Psychology Topic 5 Assignment

Race, Cardiovascular Disease, and Vascular Health Michael D. Brown and Dulce H. Gomez

College of Education, School of Kinesiology, Auburn University, Auburn, AL, USA

Non-Hispanic Blacks (NHB) have a greater prevalence cardiovascular disease (CVD) and CVD risk factors, and they appear at an earlier age compared with non-Hispanic Whites. Impaired vascular function is a major contributing factor to CVD risk, and NHB have impaired vascular function compared with non-HispanicWhites. In addition to the known biological factors, socioeconomic and environmental determinants of CVD are particularly important for NHB. Chronic exposure to racial discrimination (racialized stress) throughout the lifespan represents an allostatic load whereby the stress-response mechanism is activated repeatedly. This activates the central nervous system and other physiological systems that can cause CVD. High allostatic scores are associated with being NHB or Hispanic. The purpose of this review article is to describe the racial health disparities in the CVDs, the social determinants of CVD disparities, and how racial discrimination impacts them.

Keywords: heart disease, risk factors, health disparities, allostatic load, racism

Health disparities are preventable differences in the burden of disease, injury, violence, or opportunities to achieve optimal health that are experienced by socially disadvantaged populations (Centers for Disease Control and Prevention, 2013). They are experienced in the United States by ethnicity, race, geography, education level, and socioeconomic status (SES). The overall cost of these health disparities in the United States has been estimated to be 1.24 trillion dollars (Graham, 2015). Cardiovascular disease (CVD) arises from a complex interplay between genetic predispo- sition and environmental influences that lead to progressive dete- rioration in the structure and the function of cardiovascular tissues. During 2016–2017, the average annual direct and indirect cost of CVD in the United States was estimated to be $363.4 billion. Unfortunately, among American adults under age 75, approxi- mately 200,000 of deaths caused each year by heart disease, stroke, and hypertension are preventable (Centers for Disease Control and Prevention, 2013).

Before we discuss race and CVD, we must describe the determination and categorization of race. Most of the research in this area classifies individuals as Black, African American, or Non-Hispanic Black (NHB). However, the criteria for classifica- tion of race in much of the research lack detail. In this review, we will use the terms NHB and non-Hispanic White (NHW) to be consistent and in line with much of the literature that we cite herein.

Racial Disparities in CVD

In the United States and around the world, CVD is the leading cause of morbidity and mortality. According to the National Health and Nutrition Examination Study, the prevalence of CVD (i.e., coronary heart disease [CHD], heart failure, stroke, and hypertension) in adults ≥20 years of age was 49.2% between 2015 and 2018, or approximately126.9 million people in 2018 (Virani et al., 2021).

Over the decades, there have been important advances in the identification of CVD risk factors, and evidence-based strategies to manage CVD are now widely used. Despite these advancements, racial disparities in CVD morbidity and mortality persist in the United States. In response to the disparities identified in the report “Health, United States, 1983,” the Secretary of the U.S. Depart- ment of Health and Human Services established a Minority Health Task Force (Gibbons, 2005) that increased awareness of the vast disparity in the health of individuals belonging to minority groups compared with the White majority population (Gibbons, 2005). In 2005, the American Heart Association published an article entitled “Discovering the Full Spectrum of Cardiovascular Disease: The Minority Health Summit” (Bonow et al., 2005). The article firmly demonstrated that marked racial disparities in CVD remain (Yancy et al., 2005). No matter how CVD is measured, NHB have worse overall cardiovascular health and higher CVDmortality than NHW (Benjamin et al., 2019; Rosamond et al., 1999). The question is why?

The NHB makeup is 13.4% of the U.S. population, and they are the second largest racial/ethnic minority group behind Hispa- nics/Latinx. Of course, CVD affects individuals of all races and ethnicities; however, race/ethnicity is one factor that determines a person’s CVD risk. The prevalence of CVD in NHB males and females is 60.1% and 57%, respectively, (Benjamin et al., 2019; Virani et al., 2021) accounting for a third of the disparity in potential life-years lost between NHB and NHW (Wong et al., 2002). CVD age-adjusted death rates are 33% higher for NHB than for the overall U.S. population. NHB are nearly twice as likely to have a first stroke and much more likely to die from one than NHW (Benjamin et al., 2019). The underlying impairments contributing to the increased risk for CVD in NHB occur as early as the second decade of life before CVD manifests clinically (Benjamin et al., 2019; Heffernan et al., 2008). For these reasons, the primary focus of this review will be on the CVD disparity between NHB and NHW. To enhance understanding of the data discussed below, two definitions are provided. The National Institutes of Health defines “prevalence” as the proportion of a population who have a specific characteristic during a given time period. National Institutes of Health defines “incidence” as a measure of the number of new cases

Brown ([email protected]) is corresponding author, https://orcid.org/ 0000-0002-5374-1094.

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of a characteristic that develop in a population in a specified time period.

CHD

CHD, also called coronary artery disease, involves the reduction of blood flow to the heart muscle due to buildup of plaque (i.e., atherosclerosis) in the arteries of the heart. It is the most common of the CVDs. Types of CHD include stable angina, unstable angina, myocardial infarction, and sudden cardiac death. Currently, the overall prevalence of CHD is 6.2% affecting approximately 15.5 million people in the United States. (Benjamin et al., 2019; Virani et al., 2021). In males, CHD prevalence is lower in NHB than NHW (7.2% vs. 7.8%); however, this is reversed in females (7.0% vs. 4.6 %). Despite the lower prevalence among NHBmales, death rates from CHD are higher in NHB males and females than in NHW males and females (Benjamin et al., 2019; Virani et al., 2021). After adjustment for age, CHD death rates per 100,000 were 132.3 for NHW males, 146.5 for NHBmales, and 95.6 for Hispanic males. With respect to females, the death rates were 67.9 for NHW, 85.4 for NHB, and 54.6 for Hispanic females (Benjamin et al., 2019). The prevalence of CHD in Asians is 3.7 %, which is lower than the general population (Benjamin et al., 2019; Virani et al., 2021).

Cerebrovascular Disease/Stroke

In the United States, the incidence and mortality of cerebrovascular disease (transient ischemic attacks, ischemic stroke, and intracere- bral hemorrhage) are substantially higher in NHB compared with NHW. Stroke mortality has fallen by 80% over the past 60 years; however, there has been no meaningful decrease in the racial disparity in stroke mortality between NHB and NHW (Lackland et al., 2014). Since the 1950s, stroke mortality rates in non-Whites (predominately NHB) remain 4.5-fold higher than among NHW (Rosamond et al., 1999).

The Atherosclerosis Risk in Communities Study (ARIC Study) is one of the most significant and longest-running heart health studies and is the largest study of heart health in NHB. The study included a 15-year follow-up in the 15,069 participants that remained in the study (Rosamond et al., 1999). Most NHB subjects recruited in the ARIC Study were recruited from the southern region of the United States (Jackson, MS). Across age and sex categories, the NHB-to-NHW stroke mortality ratio was consis- tently higher for southern states than in nonsouthern states (Howard et al., 2007). Thus, it is possible that the overall U.S. NHB–NHW disparity in stroke risk is confounded by the geographic differences in stroke risk (Yang et al., 2004).

Hypertension

Nearly half of adults in the United States have hypertension defined as a systolic blood pressure ≥130 mmHg or a diastolic blood pressure ≥80 mmHg or are taking medication for hypertension. The prevalence of NHB adults with hypertension (54%) is greater than in NHW adults (46%), Asian adults (39%), or Hispanic adults (36%) and is among the highest in the world (National Center for Health Statistics, 2016). The magnitude of the association between systolic blood pressure level and stroke risk is three times greater in NHB than in NHW. A 10 mmHg difference in systolic blood pressure is associated with an 8% increase in stroke risk in NHW, but a 24% increase in stroke risk in NHB (Gaciong et al., 2013).

Interestingly, the percentage of African admixture in NHB and other racial/ethnic groups is positively associated with blood pressure levels and the prevalence of hypertension (Marden et al., 2016; Non et al., 2012). Furthermore, NHB boys and girls have higher blood pressure levels and a higher prevalence of hypertension (13.8%) compared with 8.4% in NHW and 10.4% in Hispanics boys and girls (Bao et al., 1995).

It should be noted that the data reporting on race and hyper- tension may underreport NHB. Within a racially diverse, older adult sample, it was shown that having a blood pressure item on a questionnaire tended to be problematic for NHB (Cardinal & Cardinal, 2000). One study showed that many potential partici- pants, almost entirely NHB, were screened out of the study because they answered “yes” to the original question about whether they had a blood pressure issue (Cardinal & Cardinal, 2000). Further- more, a series of studies demonstrated that by asking a less biased questions, more people were able to participate in future studies (Cardinal & Cardinal, 2000).

Sudden Cardiac Arrest/Sudden Cardiac Death

Sudden cardiac arrest is a sudden pulseless condition frequently attributable to underlying cardiac causes. Deaths due to CVD have decreased over the past five decades, but sudden cardiac death is still a leading cause of mortality in developed countries and is often the first manifestation of CVD (Fox et al., 2008; Huikuri et al., 2001; Rea et al., 2003). Sudden cardiac arrest and sudden cardiac death are higher in NHB compared with NHW. Findings from the ARIC Study show that the incidence of sudden cardiac arrest was highest in NHB men, followed by NHW men, NHB women, and NHW women (Zhao et al., 2019). NHB were younger and more likely to be uninsured; be current smokers; have a higher prevalence of hypertension, diabetes mellitus, and left ventricular hypertrophy; and have lower levels of education, alcohol consumption, triglycer- ides, and estimated glomerular filtration rate compared with NHW. Socioeconomic factors, cardiovascular risk factors, and electrocar- diographic variables explained 65.3% of the excess risk of sudden cardiac death in NHB compared with NHW. The single most important factor explaining this difference was income followed by education level. This last point highlights the important role that socioeconomic factors play in the racial disparity in CVD.

Heart Failure

Heart failure, also known as congestive heart failure, is a set of manifestations caused by the failure of the heart’s function as a pump supporting the blood flow through the body. The incidence, prevalence, and prognosis of heart failure are less favorable than CHD among NHB. The Coronary Artery Risk Development in Young Adults study reported that disparities in the incidence of heart failure are most noticeable at younger ages in NHB (Bahrami et al., 2008; Bibbins-Domingo et al., 2009). Statistical adjustment for established risk factors eliminated differences in the incidence of heart failure between NHB and NHW men. However, among women with heart failure, NHB were significantly more likely to experience CVD events within the first 7.5 years even after statistical adjustment for risk factors (Loehr et al., 2008).

Vascular Dysfunction and Race

Impaired vascular function is a major contributing factor and is a common connection in the CVDs described above (Melikian et al.,

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2007; Perregaux et al., 2000). The primary sites of dysfunction in the vasculature are the endothelium, the smooth muscle located in the blood vessel wall, and the outer layer consisting largely of structural proteins.

Vasodilator Function

The single layer of endothelial cells that line the entire circulatory system has the ability to act in both sensory and effector capacities and is critical to vascular homeostasis and thereby cardiovascular health (Hadi et al., 2005; Rajendran et al., 2013). One of these critical functions is the regulation of vessel diameter. Endothelial dysfunction is characterized by a shift in the actions of the endothelium toward reduced vessel diameter (vasodilation), and proinflammatory, pro-oxidant, and prothrombotic. The hallmark characteristic of endothelial dysfunction is a decrease in the production/bioavailability of nitric oxide (NO; Hadi et al., 2005; Rajendran et al., 2013), a potent vasodilator released by the endothelium. Endothelial cells synthesize and release NO, which diffuses into the underlying smooth muscle where it binds to guanylyl cyclase, which leads to smooth muscle dilation and thereby vasodilation. Thus, endothelial dysfunction and dimin- ished NO bioavailability are associated with most forms of CVD including hypertension, coronary artery disease, heart failure, and peripheral arterial disease (PAD; Hadi et al., 2005; Rajendran et al., 2013).

Impaired peripheral micro- and macrovascular function in the NHB population has been well documented (Campia et al., 2002, 2004; Duck & Hoffman, 2007; Heffernan et al., 2008; Hurr et al., 2015, 2018; Ozkor et al., 2014; Patik et al., 2018; Perregaux et al., 2000) and has been attributed to a decreased vasodilator capacity, largely due to reduced NO bioavailability (Jin & Loscalzo, 2010). In a review by Taherzadeh et al. (2010), a PubMed search was systematically conducted for articles on ethnic differences in vascular function and structure. The data indicate that compared with normotensive NHW, NHB have enhanced vascular reactivity to sympathetic stimulation and attenuated responses to vasodilators (Taherzadeh et al., 2010), all present in relatively young individuals (Brothers et al., 2019). Flow-mediated dilation, a measure of endothelial function, was measured in the Cardiovascular Health Study in 2,792 adults aged 72–98 years (82.7% White and 58.6% women). Flow-mediated dilation was a significant predictor of cardiovascular events after statistical adjustment for age, gender, diabetes mellitus, cigarette smoking, systolic and diastolic blood pressure, baseline CVD status, and total cholesterol (Yeboah et al., 2007). Thus, the greater prevalence of endothelial dysfunction in NHB puts them at greater risk for future CVD events.

Potential causes of reduced NO bioavailability in NHB are oxidative stress, inflammation, and uncoupling of endothelial NO synthase (eNOS). The production of NO via eNOS depends on the substrate, L-arginine, and on appropriate amounts of the essential cofactor, tetrahydrobiopterin (Holowatz & Kenney, 2011; Stanhewicz et al., 2012). If either of these is deficient, then eNOS uncoupling ensues which leads to an increased production of reactive oxygen species, reduced NO production, and thus impaired endothelial function (Delp et al., 2008; Holowatz & Kenney, 2011). Asymmetric dimethylarginine inhibits eNOS to reduce NO production. Melikian et al. (2007) found an elevated concentration of asymmetric dimethylarginine in young NHB, relative to an age- and sex-matched NHW group, which was associated with impaired endothelial function (Melikian et al., 2007).

Oxidative stress plays a role in the pathology and progression of CVD and hypertension (Griendling & FitzGerald, 2003a, 2003b). Studies have found elevated oxidative stress and superox- ide production in NHB compared with age-matched NHW (Deo et al., 2015; Kalinowski et al., 2004). Increased levels of superox- ide can react with NO such that NO is scavenged and does not diffuse to the underlying smooth muscle to cause vasodilation (Forstermann & Munzel, 2006; Kalinowski et al., 2004; Yang et al., 2009). Elevated superoxide production is associated with impaired vascular function in a variety of conditions that are related to CVD (Forstermann & Munzel, 2006; Kalinowski et al., 2004; Zou et al., 2004). We and others have found lower eNOS protein expression levels and NO production and increased oxidative stress in human umbilical vein endothelial cells in cells obtained from NHB compared with NHW (Feairheller et al., 2011; Kalinowski et al., 2004; Sapp et al., 2021).

Vasoconstrictor Responsiveness

Another possible mechanism for elevated CVD risk in NHB could be related to overactivity of the sympathetic nervous system which could result in increased peripheral vascular resistance (Adefurin et al., 2013; Sherwood et al., 2017) and an exaggerated blood pressure response to variety of acute stressor stimuli compared with NHW individuals (Calhoun et al., 1993, 1994; Hinds & Stachenfeld, 2010; Jarvis et al., 2014; Okada et al., 2012). Elevated sympathetic nerve activity precedes and is present in many of the CVDs that are more prevalent in NHB (Benjamin et al., 2019). Some (Jarvis et al., 2014; Vranish et al., 2018), but not all, studies (Calhoun et al., 1993; Marinos et al., 2017; Okada et al., 2012) suggest that there is elevated basal sympathetic nerve activity in NHB.

Endothelin-1 (ET-1) is the most potent endogenous vasocon- strictor and is implicated in the pathogenesis of hypertension, endothelial dysfunction, and CVD (DeLoach et al., 2010; Nishiyama et al., 2017; Schiffrin, 2001). The circulating concen- tration of ET and/or the sensitivity of the vasoconstrictor response to ET bioavailability are enhanced in NHB men and women (Campia et al., 2004; Ergul et al., 1999; Evans et al., 1996). Grubbs et al. (2002) found that the biosynthetic pathway of ET- 1 was activated to a higher degree and that ET Type B receptor expression was altered in the peripheral vasculature of NHB hypertensive patients. The activated synthesis and altered expres- sion of Type B receptors may contribute to the increased incidence of hypertension in NHB (Grubbs et al., 2002).

PAD

PAD is an abnormal narrowing of arteries other than those that supply the heart or brain, such as arteries supplying the legs, arms, neck, or kidneys (Olin & Sealove, 2010; Shu & Santulli, 2018). Lower-extremity PAD affects approximately 8.5 million Amer- icans above the age of 40 years and is associated with significant morbidity, mortality, and diminished quality of life (Writing Committee Members et al., 2017).

The incidence of PAD in NHB is approximately two times that of NHW (Allison et al., 2007). Even after statistical adjustment, the increased prevalence in NHB compared with NHW is not completely eliminated (Newman et al., 1993; Zheng et al., 1997). The Multi-Ethnic Study of Atherosclerosis included more than 6,000 men and women from six communities in the United States. The Multi-Ethnic Study of Atherosclerosis study found that

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the incidence of PAD was 1.67 times higher in NHB compared with NHW after statistical adjustment (Allison et al., 2007). PAD is not necessarily a direct cause of mortality but is often a reflection of the overall burden of CVD. The age-adjusted death rate resulting from PAD was higher among NHB men (24.8 per 100,000) than NHW (19.9), American Indian or Alaska Native (20.8), Hispanic (15.4), or Asian Pacific Islander (8.5) men. Similar patterns of PAD mortality were observed for NHB women (16.5) compared with NHW (13.8), American Indian or Alaska Native (16.1), Hispanic (10.7), and Asian or Pacific Islander (6.8) women (Benjamin et al., 2019).

Social Determinants, Racial Discrimination, and CVD

Race and biological/genetic factors play an undisputable role in determining CVD risk factors and subsequent CVD, but emerging data suggest that SES and environmental factors contribute sub- stantially to CVD risk (Muncan, 2018). Lower SES, social distress, and environment are fundamental causes of CVD in vulnerable and economically disadvantaged groups (Phillips & Klein, 2010), and individuals from disadvantaged backgrounds exhibit higher rates of chronic diseases and adverse physiological markers of disease risk (Adler & Ostrove, 1999; Adler & Stewart, 2010; Braveman et al., 2010; Franks et al., 2003; Hostinar et al., 2017). Individuals in specific subgroups defined by race, ethnicity, SES, and geogra- phy have a disproportionate burden of myocardial infarction, heart failure, stroke, hypertension, cardiovascular events (Graham, 2015), untreated risk factors, worse outcomes, and higher mortality rates (Bonow et al., 2005). Below, we discuss the roles that income level/employment status, education level, and environmental fac- tors (e.g., air pollution) play in the increased risk of CVD in NHB. Furthermore, we discuss how racial discrimination and chronic racialized stress negatively impact these factors, ultimately altering physiological systems that lead to CVD.

Income Level/Employment Status

It is well known that SES has a significant effect on cardiovascular health (Kucharska-Newton et al., 2011). Approximately, 26% of NHB live in poverty compared with 13% of NHW and 15% of the overall U.S. population. The median family income is $43,151 in NHB households compared with $66,632 in the U.S. population (DeNavas-Walt & Proctor, 2015). One study found that each $10,000 increase in median income of a neighborhood was asso- ciated with a 10% reduction in mortality risk (Gerber et al., 2008). A large study in the United States and Finland found an increased risk of nonfatal myocardial infarction and sudden cardiac death in the low-income groups after adjustment for smoking and alcohol consumption (Kucharska-Newton et al., 2011).

One study used data from the National Longitudinal Study of Adolescent to Adult Health to investigate whether SES during adolescence and childhood/adolescent adversities affected CVD risk (Doom et al., 2017). Both SES during adolescence and child/ adolescent adversities were significantly associated with young adult CVD risk such that a one SD increase in SES was associated with a 10% decrease in CVD risk. LaRosa et al. (2020) found an inverse relationship between annual household income and heart failure and myocardial infarction. Individuals with an annual household income <$40,000 had the greatest risk for heart failure and myocardial infarction compared with those with income

≥$100,000. Since twice the number of NHB families in the U.S. live in poverty compared with NHW, then the racial disparity in poverty is another factor that puts NHB individuals at increased risk for CVD.

Employment is a commonly used marker of SES, and unem- ployment has been associated with increased risk of CVD (Meneton et al., 2015; Mosquera et al., 2016). A study of indivi- duals with high SES relative to the general population demon- strated an increased risk of cardiovascular events in the unemployed despite adjustment for important covariates (Meneton et al., 2015). Another study found that unemployment was associated with a 35% increased risk for myocardial infarction within the first year, after which time the risk disappeared (Dupre et al., 2012). Job loss was associated with an incremental increase in myocardial infarction risk after adjustment for socioeconomic, behavioral, and clinical variables.

Overall, NHB workers are twice as likely to be unemployed as NHW workers (6.4% vs. 3.1%) (Wilson, 2019). Even NHB work- ers with a college degree are more likely to be unemployed than similarly educated NHWworkers (3.5% vs. 2.2%) (Wilson, 2019). When NHB are employed, workers with a college or advanced degree are more likely to be underemployed than their NHW counterparts (Abel & Deitz, 2016). Rose et al. (1999) examined the cross-sectional and prospective associations between employ- ment status and hypertension among middle-aged, NHB, and NHW women participating in the ARIC Study. At baseline, employed women were less likely to be hypertensive or using antihypertensive drugs than were unemployed women after con- trolling for age, body mass index, and education. In a subgroup of women who had low–normal blood pressure at baseline, employed women were less likely to develop hypertension during the 3-year period than were homemakers. The inverse association was stron- ger among NHB than NHW women. Taken together, the relatively high NHB unemployment and skill-based underemployment sug- gests that institutional racism exists in hiring practices and in the workplace. Thus, employment status is another factor contributing to the racial disparity in CVD.

Education Level

For decades, an inverse relationship between CVD and educational level has been observed (Bhatnagar, 2017). One study reported that individuals who reach higher levels of education were more likely to practice healthier behaviors (Lee & Seon, 2019) because they had better access to health-promoting resources including better neighborhoods, healthy food (Kushi et al., 1988), medication, and health care, and more healthy behaviors and social norms around exercise (He & Baker, 2005), all benefitting cardiovascular health (Fagard, 2009). For racial/ethnic minorities, the relationship between education and health is different (Liu et al., 2015; Vable et al., 2018). For example, NHB with more education report more racial discrimination than NHB with less education (Krieger, 1990). Stress and racial discrimination are associated with poorer outcomes in a variety of cardiometabolic risk factors (Association for the Study of Higher Education, 2015).

The original purpose of higher education in the United States was to serve the White majority and prepare White men for leadership roles in society (Association for the Study of Higher Education, 2015). Since then, racism has manifested in higher education policy at federal, state, and institutional levels. Racism influences precollege educational trajectories and college oppor- tunities through directing minority students into under-resourced

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schools, tracking students of color into remedial and vocational pathways as well as schools with limited access to college prepa- ratory honors, and advanced placement coursework (Association for the Study of Higher Education, 2015). State divestment from higher education, rising college costs, an increased reliance on loans, and for-profit colleges and predatory practices all create additional barriers to college affordability for low-income and minority students. An Association for the Study of Higher Educa- tion Study identified six themes on the racialized experiences of faculty of color: (a) racism in the academic pipeline, (b) racial resistance to faculty authority and expertise, (c) racial hostility in the classroom, (d) racial scrutiny of faculty research agendas, (e) racial taxation from excess faculty service, and (f) racial marginalization and isolation among faculty of color. While small improvements in the representation of persons of color among college faculty have been made in recent years, these improve- ments have primarily been due to increases of persons of color in nontenured instructor ranks (Association for the Study of Higher Education, 2015). Thus, NHB tend to face multiple barriers to education attainment, which increases their risk for CVD.

Environment

Environmental justice is the fair treatment and meaningful involve- ment of all people, regardless of race, color, national origin, or income, with respect to the development, implementation, and enforcement of environmental laws, regulations, and policies. Environmental exposure is an important contributing factor to the development and severity of CVD. Like traditional CVD risk factors, environmental exposures cause disease and mortality by activating pathophysiological processes associated with CVD, including blood pressure control, carbohydrate and lipid metabo- lism, vascular function, and atherogenesis (Cosselman et al., 2015). Specifically, exposure to air pollution is thought to lead to epige- netic modification, autonomic nervous system imbalance, or local and systemic inflammation (Cosselman et al., 2015; Hajat et al., 2015).

It is well documented that racial and ethnic minorities in the U.S. experience disproportionate exposure to toxic air emissions from industry (Mohai et al., 2009; Zwickl et al., 2014). Residence location has long been used to indicate environmental exposure to air pollution in epidemiological studies. In an early environmental justice study by the U.S. government, it was reported that a disproportionately high representation of socially disadvantaged populations resides in communities near landfills (U.S. Government Accountability Office, 2017). Furthermore, in a national sample, it was found that NHB were 1.54 times more likely to live within 1 mile of a facility listed in the Toxics Release Inventory than were NHW (Mohai et al., 2009) even after account- ing for income and education level. Finally, an Environmental Protection Agency investigation in Flint, Michigan, found that there was evidence of discriminatory treatment of NHB by the Department of Environmental Quality (Campbell et al., 2016). Thus, NHB communities are more likely to be exposed to envi- ronmental toxins putting them at increased risk for CVD.

Allostatic Load, Racial Discrimination, and CVD

An explanation for the ongoing health disparities across the socio- economic range between NHB and NHW is the multiple and unique sources of psychological stress faced byNHB. Some of the common sources of stress are job-related stress, neighborhood-related safety

concerns, socioeconomic concerns, and significant sources of psy- chological stress related to perceived racial discrimination (Black et al., 2015; Lewis et al., 2014; Sampson et al., 2016).

Allostatic load refers to the cost of an individual’s chronic exposure to fluctuating and/or heightened neuroendocrine re- sponses resulting from repeated or chronic stressful environmental challenges (Guidi et al., 2021). One study linked National Health and Nutrition Examination Study III data to the 2015 mortality data for adults 25 years or older (n = 13,673 with 6,026 deaths) and then estimated the associations of allostatic load scores (2 and ≥3 relative to ≤1) with all-cause and CVD-specific mortality. Allo- static load scores were associated with higher all-cause and CVD- specific mortality rates (Borrell et al., 2020). Others have reported that NHB exhibited a higher allostatic load mean score than NHW (Geronimus et al., 2006, 2007).

There is compelling evidence that changes in biological systems occur in response to chronic adverse daily environmental stressors and that these changes can increase chronic disease and CVD risk and mortality (Barker, 2004; Hanson & Gluckman, 2014). Studies have also identified specific pathophysiologic me- chanisms through which adverse external environments can affect the biology of an individual (Cunliffe, 2016; Schwartz, 2017). The pathophysiologic mechanisms include increased hypothalamic– pituitary–adrenal axis activity, autonomic nervous system reactiv- ity, inflammation, oxidative stress, and endothelial dysfunction (Ghiadoni et al., 2000; Gill et al., 2009; von Kanel et al., 2008; Wood, 2014).

Chronic psychological stress may cause the development of atherosclerosis (Kaplan et al., 1991) due to elevated sympathetic nerve activity, which acts directly or in combination with inflam- mation (Lewthwaite et al., 2002), elevated cortisol levels (Chrousos, 1995), and other metabolic disturbances (Brunner et al., 2002). It is also thought that autonomic reflex mechanisms, specifically baroreceptor function, may also be reduced by chronic stress, which could contribute to hypertension (Lucini et al., 2005; Mezzacappa et al., 2001). Evidence suggests that cumulative experiences of social inequality and racism among NHB leading to chronic psychological stress may affect the ability of physio- logical systems to respond and/or adapt (disrupted allostasis) to prolonged or repeated stress (Geronimus et al., 2006, 2007; McEwen, 1998).

The profound racial disparity in CVD incidence and preva- lence has compelled researchers to look beyond conventional risk factors because they do not entirely explain the increased CVD risk in NHB individuals (Brewer et al., 2013; Brewer & Cooper, 2014; Gallo et al., 2014). Researchers started to assess potential psycho- social risk factors in an effort to better understand unconventional CVD risk factors (Redmond et al., 2011). Racial and ethnic discrimination has been termed a multidimensional environmental stressor at the societal and individual levels (Brewer & Cooper, 2014) and may partially explain the increased prevalence of CVD in NHB compared with NHW. Indeed, race-related psychological stress, or racialized stress, is perceived by many NHB as an influential factor toward their elevated CVD risk (Wyatt et al., 2003).

A meta-analytic review on discrimination and health demon- strated that perceptions of discrimination were related to height- ened physiological and psychological stress responses (Pascoe & Smart Richman, 2009). Race consciousness (i.e., the awareness of one’s own race as a distinct ethnic group) is thought to be a measure of perceived racism that captures a heightened vigilance and anticipatory stress related to the threat of discrimination (Brewer

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&Cooper, 2014). Brewer et al. (2013) found that experiencing race consciousness was associated with higher diastolic blood among NHB but not NHW patients with hypertension. Hicken et al. (2014) further examined the effect of racism-related vigilance or chronic stress resulting from the anticipation of, or perseverance of, racial discrimination on hypertension. They reported that NHB with the highest vigilance levels had a higher likelihood of hypertension compared with NHW.

In addition to the SES and environmental factors that contrib- ute to the risk for CVD, discriminatory attitudes and behaviors based on race (implicit bias) by health care professionals may contribute to suboptimal diagnosis and management of CVD among patients from minority groups, particularly NHB (Mody et al., 2012). Institutional racism leads to inequities in access to and quality of health care. Studies have demonstrated widespread disparities between treatment of NHB compared with NHW in health care delivery in areas such as clinician adherence to pre- scribing guidelines, therapy intensification, and use of invasive cardiac procedures, even after controlling for clinical and socio- economic factors (Mody et al., 2012).

Finally, as mentioned above, approximately 200,000 of deaths caused each year by heart disease, stroke, and hypertension are preventable (Centers for Disease Control and Prevention, 2013). The increase in CVD prevalence over the decades is associated with a decrease in physical activity levels. Thus, CVD is a largely preventable hypokinetic disease, a disease associated with disuse (Kraus & Rabb, 1961; Lee et al., 2012). A syndemics framework examines the health consequences of identifiable disease interac- tions and the social, environmental, or economic factors that pro- mote such interaction and worsen disease (Li et al., 2020). In other words, syndemics is used to account for the interplay and synergistic nature of person, place, and timing in the development of disease (Cardinal, 2016; Singer, 2009). Community-based physical activity interventions are critically needed in minority communities in order to mitigate the risk of hypokinetic diseases such as CVD in these at- risk populations (Wallerstein & Duran, 2010).

Conclusion

It has been known for decades that NHB have worse overall cardiovascular health and higher CVD mortality than NHW. Little has changed since 2005 when noteworthy disparities in prevalence, disease management, and outcomes were reported (Bonow et al., 2005). It is not simply biologic/genetic, individual choice, or random occurrence that causes the racial disparity in CVD. The racial disparity is also caused by the biologic and physiologic consequences of systematic and institutional racism experienced by NHB. In addition, health care professionals and clinical scientists alone cannot solve racial disparities in cardiovascular health because much of the contributing causes for the disparities are deeply rooted in our society and are not merely medical issues.

Acknowledgments

The authors are grateful to Dr. Mary Rudisill for giving us the time and resources to write this manuscript.

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