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The association between particulate pollution and cardiovascular morbidity and mortality is well established. While the cardiovascular effects of nationally regulated criteria pollutants (e.g., fine particulate matter [PM 2.5 ] and nitrogen dioxide) have been well documented, there are fewer studies on particulate pollutants that are more specific for traffic, such as black carbon (BC) and particle number (PN). In this paper, we synthesized studies conducted in the Greater Boston Area on cardiovascular health effects of traffic exposure, specifically defined by BC or PN exposure or proximity to major roadways. Large cohort studies demonstrate that exposure to traffic-related particles adversely affect cardiac autonomic function, increase systemic cytokine-mediated inflammation and pro-thrombotic activity, and elevate the risk of hypertension and ischemic stroke. Key patterns emerged when directly comparing studies with overlapping exposure metrics and population cohorts. Most notably, cardiovascular risk estimates of PN and BC exposures were larger in magnitude or more often statistically significant compared to those of PM 2.5 exposures. Across multiple exposure metrics (e.g., short-term vs. long-term; observed vs. modeled) and different population cohorts (e.g., elderly, individuals with co-morbidities, young healthy individuals), there is compelling evidence that BC and PN represent traffic-related particles that are especially harmful to cardiovascular health. Further research is needed to validate these findings in other geographic locations, characterize exposure errors associated with using monitored and modeled traffic pollutant levels, and elucidate pathophysiological mechanisms underlying the cardiovascular effects of traffic-related particulate pollutants. Implications : Traffic emissions are an important source of particles harmful to cardiovascular health. Traffic-related particles, specifically BC and PN, adversely affect cardiac autonomic function, increase systemic inflammation and thrombotic activity, elevate BP, and increase the risk of ischemic stroke. There is evidence that BC and PN are associated with greater cardiovascular risk compared to PM 2.5 . Further research is needed to elucidate other health effects of traffic-related particles and assess the feasibility of regulating BC and PN or their regional and local sources.

Long-term exposure to ambient air pollution has been associated with cardiovascular morbidity and mortality. Impaired vascular responses may, in part, explain these findings, but the association of such long-term exposure with measures of both conduit artery and microvascular function has not been widely reported. We evaluated the association between residential proximity to a major roadway (primary or secondary highway) and spatially resolved average fine particulate matter (PM2.5) and baseline brachial artery diameter and mean flow velocity, flow-mediated dilation%, and hyperemic flow velocity, in the Framingham Offspring and Third Generation Cohorts. We examined 5,112 participants (2,731 [53%] women, mean age 49 ± 14 years). Spatially resolved average PM2.5 was associated with lower flow-mediated dilation% and hyperemic flow velocity. An interquartile range difference in PM2.5 (1.99 μg/m(3)) was associated with -0.16% (95% confidence interval [CI] -0.27%, -0.05%) lower flow-mediated dilation% and -0.72 (95% CI -1.38, -0.06) cm/s lower hyperemic flow velocity%. Residential proximity to a major roadway was negatively associated with flow-mediated dilation%. Compared with living ≥400 m away, living <50 m from a major roadway was associated with 0.32% lower flow-mediated dilation (95% CI -0.58%, -0.06%), but results for hyperemic flow velocity had wide confidence intervals -0.68 cm/s (95% CI -2.29, 0.93). In conclusion, residential proximity to a major roadway and higher levels of spatially resolved estimates of PM2.5 at participant residences are associated with impaired conduit artery and microvascular function in this large community-based cohort of middle-aged and elderly adults., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Inflammation and endothelial dysfunction are important risk factors for cardiovascular disease (CVD). We hypothesized that candidate genes selected for a study of asthma and chronic obstructive pulmonary disorder (COPD) are associated with markers of systemic inflammation and endothelial dysfunction in an aging population., Methods: Plasma levels of circulating C-reactive protein (CRP), fibrinogen, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were obtained from 679 elderly male participants in the Normative Aging Study. Blood samples were analyzed for 202 single nucleotide polymorphisms (SNPs) in 25 candidate genes and included both haplotype tagSNPs and functional SNPs based on literature review. Data were stratified into discovery and replication cohorts for 2-stage analysis. In the discovery cohort, the relationship between biomarker level and genotype was analyzed using linear mixed effects with random intercepts for each subject and models were adjusted for age and BMI. A positive outcome in the discovery cohort was defined as a p-value <0.1 for the SNP. SNPs that met this criterion were analyzed in the replication cohort and confirmed for those which met a criterion of significance (p<0.025)., Results: In our analyses, SNPs in the CRHR1, ITPR2, and VDR genes met significance criteria., Conclusions: Our results suggest that genes thought to play a role in the pathogenesis of asthma and COPD may influence levels of serum markers of inflammation and endothelial dysfunction via novel SNP associations which have not previously been associated with cardiovascular disease.