European journal of preventive cardiology最新文献

Aims: Air pollution remains the single largest environmental health risk factor, while atrial fibrillation (AF) is the most prevalent arrhythmia globally. The study aimed to investigate the relationship between short-term exposure to air pollution and acute AF admissions.

Methods and results: Individual data on AF hospitalization in the years 2011-20 were collected from the National Health Fund in Poland (ICD-10: I48.XX). To obtain high-resolution data on air pollution, we applied a modelling method using the GEM-AQ model. Associations between air pollution exposure and acute AF admissions were estimated using generalized additive models with Poisson regression. Over the analysed period, we recorded 252 566 acute admissions due to AF. Each 10 µg/m3 increment of particulate matter with diameters ≤2.5 (PM2.5) and nitrogen dioxide (NO2) concentration, 1 µg/m3 of sulfur dioxide and 10 ng/m3 of benzo(a)pyrene (BaP) concentration on the day of exposure resulted in 1.13% (0.70-1.55%), 1.65% (1.05-2.26%), 0.11% (0.01-0.21%), and 0.3% (0.04-0.55%) increases in acute AF admissions, respectively. The estimates are larger for women and older people. Stronger associations between PM2.5 and BaP concentrations and AF admissions in poorly urbanized areas were noted. Areas with high gross domestic product levels were more affected by the increase in NO2 concentrations, resulting in a 0.2% (1.001-1.003) increase in AF admissions. Exposure-response functions show steeper slopes of the pollutant-outcome associations in the lower ranges of exposures, far below World Health Organization (WHO) air quality guideline norms. For the zero-emission scenario, we estimate avoidable AF admissions-5873 for PM2.5 (95% confidence interval 3679 to 8047) and 3295 for NO2 (2108-4477).

Conclusion: Air pollution acts as a triggering factor and can be associated with acute AF hospitalizations. PM2.5 and NO2 have an impact on AF even at concentrations levels below WHO air quality guideline norms.

Aims: The aim was to examine the relationship between exposure to environmental metallic and metalloid pollutants and cardiovascular disease (CVD) and all-cause mortality by integrating the information currently available from systematic reviews and meta-analyses.

Methods and results: PubMed, Embase, and Web of Science for systematic reviews and meta-analyses were thoroughly searched up to 9 October 2024. Systematic reviews and meta-analyses of various kinds that evaluated the relationship between exposure to ambient metallic and metalloid pollutants and CVD and all-cause mortality were included. The methodological quality and the evidence quality were assessed using AMSTAR2 and GRADE, respectively. We identified 25 meta-analyses and 81 health outcomes-76 unique outcomes from observational studies and 5 unique outcomes from RCTs-from 8841 independent publications. Exposure to non-essential metallic and metalloid pollutants, including arsenic, lead, and cadmium as well as essential metallic and metalloid contaminants like copper, has been associated with an elevated risk of CVD events and CVD mortality, according to moderate-quality evidence. According to low-quality evidence, exposure to arsenic, lead, and cadmium increases the risk of CHD, while exposure to lead, cadmium, and copper is strongly associated with an increased risk of stroke and all-cause mortality. Further, zinc and selenium may be protective factors for CVD and all-cause mortality.

Conclusion: Despite variations in evidence gradients, environmental metallic and metalloid contaminants like arsenic, lead, cadmium, mercury, and copper are linked to CVD events and mortality, whereas zinc and selenium may offer protection.

Lay summary: Non-essential environmental metallic and metalloid contaminant exposure is associated with a higher risk of CVDs and all-cause mortality, whereas essential metallic and metalloid may confer a protective benefit.Non-essential metallic and metalloid contaminants, such as arsenic, lead, and cadmium, raise the possibility of CVD events, CHD, and all-cause mortality, with lead and cadmium associated with higher risk of stroke.Essential metallic and metalloid contaminants like zinc and selenium can protect against CVD events and CHD, but too much selenium or copper may be harmful.

Aims: Which cardiometabolic risk factors (CMRFs) primarily mediate the association between long-term fine particulate matter (PM2.5) exposure and coronary artery disease (CAD) incidence, and whether participants with high genetic risks of CMRFs are more susceptible remain unclear.

Methods and results: This study was based on the project of Prediction for Atherosclerotic Cardiovascular Disease Risk in China. Long-term PM2.5 concentration was assessed by satellite-based spatiotemporal model at 1 km resolution. Mediation analyses were conducted to assess the mediating contribution of CMRFs for PM2.5 and CAD, and then stratified by genetic risk of CMRFs. Additive interaction was additionally evaluated on modification of genetic risk for PM2.5 and CAD. During a median follow-up of 11.15 years, 941 CAD cases of 34 481 participants were recorded. Each 10 μg/m3 increase in PM2.5 exposure was associated with a 28% increased risk of CAD [hazard ratio: 1.28; 95% confidence interval (CI): 1.19-1.37]. Systolic blood pressure (SBP) and low-density lipoprotein cholesterol (LDL-C) emerged as the primary mediators, with mediating proportions of 13.02% (95% CI: 4.63-21.42) and 9.23% (95% CI: 0.34-18.12), respectively. Notably, individuals with high genetic risk exhibited greater mediating proportions at 18.99% (95% CI: 6.43-31.55) and 16.30% (95% CI: 5.11-27.52) then those with low genetic risk at 2.42% (95% CI: -16.80 to 21.64) and 6.15% (95% CI: -8.13 to 20.43). Meanwhile, the genetic risks of SBP and LDL-C also significantly exacerbated CAD risk related to PM2.5 exposure, demonstrating additive interaction (P < 0.05).

Conclusion: This study provided a combination of conventional and genetic evidence to underscore the importance of integrated management targeting blood pressure and blood cholesterol to mitigate CAD burden when PM2.5 exposure is unavoidable.

Aims: The impact of the external exposome and mental health on cardiovascular diseases (CVDs) is well documented. However, the interactions between these factors remain poorly understood. This study aims is to assess the long-term impact of the exposome on cardiovascular and mental health and to explore the interactions between them.

Methods and results: This nationwide analysis encompassed 400 million person-years of observation, using individual health data. Environmental and socioeconomic status (SES) data were derived from environmental monitoring stations, satellite-based remote sensing, and national registries. Negative binomial regression was employed. Environmental and SES were assessed as modifiers using interaction terms and stratified analyses. The association between long-term exposure to air pollution (AP) and mortality was expressed as relative risks (RRs) with 95% confidence intervals (CIs), per 10 µg/m³ annual increase in particulate matter with diameter < 2.5 μm (PM₂.₅), nitrogen dioxide (NO₂), and carbon monoxide (CO) and per 1 µg/m³ for sulfur dioxide (SO2). Between 2011 and 2020, 4 010 521 all-cause deaths were recorded, including 1 706 111 CVD-related deaths (42.5%), median age 81 (71-87), and 53.6% were female. Annual increases in AP concentrations were associated with CVD mortality: PM₂.₅ (RR, 1.023; 95% CI, 1.012-1.035), NO₂ (RR, 1.111; 95% CI, 1.072-1.151), SO₂ (RR, 1.081; 95% CI, 1.030-1.134), and CO (RR, 1.018; 95% CI, 1.013-1.023); all P < 0.001. Exposure to ambient pollutants was linked to higher rates of mental services (RR range, 1.003-1.053; all P < 0.05). Five per cent increase in forestation index (RR, 0.967; 95% CI, 0.955-0.979; P < 0.001) and recreational green spaces (RR, 0.967; 95% CI, 0.952-0.982; P < 0.001) were directly associated with lower CVD mortality. With increasing rates of psychiatric hospitalizations and depression-related services, there was weaker association between exposure to AP and mortality, while greenness exposure and SES indicators showed a mixed modifying effect depending on the pollutant, but were generally associated with risk reduction.

Conclusion: The findings indicate multidimensional interactions between AP exposure, mental health, and SES conditions in shaping mortality risk. Greater access to mental health services modified the effects of environmental exposures, attenuating the associated risk. Socioeconomic status and greenness exposure might be associated with heterogeneous modifying effects, but seem predominantly to reduce risk. Our study highlights the necessity for context-specific urban planning strategies that consider local environmental and health determinants.

Registration: ClinicalTrials.gov: NCT05198492.

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