Mice that were chronically exposed to cigarette smoke had severely damaged lungs and excessive inflammation resembling those in human smokers with emphysema, stated new study.

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Mice that were chronically exposed to cigarette smoke had severely damaged lungs and excessive inflammation resembling those in human smokers with emphysema.
"These opposing views on the safety of e-cigarettes prompted one of my graduate students, Matthew Madison, to investigate the effects of chronic exposure to e-cigarette vapors and to conventional tobacco smoke on murine lung function," said Kheradmand, who also holds the Nancy Chang, Ph.D. Endowed Professorship for the Biology of Inflammation Center at Baylor. "We also looked at the effect of vapors or smoke on the function of immune cells called macrophages residing within the lung. These cells represent a first line of defense against viral infections such as those caused by influenza virus."
The experimental design consisted of four groups of mice. One group was exposed to e-cigarette vapors containing nicotine in the common vaping solvents propylene glycol and vegetable glycerin, in the proportions (60/40) found in e-cigarettes. A second group received vapors with only solvents but no nicotine. These groups were compared with mice exposed to tobacco smoke or to clean air.
The mice were exposed to tobacco smoke or e-cigarette vapors for four months following a regimen equivalent to that of a person starting smoking at about teenage years until their fifth decade of life. This smoking regimen markedly increases the risk of people developing emphysema, a condition in which the lungs' air sacs are damaged causing shortness of breath.
Unexpectedly, Kheradmand, Madison and their colleagues found that the treatment with e-cigarette vapors made of propylene glycol and vegetable glycerin solvents only (no nicotine), which are currently considered to be safe solvents, also damaged the lungs. In this case, the researchers did not observe inflammation and emphysema; instead, they found evidence of abnormal buildup of lipids (fats) in the lungs that disrupted both normal lung structure and function.
"In summary, our experimental findings reveal that, independent of nicotine, chronic inhalation e-cigarette vapors disrupts normal murine lung function and reduces the ability of resident immune cells to respond to infection, increasing the susceptibility to diseases such as influenza," Kheradmand said. "Our experimental findings share similarities with previous multiple case reports describing the presence of lipid-laden macrophages in pulmonary fluid from people with e-cigarette-associated pneumonia. Our results support further investigations into the solvents used in vaping."
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