Thesis Abstract

Abstract
Childhood asthma is a significant public health concern with a complex etiology that involves genetic predisposition and environmental triggers. Air pollution has been identified as one of the key environmental factors that can influence the development and exacerbation of asthma in children. This study aimed to investigate the effect of early life exposure to air pollution on the development of childhood asthma. A comprehensive literature review was conducted to examine existing research on the relationship between air pollution and childhood asthma. Various air pollutants, including particulate matter (PM), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and volatile organic compounds (VOCs), were identified as potential contributors to the development of asthma in children. The mechanisms through which these pollutants can induce airway inflammation, oxidative stress, and immune dysregulation were explored. Studies have shown that exposure to air pollution during pregnancy and early childhood is associated with an increased risk of developing asthma later in life. Maternal exposure to air pollutants during pregnancy can lead to fetal programming of the immune system and respiratory pathways, making the child more susceptible to asthma development. Early life exposure to air pollution has been linked to respiratory symptoms, decreased lung function, and increased asthma incidence in children. Furthermore, genetic factors may interact with air pollution exposure to modulate the risk of childhood asthma. Polymorphisms in genes related to oxidative stress response, inflammation, and airway reactivity have been identified as potential effect modifiers in the relationship between air pollution and asthma development. Gene-environment interactions play a crucial role in determining individual susceptibility to the adverse effects of air pollution on respiratory health. In conclusion, early life exposure to air pollution is a significant risk factor for the development of childhood asthma. Efforts to reduce air pollution levels, especially in urban areas, may help mitigate the burden of asthma in children. Future research should focus on elucidating the underlying mechanisms of air pollution-induced asthma and identifying high-risk populations that may benefit from targeted interventions to prevent asthma development. By understanding the impact of air pollution on childhood asthma, public health policies can be tailored to protect vulnerable children and promote respiratory health.

Thesis Overview

 BACKGROUND:

There is increasing recognition of the importance of early environmental exposures in the development of childhood asthma. Outdoor air pollution is a recognized asthma trigger, but it is unclear whether exposure influences incident disease. We investigated the effect of exposure to ambient air pollution in utero and during the first year of life on risk of subsequent asthma diagnosis in a population-based nested case-control study.

METHODS:

We assessed all children born in southwestern British Columbia in 1999 and 2000 (n = 37,401) for incidence of asthma diagnosis up to 34 years of age using outpatient and hospitalization records. Asthma cases were age- and sex-matched to five randomly chosen controls from the eligible cohort. We estimated each individual’s exposure to ambient air pollution for the gestational period and first year of life using high-resolution pollution surfaces derived from regulatory monitoring data as well as land use regression models adjusted for temporal variation. We used logistic regression analyses to estimate effects of carbon monoxide, nitric oxide, nitrogen dioxide, particulate matter RESULTS:

A total of 3,482 children (9%) were classified as asthma cases. We observed a statistically significantly increased risk of asthma diagnosis with increased early life exposure to CO, NO, NO2, PM10, SO2, and black carbon and proximity to point sources. Traffic-related pollutants were associated with the highest risks: adjusted odds ratio = 1.08 (95% confidence interval, 1.041.12) for a 10-microg/m3 increase of NO, 1.12 (1.071.17) for a 10-microg/m3 increase in NO2, and 1.10 (1.061.13) for a 100-microg/m3 increase in CO. These data support the hypothesis that early childhood exposure to air pollutants plays a role in development of asthma.