Ambient air pollution is produced by sources including vehicular traffic, coal-fired power plants, hydraulic fracturing, agricultural production, and forest fires. It consists of primary pollutants generated by combustion and secondary pollutants formed in the atmosphere from precursor gases. Air pollution causes and exacerbates climate change, and climate change worsens health effects of air pollution. Infants and children are uniquely sensitive to air pollution, because their organs are developing and they have higher air per body weight intake. Health effects linked to air pollution include not only exacerbations of respiratory diseases but also reduced lung function development and increased asthma incidence. Additional outcomes of concern include preterm birth, low birth weight, neurodevelopmental disorders, IQ loss, pediatric cancers, and increased risks for adult chronic diseases. These effects are mediated by oxidative stress, chronic inflammation, endocrine disruption, and genetic and epigenetic mechanisms across the life span. Natural experiments demonstrate that with initiatives such as increased use of public transportation, both air quality and community health improve. Similarly, the Clean Air Act has improved air quality, although exposure inequities persist. Other effective strategies for reducing air pollution include ending reliance on coal, oil, and gas; regulating industrial emissions; reducing exposure with attention to proximity of residences, schools, and child care facilities to traffic; and a greater awareness of the Air Quality Index. This policy reviews both short- and long-term health consequences of ambient air pollution, especially in relation to developmental exposures. It examines individual, community, and legislative strategies to mitigate air pollution.

Background: Data on pediatric asthma morbidity and effective environmental interventions in U.S. agricultural settings are few. We evaluated the effectiveness of HEPA air cleaners on asthma morbidity among a cohort of rural Latino children. Methods: Seventy-five children with poorly controlled asthma and living in non-smoking homes were randomly assigned to asthma education alone or along with HEPA air cleaners placed in their sleeping area and home living room. The Asthma Control Test (ACT) score, asthma symptoms in prior 2 weeks, unplanned clinical utilization, creatinine-adjusted urinary leukotriene E4 (uLTE4 [ng/mg]), and additional secondary outcomes were evaluated at baseline, six, and 12 months. Group differences were assessed using multivariable-adjusted generalized estimating equations. Incident rate ratios of ever experiencing the metrics of poorer asthma health during follow-up (suboptimal asthma management) were estimated using Poisson regression models in secondary analysis. Results: Mean child age was 9.2 and 8.6 years in intervention and control groups, respectively, and two-thirds of participants were male. Primary analysis of repeated measures of ACT score did not differ between groups (HEPA group mean change compared to controls 10% [95% CI: − 12-39%]). A suggestion of greater decrease in uLTE4 (ng/mg creatinine) was observed (− 10% [95% CI: − 20 -1%]). Secondary analysis showed children with HEPAs were less likely to have an ACT score meeting a clinically defined cutoff for poorly controlled asthma using repeated measures (IRR: 0.45 [95% CI: 0.21–0.97]). In Poisson models, intervention participants had reduced risk of ever meeting this cutoff (IRR: 0.43 [95% CI: 0.21–0.89]), ever having symptoms in the past 2 weeks (IRR: 0.71 [95% CI: 0.52–0.98]), and lower risk of any unplanned clinical utilization (IRR: 0.35 [95% CI: 0.13–0.94]) compared to control participants. Discussion: The HAPI study showed generally improved outcomes among children in the HEPA air cleaner group. However, primary analyses did not meet statistical significance and many outcomes were subjective (self-report) in this unblinded study, so findings must be interpreted cautiously. HEPA air cleaners may provide additional benefit for child asthma health where traditional asthmagens (traffic, tobacco smoke) are not prominent factors, but larger studies with more statistical power and blinded designs are needed. Trial registration: ClinicalTrials.gov Identifier: NCT04919915. Date of retrospective registration: May 19, 2021.

Background: Increasingly studies suggest prenatal exposure to air pollution may increase risk of childhood asthma. Few studies have investigated exposure during specific fetal pulmonary developmental windows. Objective: To assess associations between prenatal fine particulate matter exposure and asthma at age 4. Methods: This study included mother–child dyads from two pregnancy cohorts—CANDLE and TIDES—within the ECHO-PATHWAYS consortium (births in 2007–2013). Three child asthma outcomes were parent-reported: ever asthma, current asthma, and current wheeze. Fine particulate matter (PM_2.5) exposures during the pseudoglandular (5–16 weeks gestation), canalicular (16–24 weeks gestation), saccular (24–36 weeks gestation), and alveolar (36+ weeks gestation) phases of fetal lung development were estimated using a national spatiotemporal model. We estimated associations with Poisson regression with robust standard errors, and adjusted for child, maternal, and neighborhood factors. Results: Children (n = 1,469) were on average 4.3 (SD 0.5) years old, 49% were male, and 11.7% had ever asthma; 46% of women identified as black and 53% had at least a college/technical school degree. A 2 μg/m³ higher PM_2.5 exposure during the saccular phase was associated with 1.29 times higher risk of ever asthma [95% confidence interval (CI): 1.06, 1.58]. A similar association was observed with current asthma (risk ratio 1.27, 95% CI: 1.04, 1.54), but not current wheeze (risk ratio 1.11, 95% CI: 0.92, 1.33). Effect estimates for associations during other developmental windows had CIs that included the null. Conclusions: Later phases of prenatal lung development may be particularly sensitive to the developmental toxicity of PM_2.5.

Background: Large-scale animal feeding operations compromise regional air quality in the rural US through emission of pollutants, such as ammonia gas. Exposure to airborne pollution from animal feeding operations may cause pediatric asthma exacerbations in surrounding communities. Objectives: To describe spatial and temporal patterns in ambient ammonia concentrations in an agricultural region, and to investigate associations between short-term fluctuations in ammonia and subsequent changes in respiratory health in children with asthma. Methods: For 13 months in the Yakima Valley of Washington State, 14 monitors sampled ammonia in outdoor air for 24-hour periods every 6 days. School-age children with asthma (n = 51) were followed for two health outcomes: biweekly reports of asthma symptoms and quick relief medication usage, and daily measurements of forced expiratory volume in 1 second. We assessed associations between each outcome and ammonia using generalized estimating equations. Results: Twenty-four-hour ammonia concentrations varied from 0.2 to 238.1 μg/m³ during the study period and displayed a strong correlation with proximity to animal feeding operations. The percentage of forced expiratory volume in 1 second was 3.8% lower (95% confidence interval = 0.2, 7.3) per interquartile increase in 1-day lagged ammonia concentration and 3.0% lower (95% confidence interval = 0.5, 5.8) for 2-day lagged concentration. We observed no associations between self-reported asthma symptoms or medication usage and estimated ammonia exposure. Conclusions: Ammonia concentrations were elevated in this community and strongly predicted by proximity to animal feeding operations. Ammonia’s association with acute lung function decrements in children with asthma in the surrounding community may be causal or, alternatively, ammonia may be a marker for other pollutants from animal feeding operations associated with respiratory effects.