Global burden of early-onset cardiovascular disease attributable to fine particulate matter pollution from 1990 to 2021: a systematic analysis for the global burden of disease study 2021 | BMC Medicine

This study provides an up-to-date evaluation on the global, regional, and national burden of early-onset CVD attributable to PM2.5 from 1990 to 2021. Males, individuals living in regions with lower SDI, and those with IHD experience a higher burden. Over the past three decades, there was a substantial decrease in early-onset CVD burden attributable to total and household PM2.5, especially in regions with higher SDI. However, the corresponding burden from ambient PM2.5 continued to rise and only began to decline since the last decade. In addition, the reduction in early-onset CVD burden was less prominent than that of late-onset CVD. Such findings underscore that even in the context of global population aging, the PM2.5-related early-onset CVD burden remains a critical concern.

Most previous studies focused on the overall CVD burden attributable to PM2.5, with few age-specific analyses and insufficient attention to younger populations [13, 15, 21]. Besides, there has been a decreasing trend in the all-age CVD death and DALY rates attributable to both ambient and household PM2.5 exposure over the past three decades [9]. However, how the early-onset CVD burden varied across different regions and time periods remains unclear. Our study is the first to fill this gap by conducting a comprehensive analysis of early-onset CVD burden attributable to PM2.5 from 1990 to 2021 at the global level. We also present the late-onset CVD burden and age-specific burden by 5-year intervals. The results show that the attributable burden was consistently higher in older age groups, suggesting their greater susceptibility. Interestingly, while the burden of both early- and late-onset CVD from total and household PM2.5 has declined, the reduction in the early-onset burden is smaller compared to the late-onset burden. Additionally, in contrast to the decline in late-onset CVD burden, the early-onset CVD burden due to ambient PM2.5 even increased slightly. This suggests a need for sustained attention to younger populations who may experience slower improvements despite lower absolute burden.

Our study reveals obvious sexual differences in the burden of early-onset CVD attributable to PM2.5 pollution. In general, males experience a higher burden compared to females, which is consistent with higher PM2.5-related CVD risk among males reported in previous researches [22,23,24]. This between-sex difference is more pronounced for ambient PM2.5 pollution and less prominent for household PM2.5. Several factors might contribute to this heterogeneity. First, there is generally a higher prevalence of traditional cardiovascular risk factors among males, such as hypertension, alcohol consumption, and smoking, which contributed to a higher overall CVD burden [9, 25, 26]. Second, social and occupational factors might also play an important role. Men are more likely to engage in outdoor labor-intensive work, leading to greater exposure to ambient air pollution. Conversely, women are more often exposed to indoor air pollution due to their involvement in household tasks such as cooking [27, 28]. These results underscore the importance of accounting for sex-specific exposure patterns when designing public health policies aimed at reducing PM2.5-related disease burdens. Reducing ambient PM2.5 exposure is particularly important for mitigating CVD burden among men, while minimizing both ambient and indoor exposure would be equally crucial for women.

Substantial variations by SDI were illustrated in the burden of early-onset CVD attributable to PM2.5 pollution. Similar to patterns observed in studies on other non-communicable diseases [29], a reversed U-shaped association was found between SDI and the early-onset CVD burden attributable to ambient PM2.5. In contrast, the corresponding burden due to household PM2.5 showed a generally decreasing trend as SDI increased. Low-SDI regions in Sub-Saharan Africa and South Asia faced the highest burden from household PM2.5, while middle-SDI regions in North Africa, the Middle East, South Asia, and East Asia experienced the greatest burden from ambient PM2.5. This pattern could be explained by the regional economic and environmental differences. Specifically, low-SDI countries, largely dependent on solid fuels, have higher household PM2.5 exposure, whereas middle-SDI countries face increased ambient pollution due to rapid urbanization and industrialization [30, 31]. High-SDI regions had the lowest burden from both ambient and household PM2.5, which might be largely due to the use of cleaner energy, stricter environmental regulations, more resources of individual protective measures, and improved public health and clinical systems. These regional differences underscore the critical influence of socioeconomic development on the early-onset CVD burden attributable to PM2.5 pollution.

To effectively mitigate the early-onset CVD burden due to PM2.5 pollution, tailored air quality policies and interventions based on regional economic and environmental contexts are warranted. In low-SDI countries, international cooperation is essential, including technology transfer to promote clean cooking stoves, clean energy use, and improved household ventilation. Global financial support is also needed to subsidize infrastructure upgrades and clean energy transitions. For middle-SDI countries undergoing rapid industrialization and urbanization, stringent air quality management plans including tightening industrial emission standards, expanding public transportation systems, and promoting clean energy transitions are needed. High-SDI countries, while facing relatively lower PM2.5 burdens, should continue strengthening environmental regulations, advancing control technologies, and investing in long-term pollutant management. They can also play a leading role in supporting global air pollution control efforts through research collaboration, funding, and cross-border policy communication.

The health effects and corresponding disease burden attributable to PM2.5 may also vary depending on its chemical composition and sources, which differ substantially across regions [32]. Previous studies reported that carbonaceous components and PM2.5 from fossil fuel combustion might pose higher cardiovascular risks [33,34,35,36], which could theoretically contribute to a higher disease burden. However, due to data limitations, our analysis focused on total PM2.5 mass and did not account for the heterogeneity in chemical constituents and sources. This limitation may also contribute to uncertainties in regional burden estimates. Future studies integrating data on PM2.5 chemical composition and source-specific toxicity are warranted to improve the precision of disease burden estimates and guide more targeted interventions.

Over the past three decades, there has been a significant decrease in the early-onset CVD burden attributable to total and household PM2.5 pollution, especially in regions with higher SDI levels. In contrast, the burden from ambient PM2.5 slightly increased at the global level, which was mainly driven by increasing burden in less-developed regions [31]. Since the year 2012, early-onset CVD burden from ambient PM2.5 has exceeded that from household PM2.5, and became the primary contributor to PM2.5-related burden. This shift illustrates the effectiveness of the global efforts in promoting cleaner energy sources including natural gas and electricity for household use, and emphasizes that stricter actions especially on ambient PM2.5 pollution are needed to reduce CVD burden in the future.

This study provides a comprehensive and up-to-date evaluation on the global, regional, and national distributions and temporal trends of early-onset CVD burden from PM2.5 exposure. Our findings offer scientific guidance for multiple fields, including public health, clinical practice, and environmental health policy, in developing targeted interventions and management strategies to promote global cardiovascular health.

There are several limitations that should be acknowledged. First, PM2.5 is a complex mixture comprising multiple constituents, each with distinct physicochemical properties [37]. The composition of PM2.5 can vary significantly by source, season, and region [38, 39]. However, the GBD 2021 study assumes spatial homogeneity in PM2.5 composition, potentially leading to inaccurate estimations in specific locations [29]. Future studies should take the heterogeneity of PM2.5 composition and source into consideration when evaluating the disease burden attributable to PM2.5. Second, our assessment of household PM2.5 pollution did not account for solid fuel use for heating, which is also an important contributor to indoor air pollution and a known risk factor for CVD [9, 40]. Thus, future studies should explore the contribution of solid fuel use for heating to the disease burden attributable to household PM2.5 pollution. Third, the effect estimates in this study rely on available epidemiological datasets, which might be limited in many low- and middle-income regions. Issues such as underdiagnosis and inadequate health care access could lead to biases in the estimation. Fourth, the current GBD 2021 dataset only evaluates burden of IHD as an aggregated category. Therefore, we were unable to estimate the disease burden by finer subtypes of IHD such as acute myocardial infarction, angina, or chronic IHD separately. In addition, most existing cohort studies on air pollution have focused on overall IHD rather than its specific subtypes, leading to insufficient evidence supporting more detailed burden estimation. Therefore, future studies with finer disease categories are warranted and would be valuable to inform targeted interventions. Last, while the relative risk estimates used in GBD 2021 were derived from epidemiological studies that adjusted for major confounders, residual confounding from unmeasured factors may still exist. In addition, potential interactions and mediation among different risk factors are not fully captured in these models. Future studies incorporating more detailed covariate data and advanced analytical methods are needed to better account for residual confounding and to explore these complex relationships.

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