Smoking a pack (or two) of cigarettes each day is obviously not good for your lungs. But for those who enjoy an occasional smoke, an obvious question is, “How many cigarettes can I smoke before I start to do some damage?”
The sobering answer: Zero.
That’s the conclusion of a new study from researchers at Weill Cornell Medical College and Cornell University in New York.
The researchers recruited 121 healthy volunteers to pee into a cup and submit to a bronchoscopy, a procedure that included removing cells from the lining of the part of the airway that would first come into contact with inhaled smoke.
Smoking status was determined based on levels of nicotine and cotinine (a chemical produced in the body as nicotine is metabolized) found in their urine. The 40 people with undetectable levels of nicotine and cotinine were classified as nonsmokers; those with low levels were considered occasional smokers or people exposed to secondhand smoke; and those with high levels were considered regular smokers.
By comparing the lung biopsies from regular smokers to those from nonsmokers, the researchers identified 372 genes whose expression was triggered by tobacco smoke. Then they checked to see what those genes were doing in the occasional smokers. It turned out that 128 of those genes (34%) had been activated -- presumably by cigarettes -- including 41 (11%) that were “significantly modified,” according to the study.
Next, the researchers checked to see how much nicotine and cotinine had to be in the urine before changes in the lung cell genes were noticeable. For nicotine, that level was a mere 1.8 nanograms per milliliter -- too low to be picked up in tests. In other words, “there was no detectable level” of nicotine that was considered harmless, the researchers wrote. For cotinine, the threshold was 11 ng/ml, only slightly higher than the amount that the most sensitive tests can detect.
Digging further, the researchers found that the two groups of genes that responded most strongly in the occasional smokers were the same two groups that are most active in regular smokers. “These changes in gene expression are likely the earliest biologic abnormalities in the small airway epithelium that lead to clinically detectable lung disease,” they wrote.
Considering that so many people are exposed to secondhand smoke or partake in an occasional cigarette, the findings are significant, they concluded.
The study was published online this month in the American Journal of Respiratory and Critical Care Medicine.
-- Karen Kaplan/Los Angeles Times