An extensive study conducted in 322 Chinese cities has revealed that prolonged exposure to air pollution is linked to a higher risk of arrhythmia or irregular heartbeat. To delve into the details of this research and address various concerns regarding the relationship between air pollution and irregular heartbeats, Patriot interviewed India’s leading cardiologist and recipient of the prestigious Padma Shri award Dr Upendra Kaul.
Q: How significant is the finding of the study suggesting that long-term exposure to air pollution is associated with an increased risk of arrhythmia?
A: The study’s finding that long-term exposure to air pollution is associated with an increased risk of arrhythmia is highly significant. It reveals that prolonged exposure to air pollution, particularly fine particulate matter, can create an arrhythmic substrate. Individuals with conditions such as high blood pressure and diabetes may experience sub-clinical ventricular dysfunction, leading to a surge in arrhythmias. The study’s findings are logical and provide valuable insights into the relationship between air pollution and arrhythmia.
Q: Can you explain what arrhythmia is and how it can progress to more serious heart disease?
A: Arrhythmia refers to a condition characterised by abnormal heart rhythms or disordered heartbeats. These can range from benign irregularities to potentially malignant and life-threatening rhythms. Malignant arrhythmias can result in sudden cardiac death. If left untreated or unmanaged, arrhythmias can progress to become more serious heart diseases, impacting the overall health and functioning of the heart.
Q: What are the main modifiable risk factors for heart disease, and the role of air pollution in causing it?
A: The main modifiable risk factors for heart disease include smoking, high levels of bad lipids (such as cholesterol), hypertension (high blood pressure), diabetes, obesity, lack of exercise, stress, and inadequate intake of fruits and vegetables. Air pollution, specifically long-term exposure to fine particulate matter, adds to these risk factors by increasing the likelihood of developing arrhythmias and potentially exacerbating other heart conditions. While each risk factor contributes differently to heart disease, air pollution’s impact on the heart should not be underestimated due to its association with arrhythmias and its potential to worsen existing heart problems.
Q: The evidence linking air pollution with arrhythmia has been inconsistent. What makes this study different from previous ones?
A: This study stands out from previous research by employing rigorous scientific methods to measure pollutants and record arrhythmias. By utilising accurate and standardised measurements, this study provides more reliable and robust evidence regarding the association between air pollution and arrhythmia. The consistency and reliability of the study’s findings strengthen the understanding of this link and contribute to the existing body of knowledge.
Q: Among the six pollutants examined, nitrogen dioxide had the strongest association with all four types of arrhythmias. Can you explain why this pollutant is particularly harmful to the heart?
A: Nitrogen dioxide, by mimicking nitric oxide, interferes with the beneficial effects of nitric oxide on arterial walls. Nitric oxide plays a vital role in maintaining proper blood vessel function, promoting vasodilation, and reducing inflammation. When nitrogen dioxide disrupts this process, it can lead to adverse effects on the heart, potentially contributing to the development of arrhythmias.
Q: The authors of the study suggest that air pollution alters cardiac electrophysiological activities by inducing oxidative stress and systemic inflammation, affecting multiple membrane channels, as well as impairing autonomic nervous function. Can you explain what these mechanisms are and how they contribute to arrhythmia?
A: Air pollution, through various mechanisms, can negatively impact cardiac electrophysiological activities and contribute to arrhythmias. One of these mechanisms is the induction of oxidative stress, which occurs when there is an imbalance between free radicals and antioxidants in the body. Oxidative stress can damage cellular components and disrupt normal heart rhythm. Systemic inflammation, another consequence of air pollution, can further disrupt the electrical activity of the heart and contribute to arrhythmias.
Air pollution can also affect multiple membrane channels involved in the conduction of electrical signals within the heart. Disruption of these channels can lead to abnormal impulses.
Q: The association between air pollution and acute onset of arrhythmia was found to be immediate. What does this mean for people living in heavily polluted areas, and what measures can they take to protect themselves?
A: People living in heavily polluted areas are at increased risk of developing arrhythmia and should take measures to protect themselves, such as wearing N95 masks, reducing outdoor activities during peak pollution periods, and improving indoor air quality. It is also important for policymakers to take steps to reduce air pollution levels.
Q: The researchers called for further reducing exposure to air pollution and prompt protection of susceptible populations worldwide. What steps do you think can be taken to achieve this goal, and what role can healthcare providers play in this effort?
A: To reduce exposure to air pollution, steps such as the preservation and expansion of green forests and reducing emissions from transportation and industry, increasing the use of renewable energy sources, and promoting public transportation can be taken. Healthcare providers can also play a role in educating patients about the risks of air pollution and providing guidance on how to protect themselves. Additionally, healthcare providers can advocate for policies and actions to reduce air pollution levels in their communities.
With more than 7 years of experience in Journalism, Tahir Bhat is Chief Sub-Editor at Patriot. Tahir has reported on Human Rights, Economy, Polity, Society, Culture.