Race,Ethnicity, and Self-Reported Hypertension: Analysis of Data From the National Health Interview Survey, 1997–2005

Objective. I estimated the association between race and self-reported hypertension among Hispanics and non-Hispanics and determined whether this association was stronger among non-Hispanics.Methods. With data from the 1997–2005 National Health Interview Survey, I used logistic regression to estimate the strength of the association between race/ethnicity and self-reported hypertension among US adults.Results. The overall prevalence of self-reported hypertension was 24.5%, with lower prevalence among Hispanics (16.7%) than among non-Hispanics (25.2%; P < .01). Blacks, regardless of ethnicity, had the highest prevalence. Compared with non-Hispanic Whites, non-Hispanic Blacks had 48% (odds ratio [OR] = 1.48; 95% confidence interval [CI] = 1.41, 1.55) greater odds of reporting hypertension; Hispanic Whites had 23% (OR = 0.81; 95% CI = 0.76, 0.88) lower odds. There was no difference in the strength of the association between race and self-reported hypertension observed among non-Hispanics (OR for Blacks = 1.47) and among Hispanics (OR for Blacks = 1.20; for interaction, P = 0.43).Conclusions. The previously reported hypertension advantage of Hispanics holds for Hispanic Whites only. As Hispanics continue their rapid growth in the United States, race may have important implications on their disease burden, because most US health disparities are driven by race and its socially patterned experiences.Hypertension affects more than 65 million US adults¹ and is a major risk factor for cardiovascular disease (CVD).^2,3 The prevalence of hypertension in the US population increased by 30% between the third National Health and Nutrition Examination Survey (NHANES III, 1988–1994) and NHANES 1999–2000.¹ Previous studies have consistently reported that, compared with non-Hispanic Whites, Hispanics have a lower prevalence of hypertension and that non-Hispanic Blacks have a higher prevalence of hypertension.^1,2,4–7 However, these studies focused mostly on Mexican Americans, ignoring the heterogeneity of the Hispanic population. For example, because of their colonization patterns, Hispanics can be of any race (i.e., White, Black, or some other race).⁸ Despite the impact of race on health in US society^9–11 and the projected growth of the Hispanic population,^12–14 there is a dearth of knowledge addressing the relationship between race and health among Hispanics. However, the evidence that does exist parallels findings observed among non-Hispanics: Hispanic Blacks experience worse health outcomes than do Hispanic Whites.^15–18 Thus, the investigation of race and health outcomes in Hispanics is imperative.Hypertension has been attributed to obesity, sodium and potassium intake, physical inactivity, alcohol consumption, smoking, and psychosocial stress.³ Of these, only psychosocial stress has been shown to be unequally distributed across racial/ethnic groups. Research suggests that racial discrimination—a trigger of psychosocial stress—is common in the everyday life of non-Hispanic Blacks and may lead to CVD.^19–26 Given this, and consistent with the historical pattern of disadvantage among non-Hispanic Blacks,^9,11,27,28 it is possible that Hispanic Blacks could be exposed to the same deleterious experiences of racial discrimination and racism as non-Hispanic Blacks because of the salience and social visibility associated with their race or dark skin color. These experiences may lead to disadvantaged life chances, which then translate into poorer health.The availability of 9 years of data from the National Health Interview Survey (NHIS, 1997–2005) afforded the opportunity to investigate the association between race and self-reported hypertension in Hispanics and non-Hispanics before and after adjustment for selected characteristics and known risk factors and to compare the strength of this association in Hispanics and non-Hispanics. If race as a social construct channels Hispanic Blacks to exposures detrimental to health as it does for non-Hispanic Blacks, the lower odds of hypertension for Hispanics observed in previous studies would apply only to Hispanic Whites whereas Hispanic Blacks would have odds of hypertension similar to those of non-Hispanic Whites or intermediate between non-Hispanic Whites and non-Hispanic Blacks. However, the magnitude of the association between race and hypertension would be stronger among non-Hispanics than among Hispanics.     

Health status, neighborhood socioeconomic context, and premature mortality in the United States: The National Institutes of Health-AARP Diet and Health Study

Objectives. We examined whether the risk of premature mortality associated with living in socioeconomically deprived neighborhoods varies according to the health status of individuals.Methods. Community-dwelling adults (n = 566 402; age = 50–71 years) in 6 US states and 2 metropolitan areas participated in the ongoing prospective National Institutes of Health–AARP Diet and Health Study, which began in 1995. We used baseline data for 565 679 participants on health behaviors, self-rated health status, and medical history, collected by mailed questionnaires. Participants were linked to 2000 census data for an index of census tract socioeconomic deprivation. The main outcome was all-cause mortality ascertained through 2006.Results. In adjusted survival analyses of persons in good-to-excellent health at baseline, risk of mortality increased with increasing levels of census tract socioeconomic deprivation. Neighborhood socioeconomic mortality disparities among persons in fair-to-poor health were not statistically significant after adjustment for demographic characteristics, educational achievement, lifestyle, and medical conditions.Conclusions. Neighborhood socioeconomic inequalities lead to large disparities in risk of premature mortality among healthy US adults but not among those in poor health.Research dating back to at least the 1920s has shown that the United States has experienced persistent and widening socioeconomic disparities in premature mortality over time.^1–5 However, it has been unclear whether socioeconomic inequalities affect the longevity of persons in good and poor health equally. Socioeconomic status (SES) and health status are interrelated,^6–8 and both are strong independent predictors of mortality.⁹ Low SES is associated with greater risk of ill health and premature death,^{1–5,8,10–13} partly attributable to disproportionately high prevalence of unhealthful lifestyle practices^10,14,15 and physical and mental health conditions.^13,16 Correspondingly, risk of premature mortality is higher in poor than in more affluent areas.^16,17 Although the association between neighborhood poverty and mortality is independent of individual-level SES,^17,18 aggregation of low-SES populations in poor areas may contribute to variations in health outcomes across neighborhoods. Conversely, economic hardships resulting from ill health may lead persons in poor physical or mental health to move to poor neighborhoods.¹⁹ This interrelatedness may create spurious associations between neighborhood poverty and mortality.Although previous studies have found that the risk of premature death associated with poor health status varies according to individuals'' SES,^20,21 no published studies have examined whether the relative risks for premature mortality associated with living in neighborhoods with higher levels of socioeconomic deprivation vary by health status of individuals. Clarifying these relationships will inform social and public health policies and programs that aim to mitigate the health consequences of neighborhood poverty.^22,23We used data from a large prospective study to examine whether the risk of premature mortality associated with neighborhood socioeconomic context differs according to health status at baseline and remains after adjustment for person-level risk factors for mortality, such as SES, lifestyle practices, and chronic medical illnesses.     

A Systematic Review of Neighborhood Disparities in Point-of-Sale Tobacco Marketing

We systematically reviewed evidence of disparities in tobacco marketing at tobacco retailers by sociodemographic neighborhood characteristics. We identified 43 relevant articles from 893 results of a systematic search in 10 databases updated May 28, 2014. We found 148 associations of marketing (price, placement, promotion, or product availability) with a neighborhood demographic of interest (socioeconomic disadvantage, race, ethnicity, and urbanicity).Neighborhoods with lower income have more tobacco marketing. There is more menthol marketing targeting urban neighborhoods and neighborhoods with more Black residents. Smokeless tobacco products are targeted more toward rural neighborhoods and neighborhoods with more White residents. Differences in store type partially explain these disparities.There are more inducements to start and continue smoking in lower-income neighborhoods and in neighborhoods with more Black residents. Retailer marketing may contribute to disparities in tobacco use. Clinicians should be aware of the pervasiveness of these environmental cues.Tobacco products and their marketing materials are ubiquitous in US retailers from pharmacies to corner stores.1 A similar presence is found across the globe, except in countries that ban point-of-sale (POS) tobacco marketing (e.g., Australia, Canada, Thailand2). In the United States, the POS has become the main communications channel for tobacco marketing3,4 and is reported as a source of exposure to tobacco marketing by more than 75% of US youths.5 Burgeoning evidence6,7 suggests that marketing at the POS is associated with youths’ brand preference,8 smoking initiation,9 impulse purchases,10,11 and compromised quit attempts.12,13The marketing of tobacco products is not uniform; it is clear from industry documents that the tobacco industry has calibrated its marketing to target specific demographic groups defined by race,14 ethnicity,15 income,16 mental health status,17 gender,18,19 and sexual orientation.20 Framed as an issue of social and environmental justice,14 research has documented historical racial, ethnic, and socioeconomic disparities in the presence of tobacco billboards,21–25 racial disparities in total tobacco marketing volume,24 and targeting of menthol cigarettes to communities with more Black residents.25,26 Targeted marketing of a consumer product that kills up to half27 of its users when used as directed exacerbates inequities in morbidity and mortality. Smoking is estimated to be responsible for close to half of the difference in mortality between men in the lowest and highest socioeconomic groups.28 However, evidence of marketing disparities is scattered across multiple disciplines and marketing outcomes, such as product availability, advertising quantity, presence of promotional discounts, and price. A synthesis of this literature would provide valuable information for intervention on tobacco marketing in the retail environment and inform etiological research on health disparities.To address this gap in the literature, we systematically reviewed observational studies that examined the presence and quantity of POS tobacco marketing to determine the extent to which marketing disparities exist by neighborhood demographic characteristic (i.e., socioeconomic disadvantage, race, ethnicity, and urbanicity).     

Life-Course Socioeconomic Position and Incidence of Diabetes Mellitus Among Blacks and Whites: The Alameda County Study, 1965�C1999

Objectives. We examined associations between several life-course socioeconomic position (SEP) measures (childhood SEP, education, income, occupation) and diabetes incidence from 1965 to 1999 in a sample of 5422 diabetes-free Black and White participants in the Alameda County Study.Methods. Race-specific Cox proportional hazard models estimated diabetes risk associated with each SEP measure. Demographic confounders (age, gender, marital status) and potential pathway components (physical inactivity, body composition, smoking, alcohol consumption, hypertension, depression, access to health care) were included as covariates.Results. Diabetes incidence was twice as high for Blacks as for Whites. Diabetes risk factors independently increased risk, but effect sizes were greater among Whites. Low childhood SEP elevated risk for both racial groups. Protective effects were suggested for low education and blue-collar occupation among Blacks, but these factors increased risk for Whites. Income was protective for Whites but not Blacks. Covariate adjustment had negligible effects on associations between each SEP measure and diabetes incidence for both racial groups.Conclusions. These findings suggest an important role for life-course SEP measures in determining risk of diabetes, regardless of race and after adjustment for factors that may confound or mediate these associations.Diabetes mellitus is a major cause of morbidity and mortality in the United States.^1,2 Type 2 diabetes disproportionately affects Hispanics, as well as non-Hispanic Black Americans, American Indians/Alaska Natives, and some Asian/Pacific Islander groups. In the United States, members of racial and ethnic minority groups are almost twice as likely to develop or have type 2 diabetes than are non-Hispanic Whites.^2–5 Significant racial and ethnic differences also exist in the rates of diabetes-related preventive services, quality of care, and disease outcomes.^6–10Researchers have attempted to determine why, relative to Whites, members of racial and ethnic minority groups are disproportionately affected by diabetes. For example, compared with White Americans, Black Americans are presumed to have stronger genetic^5,11 or physiological^11–13 susceptibility to diabetes, or greater frequency or intensity of known diabetes risk factors, such as obesity, physical inactivity, and hypertension.^14–17Black Americans also are more likely than are White Americans to occupy lower socioeconomic positions.¹⁸ Low socioeconomic position (SEP) across the life course is known to influence the prevalence^19–24 and incidence^3,19,25–30 of type 2 diabetes. The risk of diabetes also is greater for people who are obese,^3,17,31 physically inactive,^3,32 or have hypertension,^33,34 all of which are conditions more common among people with lower SEP.^16,35–37Several studies have focused on the extent to which socioeconomic factors, body composition (i.e., weight, height, body mass index, and waist circumference), and behaviors explain the excess risk of diabetes attributed to race.^4,12,19,30 For example, 2 separate studies, one with data from the Health and Retirement Study¹⁹ and the other with data from the Atherosclerosis Risk in Communities Study,³⁰ used race to predict diabetes incidence. Attempting to separate the direct and indirect effects of race on diabetes,³⁸ these studies assessed, via statistical adjustment, which socioeconomic measures and diabetes-related risk factors, when adjusted, could account for the excess risk among Black participants relative to White participants.^19,30 Adjustment for education lessened the effect of Black race on diabetes incidence in the Atherosclerosis Risk in Communities Study.³⁰ In the Health and Retirement Study, excess risk attributed to Black race was not explained by early-life socioeconomic disadvantage, but it was reduced after adjustment for education and later-life economic resources.¹⁹ The validity of this analytic approach has been challenged, however, because the socioeconomic measures used were assumed to have the same meaning across all racial/ethnic groups, a questionable assumption³⁸ in the United States, especially in 1965.We sought to explore the predictive effects of several life-course socioeconomic factors on the incidence of diabetes among both Black and White Americans. We examined demographic confounders (age, gender, marital status) and diabetes risk factors (obesity, large waist circumference, physical inactivity, high blood pressure, depression, access to health care) as possible mediators of the observed associations between SEP and incident diabetes (i.e., the development of new cases of diabetes over time).     

Socioeconomic Status,Race, and Mortality: A Prospective Cohort Study

Objectives. We evaluated the independent and joint effects of race, individual socioeconomic status (SES), and neighborhood SES on mortality risk.Methods. We conducted a prospective analysis involving 52 965 non-Hispanic Black and 23 592 non-Hispanic White adults taking part in the Southern Community Cohort Study. Cox proportional hazards modeling was used to determine associations of race and SES with all-cause and cause-specific mortality.Results. In our cohort, wherein Blacks and Whites had similar individual SES, Blacks were less likely than Whites to die during the follow-up period (hazard ratio [HR] = 0.78; 95% confidence interval [CI] = 0.73, 0.84). Low household income was a strong predictor of all-cause mortality among both Blacks and Whites (HR = 1.76; 95% CI = 1.45, 2.12). Being in the lowest (vs highest) category with respect to both individual and neighborhood SES was associated with a nearly 3-fold increase in all-cause mortality risk (HR = 2.76; 95% CI = 1.99, 3.84). There was no significant mortality-related interaction between individual SES and neighborhood SES among either Blacks or Whites.Conclusions. SES is a strong predictor of premature mortality, and the independent associations of individual SES and neighborhood SES with mortality risk are similar for Blacks and Whites.From birth through approximately age 85 years, there is a mortality rate disparity between Blacks and Whites in the United States that peaks in early adulthood and slowly narrows thereafter.1–4 Most of the excess deaths among Blacks occur in middle-aged adults, given the confluence of rising mortality rates and the disparity at those ages. During much of the 20th century, this disparity was unyielding,4–6 but recent data point to some narrowing of the gap beginning in the 1990s.7–9 Still, in 2011 the highest age-standardized death rate in the United States was that among non-Hispanic Blacks (877.4 per 100 000 standard population), followed by non-Hispanic Whites (738.1 per 100 000 standard population).10 Also, average life expectancies at birth in 2011 were 4.5 years shorter for Black than White men and 3.1 years shorter for Black than White women.10Although national mortality data are routinely reported by race/ethnicity, their interpretation must consider the determinants of race-specific mortality rates, including behavioral, social, economic, and political factors that determine the resources available to maintain health and prolong life.3 Whether socioeconomic status (SES) completely accounts for mortality differences between Blacks and Whites is not clear. Previous studies have reported that SES alone cannot fully account for the disparity, although in settings where Blacks and Whites are drawn from considerably different SES strata, confounding by SES may be difficult to overcome.11–14 By contrast, in settings where race-specific SES differences are minimal (including the current study), it has been suggested that important health indicators are quite similar by race.15–17 Individual-level SES aside, neighborhood-level SES has also been reported to influence mortality rates,18 but fewer investigations have assessed the joint contribution of individual and neighborhood SES,19–22 and analyses assessing the interplay of these 2 SES domains with race are rare.19,21We thus took the opportunity, within a large prospective study of non-Hispanic Black and White adults (residing in a large area of the United States, enrolled mainly in low-income settings but also non-low-income settings, and representing a range of SES levels), to evaluate the independent and joint contributions of race, individual SES, and neighborhood SES to overall and cause-specific mortality risk.     

Connecting Race and Place: A County-Level Analysis of White,Black, and Hispanic HIV Prevalence,Poverty, and Level of Urbanization

Objectives. We evaluated the role of poverty in racial/ethnic disparities in HIV prevalence across levels of urbanization.Methods. Using national HIV surveillance data from the year 2009, we constructed negative binomial models, stratified by urbanization, with an outcome of race-specific, county-level HIV prevalence rates and covariates of race/ethnicity, poverty, and other publicly available data. We estimated model-based Black–White and Hispanic–White prevalence rate ratios (PRRs) across levels of urbanization and poverty.Results. We observed racial/ethnic disparities for all strata of urbanization across 1111 included counties. Poverty was associated with HIV prevalence only in major metropolitan counties. At the same level of urbanization, Black–White and Hispanic–White PRRs were not statistically different from 1.0 at high poverty rates (Black–White PRR = 1.0, 95% confidence interval [CI] = 0.4, 2.9; Hispanic–White PRR = 0.4, 95% CI = 0.1, 1.6). In nonurban counties, racial/ethnic disparities remained after we controlled for poverty.Conclusions. The association between HIV prevalence and poverty varies by level of urbanization. HIV prevention interventions should be tailored to this understanding. Reducing racial/ethnic disparities will require multifactorial interventions linking social factors with sexual networks and individual risks.Within the United States, disparities in diagnosed HIV prevalence among the 3 major racial/ethnic groups (White, Black, and Hispanic) are striking. At the end of 2009, 43% of people living with an HIV diagnosis were Black, 35% White, and 19% Hispanic.1 Concurrently, Blacks constituted only 12% of the population, non-Hispanic Whites 65%, and Hispanics 16%.2 In the 46 states with confidential name-based HIV reporting since at least January 2007, the estimated diagnosed HIV prevalence rate at the end of 2009 was 952 per 100 000 people among Blacks (near the threshold for a generalized epidemic),1 320 per 100 000 among Hispanics, and 144 per 100 000 among Whites; compared with Whites, therefore, Blacks and Hispanics were respectively 6.6 times and 2.2 times more likely to be living with an HIV diagnosis.A number of mechanisms, primarily structural and social factors, have been proposed to explain these stark racial/ethnic disparities in HIV prevalence.3,4 Structural factors, such as oppression and mistrust in government, may hinder receptivity to prevention outreach and increase HIV prevalence.3 Social constructs (e.g., homophobia and HIV stigma) may discourage open discussion of risk behaviors and limit HIV testing and treatment. Additionally, limited access to health care resources has been identified as a key driver of racial/ethnic health disparities.5 Finally, Black men are more likely than White men to be both incarcerated and infected with HIV while incarcerated.6,7 All of these factors are, in turn, associated with poverty.8 However, specific relationships among these multiple factors and racial/ethnic HIV prevalence disparities, and variation of these relationships across levels of urbanization, are not well understood.Previous analyses of national surveillance and survey data in the United States have focused on associations between HIV prevalence rates, poverty, and race exclusively in urban areas, finding no disparities in poverty-adjusted HIV prevalence rates among heterosexuals in urban settings.9,10 Furthermore, among heterosexuals living in US urban areas with high AIDS prevalence, HIV prevalence rates among those living at or below the poverty line were 2.2 times as high as rates among those living above the poverty line.10 A more recent analysis of US surveillance data confirmed the complex associations between demographics, social determinants of health, and AIDS diagnosis rates.8However, variation in these factors across the urban–rural continuum may limit generalizability of these findings to nonurban settings, where similar research is lacking. In 2009, the proportions of Black and Hispanic Americans living in poverty were roughly twice that of White Americans.11 For all races/ethnicities, the proportion living in poverty is greater in rural areas than in urban areas.12 Additionally, rural areas, with lower HIV prevalence, are more likely to be medically underserved, with reduced access to HIV care and treatment.13In the context of these complex sociodemographic associations, previously observed associations in the United States between poverty and racial/ethnic disparities in HIV may differ outside of urban areas. Therefore, using publicly available county-level data, we first describe the association between poverty and HIV prevalence by race/ethnicity across levels of urbanization. We subsequently examine racial/ethnic disparities in HIV prevalence across levels of urbanization, after controlling for poverty. We hypothesized that, in all strata of urbanization, poverty-adjusted Black–White and Hispanic–White HIV prevalence rate ratios (PRRs) would statistically differ from 1.0.     

Community Poverty and Trends in Racial/Ethnic Survival Disparities Among People Diagnosed With AIDS in Florida, 1993–2004

Objectives. We described the racial/ethnic disparities in survival among people diagnosed with AIDS in Florida from 1993 to 2004, as the availability of highly active antiretroviral therapy (HAART) became widespread. We determined whether these disparities decreased after controlling for measures of community-level socioeconomic status.Methods. We compared survival from all causes between non-Hispanic Blacks and non-Hispanic Whites vis-a-vis survival curves and Cox proportional hazards models controlling for demographic, clinical, and area-level poverty factors.Results. Racial/ethnic disparities in survival peaked for those diagnosed during the early implementation of HAART (1996–1998) with a Black-to-White hazard ratio (HR) of 1.72 (95% confidence interval [CI] = 1.62, 1.83) for males and 1.40 (95% CI = 1.24, 1.59) for females. These HRs declined significantly to 1.48 (95% CI = 1.35, 1.64) for males and nonsignificantly to 1.25 (95% CI = 1.05, 1.48) for females in the 2002 to 2004 diagnosis cohort. Disparities decreased significantly for males but not females when controlling for baseline demographic factors and CD4 count and percentage, and became nonsignificant in the 2002 to 2004 cohort after controlling for area poverty.Conclusions. Area poverty appears to play a role in racial/ethnic disparities even after controlling for demographic factors and CD4 count and percentage.The HIV/AIDS epidemic has disproportionately affected the non-Hispanic Black population in the United States. In 2008, an estimated 545 000 non-Hispanic Blacks were living with HIV/AIDS.1 The estimated prevalence of HIV infection for 2008 among non-Hispanic Blacks was 18.2 per 1000 population, more than 7 times higher than the estimated rate for non-Hispanic Whites (non-Hispanic Whites; 2.4 per 1000).1 Non-Hispanic Blacks as a group not only have a higher prevalence of HIV/AIDS, but once infected also have a lower survival rate. The 3-year survival rate in the United States for people diagnosed with AIDS between 2001 and 2005 was 80% among non-Hispanic Blacks compared with 84% for non-Hispanic Whites, 83% for Hispanics, and 88% for Asians,2 further contributing to the disparities in the HIV mortality rate of 16.8 per 100 000 among non-Hispanic Blacks compared with 1.6 per 100 000 among non-Hispanic Whites during 2007.3 Race/ethnicity is a fundamentally social as opposed to a biological construct,4,5 and survival disparities between non-Hispanic Blacks and non-Hispanic Whites have not generally been seen in settings with universal health care access such as in the Veterans Administration health care system,6 the military health care system,7 or a health maintenance organization.8 Therefore, potentially modifiable social explanations for the observed racial/ethnic disparities in survival should be examined.A most remarkable advance in medical treatment in the past century was the development of highly active antiretroviral therapy (HAART). It led to a significant improvement in survival from HIV/AIDS, 9–12 but racial/ethnic disparities in HIV/AIDS survival remain2, 13–16 and in New York City appeared to widen.17 Despite these well-recognized health disparities, there is a critical gap in the knowledge about why the disparity exists. Two population-based studies, both in San Francisco, California (a city that has provided free HIV care for those who cannot afford it), found that Black race was no longer associated with survival between 1996 and 2001 after controlling for neighborhood socioeconomic status (SES), and that this SES effect seemed to be related to HAART use.18,19 However, in a study using HIV surveillance data from 33 states, racial/ethnic disparities in 5-year survival after HIV diagnosis between 1996 and 2003 persisted after adjusting for county-level SES and other factors.20 The objective of this study was to describe the racial/ethnic disparities in AIDS survival in Florida among people diagnosed with AIDS between 1993 and 2004 (a period spanning the time before and during the widespread availability of HAART) and to determine if these disparities decrease after controlling for community-level SES.     

Racial/Ethnic and Socioeconomic Differences in Short-Term Breast Cancer Survival Among Women in an Integrated Health System

Objectives. We examined the combined influence of race/ethnicity and neighborhood socioeconomic status (SES) on short-term survival among women with uniform access to health care and treatment.Methods. Using electronic medical records data from Kaiser Permanente Northern California linked to data from the California Cancer Registry, we included 6262 women newly diagnosed with invasive breast cancer. We analyzed survival using multivariable Cox proportional hazards regression with follow-up through 2010.Results. After consideration of tumor stage, subtype, comorbidity, and type of treatment received, non-Hispanic White women living in low-SES neighborhoods (hazard ratio [HR] = 1.28; 95% confidence interval [CI] = 1.07, 1.52) and African Americans regardless of neighborhood SES (high SES: HR = 1.44; 95% CI = 1.01, 2.07; low SES: HR = 1.88; 95% CI = 1.42, 2.50) had worse overall survival than did non-Hispanic White women living in high-SES neighborhoods. Results were similar for breast cancer–specific survival, except that African Americans and non-Hispanic Whites living in high-SES neighborhoods had similar survival.Conclusions. Strategies to address the underlying factors that may influence treatment intensity and adherence, such as comorbidities and logistical barriers, should be targeted at low-SES non-Hispanic White and all African American patients.Breast cancer is the most common cancer among women in the United States, and it is the second leading cause of cancer death.1 Despite significant improvements in breast cancer survival from 1992 to 2009,1,2 racial/ethnic and socioeconomic survival disparities have persisted.3,4 African American women have consistently been found to have worse survival after breast cancer,3,5–11 Hispanic women have worse or similar survival,3,9,11,12 and Asian women as an aggregated group have better or similar survival3,9,11,12 than do non-Hispanic White women. Underlying factors thought to contribute to these racial/ethnic disparities include differences in stage at diagnosis,8,12,13 distributions of breast cancer subtypes,14–16 comorbidities,12,13,17 access to and utilization of quality care,13,18 and treatment.12,13Numerous studies also have found poorer survival after breast cancer diagnosis among women residing in neighborhoods of lower socioeconomic status (SES).6,9,19,20 Research has shown that inadequate use of cancer screening services, and consequent late stage diagnosis and decreased survival, contribute to the SES disparities.21,22 Similar to racial/ethnic disparities, SES disparities have been attributed to inadequate treatment and follow-up care and comorbidities.18 Previous population-based studies have continued to observe racial/ethnic survival disparities after adjusting for neighborhood SES, but these studies have not considered the combined influence of neighborhood SES and race/ethnicity.3,9,11,12,23 These disparities may remain because information on individual-level SES, health insurance coverage, comorbidities, quality of care, and detailed treatment regimens have typically not been available.3,8,9,11,13 Even among studies using national Surveillance Epidemiology and End Results–Medicare linked data, in which more detailed information on treatment and comorbidities are available among some patients aged 65 years and older, survival disparities have remained.12,23,24 However, not all data on medical conditions and health care services are captured in Medicare claims, including data on Medicare beneficiaries enrolled in HMOs (health maintenance organizations).25,26Using electronic medical records data from Kaiser Permanente Northern California (KPNC) linked to data from the population-based California Cancer Registry (CCR), we recently reported that chemotherapy use followed practice guidelines but varied by race/ethnicity and neighborhood SES in this integrated health system.27 Therefore, to overcome the limitations of previous studies and address simultaneously the multiple social28 and clinical factors affecting survival after breast cancer diagnosis, we used the linked KPNC–CCR database to determine whether racial/ethnic and socioeconomic differences in short-term overall and breast cancer–specific survival persist in women in a membership-based health system. Our study is the first, to our knowledge, to consider the combined influence of neighborhood SES and race/ethnicity and numerous prognostic factors, including breast cancer subtypes and comorbidities, thought to underlie these long-standing survival disparities among women with uniform access to health care and treatment.     

Lifting boats without closing gaps: child health outcomes in distressed US cities from 1992-2002

Objectives. We compared cause-specific mortality and birth rates for children and youths aged younger than 18 years in 100 US cities from 1992 through 2002.Methods. We used 5 census indicators to categorize the 100 most populous US cities in 1990 as economically distressed or nondistressed. We used Poisson regression to calculate rate ratios for cause-specific mortality and birth rates, comparing distressed cities to nondistressed cities overall and by race/ethnicity from 1992 through 2002. We also calculated rates of change in these variables within each city over this period.Results. Despite improvements in health for the study population in all cities, disparities between city groups held steady or widened over the study period. Gaps in outcomes between Whites and Blacks persisted across all cities. Living in a distressed city compounded the disparities in poor outcomes for Black children and youths.Conclusions. A strong national economy during the study period may have facilitated improvements in health outcomes for children and youths in US cities, but these benefits did not close gaps between distressed and nondistressed cities.Substantial evidence has demonstrated that city residence in the late 19th and early to mid-20th centuries was associated with high rates of injury and infectious diseases.^1–6 Researchers have noted that cities have continued to impose a health penalty on their residents, with poorer outcomes among children and youth in cities than in the rest of the United States.^7–11Some have argued that this penalty was associated with the period of urban decline after 1970, during which physical infrastructures deteriorated and city government services shrank. Yet a number of scholars have noted that the decline from 1970 to 1990 set cities on different demographic and economic trajectories.^12–17 In this formulation, some cities suffered substantively different qualities of economic distress. One group of cities endured ongoing “White flight,” increasing crime rates, poorly performing schools, shrinking populations, an eroding tax base, and greater demand for health and social services.^18–22 A second group of cities experienced the same ills but less severely, and they were buoyed by new immigration.^23,24 These trajectories may have positioned cities differently to benefit from the economic prosperity that the United States experienced from 1992 through 2001.Surprisingly, even within the field of urban health, little attention has been paid to the ways in which economic and population differences among cities may be associated with poorer health outcomes and racial/ethnic health disparities among cities. To be sure, investigators have extensively studied the racial/ethnic disparities that persist despite overall gains in life expectancy and in specific health indicators in the last 15 years.^25–29 However, to our knowledge, health scholars have not investigated the different trajectories of city distress as a factor explaining health disparities and urban health. Several influential studies have demonstrated that health disparities exist between Blacks and Whites within cities,^30–32 and that the health of Blacks in cities is worse than that of Blacks in rural areas.^33,34 Much recent scholarship has demonstrated that neighborhoods of concentrated poverty in cities impose an additional health disadvantage beyond that explained by a resident''s individual poverty level.^35–39 The independent effects of neighborhood residence in urban areas have been documented across educational and social outcomes as well.^40–44We investigated the impact of different patterns of urban distress on selected mortality and birth outcomes for children and youths from 1992 through 2002. First, we assessed whether there were differences in health outcomes for children and youths in economically distressed versus nondistressed cities at the beginning of this period and whether there were racial disparities for these outcomes between different groups of cities in 1992. Next we asked whether, as the period of economic prosperity ended, all boats had risen to the same degree. That is, did improvements in health over this period narrow differences between economically distressed and nondistressed cities? Further, did disparities in health outcomes between Black and White children and youths residing in these 2 groups of cities decrease during this period? To address these questions, we investigated selected causes of mortality and birth rates for children and youths in 1992 and 2002 in 100 US cities. We also compared mortality and birth rates for Whites and Blacks in economically distressed cities versus nondistressed cities, to assess differences across this time period.     

Racial/Ethnic Disparities in Hypertension Prevalence: Reconsidering the Role of Chronic Stress

Objectives. We investigated the association between anticipatory stress, also known as racism-related vigilance, and hypertension prevalence in Black, Hispanic, and White adults.Methods. We used data from the Chicago Community Adult Health Study, a population-representative sample of adults (n = 3105) surveyed in 2001 to 2003, to regress hypertension prevalence on the interaction between race/ethnicity and vigilance in logit models.Results. Blacks reported the highest vigilance levels. For Blacks, each unit increase in vigilance (range = 0–12) was associated with a 4% increase in the odds of hypertension (odds ratio [OR] = 1.04; 95% confidence interval [CI] = 1.00, 1.09). Hispanics showed a similar but nonsignificant association (OR = 1.05; 95% CI = 0.99, 1.12), and Whites showed no association (OR = 0.95; 95% CI = 0.87, 1.03).Conclusions. Vigilance may represent an important and unique source of chronic stress that contributes to the well-documented higher prevalence of hypertension among Blacks than Whites; it is a possible contributor to hypertension among Hispanics but not Whites.Racial and ethnic disparities in hypertension are some of the most widely studied and consequential sources of social disparities in health in the United States.1–3 For example, recent prevalence estimates show that roughly 40% of Black adults but only 30% of White adults have hypertension.4 In addition, the incidence of hypertension occurs at younger ages for Blacks than Whites.1 These disparities are reflected in the larger burden of hypertension-related health and economic costs carried by non-White than White Americans. For example, mortality rates attributable to hypertension are roughly 15 deaths per 100 000 people for White men and women; the mortality rate for Black women is 40 per 100 000 and more than 50 per 100 000 for Black men.5 Among all health conditions, hypertension accounts for the greatest portion of disparities in years of lost life.6 Economically speaking, if Black Americans had the hypertension prevalence of White Americans, about $400 million would be saved in out-of-pocket health care expenses, about $2 billion would be saved in private insurance costs, and $375 million would be saved from Medicare and Medicaid—per year.7Despite the tremendous amount of research devoted to clarifying the factors that generate these disparities, most studies find that they persist after adjustment for a wide range of socioeconomic, behavioral, and biomedical risk factors.8 In fact, although disparities exist for several of these risk factors (e.g., socioeconomic status), numerous studies have shown no disparities in many others (e.g., smoking, obesity for men, lipid profile).2 Despite substantial investment in interventions to eliminate hypertension disparities, evidence suggests that these disparities have actually grown over the past few decades,9 suggesting that numerous unknown factors drive disparities in hypertension.3     

Alcohol Retail Density and Demographic Predictors of Health Disparities: A Geographic Analysis

Objectives. We examined whether the geographic density of alcohol retailers was greater in geographic areas with higher levels of demographic characteristics that predict health disparities.Methods. We obtained the locations of all alcohol retailers in the continental United States and created a map depicting alcohol retail outlet density at the US Census tract level. US Census data provided tract-level measures of poverty, education, crowding, and race/ethnicity. We used multiple linear regression to assess relationships between these variables and retail alcohol density.Results. In urban areas, retail alcohol density had significant nonlinear relationships with Black race, Latino ethnicity, poverty, and education, with slopes increasing substantially throughout the highest quartile for each predictor. In high-proportion Latino communities, retail alcohol density was twice as high as the median density. Retail alcohol density had little or no relationship with the demographic factors of interest in suburban, large town, or rural census tracts.Conclusions. Greater density of alcohol retailers was associated with higher levels of poverty and with higher proportions of Blacks and Latinos in urban census tracts. These disparities could contribute to higher morbidity in these geographic areas.The geographic density of alcohol retailers is a community risk factor that may influence behavior. Alcohol access within a neighborhood may constitute a social influence as drinking behavior is observed and social norms are created in that neighborhood; there may be an accessibility effect resulting from convenience of and proximity to opportunities to purchase alcohol; there may be increased advertising within neighborhoods that have more alcohol retail outlets¹; or the alcohol point of sale may have an influence on the neighborhood itself, changing the characteristics of the neighborhood.To date, previous work researching the impact of retail alcohol density has mainly focused on regional or local assessments, except for a study that examined urban centers at the zip code level.² The methodologies of the regional studies have also varied, with assessments at a variety of geographic levels: counties,³ cities,^4–6 zip codes,^7,8 block groups,⁹ and census tracts.^10–14 Such area-level variation may make interpretation or generalizing difficult because individuals'' activities often cross administrative boundaries. There have been no national studies on retail alcohol density in nonurban settings; previous nonurban analyses were embedded within regional or state assessments. In addition, it is not known whether potentially important findings regarding the effects of alcohol availability can be applied to locales that have not been directly studied.To better understand the association between retail alcohol density and demographic predictors of health disparities, we created a continuous density map of alcohol retailers across the continental United States, and we assessed how these points of sale related to demographic characteristics at the census tract level.     

Neighborhoods and obesity in later life

Objectives. We examined the influence of neighborhood environment on the weight status of adults 55 years and older.Methods. We conducted a 2-level logistic regression analysis of data from the 2002 wave of the Health and Retirement Study. We included 8 neighborhood scales: economic advantage, economic disadvantage, air pollution, crime and segregation, street connectivity, density, immigrant concentration, and residential stability.Results. When we controlled for individual- and family-level confounders, living in a neighborhood with a high level of economic advantage was associated with a lower likelihood of being obese for both men (odds ratio [OR] = 0.86; 95% confidence interval [CI] = 0.80, 0.94) and women (OR = 0.83; 95% CI = 0.77, 0.89). Men living in areas with a high concentration of immigrants and women living in areas of high residential stability were more likely to be obese. Women living in areas of high street connectivity were less likely to be overweight or obese.Conclusions. The mechanisms by which neighborhood environment and weight status are linked in later life differ by gender, with economic and social environment aspects being important for men and built environment aspects being salient for women.Over the past few decades the prevalence of obesity has been rising for men and women across all age groups, including the elderly.¹ For example, in 2001 to 2002 in the United States, about 1 in 3 adults 60 years or older was obese.² This trend raises concerns because excess weight is associated with a number of chronic health conditions, including diabetes, high blood pressure, asthma, and arthritis.³ Moreover, obesity can have very important implications for publicly financed health care.⁴ Recent research suggests that a number of demographic, socioeconomic, and family factors⁵ influence obesity, but the role of the neighborhood context has not been fully explored.Excess weight results from an energy imbalance in which caloric intake exceeds energy expenditures, the latter closely related to physical activity. The neighborhood environment may influence energy intake (through its influence on food availability⁶) and energy expenditure (by facilitating or impeding physical activity). For example, the presence of supermarkets in the neighborhood is associated with higher fruit and vegetable intake,⁷ whereas eating at fast-food restaurants is associated with a high-fat diet and higher body mass index (BMI; weight in kilograms divided by height in meters squared).⁸ In terms of physical activity, individuals living in neighborhoods with less crime,^9–13 higher land-use mix,¹⁴ higher street connectivity,^11,14,15 higher residential density,^11,14 a greater number of destinations,^9,16 better aesthetics,^9,10,17 and sidewalks^10,12,17,18 tend to walk more often.^19,20Only a handful of studies linking neighborhood features to late-life obesity have focused on older adults.^{11,13,16,21–23} National studies are particularly lacking for the elderly. Yet evidence from national studies of adults of all ages suggests plausible connections between obesity and neighborhood factors. Using the 1990 to 1994 waves of the National Health Interview Survey, for example, Boardman et al.²⁴ found that adults residing in neighborhoods with a high concentration of poverty and in neighborhoods with a high percentage of Blacks were more likely to be obese. In another study, Robert and Reither²⁵ found that higher community socioeconomic disadvantage was related to higher BMI among women but not among men. Because these studies had very limited characterizations of the neighborhoods, the mechanism through which poor neighborhoods result in obesity remains unclear. It could be, for instance, that poor neighborhoods tend to have fewer supermarkets^26–28 and more-limited access to places for physical activity.^29,30Using a large, nationally representative survey, we examined the relationship between the economic, built, and social environments and weight status among men and women 55 years and older. We included 8 previously validated neighborhood scales reflecting neighborhood safety and segregation, concentration of immigrants, air pollution, residential stability, connectivity, density or access, and high and low neighborhood socioeconomic status.³¹ We modeled both obesity and overweight status by using multilevel modeling techniques in which we controlled for detailed individual- and family-level confounders.     

Maternal Weathering and Risk of Preterm Delivery

Objectives. We compared the association between advancing maternal age and risk of preterm delivery across 4 groups (Black smokers, Black nonsmokers, White smokers, White nonsmokers) and within the context of neighborhood deprivation levels.Methods. We obtained data from linked census and birth records for singletons (n = 182 938) delivered by women aged 20 to 39 years in Philadelphia, Pennsylvania; Baltimore, Maryland; 16 Michigan cities; 3 Maryland counties; and 2 North Carolina counties. Results from area-specific multilevel logistic regression models were combined to obtain pooled estimates of relations between maternal age and risk of preterm delivery. We repeated the models after categorizing women by neighborhood deprivation level (low, medium, and high).Results. Among multiparous women, there was a significant age-related increase in preterm delivery in 3 of the 4 groups. The adjusted odds ratio per 5-year age increase was 1.31 in Black smokers, 1.11 in Black nonsmokers, and 1.16 in White smokers. In each group, the odds ratio increased as neighborhood deprivation increased.Conclusions. These results support the “weathering” hypothesis, suggesting that Black women, women with high-risk behaviors, and women living in high-deprivation neighborhoods may develop “accelerated aging” that increases preterm delivery risk.The elevated risks of infant mortality¹ and long-term disability² associated with preterm birth are well-documented. Studies have repeatedly shown higher preterm delivery rates among Black women in the United States³ and women in lower socioeconomic strata.^4–7 The association between preterm delivery risk and maternal age has also been frequently studied by means of data from vital records^8–12 or epidemiologic studies.^13–17 Overall, these studies suggest a curvilinear relation, with slightly higher preterm delivery risk in adolescents, lower risk in early adulthood, and increasing risk with advancing maternal age. The shape of this curve might be influenced by multiple factors, including age-related differences in maternal behaviors and physiologic and disease states. There is also self-selection in timing of pregnancies, and later-age pregnancies may include a higher proportion of women with a history of infertility or fetal loss.Building on the observations that adverse pregnancy outcomes increase with advancing maternal age, and noting the marked Black–White disparities in these adverse outcomes, Geronimus proposed a “weathering” or “accelerated aging” hypothesis.¹⁸ This hypothesis states that: (1) a decline in health status contributes to poorer reproductive outcomes as women age and (2) social inequalities lead to an earlier and disproportionately greater decline in the health status of Blacks, which results in a widening health differential between Blacks and Whites with advancing age. In support of the weathering hypothesis, Geronimus and others have shown an increase in Black–White disparities with advancing maternal age for outcomes such as neonatal mortality^18,19 and low and very low birth weight (LBW),^18,20–23 but results for preterm delivery have been inconsistent.^9,12,24 There have also been reports of increasing disparities in adverse pregnancy outcomes with advancing age when women are categorized by measures of disadvantage or socioeconomic status.^20,23,25Based on the framework described by Williams,²⁶ there are multiple potential causes in the pathway to accelerated aging among Black and disadvantaged women, such as delays in accessing health care, employment-related adverse health effects, more obstacles to and fewer opportunities for a healthy lifestyle (e.g., exercise and diet), exposure to air pollutants, high-risk coping behaviors (e.g., smoking, alcohol use, and drug use), and excess stress caused by discrimination, violence, financial troubles, housing insecurity, and lack of instrumental social support. Many of these causes are endemic, and perhaps “infectious,” in neighborhoods with high levels of deprivation.²⁷ Among previous studies that have examined effects of neighborhood poverty level on the associations among race, maternal age, and risk of LBW deliveries, results have been mixed,^20,22,23 and no study has assessed preterm delivery as the primary outcome.In our study we linked birth records to census data from a multisite project to compare the association between advancing maternal age and risk of preterm delivery across groups of women categorized by race and reported smoking status during pregnancy. Although smoking is thought to have direct effects on preterm delivery risk, we also considered smoking to be a potential indicator of high-risk coping behaviors and unhealthy lifestyle. We also examined effects of neighborhood deprivation on the age–preterm delivery relation within the different maternal groups as defined by race and smoking status. We hypothesized that the slope of increasing preterm delivery risk with advancing maternal age would be steeper for Black women, smokers, and women living in neighborhoods with high levels of deprivation.     

Associations of acculturation and socioeconomic status with subclinical cardiovascular disease in the multi-ethnic study of atherosclerosis

Objectives. We assessed whether markers of acculturation (birthplace and number of US generations) and socioeconomic status (SES) are associated with markers of subclinical cardiovascular disease—carotid artery plaque, internal carotid intima-media thickness, and albuminuria—in 4 racial/ethnic groups.Methods. With data from the Multi-Ethnic Study of Atherosclerosis (n = 6716 participants aged 45–84 years) and race-specific binomial regression models, we computed prevalence ratios adjusted for demographics and traditional cardiovascular risk factors.Results. The adjusted US- to foreign-born prevalence ratio for carotid plaque was 1.20 (99% confidence interval [CI] = 0.97, 1.39) among Whites, 1.91 (99% CI = 0.94, 2.94) among Chinese, 1.62 (99% CI = 1.28, 2.06) among Blacks, and 1.23 (99% CI = 1.15, 1.31) among Hispanics. Greater carotid plaque prevalence was found among Whites, Blacks, and Hispanics with a greater number of generations with US residence (P < .001) and among Whites with less education and among Blacks with lower incomes. Similar associations were observed with intima-media thickness. There was also evidence of an inverse association between albuminuria and SES among Whites and Hispanics.Conclusions. Greater US acculturation and lower SES were associated with a higher prevalence of carotid plaque and greater intima-media thickness but not with albuminuria. Maintenance of healthful habits among recent immigrants should be encouraged.Beginning with the Ni-Hon-San study,^1,2 which was initiated in the 1960s, research has associated increased acculturation to Western lifestyles with more-adverse cardiovascular disease (CVD) risk factor profiles and with increased CVD morbidity and mortality. Specifically, greater Western acculturation has frequently been linked to increased body mass index (BMI; weight in kilograms divided by height in meters squared),^3–5 waist circumference and abdominal obesity,^6,7 hypertension,^7–9 type II diabetes,^10,11 and CVD morbidity and mortality.^1,12,13 However, little research has explored associations between acculturation and subclinical CVD.^14,15Abundant research also exists that links low socioeconomic status (SES) to increased levels of CVD risk factors, morbidity, and mortality.^14,16–18 In general, SES has been found to be inversely related to subclinical measures of CVD, including coronary artery calcification (CAC),^14,19–22 carotid artery plaque, and intima-media thickness^20,23–26 and albuminuria.²⁷ Relations with peripheral artery disease have been inconsistent.^28–30 The extent to which these associations vary by race/ethnicity has been examined infrequently. There is, however, some evidence that the relation between SES and disease may differ across racial/ethnic groups.^14,31,32 Specifically, in the Multi-Ethnic Study of Atherosclerosis (MESA) there was a higher prevalence of CAC among Whites with low education than among those with more education, whereas the reverse was true for Hispanics.¹⁴We investigated whether acculturation and SES were associated with other measures of subclinical disease, specifically with carotid plaque and albuminuria. The relation of acculturation and SES to CAC has been described in MESA.¹⁴ Although CAC, carotid plaque, and albuminuria are all subclinical measures of CVD and are related to adverse clinical outcomes, these measures represent different aspects of the disease process and have relatively weak intercorrelations.³³ Thus, they may be differentially related to our exposures of interest.The investigation of these patterns is important from a public health perspective and may yield clues regarding the etiology of atherosclerosis. On the basis of previous work,¹⁴ we hypothesized that increased Western acculturation, as assessed by place of birth, migration history, and duration of US residence, is associated with increased carotid plaque, intima-media thickness, and albuminuria. Additionally, we expected there to be an interaction between race/ethnicity and SES with respect to their associations with subclinical CVD. Specifically, we expected Whites and Blacks at lower SES to have more-adverse subclinical CVD profiles than those at higher SES, whereas for Hispanics and Chinese, we expected the reverse to be true.     

Neighborhood social disorganization and the acquisition of trichomoniasis among young adults in the United States

Objectives. We examined relationships between neighborhood social disorganization and trichomoniasis among young US adults.Methods. We employed multilevel logistic regression modeling with secondary data from wave III of the National Longitudinal Study of Adolescent Health (2001–2002). The dependent variable—trichomoniasis—was measured via urine testing. The measures for neighborhood social disorganization were derived from the 2000 US Census—racial and ethnic composition, concentrated poverty, and residential instability. The sample comprised 11 370 individuals across 4912 neighborhoods.Results. Trichomoniasis was more likely in neighborhoods with higher concentrations of Black residents (adjusted odds ratio [AOR] = 1.16; 95% confidence interval [CI] = 1.03, 1.30). However, this association was mediated by neighborhood concentrated poverty. Furthermore, young adults who lived in neighborhoods with higher concentrations of poverty were significantly more likely to have trichomoniasis (AOR = 1.25; 95% CI = 1.07, 1.46). Neither immigrant concentration nor residential instability was significantly associated with trichomoniasis.Conclusions. These findings strengthen the evidence that neighborhood structural conditions are associated with individual sexually transmitted infection (STI) acquisition. Research is needed to explore the mechanisms through which these conditions influence STI. In addition, STI-prevention programs that include structural interventions targeting neighborhood disadvantage are needed.Adolescents and young adults are at increased risk for sexually transmitted infections (STIs) because of a complex interplay of biological, behavioral, and developmental factors.¹ Nearly half of all STIs diagnosed in the United States annually are among adolescents and young adults^1,2 despite national priority goals aimed at reducing infection rates.³ Trichomoniasis, a common and easily curable STI,¹ is of increasing concern because the infection facilitates HIV acquisition and transmission through mucosal inflammation of the genital tract and alterations in the innate immune response. ^4-7 The infection is caused by the protozoa, Trichomonas vaginalis, and is typically transmitted via penis-to-vagina or vulva-to-vulva contact.¹ Infected persons are often asymptomatic or experience only mild symptoms,¹ which can hinder early detection and treatment and increase the risk of STIs and HIV.In the United States, the prevalence of trichomoniasis is difficult to ascertain because routine screening currently is not recommended nor is the reporting of positive results required.^1,4 According to urine assay data from the National Longitudinal Study of Adolescent Health (Add Health), the prevalence of trichomoniasis among the young adult population in 2001–2002 was approximately 2.3%.⁷ The study also found that women were at greater risk than were men (2.8% vs 1.7%) as were non-Hispanic Black (6.9%) and Latino (2.1%) youths compared with their non-Hispanic White peers (1.2%).⁷ In other studies of adult women, individual risk factors for trichomoniasis included poverty, lower education, douching, non-Hispanic Black race/ethnicity, and greater numbers of lifetime sexual partners.^8,9 Among clinic samples of adolescent women, research found trichomoniasis to be associated with older male sexual partners, casual sexual activity, marijuana use, and delinquency.¹⁰However, to date, no studies have examined the role of the broader structural context in shaping trichomoniasis risk, despite theory and previous STI research suggesting that the neighborhood environment may play a role. According to social disorganization theory,^11–14 key indicators of neighborhood structural disadvantage (i.e., racial/ethnic composition, concentrated poverty, and residential instability) influence health outcomes by weakening social ties, reducing access to institutional resources, and limiting exposure to positive role models, conventional social norms, and collective efficacy. Findings from previous research examining other STIs support the hypothesis that neighborhood contexts influence STI prevalence. For example, with respect to racial and ethnic composition, studies have found that gonorrhea rates were higher in cities and neighborhoods with greater proportions of Black residents.^15,16 Furthermore, in an analysis of Chicago neighborhoods, the incidence rates of gonorrhea and chlamydia were higher for neighborhoods in which more than 60% of the residents were Black compared with those in which more than 60% of residents were Hispanic, which suggests that segregated Hispanic ethnic enclaves may be protective of STI compared with segregated Black communities.¹⁷ Researchers hypothesize that the residential segregation of Black communities has contributed to the pervasive Black-White disparities in STI through discrimination processes, which in turn has led to greater concentration of poverty, lower male-to-female gender ratios due to the disproportionate incarceration and mortality of Black men, and closed, racially segregated sexual networks that facilitate the transmission of infection.^18–20In addition, the role of community poverty in shaping STI risk has been examined extensively and found to be positively associated with rates of chlamydia, gonorrhea, syphilis, and HIV in cross-sectional^{15,17,21–23} and longitudinal analyses.¹⁶ Other socioeconomic factors, such as unemployment^17,24 and lower educational attainment,^16,17 have also been linked to higher rates of chlamydia and gonorrhea. Research on the effects of residential instability on STI is limited, but the single study that examined these relationships found greater residential instability was associated with fewer self-reported STIs among a national sample of adolescents.²⁴ Depending on the context, perhaps residential instability could increase STI risk by disrupting social support ties and informal social control measures or reduce STI risk by dispersing closed sexual networks that facilitate infection transmission.Although the aforementioned studies have illustrated links between neighborhood social disorganization and a variety of STIs, limitations exist. First, the majority have been ecological studies, in which the outcomes were measured as community STI rates and no adjustment was made for potential confounding relationships with individual-level data.^{15–17,21–23} Consequently, inferences can be made only about the community, and individual variation in the outcome cannot be ascertained.²⁵ Second, although 1 study examined individual STI, the measure was based on self-report,²⁴ which potentially increases bias because of underreporting as well as unrecognized or undiagnosed infection. In addition, the study only focused on STI in general, which could limit our understanding of unique relationships with specific infectious organisms. Third, data sources of previous research tend to be at local or state levels,^{15–17,21–23} which limits external validity of the findings. Therefore, the purpose of our research was to examine relationships between neighborhood social disorganization and trichomoniasis among young adults in the United States. Our research builds on previous studies in 3 significant ways: (1) we examined multiple levels of analysis, which enabled us to simultaneously examine the independent relationships between individual and neighborhood variables and individual acquisition of trichomoniasis, (2) we examined a more refined measure of STI through the use of urine screening, and (3) we examined data from a large national data set—Add Health.     

Race/Ethnicity,Residential Segregation,and Exposure to Ambient Air Pollution: The Multi-Ethnic Study of Atherosclerosis (MESA)

Objectives. We described the associations of ambient air pollution exposure with race/ethnicity and racial residential segregation.Methods. We studied 5921 White, Black, Hispanic, and Chinese adults across 6 US cities between 2000 and 2002. Household-level fine particulate matter (PM_2.5) and nitrogen oxides (NO_X) were estimated for 2000. Neighborhood racial composition and residential segregation were estimated using US census tract data for 2000.Results. Participants in neighborhoods with more than 60% Hispanic populations were exposed to 8% higher PM_2.5 and 31% higher NO_X concentrations compared with those in neighborhoods with less than 25% Hispanic populations. Participants in neighborhoods with more than 60% White populations were exposed to 5% lower PM_2.5 and 18% lower NO_X concentrations compared with those in neighborhoods with less than 25% of the population identifying as White. Neighborhoods with Whites underrepresented or with Hispanics overrepresented were exposed to higher PM_2.5 and NO_X concentrations. No differences were observed for other racial/ethnic groups.Conclusions. Living in majority White neighborhoods was associated with lower air pollution exposures, and living in majority Hispanic neighborhoods was associated with higher air pollution exposures. This new information highlighted the importance of measuring neighborhood-level segregation in the environmental justice literature.In the United States, race/ethnicity is highly correlated with residential location, with Whites and minorities often living segregated from one another.1,2 Differential residential location can result in important racial/ethnic differences in environmental exposures, such as air pollution.1,3–6 Epidemiological studies have consistently shown increased risk for morbidity and mortality from cardiovascular7–10 and respiratory diseases (chronic obstructive pulmonary disease, asthma, and lung cancer)8,11–14 associated with exposure to ambient air pollution, including exposure to fine particulate matter (particles < 2.5 μm in aerodynamic diameter [PM_2.5]) and nitrogen oxides (NO_X; sum of nitric oxide, nitrogen dioxide, nitrous acid, and nitric acid).15–21 Predominantly minority areas are more likely to have22,23 or be more proximal4,24,25 to hazardous sites or air pollution sources, including point sources and roadway traffic. However, few studies have investigated how individual- or household-level exposure estimates are associated with race/ethnicity.In addition to proximity to pollution sources, poor enforcement of environmental regulations in minority communities and inadequate response to community complaints may also contribute to higher exposure to environmental hazards in minority communities.1 These institutional factors reflect physical, political, social, and economic characteristics of neighborhoods that are often correlated with their racial/ethnic composition and the level of racial residential segregation. For these reasons, measures of neighborhood racial/ethnic composition and racial residential segregation may be associated with environmental exposures independently of the individual race/ethnicity of residents. Despite the importance of contextual information for advancing research for environmental justice, few studies have simultaneously examined how neighborhood characteristics and the race/ethnicity of study participants are related to environmental exposures or examined racial residential segregation as it relates to air pollution exposure.6,26Also, most studies have compared exposure among Whites and Blacks with few studies including other races/ethnicities.4,24,27–29 Our objective in this study was to describe associations of exposure to ambient air pollution, estimated by annual average PM_2.5 and NO_X concentrations at the household level, with race/ethnicity, neighborhood racial/ethnic composition, and racial/ethnic residential segregation in White, Black, Hispanic and Chinese adults who participated in the Multi-Ethnic Study of Atherosclerosis (MESA) in 6 US communities.     

Income Inequality,Alcohol Use,and Alcohol-Related Problems

Objectives. We examined the relationship between state-level income inequality and alcohol outcomes and sought to determine whether associations of inequality with alcohol consumption and problems would be more evident with between-race inequality measures than with the Gini coefficient. We also sought to determine whether inequality would be most detrimental for disadvantaged individuals.Methods. Data from 2 nationally representative samples of adults (n = 13 997) from the 2000 and 2005 National Alcohol Surveys were merged with state-level inequality and neighborhood disadvantage indicators from the 2000 US Census. We measured income inequality using the Gini coefficient and between-race poverty ratios (Black–White and Hispanic–White). Multilevel models accounted for clustering of respondents within states.Results. Inequality measured by poverty ratios was positively associated with light and heavy drinking. Associations between poverty ratios and alcohol problems were strongest for Blacks and Hispanics compared with Whites. Household poverty did not moderate associations with income inequality.Conclusions. Poverty ratios were associated with alcohol use and problems, whereas overall income inequality was not. Higher levels of alcohol problems in high-inequality states may be partly due to social context.A growing literature examines the impact of area-level income inequality on health. Inequality, or the size of the difference in income between rich and poor, is distinct from absolute income or socioeconomic status (SES).1 Recent systematic reviews have found associations between income inequality and health.2–6 Theoretical3,7 and empirical work suggests that income inequality may affect health through psychosocial pathways, whereby people compare themselves with those who are better (or worse) off,4,8–10 and neomaterial pathways, whereby inequality leads to limited public investment in social goods such as education, health services, and welfare that directly affect health.3,11,12 (The term “neomaterial” is used to acknowledge the fact that material conditions relevant to present-day health outcomes differ from those material conditions that influenced infectious diseases in the 19th century.3)Most research on income inequality and health has focused broadly on health status and mortality,2 but a few studies focus on specific health outcomes and health behaviors.2,13,14 Among these is a small literature on alcohol that suggests that income inequality is associated with increased frequency of alcohol consumption,13 volume of alcohol consumed,14,15 drinking to drunkenness,14 and death from chronic alcohol-attributable illnesses.16 Results are not unequivocal, however. Findings for alcoholic cirrhosis are mixed, with one study finding a positive association for men but not women15 and others finding no association.17,18 Another study documented a curvilinear relationship with alcohol-related hospitalization, suggesting an initial decline in hospitalizations followed by a rapid rise as inequality increases.16 Finally, one study found that state-level income inequality was negatively associated with women’s alcohol dependence, but not after adjustment for state beer taxes.19To date, this literature on income inequality and alcohol has not examined whether income inequality affects alcohol consumption and related problems equally across SES and race/ethnicity. Furthermore, it has primarily measured income inequality using the Gini coefficient, a measure that captures the difference between an observed income distribution and a condition of complete equality.1 We have expanded on the existing literature by examining SES and race/ethnicity as moderators of associations between income inequality and alcohol outcomes, and by examining race-based measures of income inequality in addition to the Gini coefficient.Income inequality may not affect everyone in the same way.2,20 Affluent individuals may benefit from2 or be immune to the negative effects of²¹ living in unequal areas, whereas poorer people and Black and Hispanic people may suffer a “double jeopardy” in unequal areas.20,21 This double jeopardy hypothesis, however, may be specific to certain health and social outcomes.18 For example, compared with more egalitarian areas, areas with more unequal income distribution have stronger inverse associations between individual SES and adolescent literacy21 as well as mortality from alcoholic liver disease.18 These studies indicate that there is an interaction of individual SES and income inequality for certain outcomes. By contrast, some evidence suggests largely uniform (rather than differential) effects of income inequality on poor self-rated health22; however, most alcohol studies have not examined possible moderators of effects of income inequality.Income inequality can be measured overall or by comparing the status of 2 groups. Overall measures incorporate the range and distribution of incomes with the extent of inequality. The most commonly used overall measure is the Gini coefficient.1 By contrast, relative measures emphasize income or poverty differences between groups based on demographic characteristics. For example, between-race income inequality measures summarize differentials in income between various racial/ethnic groups living in the same area and have been used in the criminology literature.23,24 In the United States, there are stark differences in income and poverty status between Whites, Blacks, and Hispanics. In 2000, the ratio of per capita income of Whites to Blacks was 1.66 and of Whites to Hispanics was 1.97, with 15% of Whites, almost 30% of Blacks, and more than 20% of Hispanics having family incomes below the federal poverty threshold.25 Use of these relative measures seems especially relevant given our interest in examining whether race/ethnicity moderates the associations between income inequality and alcohol outcomes.We examined whether income inequality, measured by the Gini coefficient and 2 between-race measures, is associated with light to moderate alcohol consumption, heavy alcohol consumption, alcohol-related consequences, and alcohol dependence. Although not tested explicitly here, heavy (but not light) alcohol consumption may be linked to income inequality primarily through the psychosocial pathway (such as drinking to cope with stress), whereas alcohol problems additionally may be influenced by neomaterial effects of inequality (such as increased policing24 or decreased funding for alcohol treatment services). We also investigated whether associations with inequality were most detrimental for disadvantaged individuals (people in poor neighborhoods, with low household income, or racial/ethnic minority status), which also may suggest neomaterial effects of inequality.3     

Racial residential segregation and low birth weight in Michigan's metropolitan areas

Objectives. We examined the influence of racial residential segregation, independent of neighborhood economic factors, on the overall and specific etiological risks of low birth weight.Methods. We geocoded all singleton births in Michigan metropolitan areas during 2000 to census tracts. We used hierarchical generalized linear models to investigate the association between low birth weight (< 2500 g) and neighborhood-level economic and racial segregation, controlling for individual and neighborhood characteristics. We analyzed competing risks of the 2 etiologies of low birth weight: intrauterine growth restriction and preterm birth.Results. Living in a Black segregated area was associated with increased odds (odds ratio [OR] = 1.15; 95% confidence interval [CI] = 1.03, 1.29; P < .05) of low birth weight after adjusting for individual- and tract-level measures. The analysis suggested that the association between low birth weight and racial segregation was attributable primarily to increased risk of intrauterine growth restriction (OR = 1.19; 95% CI = 1.03, 1.37; P < .05).Conclusions. Odds of low birth weight are higher in racially segregated Black neighborhoods in Michigan''s metropolitan areas, independent of economic factors. The association appears to operate through intrauterine growth restriction rather than preterm birth.As the leading cause of death among non-Hispanic Black infants and second-leading cause of death among non-Hispanic White infants, complications related to short gestation and low birth weight represent a significant clinical and public health issue.^1–3 Low birth weight also leads to long-term health consequences through increased rates of childhood and adult chronic diseases.^3–6 Racial disparities in rates of low birth weight have persisted even as total infant mortality has declined and prenatal care utilization among women of color has increased.^1–3 Because differences in individual-level risk factors cannot completely explain the differences in outcomes for White and Black mothers,^3,7 researchers have begun investigating contextual influences on racial disparities in birth outcomes.^3,8Racial segregation is a contextual factor that might contribute to racial disparities in low birth weight by isolating Blacks from the resources and opportunities found more frequently in White communities.^9–13 Residents in Black segregated neighborhoods accumulate less home equity,^14,15 have decreased access to quality primary education,¹⁶ and are exposed to greater residential and economic instability than are residents of nonsegregated communities.⁹ The accumulation of disadvantages in racially isolated neighborhoods could lead to negative birth outcomes for women by limiting opportunities associated with improved health (e.g., educational opportunities or access to quality medical care) and by exposing them to increased stress from neighborhood-level factors.Evidence from a small number of studies suggests that low birth weight is associated with racial residential segregation.^17–24 With few exceptions,^17,25,26 studies link metropolitan-level segregation or the percentage of Black residents in a community to low birth weight. However, because isolation is inherently spatial, to understand how the racial isolation of an individual mother''s neighborhood affects her pregnancy outcomes, isolation is most appropriately measured by considering her neighborhood along with its immediate surroundings (e.g., bordering neighborhoods) rather than by the metropolitan area or a single neighborhood.¹⁷Some authors have argued that racial segregation simply serves as a proxy for economic segregation.^27,28 By contrast, we posit that racial segregation is a distinct form of neighborhood-level disadvantage that presents an increased risk for low birth weight beyond that caused by economic segregation. Sociologists have shown that, even in the presence of economic segregation, the circumstances of racially segregated Black neighborhoods differ from those of White neighborhoods at similar socioeconomic levels.^29–32 This means that although residents of Black middle-class neighborhoods may live in residential areas that are separate from poor Black neighborhoods, they have greater exposure than do middle-class Whites to negative contextual factors and have fewer resources in their vicinity. This also suggests that any attempt to distinguish between the effects of racial and economic segregation on low birth weight requires that economic segregation also be measured spatially, taking a mother''s neighborhood and its immediate surroundings into account.It is also important to consider that the drivers of low birth weight—preterm birth and intrauterine growth restriction—have distinct physiological mechanisms.^33–35 Assessing the degree to which racial isolation is associated with each can provide important insight into the etiological mechanisms relating racial segregation to low birth weight. Spontaneous preterm birth is commonly precipitated by an infection,^36–40 which could be associated with racial segregation if, for instance, racial segregation reduces access to quality care.²⁵ Intrauterine growth restriction, on the other hand, typically stems from a chronic deficiency in oxygen and nutrient delivery to the fetus.^41–46 Chronic stress associated with the circumstances of racially isolated neighborhoods might affect placental vasculature function, creating an oxygen–nutrient insufficiency that leads to intrauterine growth restriction.⁴⁷ We know of no research that has considered the competing risks of growth restriction and preterm birth in the relationship of neighborhood environments with low birth weight.We examined births to mothers living in Michigan metropolitan areas to ascertain whether neighborhood racial segregation was associated with low birth weight independent of economic factors. We explicitly captured the spatial nature of both racial and economic segregation through a localized segregation index. We also analyzed the degree to which racial segregation was associated with different etiologies of low birth weight.     

Neighborhood Incarceration Rate and Asthma Prevalence in New York City: A Multilevel Approach

Objectives. We examined the association between neighborhood incarceration rate and asthma prevalence and morbidity among New York City adults.Methods. We used multilevel modeling techniques and data from the New York City Community Health Survey (2004) to analyze the association between neighborhood incarceration rate and asthma prevalence, adjusting for individual-level sociodemographic, behavioral, and environmental characteristics. We examined interactions between neighborhood incarceration rate, respondent incarceration history, and race/ethnicity.Results. The mean neighborhood rate of incarceration was 5.4% (range = 2.1%–12.8%). Neighborhood incarceration rate was associated with individual-level asthma prevalence (odds ratio [OR] = 1.06; 95% confidence interval [CI] = 1.03, 1.10) in unadjusted models but not after adjustment for sociodemographic characteristics (OR = 1.01; 95% CI = 0.98, 1.04). This association did not differ according to respondent race/ethnicity.Conclusions. Among New York City adults, the association between neighborhood incarceration rate and asthma prevalence is explained by the sociodemographic composition of neighborhoods and disparities in asthma prevalence at the individual level. Public health practitioners should further engage with criminal justice professionals and correctional health care providers to target asthma outreach efforts toward both correctional facilities and neighborhoods with high rates of incarceration.In the United States, asthma disproportionately affects non-White individuals living in urban areas and living in poverty.1 Because low socioeconomic status (SES) and racial/ethnic minority group status are closely intertwined with residence in an inner-city environment, characteristics of these inner-city neighborhoods have received much attention in the effort to explain patterns of asthma prevalence and morbidity.2,3 Epidemiological studies have highlighted the influence of poor housing, which may increase exposure to indoor allergens such as rat droppings4; greater likelihood of tobacco smoke exposure5; and overcrowding, which may predispose people to viral respiratory illness.2Because features of the physical environment do not completely explain observed patterns in asthma prevalence, features of the social environment have emerged as important asthma risk factors.6 Observational studies have demonstrated the association between asthma, psychological stress, and exposure to violent neighborhoods.7–9 For example, exposure to violence may influence an individual’s impulse control and risk-taking behavior, resulting in the adoption of coping behaviors, such as smoking, a known trigger for asthma.8–10 Psychological stress may be further compounded by the presence of overburdened or absent social supports and a perceived lack of control over one’s self or environment.6,11 Neighborhood-level constructs such as social capital and social cohesion have been linked to important health outcomes and may have an impact on asthma prevalence.12A natural but overlooked extension of this work is the potential impact of the criminal justice system on communities. Incarceration has a disproportionate impact on poor communities of color and has been linked to increased rates of asthma at the level of the individual.13–15 In addition to the effects on the individuals directly involved with the criminal justice system, neighborhood incarceration rates may play a role in shaping the social environment and thereby affect asthma prevalence. Exposure to high rates of neighborhood violence and crime often accompany exposure to incarceration. Recidivism and the risks of community reentry may further exacerbate this exposure.16 Incarceration has been shown to lead to long-term psychological stress for those affected17,18 and holds significant consequences for their families, creating further stress by removing social supports and weakening families.19 Individuals released from prison face legal barriers to employment, housing, public entitlements, and educational opportunities and various restrictions on political and social rights,20,21 further diminishing the social capital of their communities.Therefore, we sought to examine the association between neighborhood-level incarceration rates and several individual-level asthma outcomes. We hypothesized that increased neighborhood incarceration rates would be associated with increased asthma prevalence. Additionally, we proposed that increased neighborhood incarceration rates would be associated with increased asthma morbidity. We specifically examined factors potentially correlated with both neighborhood incarceration rate and asthma prevalence, such as SES, smoking, and poor housing conditions.     

Trust in the health care system and the use of preventive health services by older black and white adults

Objectives. We sought to find racial differences in the effects of trust in the health care system on preventive health service use among older adults.Methods. We conducted a telephone survey with 1681 Black and White older adults. Survey questions explored respondents'' trust in physicians, medical research, and health information sources. We used logistic regression and controlled for covariates to assess effects of race and trust on the use of preventive health services.Results. We identified 4 types of trust through factor analysis: trust in one''s own personal physician, trust in the competence of physicians'' care, and trust in formal and informal health information sources. Blacks had significantly less trust in their own physicians and greater trust in informal health information sources than did Whites. Greater trust in one''s own physician was associated with utilization of routine checkups, prostate-specific antigen tests, and mammograms, but not with flu shots. Greater trust in informal information sources was associated with utilization of mammograms.Conclusions. Trust in one''s own personal physician is associated with utilization of preventive health services. Blacks'' relatively high distrust of their physicians likely contributes to health disparities by causing reduced utilization of preventive services. Health information disseminated to Blacks through informal means is likely to increase Blacks'' utilization of preventive health services.There is strong empirical evidence of health care disparities between Black and White Americans. Blacks are less likely than are Whites to receive many needed services, including routine preventive care.^1–5 The causes of disparities in health care are complex and have been the subject of considerable research; socioeconomic differences and structural characteristics (such as lack of access to care) are important sources of care disparities, and there is significant evidence that racial bias in the health care system is also a major factor in disparities in care between Blacks and Whites.¹Blacks'' distrust of physicians and the health care system may also contribute to health care disparities. Studies have demonstrated that Blacks exhibit less trust in the health care system.^6–9 There are a variety of mechanisms through which this distrust may occur, including Blacks'' personal experiences with racism, their knowledge of a history of racism in the health care system—including circumstances in which Blacks were victimized, such as the Tuskegee Syphilis Study^10–12—and social and cultural distance between Black patients and White physicians.¹³ Taken together, these individual experiences constitute a broader cultural memory of abuse that may contribute to belief in conspiracy theories among Blacks.^14,15 Goertzel reported that belief in conspiracies was correlated with lack of interpersonal trust and that Blacks were more likely to believe in conspiracy theories than were Whites.¹⁶Trust plays a central role in all medical relationships and is an important contributor to positive therapeutic outcomes.^17–20 Lack of patient trust is associated with less doctor–patient interaction, poor clinical relationships that exhibit less continuity, reduced adherence to recommendations, worse self-reported health, and reduced utilization of health care services^17–22; thus, Blacks'' relatively lower trust in the health care system puts them at greater risk of all these negative outcomes. When O''Malley et al.²² evaluated respondents'' answers to a global question assessing overall trust in personal physicians, they found that greater trust was associated with higher overall use of a number of preventive services among low-income Black women 41 years and older.However, little is known about whether distrust affects use of specific preventive services differently. Because trust in the health care system is conceived as consisting of a number of types and dimensions,^17,19,20 it is also possible that different aspects of trust may affect service use differently, thus warranting more detailed study of how the dimensions of trust may affect use of preventive services among various populations. Because of its likely origins in racial bias, Blacks'' health care–related distrust may have somewhat different effects from that of Whites, perhaps manifesting as institutional distrust as opposed to interpersonal distrust.We explored these issues by examining the association of different aspects of health care–related trust with receipt of preventive health services among older Blacks and Whites. We focused on older adults because preventive services such as immunizations, routine physical examinations, and screening for cancer and other diseases can greatly reduce premature mortality and morbidity among this population and are critical to sustaining older adults'' health.²³ Thus, disparities in receipt of preventive services are an especially strong contributor to disparities in health outcomes for older adults.