2026

Air pollution exposure may raise risk of adverse pregnancy outcomes by increasing inflammation, study finds


UCLA Fielding School of Public Health-led research shows biological effects of polycyclic aromatic hydrocarbons.

Air pollution exposure may raise risk of adverse pregnancy  outcomes by increasing inflammation, study finds

Exposure to a common environmental pollutant contributes to inflammation among pregnant women, which is thought to play a role in adverse pregnancy outcomes such as preterm birth, low birth weight, and developmental issues in children, a UCLA Fielding School of Public Health-led study has found. 

While previous research has identified associations between air pollution exposure during pregnancy and increased risk of such outcomes, the newly published findings offer insight on the potential biological factors involved. The results appear in the peer-reviewed journal Environmental Research Health.

The new study, led by Dr. Beate Ritz, professor in UCLA Fielding’s epidemiology and environmental health sciences departments, examined the impact of polycyclic aromatic hydrocarbons (PAHs) on a cohort of 159 pregnant women, using urine samples to measure both PAH levels and the levels of inflammatory markers at up to three points during their pregnancy. PAHs are most produced from vehicular combustion, although individuals can also be exposed through wildfire or cigarette smoke, industrial emissions, and high-temperature grilled or charred meats, such as from barbecues. 

“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,” Ritz said. “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.”

For the study, Ritz’s group collected urine samples up to three times during the pregnancy - in the early, middle, and later gestational periods. They measured both PAH metabolites and inflammatory markers (molecules showing an activation of the immune system). At all three points in time, higher PAH levels were associated with increased inflammatory activity - specifically, for every doubling of PAH exposure there was a 10-50% increase in the level of inflammatory markers. 

Importantly, the type of inflammatory activity changed during the pregnancy: Associations with pro-inflammatory markers were strongest during the early and middle gestation periods, while increases in an anti-inflammatory marker known as IL-10 were more evident later in the pregnancy. 

“IL-10 suppresses inflammation, which is important in preventing preterm birth,” Ritz 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.”

At the individual level, Ritz said, pregnant women can reduce their risk through such measures as minimizing time spent near heavy traffic, staying indoors or evacuating during active wildfires, and using indoor air filters when possible.

Healthy eating may also have a protective effect - for example, she noted, green leafy vegetables have been shown to increase metabolism, which can help to rid the body of PAHs more rapidly. She added that more research is needed to look at other potential protective factors, as well as to further clarify how PAH-related inflammatory changes during pregnancy translate to long-term health risks for the mother and child.

Funding and authors

The study was funded by the National Institute of Child Health and Human Development, part of the National Institutes of Health. Other authors included Yoojin Cho, Qi Meng, Kasey E. Yu, Irish Del Rosario, and Sanjali Mitra from the UCLA Fielding School of Public Health; and the UCLA David Geffen School of Medicine’s Carla Janzen and Sherin U. Devaskar.