Rationale: The relationship between air pollution and pneumonia is poorly understood. Objectives: To examine relationships between short-term air pollution exposure and number and severity of pneumonia cases along the Wasatch Front in Utah, a region with periodic high levels of outdoor air pollution. Methods: We applied time-stratified case–crossover analyses with distributed lag to patients presenting to seven emergency departments with pneumonia over a 2-year period. We compared levels of particulate matter less than or equal to 2.5 μm in aerodynamic diameter, nitrogen dioxide, and ozone at patient residences with emergency department cases, hospitalizations, objectively defined severe pneumonia, and mortality. We calculated direct cost impacts of particulate matter less than or equal to 2.5 μm in aerodynamic diameter reduction. Results: We evaluated 4,336 pneumonia cases in seven hospitals. Among adults aged 65 years and older, we found consistently positive associations between particulate matter less than or equal to 2.5 μm in aerodynamic diameter within 6 days of presentation and instances of pneumonia (Lag Day 1 adjusted odds ratio, 1.35 per 10 μg/m3 over 12 μg/m3; 95% confidence interval, 1.16–1.57), severe pneumonia (Lag Day 1 adjusted odds ratio, 1.38; 95% confidence interval, 1.06–1.80), and inpatient mortality (Lag Day 5 adjusted odds ratio, 1.50; 95% confidence interval, 1.03–2.16). Smaller associations were found between nitrogen dioxide exposure and pneumonia occurrence, severity, and inpatient and 30-day mortality. Ozone exposure was modestly associated with increased instance and severity of pneumonia in younger adults. Particulate matter less than or equal to 2.5 μm in aerodynamic diameter and nitrogen dioxide effects were greatest in colder months, and ozone effects were greatest in warmer months. Reduction of particulate matter less than or equal to 2.5 μm in aerodynamic diameter levels to less than 12.0 mg/m3 could prevent 76–112 cases of pneumonia per year in these hospitals serving approximately half of the Wasatch Front’s population, reducing direct medical facility costs by $807,000 annually. Conclusions: Among older adults, short-term ambient particulate matter less than or equal to 2.5 μm in aerodynamic diameter exposure is associated with more emergency department visits and hospitalizations for pneumonia, severe pneumonia, increased mortality, and increased healthcare costs. Nitrogen dioxide and ozone modestly increase pneumonia risk and illness severity.

This study aimed to determine if short-term exposure to particulate matter (PM_2.5) and ozone (O₃) is associated with increased symptoms or lung function decline in fibrotic sarcoidosis. Sixteen patients with fibrotic sarcoidosis complicated by frequent exacerbations completed pulmonary function testing and questionnaires every three months for one year. We compared 7-, 10-, and 14-day average levels of PM_2.5 and O₃ estimated at patient residences to spirometry (forced expiratory volume in 1 s (FEV1), to forced vital capacity (FVC), episodes of FEV1 decline > 10%) and questionnaire outcomes (Leicester cough questionnaire (LCQ), Saint George Respiratory Questionnaire (SGRQ), and King’s Sarcoidosis Questionnaire (KSQ)) using generalized linear mixed effect models. PM_2.5 level averaged over 14 days was associated with lower KSQ general health status (score change −6.60 per interquartile range (IQR) PM_2.5 increase). PM_2.5 level averaged over 10 and 14 days was associated with lower KSQ lung specific health status (score change −6.93 and −6.91, respectively). PM_2.5 levels were not associated with FEV₁, FVC, episodes of FEV₁ decline > 10%, or respiratory symptoms measured by SGRQ or LCQ. Ozone exposure was not associated with any health outcomes. In this small cohort of patients with fibrotic sarcoidosis, PM_2.5 exposure was associated with increased severity of respiratory and quality of life symptoms.

Asthma and obesity are among the most prevalent chronic health conditions in children. Although there has been compelling evidence of co-occurrence of asthma and obesity, it is uncertain whether asthma contributes to the development of obesity or obesity contributes to the onset of asthma or both. In this study, we used a joint transition modeling approach with cross-lagged structure to understand how asthma and obesity influence each other dynamically over time. Subjects for this study included 5,193 kindergarten and first-grade students enrolled from 13 communities in 2002–2003 in the Southern California Children’s Health Study, with up to 10 years of follow-up. We found that nonobese children with diagnosed asthma at a study visit were at 37% higher odds of becoming obese by the next annual visit compared with children without asthma (odds ratio = 1.38; 95% credible interval: 1.12, 1.71). However, the presence of obesity at the current visit was not statistically significantly associated with asthma onset in the next visit (odds ratio = 1.25; 95% credible interval: 0.94, 1.62). In conclusion, childhood asthma appears to drive an increase in the onset of obesity among schoolchildren, while the onset of obesity does not necessarily imply the future onset of asthma, at least in the short term.

The fractional concentration of exhaled nitric oxide (FeNO) is a biomarker of airway inflammation that has proved to be useful in investigations of genetic and epigenetic airway susceptibility to ambient air pollutants. For example, susceptibility to airway inflammation from exposure to particulate matter with aerodynamic diameter < =2.5 μm (PM2.5) varies by haplotypes and promoter region methylation in inducible nitric oxide synthase (iNOS encoded by NOS2). We hypothesized that PM2.5 susceptibility associated with these epigenetic and genetic variants may be greater in children with high FeNO from inflamed airways. In this study, we investigated genetic and epigenetic susceptibility to airborne particulate matter by examining whether the joint effects of PM2.5, NOS2 haplotypes and iNOS promoter methylation significantly vary across the distribution of FeNO in school children. The study included 940 school children in the southern California Children’s Health Study who provided concurrent buccal samples and FeNO measurements. We used quantile regression to examine susceptibility by estimating the quantile-specific joint effects of PM2.5, NOS2 haplotype and methylation on FeNO. We discovered striking differences in susceptibility to PM2.5 in school children. The joint effects of short-term PM2.5 exposure, NOS2 haplotypes and methylation across the FeNO distribution were significantly larger in the upper tail of the FeNO distribution, with little association in its lower tail, especially among children with asthma and Hispanic white children. School-aged children with higher FeNO have greater genetic and epigenetic susceptibility to PM2.5, highlighting the importance of investigating effects across the entire distribution of FeNO.

Some chemotherapies that treat childhood cancers have pulmonary-toxic properties that increase risk for adverse respiratory-health outcomes. PM_2.5 causes similar outcomes but its effect among pulmonary compromised cancer survivors is unknown. This case-crossover study identified the PM_2.5-associated odds for primary-respiratory hospitalizations and emergency department visits among childhood cancer survivors in Utah. We compared risk among chemotherapy-treated survivors to a cancer-free sample. We calculated 3-day-average PM_2.5 by ZIP code and county for event and control days. Conditional logistic regression estimated odds ratios. Models were stratified by cause of admission (infection, respiratory disease, asthma), previous chemotherapy, National Ambient Air Quality Standard (NAAQS), and other variables. Results are presented per 10 µg/m³ of PM_2.5. 90% of events occurred at 3-day PM_2.5 averages <35.4 µg/m³, the NAAQS 24-h standard. For survivors, PM_2.5 was associated with respiratory hospitalizations (OR = 1.84, 95% CI = 1.13–3.00) and hospitalizations from respiratory infection (OR = 2.09, 95% CI = 1.06–4.14). Among chemotherapy-treated survivors, the PM_2.5-associated odds of respiratory hospitalization (OR = 2.03, 95% CI = 1.14–3.61) were significantly higher than the cancer-free sample (OR = 0.84, 95% CI = 0.57–1.25). This is the first study to report significant associations between PM_2.5 and respiratory healthcare encounters in childhood cancer survivors. Chemotherapy-treated survivors displayed the highest odds of hospitalization due to PM_2.5 exposure and their risk is significantly higher than a cancer-free sample.