Tobacco Center Faculty Blog

September 10, 2019

Stanton A. Glantz, PhD

The Washington Post just published my oped arguing that the most important thing to come out of tobacco litigation was the truth; attorneys general and others suing drug and fossil fuel companues need to follow the tobacco precident.  Read the oped here.

September 7, 2019

Stanton A. Glantz, PhD

As health officials struggle to understand the increasing number of serious lung disease, a new experimental study using mice may provide some clues about what is going on.

Matthew Madison and his colleagues published “Electronic cigarettes disrupt lung lipid homeostasis and innate immunity independent of nicotine” in Journal of Clinical Investigation.  They exposed mice to e-cigarette aerosol without and with nicotine and found that the aerosol altered lipid (fat) balance in the lungs in ways that depressed the ability of the lung macrophages to fight infections and disrupted normal production of surfactants, chemicals in lungs that help keep the airsacs from collapsing.   This effect did not depend on the nicotine, but was related to the propylene glycol and vegetable glycerin that are the primary carriers in e-cigarettes.

September 4, 2019

Stanton A. Glantz, PhD

This ad ran in Variety and Hollywood Reporter this week.  You can download the ad and learn more here.

August 31, 2019

Stanton A. Glantz, PhD

Alessandra Caporale and colleagues recently published “Acute Effects of Electronic Cigarette Aerosol Inhalation on Vascular Function Detected at Quantitative MRI” that shows that exposure to nicotine free e-cigarette aerosol immediately inhibits normal function of blood vessels in ways similar to exposure to cigarette smoke or secondhand cigarette smoke.

They had 31 young adult never-smokers who were in good health use a nicotine-free e-cigarette, then measured the ability of their blood vessels to dilate (get bigger) in response to increased demands for blood flow.  There was also evidence that their arteries got stiffer.  These effects appeared immediately after using the e-cigarette.

These changes (reductions in so-called flow mediated dilation) are a risk factor for long-term development of heart disease and, if it occurs in people at risk of a heart attack, can be involved in triggering an event.

The fact that they found these effects in nicotine-free aerosol is more evince that other elements of the e-cigarette aerosol are causing the problems.

Here is the abstract:

August 31, 2019

Stanton A. Glantz, PhD

Robert Tarran and his colleagues at UNC recently published “Chronic E-Cigarette Use Increases Neutrophil Elastase and Matrix Metalloprotease Levels in the Lung” in American Journal of Respiratory and Critical Care Medicine.  They inserted bronchoscopes into the lungs of 14 e-cigarette users and measured levels of enzymes in their lungs.  They found high levels of protease, an enzyme that, when too high, cause emphysema by essentially dissolving lung tissue.  The levels were as high as observed in smokers.

They also studied the effect of nicotine on cultured immune cells from lungs and found that higher levels of nicotine produced more proteases.

These findings challenge the conventional wisdom among e-cigarette enthusiasts (and the FDA) that e-cigarettes are safer than cigarettes and that nicotine per se does not have any adverse health effects beyond being an addictive drug.

Here is the abstract:

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