Abstract and Introduction
Abstract
Aims: Living close to high traffic has been linked to subclinical atherosclerosis, however it is not clear, whether fine particulate matter (PM) air pollution or noise, two important traffic-related exposures, are responsible for the association. We investigate the independent associations of long-term exposure to fine PM and road traffic noise with thoracic aortic calcification (TAC), a reliable measure of subclinical atherosclerosis.
Methods and results: We used baseline data (2000–2003) from the German Heinz Nixdorf Recall Study, a population-based cohort of 4814 randomly selected participants. We assessed residential long-term exposure to PM with a chemistry transport model, and to road traffic noise using façade levels from noise models as weighted 24 h mean noise (Lden) and night-time noise (Lnight). Thoracic aortic calcification was quantified from non-contrast enhanced electron beam computed tomography. We used multiple linear regression to estimate associations of environmental exposures with ln(TAC+1), adjusting for each other, individual, and neighbourhood characteristics. In 4238 participants (mean age 60 years, 49.9% male), PM2.5 (aerodynamic diameter ≤2.5 μm) and Lnight are both associated with an increasing TAC-burden of 18.1% (95% CI: 6.6; 30.9%) per 2.4 μg/m PM2.5 and 3.9% (95% CI 0.0; 8.0%) per 5dB(A) Lnight, respectively, in the full model and after mutual adjustment. We did not observe effect measure modification of the PM2.5 association by Lnight or vice versa.
Conclusion: Long-term exposure to fine PM and night-time traffic noise are both independently associated with subclinical atherosclerosis and may both contribute to the association of traffic proximity with atherosclerosis.
Introduction
Long-term fine particulate matter (PM) air pollution and long-term exposure to high ambient noise levels are environmental exposures, which share similar sources, often occur conjointly and affect large portions of the population. Both exposures, occurring over years, are linked to the incidence of acute cardiovascular events. Due to their overlapping sources such as road traffic, it has been difficult to tease apart the independent effects of long-term PM and noise exposure. Furthermore, PM and noise exposure share many hypothesized biological pathways, including the elicitation of autonomic imbalance with sympathetic preponderance, an increase of arterial blood pressure, and increased blood coagulability.
Recently, two studies have shown an association of high residential traffic exposure—the most important source of inner-urban variability of PM and noise—with different measures of atherosclerosis of the coronary and large conduit vessels. Other studies have suggested that long-term fine PM exposure is associated with atherosclerosis of the larger vessels and with narrowing of the microvasculature. While these studies built on elaborate assessments of long-term residential PM exposure, none has been able to adequately control for the simultaneous occurrence of traffic noise and therefore has not been able to tease apart the detrimental effects of particle and noise exposure.
In this analysis, we use long-term exposure estimates for traffic noise and for fine PM exposure concurrently to investigate their independent associations with thoracic aortic calcification (TAC), a measure of subclinical atherosclerosis, in a large cardiovascular cohort study. While sharing cardiovascular risk factors with coronary calcification, which has been studied by our group before, TAC is independently related to the incidence of cardiovascular events. Furthermore, TAC has a higher prevalence among middle-aged adults than coronary calcification, making it specifically suitable for epidemiological analyses.
We investigate whether long-term residential exposure to PM and traffic noise are independently associated with the degree of TAC, and whether concurrent traffic noise exposure modifies the association of PM with subclinical atherosclerosis or vice versa. The study extends prior analyses of coronary calcification in the Heinz Nixdorf Recall Study, a well-characterized, ongoing population-based prospective cohort in Germany, which has been subjected to intense state-of-the-art fine PM and noise exposure assessment campaigns.