摘要：Background: 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. Objectives: To examine the association of long-term air pollutants with three urinary catecholamines: dopamine (DA), epinephrine (EPI), and norepinephrine (NE). As a secondary aim, we also examined the association between short-term (or acute) exposure to fine particulate matter [particulate matter with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 )] and those catecholamines. Methods: We used data from the Multi-Ethnic Study of Atherosclerosis (MESA) and two of its ancillary studies, the MESA Air Pollution Study and the MESA Stress Study, to provide exposure and outcome data. DA, EPI, and NE from urine samples were collected from 2004 to 2006 from 1,002 participants in the New York, New York, and Los Angeles, California, study sites. Spatiotemporal models incorporated cohort-specific monitoring and estimated annual average pollutant concentrations ( PM 2.5 , NO 2 , NO x and black carbon) at participants’ homes the year prior to urine collection. Secondarily, short-term PM 2.5 was evaluated (day of, day prior, and 2- to 5-d lags prior to urine collection). Several covariates were considered confounders (age, race, sex, site, socioeconomic status, cardiovascular disease risk factors, psychosocial stressors, and medication use) in linear regression models. Results: A 17 ppb higher annual NO x concentration was associated with 6.3% higher mean EPI level [95% confidence interval (CI): 0.3%, 12.6%]. A 2- μ g / m 3 higher annual ambient PM 2.5 concentration was associated with 9.1% higher mean EPI (95% CI: 3.2%, 15.3%) and 4.4% higher DA level (95% CI: 1%, 7.9%). NO 2 , black carbon, and short-term PM 2.5 exposures were not significantly associated with any of the catecholamines. Conclusions: We found an association between EPI and long-term concentrations of PM 2.5 and NO x and an association between DA and long-term ambient PM 2.5 . These novel findings provide modest support for the hypothesis that air pollutant exposures are related to sympathetic nervous system activation.
