Colorado is regularly impacted by long-range transport of wildfire smoke from upwind regions. This smoke is a major source of ambient PM_2.5. Maternal exposure to total PM_2.5 during pregnancy has been linked to decreased birth weight and other adverse outcomes, although the impact of wildfire smoke contribution has only recently been investigated. The objective of this study was to estimate associations between adverse pregnancy outcomes and ambient wildfire smoke PM_2.5. Wildfire smoke PM_2.5 exposures were estimated using a previously published method incorporating ground-based monitors and remote sensing data. Logistic regression models stratified by ZIP code and mixed models with random intercept by ZIP code were used to test for associations. The primary outcomes of interest were preterm birth and birth weight. Secondary outcomes included gestational hypertension, gestational diabetes, neonatal intensive care unit admission, assisted ventilation, small for gestational age, and low birth weight. Exposure to wildfire smoke PM_2.5 over the full gestation and during the second trimester were positively associated with pre-term birth (OR = 1.076 (μg/m³)⁻¹ [95% CI = 1.016, 1.139; p = 0.013] and 1.132 (μg/m³)⁻¹ [95% CI = 1.088, 1.178]; p < 0.0001, respectively), while exposure during the first trimester was associated with decreased birth weight (−5.7 g/(μg/m³) [95% CI: −11.1, −0.4; p = 0.036]). Secondary outcomes were mixed.

Multi-city population-based epidemiological studies have observed heterogeneity between city-specific fine particulate matter (PM2.5)-mortality effect estimates. These studies typically use ambient monitoring data as a surrogate for exposure leading to potential exposure misclassification. The level of exposure misclassification can differ by city affecting the observed health effect estimate. The objective of this analysis is to evaluate whether previously developed residential infiltration-based city clusters can explain city-to-city heterogeneity in PM2.5 mortality risk estimates. In a prior paper 94 cities were clustered based on residential infiltration factors (e.g. home age/size, prevalence of air conditioning (AC)), resulting in 5 clusters. For this analysis, the association between PM2.5 and all-cause mortality was first determined in 77 cities across the United States for 2001–2005. Next, a second stage analysis was conducted evaluating the influence of cluster assignment on heterogeneity in the risk estimates. Associations between a 2-day (lag 0–1 days) moving average of PM2.5 concentrations and non-accidental mortality were determined for each city. Estimated effects ranged from −3.2 to 5.1% with a pooled estimate of 0.33% (95% CI: 0.13, 0.53) increase in mortality per 10 μg/m3 increase in PM2.5. The second stage analysis determined that cluster assignment was marginally significant in explaining the city-to-city heterogeneity. The health effects estimates in cities with older, smaller homes with less AC (Cluster 1) and cities with newer, smaller homes with a large prevalence of AC (Cluster 3) were significantly lower than the cluster consisting of cities with older, larger homes with a small percentage of AC. This is the first study that attempted to examine whether multiple exposure factors could explain the heterogeneity in PM2.5-mortality associations. The results of this study were found to explain a small portion (6%) of this heterogeneity.

Background: The impact of dust storms on human health has been studied in the context of Asian, Saharan, Arabian, and Australian storms, but there has been no recent population-level epidemiological research on the dust storms in North America. The relevance of dust storms to public health is likely to increase as extreme weather events are predicted to become more frequent with anticipated changes in climate through the 21st century. Objectives: We examined the association between dust storms and county-level non-accidental mortality in the United States from 1993 through 2005. Methods: Dust storm incidence data, including date and approximate location, are taken from the U.S. National Weather Service storm database. County-level mortality data for the years 1993–2005 were acquired from the National Center for Health Statistics. Distributed lag conditional logistic regression models under a time-stratified case-crossover design were used to study the relationship between dust storms and daily mortality counts over the whole United States and in Arizona and California specifically. End points included total non-accidental mortality and three mortality subgroups (cardiovascular, respiratory, and other non-accidental). Results: We estimated that for the United States as a whole, total non-accidental mortality increased by 7.4% (95% CI: 1.6, 13.5; p = 0.011) and 6.7% (95% CI: 1.1, 12.6; p = 0.018) at 2- and 3-day lags, respectively, and by an average of 2.7% (95% CI: 0.4, 5.1; p = 0.023) over lags 0–5 compared with referent days. Significant associations with non-accidental mortality were estimated for California (lag 2 and 0–5 day) and Arizona (lag 3), for cardiovascular mortality in the United States (lag 2) and Arizona (lag 3), and for other non-accidental mortality in California (lags 1–3 and 0–5). Conclusions: Dust storms are associated with increases in lagged non-accidental and cardiovascular mortality. Citation: Crooks JL, Cascio WE, Percy MS, Reyes J, Neas LM, Hilborn ED. 2016. The association between dust storms and daily non-accidental mortality in the United States, 1993–2005. Environ Health Perspect 124:1735–1743; http://dx.doi.org/10.1289/EHP216

Air pollution is a major risk factor for cardiovascular disease, of which ozone is a major contributor. Several studies have found associations between ozone and cardiovascular morbidity, but the results have been inconclusive. We investigated associations between ozone and changes across biological pathways associated with cardiovascular disease. Using a panel study design, 13 participants with coronary artery disease were assessed for markers of systemic inflammation, heart rate variability and repolarization, lipids, blood pressure, and endothelial function. Daily measurements of ozone and particulate matter (PM2.5) were obtained from central monitoring stations. Single (ozone) and two-pollutant (ozone and PM2.5) models were used to assess percent changes in measurements per interquartile ranges of pollutants. Per interquartile increase in ozone, changes in tissue plasminogen factor (6.6%, 95% confidence intervals (CI) = 0.4, 13.2), plasminogen activator inhibitor-1 (40.5%, 95% CI = 8.7, 81.6), neutrophils (8.7% 95% CI = 1.5, 16.4), monocytes (10.2%, 95% CI = 1.0, 20.1), interleukin-6 (15.9%, 95% CI = 3.6, 29.6), large-artery elasticity index (−19.5%, 95% CI = −34.0, −1.7), and the baseline diameter of the brachial artery (−2.5%, 95% CI = −5.0, 0.1) were observed. These associations were robust in the two-pollutant model. We observed alterations across several pathways associated with cardiovascular disease in 13 coronary artery disease patients following ozone exposures, independent of PM2.5. The results support the biological plausibility of ozone-induced cardiovascular effects. The effects were found at concentrations below the EPA National Ambient Air Quality Standards for both ozone and PM2.5.

Purpose: Immune-related cutaneous adverse events (ircAE) occur in ≥50% of patients treated with checkpoint inhibitors, but the underlying mechanisms for ircAEs are poorly understood. Experimental Design: Phenotyping/biomarker analyses were conducted in 200 patients on checkpoint inhibitors [139 with ircAEs and 61 without (control group)] to characterize their clinical presentation and immunologic endotypes. Cytokines were evaluated in skin biopsies, skin tape strip extracts, and plasma using real-time PCR and Meso Scale Discovery multiplex cytokine assays. Results: Eight ircAE phenotypes were identified: pruritus (26%), maculopapular rash (MPR; 21%), eczema (19%), lichenoid (11%), urticaria (8%), psoriasiform (6%), vitiligo (5%), and bullous dermatitis (4%). All phenotypes showed skin lymphocyte and eosinophil infiltrates. Skin biopsy PCR revealed the highest increase in IFNγ mRNA in patients with lichenoid (P < 0.0001) and psoriasiform dermatitis (P < 0.01) as compared with patients without ircAEs, whereas the highest IL13 mRNA levels were detected in patients with eczema (P < 0.0001, compared with control). IL17A mRNA was selectively increased in psoriasiform (P < 0.001), lichenoid (P < 0.0001), bullous dermatitis (P < 0.05), and MPR (P < 0.001) compared with control. Distinct cytokine profiles were confirmed in skin tape strip and plasma. Analysis determined increased skin/plasma IL4 cytokine in pruritus, skin IL13 in eczema, plasma IL5 and IL31 in eczema and urticaria, and mixed-cytokine pathways in MPR. Broad inhibition via corticosteroids or type 2 cytokine–targeted inhibition resulted in clinical benefit in these ircAEs. In contrast, significant skin upregulation of type 1/type 17 pathways was found in psoriasiform, lichenoid, bullous dermatitis, and type 1 activation in vitiligo. Conclusions: Distinct immunologic ircAE endotypes suggest actionable targets for precision medicine-based interventions.

Wildfires are a growing threat in the United States. At a population level, exposure to ambient wildfire smoke is known to be associated with severe asthma outcomes such as hospitalizations. However, little work has been done on subacute clinical asthma outcomes, especially in sensitive populations. This study retrospectively investigated associations between ambient wildfire smoke exposure and measures of lung function and asthma control, Forced Expiratory Volume in 1 Second (FEV1) and the Asthma Control Test (ACT) and Children's Asthma Control Test (CACT) test scores, during nonurgent clinic visits. The study population consisted of pediatric asthma patients (ages 4–21;n = 1,404 for FEV1 andn = 395 for ACT/CACT) at National Jewish Health, a respiratory referral hospital in Denver, Colorado, and therefore represents a more severe asthma phenotype than the general pediatric asthma population. Wildfire smoke‐related PM_2.5at patients' residential ZIP codes was characterized using satellite‐derived smoke polygons from NOAA's Hazard Mapping System combined with kriging of ground‐based U.S. EPA monitors. Mixed effect models were used to estimate associations between clinical outcomes and smoke PM_2.5exposure, controlling for known risk factors and confounders. Among older children aged 12–21 we found that wildfire PM_2.5was associated with lower FEV1 the next day but higher FEV1 the day after. We found no associations between wildfire PM_2.5and FEV1 in younger children or between wildfire PM_2.5and asthma control measured by the ACT/CACT in all ages. We speculate that rescue medication usage by older children may decrease respiratory symptoms caused by wildfire smoke.