Study Finds Air Pollution and Noise Pollution Increase Cardiovascular Risk

Released: 5/13/2013 1:00 PM EDT
Embargo expired: 5/20/2013 2:00 PM EDT
Source Newsroom: American Thoracic Society (ATS)
Contact Information

Available for logged-in reporters only

Citations American Thoracic Society 2013 International Conference

Newswise — ATS 2013, PHILADELPHIA ─ Both fine-particle air pollution and noise pollution may increase a person’s risk of developing cardiovascular disease, according to German researchers who have conducted a large population study, in which both factors were considered simultaneously.

“Many studies have looked at air pollution, while others have looked at noise pollution,” said study leader Barbara Hoffmann, MD, MPH, a professor of environmental epidemiology at the IUF Leibniz Research Institute for Environmental Medicine in Germany. “This study looked at both at the same time and found that each form of pollution was independently associated with subclinical atherosclerosis.”

The research will be presented at ATS 2013.

“This study is important because it says that both air pollution and noise pollution represent important health problems,” said Dr. Philip Harber, a professor of public health at the University of Arizona who was not involved in the research. “In the past, some air pollution studies have been dismissed because critics said it was probably the noise pollution that caused the harm, and vice versa. Now we know that people who live near highways, for instance, are being harmed by air pollution and by noise pollution.”

Using data from the Heinz Nixdorf Recall study, an ongoing population study from three neighboring cities in the Ruhr region of Germany, Dr. Hoffmann and her colleagues assessed the long-term exposure to fine particulate matter with an aerodynamic diameter <2.5 µm (PM2.5) and long-term exposure to traffic noise in 4238 study participants (mean age 60 years, 49.9% male).

The exposure to air pollutants was calculated using the EURopean Air Pollution Disperson, or EURAD, model. Exposure to traffic noise was calculated using European Union models of outdoor traffic noise levels. These levels were quantified as weighted 24-hour mean exposure (Lden) and nighttime exposure (Lnight).

To determine the association of the two variables with cardiovascular risk, the researchers looked at thoracic aortic calcification (TAC), a measure of subclinical atherosclerosis.

TAC was quantified using non-contrast enhanced electron beam computed tomography. Using multiple linear regression, the researchers controlled for other cardiovascular risk factors, including age, gender, education, unemployment, smoking status and history, exposure to second-hand smoke, physical activity, alcohol use and body mass index.

After controlling for these variables, the researchers found that fine-particle air pollution was associated with an increase in TAC burden by 19.9 % (95%CI 8.2; 32.8%) per 2.4µg/m3. (To put that increase in perspective: in the United States, the Environmental Protection Agency recently revised the overall limit downward from 15 to 12µg/m 3).

The researchers also found that nighttime traffic noise pollution increased TAC burden by 8% (95% CI 0.8; 8.9%) per 5 dB. (An average living room would typically have a noise level of about 40 A-weighted decibels, or dB(A), an expression of the relative loudness of sounds as perceived by the human ear, while busy road traffic would generate about 70-80dB(A)). Mean exposure to traffic noise over 24 hours was not associated with increased TAC.

Among subgroups of participants, the researchers found even stronger associations. The interaction of PM2.5 and TAC was clearer among those younger than 65, participants with prevalent coronary artery disease and those taking statins. In contrast, the effect of Lnight was stronger in participants who were not obese, did not have coronary artery disease and did not take statins.

Although the cross-sectional design of this study limits the causal interpretation of the data, Dr. Hoffmann said, “both exposures seem to be important and both must be considered on a population level, rather than focusing on just one hazard.”

She added that her research group plans to conduct a longitudinal analysis with repeated measures of TAC over time.

* Please note that numbers in this release may differ slightly from those in the abstract. Many of these investigations are ongoing; the release represents the most up-to-date data available at press time.

Abstract 40036
Searching For The Culprit: Is Urban Particulate Air Pollution Or Road Traffic Noise Responsible For The Association Of Traffic Proximity With Subclinical Atherosclerosis - Results From The Heinz Nixdorf Recall Study
Type: Scientific Abstract
Category: 06.01 - Air Pollution: Epidemiology and Mechanisms (EOH)
Authors: B. Hoffmann1, F. Hennig2, S. Moebus3, S. Mohlenkamp4, N. Dragano5, H. Jakobs6, R. Erbel4, K.-H. Jockel3, H. Kalsch4; 1IUF Leibniz Research Institute for Environmental Medicine - Dusseldorf/DE, 2IUF Leibniz Research Institute for Environmental Medicine - Düsseldorf/DE, 3University of Duisburg-Essen - Essen/DE, 4West-German Heart Center - Essen/DE, 5University of Duesseldorf - Duesseldorf/DE, 6Rhenish Institute for Environmental Research - Cologne/DE

Abstract Body
Rationale: Long-term particulate matter (PM) air pollution and high ambient noise levels are traffic-related environmental exposures, which often occur concurrently. Traffic proximity has been linked to subclinical atherosclerosis; however until now, no study has investigated, whether PM or road traffic noise is responsible for this association. We aimed to investigate the independent associations of PM and road traffic noise with thoracic aortic calcification (TAC), a measure of subclinical atherosclerosis.
Methods: We used baseline data (2000-2003) from the German Heinz Nixdorf Recall Study, a population-based cohort of 4814 participants. We assessed long-term exposure to fine particulate matter with an aerodynamic diameter <2.5 µm (PM2.5) with a chemistry transport model (EURAD), and long-term exposure to road traffic noise with façade levels from validated noise models according to the European Union noise directive. Long-term traffic noise exposure was quantified as weighted 24 h mean exposure (Lden) and night-time exposure (Lnight) TAC 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), controlling for PM2.5 and long-term traffic noise, respectively, and age, sex, education, neighbourhood unemployment rate, smoking status, cumulative cigarette exposure, environmental tobacco smoke, physical activity, weekly alcohol consumption and body mass index. Effect modification of the PM2.5 and noise associations was investigated using product terms of continuous PM2.5, respectively traffic noise exposure, with dichotomized values of the respective other exposure, as well as dichotomized terms for age, sex, BMI, prevalence of coronary artery disease (CAD), intake of statins and prevalence of Diabetes mellitus.
Results: In 4238 included participants (mean age 60 years, 49.9% male), TAC score had a highly skewed distribution with a median Agatston-score of 20.04 (IQR: 143.31). PM2.5, and Lnight were independently associated with increasing TAC-burden (19.9% [95%CI 8.2; 32.8%] per 2.4µg/m3 PM2.5, and 4.8% [95%CI 0.8; 8.9%] per 5 dB Lnight, respectively), while Lden was not associated with TAC. The effect of PM on TAC was not modified by high traffic noise exposure and vice versa. We observed an interaction of PM2.5 with several personal participant characteristics, displaying clearly stronger associations for younger participants (<65 years), participants with prevalent CAD and participants taking statin medication. In contrast, the effect of Lnight was stronger in non-obese, participants without CAD and without statin medication.
Conclusions: Long-term exposure to fine PM air pollution and night-time road traffic noise are independently associated with thoracic aortic calcification, a measure of subclinical atherosclerosis.