Exposure to green space has been proposed to be beneficially associated with cardiovascular morbidity and mortality. Many studies have explored this topic, but the results remain conflicting. We aimed to evaluate the epidemiological evidence on this topic by performing a systematic review with meta-analysis. We searched PubMed, Web of Science and Embase for studies on the association between green space and cardiovascular disease (CVD) that were published till January 2022. Two authors independently performed study selection, data extraction, quality assessment, and risk of bias assessment. For studies providing detailed numeric data, we also conducted quantitative meta-analyses and calculated the pooled odd ratios (ORs) for associations between the most commonly used exposure estimate (normalized difference vegetative index [NDVI]) and five CVD events: CVD mortality, ischemic heart disease (IHD) mortality, cerebrovascular disease (CBVD) mortality, and stroke incidence/prevalence. Additional analyses were conducted to explore the geographical scale effects of NDVI. Publication bias tests were also conducted. Of the 6787 records identified, 53 studies were eligible for inclusion. These studies covered 18 countries and included data from more than 100 million persons. Meta-analyses showed that a 0.1 increase in NDVI was significantly associated with 2–3% lower odds of CVD mortality (OR: 0.97, 95% CI: 0.96–0.99), IHD mortality (OR: 0.98, 95% CI: 0.96–1.00), CBVD mortality (OR: 0.98, 95% CI: 0.97–1.00), and stroke incidence/prevalence (OR: 0.98, 95% CI: 0.96–0.99). There was no significant difference between the pooled estimates for different buffer sizes. No evidence of publication bias was detected. We provide strong and robust evidence for the beneficial effects of green space exposure on cardiovascular health. More prospective studies and mechanistic studies, especially that conducted in low- and middle-income countries, are merited to strengthen our conclusions.

Public health is threatened by air pollution and high temperature, especially in urban areas and areas impacted by climate change. Well-designed urban forms have co-benefits on promoting human health and mediating atmospheric environment-related threats (e.g., high temperature and air pollution). Previous studies overlooked these mediating effects of urban form on suicide mortality. This study used partial least squares modeling and countywide data in Taiwan to identify the crucial influences and pathways of urban environment, socioeconomic status, and diseases on suicide mortality. The model considered the impact of the characteristics of urban form (i.e., urban development intensity, land mix, and urban sprawl), urban industrial status (i.e., industrial level), urban greening (i.e., green coverage), disease (i.e., important diseases morbidity of human immunodeficiency virus [HIV], cerebrovascular disease [CVD], chronic liver disease and cirrhosis [CLDC], nephritis, nephrotic syndrome and nephrosis [NNSN], malignant tumor [MT]), socioeconomic status (i.e., income level and aging population rate), and the atmospheric environment (i.e., air pollution and high temperature) on suicide mortality. Optimizing land mix and minimizing urban development intensity and urban sprawl have been found to reduce suicide mortality. The mediating effect of urban form on suicide mortality originated from air pollution and high temperature, and mediating air pollution was greater than high temperature. Furthermore, industrial level, important diseases (HIV, CVD, CLDC, NNSN, and MT) morbidity, an aging population rate, air pollution, and high temperature were associated with an increase in suicide mortality, whereas green coverage and income level were associated with a reduction in suicide rates. The findings demonstrate that appropriate urban policy and urban planning may lower suicide mortality, be useful strategies for suicide prevention, and be a foundation for building a healthy city. Moreover, this study provides clarity on the complex relationship of suicide and the urban environment while identifying crucial factors.

In China, PM₂.₅ pollution has caused extensive death and economic loss. Thus, an accurate assessment of the spatial distribution of these losses is crucial for delineating priority areas for air pollution control in China. In this study, we assessed the PM₂.₅ exposure-related health effects according to the integrated exposure risk function and non-linear power law (NLP) function in 338 prefecture-level cities in China by utilizing online monitoring data and the PM₂.₅ Hindcast Database (PHD). Our results revealed no significant difference between the monitoring data and PHD (p value = 0.66 > 0.05). The number of deaths caused by PM₂.₅-related Stroke (cerebrovascular disease), ischemic heart disease, chronic obstructive pulmonary disease, and lung cancer at the national level estimated through the NLP function was 0.27 million (95% CI: 0.06–0.50), 0.23 million (95% CI: 0.08–0.38), 0.31 million (95% CI: 0.04–0.57), and 0.31 million (95% CI: 0.16–0.40), respectively. The total economic cost at the national level in 2016 was approximately US$80.25 billion (95% CI: 24.46–132.25). Based on a comparison of Z statistics, we propose that the evaluation results obtained using the NLP function and monitoring data are accurate. Additionally, according to scenario simulations, Beijing, Chongqing, Tianjin, and other cities should be priority areas for PM₂.₅ pollution control to achieve considerable health benefits. Our statistics can help improve the accuracy of PM₂.₅-related health effect assessments in China.

Long-term exposure to air pollution has been associated with increased natural-cause mortality, but the evidence on diagnoses-specific mortality outcomes is limited. Few studies have examined the potential synergistic effects of exposure to pollutants and greenness. We investigated the association between exposure to air pollution and greenness with nervous system related mortality, cardiometabolic and chronic obstructive pulmonary diseases (COPD) mortality in Greece, using an ecological study design. We collected socioeconomic and mortality data for 1035 municipal units from the 2011 Census. Annual PM₂.₅, NO₂, BC and O₃ concentrations for 2010 were predicted at 100 × 100 m grids by hybrid land use regression models. The normalized difference vegetation index (NDVI) was used for greenness. We applied single and two-exposure Poisson regression models on standardized mortality rates accounting for spatial autocorrelation. We assessed interactions between pollutants and greenness. An interquartile range increase in PM₂.₅, NO₂ and BC was associated with increased risk in mortality from diseases of the nervous system (relative risk (RR): 1.14, 95% confidence interval (CI): 1.01, 1.28); 1.03 (95% CI: 0.99, 1.07); 1.05 (95% CI: 1.00, 1.10) respectively) and from cerebrovascular disease (RR: 1.14, 95% CI: 1.10, 1.18); 1.02 (95% CI: 1.01, 1.04); 1.02 (95% CI: 1.00, 1.04) respectively). PM₂.₅ was associated with ischemic heart disease mortality (RR: 1.05, 95% CI: 1.01, 1.10). We estimated inverse associations for all outcomes with O₃ and for mortality from diseases of the nervous system or COPD with greenness. Estimates were mostly robust to co-exposure adjustment. Interactions were identified between NDVI and O₃ or PM₂.₅ on mortality from the diseases of the nervous system, with higher effect estimates in greener areas.Our findings support the adverse effects of air pollution and the beneficial role of greenness on cardiovascular and nervous system related mortality. Further research is needed on diabetes mellitus.

Epidemiological evidence has shown a significant association between short-term exposure to air pollution and mortality risk for circulatory system diseases (CSD). However, informative insights on the significance and magnitude of its relationship in the process of government interventions on abating air pollution are still lacking, particularly in a burgeoning Chinese city. In this study, we conducted a time series study in Lishui District, Nanjing, to examine the effect of ambient particulate matter (PM), e.g., PM₂.₅ and PM₁₀, on daily death counts of CSD which included cardiovascular disease (CVD), cerebrovascular disease (CEVD), and arteriosclerotic heart disease (ASHD) mortality from January 1, 2015, to December 31, 2019. The results revealed that each 10 μg/m³ increase in PM₂.₅ and PM₁₀ concentration at lag0 day was associated with an increase of 1.33% (95% confidence interval, 0.08%, 2.60%) and 1.12% (0.43%, 1.82%) in CSD mortality; 2.42% (0.44%, 4.43%) and 1.43% (0.32%, 2.55%) in CVD mortality; 1.20% (− 0.31%, 2.73%) and 1.21% (0.38%, 2.05%) in CEVD mortality; and 2.78% (0.00%, 5.62%) and 1.66% (0.14%, 3.21%) in ASHD mortality, respectively. For cumulative risk, the corresponding increase in daily mortality for the same change in PM₂.₅ concentration at lag03 day was significantly associated with 1.94% (0.23%, 3.68%), 3.17% (0.58%, 5.84%), 2.38% (0.17%, 4.63%), and 4.92% (1.18%, 8.81%) for CSD, CVD, CEVD, and ASHD, respectively. The exposure–response curves were approximately nonlinear over the entire exposure range of the PM concentrations. We also analyzed the effect modifications by season (warm or cold), age group (0–64 years, 65–74 years, or ≥ 75 years), and sex (male or female). Although not statistically significant, stratified analysis showed greater vulnerability to PM exposure for cold season, population over 65 years of age, and female group.

Although it is biologically plausible, findings relating radon exposure to the risk of cerebrovascular disease (CeVD) are inconsistent and inconclusive. To investigate whether radon exposure was associated with the risk of CeVD, we qualitatively and quantitatively summarized the literature on radon and CeVD in both occupational and general populations. A search of PubMed, Embase, Scopus, and Web of Science was performed for peer-reviewed articles published through March 2022. Studies were excluded if radon exposure was not assessed separately from other ionizing radiation. In the meta-analysis, excess relative risks (ERRs) were converted to relative risks (RRs), and the pooled RRs and 95% confidence intervals (CIs) were determined using the random-effects model (DerSimonian and Laird). In the systematic review, nine eligible studies were summarized. Six occupational studies indicated inconsistent associations between cumulative radon exposure and CeVD mortality among mine workers. With available data from four updated occupational studies (99,730 mine workers and 2745 deaths), the pooled RR of radon exposure with CeVD mortality showed a non-significant association (1.10, 95% CI 0.92, 1.31). Three studies (841,270 individuals and 24,288 events) conducted in general populations consistently demonstrated a significant inverse relationship between residential radon exposure and risk of CeVD. The existing literature suggested a potential link between radon exposure and CeVD risk in general population. The inconsistent association in occupationally exposed populations may be explained by different methods of radon assessment and other methodological issues. Since radon exposure is a common public health issue, more rigorously designed epidemiologic studies, especially in the general population are warranted.

Considering the increasing rate of hospitalization due to the symptoms intensification, and the increasing trend of air pollution, this study aimed to determine the relationship between the amount of air pollutants and the incidence of cardiovascular disease leading to hospitalization. This case-crossover study was carried out on the data of admitted patients with cardiovascular disease such as hypertension, ischemic heart disease, and cerebrovascular disease in Urmia during 2011–2016. Weather data about air pollutants (NO2, PM10, SO2, and CO) were obtained from the meteorological department of Urmia. The data were coded for each patient and matched with the meteorological data for statistical modeling. The data were analyzed through STATA version 14. Conditional logistic regression was used to estimate the effects of air pollutants on cardiovascular disease adjusted to air temperature, relative humidity, and air pollutants. The final analysis was performed on 43,424 patients with cardiovascular disease using code I10-I99 including ischemic heart disease, hypertension, and cerebrovascular disease adjusted to air temperature and relative humidity. Of all pollutants, CO with each increase 10 μg/m³ had a meaningful relationship with the incidence of cardiovascular hospitalization. By selecting the window of exposure, 1, 2, and 6 days before admission, lag 6 (6 days) was the best estimation for exposure time in the patients with cardiovascular patients (OR 1.0056, CI 1.0041–1.007), and in the patients with ischemic heart disease (OR 1.000055, CI 1.000036–1.000075) and in the patients with hypertension (OR 1.000076, CI 1.00002–1.000132). Regarding cerebrovascular disease, no statistically significant association was observed. The results showed that only CO was associated with an increased risk of admission in patients with cardiovascular disease, ischemic heart disease, and hypertension, and there was no clear evidence for pollution effects on cerebrovascular diseases.

Short-term exposures to air pollution have been associated with various adverse health effects. In this study, we investigated the associations between ambient air pollutants with the number of hospital admissions and mortality from cardiovascular diseases (CVDs). This time series study was conducted in Tehran for the years 2014–2017 (1220 day). We collected the ambient air pollutant concentration data from the regulatory monitoring stations. The health data were obtained from the Ministry of Health and Medical Education. A distributed lag non-linear model (DLNM) was used for the analyses. Total CVDs and ischemic heart disease (IHD) admissions were associated with CO for each 1 mg/m³ increase at lags of 6 and 7 days. Also, there was a positive association between total CVDs (RR 1.01; 1.001 to 1.03), IHD (RR 1.04; 1.006 to 1.07), and cerebrovascular diseases (RR 1.03; 1.005 to 1.07) mortality with SO₂ at a lag of 4 days. PM₂.₅ and PM₁₀ were associated with cerebrovascular disease admissions in females aged 16–65 years and 16 years and younger for each 10 µg/m³ increase, respectively. Short-term exposure to SO₂, NO₂, and CO was associated with hospital admissions and mortality for CVDs, IHD, cerebrovascular diseases, and other cardiovascular diseases at different lags. Moreover, females were more affected by ambient air pollutants than males in terms of their burden of CVDs. Therefore, identifying the likely harmful effects of pollutants given their current concentrations requires the planning and implementation of strategies to reduce air pollution.

Most studies of short-term exposure to ambient air pollution and cerebrovascular diseases focused on specific stroke-related outcomes, and results were inconsistent due to data unavailability and limited sample size. It is unclear yet how ambient air pollution contributes to the total cardiovascular mortality in central China. Daily deaths from cerebrovascular diseases were obtained from the Disease Surveillance Point System (DSPs) of Wuhan Center for Disease Control and Prevention during the period from 2013 to 2019. Air pollution data were obtained from Wuhan Ecology and Environment Institute from 10 national air quality monitoring stations, including average daily PM₂.₅, PM₁₀, SO₂, NO₂, and O₃. Average daily temperature and relative humidity were obtained from Wuhan Meteorological Bureau. We performed a Poisson regression in generalized additive models (GAM) to examine the association between ambient air pollution and cerebrovascular disease mortality. We observed a total of 84,811 deaths from cerebrovascular diseases from 1 January 2013 to 31 December 2019 in Wuhan. Short-term exposure to PM₂.₅, PM₁₀, SO₂, and NO₂ was positively associated with daily deaths from cerebrovascular diseases, and no significant association was found for O₃. The largest effect on cerebrovascular disease mortality was found at lag0 for PM₂.₅ (ERR: 0.927, 95% CI: 0.749–1.105 per 10 μg/m3) and lag1 for PM₁₀ (ERR: 0.627, 95% CI: 0.493–0.761 per 10 μg/m³), SO₂ (ERR: 2.518, 95% CI: 1.914, 3.122 per 10 μg/m³), and NO₂ (ERR: 1.090, 95% CI: 0.822–1.358 per 10 μg/m³). The trends across lags were statistically significant. The stratified analysis demonstrated that females were more susceptible to SO₂ and NO₂, while elder individuals aged above 65 years old, compared with younger people, suffered more from air pollution, especially from SO₂. Short-term exposure to PM₂.₅, PM₁₀, SO₂, and NO₂ were significantly associated with a higher risk of cerebrovascular disease mortality, and elder females seemed to suffer more from air pollution. Further research is required to reveal the underlying mechanisms.

High blood pressure (BP) is known as the main determinant of high cerebrovascular disease levels in China. Many studies discovered the associations between short-term exposure to PM₂.₅ and BP, while most of those focused on low or medium PM₂.₅ concentration. The aim of this study was to reveal the association between extremely high level ambient PM₂.₅ exposure and BP. We conducted a repeated-measures panel study in Beijing, China, during December 1, 2016 to December 28, 2016. BP was monitored daily for all 133 participants. Daily concentration of PM₂.₅ was obtained from local monitoring sites. A linear mixed-effect model combined with the distributed lag non-linear model was used to evaluate the associations between PM₂.₅ and daily variations in BP. This study showed short-term exposure to PM₂.₅ that was significantly associated with increased DBP (on lags of 0–8 days, Beta = 0.12, 95% confidence interval 0.04, 0.20). The single day effect of PM₂.₅ on DBP had a 2-day lag, and the cumulative effect lags 5 days. The effects of PM₂.₅ on SBP and DBP on hypertensive adults were significant. The cumulative effect of PM₂.₅ on SBP and DBP had 2 rapidly increasing periods in hypertensive adults: lags of 0–2 days and lags of 0–7 days to lags of 0–11 days. Our study revealed that short-term exposure in the extreme high level of ambient PM₂.₅ may increase BP among adults. Hypertensive adults may more sensitive than normotensive adults. The periodic high concentration of ambient PM₂.₅ might magnify the effect of PM₂.₅ on BP increase.