Abstract P067: Early Exposure to PM 2.5 and Ozone During the Menopausal Transition as Predictor of Subclinical Atherosclerosis in Late Midlife Women: the Study of Women’s Health Across the Nation (SWAN)

Abstract

Introduction: Long-term air pollution may be a risk factor for CVD mortality, but few studies have investigated its effect on subclinical atherosclerosis. Moreover, data among women transitioning the menopause are lacking. Hypothesis: We hypothesized that mid-life women exposed to higher levels of air pollution across a 5-year period may have a greater burden of subclinical atherosclerosis (higher common carotid intima-media thickness (CIMT), inter-adventitial diameter (AD) and plaque) 5 to 7 years later compared to women exposed to lower levels. Methods: This longitudinal study was conducted among 1,188 women from the Study of Women’s Health Across the Nation (SWAN) with available data on both air pollution exposure and CIMT. We excluded participants who had an MI and stroke before the carotid ultrasound scan. Yearly cumulative exposure levels of two air pollutants, particulate matter ≤2.5 μm (PM 2.5 ) and ozone (O 3 ), were collected from monitors 20km within the participant’s residential address at SWAN visit 3 – 7 (1999-2005). Corresponding years cumulative levels of continuous CVD risk factors were used as covariates. CIMT, AD and plaque presence were assessed at visits 12/13 (2010-2012). Linear regression models were used to estimate the effect of early exposure to PM 2.5 and O 3 on mean and maximum CIMT. Logistic regression was applied to assess the effects of air pollutants on plaque presence. Full models were adjusted for CVD risk factors, including BMI, smoking, cholesterol, triglyceride, HDL-C, menopause status, hormone use, fasting blood glucose, insulin, diabetic medication and hypertension, and the extended models were further adjusted for SBP and inflammatory biomarkers (tPA, PAI-1 and CRP). Results: At time of carotid scan, women were on average 59.6±2.7 years old and a majority were postmenopausal (88.4%). The women were White (48.4%), Black (31.2%), Chinese (13.3%) and Hispanic (7.1%). Cumulative PM 2.5 significantly predicted maximum CIMT adjusting for CVD risk factors such that 1 μg/m 3 higher cumulative exposure to PM 2.5 over 5 years was associated with a 7.4 μm (95% CI: 0.4 – 14.4) greater maximum CIMT. The association was not significant after adjusting for SBP but was not attenuated by adjusting for inflammatory biomarkers. PM 2.5 was related to mean CIMT and AD when adjusting for site, SES and age, but not after adjusting for other CVD risk factors. Ozone levels were not associated with any of the outcomes. No association was found between air pollution exposure and plaque presence. Conclusion: Early cumulative PM 2.5 exposure was associated with maximum CIMT later in the post-menopausal period. This association was largely explained by SBP suggesting that early exposure to air pollutants may relate to higher values of CIMT potentially by increasing SBP.