May 16, 2011

How Secondhand Smoke Affects the Brain

PET scan images of 2 human brains, with the top brain showing a patch of red at center When not exposed to smoke (top image), brains show high levels (red and yellow) of a tracer molecule that binds to empty nicotine receptors. After 1 hour of exposure to secondhand smoke (bottom), nicotine displaces and reduces the level of tracer molecules.Brody et al., Archives of General Psychiatry.

Secondhand smoke has a direct, measurable impact on the brain similar to what’s seen in the person doing the smoking, according to a new study. The finding highlights the importance of limiting exposure to secondhand smoke in cars and other enclosed spaces.

Tobacco is the leading cause of preventable death nationwide. People who smoke are up to 6 times more likely than non-smokers to suffer a heart attack. Tobacco is also one of the strongest cancer-causing agents. Up to 90% of lung cancer deaths are attributed to smoking.

But the smoker isn’t the only one harmed by cigarette smoke. According to the U.S. Centers for Disease Control and Prevention, almost 50,000 deaths per year can be attributed to secondhand smoke. A Surgeon General’s Report in 2006 concluded that secondhand smoke causes heart disease and lung cancer in nonsmoking adults. It also causes serious health conditions in children, including sudden infant death syndrome, respiratory infections and more severe asthma.

Previous research has shown that exposure to secondhand smoke increases the likelihood that children will become teenage smokers and makes it more difficult for adult smokers to quit. Laboratory studies give some insight into the mechanisms at work. Nicotine, a chemical found in all tobacco products, is addictive. Long-term exposure to cigarette smoke leads to nicotine dependence in rats and an increase in nicotinic acetylcholine receptors (nAChRs) in the brain.

A team led by Dr. Arthur Brody of the University of California, Los Angeles, set out to study how secondhand smoke affects the human brain. They used an imaging technique to visualize when nicotine occupies brain nAChRs. The method depends on a special tracer molecule that binds specifically to nAChRs and can be detected by positron emission tomography (PET). Nicotine displaces the tracer molecule at the receptor, so the more nicotine that binds to nAChRs, the lower the tracer signals.

The scientists recruited 24 young adult participants — 11 moderately dependent cigarette smokers and 13 nonsmokers. The participants were given the tracer molecule and then asked to sit in the passenger’s seat of a car for 1 hour. They did this twice, a week apart. In 1 session, they were exposed to moderate secondhand smoke; in the other they weren’t. Afterward, they underwent PET scans. The study, which was partly funded by NIH’s National Institute on Drug Abuse (NIDA), appeared online on May 2, 2011, in Archives of General Psychiatry.

The researchers found that about 1 in 5 nAChRs in the brains of both smokers and non-smokers became occupied by nicotine after 1 hour of exposure to secondhand smoke. The smokers also had a significant increase in craving following exposure to secondhand smoke.

“These results show that even limited secondhand smoke exposure delivers enough nicotine to the brain to alter its function,” says NIDA Director Dr. Nora D. Volkow. “Chronic or severe exposure could result in even higher brain nicotine levels, which may explain why secondhand smoke exposure increases vulnerability to nicotine addiction.”

“This study gives concrete evidence to support policies that ban smoking in public places, particularly enclosed spaces and around children,” Brody says.

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