Polycyclic Aromatic Hydrocarbons (PAH) Exposure Trends, and Evidence of Adverse Health Effects in Infants and Children from Prenatal/Early-Life PAH Exposure
Polycyclic aromatic hydrocarbons (PAHs) are complex mixtures that form when organic matter is burned. Humans are primarily exposed to PAHs via air pollution from incomplete combustion of fossil fuels and biomass, such a motor vehicle exhaust, cigarette smoke, wood smoke, or industrial emissions; or via ingestion of PAHs bound to particles in household dust, or from grilled or smoked food. Chronic PAH exposure is linked to many adverse health outcomes, including cancer, cardiovascular disease, and respiratory illness. Concern regarding the adverse health effects of PAHs prompted public health surveillance and regulatory measures to monitor and control PAH exposure. Recent air monitoring studies in the U.S. showed PAH levels in ambient air have decreased since the 1990s, but few studies have utilized biomarkers as a measure of internal dose to evaluate if decreased PAHs in ambient air equates to decreased human exposure. Recent toxicological studies in animals, and epidemiologic studies in humans, revealed that PAHs can cross the placenta, and there is a growing epidemiological evidence that prenatal and early-life PAH exposure is linked with adverse human development outcomes, such as low birth weight in infants, and lower IQ scores in children. However, there are few studies that have attempted to address these conflicting results by summarizing the available evidence. The overarching goal of this dissertation is to summarize the global weight of evidence regarding prenatal and early-life PAH exposure on infant/child health, and to evaluate the effectiveness of U.S. environmental health policies in reducing PAH exposure. The first study of this dissertation provides evidence that, while U.S. policies, such as the U.S. Clean Air Act Amendments (1990, as amended), have been successful in reducing ambient PAH concentration, exposure of two semi-volatile PAHs, Naphthalene, and Pyrene, increased in non-smokers from 2001-2014. This study also provides evidence that, compared to Non-Hispanic Whites, a persistent disparity exists in PAH exposure for Non-Hispanic Blacks and Mexican Americans, suggesting these ethnic groups have not benefited to the same extent from U.S. policies to reduce PAH exposures. The second study is a systematic review and meta-analysis that evaluated prenatal PAH exposure on selected birth outcomes in infants. The results of this study indicate there is sufficient human evidence that prenatal PAH exposure adversely affects birth length, head circumference, and ponderal index. The third study is a systematic reviews and meta-analysis that evaluated prenatal and early-life PAH exposure on neurodevelopment outcomes in children. The results of this study indicate there is sufficient human evidence that prenatal and early-life PAH exposure adversely affects cognitive function, motor function, and behavioral outcomes in children.
These results provide evidence that prenatal and early-life PAH exposure can influence human development, and that, while evidence that U.S. public health efforts to reduce ambient PAH exposure have been successful, the internal dose of Naphthalene and Pyrene have increased over time, especially in minority populations. A persistent disparity exists in PAH exposure for Non-Hispanic Blacks and Mexican Americans, suggesting these groups have not benefited to the same extent from U.S. policies to reduce PAH exposures. Our research also suggests that environmental sources of PAHs have changed over time. Overall, these results will guide future research and inform regulatory guidelines to help further identify sources of PAH exposure and reduce exposure, particularly during pregnancy