Research has suggested that there could be a causal relationship between air pollution and heart attacks. Read to know more.
According to a study, sudden braking and exhaust fumes may dramatically raise the risk of heart attacks. Nitric oxide, a common traffic-related pollutant, has been linked in a study on nearly 18,000 people in Germany to an increased risk of having an attack. Every 10 g of air pollution above the daily average increased the risk of having a heart attack by 1%, and a three-day period of high pollution elevated that risk by 4%.
The researchers claimed that the smokers did not appear affected by the smog– this was likely because they were already used to smoking toxic fumes continuously. It comes following warnings that up to 11,000 fatalities from heart disease and circulatory diseases may occur annually in the UK as a result of air pollution.
The study, which will be presented this weekend at the European Society of Cardiology’s annual congress in Barcelona, claims that heart attacks decline in hot weather. The study included 17,873 people who had a heart attack between 2008 and 2014. Furthermore, a temperature increase of 10°C was associated with a 6% reduction in the frequency of heart attacks.
Traffic pollutants must be minimalized to reduce the risk of heart attack
The study comes to the conclusion that if we want to lower the risk of acute myocardial infarction, traffic and pollutants must be minimized. An observational study cannot prove a causal relationship. It is conceivable that air pollution causes myocardial infarction given that nitric oxide and PM10 promote inflammation, atherosclerosis is largely caused by inflammatory processes, and no connections were detected in smokers.
However, there was another study conducted back in 2011 that looked at the cardiovascular effects of exposure to air pollution. The study discovered that the risk was temporary, lasting one to six hours. Rather than raising the overall risk of having a heart attack, pollution exposure appeared to trigger cardiac events in persons who were already at higher-than-average risk.
