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Exposure to air pollution in childhood was directly associated with bronchitic symptoms in adulthood, according to findings from a decades-long study from California.

In fact, each standard deviation (SD) increase in mean childhood exposure to nitrogen dioxide (NO₂) -- a common byproduct from fossil fuel combustion -- was associated with a 51% higher odds of cough, phlegm, and bronchitis symptoms in adulthood (OR 1.51, 95% CI 1.00-2.27).

And each SD increase in mean exposure to particulate matter smaller than 10 μm in diameter (PM₁₀) -- which can stem from pollen, wildfire ash, dust, and other sources -- was linked with a 69% higher odds bronchitic symptoms later in life (OR 1.69, 95% CI 1.14-2.49), reported researchers led by Erika Garcia, PhD, MPH, of the Keck School of Medicine of the University of Southern California (USC) in Los Angeles.

These links largely persisted when the researchers adjusted for asthma and bronchitic symptoms in childhood, a surprise to the study authors, who detailed their findings in the .

"We would expect that these observable impacts on childhood respiratory health would explain the relationship," Garcia said in a "Our results suggest that childhood air pollution exposure has more subtle effects on our respiratory system that still impact us in adulthood."

Few studies have looked at the impacts of long-term air pollution exposure in childhood on adult respiratory health, the authors explained, though research from , and has demonstrated links between pollution in childhood and later-life asthma. The current study, said Garcia and co-authors, adds to the literature by "providing evidence for a pathway from childhood air pollution exposure to adult respiratory outcomes that is not related to prior childhood respiratory effects."

Still, the study found that participants who did have asthma in childhood had an even greater odds of bronchitis symptoms in adulthood with increasing exposure to air pollution:

• NO₂: OR 2.27 for each SD increase in childhood exposure (95% CI 1.38-3.71)
• PM₁₀: OR 2.34 for each SD increase (95% CI 1.39-3.96)

"This study highlights the importance of lowering air pollution, and especially exposure during the critical period of childhood," said Garcia. "Because there's only so much that we can do as individuals to control our exposure, the need to protect children from the adverse effects of air pollution is better addressed at the policy level."

Of note, the average childhood exposure to NO₂ for the participants who later reported bronchitis symptoms as adults -- 26.8 parts per billion (ppb) -- was only a little more than half that of the annual limits in the Environmental Protection Agency's standards, which were set in 1971.

Commenting on the study, Elizabeth Gibb, MD, MPhil, of the University of California San Francisco–Benioff Children's Hospitals in Oakland, California, told MedPage Today that air pollution can cause airway inflammation, impaired mucociliary clearance, and direct injuries to the respiratory epithelium.

"This damage to the respiratory tract can lead to airway remodeling over time. It's not surprising that these changes in children's airways have long-term effects on their airways as adults," said Gibb, who was not involved in the research.

Lisa Patel, MD, MESc, of Stanford Medicine Children's Health in Pleasanton, California, who also was not involved with the study, emphasized the need to move toward renewable energy and said air pollution counseling should be standard in clinical practice, especially for infants, young children, and those with respiratory conditions.

"For children who have been hospitalized with wheeze, asthma, or pneumonia, this is also a critical opportunity for counseling," she told MedPage Today via email. "I talk to my families about how to read the air quality index, what precautions they should take (like purchasing an air purifier, or DIY if they can't afford one), and the dangers of gas stoves, which produce nitrous oxide and a host of other pollutants."

For their study, Garcia and colleagues relied on data from three cohorts in the decades-long , ultimately including 1,308 participants recruited (during the 1990s and early 2000s) as children from 16 communities across Southern California.

Exposure to air pollution was assessed by inverse-distance-squared spatial interpolation based on residential histories during childhood based on recorded patterns for their region. Participants needed to have completed an online survey during adulthood with bronchitic symptoms recorded for inclusion.

Overall, 60% were female and a majority (56%) were non-Hispanic white, with 32% Hispanic and 3% non-Hispanic Black.

During childhood, 28% reported mold/mildew in the home, 12% reported exposure to smoking in the womb, 13% had exposure to smoking in the home, 19% had bronchitic symptoms, 18% had an asthma diagnosis, and 19% had a parent with asthma. Mean pollutant exposure was 26.1 ppb for NO₂, 49.1 ppb for O₃, and 41.9 μm/m³ for PM₁₀. SDs for each were 11.1 ppb, 10.3 ppb, and 14.2 mg/m³, respectively.

No significant associations were observed between ozone (O₃) pollution and adult bronchitic symptoms, and too few participants had valid estimates of PM_2.5 exposure for analysis, according to the researchers.

During the adult assessment (mean age 32 years), 49% reported having allergies, 18% were smokers, and 25% reported bronchitic symptoms in the past 12 months: most commonly being congested or bringing up phlegm (15%) followed by cough throughout the day (8%), cough first thing in the morning (7%), and having previously had bronchitis (7%).

The main analysis adjusted for differences in a host of factors, including age, income, education, race/ethnicity, smoking or mold/mildew in the childhood home, maternal smoking in pregnancy, most recent smoking status, and BMI in adulthood.

Limitations cited by Garcia and colleagues included that adult bronchitic symptoms were recorded at a single moment in time, with the possibility of misclassification; an inability to adjust for current air pollution levels; and that there was limited monitoring of PM_2.5 during the time that the baseline and follow-up questionnaires were conducted.

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