Aside from the material/physical environment, an attribute of the neighborhood social environment that may potentially shape CHD risk is social cohesion, defined as the presence of strong social bonds, including interpersonal trust (13). Posited mechanisms for health effects include diffusion of knowledge about health-related behaviors (e.g., dietary practices), maintenance of healthy behaviors through informal social control, generation of psychosocial processes including social support, and greater collective efficacy in improving local amenities and services (13). Social cohesion (or the related concept of social capital) at the state and community levels has predicted wide-ranging health outcomes, including obesity (14), self-rated health (15, 16), smoking (17), depression (18), and CHD incidence (19).

While researchers have explored the associations between neighborhood socioeconomic deprivation, social cohesion/capital, and individual health endpoints, few investigators have studied these neighborhood attributes in relation to coronary artery calcification (CAC), a marker for underlying CHD; to our knowledge, no investigators have done so in younger adult populations. Prospective analyses of asymptomatic adults have shown CAC to predict CHD (20–22).

The relations between neighborhood deprivation, cohesion, and individual CAC may vary by gender and race/ethnicity, as findings for related endpoints suggest. For instance, several studies have found stronger associations of neighborhood characteristics with CHD outcomes in women than in men (3, 5, 23) and in whites than in blacks (24). Neighborhood deprivation and low social cohesion may further act synergistically to affect health (25).

We used data from a population-based sample of younger adults to investigate associations of neighborhood deprivation and low perceived neighborhood cohesion with CAC. We hypothesized that higher deprivation and lower cohesion would each be associated with higher CAC prevalence. We looked for heterogeneous associations by gender (hypothesizing stronger associations in women) and race/ethnicity (positing stronger associations in whites) and explored whether associations of neighborhood cohesion with CAC were modified by neighborhood deprivation. We also investigated the extent to which psychosocial, behavioral, and biologic factors could explain the neighborhood associations.

The mean age of the overall sample in 2000 was 45.3 years (range, 32–50 years); 57.1% were female, 54.6% were white, and 45.4% were African-American. Women were more likely to be African-American and to report lower income and education, although gender differences by income and education were not large. There were no substantial differences in neighborhood characteristics between men and women. CAC prevalence was substantially lower in women (10.9% in women vs. 28.9% in men). A comparison of the 2005 and 1985 baseline samples of women and men (by race/ethnicity, income, and education) suggested greater selective attrition in men.

Internal consistency reliability estimates for the neighborhood SEP and cohesion measures were high (Cronbach's α values were 0.94 and 0.82, respectively). In the overall sample, neighborhood SEP scores were strongly inversely correlated with the percentage of black residents (r = −0.63), weakly inversely correlated with the percentage of immigrants (r = −0.13), and positively correlated with residential stability (r = 0.21). Higher neighborhood SEP and residential stability were positively correlated with neighborhood cohesion (r = 0.26 and r = 0.17, respectively). Being female, being white, having a higher income, being widowed, divorced, or separated, and never being married were also related to higher cohesion.

In women (Table 2), the highest quartile of neighborhood deprivation was associated with 2.49 times’ higher odds of CAC, controlling for covariates and perceived neighborhood cohesion (P for trend = 0.03; model 2). Persons in the quartile corresponding to the lowest level of cohesion had 1.87 times’ higher adjusted odds of CAC than persons in the quartile of highest cohesion (P for trend = 0.02; model 2). Associations of neighborhood deprivation and cohesion with CAC were very similar before and after adjustment for individual sociodemographic and socioeconomic characteristics (compare model 1 with model 2). Additional adjustment for physical activity and smoking slightly attenuated associations with neighborhood deprivation (model 3), and separate adjustment for Center for Epidemiologic Studies Depression Scale score slightly attenuated associations with cohesion (model 4), although both main effects remained statistically significant. Adjustment for biologic factors (model 5) also resulted in minor changes. When all potential risk-factor mediators were added, the neighborhood associations remained but were no longer statistically significant for deprivation (for quartile of highest deprivation, odds ratio (OR) = 2.02, 95% confidence interval (CI): 0.95, 4.32 (P for trend = 0.16); for quartile of lowest cohesion, OR = 1.80, 95% CI: 1.02, 3.16 (P for trend = 0.04)).

Neighborhood deprivation was not associated with CAC in men (Table 3). Men in quartiles 2, 3, and 4 of neighborhood cohesion (indicating lower levels of cohesion) had higher CAC odds than those in the lowest quartile, but confidence intervals were wide and only the estimate for quartile 2 was statistically significant; there was no dose-response trend. These estimates were largely unchanged after adjustment for individual-level risk factors.

Table 4 shows associations of neighborhood cohesion with CAC for men in deprived and nondeprived neighborhoods separately. The interaction between neighborhood deprivation and cohesion was statistically significant (P = 0.03). In deprived neighborhoods, all 3 lower quartiles of cohesion were associated with higher odds of CAC in comparison with the highest quartile, with a marginally statistically significant trend (P = 0.07). No association between social cohesion and CAC was seen in men in nondeprived neighborhoods (model 1). For women, lower cohesion predicted higher odds in both deprived and nondeprived neighborhoods, although associations were significant only in nondeprived neighborhoods (data not shown; for interaction between neighborhood deprivation and cohesion, P = 0.34).

After restricting the main analyses to persons living in the same homes in 1995 and 2000, neighborhood deprivation associations adjusted for demographic/socioeconomic covariates and neighborhood cohesion became stronger in women (for quartile of highest deprivation, OR = 3.93, 95% CI: 1.52, 10.13) and were relatively unchanged in men.

In multiple imputation analyses, odds ratio point estimates for neighborhood deprivation and cohesion differed by less than 10% in comparison with corresponding estimates from models without imputation.

A key strength of our analysis was the investigation of an established marker of subclinical atherosclerosis in young adults. This helped us to avoid biases that may occur in cross-sectional analyses of prevalent clinical outcomes when clinical symptomatic disease influences residential location. Moreover, the investigation of CAC in a young adult sample allows the detection of associations with very early disease, long before it becomes symptomatic. Thus, our analyses demonstrated that, particularly in women, neighborhood characteristics predict the presence of very early disease.

Our finding that neighborhood characteristics predict very early CHD agrees with past studies of neighborhood deprivation and subclinical atherosclerosis (33–36). To our knowledge, this study is among the first to document this relation in younger adults, and represents the first US study of these characteristics and coronary calcification. Our findings are also consistent with the magnitude of associations between neighborhood deprivation and CHD incidence/mortality documented in prospective studies (3, 5, 36). They add substantially to the limited existing research on the relation between social cohesion/capital and CHD, which is largely confined to ecologic studies and non-US studies that used single-item measures of social cohesion/capital (37, 38). The present study advances the literature by showing that social cohesion predicts subclinical atherosclerosis, even in a relatively young adult sample.

We estimated neighborhood characteristics 5 years before CAC assessment, making the temporal relation in our data compatible with causation. Strengths of our analysis include the use of a demographically and socioeconomically diverse sample. Furthermore, we adjusted for multiple neighborhood- and individual-level potential confounders and predictors of CAC, which should have limited residual confounding.

In several prospective studies of neighborhood deprivation and CHD incidence and mortality, researchers have found stronger associations in women than in men (3, 5, 23). Similar differences have been observed in analyses of subclinical carotid artery intima-media wall thickness (34, 36). In a German study of neighborhood deprivation and coronary calcification, Dragano et al. (35) found a less clear pattern, although they primarily used the neighborhood unemployment rate as the measure of neighborhood SEP. Empirical evidence also suggests that dietary factors, physical activity, and smoking behaviors are more responsive to neighborhood socioeconomic environments in women than in men (39, 40). These gender differences could result from gender differences in health-related behavioral responses to neighborhood perceptions (e.g., varying perceptions of crime/physical safety contributing to differential levels of physical activity). Furthermore, the gender discrepancies could be due to differences in the degree and type of neighborhood exposures, which in turn may be shaped by domestic and work-related gender roles. For example, women may be less likely to be employed full-time and may plausibly spend greater proportions of time in the neighborhood due to child care and domestic chores. Conversely, men may be more likely to work full-time and to be exposed to psychosocial stressors in the workplace, some of which may be linked to CHD incidence (e.g., job strain) (41, 42). In a supplementary exploratory analysis, employment status modified the estimated effects of neighborhood deprivation in women (in the full-time stratum, highest-quartile OR = 1.12, 95% CI: 0.44, 2.82; in the non-full-time stratum, highest-quartile OR = 7.15, 95% CI: 1.49, 34.4 (P for interaction = 0.02)). No effect modification was seen in men, although the sample size in the non-full-time stratum was limited (n = 161) (data not shown).

Our study suggested only partial mediation of neighborhood effects by risk factors, at best. There were suggestions of modest mediation of neighborhood deprivation effects by behavioral factors (i.e., smoking, physical activity) and of social cohesion effects by depression. Evidence of mediation by biologic factors was also limited. While previous studies have similarly found limited evidence of mediation by modifiable risk factors (3), our ability to examine mediation may have been compromised by measurement error, the timing of measures, and the particular potential mediators considered. In addition, while we hypothesized these sets of risk factors primarily as potential mediators, our study design could not allow us to distinguish mediation from confounding. A fuller account of mediating pathways would require data different from those available to us (including longitudinal assessments of mediators and assessments of confounders of the mediator-CAC relations).

Lower neighborhood cohesion predicted higher CAC prevalence among men in poorer (but not richer) neighborhoods. Plausibly, resources available in richer neighborhoods (e.g., abundant green spaces for leisure) may buffer the adverse effects of low cohesion on CAC. The similar associations observed for the 3 lowest quartiles versus the highest quartile might reflect a threshold effect. We lack a clear explanation for why this effect modification was observed in men only, and replication in other studies is needed. We did not find that high family income versus low family income had a similar modifying effect on the associations for low cohesion in men (data not shown), suggesting that individual income was not driving the observed interaction.

Previous studies, including the Whitehall studies, have found graded associations between individual SEP and CHD which persist after controlling for behavioral and biologic risk factors (43). The persistence of this gradient across places and time periods suggesting multiple pathways to disease has characterized individual SEP as a “fundamental cause” of health and disease (44). To the extent that neighborhood SEP and cohesion may mobilize and shape more proximal specific neighborhood dimensions (such as access to healthy foods and recreation (45, 46) or neighborhood sources of stress) over time, which may in turn shape individual-level risk factors, neighborhood SEP and cohesion may be considered contextual “fundamental causes” of health (44, 47). Therefore, explaining the associations between these key neighborhood attributes and disease according to selected risk factors may be particularly challenging. Nevertheless, in future work, investigators should attempt to carefully elucidate the specific pathways through which these distal causes may operate in order to identify promising interventions for CHD prevention. Furthermore, corresponding to these factors as “fundamental causes,” more fundamental approaches (e.g., mixed-income housing initiatives) to reduce gaps in neighborhood SEP and social capital should be explored for their potential to reduce CHD inequalities.

Our study had several limitations. First, participants’ residential addresses were ascertained in 1995 and characterized on the basis of 2000 US Census data. Some study participants had moved into other neighborhoods by the time of CAC assessment in 2005. If the relevant exposure time frame for the development of CAC is between neighborhood assessment and CAC assessment, misclassification related to residential mobility subsequent to the 1995 assessment could have led to underestimation of the true associations. On the basis of information corresponding to residence in 1995 and 2000, we did in fact observe stronger associations for neighborhood deprivation among women who did not move. However, if neighborhood of residence assessed in 1995 is a reliable proxy for prior (life-course) exposures related to CAC development, subsequent residential mobility may not have introduced substantial bias. Second, despite the diverse characteristics of the cohort at inception, both nonresponse and cohort attrition may have limited the generalizability of the findings to younger-to-middle-aged US adult urban populations. Third, because of insufficient numbers of participants per neighborhood, perceived neighborhood cohesion was modeled at the individual level, not the neighborhood level. Unadjusted individual-level characteristics (such as affective states) may have influenced such perceptions while also determining CAC, resulting in residual confounding.