Date of Award

Fall 12-7-2020

Degree Type

Thesis

Degree Name

Master of Public Health (MPH)

Department

Public Health

First Advisor

Roby Greenwald, PhD

Second Advisor

Matthew Hayat, PhD

Third Advisor

Donghai Liang, PhD

Abstract

INTRODUCTION: Air pollution is a major public health concern. Reducing air pollution exposure can reduce the burden of disease and improve cardiovascular and respiratory health. Traffic related air pollution (TRAP) is a significant contributor to air pollution globally. TRAP and physical activity have a dynamic relationship with interacting and opposing effects that are not fully understood.

AIM: This study investigates the relationship between physical activity and exposure to TRAP by identifying the metabolic pathways associated with important TRAP components including Black Carbon (BC), Ozone (O3), Fine Particulate Matter

METHODS: Saliva samples were collected from 57 study participants playing sports outdoors near major roadways in Atlanta, GA in 2016. Outdoor air pollution measurements were taken along with participants’ physical activity level and breathing metrics. Liquid chromatography coupled with high resolution mass spectrometry was used to process the saliva samples. Mummichog, a pathway analysis tool, was used to identify the metabolic pathways activated.

RESULTS: Ninety-seven pathways were found to be activated as a result of exposure to TRAP and covariates. Acute air pollution exposure was found to be significant in activating metabolic pathways a total of 81 times, with 14 metabolic pathways that showed significant correlation with acute TRAP: Vitamin B6, Beta-Alanine metabolism, Pyruvate metabolism, Selenoamino acid metabolism, Drug metabolism pathway, Saturated fatty acids beta-oxidation, Fatty acid activation metabolism, Glyoxylate and dicarboxylate, TCA cycle metabolism, Vitamin B3 metabolism, Propanoate, Bile acid biosynthesis, Caffeine metabolism, Glyoxylate and dicarboxylate metabolism. One-day lagged PM2.5 exposure has a higher number of pathways activated when compared to acute pollutant exposure.

DISCUSSION: The lower degree of acute exposure pathway activation may be due to insufficient time for changes in metabolic activity to be expressed in saliva compared to long-term exposure or ongoing biological processes. While acute exposure to air pollution may contribute to activating less metabolic pathways than long term exposure, heat index and other covariates all contribute to activating metabolic pathways in addition to the effects of static covariates. There is limited research in untargeted, high-resolution metabolomics data of the effects of air pollution in activating metabolic pathways, but this study offers a glimpse into this relationship for future studies to build upon.

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