Researchers from China’s Huazhong University of Science and Technology have linked the risk of atrial fibrillation (AF) to the impacts of air pollution. In a study that was published in PNAS under the title “Air pollution, genetic susceptibility, and the risk of atrial fibrillation: A large prospective cohort study,” the research team discovered that long-term exposure to air pollutants increased the risk of AF, especially in people who have a high genetic predisposition to the condition.
Air pollutants have long been associated with cardiovascular diseases. Recent investigations have connected acute AF exacerbations and short-term exposure to these contaminants. However, these risk factors only account for roughly half of AF instances, according to studies on twins, which indicate that genetic predisposition plays a significant role in AF risk.
The current study focuses on the cumulative harm brought on by long-term exposure to these pollutants and finds a link between elevated levels of particulate matter with aerodynamic diameters less than 2.5 μm (PM2.5), particulate matter with diameters of 10 μm (PM10), nitrogen dioxide (NO2), and nitrogen oxide and the underlying genetic risk of AF.
Particle pollution is made up of tiny non-visible materials under 10 m, and these can travel deep into the lungs despite the visible haze that can accompany smoke, dust, or vehicle emissions. For comparison, a human hair’s typical width is about 70 μm.
Depending on where they came from, the particles may be hundreds of different substances. Direct emissions from building sites, fires, or agricultural, automotive, or industrial facilities will represent what is coming from those sources.
Sulfur dioxide and nitrogen oxides can be produced in the atmosphere by reactions between more environmentally complex sources such those released from power plants, heavy industries, and automotive emissions.
UK Biobank, a study cohort of over 500,000 participants aged 37 to 73 from across the United Kingdom, was used to create a polygenic risk score aggregating multiple genetic variants associated with AF. As expected, those at medium or high genetic risk had elevated AF risk.
When combining genetic susceptibility with high air pollutant levels, participants exposed to high air pollutants with high genetic risk had approximately 149–182% higher risk of AF than individuals with low genetic risk factors.
The study also found a significant additive risk interaction between PM10 and NO2 and genetic risk, with approximately 16.4–35.1% of cases attributable to the joint effects of these pollutants and genetic predisposition.
The combined impacts of genetic risk and air pollution exhibited a dose-response relationship, such that exposure to high levels of genetic risk and exposure to high levels of air pollution led to high odds of developing AF.
