Early Gestational Wildfire-Related PM2.5 Exposure Is Associated with Lung Function in Offspring of Mothers with Asthma

Abstract

Highlights: Public health relevance—How does this work relate to a public health issue? Wildfire-related air pollution is an increasing global public health concern due to climate change, with pregnant women and infants representing particularly vulnerable populations. This study examines prenatal exposure to wildfire-related PM2.5 during a critical developmental window and its association with early-life lung function and subsequent respiratory health. Public health significance—Why is this work of significance to public health? Early gestational wildfire-related PM2.5 exposure was associated with differences in tidal breathing patterns in infancy. Infant inspiratory flow measures were also associated with airway reactance and asthma outcomes at six years. These findings suggest early gestation may be an important exposure window and highlight the need to understand how environmental hazards intersect with maternal asthma in shaping child respiratory health. Public health implications—What are the key implications or messages for practitioners, policy makers and/or researchers in public health? Pregnant women with asthma may represent a group at increased vulnerability to wildfire smoke exposure, warranting consideration in public health planning. These findings support the integration of environmental exposure assessment into maternal and child health research and inform policies aimed at reducing health impacts of climate-driven air pollution. Background: Prenatal exposure to air pollutants may increase the risk of adverse respiratory outcomes, particularly in offspring of asthmatic mothers. Evidence on wildfire-related PM2.5 exposure during pregnancy remains limited. This study investigated associations between early gestational wildfire-related PM2.5 exposure, infant lung function, and respiratory outcomes at 6 years. Methods: Gestational wildfire-related PM2.5 exposure patterns were characterised using group-based trajectory modelling and linked to infant lung function outcomes. Infant respiratory measurements were obtained at six weeks of age during behaviourally defined quiet sleep using tidal-breathing flow–volume loops (TBFVL). Airway mechanics at six years were assessed by impulse oscillometry (IOS) following international guideline standards. Trajectory modelling of PM2.5 during gestation was conducted in SAS (PROC TRAJ); all additional statistical analyses were performed in Stata IC 16.1. Results: Increased mean tidal inspiratory flow (MTIF, beta coefficient [β]: 10.51 mL/s, 95% CI: 3.66 to 17.36, p = 0.003) and peak tidal inspiratory flow (PTIF, β: 12.49 mL/s, 95% CI: 2.48 to 22.51, p = 0.014) were observed in infants born to mothers with higher wildfire-related PM2.5 exposure during early gestation (n = 420; n = 411 not exposed, n = 9 exposed). β-coefficients from infant mixed models were then used as proxy indicators and applied in linear regression models and associated with higher reactance at 5 Hz frequency (n = 73) at 6 years of age (PTIF: β: 9.88 mL/s, 95% CI: 0.10 to 19.67, p = 0.048 and MTIF: β: 13.43 mL/s, 95% CI: 1.43 to 25.44, p = 0.029). PTIF was further associated with asthma diagnoses at 6 years (aOR: 1.36, 95% CI: 1.07 to 1.73, p = 0.012; n = 259; n = 116 asthma). Conclusion: Early gestational exposure to wildfire-related PM2.5 may be linked with altered respiratory patterns in infancy and differences in airway reactance during childhood. Findings also suggest a relationship with asthma risk, although mechanisms remain uncertain.