This project pursues the hypothesis that lifetime cumulative exposure to ambient air pollution is associated with sonographically measured carotid intima-media thickness (CIMT) at age 18-20. CIMT is an established marker of subclinical atherosclerosis - the primary pathogenic process of cardiovascular diseases (CVD). CIMT gradually increases from birth to death and is associated with subclinical inflammation at all ages, and is a strong determinant of CVD. Ambient air pollution is associated with cardiovascular mortality and morbidity and is a cause of pulmonary and systemic inflammation - a hallmark of atherosclerosis. Significant associations between air pollution and CIMT have been reported in adults. Long-term exposure to air pollution also adversely affects lung function (LF) which is a strong predictor of CVD mortality. Both pulmonary and systemic inflammation is an important correlate of poor LF. Poor LF also modifies the distribution and uptake of pollutants in the respiratory tract, leading to higher tissue dose. Given systemic inflammation affecting CIMT, LF and dyslipidemia, low LF, high C-reactive protein (CRP) and high lipids (LDL) these markers will be used to those most susceptible to atherogenic effects of air pollution. CIMT, lifetime residential history, cardio-respiratory covariates, LF, LDL and CRP will be assessed among 800 non-smoking USC College students with lifetime California residencies. Statewide air pollution monitoring information will be assembled to interpolate monthly fine particulate matter (PM2.5), nitrogen- dioxide (NO2) and ozone (O3) concentrations to each residence across lifetime. Concentrations will be weighted by activity levels and time spent indoors and outdoors to individually derive estimates of lifetime exposure. The association between exposure and CIMT and the interaction with LF, CRP and LDL will be investigated with multivariate regressions, tests for interactions, and structural equation modeling. The American Heart Association recommends focusing on prevention of atherosclerosis in early life. Air pollutants represent ubiquitous inflammatory exposures, and millions of young Americans live in areas that exceed current government standards. Small differences in CIMT and LF at a young age translate into clinically relevant diseases, including CVD - the leading cause of mortality in the U.S. ? ? ?
| Brandt, Sylvia; Dickinson, Brenton; Ghosh, Rakesh et al. (2017) Costs of coronary heart disease and mortality associated with near-roadway air pollution. Sci Total Environ 601-602:391-396 |
| Breton, Carrie V; Mack, Wendy J; Yao, Jin et al. (2016) Prenatal Air Pollution Exposure and Early Cardiovascular Phenotypes in Young Adults. PLoS One 11:e0150825 |
| Breton, Carrie V; Park, Caron; Siegmund, Kim et al. (2014) NOS1 methylation and carotid artery intima-media thickness in children. Circ Cardiovasc Genet 7:116-22 |
| Breton, Carrie V; Yin, Fen; Wang, Xinhui et al. (2014) HDL anti-oxidant function associates with LDL level in young adults. Atherosclerosis 232:165-70 |
| Breton, Carrie V; Wang, Xinhui; Mack, Wendy J et al. (2013) Response to letter regarding article, “Childhood air pollutant exposure and carotid artery intima–media thickness in young adults”. Circulation 127:e659 |
| Dratva, Julia; Breton, Carrie V; Hodis, Howard N et al. (2013) Birth weight and carotid artery intima-media thickness. J Pediatr 162:906-11.e1-2 |
| Breton, Carrie V; Wang, Xinhui; Mack, Wendy J et al. (2012) Childhood air pollutant exposure and carotid artery intima-media thickness in young adults. Circulation 126:1614-20 |
| Bradfield, Jonathan P; Taal, H Rob; Timpson, Nicholas J et al. (2012) A genome-wide association meta-analysis identifies new childhood obesity loci. Nat Genet 44:526-31 |
| Breton, Carrie V; Wang, Xinhui; Mack, Wendy J et al. (2011) Carotid artery intima-media thickness in college students: race/ethnicity matters. Atherosclerosis 217:441-6 |
| Gauderman, W James; Thomas, Duncan C; Murcray, Cassandra E et al. (2010) Efficient genome-wide association testing of gene-environment interaction in case-parent trios. Am J Epidemiol 172:116-22 |
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