As anti-smoking groups like the American Council on Science and Health have long contended, while nicotine may be addictive, so are lots of things, from video games to coffee. It's the toxins in cigarette smoke that will kill you.
For that reason, public-health oriented anti-smoking groups have embraced nicotine vaping devices ("e-cigarettes") as one tool in the tool chest of harm reduction and (preferably) smoking cessation. Yet some smoking groups, and even the U.S. Centers for Disease Control and Prevention, have migrated from being a war on cigarettes to being in war on some tobacco products, including nicotine vapor yet, oddly, not nicotine gums and patches.
New evidence shows that in at least one area, gene expression, those groups should abandon their 'quit or die' mentality that bolsters cigarette companies. A new study found changes in the expression levels of 123 genes when reconstituted lung tissue was exposed to cigarette smoke, compared to only two genes following exposure to e-cigarette aerosols.
The paper also reported increased levels of several cytokines, which are biomarkers of inflammation, in the lung tissue model exposed to cigarette smoke. Expression doesn't mean a bad thing, but as the Atlanta Falcons discovered in the Super Bowl yesterday, what Woody Hayes long said about passing the ball was true; three things can happen when you throw the ball, and two of them are bad.
And in gene expression, things are just as tricky, so the less of it the better when you don't know what will happen or why.
Anisha Banerjee and coauthors from British American Tobacco R&D Centre (Southampton, U.K.) used a commercially available 3D airway culture system comprised of reconstituted human epithelium, which mimics the structure and functions of human lung tissue.
The researchers demonstrated how this model system, together with a protocol designed to deliver matched, repeated exposures to smoke or aerosol over a short period, can be applied in the laboratory to assess potential toxicity.
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