Significance: Estimation of the chronic health effects of PM _2.5 exposure has been hindered by the lack of long-term PM _2.5 data in China. To support this, high-performance machine-learning models were developed to estimate PM _2.5 concentrations at 1-km resolution in China from 2000 to 2016, based on satellite data, meteorological conditions, land cover information, road networks, and air pollution emission indicators. By adopting imputation techniques, relatively unbiased spatiotemporally continuous exposure estimates were generated. Annual mortality burdens attributable to long-term PM _2.5 exposure were estimated at the provincial scale, and the national total adult premature deaths were estimated at 30.8 million over the 17-y period in China.

Importance: Although cumulative evidence suggests that elevated urinary albumin-to-creatinine ratio (UACR) in the normal range (<30 mg/g) may be associated with an increased risk of mortality, few studies have investigated whether cardiovascular health (CVH) modifies the harmful outcomes of high-normal UACR.Objective: To investigate associations of traditionally normal UACR and CVH with all-cause mortality.Design, Setting, and Participants: This cohort study used National Health and Nutrition Examination Survey data from 2005 through 2018 and linked mortality information until 2019. Data were analyzed from March 1 through October 31, 2023. The study included adult participants aged 20 to 79 years with a normal UACR (<30 mg/g) based on Kidney Disease: Improving Global Outcomes criteria.Exposures: The UACR was treated as a continuous variable and categorized into tertiles delineated as low (<4.67 mg/g), medium (4.67-7.67 mg/g), and high (7.68 to <30 mg/g). Cardiovascular health was assessed using Life’s Essential 8 scores and grouped as poor (0-49 points), moderate (50-79 points), and ideal (80-100 points).Main Outcomes and Measures: Multivariable Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95% CIs for associations of UACR with all-cause mortality in total participants and as stratified by CVH groups.Results: The study included 23 697 participants (mean [SD] age, 45.58 [15.44] years; 11 806 women [49.7%] and 11 891 men [50.3%]). During the median 7.8 years (range, 4.5-11.1 years) of follow-up, 1403 deaths were recorded. Near-linear associations were observed for continuous UACR and CVH with all-cause mortality. Compared with the low UACR group, high UACR in the normal range showed an increased mortality risk in the moderate and poor CVH groups (CVH [50-79]: HR, 1.54 [95% CI, 1.26-1.89]; CVH [0-49]: HR, 1.56 [95% CI, 1.10-2.20]), with a significant multiplicative interaction of UACR and CVH (P < .001).Conclusions and Relevance: The findings suggest that high UACR within the normal range is associated with a significantly increased risk of all-cause mortality, with the association more pronounced in adults with poor CVH status. These findings highlight the importance of risk management for early kidney dysfunction, particularly among individuals with poor CVH.

Background: Established evidence suggests risks of developing cardiovascular disease are different by sex. However, it remains unclear whether associations of PM_2.5 with cardiovascular risk are comparable between women and men. The meta-analysis aimed to examine sex differences in associations of ischemic heart disease (IHD) and stroke with long-term PM_2.5 exposure.Methods: PubMed, EMBASE and Cochrane Library were searched until May 2, 2021. We included cohort studies reporting sex-specific associations of long-term PM_2.5 exposure (e.g., ≥1 year) with IHD and stroke. The primary analysis was to estimate relative risk (RR) of PM_2.5-outcome in women and men separately, and the additional women-to-men ratio of RR (RRR) was explored to compare sex differences, using random-effect models.Results: We identified 25 eligible studies with 3.6 million IHD and 1.3 million stroke cases among 63.7 million participants. A higher level of PM_2.5 exposure was significantly associated with increased risk of IHD in both women (RR = 1.21; 95% CI, 1.15–1.27) and men (RR = 1.12; 95% CI, 1.07–1.17). The women-to-men RRR of IHD was 1.05 (95% CI, 1.02–1.08) per 10 μg/m³ increment in PM_2.5 exposure, indicating significant excess risk of IHD in women. The significant risks of stroke associated with PM_2.5 were obtained in both women (RR = 1.11; 95% CI, 1.08–1.13) and men (RR = 1.11; 95% CI, 1.07–1.14), but no significant women-to-men RRR was observed in stroke (RRR = 1.00; 95% CI, 0.96–1.04).Conclusions: The study identified excess risk of IHD associated with long-term PM_2.5 exposure in women. The findings would not only have repercussions on efforts to precisely evaluate the burden of IHD attributable to PM_2.5, but would also provide novel clues for cardiovascular risk prevention accounting for sex-based differences.

The causal effects of moderate alcohol consumption on cardiovascular diseases (CVDs) are continuously debated, especially on coronary artery disease (CAD). We aimed to explore the causal associations of alcohol consumption with CVDs and all-cause mortality among Chinese males. A prospective cohort study was conducted in 40,386 Chinese males, with 17,676 being genotyped for the rs671 variant in the aldehyde dehydrogenase 2 (ALDH2) gene. A Cox proportional hazards model was conducted to estimate the effects of self-reported alcohol consumption. Mendelian randomization (MR) analysis was performed to explore the causality using rs671 as an instrumental variable. During the follow-up of 303,353 person-years, 2406 incident CVDs and 3195 all-cause mortalities were identified. J-shaped associations of self-reported alcohol consumption with incident CVD and all-cause mortality were observed, showing decreased risks for light (≤25 g/d) and moderate drinkers (25−≤60 g/d). However, MR analyses revealed a linear association of genetically predicted alcohol consumption with the incident CVD (P-trend = 0.02), including both CAD (P-trend = 0.03) and stroke (P-trend = 0.02). The HRs (95% CIs) for incident CVD across increasing tertiles of genetically predicted alcohol consumption were 1 (reference), 1.18 (1.01, 1.38), and 1.22 (1.03, 1.46). After excluding heavy drinkers, the risk of incident CVD and all-cause mortality was increased by 27% and 20% per standard drink increment of genetically predicted alcohol consumption, respectively. Our analyses extend the evidence of the harmful effect of alcohol consumption to total CVD (including CAD) and all-cause mortality, highlighting the potential health benefits of lowering alcohol consumption, even among light-to-moderate male drinkers.

Although multiple genetic markers associated with blood pressure have been identified by genome-wide association studies, their aggregate effect on risk of incident hypertension and cardiovascular disease is uncertain, particularly among East Asian who may have different genetic and environmental exposures from Europeans. We aimed to examine the association between genetic predisposition to higher blood pressure and risk of incident hypertension and cardiovascular disease in 26 262 individuals in 2 Chinese population-based prospective cohorts. A genetic risk score was calculated based on 22 established variants for blood pressure in East Asian. We found the genetic risk score was significantly and independently associated with linear increases in blood pressure and risk of incident hypertension and cardiovascular disease ( P range from 4.57×10 ^–3 to 3.10×10 ^–6 ). In analyses adjusted for traditional risk factors including blood pressure, individuals carrying most blood pressure–related risk alleles (top quintile of genetic score distribution) had 40% (95% confidence interval, 18–66) and 26% (6–45) increased risk for incident hypertension and cardiovascular disease, respectively, when compared with individuals in the bottom quintile. The genetic risk score also significantly improved discrimination for incident hypertension and cardiovascular disease and led to modest improvements in risk reclassification for cardiovascular disease (all the P <0.05). Our data indicate that genetic predisposition to higher blood pressure is an independent risk factor for blood pressure increase and incident hypertension and cardiovascular disease and provides modest incremental information to cardiovascular disease risk prediction. The potential clinical use of this panel of blood pressure–associated polymorphisms remains to be determined.