While the health impacts of larger particulate matter, such as PM₁₀ and PM₂.₅, have been studied extensively, research regarding ultrafine particles (UFPs or PM₀.₁) and particle surface area concentration (PSC) is lacking. This case-crossover study assessed the associations between exposure to PSC and UFP number concentration (UFPnc) and hospital admissions for cardiovascular diseases (CVDs) in New York State (NYS), 2013–2018. We used a time-stratified case-crossover design to compare the PSC and UFPnc levels between hospitalization days and control days (similar days without admissions) for each CVD case. We utilized NYS hospital discharge data to identify all CVD cases who resided in NYS. UFP simulation data from GEOS-Chem-APM, a state-of-the-art chemical transport model, was used to define PSC and UFPnc. Using a multi-pollutant model and conditional logistic regression, we assessed excess risk (ER)% per inter-quartile change of PSC and UFPnc after controlling for meteorological factors, co-pollutants, and time-varying variables. We found immediate and lasting associations between PSC and overall CVDs (lag0–lag0-6: ERs% (95% CI%) ranges: 0.4 (0.1,0.7) - 0.9 (0.7–1.2), and delayed and prolonged ERs%: 0.1–0.3 (95% CIs: 0.1–0.5) between UFPnc and CVDs (lag0-3–lag0-6). Exposure to larger PSC was associated with immediate ER increases in stroke, hypertension, and ischemic heart diseases (1.1%, 0.7%, 0.8%, respectively, all p < 0.05). The adverse effects of PSC on CVDs were highest among children (5–17 years old), in the fall and winter, and during cold temperatures. In conclusion, we found an immediate, lasting effects of PSC on overall CVDs and a delayed, prolonged impact of UFPnc. PSC was a more sensitive indicator than UFPnc. The PSC effects were higher among certain CVD subtypes, in children, in certain seasons, and during cold days. Further studies are needed to validate our findings and evaluate the long-term effects.

Responses to COVID-19 altered environmental exposures and health behaviours associated with non-communicable diseases. We aimed to (1) quantify changes in nitrogen dioxide (NO₂), noise, physical activity, and greenspace visits associated with COVID-19 policies in the spring of 2020 in Barcelona (Spain), Vienna (Austria), and Stockholm (Sweden), and (2) estimated the number of additional and prevented diagnoses of myocardial infarction (MI), stroke, depression, and anxiety based on these changes. We calculated differences in NO₂, noise, physical activity, and greenspace visits between pre-pandemic (baseline) and pandemic (counterfactual) levels. With two counterfactual scenarios, we distinguished between Acute Period (March 15th – April 26th, 2020) and Deconfinement Period (May 2nd – June 30th, 2020) assuming counterfactual scenarios were extended for 12 months. Relative risks for each exposure difference were estimated with exposure-risk functions. In the Acute Period, reductions in NO₂ (range of change from −16.9 μg/m³ to −1.1 μg/m³), noise (from −5 dB(A) to −2 dB(A)), physical activity (from −659 MET*min/wk to −183 MET*min/wk) and greenspace visits (from −20.2 h/m to 1.1 h/m) were largest in Barcelona and smallest in Stockholm. In the Deconfinement Period, NO₂ (from −13.9 μg/m³ to −3.1 μg/m³), noise (from −3 dB(A) to −1 dB(A)), and physical activity levels (from −524 MET*min/wk to −83 MET*min/wk) remained below pre-pandemic levels in all cities. Greatest impacts were caused by physical activity reductions. If physical activity levels in Barcelona remained at Acute Period levels, increases in annual diagnoses for MI (mean: 572 (95% CI: 224, 943)), stroke (585 (6, 1156)), depression (7903 (5202, 10,936)), and anxiety (16,677 (926, 27,002)) would be anticipated. To decrease cardiovascular and mental health impacts, reductions in NO₂ and noise from the first COVID-19 surge should be sustained, but without reducing physical activity. Focusing on cities’ connectivity that promotes active transportation and reduces motor vehicle use assists in achieving this goal.

This study aims to examine the association between short-term exposures to PM₁, PM₂.₅ and PM₁₀ (particulate matter with aerodynamic diameters ≤1 μm, ≤2.5 μm and ≤10 μm, respectively) and hospital admission for ischemic stroke in China. Daily counts of hospital admission for ischemic stroke were collected in 5 hospitals in China during November 2013 to October 2015. Daily concentrations of PM₁, PM₂.₅ and PM₁₀ were collected in 5 cities where the hospitals were located. A time-stratified case-crossover design was used to examine the hospital-specific PM-ischemic stroke association after controlling for potential confounders. Then the effect estimates were pooled using a random-effect meta-analysis. A total of 68,122 hospital admissions for ischemic stroke were identified from 5 hospitals during the study period. The pooled results showed that exposures to PM₁, PM₂.₅ and PM₁₀ were significantly associated with increased hospital admission for ischemic stroke on the current day and previous 1 day. The RRs (relative risk associated with per 10 μg/m³ increase in each pollutant) and 95%CIs (confidence intervals) for the cumulative effects of PM₁, PM₂.₅ and PM₁₀ on ischemic stroke during lag 0–1 days were 1.014 (1.005, 1.0023), 1.007 (1.000, 1.014) and 1.005 (1.001, 1.009), respectively. In total, 3.5%, 3.6% and 4.1% of hospital admissions for ischemic stroke could be attributable to PM₁, PM₂.₅ and PM₁₀, respectively. Exposures to ambient PM₁, PM₂.₅ and PM₁₀ pollution showed acute adverse effects on hospital admission for ischemic stroke. The health effects of PM₁ should be considered by policy-makers.

Short-term exposure to air pollution has pro-thrombotic effects and triggers thrombo-embolic events such as myocardial infarction or stroke in adults. This study evaluates the association between short-term variation in air pollution and treatments for acute thrombo-embolic events among the whole Belgian population. In a bidirectional time-stratified case-crossover design, we included 227,861 events treated with endovascular intervention and 74,942 with antithrombotic enzymes that were reimbursed by the Belgian Social Security between January 1st, 2009 and December 31st, 2013. We compared the concentrations of particulate matter (PM) air pollution (PM₁₀ and PM₂.₅), as estimated at the municipality level on the day of the event (lag 0) and two days earlier (lag 1 and lag 2) with those of control days from the same month, matched by temperature and accounting for day of the week (weekend vs week days). We applied conditional logistic regression models to obtain odds ratios (OR) and their 95% CI for an increase of 10 μg/m³ (PM₁₀) or 5 μg/m³ (PM₂.₅) in pollutant concentrations over three lag days (lag 0, 1 and 2). We observed significant associations of PM₁₀ and PM₂.₅ with treatment of acute thrombo-embolic events at the three lags. The strongest associations were observed for air pollution concentrations on the day of the event (lag0). Increases of 10 μg/m³ PM₁₀ and 5 μg/m³ PM₂.₅ on lag0 increased the odds of events treated with endovascular intervention by 2.7% (95%CI:2.3%–3.2%) and 1.3% (95%CI:1%–1.5%), respectively, and they increased the odds of events treated with antithrombotic enzymes by 1.9% (95%CI:1.1–2.7%) and 1.2% (95%CI:0.7%–1.6%), respectively. The associations were generally stronger during autumn months and among children. Our nationwide study confirms that acute exposure to outdoor air pollutants such as PM₁₀ or PM₂.₅ increase the use of medication and interventions to treat thrombo-embolic events.

Knowledge of environmental risk factors for stroke and their role are limited. We performed a case-cohort study to evaluate the association between serum persistent organic pollutants (POPs) level and stroke risk.526 subcohort members and 111 stroke incidence cases were identified from the Korean Cancer Prevention Study-II. Serum levels of POPs were measured using gas chromatography/high-resolution mass spectrometry. The hazard ratios (HRs) for stroke (ischemic, hemorrhagic, and all stroke types) were estimated using the weighted Cox regression model. Age, sex, body mass index, smoking status, physical activity, family history of cardiovascular disease, and hypertension were adjusted in the weighted Cox regression model.After adjusting for potential confounding factors, increased risk for stroke was observed among participants with serum concentration of p,p'-DDE in the highest tertile compared to those in the lowest tertile (HR = 4.10, 95% CI: 1.58, 10.59). A similar association was estimated for PCB118 (HR = 2.33, 95% CI: 1.04, 5.22), PCB156 (HR = 3.42, 95% CI: 1.42, 8.23), and PCB138 (HR = 3.80, 95% CI: 1.48, 9.76). For TEQ, stroke was three times as likely to occur among subjects with TEQ in the highest tertile compared to those in the lowest tertile (HR = 3.12, 95% CI: 1.27, 7.65). PCBs were positively associated with ischemic stroke, but not with hemorrhagic stroke.Elevated serum POPs levels were associated with an increased risk of stroke, especially ischemic stroke.

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.

There is growing interest in the association between ambient air pollution and stroke, but few studies have investigated the association in developing countries. The primary objective of this study was to examine the association between levels of ambient air pollutants and hospital admission for stroke in China. A time-stratified case-crossover analysis was conducted between 2014 and 2015 in 14 large Chinese cities among 200,958 ischemic stroke and 41,746 hemorrhagic stroke hospitalizations. We used conditional logistic regression to estimate the percentage changes in stroke admissions in relation to interquartile range increases in air pollutants. Air pollution was positively associated with ischemic stroke. A difference of an interquartile range of the 6-day average for particulate matter less than 10 μm in aerodynamic diameter, sulfur dioxide, nitrogen dioxide, carbon monoxide, and ozone corresponded to 0.7% (95% CI: 0%, 1.4%), 1.6% (95% CI: 1.0%, 2.3%), 2.6% (95% CI: 1.8%, 3.5%), 0.5% (95% CI: −0.2%, 1.1%), and 1.3% (95% CI: 0.3%, 2.3%) increases in ischemic stroke admissions, respectively. For hemorrhagic stroke, we observed the only significant association in relation to nitrogen dioxide on the current day (percentage change: 1.6%; 95% CI: 0.3%, 2.9%). Our findings contribute to the limited scientific literature concerning the effect of ambient air pollution on stroke in developing countries. Our findings may have significant public health implications for primary prevention of stroke in China.

In the past decade, particulate matter with aerodynamic diameter less than 2.5 μm (PM₂.₅) has reached unprecedented levels in China and posed a significant threat to public health. Exploring the long-term trajectory of the PM₂.₅ attributable health burden and corresponding disparities across populations in China yields insights for policymakers regarding the effectiveness of efforts to reduce air pollution exposure. Therefore, we examine how the magnitude and equity of the PM₂.₅-related public health burden has changed nationally, and between provinces, as economic growth and pollution levels varied during 2005–2017. We derive long-term PM₂.₅ exposures in China from satellite-based observations and chemical transport models, and estimate attributable premature mortality using the Global Exposure Mortality Model (GEMM). We characterize national and interprovincial inequality in health outcomes using environmental Lorenz curves and Gini coefficients over the study period. PM₂.₅ exposure is linked to 1.8 (95% CI: 1.6, 2.0) million premature deaths over China in 2017, increasing by 31% from 2005. Approximately 70% of PM₂.₅ attributable deaths were caused by stroke and IHD (ischemic heart disease), though COPD (chronic obstructive pulmonary disease) and LRI (lower respiratory infection) disproportionately affected poorer provinces. While most economic gains and PM₂.₅-related deaths were concentrated in a few provinces, both gains and deaths became more equitably distributed across provinces over time. As a nation, however, trends toward equality were more recent and less clear cut across causes of death. The rise in premature mortality is due primarily to population growth and baseline risks of stroke and IHD. This rising health burden could be alleviated through policies to prevent pollution, exposure, and disease. More targeted programs may be warranted for poorer provinces with a disproportionate share of PM₂.₅-related premature deaths due to COPD and LRI.

Several studies have reported associations between exposure to particulate matter and incidence of out-of-hospital cardiac arrest (OHCA) and some have observed associations with ozone (O3). There are no studies investigating susceptibility based on previous disease history to short-term O3 exposure and the risk of OHCA.To investigate the role of previous cardiovascular-related hospitalizations in modifying the associations between the risk of OHCA and short-term increase in O3 concentrations.A time-stratified case-crossover analysis of 11,923 OHCA registered in the Swedish Register for Cardiopulmonary Resuscitation from 2006 to 2014 was performed. Using personal identification numbers, OHCA were linked to all previous hospitalizations in Sweden since 1987 to create susceptible groups based on the principal diagnosis code at discharge. Susceptibility was based on hospitalization for i) acute myocardial infarction; ii) heart failure; iii) arrhythmias; iv) diabetes; v) hypertension; and vi) stroke. Moving 2 and 24-h averages for O3, PM2.5, PM10, and NO2 were constructed from hourly averages.A 10 μg/m3 higher 2-h average O3 concentration was associated with a 2% higher risk of OHCA (95% CI, 0% 3%). Associations were similar for 24-h average O3 and in individuals with or without hospitalizations for AMI, heart failure, diabetes, hypertension or stroke. Individuals with previous hospitalizations for arrhythmias had a lower risk of OHCA with higher O3. No associations were observed for other pollutants.Short-term exposure to O3 was associated with an elevated risk of OHCA, however, previous hospitalizations for cardiovascular diseases were not associated with additionally augmented risks.

The estimation of PM₂.₅-related mortality is becoming increasingly important. The accuracy of results is largely dependent on the selection of methods for PM₂.₅ exposure assessment and Concentration-Response (C-R) function. In this study, PM₂.₅ observed data from the China National Environmental Monitoring Center, satellite-derived estimation, widely collected geographic and socioeconomic information variables were applied to develop a national satellite-based Land Use Regression model and evaluate PM₂.₅ exposure concentrations within 2013–2015 with the resolution of 1 km × 1 km. Population weighted concentration declined from 72.52 μg/m³ in 2013 to 57.18 μg/m³ in 2015. C-R function is another important section of health effect assessment, but most previous studies used the Integrated Exposure Regression (IER) function which may currently underestimate the excess relative risk of exceeding the exposure range in China. A new Shape Constrained Health Impact Function (SCHIF) method, which was developed from a national cohort of 189,793 Chinese men, was adopted to estimate the PM₂.₅-related premature deaths in China. Results showed that 2.19 million (2013), 1.94 million (2014), 1.65 million (2015) premature deaths were attributed to PM₂.₅ long-term exposure, different from previous understanding around 1.1–1.7 million. The top three provinces of the highest premature deaths were Henan, Shandong, Sichuan, while the least ones were Tibet, Hainan, Qinghai. The proportions of premature deaths caused by specific diseases were 53.2% for stroke, 20.5% for ischemic heart disease, 16.8% for chronic obstructive pulmonary disease and 9.5% for lung cancer. IER function was also used to calculate PM₂.₅-related premature deaths with the same exposed level used in SCHIF method, and the comparison of results indicated that IER had made a much lower estimation with less annual amounts around 0.15–0.5 million premature deaths within 2013–2015.