[Truncated abstract] According to the fetal origins hypothesis, our health is influenced not only by diet, exercise or genes inherited at conception but also by the exposures experienced in utero, which happen to be well represented by fetal growth. It is widely accepted that exposure to toxic agents during pregnancy restricts fetal growth; with repeated acute exposure to tobacco smoke being one of the most well documented examples. However, the influence of cumulative long-term exposure to typically lower levels of air pollutants is less well understood. In most urbanised locations, motor vehicles are the single largest contributor to anthropogenic ambient air pollution. This thesis investigates the association between restricted fetal growth and exposure to motor vehicle emissions at a location where most time is spent – home. Much can be learned from prior research on the associations between traffic emissions and exacerbation of certain respiratory conditions, for which a number of reviews have concluded that there is a causal association. There is a reasonable, albeit putative, expectation that there would be greater power to detect an effect for respiratory exacerbation. This offered the opportunity to develop and test methods to model air pollution and map disease risk using emergency department presentations for asthma that could be later applied to examine associations with fetal growth. Risk of asthma emergency department presentation was found to be elevated for children who lived closer to the two cities in the study area. This geographic pattern in risk remains unexplained but offers opportunity for further investigation in a future study. There was a 70% increase in risk of emergency department presentation among the youngest children (aged less than 5 years) for elevated previous day exposure to traffic-related air pollution. This association was stronger than those reported by previous studies.
|Doctor of Philosophy
|Unpublished - 2011