Aircraft noise pollution harms arteries, but heart drugs show promise in animal model research

Discover how common heart medications combat oxidative stress and inflammation from aircraft noise pollution.

Image Credit: Steve Mann / Shutterstock

In a recent article in the journal Antioxidants, researchers in Germany investigated whether cardiovascular drugs such as alpha-blockers and beta-blockers can protect against the complications caused by short-term exposure to aircraft noise. Their findings indicate that these drugs may effectively reduce oxidative stress and inflammation in heart and brain tissue and lower pulse pressure but may not protect against hypertension.

Background

Due to advances in hygiene and medical care, non-communicable diseases (NCDs) are now a major health concern globally. Traffic noise, one of the environmental risk factors contributing to NCDs, has gained attention, especially in densely populated urban areas.

In the European Union, over 20% of people reside in areas with transportation noise levels exceeding 55 decibels, which is considered harmful. Aircraft noise, in particular, is disruptive due to its unpredictability and high intensity, causing sleep disturbances and annoyance. This type of noise has been linked to increased risks of cardiovascular disease, including hypertension, heart disease, and stroke.

Noise-induced cardiovascular issues are thought to arise from stress responses that activate the sympathetic nervous system, leading to the release of stress hormones like adrenaline. These hormones trigger oxidative stress and inflammation through the activation of enzymes such as NADPH oxidase and pathways like the hypothalamic-pituitary-adrenal (HPA) axis. This contributes to blood vessel constriction and endothelial dysfunction, key precursors to heart problems.

Alpha- and beta-blockers, common medications for heart conditions, work by blocking the receptors that these stress hormones bind to, reducing blood pressure and improving heart function. Limited data exist regarding the effectiveness of these drugs in mitigating cardiovascular issues induced by noise exposure. However, previous studies suggest they may be beneficial, prompting further investigation into their potential protective effects for people exposed to noise pollution.

About the Study

This study aimed to investigate the potential improvements in vascular dysfunction caused by aircraft noise and the brain-heart connection, focusing on oxidative stress and inflammation. Male mice were used for the experiments, housed under standard conditions, and exposed to aircraft noise 24 hours a day for four days.

The noise protocol simulated takeoffs and landings, with sound levels averaging 72 dB(A) to the human ear, a level chosen to mimic real-world exposure without causing hearing loss. This approach ensured measurable biochemical and functional changes within a short time frame.

The mice received either propranolol (a beta-blocker) or phenoxybenzamine (an alpha-receptor antagonist) via subcutaneous osmotic pumps to study the effects on cardiovascular function. Non-invasive blood pressure was measured using a tail-cuff method, while vascular function was assessed through isometric tension studies of the aorta and video microscopy of cerebral arterioles. Oxidative stress was evaluated using dihydroethidium staining, and protein expression related to inflammation and oxidative stress was analyzed through Western blot and dot blot techniques. This multi-faceted experimental design allowed researchers to isolate the molecular and functional impacts of noise exposure.

Findings

Exposure to aircraft noise increased systolic blood pressure, which remained elevated despite treatment with propranolol or phenoxybenzamine. Diastolic pressure showed a rising trend with noise exposure but no significant improvement with these treatments. Only pulse pressure showed some improvement.

Noise exposure caused endothelial dysfunction, as seen in impaired aortic relaxation to acetylcholine, but both drugs mitigated this effect. Nitroglycerin-induced relaxation remained unchanged, indicating unaffected smooth muscle function. Noise exposure also increased reactive oxygen species (ROS) in the aorta, a sign of oxidative stress. Both drugs significantly reduced ROS levels, with propranolol even bringing them below control levels.

Noise impaired endothelium-dependent dilation in cerebral arterioles, but propranolol and phenoxybenzamine restored this. Noise also elevated oxidative stress and inflammation markers, such as NOX2 and IL-6, in brain and heart tissues. Both drugs significantly reduced these markers, showcasing their ability to protect against noise-induced molecular damage.

On a molecular level, noise exposure increased oxidative stress and inflammation markers in cardiac and brain tissues. However, the absence of blood pressure improvement may reflect compensatory mechanisms such as reflex tachycardia or persistent cortisol signaling, which are unaffected by alpha- and beta-blockers. These findings suggest that while vascular function improves, hypertension may require additional interventions.

Conclusions

In this study, researchers examined how alpha- and beta-blockers might counter the negative impacts of aircraft noise on cardiovascular health. They found that using phenoxybenzamine or propranolol helped reduce noise-induced damage to blood vessels in the brain and aorta, specifically by decreasing oxidative stress and inflammation. However, these interventions did not lower blood pressure.

The study revealed that noise exposure triggers a stress response, activating the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system. This leads to oxidative stress and inflammation, which contribute to endothelial dysfunction. Blocking alpha—and beta-adrenergic receptors helped reduce oxidative stress and inflammation in the brain and cardiovascular tissues.

Despite the positive impact on vascular function, the treatments did not prevent the noise-induced increase in blood pressure, possibly due to compensatory mechanisms. Nonetheless, the findings highlight the drugs’ potential to mitigate noise-induced vascular damage in vulnerable groups, particularly those at risk for stroke or pre-existing cardiovascular conditions.

Journal reference:
  • Kuntić, M., Kuntić, I., Zheng, J., Nardi, L., Oelze, M., Valar, A., Mihaliková, D., Strohm, L., Ubbens, H., Tang, Q., Zhang, L., Horta, G., Stamm, P., Hahad, O., Li, H., Steven, S., Gericke, A., Schmeisser, M. J., Münzel, T., . . . Daiber, A. (2024). Interventions by Cardiovascular Drugs Against Aircraft Noise-Induced Cardiovascular Oxidative Stress and Damage. Antioxidants, 14(1), 59. DOI: 10.3390/antiox14010059, https://www.mdpi.com/2076-3921/14/1/59
Priyanjana Pramanik

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Priyanjana Pramanik

Priyanjana Pramanik is a writer based in Kolkata, India, with an academic background in Wildlife Biology and economics. She has experience in teaching, science writing, and mangrove ecology. Priyanjana holds Masters in Wildlife Biology and Conservation (National Centre of Biological Sciences, 2022) and Economics (Tufts University, 2018). In between master's degrees, she was a researcher in the field of public health policy, focusing on improving maternal and child health outcomes in South Asia. She is passionate about science communication and enabling biodiversity to thrive alongside people. The fieldwork for her second master's was in the mangrove forests of Eastern India, where she studied the complex relationships between humans, mangrove fauna, and seedling growth.

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