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A study found that higher PM2.5 exposure during the first year after NICU discharge increased asthma risk in children with bronchopulmonary dysplasia by age 5.
Higher ambient fine particulate matter (PM2.5) exposure during the year following NICU discharge was linked to an increased risk of asthma by 5 years old in children with bronchopulmonary dysplasia, a new study revealed.1
“Importantly, our results build upon evidence that links ambient PM2.5 to wheeze, respiratory deficits, and asthma in infants born preterm, and demonstrate that, among children with compromised lung function, air pollution may influence asthma susceptibility later on in childhood,” wrote study investigator Lizbeth F. Gomez, PhD, MPH, from the division of pulmonary, allergy, and critical care of medicine at the University of Pennsylvania, Philadelphia, and colleagues.1 “Specifically, our findings add to the small but growing literature suggesting that post‑discharge PM2.5 exposure may influence long-term respiratory outcomes among infants with [bronchopulmonary dysplasia].”
Earlier research has found that children born preterm had lower FEV1 than healthy controls and that prenatal exposure to air pollutants, such as PM2.5, PM10, and NO2, can further impact postnatal lung function.2 These findings suggest that infants may have a reduced capacity to handle oxidative stress, making them more susceptible to respiratory inflammation and long-term impairment from pollution.
However, most prior studies used prenatal air pollution exposure as a proxy for postnatal exposure, and few have specifically examined postnatal ambient pollutants. In this retrospective cohort study, investigators evaluated whether higher mean ambient PM2.5 exposure in the first 12 months after hospital discharge was associated with asthma by age 5 in children with bronchopulmonary dysplasia, hypothesizing that greater postnatal exposure would increase the risk of developing asthma.1
The study included 337 infants with bronchopulmonary dysplasia, born between 2010 and 2019, who were discharged from and followed up at the Children’s Hospital of Philadelphia Care Network until age 5. The sample was 59% male, 61% born after 2014, 62% with public insurance, and 52% identified as non-Hispanic Black. The mean gestational age at birth was 27 weeks (range, 25 – 28), the median birth weight was 771 grams, and infants had a mean age of 156 days after NICU discharge.
Although most infants were discharged without inhaled respiratory medications, 17% received albuterol, and 11% were prescribed albuterol and inhaled corticosteroid. About one-fourth required respiratory support at discharge, either oxygen (12%) or tracheostomy (14%).
Investigators estimated daily residential census block group PM2.5 exposures using a spatiotemporal machine-learning model. Estimates were averaged over the first year following the NICU discharge. The study reported that the mean annual PM2.5 exposure was 8.8 µg/m3.
Half of the infants received an asthma diagnosis by 5 years old. In an analysis adjusted for neonatal clinical factors, insurance, neighborhood deprivation, and race/ethnicity, every µg/m3 increment of PM2.5 was associated with a greater asthma risk (adjusted rate ratio [aRR], 1.19, 95% CI: 1.03–1.37). Infants with the most exposure were more likely to be male, born in 2014 or after, receive public insurance, be diagnosed with grade 1 bronchopulmonary dysplasia, and not require supplemental respiratory support at the time of NICU discharge.1
Asthma incidence tended to rise with increasing PM2.5 exposure. Relative to the lowest tertile (mean 7.6 µg/m³), tertile 2 (mean 8.7 µg/m³) had an aRR of 1.31 (95% CI: 0.98–1.74), and tertile 3 (mean 10.0 µg/m³) had an aRR of 1.68 (95% CI: 1.17–2.4).1
“Average annual PM2.5 exposure in the cohort was less than the current EPA threshold of 9 μg/m3,” investigators noted.1 “Therefore, it is important to note that the adverse health effects of fine PM exposure may remain even at relatively low concentrations.”
The study showed that small reductions in average ambient pollen exposure, even as little as 1 µg/m3, may offer meaningful long-term respiratory benefits for children with bronchopulmonary dysplasia.1
“These findings suggest that creating guidance to decrease fine PM exposure during a pivotal phase of lung growth may offer an actionable pathway to mitigate long‑term respiratory morbidity among high-risk neonates with [bronchopulmonary dysplasia],” investigators concluded.1 “Given that environmental exposures may be modifiable with personal exposure mitigation and environmental policy, these results have important implications for developing targeted interventions to improve long-term health outcomes in children with [bronchopulmonary dysplasia].”
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