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Traffic fumes may boost stroke risk

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Traffic fumes may increase the risk of stroke by narrowing the arteries that carry blood to the brain, a study has found.

Tests showed that increased exposure to sooty particles from diesel exhausts led to faster thickening of the common carotid artery.

The effect was closely tied to pollution levels, so that a reduction in exposure over time led to slower progression of blood vessel narrowing.

The right and left carotid arteries provide a vital lifeline from the heart to the head and brain.

Atherosclerosis, or thickening, of the carotid artery wall is known to increase the risk of strokes caused by depriving the brain of blood.

Previous research has also linked sooty traffic pollution to premature death, heart disease and strokes.

“Our findings help us to understand how it is that exposure to air pollution may cause the increases in heart attacks and strokes observed by other studies,” said US lead scientist Dr Sara Adar, from the University of Michigan.

The research, part of the Multi-Ethnic Study of Atherosclerosis and Air Pollution (Mesa Air), involved 5,362 people aged 45 to 84 with no history of heart disease.

Air pollution levels at the home address of each participant were estimated and linked to the results of ultrasound measurements of blood vessel thickness.

After adjusting for other factors such as smoking , the researchers found an association between higher exposure to fine sooty particles called PM2.5s and faster thickening of the carotid artery.

Even people living in the same urban district who had different levels of exposure were affected differently.

The particles, measuring up to 2.5 micrometres across, can easily lodge deep within the lungs.

“Linking these findings with other results from the same population suggests that persons living in a more polluted part of town may have a 2% higher risk of stroke as compared to people in a less polluted part of the same metropolitan area,” said Dr Adar.

Writing in the online journal Public Library of Science Medicine, the authors concluded: “If confirmed by future analysis of the full 10 years of follow-up in this cohort, these findings will help to explain certain associations between long-term PM2.5 concentrations and clinical cardiovascular events.”

Commenting on the results, Australian expert Professor Michael Moore, former director of the National Research Centre for Environmental Toxicology at the University of Queensland, said: “This is an important paper which provides further evidence of the malign effects of poor air quality.

“The association between particulates and carotid artery thickness, cannot prove that the weight measure, PM2.5, is the causative factor.

“PM2.5 may well be an indicator of other components of pollution such as nitrogen oxides, carbon monoxide or ozone. It may also be a surrogate for ultra-fine particulates.

“Future studies of concurrent pollution factors will resolve the likely mechanistic rationale for these effects.”

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