Exposure to traffic noise - independent of air pollution levels - may increase the risk of having a myocardial infarction (MI), a Danish study showed.

For every 10-decibel increase in traffic noise near an individual’s home, the risk of MI over a 10-year period was a relative 12% higher, according to Mette Sørensen, PhD, of the Danish Cancer Society in Copenhagen, and colleagues.

The relationship was linear and dose-dependent across the range of noise exposures (42 to 84 dB), the researchers reported online in PLoS One.

Previous studies have shown associations between ischemic heart disease risk and both traffic noise and ambient air pollution, but only a few studies have included both measures, with conflicting results.

To further explore the issue, Sørensen and colleagues looked at data from the Diet, Cancer, and Health cohort, a population-based study of Copenhagen residents who were ages 50 to 64 at baseline. The current analysis included 50,614 people who were free from cancer and coronary artery disease at baseline.

The researchers estimated traffic noise using the participants’ home addresses and used estimated levels of nitrogen oxides as a measure of air pollution exposure.

Through an average follow-up of 9.8 years, there were 1,600 first-ever MIs identified through national registries and medical records.

MIs were more likely at higher levels of traffic noise exposure, whether the exposure was measured at the time of diagnosis (incidence rate ratio 1.12, 95% CI 1.02 to 1.22) or averaged over the 5 years preceding the event (incidence rate ratio 1.12, 95% CI 1.02 to 1.23).

Those associations were adjusted for air pollution exposure, age, sex, education, smoking status, duration, and intensity, fruit and vegetable intake, body mass index, alcohol use, physical activity levels, calendar year, and railway and airport noise.

When looking at fatal MIs, the unadjusted incidence rate ratio for every 10-dB increase in traffic noise was 1.25 (95% CI 1.07 to 1.46). After adjustment, it fell short of statistical significance (incidence rate ratio 1.17, 95% CI 0.96 to 1.43).

Although the results cannot definitively establish a cause-and-effect association between traffic noise and MI risk, the researchers noted that noise in general induces a stress response “with hyperactivity of the sympathetic autonomic nervous system followed by elevated blood pressure, heart rate, and vasoconstriction,” which could represent an underlying mechanism connecting the two.

“Furthermore, noise affects the hypothalamus-pituitary-adrenal axis, leading to increased levels of cortisol,” they continued. “In addition, exposure to noise during the night at normal urban levels has been associated with sleep disturbances, which might affect metabolic and endocrine function and impair the immune system.”

They acknowledged some limitations of the study, including the fact that the mainly urban study population is not representative of the wider Danish population, the possible influence of death from other causes on the findings, uncertainty in the assessments of noise exposure, the lack of information on other sources of noise, and possible residual confounding from unmeasured factors, such as family history of MI.

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