Objective: To investigate the effects of fine particulate matter (PM2.5) exposure on acute myocardial infarction (AMI) mortality and years of life lost (YLL). Methods: Mortality data in Haizhu District, Guangzhou City from 2020 to 2024 were collected by the China Population Death Information Registration Management System and Guangdong Death Certificate Management System. Air pollution and meteorological data of the same period were obtained from the national environmental monitoring sites on the National Real-time Air Quality Release Platform and the Guangzhou Observatory, respectively. The single-pollutant model and multi-pollutant model were established by distributed lag non-linear model to analyze the effects of PM2.5 on AMI mortality and YLL. Results: From 2020 to 2024, there were 2 466 AMI death cases in Haizhu District, including 949 males and 1 517 females. Among them, 530 cases were aged <65 years, 494 cases were aged 65-74 years, and 1 442 cases were aged >74 years. The median daily average number of deaths was 1.3 (interquartile range, 2.0) cases, and the median daily average YLL was 16.4 (interquartile range, 24.8) person years. The median daily average mass concentration of PM2.5 was 24.3 (interquartile range, 18.0) μg/m3. In single-pollutant models, the maximum effects of PM2.5 on AMI mortality and YLL were observed at a cumulative lag of 7 days. For per 10 μg/m3 increment in the daily average concentration of PM2.5, the excess risk of AMI mortality increased by 8.793% (95%CI: 4.201% to 13.588%), and YLL increased by 2.059 (95%CI: 1.081 to 3.037) person-years. Gender-stratified analyses showed that PM2.5 significantly affected AMI mortality in males and YLL in males and females (all P<0.05). Age-stratified analyses revealed that PM2.5 significantly affected AMI mortality and YLL among residents aged <65 years and 65-74 years (all P<0.05). However, the difference between genders or the two age groups was not statistically significant (both P>0.05). In multi-pollutant models, when NO2, SO2, or O3 were introduced respectively at a cumulative lag of 7 days, the effects of PM2.5 on AMI mortality and YLL were enhanced compared to the single-pollutant model (all P<0.05). When PM10 was introduced alone or in combination with PM10, SO2, NO2, and O3, the effects of PM2.5 on AMI mortality and YLL were not statistically significant (all P>0.05). Conclusion Exposure to PM2.5 may increase the risk of AMI mortality and YLL, with varying effects across populations of different genders and ages.

Background Researchers are paying increasing attention to the effect of cellular senescence in vascular dysfunctional diseases,and it is hypothesized that cellular senescence may also be involved in the development of diabetes related vascular complications.The outstanding feature of cellular senescence is the upregulation of beta-galactosidase.Objective This study was to investigate the effects of high glucose on cell senescent in vitro and in vivo on bovine retinal endothelial cells (BRVECs) and mouse retina.Methods BRVECs were cultured and passaged,and the seventh generation of cells were employed in this study.The cells were divided into the control group and the high glucose culture group and cultivated using M199 medium containing 5.5 mmol/L or 25.0 mmol/L glucose,respectively.5-bromine-chlorine-4-3-indole-beta D galactose glucoside (X-Gal) staining was used to examine the expression of beta-galactosidase in the cells.Diabetic models were established in the SPF male C57BL/6J mice aged 8-10 weeks by intraperitoneal injection of streptozotocin (STZ),and the age-and gendermatched normal mice served as controls.The mouse retinas were collected and starched in the 48-well plates 3 months later.X-Gal staining was employed to calculate the positive cells.Results BRVECs grew well 24 hours after culture but showed irregular arrangement.Forty-eight hours later,the cells reached confluence with a tight connect.The ratios of positive BRVECs and total cells were (51.4±5.4) ％ and (36.6-±3.8) ％ in the high glucose culture group and the control group,with a significant difference between the two groups (t =-3.204,P =0.033).The number of positive cells for X-Gal in mouse retinas was (94.0± 15.1) /field in the diabetic group,which was higher than that in the control group ([60.0 ± 5.7]/field) (t =-2.974,P =0.041).Conclusions High glucose environment accelerates senescence of retinal cells,and high glucose induces premature cell senescence,which likely plays an important role in the pathogenesis of diabetic retinopathy.