O1011: Maternal Exposure to Ethylene Oxide Emissions and Congenital Heart Defects: A Case–Control Study.

Background: Congenital heart defects (CHD) affect nearly 1% of U.S. births and are a leading cause of infant mortality. The etiology of most CHD cases is unknown, and the potential role of residential exposure to industrial pollution is largely unexplored. There are no studies of pollution and CHD in Louisiana, a state with among the highest industrial emissions and worst birth outcomes in the nation. Our study aimed to investigate the possible relationship between residential exposure to industrial air pollution and CHD incidence among Louisiana births.

Methods: We conducted a matched case-control study of 5,198 live births in Louisiana from 2018-2021 (916 CHD cases and 4,282 controls, excluding those with records of maternal smoking, alcohol, or drug use), using hospital records for CHD cases and state birth data for controls. Our pollution metrics were annual average ambient ethylene oxide concentrations and overall air toxicity values (accounting for >400 pollutants) at the maternal residence, as estimated by the U.S. Environmental Protection Agency and reported in the Risk Screening Environmental Indicators Microdata Version 2.3.12. We evaluated the association between each pollution metric and CHD risk using logistic regressions conditioned on matched variables (race, birth
year, and Louisiana Department of Health region) with maternal diabetes status, infant sex, and birth year included as covariates. We conducted a supplemental analysis limited to CHD cases that resulted in surgery or death. To address potential bias from loss to out-of-state treatment, we conducted a sensitivity analysis that excluded cases covered by private insurance.

Results: Estimated ethylene oxide concentrations ≥2.0 ng/m3 (90th percentile) were associated with a >300% higher risk of septal defects (adjusted OR = 3.13, 95% CI: 1.51, 6.51). Associations with other defect types were non-significant, though statistical power was more limited for these comparisons. Risk of CHD overall (any defect) increased with ethylene oxide concentrations in a dose-response manner (99th percentile adjusted OR = 3.65; 95% CI: 1.75, 7.57). A similar pattern was observed for overall toxicity, though these associations were generally weaker. The results of sensitivity analyses supported the main findings.

Conclusion: To our knowledge, this is the first study to investigate the relationship between industrial ethylene oxide emissions and CHD, or any birth defect, in a residential population. We found that ethylene oxide levels representative of current environmental conditions in Louisiana are associated with a substantially increased risk of CHD, particularly septal defects.