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Pollution-Caused Cell Messengers Linked To CP Disease

Proinflammatory cell messengers caused by atmospheric pollutants could play an important role in cardiopulmonary disease, according to a new study.

Canadian scientists report that tiny atmospheric particles (PM10) and other forms of acute atmospheric pollution stimulate large scavenger cells in the tiny air sacs of the lung (alveolar macrophages) to produce proinflammatory intercellular messengers called cytokines which they believe play an important role in increased cardiopulmonary illness and mortality.

Epidemiological studies have shown a significant association between exposure to tiny ambient air particles and greater illness and death from cardiopulmonary disease.

The researchers cite alveolar macrophages as the most likely link between the lung inflammation process caused by air pollution and the human systemic response because these cells are responsible for ingesting and clearing inhaled particles.

Writing in the first issue for September of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine, Stephen F. van Eeden, M.D., of the Pulmonary Research Laboratory, University of British Columbia in Canada measured the proinflammatory cytokines produced by human alveolar macrophages exposed to ambient atmospheric particles of different composition and size.

The cytokines produced by the alveolar macrophages are a group of small, short-lived proteins released by one cell to regulate the function of another cell, thereby acting as intercellular messengers.

"An intriguing aspect of the epidemiologic data is that the particle health effects are also associated with disease of the cardiovascular system that does not come in contact with the particles," said Dr. van Eeden.

The researchers studied serum samples from 30 healthy males, 19 to 24 years of age, taken at the time they fought serious fires in Southeast Asia in 1997.

They also incubated other human alveolar macrophages with particle suspensions of residual oil fly ash, ambient urban particles from a large Canadian city, inert carbon particles and latex particles of various sizes.

They found that the same cytokines that elicited a systemic proinflammatory response when alveolar macrophages were exposed to urban particles were present in the serum samples collected from the young adult males during the hazy smoke period of serious Southeast Asian fires.

They postulate that these cytokines contribute to the systemic response caused by air pollution. They believe that further studies are required to establish a clear link between circulating cytokines and the adverse cardiopulmonary effects in susceptible individuals exposed to air pollution.

[Contact: Dr. Stephen F. van Eeden]






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