Short-term variations in particulate matter (PM) and traffic-related air pollutants (e.g., nitrogen dioxide, NO2) have been associated with daily mortality and cardiovascular health outcomes in previous studies. We aimed to evaluate whether short-term changes in PM in three size fractions (PM2.5 , PM2.5-10 , and PM10) and NO2 were associated with systolic and diastolic arterial blood pressure (SBP and DBP, respectively) in the Women’s Health Initiative Observational Study (OS) and Clinical Trials (CT).
We used linear mixed-effect models to estimate the association between short-term air pollution concentrations and repeated measures of arterial blood pressure.
We found statistically significant positive associations between short-term measures (lag days 3-5) of PM2.5 as well as NO2 for both SBP and DBP in fully adjusted models when not controlling for calendar time. Also, in only the CT, PM10 and PM2.5-10 were associated with DBP but not SBP. In fully adjusted models controlling for calendar time, associations with PM2.5-10 and NO2 remained statistically significant for DBP (except for PM2.5-10 in the OS). Specifically, in the CT group, each IQR increase in lag 3-5 NO2 exposure (9.88 ppb) was associated with a 0.13 mm Hg increase in DBP. Also, each IQR increase in lag 3-5 PM2.5-10 exposure (8.46 µg m -3) was associated with a 0.05 mm Hg increase in DBP. Effect modification was found for body mass index (BMI), socioeconomic position (SEP), diabetes, dietary sodium intake, combined fruit and vegetable consumption, and long-term PM2.5 for PM2.5 , PM10 , and NO2 . Shorter lag periods (lag 0 through lag 2) typically exhibited lesser and, especially for SBP, sometimes negative associations. In two-pollutant models of exposures lagged over 3-5 days, NO2 associations with DBP were stronger (0.20 mm Hg per IQR), but those for PM2.5-10 were attenuated to null, as compared to single-pollutant models.
Our findings are consistent with short-term (lag days 3-5) PM2.5-10 and NO2 levels as risk factors for acute cardiovascular outcomes and cardiovascular disease, though two-pollutant model results suggest NO2 is more likely responsible for the observed effects.