WINSTON-SALEM -- New research from one of the most comprehensive studies ever of middle-age Americans indicates that people who once smoked may continue to suffer from the effects of smoking even if they had quit years before.
Progression of atherosclerosis -- hardening of the arteries -- among past smokers continued at a faster rate than among nonsmokers even though the past smokers had quit smoking before the study began, said George Howard, Dr. P.H., professor of public health sciences and neurology at the Wake Forest University Baptist Medical Center.
"Atherosclerosis progression appears to be largely related to the pack-years of cigarette exposure and not to the present smoking status," Howard and his colleagues reported in today's issue of the Journal of the American Medical Association (JAMA). A pack year is the average number of packs smoked per day over the course of a year; thus a two pack-a-day smoker accumulates two pack years.
"These observations suggest that the effect of smoking on atherosclerosis may be cumulative, proportional to lifetime pack-years of exposure, and perhaps irreversible," Howard and his colleges wrote. "If this is true, the primary benefit of quitting smoking on the progression of atherosclerosis would be to prevent further accumulation of exposure."
The study also found that the effects of secondhand smoke "was surprisingly large." The rate of progression of atherosclerosis was 20 percent higher than among those who were not exposed.
The study involved 10,914 participants in Atherosclerosis Risk in Communities (ARIC) in Forsyth County, N.C., Jackson, Miss., Hagerstown, Md. and suburban Minneapolis, Minn. ARIC is an National Institutes of Health-sponsored study conceived as a successor to the famed Framingham Heart Study.
ARIC participants, all between 45 and 65 when the trial began, were carefully chosen at random from their communities at large and volunteers were not accepted, which means that ARIC can be considered an accurate reflection of the population of these four communities.
ARIC is an observational study. The health of the participants is monitored regularly, and physical condition, lifestyle, diet and other parameters are recorded, but diagnosis and treatment is left in the hands of personal physicians.
"These data represent the first report from a large population-based study of the impact of active smoking and exposure to environmental tobacco smoke on the progression of atherosclerosis," the researchers said.
The study also found:
The impact of smoking on progression of atherosclerosis was greater among people with diabetes than among nondiabetics. "A synergistic effect of smoking that may accelerate the atherosclerotic process in diabetics is plausible, given that diabetics are more likely to have widespread vascular [blood vessel] damage as a consequence of their disease," the researchers said.
Patients with high blood pressure already are more susceptible to atherosclerosis, and smoking accelerated that progression.
The degree of atherosclerosis was determined by using ultrasound to measure how much the walls of arteries thickened over a three-year period. The researchers measured the walls of the carotid artery in the neck, which runs close to the surface and supplies blood to the brain.
People were classified as exposed to secondhand smoke, known scientifically as environmental tobacco smoke (ETS), if they were in close contact with people who were smoking for more than one hour a week.
Of the 10,914 participants, 27 percent were current smokers, 17 percent were past smokers exposed to environmental tobacco smoke (ETS), 12 percent were past smokers not exposed to ETS, 22 percent were nonsmokers exposed to ETS, and 21 percent were nonsmokers who had never been exposed to ETS.
Over the three year period of the study, the walls of the arteries of current smokers thickened by an average of 41 microns, past smokers exposed to ETS by 39.6 microns, past smokers not exposed to ETS by 32.5 microns, and nonsmokers exposed to ETS by 33.2 microns.
Atherosclerosis progresses naturally anyway, averaging 27 microns over the three years of the study in the nonsmokers not exposed to ETS. A micron is .000039 inch.
So exposure to ETS increased the progression rate of atherosclerosis by a average of 6.7 microns over the three years of the study, a difference that was statistically significant. When adjusted for other cardiovascular risk factors and lifestyle factors, "the relationship between increased progression of atherosclerosis and smoking exposure was clear and consistent."
Howard and his colleagues added, "The increase in atherosclerosis attributable to this modifiable risk factor is among the most substantial of any of the cardiovascular risk factors assessed by the ARIC study."
Contact: Robert Conn, Mark Wright or Jim Steele at 910-716-4587
Journal
JAMA