Though arteries and veins move large flows of blood around the body, tinier vessels called arterioles distribute blood to the capillaries in tissues. To regulate this microflow minute to minute according to tissues’ needs, arterioles continually dilate and constrict. An animal experiment now indicates that breathing soot and other airborne particles compromises the arterioles’ capacity to dilate.
The finding, reported in Pittsburgh in October at the Society of Environmental Journalists annual meeting, offers one explanation for epidemiological studies that have linked cardiovascular disease and polluted air (SN: 8/2/03, p. 72: Air Sickness).
A wallpaper-thin layer of cells lining arterioles throughout the body makes contact with blood. When that blood transfers dissolved nitric oxide, a molecule that carries signals between healthy tissues, this lining normally relaxes and the arteriole expands, explains Timothy R. Nurkiewicz of the West Virginia University School of Medicine in Morgantown. However, when his research team delivered tiny quantities of oily soot to the lungs of rats, arterioles in the rodents’ back muscles lost much of their responsiveness to nitric oxide. The pollutant particles were less than 2.5 micrometers in diameter, a size that can be inhaled deeply into lungs and is not now regulated as air pollution.
To check whether soot’s chemical reactivity had caused the effect on the arterioles, the scientists exposed the lungs of other mice to ostensibly inert particles of titanium dioxide. To the researchers’ great surprise, Nurkiewicz says, the vessels again proved largely unresponsive to nitric oxide.