Air pollution causes healthy blood vessels to constrict

Air pollution has long been associated with respiratory and cardiovascular illness, but, until now, there has been a lack of understanding as to how the association occurs physiologically. Dr Robert D Brook, co-author of the study and Assistant Professor of Internal Medicine in the Division of Hypertension and Vascular Medicine Program at the University of Michigan, Ann Arbor, explained the significance of the study to edie: “The findings may suggest a possible reason why the rate of heart attacks and other cardiovascular events increases with exposure to air pollution for people with known heart and blood vessel disease.”

The experiment focused on 25 healthy individuals who inhaled a set concentration of atmospheric pollution consisting of fine particles and ozone. After two hours of exposure, the volunteers’ blood vessels had constricted between 2% and 4% on average. Their blood vessels did not, however, constrict following exposure to air that was free of ozone and fine particles.

The researchers used ultrasound to measure the changing diameter of the brachial artery, which runs from the shoulder to the elbow.

The study was conducted at the University of Toronto, one of the few facilities worldwide that is currently using human volunteers and which is able to accurately set desired concentrations of outdoor fine urban air particles inside special air chambers used for controlled experiments.

Fine particles belong to the size range of a diameter less than 2.5 micrometers. The majority of fine particles in the urban atmosphere are produced anthropogenically, through the burning of fossil fuels, car exhausts and industrial processes. Ozone is formed when the sun shines on these emissions. Tiny particles in the 2.5 micrometers size range have the greatest implication for the human respiratory system because they are small enough to be inhaled into the alveoli, deep inside the lungs.

The volunteers inhaled a concentration of 150 micrograms per cubic meter, about twice the level suggested by the Environmental Protection Agency (EPA) for 24 hours of exposure. Brook suggested that this exposure was equivalent to levels found in urban areas during peak pollution times such as rush-hour traffic.

All the volunteers in this experiment were healthy individuals, with an average age of 35. “Although the degree of constriction in and of itself is unlikely to produce significant problems in healthy individuals, such a constriction could conceivably trigger cardiac events in those individuals who have or are at risk of heart disease,” Brook observed.

In the U.S. the EPA estimates that in 1996 alone, air pollution contributed to 60 thousand heart-related deaths, according to figures in the federal register.

Brook explained to edie the need for more research in order to fully understand the negative effects on blood vessels caused by air pollution, and to clarify the public health implications of the findings of these initial studies. “The next stage in our research is to figure out what are the exact physiological process that are causing the vascular constriction – to see if it’s an inflammatory response to the PM 2.5,” he explained. “We also need to figure out what are the exact components of the PM 2.5 which are causing these effects – the actual components of the air pollution mixture.”

“We also need to know at what levels they affect humans,” Brook added. “We used quite high levels of atmospheric pollution, but effects may occur at much lower levels.”

In the light of increasing traffic congestion and atmospheric pollution in major cities, studies such as this will prove crucial to our understanding of the possible health implications imposed on urban populations.