NEW YORK, Jul 07 (Reuters) -- African-American smokers tend to have higher levels of cotinine, a breakdown product of nicotine, in their blood than whites, according to a study in the July 8th issue of The Journal of the American Medical Association.
And a second report in the same journal suggests that blacks process cotinine more slowly than whites or Mexican Americans.
These factors may help explain why black smokers have a lower success rate in stopping smoking, and why they are at greater risk than whites for developing and dying from lung cancer, say researchers.
In the first report, Dr. Eliseo J. Perez-Stable and colleagues, of the University of California at San Francisco, gave infusions of nicotine and cotinine to 40 non-Latino blacks and 39 non-Latino whites, then analyzed blood and urine samples. Both groups of smokers averaged about 14 cigarettes per day.
Laboratory results showed that cotinine levels were 50% higher in blacks than in whites, the California researchers report, even though the two groups smoked similar numbers of cigarettes.
The investigators estimated that nicotine intake per cigarette was 30% greater in blacks than in whites. They also found that cotinine was slower to leave the bodies of black smokers than those of white smokers.
"One possible explanation for these differences is that there may be a racial genetic difference in cotinine metabolism," Perez-Stable's group proposes.
In the second report, Dr. Ralph S. Caraballo and colleagues at the Centers for Disease Control and Prevention in Atlanta, Georgia, found racial differences in blood levels of cotinine irrespective of the number of cigarettes smoked.
The researchers reviewed data from 2,136 smokers, aged 17 years or older, who had their blood levels of cotinine measured as part of a nationwide healthy survey. All subjects reported smoking at least one cigarette in the 5 days before the cotinine measurement, and they had not used other sources of nicotine.
Black smokers had significantly higher cotinine levels than white or Mexican American smokers at all levels of cigarette exposure, the research team found. The difference persisted after the researchers adjusted the data for the effects of secondhand smoke exposure at home and at work.
Caraballo's group calls for additional research to determine whether high cotinine levels indicate "higher nicotine intake and absorption," or perhaps "higher exposure to other cigarette components," such as cancer-causing substances in cigarette smoke.
There are genetic variations in the enzymes that break down nicotine and cotinine into inactive substances, Dr. Edward M. Sellers, of the University of Toronto, Ontario, Canada, explains in an accompanying editorial.
Sellers concludes that "these variants may contribute to the risk of becoming addicted to nicotine and influence individual risks for smoking- related health consequences."
"For individuals who smoke, an understanding of the risk factors that lead to tobacco dependence should lead to improved strategies for harm reduction," Sellars concludes.
SOURCE: The Journal of the American Medical Association 1998;280:135-139,152-156,179-180.
