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Exposure to Polycyclic Aromatic Hydrocarbons and Early Cardiovascular Effects


Polycyclic aromatic hydrocarbons (PAHs) are a group of combustion-originated chemicals with two or more fused aromatic rings, which ubiquitously present in the ambient air. Substantial evidence indicates that PAHs cause cancers due to their carcinogenesis and mutagenesis, however, less understood is to what extent PAHs influences cardiovascular (CV) health. While previous animal studies have demonstrated that PAHs caused CV diseases, comparable evidence in humans is lacking. Most human studies on the relationship between PAHs and CV diseases were with a cross-sectional study design and yielded inconsistent results, which might be at least partially due to the lack of exposure contrast. Previous studies have documented a more than 10-fold difference in airborne PAHs between Los Angeles (< 10 ng/m3) and Beijing (>100 ng/m3), providing a dramatic exposure contrast among the international travelers between the two cities. This dissertation took advantages of a natural experiment among international travelers between Los Angeles and Beijing to determine the early CV effects associated with PAHs exposures. This work is subdivided into the following five chapters: an introduction (Chapter 1), three chapters of original research (Chapters 2 - 4), and a discussion of the conclusions of the work (Chapter 5).

Chapter 2 evaluated the alteration of PAHs exposure among ten healthy human subjects who traveled between Los Angeles and Beijing in 2012 and explored the associated health effects. This pilot study has demonstrated elevated exposure to PAHs in Beijing as compared with Los Angeles and identified lipid peroxidation as one of the early CV effects that were associated with PAHs exposure. This chapter provide experimental basis for later works and justify larger studies in chapters 3 and 4.

Chapter 3 systematically tested a panel of circulating biomarkers indicative of systemic inflammation and oxidation in response to changes in PAHs exposures among 26 healthy international travelers in 2014 and 2015. The results indicated that traveling to Beijing led to increased lipid peroxidation and inflammation in associations with urinary PAHs metabolites. This study also suggested hydroxyeicosatetraenoic (HETE), hydroxyoctadecadienoic (HODE) acids, and paraoxonase 1 (PON1) enzymatic activities have potentials to serve as sensitive biomarkers to detect early CV effects induced by environmental exposures.

Chapter 4 extended previous works to 2017 and investigated the temporal trends of PAHs exposure in Los Angeles and Beijing. The results indicated that exposure to PAHs didn’t change in Los Angeles, but significantly decreased in Beijing from 2012 to 2017. This study discussed the potential driving forces of the temporal trends in each city, aiming to achieve a better understanding on how chemical regulations influence human exposure to PAHs.

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