Rationale: Fine particulate matter air pollution of 2.5 μm or less in diameter (PM2.5) has been associated with an increased risk of respiratory disease, but assessments of specific respiratory infections in adults are lacking. Objectives: To estimate the rate of respiratory infection healthcare encounters in adults associated with acute increases in PM2.5 concentrations. Methods: Using case–crossover methods, we studied 498,118 adult New York State residents with a primary diagnosis of influenza, bacterial pneumonia, or culture-negative pneumonia upon hospitalization or emergency department (ED) visit (2005–2016). We estimated the relative rate of healthcare encounters associated with increases in PM2.5 in the previous 1–7 days and explored differences before (2005–2007), during (2008–2013), and after (2014–2016) implementation of air quality policies and economic changes. Results: Interquartile range increases in PM2.5 over the previous 7 days were associated with increased excess rates (ERs) of culture-negative pneumonia hospitalizations (2.5%; 95% confidence interval [CI], 1.7–3.2%) and ED visits (2.5%; 95% CI, 1.4–3.6%), and increased ERs of influenza ED visits (3.9%; 95% CI, 2.1–5.6%). Bacterial pneumonia hospitalizations, but not ED visits, were associated with increases in PM2.5 and, though imprecise, were of a similar magnitude to culture-negative pneumonia (Lag Day 6 ER, 2.3%; 95% CI, 0.3–4.3). Increased relative rates of influenza ED visits and culture-negative pneumonia hospitalizations were generally larger in the “after” period (P < 0.025 for both outcomes), compared with the “during” period, despite reductions in overall PM2.5 concentrations. Conclusions: Increased rates of culture-negative pneumonia and influenza were associated with increased PM2.5 concentrations during the previous week, which persisted despite reductions in PM2.5 from air quality policies and economic changes. Though unexplained, this temporal variation may reflect altered toxicity of different PM2.5 mixtures or increased pathogen virulence.

Previous studies reported triggering of acute cardiovascular events by short-term increasedPM2.5 concentrations. From 2007 to 2013, national and New York state air quality policies and economic influences resulted in reduced concentrations of PM2.5 and other pollutants across the state. We estimated the rate of cardiovascular hospital admissions associated with increased PM2.5 concentrations in the previous 1-7 days, and evaluated whether they differed before (2005-2007), during (2008-2013), and after these concentration changes (2014-2016). Using the Statewide Planning and Research Cooperative System (SPARCS) database, we retained all hospital admissions with a primary diagnosis of nine cardiovascular disease (CVD) subtypes, for residents living within 15 miles of PM2.5 monitoring sites in Buffalo, Rochester, Albany, Queens, Bronx, and Manhattan from 2005 to 2016 (N = 1,922,918). We used a case-crossover design and conditional logistic regression to estimate the admission rate for total CVD, and nine specific subtypes, associated with increased PM2.5 concentrations. Interquartile range (IQR) increases in PM2.5 on the same and previous 6 days were associated with 0.6%-1.2% increases in CVD admission rate (2005-2016). There were similar patterns for cardiac arrhythmia, ischemic stroke, congestive heart failure, ischemic heart disease (IHD), and myocardial infarction (MI). Ambient PM2.5 concentrations and annual total CVD admission rates decreased across the period. However, the excess rate of IHD admissions associated with each IQR increase in PM2.5 in previous 2 days was larger in the after period (2.8%; 95%CI = 1.5%-4.0%) than in the during (0.6%; 95%CI = 0.0%-1.2%) or before periods (0.8%; 95%CI = 0.2%-1.3%), with similar patterns for total CVD and MI, but not other subtypes. While pollutant concentrations and CVD admission rates decreased after emission changes, the same PM2.5 mass was associated with a higher rate of ischemic heart disease events. Future work should confirm these findings in another population, and investigate whether specific PM components and/or sources trigger IHD events.

Previous work reported increased rates of acute cardiovascular hospitalizations associated with increased PM2.5 concentrations in the previous few days across urban centers in New York State from 2005 to 2016. These relative rates were higher after air quality policies and economic changes resulted in decreased PM2.5 concentrations and changes in PM composition (e.g. increased secondary organic carbon), compared to before and during these changes. Changes in PM composition and sources may explain this difference. To estimate the rate of acute cardiovascular hospitalizations associated with increases in source specific PM2.5 concentrations. Using source apportioned PM2.5 concentrations at the same NYS urban sites, a time-stratified case-crossover design, and conditional logistic regression models adjusting for ambient temperature and relative humidity, we estimated the rate of these acute cardiovascular hospitalizations associated with increases in mean source specific PM2.5 concentrations in the previous 1, 4, and 7 days. Interquartile range (IQR) increases in spark-ignition emissions (GAS) concentrations were associated with increased excess rates of cardiac arrhythmia hospitalizations (2.3%; 95% CI = 0.4%, 4.2%; IQR = 2.56 μg/m3) and ischemic stroke hospitalizations (3.7%; 95% CI = 1.1%, 6.4%; 2. 73 μg/m3) over the next day. IQR increases in diesel (DIE) concentrations were associated with increased rates of congestive heart failure hospitalizations (0.7%; 95% CI = 0.2% 1.3%; 0.51 μg/m3) and ischemic heart disease hospitalizations (0.8%; 95% CI = 0.3%, 1.3%; 0.60 μg/m3) over the next day, as hypothesized. However, secondary sulfate PM2.5 (SS) was not. Increased acute cardiovascular hospitalization rates were also associated with IQR increases in concentrations of road dust (RD), residual oil (RO), and secondary nitrate (SN) over the previous 1, 4, and 7 days, but not other sources. These findings suggest a role of several sources of PM2.5 in New York State (i.e. traffic emissions, non-traffic emissions such as brake and tire wear, residual oil, and nitrate that may also reflect traffic emissions) in the triggering of acute cardiovascular events.

Prior studies reported that exposure to increased concentrations of fine particulate matter (PM2.5) were associated with increased rates of hospitalization and emergency department (ED) visits for asthma and chronic obstructive pulmonary disease (COPD). In this study, rates were examined from 2005 to 2016 using a case-crossover design to ascertain if there have been changes in the rates per unit mass exposure given substantial reductions in PM2.5 concentration and changes in its composition. PM2.5 concentrations were reduced through a combination of policies designed to improve air quality and economic drivers, including the 2008 economic recession and shifts in the relative costs of coal and natural gas. The study period was split into three periods reflecting that much of the emissions changes occurred between 2008 and 2013. Thus, the three periods were defined as: BEFORE (2005 to 2007), DURING (2008-2013), and AFTER (2014-2016). In general, the number of hospitalizations and ED visits declined with the decreased concentration of PM2.5. However, the rate of COPD hospitalizations and asthma ED visits associated with each interquartile range increase in ambient PM2.5 concentration was larger in the AFTER period than the DURING and BEFORE periods. For example, each 6.8 μg/m3 increase in PM2.5 on the same day was associated with 0.4% (0.0%, 0.8%), 0.3% (-0.2%, 0.7%), and 2.7% (1.9%, 3.5) increases in the rate of asthma emergency department visits in the BEFORE, DURING, and AFTER periods, respectively, suggesting the same mass concentration of PM2.5 was more toxic in the AFTER period.

Background: More intense and longer‐lasting heat events are expected in the United States as a consequence of climate change. This study aimed to project the potential changes in maternal heat exposure during early pregnancy (3–8 weeks post conception) and the associated burden of congenital heart defects ( CHD s) in the future. Methods and Results: This study expanded on a prior nationwide case‐control study that evaluated the association between CHD s and maternal heat exposure during early pregnancy in summer and spring. We defined multiple indicators of heat exposure, and applied published odds ratios obtained for the matching season of the baseline (1995–2005) into the projection period (2025–2035) to estimate potential changes in CHD burden throughout the United States. Increases in maternal heat exposure were projected across the United States and to be larger in the summer. The Midwest will potentially have the highest increase in summer maternal exposure to excessively hot days (3.42; 95% CI, 2.99–3.88 per pregnancy), heat event frequency (0.52; 95% CI, 0.44–0.60) and heat event duration (1.73; 95% CI, 1.49–1.97). We also found large increases in specific CHD subtypes during spring, including a 34.0% (95% CI, 4.9%–70.8%) increase in conotruncal CHD in the South and a 38.6% (95% CI , 9.9%–75.1%) increase in atrial septal defect in the Northeast. Conclusions: Projected increases in maternal heat exposure could result in an increased CHD burden in certain seasons and regions of the United States.