Ozone pollution and cardiovascular mortality in the elderly: A time-series analysis in Jinan, China (2015–2023)
- VernacularTitle:2015—2023年济南市臭氧污染对老年人心血管疾病死亡的影响
- Author:
Yan ZHANG
1
;
Yunjing LI
1
;
Weimei GONG
1
;
Ying WANG
1
;
Xiumiao PENG
1
;
Jingwen ZHOU
1
;
Yingjian ZHANG
1
Author Information
- Publication Type:Selectedarticle
- Keywords: air pollution; ozone; cardiovascular disease; elderly; risk of death; time-series analysis; interactive effect
- From: Journal of Environmental and Occupational Medicine 2025;42(11):1289-1298
- CountryChina
- Language:Chinese
-
Abstract:
Background Ozone (O3), a key air pollutant, significantly contributes to cardiovascular disease (CVD)-related mortality, with particularly pronounced effects in the elderly. Objective To explore the association between acute O3 exposure and mortality from CVD and its subtypes in the elderly population in Jinan, and to investigate the modifying effects of gender,age, and seasonal factors on O3-related effects, as well as to clarify the interaction with other air pollutants. Methods Daily mortality data for CVD, air pollutants, and meteorological parameters were collected in Jinan from 2015 to 2023. Generalized additive models (GAM) combined with distributed lag nonlinear models (DLNM) were used to analyze the lag effects of acute O3 exposure on mortalities from CVD, ischemic heart disease (IHD), and stroke in elderly individuals aged ≥60 years. Subgroup analyses were conducted to explore effect differences by gender (male vs. female), age (non-high-aged elderly<80 years vs. high-aged elderly ≥80 years), and season (warm season: April–September vs. cold season: October–March of the following year). Relative excess risk due to interaction (RERI), attributable proportion of interaction (API), and Synergy index (SI) were used to assess the interactions of O3 with PM2.5 and NO2. Results During the study period, the mean daily concentration of ozone reached (105.01 ± 54.18) μg·m−3, exceeding the Grade I limit value specified in Ambient Air Quality Standard (GB 3095–2012). Among the
203834 CVD deaths, IHD (53.07%) and stroke (33.33%) were the predominant mortality subtypes. The single-day lag analysis revealed peak excess risk (ER) for CVD mortality at lag0 (ER=0.64%, 95%CI: 0.29%, 1.00%) per 10 μg·m−3 O3 increase. The cumulative effects peaked at lag04 (ER=1.61%, 95%CI: 0.77%, 2.46%). The subtype-specific analyses showed the maximal single-day effects at lag0 were identified for both IHD (ER=0.61%, 95%CI: 0.20%, 1.03%) and stroke (ER=0.65%, 95%CI: 0.19%, 1.11%), while the cumulative risks peaked at lag04 for IHD (ER=1.54%, 95%CI: 0.56%, 2.54%) and lag03 for stroke (ER=1.74%, 95%CI: 0.76%, 2.73%). The gender subgroup analyses suggested that both male and female subgroups showed the most significant impact on CVD mortality at lag0, with ER values of 0.53% (95%CI: 0.11%, 0.95%) and 0.75% (95%CI: 0.33%, 1.18%), respectively, but the differences were not statistically significant (P>0.05). No statistically significant difference in effect values was found between high-aged and non-high-aged elderly (P>0.05) after age subgroup analyses. The seasonal subgroup analyses indicated that the effects of O3 on CVD and its subtypes in the warm season were significantly higher than those in the cold season (P<0.05). At lag0 in the warm season, the ER values for CVD, IHD, and stroke mortality were 0.86% (95%CI: 0.57%, 1.14%), 0.84% (95%CI: 0.49%, 1.19%), and 0.84% (95%CI: 0.43%, 1.26%), respectively. The interaction analyses revealed an antagonistic effect between O3 and PM2.5 on stroke mortality in the elderly [RERI=−4.64% (95%CI: −9.27%, −0.01%), API=−4.39% (95%CI: −8.77%, −0.01%), SI=0.55 (95%CI: 0.26, 0.84)]. The O3 effect remained robust in the multi-pollutant models (P<0.05). Conclusion Acute O3 exposure increases the risk of mortality from CVD and its subtypes in the elderly, and this effect is amplified in the warm season. Additionally, O3 and PM2.5 have an antagonistic effect on stroke mortality in the elderly.
