UTHealth Houston researcher reviews evidence on how “forever chemicals” may shape congenital heart defect risk
A UTHealth Houston researcher reviewed existing scientific evidence on how exposure to “forever chemicals,” including per- and polyfluoroalkyl substances (PFAS) and polycyclic aromatic hydrocarbons (PAHs), may influence the risk of congenital heart defects in fetal cardiac development.
The findings were recently published in a study in Clinical Chemistry.
Authored by Jenil Patel, MBBS, MPH, PhD, assistant professor of epidemiology at UTHealth Houston School of Public Health, the paper synthesizes current research on how environmental exposures during critical periods of pregnancy may interfere with fetal heart development.
Congenital heart defects are the most recorded birth defects in the U.S., affecting about 1% of all live births and contributing significantly to infant illness and death, according to the CDC. While genetic factors explain some cases, a growing body of research increasingly points to environmental exposures during pregnancy as potential contributors.
“The developing heart is extremely sensitive to its environment, especially in early pregnancy,” said Patel. “This review brings together what we currently know about how environmental chemicals may influence that process.”
The review focuses on chemicals that are widespread, measurable in human populations, and supported by biological evidence indicating potential effects of heart damage. In addition to PFAS and PAHs, the authors summarize findings related to air pollution, nitrates in drinking water, and endocrine-disrupting chemicals such as phthalates and bisphenol A.
Environmental chemicals may affect how a baby’s heart forms by disrupting the body’s standard hormone systems. Hormones such as estrogen and thyroid hormones act like chemical messengers, helping direct when and how organs develop. Certain substances, such as PFAS and PAHs, can disrupt hormones that guide early development.
“When developmental signals are disturbed, the instructions that tell heart cells where to migrate and how to organize can be altered,” Patel said. “Evidence from human and animal studies suggests that PFAS exposure can interfere with thyroid hormone signaling, which is essential for proper heart development, including the formation of heart chambers.” Although advances in pediatric cardiology have improved survival rates among children born with CHDs, the underlying causes of many defects remain unclear. Environmental exposures during early pregnancy, when the fetal heart is forming, may disrupt the developmental processes.
“This is one of the most complex and carefully timed processes in human development,” Patel said. “Understanding how environmental chemicals may interfere with it is critical for identifying preventable risk factors.”
The authors emphasize the need for future research that follows individuals from before pregnancy through birth to better identify when harmful exposures occur and how they overlap with key stages of heart development. They also highlight the importance of combining environmental monitoring data, residential history, and biological measurements to improve exposure assessment.
By combining detailed information about where people live, how they move through their environments, and local pollution levels, researchers can identify potential contributors to CHDs at a more finite level.
The review was conducted in collaboration with researchers from the Arkansas Center for Birth Defects Research and Prevention at the University of Arkansas for Medical Sciences. Corresponding author included alumna Wendy N. Nembhard, PhD, Chair of Epidemiology at Fay W. Boozman College of Public Health.