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Researchers discovered a causal relationship between air pollutants and increased cardiovascular disease (CVD) risk, highlighting the need for protective measures to mitigate exposure.
A causal relationship exists between air pollutants and cardiovascular diseases (CVDs), according to a study published in Global Heart.1
The researchers explained that CVD is the leading cause of morbidity and mortality worldwide; in particular, it is the most common cause of mortality in wealthy countries.2,3 Well-established CVD risk factors include hypertension and dyslipidemia. However, various past studies showed that increased air pollution levels could augment cardiovascular morbidity and mortality because of ischemic events, more frequent hospitalizations, and the worsening of heart failure and arrhythmias.4
Therefore, the relationship between environmental pollution and CVD has become the focus of epidemiologists and clinicians; worldwide consequences could occur if air pollution becomes a relevant CVD factor. Consequently, the researchers used a 2-sample Mendelian randomization (MR) approach to investigate the causal relationship between environmental pollution and CVD risk.1
The researchers analyzed several environmental pollutants, including particulate matter 2.5 (PM2.5) air pollution, PM10 air pollution, noise pollution, and nitrogen dioxide air pollution. They sourced the summary genetic data for environmental pollutants from the publicly available UK Biobank genome-wide association studies (GWAS), which involved 456,380 participants of European descent.
Additionally, the researchers incorporated 13 CVDs into the study with varying case numbers, ranging from 556 (hypertrophic cardiomyopathy) to 122,733 (coronary artery disease). They sourced this data from several different databases.
More specifically, the researchers sourced information about myocardial infarction and coronary artery disease from the Coronary Artery Disease Genome-Wide Replication and Meta-analysis plus the Coronary Artery Disease Genetics (CARDIoGRAMpluesC4D) consortium. Also, they sourced heart failure information from the Heart Failure Molecular Epidemiology for Therapeutic Targets consortium and atrial fibrillation information from the Atrial Fibrillation Gen consortium. Lastly, the researchers obtained GWAS summary statistics for the remaining CVDs, including hypertension, ischemic heart disease, and cardiomyopathy, from the FinnGen-R5 consortium.
To analyze the MR data, the researchers primarily used the inverse variance weighted method. Also, to ensure the robustness of their findings, they conducted various sensitivity analyses using maximum likelihood, weighted median, MR-Egger regression, and weighted model methods.
Overall, the researchers found that a 1-SD increase in PM2.5 exposure raised heart failure risk (OR, 1.40; 95% CI, 1.02-1.93; P = .0386). Similarly, a 1-SD increase in PM10 exposure escalated the risk of hypertension (OR, 1.45; 95% CI, 1.02-2.05; P = .03598) and atrial fibrillation (OR, 1.41; 95% CI, 1.03-1.94; P = .03461).
Lastly, the researchers determined that being exposed to chemical or other fumes in the workplace increased the risk of hypertension (OR, 3.08; 95% CI, 1.40-6.78; P = .005218), coronary artery disease (OR, 1.81; 95% CI, 1.00-3.26; P = .04861), coronary heart disease (OR, 3.15; 95% CI, 1.21-8.16; P = .0183), and myocardial infarction (OR, 3.03; 95% CI, 1.13-8.17; P = .02802). Conversely, they did not find a causal effect of nitrogen dioxide air pollution or noise pollution on an increased CVD risk.
The researchers also acknowledged their limitations, the most notable being their study population. It consisted solely of patients of European ancestry, limiting the generalizability of their findings. Despite their limitations, the researchers made suggestions based on their findings.
“…the use of portable air cleaners or respirators could significantly reduce fine PM exposures on blood pressure and heart rate variability, which could reduce the risk of hypertension and other CVDs,” the authors wrote.
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