The Effect of Transportation-Related Air Pollution on the HPA Axis and Adverse Birth Outcomes
- Author(s): Wing, Samuel
- Advisor(s): Ritz, Beate
- et al.
Exposure to air pollution causes dysfunction in human physiology, including in the endocrine system and reproductive process. Transportation-related air pollutants are products of combustion engines, which can come from mobile ground and air sources. Los Angeles County is home to the world’s fourth busiest passenger airport and almost 22,000 miles of maintained roadway, of which approximately 500 miles are freeway. Communities located proximal to these sources experience a considerable health burden from these exposures, especially among sensitive populations like children and pregnant mothers.
The first study of this dissertation examines the role of traffic-related air pollution in dysregulation of the hypothalamus-adrenal-pituitary gland (HPA) axis. Subjects were adolescents enrolled in the Los Angeles Family and Neighborhood Survey (LAFANS) between 2006 and 2008. We built a land use regression (LUR) model to estimate chronic nitrogen dioxide (NO2) exposure, a marker of traffic-related air pollution. We then generated model-based estimates of the association between the cortisol, a measure of HPA axis functioning, and NO2 exposure one year prior to cortisol sampling. Our results indicate that increased exposure to NO2 was associated with a flattened diurnal slope of cortisol, an indicator of an abnormal cortisol response. We hypothesize that this may be a mechanism through which air pollution may affect respiratory function and asthma in adolescents.
The second and third studies of this dissertation use birth outcome data from birth certificates supplied by the California Department of Public Health and exposure data from novel ultrafine particle (UFP) dispersion model. The second study estimates the association between in utero exposure to aircraft-related UFPs from planes landing at Los Angeles International Airport and preterm birth (PTB). Women were included in this study if they delivered babies between 2008 and 2016 and lived within 15 km of the airport. Controlling other pollutants and demographic factors, we found that the risk of PTB was elevated among women more highly exposed to aircraft-related UFPs during their pregnancy. This association was strongest among foreign-born women, especially those of Hispanic and Asian descent.
The third study is a causal mediation analysis, that examines the role of pregnancy-induced hypertension (PIH), including preeclampsia, as a mediator in the previously described relationship between UFP and PTB. We used a weighted marginal structural models approach to estimate the natural direct and indirect effects of UFP on PTB risk, with PIH as a mediating factor. We found that approximately 13% of the UFP-PTB relationship was mediated through UFP exposure-caused hypertensive disorders. We hypothesize that UFP exposure may lead to an inflammatory response which puts expectant mothers at greater risk for hypertensive disorders that can lead to iatrogenic preterm births.
In conclusion, our findings present evidence of the detrimental effects of exposure to air pollution both in utero and during adolescence. These environmental exposures are widespread in urban settings like Los Angeles and impact large populations. The burden of these health effects is often carried by low socioeconomic status communities co-exposed to other pollutants. This research exposes potential processes through which air pollution impacts human health, adding plausible biologic mechanisms that strengthen the understanding of how transportation-related emissions impact a city’s most vulnerable groups.