Date on Master's Thesis/Doctoral Dissertation


Document Type

Doctoral Dissertation

Degree Name

Ph. D.


Environmental and Occupational Health Sciences

Degree Program

Public Health Sciences with a specialization in Environmental Health, PhD

Committee Chair

Bhatnagar, Aruni

Committee Co-Chair (if applicable)

Hoyle, Gary

Committee Member

Taylor, Kira

Committee Member

Zhang, Qunwei

Committee Member

Rai, Shesh

Committee Member

Srivastava, Sanjay

Author's Keywords

volatile organic compounds; air pollution; toxic release inventory; mixtures; cardiovascular disease; heart disease


Cardiovascular disease (CVD) is the leading cause of death from environmental exposures. Although exposure to PM2.5 is an established risk factor for CVD, the contribution of other hazardous pollutant exposure to CVD is less clear. Overall, this work aimed to examine the effect of pollutants with lesser documented effects on cardiovascular disease using a multi-pronged approach to exposure assessment. The three aims were to examine the relationship between county-level toxic chemical releases and CVD mortality in the contiguous United States between 2002 and 2012, to assess the relationship between individual-level VOC metabolites and vascular function, and to build multipollutant models from the previous two aims to assess the role of mixtures and mixture components in CVD mortality and vascular function. In our national, county-level study, we found that for every 25% increase in annual county-level toxic release, we found a 2.8% (1.2, 4.4; p-value=0.0006) increase in CVD mortality rate. We also found that for every 25% increase in annual county-level risk score, there was a 3.0% (95%CI 1.3, 4.6; p-value=0.0003) increase in CVD mortality. Using the multipollutant method, elastic net, we identified five out of 467 potentially toxic chemicals at the county-level: bromoform, dichlorobromomethane, dichlorotrifluoroethane, nitrophenol, and thallium. In our study of individual-level VOC metabolites, we found that the acrolein metabolite, 3HPMA, was positively associated with systolic BP (+0.98 per SD of 3HPMA; CI: 0.04, 1.91; P=0.04). For each IQR of 3HPMA or DHBMA (a 1,3-butadiene metabolite), there was a 3.3% (CI: -6.18, -0.37; p-value: 0.03) or a 4.0% (CI: -7.72, -0.12; P=0.04) decrease in endothelial function. Urinary levels of the 1,3-butadiene metabolite, MHBMA3, were positively associated with a 2.9% increase in urinary epinephrine (CI: 0.48, 5.37; P=0.02). Using the multipollutant method, Bayesian Kernel Machine Regression, we found that the whole mixture of VOC metabolites (CEMA, 3HPMA, DHBMA, MHBMA3, and HPMMA) was significantly associated with blood pressure, which was primarily driven by 3HPMA. Taken together, these findings suggest that exposure to under regulated pollutants like TRI chemicals and VOCs contribute to CVD mortality and vascular dysfunction. Further research is required to corroborate these findings.