Racial Discrimination, Disease Activity, and Organ Damage: The Black Women's Experiences Living With Lupus (BeWELL) Study

David H. Chae; Connor D. Martz; Thomas E. Fuller-Rowell; Erica C. Spears; Tianqi Tenchi Gao Smith; Evelyn A. Hunter; Cristina Drenkard; S. SamLim


Am J Epidemiol. 2019;188(8):1434-1443. 

In This Article

Abstract and Introduction


Black women are disproportionately affected by systemic lupus erythematosus (SLE), a chronic, potentially debilitating autoimmune disease, and they also experience more rapid progression and worse outcomes compared with other groups. We examined if racial discrimination is associated with disease outcomes among 427 black women with a validated diagnosis of SLE, who live in the Atlanta, Georgia, metropolitan area, and were recruited to the Black Women's Experiences Living with Lupus Study (2015–2017). Frequency of self-reported experiences of racial discrimination in domains such as employment, housing, and medical settings was assessed using the Experiences of Discrimination measure. SLE activity in the previous 3 months, including symptoms of fatigue, fever, skin rashes, and ulcers, was measured using the Systemic Lupus Activity Questionnaire; irreversible damage to an organ or system was measured using the Brief Index of Lupus Damage. Results of multivariable linear regression analyses examining the Systemic Lupus Activity Questionnaire and log-transformed Brief Index of Lupus Damage scores indicated that increasing frequency of racial discrimination was associated with greater SLE activity (b = 2.00, 95% confidence interval: 1.32, 2.68) and organ damage (b = 0.08, 95% confidence interval: 0.02, 0.13). Comprehensive efforts to address disparities in SLE severity should include policies that address issues of racial discrimination.


Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with potentially debilitating health consequences.[1] It is characterized by periods of disease activity that include a vast array of clinical manifestations, such as skin rashes, oral ulcers, fever, vasculitis, myositis, and inflammatory arthritis.[2,3] Organ damage and comorbid conditions may emerge as consequences of uncontrolled disease activity and chronic inflammation.[4] The number of people living with SLE in the United States is estimated at between 161,000 and 322,000;[5] still, the epidemiology of SLE is marked by significant disparities along racial and sex lines.[6–9] In the state of Georgia, the prevalence of SLE among women is nearly 9 times greater than among men, and it is more than 3 times greater among blacks compared with whites.[6] Moreover, there are wide variations in severity and progression between blacks and whites with SLE. For example, the prevalence of renal and cardiovascular damage in SLE is 2 to 4 times greater among blacks compared with whites,[10,11] and blacks suffer these complications 3 to 9 years earlier, on average.[12,13] Blacks with SLE also have overall death rates that are up to 3 times higher than those of whites, and blacks with SLE die earlier.[14] Moreover, according to US death trend data between 1968 and 2013, there was a relatively smaller decrease in SLE-related death among blacks (13.3%) than in whites (33.3%), suggesting that racial disparities in SLE outcomes have been increasing over time.[15]

The reasons for racial disparities in SLE outcomes are multifactorial. However, genetic evidence for these differences is lacking; in fact, psychosocial factors have been more clearly identified as having a role in disease progression.[16,17] Socioeconomic stressors are associated with SLE severity and death.[18–20] Geographic clusters with higher SLE death rates are concentrated in areas with higher poverty and numbers of racial minorities, implicating the role of environmental factors in SLE outcomes.[17,21–23] Compared with their white counterparts, black women are more likely to experience psychosocial stressors shown to exacerbate SLE, including those associated with poverty, unemployment, exposure to violence, and physical victimization.[24–28] Black women also disproportionately experience environmental stressors and area-level deprivation associated with racial residential segregation and poverty concentration.[29–31]

The constellation of psychosocial risk factors experienced by black women with SLE compound those more generally associated with the management of a chronic disease, leading to worse disease trajectories in this population.[32] Among these stressors is the interpersonal experience of racial discrimination, a distinct, qualitatively unique, and salient form of psychosocial stress that also may increase the risk of poor SLE outcomes.[33–35] Racial discrimination can be experienced in multiple societal domains, such as employment, housing, education, health care, and legal contexts; these experiences may proliferate stress by diminishing socioeconomic attainment.[33,36–38] Experiences of racial discrimination in housing markets can also undermine health through segregation into worse neighborhood conditions.[36,38] Disparate treatment in health care can directly affect health. Patient-reported racial discrimination by physicians has been associated with heightened SLE activity and depression.[39,40] Chronic stress associated with racial discrimination, particularly when it is viewed as being outside of personal control, may compromise psychological adjustment and result in maladaptive coping responses, such as smoking and problem drinking, which negatively affect the progression of chronic diseases.[33,38,41] Depression resulting from racial discrimination may lead to accelerated declines in health among women with SLE.[39,40] Indeed, studies have most consistently found associations for adverse mental health consequences of racial discrimination.[42,43] Accordingly, racial discrimination may increase disease severity through these mental health and behavioral channels.

As a source of psychosocial stress, racial discrimination can also elicit a cascade of biological responses that damage stress-response systems over time and, over one's life, can contribute to "weathering" or accelerated physiologic deterioration.[44,45] Discrimination is associated with a range of inflammatory markers.[46–49] Repeated experiences of racial discrimination may lead to chronically elevated levels of proinflammatory cytokines and acute-phase proteins, contributing to a heightened inflammatory state.[50,51] These biological conditions may increase the risk of diseases characterized by inflammatory processes. For example, racial discrimination has been associated with increased cardiovascular risk, as well as biological processes and other health conditions that are sensitive to inflammation.[52–56] Several indicators of inflammation are involved in the etiopathogenesis of SLE activity and organ damage, and the maintenance of inflammation.[57–62] Accordingly, racial discrimination may have consequences for more acute SLE outcomes, such as disease activity. In addition, the tolls of racial discrimination on biological systems critical for regulating the stress response may accumulate and place black women at greater risk for earlier onset of SLE complications and disease damage. For example, experiences of contemporaneous unfair treatment attributed to racial as well as nonracial causes were associated with greater irreversible organ damage among black women with SLE.[63] The purpose of the current study was to examine the association among racial discrimination, cumulative organ damage, and disease activity among black women with SLE from a large, population-based cohort.