Maternal Occupational Exposure to Polycyclic Aromatic Hydrocarbons: Effects on Gastroschisis among Offspring in the National Birth Defects Prevention Study

Background: Exposure to polycyclic aromatic hydrocarbons (PAHs) occurs in many occupational settings. There is evidence in animal models that maternal exposure to PAHs during pregnancy is associated with gastroschisis in offspring; however, to our knowledge, no human studies examining this association have been conducted

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

Polycyclic aromatic hydrocarbons in maternal and cord blood plasma.

Polycyclic aromatic hydrocarbons (PAH) are chemicals generated from the incomplete combustion of organic materials, including tobacco smoke. Some PAH are known to be mutagenic and carcinogenic in humans, and of concern for the fetus when women smoke during pregnancy. Known consequences of smoking during pregnancy include low birth weight and preterm delivery. It is unknown if PAH are related to these outcomes. This pilot study was designed to measure concentrations of 3 PAH (anthracene, benzo(a)pyrene and 1-hydroxypyrene) in paired maternal and cord blood samples as well as any correlations between the two matrices. Plasma cotinine was used as a biomarker of tobacco exposure. Additionally, we asked if there is any relationship between the PAH concentrations and low birth weight or preterm delivery. Results showed that all 3 PAH could be found in maternal and cord plasma. Anthracene was consistently shown to be significantly elevated in cord plasma compared to maternal plasma in subgroups based on increasing cotinine concentrations. However, none of the compounds studied were correlated with either birth weight or gestational age

Birth Defects Res A Clin Mol Teratol

BackgroundEvidence in animal models and humans suggests that exposure to polycyclic aromatic hydrocarbons (PAHs) may lead to birth defects. To our knowledge, this relationship has not been evaluated for craniosynostosis, a birth defect characterized by the premature closure of sutures in the skull. We conducted a case-control study to examine associations between maternal occupational exposure to PAHs and craniosynostosis.MethodsWe used data from craniosynostosis cases and control infants in the National Birth Defects Prevention Study (NBDPS) with estimated delivery dates from 1997\ue2\u20ac\u201c2002. Industrial hygienists reviewed occupational data from the computer-assisted telephone interview and assigned a yes/no rating of probable occupational PAH exposure for each job from one month before conception through delivery. We used logistic regression to assess the association between occupational exposure to PAHs and craniosynostosis.ResultsThe prevalence of exposure was 5.3% in case mothers (16/300) and 3.7% in control mothers (107/2,886). We observed a positive association between exposure to PAHs during the one month before conception through the third month of pregnancy and craniosynostosis [odds ratio (OR) = 1.75; 95% confidence interval (CI): 1.01, 3.05] after adjusting for maternal age and maternal education. The number of cases for each craniosynostosis subtype limited subtype analyses to sagittal craniosynostosis; the odds ratio remained similar (OR = 1.76, 95% CI: 0.82\ue2\u20ac\u201c3.75), but was not significant.ConclusionsOur findings support a moderate association between maternal occupational exposure to PAHs and craniosynostosis. Additional work is needed to better characterize susceptibility and the role PAHs may play on specific craniosynostosis subtypes.200-2000-08018/PHS HHS/United StatesCC999999/Intramural CDC HHS/United StatesDYT1/Intramural CDC HHS/United StatesL40 DE023736/DE/NIDCR NIH HHS/United StatesP30 ES005605/ES/NIEHS NIH HHS/United StatesP30 ES023512/ES/NIEHS NIH HHS/United StatesR03 DE021739/DE/NIDCR NIH HHS/United StatesR03DE021739/DE/NIDCR NIH HHS/United StatesU01DD000494/DD/NCBDD CDC HHS/United States2017-01-01T00:00:00Z26033890PMC466822

Traffic-Related Air Toxics and Term Low Birth Weight in Los Angeles County, California

Background: Numerous studies have linked criteria air pollutants with adverse birth outcomes, but there is less information on the importance of specific emission sources, such as traffic, and air toxics