In a recent study from Massachusetts General Hospital, scientists found a mechanism through which long-term exposure to noise leads to inflammation, blood vessel damage, and heart disease.
They found that high noise levels lead to activation of the amygdala, a deep brain structure that plays a central role in processing emotions and responding to stress.
Long-term exposure to environmental noise—think planes, trains, and automobiles—has been linked in multiple studies to adverse health effects such as poor sleep, psychiatric disorders, and diabetes.
In the study, researchers used advanced PET-CT imaging to study the brains and arteries of 498 adults and followed them for 5 years to see whether higher levels of noise exposure were associated with a major adverse cardiovascular event, commonly abbreviated as “MACE.”
MACE was defined as CVD-related death, heart attack (myocardial infarction), severe uncontrolled chest pain (unstable angina), stroke, heart failure, or the need for an intervention to reopen blocked coronary or peripheral arteries.
They found that stress-associated brain centers, specifically the amygdala, potentially serve as the conduit by which noise triggers changes that lead to disease.
Over about 4 years, 40 of the 498 people (8%) experienced MACE, and when the team looked at noise exposure for these individuals, they found that every 5-decibel increase in noise predicted MACE.
The association between noise levels and MACE remained strong even when they took into account other potential risk factors for CVD.
Importantly, the PET-CT imaging showed that higher levels of noise exposure were linked to an increase in activity in the amygdala and an increase in inflammation of arteries, an early and critical event in the development of CVD.
These findings suggest a need to help people who may be at risk for CVD understand that chronic noise exposure where they live may increase their risk of disease.
Future work needs to study the link between noise exposure and other diseases (including diabetes and obesity) with an eye toward developing interventions to mitigate disease.
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The study was published in the European Heart Journal and conducted by Michael T. Osborne et al.
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