Related Experiment Video
Updated: Jul 16, 2025
Measuring Carbon Content in Airway Macrophages Exposed to Carbon-Containing Particulate Matters
Published on: July 12, 2024
Causality of particulate matter on cardiovascular diseases and cardiovascular biomarkers
Qiubo Wang1,2, Zhimiao Wang1, Mingyou Chen1
1Department of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, China.
Background:
Previous observational studies have shown that the prevalence of cardiovascular diseases (CVDs) is related to particulate matter (PM). However, given the methodological limitations of conventional observational research, it is difficult to identify causality conclusively. To explore the causality of PM on CVDs and cardiovascular biomarkers, we conducted a Mendelian randomization (MR) analysis.
Method:
In this study, we obtained summary-level data for CVDs and cardiovascular biomarkers including atrial fibrillation (AF), heart failure (HF), myocardial infarction (MI), ischemic stroke (IS), stroke subtypes, body mass index (BMI), lipid traits, fasting glucose, fasting insulin, and blood pressure from several large genome-wide association studies (GWASs). Then we used two-sample MR to assess the causality of PM on CVDs and cardiovascular biomarkers, 16 single nucleotide polymorphisms (SNPs) for PM2.5 and 6 SNPs for PM10 were obtained from UK Biobank participants. Inverse variance weighting (IVW) analyses under the fixed effects model were used as the main analytical method to calculate MR Estimates, followed by multiple sensitivity analyses to confirm the robustness of the results.
Results:
Our study revealed increases in PM2.5 concentration were significantly related to a higher risk of MI (odds ratio (OR), 2.578; 95% confidence interval (CI), 1.611-4.127; p = 7.920 × 10-5). Suggestive evidence was found between PM10 concentration and HF (OR, 2.015; 95% CI, 1.082-3.753; p = 0.027) and IS (OR, 2.279; 95% CI,1.099-4.723; p = 0.027). There was no evidence for an effect of PM concentration on other CVDs. Furthermore, PM2.5 concentration increases were significantly associated with increases in triglyceride (TG) (OR, 1.426; 95% CI, 1.133-1.795; p = 2.469 × 10-3) and decreases in high-density lipoprotein cholesterol (HDL-C) (OR, 0.779; 95% CI, 0.615-0.986; p = 0.038). The PM10 concentration increases were also closely related to the decreases in HDL-C (OR, 0.563; 95% CI, 0.366-0.865; p = 8.756 × 10-3). We observed no causal effect of PM on other cardiovascular biomarkers.
Conclusion:
At the genetic level, our study suggested the causality of PM2.5 on MI, TG, as well HDL-C, and revealed the causality of PM10 on HF, IS, and HDL-C. Our findings indicated the need for continued improvements in air pollution abatement for CVDs prevention.
Insights
This Mendelian randomization study found that exposure to fine particulate matter (PM2.5) increases the risk of myocardial infarction and affects lipid levels. Coarser particulate matter (PM10) was linked to heart failure, ischemic stroke, and reduced HDL cholesterol.
Area of Science:
- Environmental Epidemiology
- Genetic Epidemiology
- Cardiovascular Research
Background:
- Observational studies suggest a link between particulate matter (PM) and cardiovascular diseases (CVDs).
- Methodological limitations in previous studies hinder conclusive causal inference.
- Mendelian randomization (MR) offers a robust approach to investigate causality.
Purpose of the Study:
- To determine the causal effect of PM2.5 and PM10 exposure on CVDs.
- To assess the impact of PM exposure on key cardiovascular biomarkers.
- To leverage genetic variants as instrumental variables for PM exposure.
Main Methods:
- Two-sample Mendelian randomization analysis using summary-level data from large genome-wide association studies (GWASs).
- Utilized 16 single nucleotide polymorphisms (SNPs) for PM2.5 and 6 SNPs for PM10.
- Employed inverse variance weighting (IVW) as the primary method, with sensitivity analyses for robustness.
Main Results:
- PM2.5 exposure significantly increased the risk of myocardial infarction (MI) and triglyceride (TG) levels, while decreasing high-density lipoprotein cholesterol (HDL-C).
- PM10 exposure showed suggestive links with heart failure (HF) and ischemic stroke (IS), and significantly decreased HDL-C.
- No causal effects were observed for other CVDs or cardiovascular biomarkers.
Conclusions:
- Genetic evidence supports a causal role of PM2.5 in MI, TG, and HDL-C.
- Genetic evidence suggests PM10 causally influences HF, IS, and HDL-C.
- Findings underscore the importance of air pollution control for cardiovascular disease prevention.
More Related Videos
07:35Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
Published on: December 10, 2021
10:11Fundus Photography as a Convenient Tool to Study Microvascular Responses to Cardiovascular Disease Risk Factors in Epidemiological Studies
Published on: October 22, 2014
Related Concept Videos
01:19Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
01:30Coronary Artery Disease I: Introduction
01:21Causality in Epidemiology
01:27Psychoneuroimmunology: Cardiovascular Disease
A key area of focus in PNI is the relationship between stress and coronary...
01:20Blood Studies for Cardiovascular System I: Cardiac Biomarkers
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
01:28Criteria for Causality: Bradford Hill Criteria - II