Air pollution exposure and novel biomarkers of inflammation and cardiac stress in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air)

Marnie Hazlehurst | 2016

Advisor: Joel D. Kaufman

Research Area(s): Environmental & Occupational Health, Epidemiologic Methods


Epidemiologic evidence indicates a causal association between long-term air pollution exposure and cardiovascular disease (CVD), but the mechanisms underlying this process are not fully understood. Inflammation in the lungs that spreads to the rest of the body may result in systemic oxidative stress and inflammation. Subsequently, this inflammatory state may lead to endothelial dysfunction, atherosclerosis, increased coagulation, and activation of the renin-angiotensin system. Some studies have utilized measures of subclinical disease or biomarkers to support these potential mechanisms for the effect of air pollution on the development of CVD. This analysis investigated the effects of long-term exposure to air pollution, specifically four pollutants: fine particulate matter (PM2.5), oxides of nitrogen (NOx), nitrogen dioxide (NO2), and black carbon (BC). This paper examined the association between long-term exposure and the following novel biomarkers of cardiac stress and inflammation: (1) N-terminal-pro-B-type natriuretic peptide (NT-proBNP), (2) Pentraxin-3 (PTX3), and (3) Serum Amyloid P (SAP). As a secondary aim, this paper examined the association between short-term exposures to PM2.5 and each of the biomarkers of interest. Data from a prospective cohort study, the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) in six US cities, were used for this analysis. Likelihood-based spatiotemporal models were used to calculate air pollution exposures at participant residences. NT-proBNP was measured at baseline (n=5,597) and again at a follow-up exam (n=4,694), which was on average three years after baseline. PTX3 and SAP were both measured at the baseline exam in a subset of participants (n=2,878) selected in equal proportions from each racial/ethnic group. NT-proBNP and PTX3 were log-transformed for analysis; SAP was modeled on the natural scale. No association was found between air pollution and NT-proBNP in a repeated measures analysis, but an association was observed between air pollution and elevated levels (≥125 pg/mL) of NT-proBNP at Exam 3 among those with a normal NT-proBNP level at baseline (i.e. reflecting incident cases of sub-clinical cardiac stress and/or sub-clinical heart failure). For a 15 ppb increase in NO2 exposure, the odds ratio was 1.88 (95% CI: 1.20, 2.95; p=0.006) and for a 0.7 10-5 m-1 increase in BC exposure the odds ratio was 1.72 (95% CI: 1.07, 2.76; p=0.026). Increased exposure to PM2.5 was associated with a 2.5 µg/mL increase in SAP (95% CI: 0.3, 4.8; p=0.025), though no associations were found with NOx, NO2, or BC. In cross-sectional analyses, no association was observed between air pollution and PTX3. No associations were found between short-term exposure to PM2.5 and NT-proBNP, PTX3, or SAP.