Research currently be conducted by University of Louisville (UofL) professor Daniel J. Conklin, Ph. D, has sparked a national multi-billion dollar industry debate against regulators and health advocates. Daniel J. Conklin, Ph. D, professor in UofL’s Division of Cardiovascular Medicine, stated that he has found more potential harmful effects which indicates an exposure to e-cigarette vapor damages blood vessels within mice.
There’s evidence coming out that e-cigarette use has … genetic effects in humans that are like smoking to some degree, and that the effects in animals show … poor outcomes..
Dr. Conklin presented part of his research during an annual meeting of the American Association for the Advancement of Science in Washington, D.C. this month. An unnamed e-cigarette industry spokesman stated that e-cigarettes are still safer and continue help cigarette smokers quit, but it is the government agencies and health organizations that are voicing concerns, especially in regards to e-cigarettes luring teens into nicotine addiction.
Dr. Conklin shared new data showing that e-cigarettes have been shown to speed up atherosclerosis, a plaque-causing disease that leads to heart attack, stroke and peripheral arterial disease. Once atherosclerosis affects the arteries within the heart, it becomes coronary artery disease, a condition affecting more than 15 million Americans and causes 500,000 deaths annually. Dr. Conklin went on to say:
Currently, we do not know whether e-cigarettes are harmful. They do not generate smoke as do conventional cigarettes but they do generate an aerosol – the vapor – that alters indoor air quality and contains toxic aldehydes. We investigated the direct effects of these toxins on cardiovascular disease in the laboratory.
Dr. Conklin and his team exposed a set of mice to varying levels of e-cigarette aerosol, tobacco smoke, smokeless tobacco or to an aldehyde produced by tobacco, acrolein, which is thought to pose 80 to 85 percent of the non-cancer health risk of tobacco smoke. Another set of mice was exposed to nicotine alone to understand whether nicotine by itself had any effect. Not surprisingly and consistent with previous studies, exposure to tobacco smoke increased the amount of atherosclerosis in mice. At the same time, the research team found that either e-cigarette aerosol or smokeless tobacco exposure alone also increased atherosclerosis.
Conklin was particularly intrigued by the results seen with exposure to acrolein or nicotine alone and went on to state:
Somewhat surprising was the finding that either nicotine alone or acrolein alone at levels equivalent to those present in smokeless tobacco or mainstream smoke also increased atherosclerosis in mice. These findings indicate that multiple tobacco-derived constituents have cardiovascular disease-causing potential.