shows the demographic and clinical characteristics of the sample. The average age of participants in the study sample was 62 years, and a little more than half were women. About half the participants had ever smoked, and about 36% reported any ETS exposure. No important differences in key characteristics existed between the analysis sample and the full MESA cohort (n = 6,814; data not shown). The study sample had fewer Chinese and Hispanic participants than did the full cohort (which had 11.8% and 22% of these ethnicities) because many in these groups were recent immigrants whose average long-term exposure could not be estimated. Correlations among all three arterial stiffness variables were −0.26 and −0.17 between YM and C1 and C2, respectively, and 0.48 between C1 and C2 (all p < 0.0001). Clinical measures were consistent with expectation.
Demographic and clinical characteristics and tobacco smoke exposure for participants included in the analyses (n = 3,996): MESA, 2000–2002.
shows the pollution levels and outcome variables by site. Los Angeles had the highest mean pollution levels, and Winston-Salem and St. Paul had the lowest. For the pollution levels estimated in the two decades before the MESA baseline exam, the imputed and directly observed PM10 levels are comparable, with the imputed levels slightly lower on average than the observed. Measures of arterial stiffness differed by study site: They were most unfavorable (higher for YM, lower for C1 and C2) in New York City (YM), Baltimore (C1), and Winston-Salem (C2).
Long-term PM exposure and outcomes (mean ± SD) averaged across all sites and by individual site for participants included in the analyses (n = 3,996): MESA, 2000–2002.
In the multivariable linear regression models that did not include the pollutant values (), age was associated with stiffer arteries, and women had stiffer arteries than did men for all three measures of stiffness examined. Chinese, Hispanic, and African American participants tended to have stiffer arteries than did Caucasians based on YM and C2, but we observed the opposite for C1, although differences were sometimes not statistically significant. YM was lower in former and current smokers than in never smokers, which indicated less stiff arteries. However, current smoking was associated with greater arterial stiffness as assessed by C2. Smoking status was not associated with stiffness as assessed by C1. Exposure to ETS and smoking exposure represented by pack-years were not associated with increased arterial stiffness for any of the outcome variables. Associations of smoking status and pack-years with the outcomes were generally similar when both variables were not simultaneously in the same model. Greater MAP was associated with greater stiffness by all three measures. Physical activity was not significantly associated with any of the outcomes, nor was diabetes status, glucose, or triglycerides.
Percent difference (95% CI) in three arterial stiffness outcomes, not adjusted for pollution (n = 3,996): MESA, 2000–2002.
In all of the models, including those adjusted for all covariates (for which none of the variance inflation factors exceeded 3), average long-term exposure to PM10 was not associated with greater arterial stiffness measured by YM (). The same was true for the compliance outcomes C1 and C2 at all sites. The 2001 nearest-monitor average PM10 and PM2.5 were also not associated with the outcomes for any of the sites.
Percent difference (95% CI) in three arterial stiffness outcomes per 10-μg/m3 PM increment in preceding two decades and 2001 PM exposure under various covariate adjustment schemes: MESA, 2000–2002.
We then took study site into consideration. Patterns of association calculated for the six sites in site-stratified models were generally consistent with no associations for all pollution metrics and covariate adjustment schemes (,). Although a scattering of associations were significant, they were not robust to the covariate adjustments for all the models.
Percent difference (95% CI) in three arterial stiffness outcomes per 10-μg/m3 increment in long-term PM exposure under various covariate adjustment schemes, stratified by study site: MESA, 2000–2002.
Percent difference (95% CI) in three arterial stiffness outcomes per 10-μg/m3 increment in 2001 PM exposure under various covariate adjustment schemes, stratified by study site: MESA, 2000–2002.
Analyses with adjustment for shorter term PM exposure did not alter the patterns in the observed associations (data not shown). Analyses restricted to participants residing within 10 km of the nearest monitor (n = 2,518) were consistent with the analysis of the complete data set (data not shown).
We examined heterogeneity by BMI, waist:hip ratio, diabetes, physical activity, sex, race/ethnicity, and age in fully adjusted models. Race had significant interaction terms for YM and C1 and diabetes for C1 and C2. None of the other variables showed evidence of effect modification.
We fitted fully adjusted random effects models stratified by race and diabetes for the outcomes for which interaction terms were significant. Among black participants, the percent difference in YM with a 10-μg/m3 increase in nearest-monitor PM10 was 14.8% [95% confidence interval (CI), 1.3–30.2%] and with a 10-μg/m3 increase in imputed PM10 was 16.9% (95% CI, 1.9–34.1%). CIs for corresponding estimates for the other race/ethnic groups did not include the point estimates for blacks for these metrics, except for Chinese participants and nearest-monitor PM10 (1.2%; 95% CI, −10.9% to 15.0%). We observed no significant associations for YM in other race/ethnic groups; in general, the point estimates of effect were lowest for Hispanics for YM for all three metrics. For C1, white participants had a significant positive association with imputed PM2.5 (4.4%; 95% CI, 0.2–8.9%), and Chinese participants, for imputed PM10 (13.5%; 95% CI, 3.5–24.4%). We observed no other consistent patterns of point estimates by race/ethnicity. For diabetes-stratified analyses, patterns of association were inconsistent when comparing pollution metrics and outcomes, with two positive and one negative significant association among those with no diabetes and those with impaired glucose tolerance, respectively.
For the results stratified by smoking status, we found only two significant associations. Among the 1,519 former smokers, C1 was associated with both observed −8.9% (95% CI, −16.4% to −0.7%) and imputed −8.9% (95% CI, −16.8% to −0.4%) PM10. No other associations were significantly different from zero, and point estimates showed no consistent trends by smoking status.