Both smoking and passive exposure to tobacco smoke can accelerate irreversible hardening of the arteries, according to the largest study ever to examine tobacco’s effects on atherosclerosis.
Smoking is one of the most important risk factors contributing to atherosclerosis, which causes heart attacks and strokes, according to a report to be published in today’s Journal of the American Medical Association.
The findings, according to the American Heart Association, provide strong evidence to support bans on smoking in public places.
A team headed by epidemiologist George Howard of Wake Forest University studied 10,914 people enrolled in a study of all risk factors for atherosclerosis.
They found that smokers had a 50 percent increase in the rate of plaque accumulation in the carotid arteries, ex-smokers had a 25 percent acceleration, and people passively exposed to smoke had a 20 percent increase.
The finding is surprising because scientists had not known that, unlike cigarette-induced lung damage, the cardiovascular damage may be irreversible. Nor had they previously had hard evidence that secondhand smoke could cause this type of artery damage, the researchers said.
“This is pretty striking evidence,” said Dr. Sidney Smith of the University of North Carolina, Chapel Hill. “We knew that populations who smoked had an increase in heart disease. Now we know why.”
“This is a good study … that went right to the heart of the matter,” said Dr. Aubrey Taylor of the University of South Alabama College of Medicine in Mobile. “It will be very difficult for the tobacco companies to argue it away,” added Taylor.
But Tom Lauria, a spokesman for the tobacco industry’s Tobacco Institute, argued that earlier studies “do not show any increased risk for nonsmokers. We consider the science to be inconclusive.”
The nearly 11,000 people in the Atherosclerosis Risk in Communities study were drawn from Minnesota, Maryland, Mississippi and North Carolina. All were between the ages of 45 and 64.
At the beginning of the study, researchers used ultrasound to measure the thickness of the walls of the carotid arteries, which supply blood to the brain. Three years later, the thickness was measured again.
When the team compared measurements at the beginning and end of the study, they found that the carotid artery walls of smokers had grown by 50 percent more than those of non-smokers. Those of people who had quit smoking before the study began grew by 25 percent more than those of nonsmokers.
But they found that the rate of thickening was less dependent on whether a person was smoking at the time of the study than on how much they had smoked over the course of their lifetime, as measured in pack-years. (Two packs a day for one year, for example, equals two pack-years.)
Smokers and ex-smokers who had accumulated the same number of pack-years showed the same rates of thickening. This suggests, Howard said, that the smoke triggers an irreversible process that continues long after a smoker has kicked the habit.
The researchers also found that nonsmokers exposed to significant amounts of secondhand smoke showed 20 percent more thickening than other nonsmokers.