a state of community vulnerability (community stress). Community-level vulnerability, in turn, may translate to individual vulnerability, such as when individuals lose their jobs or become anxious about perceived toxic exposures. When personal coping resources do not adequately counterbalance these external insults, individual stress and illness may result. Individual illness, in turn, may lead to further individual vulnerability, such as by reducing the ability to exercise. Additionally, individuals may affect their communities, such as when disaffected individuals cease participating in neighborhood organizations. Health disparities may arise because minorities are segregated into neighborhoods with high levels of community stress.
We do not explicitly examine the issue of genetic susceptibility in this framework for three reasons. First, we focus on factors that are amenable to policy change and social action. Second, genetic susceptibility is partly subsumed in the exposure–disease paradigm because it is presumed to partially determine one’s ability to defend against hazards. Third, although genetic factors are important in the etiology of many illnesses, it is likely that genetic factors do not explain racial health disparities (Cooper 1984
; Cooper et al. 2003
; Garte 2002
; LaVeist 1994
). It is often acknowledged that race is a social construct. What that means is that racial groups are not inherent biological taxons, but represent societally defined categories during a particular point in history and place. For example, before 1989, the child of a black father and a white mother would be classified as black, but after 1989, the same child would be classified as white (LaVeist 1994
). Further, a child born in Brazil, rather than the United States, would be classified as mulatto. Thus, racial designations are the product of social consensus and public policy, rather than biology per se.
Additionally, “genetically identified” groups tend to correlate poorly with socially identified groups because there is more genetic variation within than between groups (Garte 2002
; Lewontin 1982
; Mountain and Cavalli-Sforza 1997
). For example, genetic differences between any two Italians appear to be 5-fold greater than the difference between an Italian and a Japanese, African, or New Guinean (Mountain and Cavalli-Sforza 1997
). Observations such as these have led Cooper et al. (2003)
to conclude that race “has not shown to provide a useful categorization of genetic information about the response to drugs, diagnosis, or causes of disease.”
We now review the science that informs this framework, beginning with the exposure–disease paradigm.
The Exposure–Disease Paradigm
The exposure–disease paradigm is a well-known model that shows how environmental toxicants might cause disease (Lioy 1990
; Lioy and Pellizzari 1995; National Research Council, 1991a
; Wagener 1987
). It is a continuum that includes the emission of a contaminant from a source through human exposure to the occurrence of a health effect.
Susceptibility/vulnerability intersects the continuum, increasing or decreasing resistance to absorption and/or effect from toxicants. The term “susceptibility/vulnerability” has been used broadly to cover both biological and non-biological factors, including genetic predisposition, pre-existing health conditions, and social conditions. The exact susceptibility/ vulnerability factors and their pathways intersecting the exposure–disease paradigm are not well understood. We argue later that community and individual stress is one type of susceptibility factor.
Race and Residential Location
Segregation, the spatial separation of the residences of racial groups from one another, has persisted for many decades (Iceland et al. 2002
; Massey 2001
; Massey and Denton 1993
). shows the segregation of blacks, Hispanics, Native Americans, and Asians compared with whites from 1980 to 2000 for metropolitan areas, as measured with the index of dissimilarity (Logan 2003
; U.S. Census Bureau 2003
). Scored from 0 to 100, a given value of the index indicates the percentage of that group who would have to move to integrate the metropolitan area.
Segregation of ethnic minorities compared with whites, United States, 1980–2000.
Segregation from whites is highest for African Americans, followed by Hispanics, Asian Americans, and Native Americans. In the average U.S. metropolis in the year 2000, about two-thirds of blacks (or whites) would have to move to another neighborhood in order to desegregate that metropolis.
Black–white and Native-American–white segregation has declined since the 1980s, but segregation levels for Hispanics and Asians have remained stable. Further, most of the decline in black–white segregation has occurred in metropolitan areas with the fewest numbers of blacks (Logan 2003
The causes of segregation are still debated. Some have suggested that segregation is an artifact of broader shifts in the economy—including the decline of manufacturing jobs and suburbanization—that have left behind a cadre of the poor that are disproportionately racial minorities (Wilson 1987
). Others have postulated that segregation results from personal preferences of homebuyers to cluster together (Schelling 1971
). Most research has argued that segregation results from institutionalized discriminatory practices in the housing market (e.g., mortgage redlining, racialized “steering”) that persists to the current day (Massey and Denton 1993
; Meyer 2000
; Munnell et al. 1996
; Schwartz 1998
; Squires 1994
; Squires and Velez 1996
Some evidence suggests that the mechanisms for segregation vary by ethnic group and region, but most ethnic groups have encountered discriminatory treatment historically and currently (Squires 1994
; Feagin and McKinney 2003
; Krieger et al. 1993
; Williams et al. 1997
). For example, a recent audit study suggested that consistent adverse treatment in home buying was similar for Asian-American and African-American homebuyers, with one in five potential homebuyers disfavored compared with whites (Turner and Skidmore 2001
). The causes of segregation notwithstanding, it is clear that neighborhoods do cluster on the basis of race and ethnicity.
Studies have reported that segregation is associated with numerous outcomes, including infant mortality [Centers for Disease Control and Prevention (CDC) 2002
; LaVeist 1989
], adult mortality (Hart et al. 1998
; Jackson et al. 2000
; Polednak 1991
), tuberculosis (Acevedo-Garcia 2003
), homicide (Peterson and Krivo 1993
), teenage childbearing (Sucoff and Upchurch 1998
), exposure to tobacco and alcohol advertising (Alaniz 1998
; Luke et al. 2000
; U.S. DHHS 1998
), and increased exposure to air pollution (Lopez 2002
Segregation may thus be one critical link between race and environmental health disparities because racial groups, on average, occupy different residential areas. This may lead to differential exposure to health risk factors as well as differential access to resources. Segregation is multifactorial, often conceptualized around five dimensions (Acevedo-Garcia 2000
; Massey and Denton 1988
) evenness, the inequitable distribution of groups over an area and the dimension receiving the greatest empirical study; b
) isolation, the degree of potential contact between two groups within a city; c
) concentration, the extent to which minority groups are confined to a compact area within the city; d
) centralization, the degree to which minorities are clustered around the center of a city; and e
) clustering, the extent to which minority neighborhoods are adjacent to one another. Our discussion refers to the general principle of segregation, although it will be an important research endeavor to examine which specific dimensions of segregation are related to environmental health disparities.
Having established a link between race and residence, we now turn to the proximal mechanisms that may account for the relationship between environmental conditions and racial health disparities.
Environmental Hazards and Pollutants
Briefly, environmentally relevant disparities are evident in a variety of outcomes, including asthma, cancer, and chemical poisoning (Institute of Medicine 1999
). Although debated, the main hypothesis explaining these disparities is that disadvantaged communities encounter greater exposure to environmental toxicants such as air pollution, pesticides, and lead (Burger et al. 2001
; Calderon et al. 1993
; Corburn 2002
; Fitzgerald et al. 1998; Institute of Medicine 1999
; Morello-Frosch 2001
; Moses et al. 1993
; Northridge et al. 2003
; Perera 2003
; Pirkle et al. 1998
; Woodruff et al. 2003
). Mediators of the relationship between toxic exposure and disadvantaged status include the siting of pollution sources (e.g., waste incinerators), illegal dumping, poor enforcement of environmental regulations, and inadequate response to community complaints (Anderton et al. 1994
; Bullard 1983
; Bullard and Wright 1993
; Goldman and Fitton 1994
; Institute of Medicine 1999
; Maantay 2001
; Mohai and Bryant 1992
; Perlin et al. 1999
, 2001; United Church of Christ 1987
; U.S. General Accounting Office 1983
Structural factors refer to the historically evolving infrastructure that provides boundaries for health promotion. That is, structural factors are constraints that shape how new conditions emerge as “salutogens” (factors that support health) or pathogens in a community. The local economy, for example, is a structural factor that will help determine a community’s ability to mobilize resources in order to reject undesirable changes (e.g., introduction of a waste facility) or develop desirable ones (e.g., construction of a park). Structural factors that may be especially pertinent to environmental health disparities include the local and national economy, neighborhood physical conditions, land use patterns, and health infrastructure. This is not an exhaustive list, but rather is meant to be illustrative.
One primary effect of residential segregation may be to concentrate disadvantage (Massey and Denton 1993
). Compared with whites, minorities are overrepresented in neighborhoods with diminishing and constrained economic opportunities (Jargowsky 1997
; Wilson 1987
). For example, in Los Angeles, California, in 1990, only 4.9% of blacks lived in high-job-growth areas, compared with 52.3% of whites (Pastor 2001
). Cutler and Glaeser (1997)
reported that a decrease in segregation by one standard deviation (13%) would eliminate one-third of the black–white differences in education and employment. Thus, segregation not only may concentrate poverty but also may be partly responsible for the production of poverty among racial minorities (Massey and Denton 1993
; Williams and Collins 2001
Neighborhood economic deprivation may compromise health-promoting resources (Diez-Roux et al. 2001
). For example, poor and minority neighborhoods tend to have fewer grocery stores with healthy foods (Morland et al. 2002
) and fewer pharmacies with needed medications (Morrison et al. 2000
). Poor nutrition can increase susceptibility to environmental pollutants by compromising immune function (Beck and Weinstock 1988
; Rios et al. 1993
). Additionally, disadvantaged neighborhoods are also exposed to greater health hazards, including tobacco and alcohol advertisements, toxic waste incinerators, and air pollution (Morello-Frosch et al. 2002
). Finally, economic stress within a community may exacerbate tensions between social groups, magnify workplace stressors, and induce “maladaptive” coping behaviors, such as smoking and alcohol use (Brenner 1995
). Tobacco and alcohol use can increase susceptibility to environmental toxicants that are normally metabolized by impairing host defense (Rios et al. 1993
In general, racial minorities have lower socioeconomic position compared with whites. Although it is intuitive to hypothesize that disparities in health arise because of socioeconomic differences between racial groups, studies often find that racial disparities persist even after accounting for socioeconomics factors (Hayward et al. 2000
; Sorlie et al. 1995
; Williams 1999
Although socioeconomic differences do not completely explain racial disparities, it is often argued that social class is an important mediator. That is, it is hypothesized that race determines one’s economic resources, which in turn determine health (Williams and Collins 1995
). Thus, although socioeconomic conditions do not fully account for health disparities, they are a necessary part of the equation.
Neighborhood physical conditions present another structural factor that may contribute to health disparities (Cohen et al. 2003
). Minorities are more likely to live in areas with building code violations and neighborhoods with deteriorated housing (Perera et al. 2002
; Rosenbaum et al., unpublished data). In 1999, 3.4% of blacks, 3.8% of Hispanics, and 1.7% of Asian Americans and Pacific Islanders reported living in housing units with severe problems with heating, plumbing, electricity, public areas, or maintenance, compared with 1.5% of whites (U.S. Census Bureau 2000
). Substandard housing may contribute to a variety of problems, including exposure to toxicants, increased risk of injuries from falls and fires, and illness due to ineffective waste disposal and presence of disease vectors (Bashir 2002
; Jacobs et al. 2002
; Krieger and Higgins 2002
; Northridge et al. 2003
Urban minorities tend to fare worse than their counterparts in rural areas (Geronimus et al. 1999
; Geronimus et al. 2001
). This may be due in part to land use patterns in urban areas. In Detroit, many minority neighborhoods exist next to highways that expose residents to hazards (Schulz et al. 2002
). Sugrue (1996) argues that
Detroit’s highway planners were careful to ensure that construction of new … expressways would only minimally disrupt middle-class residential areas, but they had little such concern for black neighborhoods.
Similarly, New York City rezoned its neighborhoods between 1961 to 1998 so as to increase manufacturing zones in areas with higher minority populations and to decrease those zones in areas with fewer minorities (Maantay 2001
). Those rezoning efforts led to a higher concentration of industrial burden within manufacturing-designated areas. Further, some policies that appear neutral prima facie may result in adverse impacts on already disadvantaged communities, as in the example of emissions trading systems and their potential to create pollution “hot spots” (Schmidt 2001
; Soloman and Lee 2000
Health infrastructure may also be associated with race. Minorities tend to reside in areas with a lower physician-per-population ratio and lower medication supply (Morrison et al. 2000
; Rosenbaum et al., unpublished data; Schulz et al. 2002
). Community hospitals are more likely to close in urban minority communities (Whiteis 1992
). These findings suggest that segregated communities face structural disadvantages in the provision of health services.
Community Stressors Health effects of stress.
Stressors can trigger the sympathoadrenal system, whose hallmark is rapid release of adrenalin and noradrenalin, which leads to various “fight or flight” responses, including arousal, bronchodilation, tachycardia, and increased blood pressure. The hypothalamic–pituitary–adrenal system is also activated, signified by release of corticotrophin-releasing factor, adrenocorticotropic hormone, and cortisol. These glucocorticoids have several metabolic and psychological effects, including the mobilization of energy reserves, suppression of the immune system, and heightened vigilance. Chronic activation of the stress system is believed to lead to allostatic load, which is the “wear and tear” on organ systems resulting from stress (McEwen 1998
). A full discussion of the biology of stress is beyond the scope of this article but can be found in several publications (Brunner 2000
; Hadley 1992
; McEwen 1998
The key point is that stressors can cause illness by weakening the body’s ability to defend against external challenges. As an example, Cohen et al. (1991)
asked volunteers to self-rate their levels of stress and then randomized them to receive nasal drops containing either placebo or respiratory viruses. Rates of respiratory infection and clinically diagnosed colds followed a positive dose response with level of psychological stress. Findings from this controlled experiment were unaffected by controlling for a variety of factors (e.g., allergic status).
Intriguingly, some evidence suggests that stress may influence the internal dose of a given toxicant. This is because stress may a
) increase the absorption of toxicants into the body through increased respiration, perspiration, and consumption (Gordon 2003
) compromise host defense systems (McEwen 1998
); and c
) directly cause illness, which in turn may lead to an amplification loop whereby sick individuals are less likely to cope with environmental toxicants (Rios et al. 1993
; U.S. EPA 2003b
). Stress may induce or unmask a latent effect of a toxicant, possibly altering basal levels of neurofunctioning and shifting the threshold for neurotoxicity [Agency for Toxic Substances and Disease Registry (ATSDR) 1995
Two factors are purported to determine individual response to stress: how one appraises the situation, and their general state of physical health (Lazarus and Folkman 1984
; McEwen 1998
). Coping resources, such as social support, help determine the extent to which a stressor is perceived as a threat and subsequent health responses (Israel et al. 2002
). For example, workers with high levels of job strain and low levels of co-worker support have higher risk of cardiovascular disease than do those with similar levels of strain and more support (Johnson et al. 1996
). Additionally, physical illness will impair an individual’s ability to respond to stressors. Individual stress and coping have macro-level analogs, community stressors and neighborhood resources.
Types of community stressors.
Community stressors can be categorized into two major types, physical and psychosocial. Physical conditions, including noise, temperature, humidity, barometric/water pressure, visible light, geomagnetism, radiation, and particulate matter, may contribute to stress (Gordon 2003
). These stressors can induce a physiological response that makes the body more susceptible to illness. Heat stress, for example, induces sweating and increased skin blood flow, which in turn can facilitate the transcutaneous absorption of pesticides (Chang et al. 1994
; Funckes et al. 1963
; Wester et al. 1996
). Individuals subject to ambient noise have higher levels of noradrenalin, a stress biomarker (Babisch et al. 2001
). In a natural experiment, Evans et al. (1998)
found that the chronic exposure to aircraft noise elevated resting blood pressure, norepinephrine, and epinephrine biomarker levels and decreased self-reported quality of life over a 2-year period.
Psychosocial conditions—including crowding, social disorganization, racial discrimination, fear, and economic deprivation—may also be sources of stress (Krieger and Higgins 2002
; Macintyre et al. 2002
). One stressor that has received extensive attention is fear of crime (Morenoff 2003
; Warr and Ellison 2000
). Minority neighborhoods tend to have higher crime rates, which may contribute to health disparities. Perceptions of crime and disorder within an individual’s community has been associated with numerous outcomes, including anxiety depression, posttraumatic stress disorder, and substance use (Aneshensel and Sucoff 1996
; Cutrona et al. 2000
; Fick and Thomas 1995
; Geis and Ross 1998
; Ross et al. 2000
; Ross and Jang 2000
). Morenoff (2003)
found that the neighborhood violent crime rate was one of the “most robust” environmental predictors of infant birth weight, after controlling for both individual (e.g., smoking during pregnancy) and neighborhood (e.g. percentage of poor families) characteristics.
Physical and psychosocial stressors may interact with one another, as seen with natural and technological disasters (Ginexi et al. 2000; Kaniasty and Norris 2000
). For example, the trauma of the Love Canal incident in New York resulted from both the chemical hazards and public perceptions (Edelstein and Wandersman 1987
; Gibbs 1983
; Holden 1980
). Further, the relationship between environmental and subjective stressors occurs not only for highly salient events but also for everyday events. Gee and Takeuchi (2004)
, using multilevel models, reported that persons perceiving stress due to automobile traffic had greater psychological distress and lowered general health status than did those perceiving less stress. However, these outcomes were worst for persons perceiving high stress and living in high traffic areas.
Racial disparities in exposure to stressors.
Racial and ethnic minorities tend to receive a lower quality of healthcare than non-minorities, even when access-related factors, such as patients’ insurance status and income are controlled.… [T]he study committee found evidence that stereotyping, biases, and uncertainty on the part of healthcare providers can all contribute to unequal treatment.
The conjunction of high prevalence and strong impact would mean that discrimination is among the most important of all the stressful experiences that have been implicated as causes of mental health problems.
Although a common argument is that segregation is harmful to the health of minorities, there is some indication that segregation may have a counterbalancing effect by concentrating social resources, such as black political power (LaVeist 1993
). Others have reported that the clustering of ethnic groups may build a sense of collective identity that helps mitigate trauma (Mazumdar et al. 2000
). Thus, supportive social relationships within minority communities may help promote health and well-being and ameliorate the effects of community risks. Our view is that segregation concentrates both risks and resources. It is not a matter of whether segregation is either “bad” or “good,” but to what degree the negative effects of segregation outweigh positive effects.
Neighborhood resources buffer community stressors (Israel et al. 1998
; Kretzman and McKnight 1993
). Generally, these resources have been conceptualized in terms of relationships among residents, including social cohesion, social capital, psychological sense of community, informal social control, and community empowerment (Berkman and Clark 2003; Kawachi et al. 1999
; Ross and Jang 2000
; Sampson et al. 1997
). “Social cohesion” is the “extent of connectedness and solidarity among groups in society” (Kawachi and Berkman 2000
). Essentially, a community with a high degree of social cohesion has strong social ties between members and minimal conflict. “Social capital” can be considered a type of resource that emerges from socially cohesive groups that facilitates collective action. These resources include norms of reciprocity, aid, and interpersonal trust.
Collective efficacy, defined as “mutual trust and willingness to intervene for the common good” (Sampson et al. 1997
), may mediate the adverse effects of concentrated disadvantage and fear (Ross and Jang 2000
). Pastor et al. (2001)
suggested that social capital was stronger in communities with less “ethnic churning,” referring to the replacement of one minority group with another within a community. They argued that ethnic churning may “weaken the usual social bonds constituted by race and make an area more susceptible to siting of noxious land uses.” Their data indicated that ethnic churning in Los Angeles was associated with the siting of hazardous waste storage and disposal facilities over a two-decade period, after adjusting for economic factors.
Another potential resource is residents’ ability to control their environment, which may mitigate community problems in two ways. First, empowered communities may be able to protect themselves from the instruction of new hazards and eliminate extant ones (Bullard and Wright 1993
; Lee 1993
; Morello-Frosch et al. 2002
; Phoenix 1993
; Rich et al. 1995
; Zimmerman 2000
). These communities may also be able to control the political arena that shapes their health beyond the effect of environmental pollutants. Black political participation, defined by the presence of African-American legislators, has been associated with lower mortality rates in African-American communities (LaVeist 1993
). This is possibly due to a higher preponderance among African-American communities to provide a wider range of social services compared with white communities (Schneider and Logan 1982
). Second, control per se may be an important factor determining stress and health. Workers with greater control over their work process have lower risk of cardiovascular disease than do workers with less control (Karasek and Theorell 1990
; Kuper and Marmot 2003
; Landsbergis et al. 1997
). Further, collective control by workers and their unions may also provide health benefits (Johnson 1989
; Sorensen et al. 2004
The cumulation of environmental pollutants, structural process, community stressors, and neighborhood resources is community stress. Community stress is a state of ecological vulnerability. Community resources help buffer community stressors and protect against environmental exposure, but when resources are inadequate, community stress arises. Structural factors constrain the limits of resources and stressors.
Although several factors cross the threshold from “community” to “individual,” we focus on the intersection between community stress and individual stress. In particular, community stress may itself lead to individual stressors. These individual stressors may in turn lead to individual stress and subsequent illness. The terrorist attacks of 11 September 2001 provide an extreme example of how community stress can translate to individuals. The attack was a threat to the American “community.” Although most citizens were not close to the epicenter, many individuals across the United States felt some measure of distress from the attack (Schlenger et al. 2002
; Schuster et al. 2001