Isabella Hornick
2026-01-30 12:47:00
January 30, 2026
3 min read
Key takeaways:
- The prenatal timeframe in which PM2.5 exposure negatively impacted offspring lung function differed based on lung function measure.
- This was also true for nitrogen dioxide exposure.
Elevated fine particulate matter and nitrogen dioxide exposure in the early to middle weeks of pregnancy had links to lower lung function measures in offspring aged 8 to 14 years, according to results published in CHEST.
Maria José Rosa
“We found that exposure to air pollution during mid-gestation is associated with lower lung function outcomes in childhood,” Maria José Rosa, DrPH, environmental epidemiologist and associate professor in the department of environmental medicine at the Icahn School of Medicine at Mount Sinai, told Healio.
PM2.5 exposure during pregnancy linked to lower lung function in offspring at age 8 to 14 years.” class=”figure-img img-fluid” width=”800″/>
Data were derived from Hu CY, et al. CHEST. 2025;doi:10.1016/j.chest.2025.08.022.
In this study, Rosa and colleagues evaluated 429 mother-child pairs (mother mean age, 27.5 years; offspring mean age, 10.7 years; 54.1% male) from the Mexico City Programming Research in Obesity, Growth, Environment and Social Stressors birth cohort to determine the prenatal timeframes in which higher fine particulate matter (PM2.5) and nitrogen dioxide exposure negatively impact lung function measures in their offspring at 8 to 14 years. They also assessed the impact of extreme temperatures.
Satellite-based models generated daily residential PM2.5, nitrogen dioxide and temperature exposures during pregnancy, according to the study.
“Air pollution is a key environmental risk factor for disease, particularly in Mexico City where pollution levels regularly exceed regulatory standards,” Rosa said. “We also know that air pollution may impact lung development starting in utero, potentially impacting lung health in childhood and adulthood.”
Researchers found that the prenatal timeframe in which increased PM2.5 exposure negatively impacted lung function depended on the lung function measure. For example, the link between this exposure type and a decreased FEV1 z score adjusted for age, height and sex was reported at gestational weeks 1 to 21 (cumulative change, –0.23; 95% CI, –0.39 to –0.07).
For the forced expiratory flow at 25% to 75% of vital capacity (FEF25-75%) z score, the gestational window for PM2.5 exposure was weeks 1 to 20 (cumulative change, –0.2; 95% CI, –0.36 to –0.04).
Additionally, the link between PM2.5 and a lower FVC z score was found at gestational weeks 13 to 19 (–0.04; 95% CI, –0.08 to 0), whereas the link to a lower FEV1/FVC ratio was reported at gestational weeks 6 to 16 (–0.57; 95% CI, –0.11 to –0.04).
Similar to PM2.5 exposure, researchers noted that the prenatal timeframe in which elevated nitrogen dioxide exposure negatively impacted lung function depended on the measure. For example, the link between this exposure type and a decreased FEV1 z score was found at gestational weeks 1 to 16 (cumulative change, –0.16; 95% CI, –0.31 to –0.02).
Further, the study reported that the link between nitrogen dioxide and a lower FEF25-75% z score was found at gestational weeks 13 to 16 (cumulative change, –0.02; 95% CI, –0.04 to –0), whereas the link between this exposure and a lower FEV1/FVC ratio was reported at gestational weeks 6 to 15 (–0.48; 95% CI, –0.96 to –0.01).
Switching to temperature, the FVC z score went up with warmer temperatures at gestational weeks 1 to 8 (0.57; 95% CI, 0.03-1.11) and with colder temperatures at gestational weeks 9 to 18 (0.51; 95% CI, 0.04-0.97).
After dividing the children by sex, researchers found links between PM2.5 and changes in FEV1, FVC and FEF25-75% z scores in boys, and links between this pollutant and changes in FEV1 z score and FEV1/FVC ratio in girls. Notably, only girls had a lower FEV1 z score and FEV1/FVC ratio with nitrogen dioxide exposure.
Prenatal air pollution and temperature exposures did not interact, according to the study.
“We would have expected to see more evidence for joint effects of air pollution and temperature, but the lack of evidence for synergy might be due to the moderate temperatures seen in Mexico City,” Rosa told Healio.
“Future studies should continue to track lung function into adulthood in order to determine if these reductions persist and further gauge the impact of air pollution on lung growth trajectories,” Rosa added.
For more information:
Maria José Rosa, DrPH, can be reached at [email protected].
Perspective
This study by Hu and colleagues provides compelling and clinically meaningful evidence that the timing of prenatal environmental exposures is critical, with early to mid-gestation representing a particularly vulnerable window for lung development.
Although the association between prenatal air pollution and impaired childhood lung function is not unexpected, the precise identification of critical exposure windows represents a major strength and a significant advance over prior trimester-averaged approaches. The use of distributed lag nonlinear models enables the authors to demonstrate that PM2.5 and nitrogen dioxide exert their strongest effects during specific, and sometimes relatively brief, gestational periods — information that is far more actionable for clinicians and policymakers. Notably, sensitivity analyses adjusting for postnatal exposures did not meaningfully alter the results, underscoring the lasting impact of early-life environmental exposures during key stages of lung development.
While not entirely surprising, the sex-specific findings — showing stronger associations in female children — are particularly striking. We and others have previously demonstrated increased susceptibility of the female sex to ozone exposure and oxidative stress in animal models. Although sex-based differences in lung development are well recognized, these findings suggest that prenatal environmental programming may differentially shape long-term respiratory trajectories in ways that remain incompletely understood and warrant further investigation. From a clinical standpoint, these data reinforce the growing recognition that a “one-size-fits-all” approach to risk assessment may be inadequate when counseling families about environmental exposures during pregnancy.
The temperature-related findings are also intriguing. Both warmer and colder prenatal exposures were associated with improved FVC, and contrary to some prior studies, no interaction between temperature and air pollution was observed. These seemingly paradoxical results may reflect the relatively moderate temperature range in the study setting and may limit generalizability to regions experiencing more extreme climatic conditions.
Several limitations merit consideration. Exposure assessment relied on residential location and could not account for maternal mobility or indoor exposures, potentially biasing estimates toward the null. In addition, the inability to adjust for potential mediators such as gestational age and birth weight may limit clinical interpretability and introduce residual confounding.
Future research should focus on replication in diverse populations, mechanistic studies to elucidate sex-specific vulnerability, and longitudinal follow-up into adulthood to determine whether early lung function deficits translate into clinically significant respiratory disease. For clinicians, these findings emphasize the importance of counseling pregnant patients — particularly early in gestation — about air quality and environmental risk mitigation, while highlighting the need for broader structural interventions to reduce pollution exposure at the population level.
Chintan K. Gandhi, MD, MBBS
Disclosures: Gandhi reports no relevant financial disclosures.
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