Cardiovascular disease (CVD) has been highlighted as a significant public health challenge due to its high morbidity, disability, and mortality rates (1). In 2019, the global prevalence of CVD increased to 523 million, and the global deaths from CVD increased to 18.6 million (2). The burden of CVD is expected to rise further, driven by the dual pressures of an aging population and the growing prevalence of metabolic risk factors. Identifying modifiable risk factors is therefore essential to mitigate the adverse effects of CVD.

The detrimental effects of air pollution on CVD have been confirmed by epidemiologic and clinical studies (3–5). Rapid global economic development has resulted in nearly 90% of the world’s population residing in areas with air quality below World Health Organization (WHO) standards (6). As an essential component of air pollution, fine particulate matter mass ≤ 2.5 μm (PM_2.5) is considered to play a vital role in the risk of developing CVD (7). A meta-analysis showed that every 10 μg/m³ increment of PM_2.5 exposure had a 12% (95% CI: 1.08–1.16) increased risk of CVD mortality (8). In addition, air temperature is also one of the significant risk factors for CVD. At low ambient temperatures, particularly in winter, the risk of CVD rises considerably (9). Hospitalization rates for CVD can also be influenced by air temperature (10, 11). Interestingly, some studies have suggested that temperature might modify the mortality effects of PM_2.5 (12, 13)_. A study concerning the effects of daily temperature and daily PM_2.5 on mortality found that low air temperature significantly enhances the impact of PM_2.5 on CVD mortality (14).

Existing studies on the effects of air temperature and PM_2.5 on CVD have focused on short-term effects (15, 16) or cross-sectional studies (17, 18) on CVD mortality (8, 19). There are still significant gaps in our understanding. One of the major gaps is the lack of comprehensive data on how different levels of PM_2.5 exposure, in combination with various temperature ranges, interact to influence the onset and progression of CVD in different population subgroups. For example, individuals with cardiometabolic risk factors (age, gender, obesity, hypertension, diabetes) may be more vulnerable. Another gap lies in the long—term cumulative effects. While some short—term associations have been explored, the long—term impact of continuous exposure to PM_2.5 and temperature fluctuations on CVD development is not well-defined.

In this study, we investigated the longitudinal relationship between ambient PM_2.5 exposure, temperature, and CVD morbidity among Chinese adults using detailed data from the China Health and Retirement Longitudinal Study (CHARLS), considering long-term exposure and analyzing different population subgroups.

Based on the CHARLS survey, this study investigated the individual and combined impacts of ambient PM_2.5 exposure and air temperature with CVD in the Chinese population for the first time. We presented further proof of the harmful effects of high PM_2.5 exposure and low temperatures on CVD morbidity. Subgroup analysis showed that age, gender, obesity, hypertension, diabetes and dyslipidemia did not change these association. Furthermore, we discovered that long-term PM_2.5 exposure and low air temperatures together enhanced the risk of CVD. Therefore, it is necessary for continued air pollution abatement efforts. Better defense against low temperatures may also help reduce the risk of CVD.

The current study found a positive association between long-term PM_2.5 exposure and the risk of CVD, aligning with existing evidence. Several cross-sectional studies indicate that long-term PM_2.5 exposure is correlated with an increased likelihood of developing CVD (23, 24). Siregar et al. demonstrated that a 10 μg/m³ increase in PM_2.5 was significantly associated with 29% higher odds of having CVD (OR = 1.29; 95% CI: 1.02, 1.47) among 2,324 participants who were aged ≥40 years old (23). Many studies have reported a positive association between long-term PM_2.5 exposure and CVD mortality (25–27). Several studies also reported the effects of long-term exposure to PM_2.5 on CVD events across various populations (28–31). Liang et al. reported that every 10 μg/m³ increase in PM_2.5 exposure increased the risk of CVD incidence (HR = 1.25; 95% CI: 1.22–1.28) and CVD mortality (HR = 1.16; 95% CI: 1.12–1.21) (29). A study using a population-based and nationwide cohort in South Korea also reported that a 10 μg/m³ increase in 5-y PM_2.5 was associated with a 4% higher risk of CVD (95% CI: 0–9%) (32). However, existing studies have not considered the effects of indoor air pollution and temperature on CVD, which may influence the association between PM_2.5 exposure and CVD risk. In the present study, we supplemented this evidence among the middle-aged and older population in China. Additionally, we identified a nonlinear association between long-term PM_2.5 exposure and CVD incidence across the entire exposure range, consistent with the findings of Liang et al. (29).

Existing studies have focused on the effects of short-term air temperature on CVD hospitalization rates and CVD mortality (33–35), showing that low or high temperatures were associated with higher rates of CVD hospitalization and mortality. Evidence regarding the long-term effects of air temperature on CVD morbidity is limited. A study conducted on an open cohort of the older adult American population from 2000 to 2016 found that higher average summer temperatures and lower average winter temperatures were associated with an increased risk of CVD hospitalization (36). Our study found that lower annual average air temperatures were associated with a higher risk of CVD. Findings from the China Kadoorie Biobank (CKB) study indicated that lower temperatures increased CVD risk by regulating blood pressure (37). A survey in subtropical southern China showed a U-shaped association between CVD admissions and temperature (34). Our results demonstrated a U-shaped association between air temperatures and stroke morbidity. In contrast, we observed nonlinear associations for CVD morbidity, showing a strong inverse relationship at low to moderate temperatures, but weaker association at higher temperatures. These findings highlight inconsistencies in the effects of higher temperatures on CVD (37). Variations in results may arise from differing exposure estimates or distinct definitions of outcomes.

Previous studies have reported that the association between long-term PM_2.5 exposure and CVD may be modified by cardiometabolic risk factors (29, 38, 39). In the present study, we explored the modifying effects of age, gender, overweight or obesity, hypertension, type 2 diabetes, and dyslipidemia on the impact of PM_2.5 exposure and air temperature on CVD incidence. Our findings indicated that the harmful effects of PM_2.5 exposure and low air temperatures on CVD can be altered by age, gender, and cardiovascular risk factors. Older individuals, those with obesity, hypertension, or diabetes are more susceptible to the cardiovascular risks posed by PM_2.5 exposure due to various factors. For older adults, a decline in physiological function and the presence of comorbidities make them more vulnerable to inflammation and oxidative stress caused by PM_2.5. Obesity is linked to a chronic inflammatory state and metabolic disorders, both of which are aggravated by PM_2.5, leading to endothelial dysfunction and greater CVD risk. Hypertension causes vascular damage and impaired endothelial function, making blood vessels more susceptible to the harmful effects of PM_2.5. Diabetes results in vascular and nerve damage as well as abnormal glucose metabolism, which, when combined with PM_2.5 exposure, increases oxidative stress and inflammation, further heightening the risk of CVD. Several studies hypothesized that cardiometabolic risk factors act as mediators in the relationship between air pollution and CVD which aligns with our results (39, 40). Besides, we detected younger people, females, and those with obesity, hypertension, diabetes, or dyslipidemia were sensitive for the associations between low temperatures and CVD incidence. Studies conducted in two aging populations found that lower air temperatures had detrimental effects on cholesterol levels and blood pressure (41). However, we found that younger individuals, rather than older ones, had a higher risk of developing CVD at low temperatures. One possible explanation is that older individuals are more aware of keeping warm. Additionally, we detected stronger associations between low temperatures and CVD incidence in females. The reasons for the different results by age and sex remain unclear. However, they may be related to lifestyle factors (e.g., the thickness of clothing and outdoor physical activity) and biological differences (e.g., inflammation responses and primary metabolism) (42).

We found a significant additive interaction between high PM_2.5 exposure and low air temperatures with CVD incidence. Individuals in the highest PM_2.5 exposure percentile and the lowest air temperature percentile exhibited the highest risk of CVD morbidity. Studies investigating the interaction effects of air pollution and temperature on public health suggest that temperature may modify the association between air pollution and various diseases (14, 43). Although the mechanisms of the influence of PM_2.5 exposure and temperature on CVD not yet fully understood, there have been several studies addressing this aspect. Several studies hypothesize that the potential mechanisms linking air pollution to CVD include the following: promoting inflammation and oxidative stress (44), mitochondrial dysfunction (45), vascular dysfunction (46), and epigenetic dysregulation of gene expression (47). Current research on possible mechanisms of low temperature-induced CVD involves a variety of physiopathological modulations, including enhanced sympathetic responses to cold (48), activation of the renin-angiotensin system (RAS) (49), and cold-mediated dehydration (50).

Our study further confirmed the harmful effects of high PM_2.5 exposure and low temperatures on CVD morbidity, which could provide a reference basis for the formulation of public health policies. Firstly, we can provide a scientific basis for setting stricter regulations on PM_2.5-emitting sources, simultaneously increase keep-warm measures. Secondly, public health campaigns can be designed more effectively. Population who are vulnerable to the effects of high PM_2.5 exposure and low temperatures on CVD (such as the older adult or those with cardiometabolic risks), targeted educational programs can be developed. These programs can inform these at high-risk groups about the potential risks of high PM_2.5 exposure and low temperatures and how to reduce their exposure, such as staying indoors during peak PM_2.5 h and cold weather or using air purifiers.

This study had several advantages. It is the first time that the effects of long-term PM_2.5 exposure and air temperature on CVD morbidity among Chinese adults were quantified based on a large and representative cohort with 7 years of follow-up. In addition, the modifying effect of cardiometabolic risk factors on these associations was also explored. Furthermore, the association of combined exposures to PM_2.5 and air temperature with CVD, which has been ignored in other studies, was assessed. Our study had important public health implications, as exposure to PM_2.5 and low temperature is potentially modifiable, for example, via air conditioning and keeping warm. However, our study is susceptible to some restrictions. First, we examined air temperature and PM_2.5 exposure at the city level rather than directly measuring pollutant concentrations and temperature at homes, which could cause issues with exposure classification. Second, information on CVD and other disease histories was collected through participants’ self-reports, which might ignore some individuals with CVD. However, we have confirmed whether the answers to the self-reported diseases from the previous survey were correct during each survey, and repeating the confirmation can reduce some bias. In addition, when analyzing the data, we focused on overall trends rather than individual event accuracy. Since our study had a relatively large sample size, the impact of individual inaccuracies in self—reporting on the overall results was likely to be minimized. For example, if a small number of patients misreported CVD events, it would not significantly distort the general patterns of CVD prevalence or associations with other factors in the study population as a whole. Third, prospective cohort studies can be time—consuming and costly. There may be issues with confounding factors not fully accounted for. For example, our study did not control for other air pollution and climate factors confounders, which may affect our results. In addition, the effects of PM_2.5 exposure and low temperatures on CVD may be influenced by the indoor living environment and time spent outdoors, which were not included in our research. Fourth, the cohort may not be truly representative of the general population, limiting the generalizability of the findings. Last but not the least, the interpretation of results might be over—simplified. Just because an association was found between PM_2.5 exposure and air temperature on CVD risk, it does not necessarily mean there is a causal relationship. There may be potential mechanisms that have not been fully explored, and further research is needed to confirm them in the future. Finally, during our investigations, we discovered that when we attempted to examine and control for spatially auto—correlation, the performance of our models deteriorated significantly.

In summary, we discovered that long-term exposure to high-level PM_2.5 and low air temperatures adversely affected CVD morbidity in Chinese adults, with cardiovascular metabolic risk factors not altering these associations. The combination of high PM_2.5 exposure and low temperatures significantly enhances the risk of CVD. Our findings are essential for assisting governments in formulating effective public health interventions aimed at addressing environmental pollution and temperature-related health risks.