We found independent, graded associations of higher neighborhood deprivation and lower social cohesion with the presence of CAC 5 years later in women. No associations were observed in men overall. However, low social cohesion was associated with higher odds of CAC among men living in poorer neighborhoods, although no clear dose-response was found.
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
). 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
). 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
). 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
). Similar differences have been observed in analyses of subclinical carotid artery intima-media wall thickness (34
). 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
). 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
). 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
) 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
). 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.
In summary, this study offers novel evidence on the associations of neighborhood deprivation and low cohesion with CAC in younger, asymptomatic adults. The associations appear to be relatively uniformly present in women, whereas in men the adverse effects of low cohesion seem confined to those living in deprived neighborhoods. Future investigations should build on these findings, including gender differences and mediating pathways, to better elucidate the contextual and individual-level determinants of CHD and thereby optimize the design of effective prevention strategies.