Abstract
Introduction: Autonomic nervous system effects have been hypothesized as a mechanism of air pollutant health effects, though scant prior epidemiologic research has examined the association between air pollutants and catecholamines. Methods: We examined the association between air pollutants and urinary catecholamines in the Multi-Ethnic Study of Atherosclerosis (MESA), a cohort study with participants from six US areas. Data from two ancillary studies, the MESA Air Study and the MESA Stress Study, provide exposure and outcome data. Dopamine (DA), epinephrine (EPI), norepinephrine (NE) data were collected from 2004 – 2006 from 1002 white, black and Hispanic participants from the New York and Los Angeles study sites. Urinary analyte concentrations were adjusted for creatinine and log-transformed for analysis. Spatio-temporal models incorporated cohort-specific monitoring and modeled estimated annual average pollutant concentrations (PM2.5 and NOx) at participant's homes the year prior to urine collection. Several covariates were considered confounders: age, race, sex, site, socioeconomic status, cardiovascular disease risk factors (smoking, second hand smoke, BMI, alcohol use and hypertension) and psychosocial stressors (depression, social support, anxiety, anger and chronic stress) and linear regression models were employed. Results: Preliminary models show a 40 ppb higher NOx concentration was associated with 10% higher NE (95% confidence interval (CI): 4%, 20%) and 17% higher EPI level (95% CI: 3%, 33%). A 5 µg/m3 higher PM2.5 concentration was associated with 23% higher EPI (95% CI: 8%, 41%) and 14% higher DA level (95% CI: 5%, 23%). Conclusions: We found a cross-sectional association between several urinary catecholamines and long-term residential concentrations of PM2.5 and NOx. These novel finding support the hypothesis that air pollutant exposures are related to sympathetic nervous system activation; however, additional investigation is warranted.
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