ArticleGlobal heart2024
Causal Associations of Environmental Pollution and Cardiovascular Disease: A Two-Sample Mendelian Randomization Study.
Article in Global heart, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Article
- Uridine, a Therapeutic Nucleoside, Exacerbates Alcoholic Liver Disease via SRC Kinase Activation: A Network Toxicology and Molecular Dynamics Perspective.International journal of molecular sciences · 2025Article
- Effect modification by cardiovascular and metabolic disease onset on long-term PMScientific reports · 2025Article
- Air Pollution and Its Impact on Health and Performance in Football Players.Sports (Basel, Switzerland) · 2025Review
- Air pollution and cardiovascular diseases: mechanisms, evidence, and mitigation strategies.Journal of medicine and life · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: There is growing evidence that concentrations of environmental pollutants are previously associated with cardiovascular disease; however, it is unclear whether this association reflects a causal relationship. Methods: We utilized a two-sample Mendelian randomization (MR) approach to investigate how environmental pollution affects the likelihood of developing cardiovascular disease. We primarily employed the inverse variance weighted (IVW) method. Additionally, to ensure the robustness of our findings, we conducted several sensitivity analyses using alternative methodologies. These included maximum likelihood, MR-Egger regression, weighted median method and weighted model methods. Results: Inverse variance weighted estimates suggested that an SD increase in PM2.5 exposure increased the risk of heart failure (OR = 1.40, 95% CI 1.02-1.93, p = 0.0386). We found that an SD increase in PM10 exposure increased the risk of hypertension (OR = 1.45, 95% CI 1.02-2.05, p = 0.03598) and atrial fibrillation (OR = 1.41, 95% CI 1.03-1.94, p = 0.03461). Exposure to chemical or other fumes in a workplace was found to increase the risk of hypertension (OR = 3.08, 95% CI 1.40-6.78, p = 0.005218), coronary artery disease (OR = 1.81, 95% CI 1.00-3.26, p = 0.04861), coronary heart disease (OR = 3.15, 95% CI 1.21-8.16, p = 0.0183) and myocardial infarction (OR = 3.03, 95% CI 1.13-8.17, p = 0.02802). Conclusion: This study reveals the causal relationship between air pollutants and cardiovascular diseases, providing new insights into the protection of cardiovascular diseases.
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Registered trials
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