Air pollution is major environmental health risk, which contributes significantly to global morbidity and mortality. Although the primary focus of connected resources is the impact of pollution air on heart health, it is essential to realize that Climate change and air pollution are deeply interconnected. This linkage is because air pollutants, such as fine particles, are often released into the atmosphere along with greenhouse gases. The main sources of both problems are common, including the burning of fossil fuels, smoke from forest fires and other human activities that release harmful pollutants. This synergy means that efforts to address one problem can often contribute to improving the other.

The level of exposure to air pollution is practically ubiquitous; in 2019, up to 99% of the world's population lived in areas that did not meet air quality standards set by the World Health Organization (WHO)The global cost of health damage associated with exposure to air pollution is estimated at $8.1 trillion, equivalent to 6.1 % of global gross domestic product. This underlines not only the health but also the enormous economic burden associated with this environmental problem.

Among the various components of air pollution, the most thoroughly studied are fine particles with an aerodynamic diameter of 2.5 µm or less (PM2.5). These particles are associated with an increased risk of cardiovascular disease – including myocardial infarction, heart failure and stroke – and promote the development of cardiovascular risk factors such as hypertension and diabetes. WHO estimates that up to 31% of cardiovascular disease deaths can be attributed to environmental factors, with air pollution being the most significant, accounting for 119 million disability-adjusted life years. In 2019, almost 70% of the 4.2 million deaths attributed to air pollution were due to cardiovascular disease. Although the precise pathophysiological mechanisms by which exposure to PM2.5 leads to adverse cardiovascular outcomes are not fully understood, Hypothetical mechanisms include oxidative stress, inflammation, and autonomic stimulation, which may lead to activation of cardiac fibroblasts and increased deposition of extracellular matrix proteins.

New retrospective study focused on the relationship between long-term exposure to PM2.5 and the extent of diffuse myocardial fibrosis, quantified using cardiac magnetic resonance imaging (MRI). The results showed that higher long-term exposure to PM2.5 is associated with greater diffuse myocardial fibrosis on native T1 cardiac MRI. This was true not only for patients with dilated cardiomyopathy (DCM) but also for healthy controls. Specifically, each 1 µg/m³ increase in average PM2.5 exposure was associated with a 0.30 higher native T1 z-score in patients with DCM and a 0.27 higher native T1 z-score in controls.

In absolute terms, each 1 µg/m³ increase in average annual PM2.5 exposure was associated with a 9.1 ms higher native T1 at 1.5 T and a 12.1 ms higher native T1 at 3 T. In addition to diffuse myocardial fibrosis, this exposure was also associated with a 40 % higher likelihood of late gadolinium enhancement (LGE), indicative of substitution fibrosis, a 3.6 ml/m² higher left ventricular end-diastolic volume (LVEDVI) and a 2.2 % lower left ventricular ejection fraction (LVEF) in the overall cohort. In patients with DCM, PM2.5 exposure was also associated with a 25 % higher likelihood of LGE.

Stratified analyses of the study revealed that The largest effect sizes for the association of PM2.5 exposure with native T1 z-scores were observed in women (β coefficient: 0.49), smokers (β coefficient: 0.43), and patients with hypertension (β coefficient: 0.48).. These findings suggest that some population subgroups may be particularly vulnerable to long-term exposure to air pollution, contributing to health inequalities. Importantly, adverse effects of fine particle air pollution on the heart were observed even at exposures below current Canadian Ambient Air Quality Standards (CAAQS), reinforcing the conclusion that there are no safe exposure limitsSince myocardial fibrosis is considered an irreversible process, it is it is essential to implement robust measures to reduce exposure to long-term air pollution, especially in the most vulnerable patients.

In conclusion, this study provides important empirical data in human patients on the association between air pollution and myocardial fibrosis, which may be an underlying pathophysiological mechanism leading to adverse cardiovascular outcomes. Given the linkages with climate change and the ubiquity of air pollution, Extensive public health measures are needed to reduce long-term exposure to fine particle air pollution, especially in vulnerable patients. At the same time, medical imaging can serve as a noninvasive tool to assess the underlying mechanisms of climate- and environment-related diseases. Future studies should continue to evaluate the associations and potential interventions in this important environmental and health context. Spring