Exposure to a common air pollutant found in vehicle exhaust and wildfire smoke triggers inflammation in pregnant women, potentially raising the risk of preterm birth, low birth weight and developmental problems in children, according to a new study led by UCLA researchers.
The study, published Monday in the peer-reviewed journal Environmental Research Health, is among the first to identify a biological mechanism explaining why pregnant women exposed to higher levels of air pollution face worse outcomes — moving beyond statistical associations to examine what is actually happening inside the body.
Researchers focused on polycyclic aromatic hydrocarbons, or PAHs, a class of chemicals released primarily through the burning of fuel in vehicle engines. PAHs are also produced by wildfires, cigarette smoke, industrial emissions and high-temperature cooking methods such as grilling or charring meat.
"These findings provide biological evidence that PAHs influence the immune system and inflammatory processes during pregnancy, and we know that increased inflammation can contribute to negative pregnancy outcomes," said Dr. Beate Ritz, a professor in UCLA Fielding School of Public Health's epidemiology and environmental health sciences departments and the study's lead researcher. "Given how widespread PAHs are in urban air pollution, it underscores the need for policies that reduce exposures to these pollutants for this vulnerable population."
The research team tracked 159 pregnant women, collecting urine samples at up to three points during their pregnancies — in the early, middle and later stages of gestation. Scientists measured both PAH metabolites, which indicate how much of the chemical a person has absorbed, and inflammatory markers, molecules that signal activation of the immune system.
At every stage of pregnancy, higher PAH levels corresponded with greater inflammatory activity. For every doubling of PAH exposure, inflammatory markers rose by 10 to 50 percent.
The type of inflammation, however, shifted as pregnancies progressed. Pro-inflammatory responses were strongest during the early and middle stages of gestation. Later in pregnancy, researchers observed elevated levels of interleukin-10, or IL-10, a marker that works to suppress inflammation.
Ritz said that late-pregnancy rise in IL-10 represents the body responding as it should. "IL-10 suppresses inflammation, which is important in preventing preterm birth," she said. "The higher IL-10 levels toward the end of the pregnancy meant the mother's body was doing what we would want in response to the PAHs. But we can assume that in cases where the IL-10 wasn't increased at the end of the pregnancy, that is how air pollution would contribute to an adverse outcome."
On the policy front, Ritz said current air quality standards may be less of a concern than geographic hotspots where pollution is concentrated. "General air pollution standards are less of a problem than geospatial hot spots for high exposures near sources such as closer to traffic, ports and airports," she said. She called for "reductions in combustion and traffic related pollution and public health recommendations for air filters during wildfires as interventions in vulnerable populations, such as pregnant women."
At the individual level, Ritz said pregnant women can take steps to limit their exposure by avoiding time spent near heavy traffic, staying indoors during active wildfires and using indoor air filtration when available. Diet may also offer some protection — green leafy vegetables have been shown to accelerate the body's metabolism of PAHs, helping to eliminate them more quickly.
Ritz cautioned that while the study cohort was not representative of the broader population of pregnant women, the immune responses observed are considered universal. "We have shown many times that air pollution is related to adverse birth outcomes in all of California pregnant women," she said. The study, she added, was focused specifically on the biological mechanisms at work — examining "whether PAH increase immune responses" — rather than broader demographic patterns.
The study was funded by the National Institute of Child Health and Human Development, part of the National Institutes of Health. Additional authors came from UCLA's Fielding School of Public Health and the David Geffen School of Medicine.
Ritz said further research is needed to identify additional protective factors and to better understand how PAH-related inflammation during pregnancy translates into long-term health risks for both mothers and children.