Meeting News Coverage

Long-term traffic pollution exposure linked to atherosclerosis

New data suggest that long-term exposure to fine particulate matter from traffic pollution may be associated with increased risk for subclinical atherosclerosis.

Previous research has shown that close proximity to traffic noise increased risk for MI; however, the specific cause of this increased risk was unknown.

Hagen Kälsh, MD, from West-German Heart Center in Essen, Germany, and colleagues examined the cause of increased CV risk associated with traffic — traffic noise, particle pollution or both. Researchers used baseline data (2000-2003) from the population-based German Heinz Nixdorf Recall Study of 4,814 participants (mean age, 60 years). Participants were assessed based on proximity to high traffic volume and measured via CT for thoracic aortic calcification as an indicator of atherosclerosis.

Results showed that proximity to major roads and small particulate matter (PM2.5) were associated with increasing thoracic aortic calcification. For every increase in particle volume up to 2.4 mcg/m3, the degree of calcification increased by 20.7%. For every 100-m proximity to heavy traffic, the degree of calcification increased by 10%. The researchers also observed a borderline increase in thoracic aortic calcification for nighttime noise (3.2% per 5 decibels). Associations of PM2.5 and road traffic noise were independent of each other.

The results were presented at EuroPrevent 2013.

“These two major types of traffic emissions [fine particulate matter air pollution and traffic noise] help explain the observed associations between living close to high traffic and subclinical atherosclerosis,” Kälsh said in a press release.

In another study presented at the meeting, French researchers reported that all main air pollutants, including carbon monoxide, nitrogen dioxide, sulfur dioxide and particulate matter measured as PM10 or PM2.5, were significantly associated with increased risk for MI. The only pollutant not implicated was ozone.

For more information:

Kälsh H. Abstract P307.

Mustafic H. Abstract P89. Both presented at: EuroPrevent; April 18-20, 2013; Rome.

Disclosure: The researchers report no relevant financial disclosures.

New data suggest that long-term exposure to fine particulate matter from traffic pollution may be associated with increased risk for subclinical atherosclerosis.

Previous research has shown that close proximity to traffic noise increased risk for MI; however, the specific cause of this increased risk was unknown.

Hagen Kälsh, MD, from West-German Heart Center in Essen, Germany, and colleagues examined the cause of increased CV risk associated with traffic — traffic noise, particle pollution or both. Researchers used baseline data (2000-2003) from the population-based German Heinz Nixdorf Recall Study of 4,814 participants (mean age, 60 years). Participants were assessed based on proximity to high traffic volume and measured via CT for thoracic aortic calcification as an indicator of atherosclerosis.

Results showed that proximity to major roads and small particulate matter (PM2.5) were associated with increasing thoracic aortic calcification. For every increase in particle volume up to 2.4 mcg/m3, the degree of calcification increased by 20.7%. For every 100-m proximity to heavy traffic, the degree of calcification increased by 10%. The researchers also observed a borderline increase in thoracic aortic calcification for nighttime noise (3.2% per 5 decibels). Associations of PM2.5 and road traffic noise were independent of each other.

The results were presented at EuroPrevent 2013.

“These two major types of traffic emissions [fine particulate matter air pollution and traffic noise] help explain the observed associations between living close to high traffic and subclinical atherosclerosis,” Kälsh said in a press release.

In another study presented at the meeting, French researchers reported that all main air pollutants, including carbon monoxide, nitrogen dioxide, sulfur dioxide and particulate matter measured as PM10 or PM2.5, were significantly associated with increased risk for MI. The only pollutant not implicated was ozone.

For more information:

Kälsh H. Abstract P307.

Mustafic H. Abstract P89. Both presented at: EuroPrevent; April 18-20, 2013; Rome.

Disclosure: The researchers report no relevant financial disclosures.

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