Date of Award

Spring 5-13-2016

Degree Type


Degree Name

Master of Public Health (MPH)


Public Health

First Advisor

Dr. Roby Greenwald

Second Advisor

Dr. Matt Hayat


INTRODUCTION: Airway inflammatory response is widely believed to be a central mechanism in the development of adverse health effects related to air pollution exposure. Increased ventilation and inspiratory flow rates due to physical activity in the presence of air pollution will increase the inhaled dose of air pollutants. However, physical activity can also affect lung function and may moderate the relationship between air pollution and lung function. The mechanisms that underpin the complex interplay between air pollution, physical activity, and lung function may be more sensitive to the inhaled dose of air pollution than to ambient air pollution exposure alone. Despite this, the majority of literature on the topic measures only the ambient concentration of air pollution.

AIM: This study aims to characterize the relationship between inhaled air pollution dose, physical activity, and respiratory response markers of lung function, oxidative stress and inflammation among healthy adolescents. Respiratory response measures include exhaled nitric oxide (eNO), percent oxidized exhaled breath condensate glutathione (%GSSG), percent oxidized exhaled breath condensate cysteine (%CYSS), the percentage of total oxidized compounds (%Oxidized), and changes in pulmonary function, namely, forced vital capacity (FVC), forced expiratory volume (FEV1), and forced expiratory flow (FEF25-75). Air pollution measures include cumulative inhaled doses of fine particulate matter (PM2.5), ozone (O3), black carbon (BC), and particle number total (PNT).

METHODS: Using a non-probability sample of high school athletes, outcomes were measured prior to and after participation in extracurricular sports practice. The inhaled dose of air pollutants during the sports practice was estimated for each participant using a novel method developed by Dr. Roby Greenwald. This observational study estimates the association between air pollution dose and outcome measures using general linear mixed models with an unstructured covariance structure and a random intercept for subject to account for repeated measures within subjects. All data analysis was completed using SAS.

RESULTS: A one IQR (i.e. 345.64 µg) increase in O3 inhaled dose is associated with a 29.16% average decrease from baseline in %Oxidized. A one IQR (i.e. 2.368E+10 particle) increase in PNT inhaled dose is associated with an average decrease in FEF25-75 of 0.168 L/second from baseline. The relationship between PNT inhaled dose and eNO is moderated by activity level, with increasing activity levels attenuating the relationship. Similarly, the relationship between O3 inhaled dose and %CYSS is attenuated by activity level, with increasing activity levels corresponding to smaller changes from baseline for a constant O3 inhaled dose.

DISCUSSION: Someone who inhales a high cumulative dose despite a low activity level is likely breathing in a higher concentration of air pollution in a shorter period of time than a person who receives the same dose with a high activity level. The moderating effects of activity level suggest that peaks of high concentration doses of air pollution may overwhelm cells’ endogenous redox balance resulting in increased airway inflammation. Further research that examines the relationships between dose peaks over time and inflammation could help to determine whether a high concentration dose over a short period of time has a different effect than a lower concentration dose over a longer period of time.