Article Impact Level: HIGH Data Quality: STRONG Summary of Clinical Cardiology, 46(11), 1319–1325. https://doi.org/10.1002/clc.24111 Dr. Shiva Tabaghi et al.
Points
- A study in Tehran, Iran, assessed the short-term effects of PM2.5 and PM10 on acute myocardial infarction (AMI) in 982 patients presenting to emergency departments.
- Case-crossover design and conditional logistic regression were used to analyze associations between air pollutant concentrations and AMI occurrence.
- Significant associations were found between increased PM2.5 and PM10 levels and the occurrence of AMI, independent of temperature and humidity.
- Subgroup analysis revealed positive associations between PM2.5 and PM10 concentrations and increased AMI events across various subgroups, except for the diabetic subgroup.
- Findings emphasize the detrimental impact of ambient air pollution on cardiovascular health, highlighting the need for targeted interventions to mitigate the adverse cardiovascular effects of particulate matter exposure.
Summary
The research aimed to assess the short-term effects of air pollutants, specifically particulate matter with aerodynamic diameters ≤2.5 μm (PM2.5) and ≤10 μm (PM10), on the occurrence of acute myocardial infarction (AMI) in patients presenting to emergency departments in Tehran, Iran. A total of 982 patients with documented AMI between July 2017 and March 2019 were included in the study. The case-crossover design utilized a specific case report sheet to define case and referent periods, enabling the evaluation of associations between PM2.5 and PM10 concentrations and AMI occurrence. The analysis, conducted using conditional logistic regression, revealed a significant association between increased PM2.5 and PM10 levels and the occurrence of AMI, even after adjusting for temperature and humidity. Furthermore, subgroup analysis indicated positive associations between PM2.5 and PM10 concentrations and increased AMI events across various subgroups, except for the diabetic subgroup, where PM10 did not show a significant increase in AMI events.
The findings of this study, which are novel in their comprehensive evaluation of the associations between air pollutant concentrations and AMI occurrence, underscore the significant impact of acute exposure to ambient air pollution, particularly PM2.5 and PM10, on the risk of AMI, independent of temperature and humidity. The robust methodology, including the use of a case-crossover design and conditional logistic regression, further enhances the credibility of these findings. The results provide valuable insights into the potential health implications of air pollution, emphasizing the need for targeted interventions to mitigate the adverse cardiovascular effects of particulate matter exposure. These findings contribute to the growing body of evidence highlighting the detrimental impact of ambient air pollution on cardiovascular health, particularly in the context of acute myocardial infarction.
In summary, the research demonstrates a clear association between increased PM2.5 and PM10 concentrations and the risk of AMI and underscores the adverse cardiovascular effects of ambient air pollution. These findings have immediate and significant implications for public health, highlighting the urgent need for effective strategies to reduce air pollutant levels and mitigate the associated cardiovascular risks, particularly in urban environments like Tehran, Iran. Policymakers and public health officials can use these findings to inform and guide their decisions on air quality management and public health interventions.
Link to the article: https://onlinelibrary.wiley.com/doi/10.1002/clc.24111
References Tabaghi, S., Sheibani, M., Khaheshi, I., Miri, R., Haji Aghajani, M., Safi, M., Eslami, V., Pishgahi, M., Alipour Parsa, S., Namazi, M. H., Beyranvand, M. R., Sohrabifar, N., Hassanian‐Moghaddam, H., Pourmotahari, F., Khaiat, S., & Akbarzadeh, M. A. (2023). Associations between short-term exposure to fine particulate matter and acute myocardial infarction: A case-crossover study. Clinical Cardiology, 46(11), 1319–1325. https://doi.org/10.1002/clc.24111
