Background: Fine particulate matter (PM2.5) exposure is associated with increased morbidity and mortality, particularly for cardiovascular disease. The association between long-term exposure to PM2.5 and measures of lipoprotein subfractions remains unclear. Therefore, we examined associations between long-term PM2.5 exposure and traditional and novel lipoprotein measures in a cardiac catheterization cohort in North Carolina. Methods: This cross-sectional study included 6587 patients who had visited Duke University for a cardiac catheterization between 2001 to 2010 and resided in North Carolina. We used estimates of daily PM2.5 concentrations on a 1km-grid based on satellite measurements. PM2.5 predictions were matched to the address of each patient and averaged for the year prior to catheterization date. Serum lipids included HDL, LDL, and triglyceride-rich particle, and apolipoprotein B concentrations (HDL-P, LDL-P, TRL-P, and apoB, respectively). Linear and quantile regression models were used to estimate change in lipoprotein levels with each μg/m3 increase in annual average PM2.5. Models were adjusted for age, sex, race/ethnicity, history of smoking, area-level education, urban/rural status, body mass index, and diabetes. Results: For a 1-μg/m3 increment in PM2.5 exposure, we observed increases in total and small LDL-P, LDL-C, TRL-P, apoB, total cholesterol, and triglycerides. The percent change from the mean outcome level was 2.00% (95% CI: 1.38%, 2.64%) for total LDL-P and 2.25% (95% CI: 1.43%, 3.06%) for small LDL-P. Conclusion: Among this sample of cardiac catheterization patients residing in North Carolina, long-term PM2.5 exposure was associated with increases in several lipoprotein concentrations. This abstract does not necessarily reflect U.S. EPA policy.

Background Epidemiological studies have identified associations between long-term PM2.5 exposure and cardiovascular events, though most have relied on concentrations from central-site air quality monitors. Methods We utilized a cohort of 5,679 patients who had undergone cardiac catheterization at Duke University between 2002-2009 and resided in North Carolina. We used estimates of daily PM2.5 concentrations for North Carolina during the study period based on satellite derived Aerosol Optical Depth (AOD) measurements and PM2.5 concentrations from ground monitors, which were spatially resolved with a 10 × 10 km resolution, matched to each patient's residential address and averaged for the year prior to catheterization. The Coronary Artery Disease (CAD) index was used to measure severity of CAD; scores >23 represent a hemodynamically significant coronary artery lesion in at least one major coronary vessel. Logistic regression modeled odds of having CAD or an MI with each 1 μg/m3 increase in annual average PM2.5, adjusting for sex, race, smoking status and socioeconomic status. Results In adjusted models, a 1μg/m3 increase in annual average PM2.5 was associated with an 11.1% relative increase in the odds of significant CAD (95% CI: 4.0%-18.6%) and a 14.2% increase in the odds of having a myocardial infarction (MI) within a year prior (95% CI: 3.7% -25.8%). Conclusions Satellite-based estimates of long-term PM2.5 exposure were associated with both coronary artery disease (CAD) and incidence of myocardial infarction (MI) in a cohort of cardiac catheterization patients.

Rationale: Risk factors for COVID-19 mortality may include environmental exposures, such as air pollution.Objectives: Determine whether, amongst adults hospitalized with PCR-confirmed COVID-19, long-term air pollution exposure is associated with risk for mortality, intensive care unit (ICU) admission or intubation. Methods:We performed a retrospective analysis of SARS-CoV-2 PCR positive patients admitted to seven New York City hospitals from March 8, 2020 to August 30, 2020. The primary outcome was mortality; secondary outcomes were ICU admission and intubation. We estimated the annual average fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ) and black carbon (BC) concentrations at patients' residential addresses. We employed double-robust Poisson regression to analyze associations between annual average PM 2.5 , NO 2 and BC exposure and COVID-19 outcomes, adjusting for age, sex, race/ethnicity, hospital, insurance and time from onset of the pandemic.Results: Of the 6,542 patients, 41% were female and aged median 65 years (IQR 53, 77). Over 50% selfidentified as a person of color [N=1,687 (26%) Hispanic, N=1,659 (25%) Black]. Air pollution exposures were generally low. Overall, 31% (N=2,044) of the cohort died, 19% (N=1,237) were admitted to the ICU and 16% (1,051) were intubated. In multivariable models, higher long-term exposure to PM 2.5 was associated with increased risk of mortality (RR 1.11, 95% CI 1.02, 1.21 per 1µg/m 3 increase in PM 2.5 ) and ICU admission (RR 1.13, 95% CI 1.00, 1.28 per 1µg/m 3 increase in PM 2.5 ). In multivariable models, neither NO 2 nor BC exposure was associated with COVID-19 mortality, ICU admission or intubation.Conclusions: Amongst patients hospitalized with COVID-19, higher long-term PM 2.5 exposure was associated with increased risk of mortality and ICU admission.

Background Bisphenol A (BPA) is an environmental estrogen used in the manufacture of polycarbonate plastics and epoxy resins used to make food and beverage packaging. Increasing evidence suggests that BPA mimics estrogens in the body and may be associated with putative markers of breast cancer risk. Objectives We analyzed the National Health and Nutrition Examination Survey (NHANES) 2003–2010 data to investigate the association of BPA with age at menarche in adolescent girls. We hypothesized that urinary BPA, as a surrogate biomarker for BPA exposure, is associated with earlier age at menarche, and that body mass index (BMI) may modulate this association. Methods We conducted cross-sectional analyses of urinary BPA, BMI and age of menarche in a subsample of 987 adolescent girls aged 12–19, using pooled data from the 2003–2010 NHANES. Unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CI) for the association between urinary BPA and early onset of menarche, with adjustment for sampling design. We additionally assessed interaction of BPA with BMI. Results Adolescent girls with moderate BPA levels appeared to be less likely to have early onset of menarche than those with the lowest levels (OR=0.57; 95% CI=0.30, 1.08) after adjusting for age, race/ethnicity, parental education, country of birth, NHANES cycle, BMI and creatinine. BMI appeared to modify the BPA-menarche association. Conclusions Although a non-significant trend suggests increasing urinary BPA may be associated with delayed menarche in adolescent girls, these results are based on cross-sectional data. Results should be clarified in carefully designed longitudinal cohort studies.