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.

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.

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.

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.

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.

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.

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.

Living in walkable neighborhoods has been reported to be associated with a lower risk of cardiovascular disease. Features of walkable neighborhoods, however, may be related to particulate matter with an aerodynamic diameter ≤2.5 μm (PM₂.₅), which could increase risk of cardiovascular disease. The interaction effect between walkability and PM₂.₅ on risk of ischemic stroke remains to be elucidated. In this study, we recruited a total of 27,375 participants aged ≥40 years from Yinzhou District, Ningbo, Zhejiang Province, China to investigate the associations of walkability and PM₂.₅ with risk of ischemic stroke. We used amenity categories and decay functions to evaluate walkability and high-spatiotemporal-resolution land-use regression models to assess PM₂.₅ concentrations. We used Cox proportional hazards regression models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). During a median follow-up of 4.08 years, we identified a total of 637 incident cases of ischemic stroke in the entire cohort. Higher walkability was associated with a lower risk of ischemic stroke (quartile, Q4 vs. Q1 walkability: HR = 0.59, 95% CI: 0.47–0.75), whereas PM₂.₅ was positively associated with risk of ischemic stroke (Q4 vs. Q1 PM₂.₅: HR = 1.70, 95% CI: 1.29–2.25). Furthermore, we observed a significant interaction between walkability and PM₂.₅ on risk of ischemic stroke. Walkability was inversely associated with risk of ischemic stroke at lower PM₂.₅ concentrations, but this association was attenuated with increasing PM₂.₅ concentrations. Although walkable neighborhoods appear to decrease the risk of ischemic stroke, benefits may be offset by adverse effects of PM₂.₅ exposure in the most polluted areas. These findings are meaningful for future neighborhood design, air pollution control, and stroke prevention.

Only a few prospective studies have investigated the relationship between solid fuel use and cardiovascular disease (CVD) and mortality, and they have reported inconsistent conclusions. This study aimed to investigate the effect of solid fuel heating on the risk of CVD events and all-cause mortality among non-smokers. Data of this sub-study were obtained from the China Hypertension Survey (CHS), and 13,528 non-smoking participants aged 35 or above without self-reported medical history of CVD were enrolled between October 2012 and December 2015. CVD events and all-cause mortality were followed up in 2018 and 2019. The type of primary heating fuel was categorized as clean fuel (natural gas and electricity) and solid fuel (coal, wood, and straw). Cox regression was applied to evaluate the relationship between solid fuel use and CVD events and all-cause mortality. Of the 13,528 non-smoking participants, the mean age was 55.4 ± 13.1 years. During the median follow-up of 4.93 years, 424 participants developed fatal or nonfatal CVD (stroke, 273; coronary heart disease, 119; and other cardiovascular events, 32) and 288 died from all causes. The cumulative incidence of fatal and nonfatal CVD and all-cause mortality were 6.78 and 4.62 per 1000 person-years, respectively. Solid fuel heating was independently associated with an increased risk of fatal or nonfatal stroke and all-cause mortality compared with the use of clean fuels, the fully adjusted hazard ratios (HRs), and 95% confidence intervals (CI) were 1.44 (1.00–2.08) and 1.55 (1.10–2.17), respectively. The relationship between solid fuel heating and fatal and nonfatal CVD events was non-significant (HR = 1.19; 95% CI: 0.89–1.59). Solid fuel heating is longitudinally associated with a higher risk of stroke and all-cause mortality in non-smoking Chinese. Switching to cleaner energy sources for heating may be important for reducing the risk of CVD and mortality.

We aimed to update the evidence-base of long-term noise exposures from road, rail, and aircraft traffic on both non-accidental and cardiovascular mortality.A systematic review and meta-analysis were conducted following PRISMA guidelines. The literature was searched using PubMed, Scopus, Web of Science, and EMBASE for the period between January 01, 2000 and October 05, 2020. 13 studies were selected for final review. The risk of bias and overall quality of evidence was evaluated using a pre-defined list of criteria. Risk estimates from each study were converted into per 10 dB higher of Ldₑₙ for each traffic source. Inverse-Variance heterogeneity (I-Vhet) meta-analysis was used to pool these individual risk estimates, along with assessment of heterogeneity and publication bias. Sensitivity analyses include using random-effect model and leave-one-out meta-analysis. Subgroup analyses by study design and noise exposure assessment were conducted to explore potential sources of heterogeneity.For road traffic, the pooled relative risk (RR) per 10 dB higher Ldₑₙ for mortality from non-accidental causes was 1.01 (95% CI: 0.98, 1.05) (5 studies, I² = 78%), CVD was 1.01 (95% CI: 0.98, 1.05) (5 studies, I² = 41%), ischemic heart disease (IHD) was 1.03 (95% CI: 0.99, 1.08) (7 studies, I² = 46%), and stroke was 1.05 (95% CI: 0.97, 1.14) (5 studies, I² = 62%). The overall quality of evidence for most meta-analyses was rated as very low to low, except for CVD or IHD mortality, for which the quality of evidence was rated as moderate. A possible threshold of 53 dB was visually suggested for CVD-related mortality from road traffic noise in the trend analysis. For aircraft noise, pooled estimates were based on fewer studies and varied by mortality outcomes.Evidence of long-term exposure to traffic noise on mortality remains weak except the association between road traffic noise and IHD mortality. High-quality longitudinal studies are required to better characterise mortality effects of traffic noise.