I was thinking since the good doctor is doing so much for vaping he should have his own thread dedicated just to him and his studies!
I'll start with his latest:
A new study in mice provides no information for smokers but verifies e-cigarettes are less harmful
A new study published today in PLoS One, evaluated the effects of 2 weeks exposure to e-cigarettes on lung inflammation and immune defense against bacteria and viruses.
The authors evaluated 2 groups of mice: one exposed to clean air and one exposed to e-cigarettes. They report cotinine levels in mice similar to e-cigarette users. They evaluated pulmonary response and antibacterial (against Streptococcus pneumonia) and antiviral (against H1N1 influenza) defenses, by exposing the animals to these agents. Additionally, they measured free radicals in e-cigarette aerosol which was collected in Cambridge filters.
Concerning pulmonary response, the only effect that was statistically significant was an elevation in inflammatory cells in the bronchoalveolar lavage. Inflammatory mediators were not elevated in the e-cigarette group compared to the control group.
Concerning infection, the e-cigarette group showed impaired clearance of infectious agents and slower recovery. Mortality was elevated in e-cigarette group but was not statistically different from the control group.
Concerning free radicals, the authors found 7x1011 spins/puff compared to 1014 spins/puff for smoking (other reports have measured up to 1017 spins/puff for smoking). That is about 150 times lower compared to tobacco cigarettes.
So, what information does this study provide? Very limited I should say. First of all, the conclusions made by the authors are completely irrelevant to the study design and findings. The authors mention: “In conclusion, E-cig exposure results in immunomodulatory effects that are similar to those observed after exposure to cigarette smoke. Since bacterial and viral exacerbations are major drivers of COPD disease progression, this study raises a concern that COPD patients who switch from cigarettes to E-cigs may not observe substantial improvement in their disease progression”. This is irrelevant because they did not assess switching from tobacco to e-cigarette use. That would need a group of mice to be exposed to tobacco cigarettes, and then randomly select half of the mice to switch to e-cigarettes while the others will continue to be exposed to tobacco cigarettes. They did not do that. Moreover, they did not even include a group of mice exposed to tobacco cigarettes as a comparison. I am sure we would have seen some impressive differences. Thus, the information provided by this study is limited and irrelevant to the conclusion presented. It seems that researchers have yet to realize that e-cigarettes are marketed as smoking substitutes. Studying healthy non-smoking populations (humans or animals) to evaluate the effects of e-cigarette exposure is of limited value.
Furthermore, I have serious doubts about the findings of free radicals in e-cigarette vapor. Studies evaluating cigarette smokehave confirmed that the free radicals are derived from catechol (in the gas phase of the smoke) and from hydroquinone (in the particulate matter of the smoke). Recently, we assessed 21 e-liquids for the presence of phenols, including catechol and hydroquinone. Hydroquinone was not found in any of the liquids, while catechol was present in only 2 e-liquids, at minute quantities (the study is currently under review for publication).
The only conclusions that can be drawn from this study is that e-cigarettes should only be used by smokers as a smoking substitute and that they are by far less harmful than tobacco cigarettes (based on emitting 150 times less radicals). Any other conclusions about the probable effects of e-cigarette use on COPD patients are totally irrelevant.
http://www.ecigarette-research.com/research/index.php/whats-new/whatsnew-2015/192-ecig-mice
I'll start with his latest:
A new study in mice provides no information for smokers but verifies e-cigarettes are less harmful
A new study published today in PLoS One, evaluated the effects of 2 weeks exposure to e-cigarettes on lung inflammation and immune defense against bacteria and viruses.
The authors evaluated 2 groups of mice: one exposed to clean air and one exposed to e-cigarettes. They report cotinine levels in mice similar to e-cigarette users. They evaluated pulmonary response and antibacterial (against Streptococcus pneumonia) and antiviral (against H1N1 influenza) defenses, by exposing the animals to these agents. Additionally, they measured free radicals in e-cigarette aerosol which was collected in Cambridge filters.
Concerning pulmonary response, the only effect that was statistically significant was an elevation in inflammatory cells in the bronchoalveolar lavage. Inflammatory mediators were not elevated in the e-cigarette group compared to the control group.
Concerning infection, the e-cigarette group showed impaired clearance of infectious agents and slower recovery. Mortality was elevated in e-cigarette group but was not statistically different from the control group.
Concerning free radicals, the authors found 7x1011 spins/puff compared to 1014 spins/puff for smoking (other reports have measured up to 1017 spins/puff for smoking). That is about 150 times lower compared to tobacco cigarettes.
So, what information does this study provide? Very limited I should say. First of all, the conclusions made by the authors are completely irrelevant to the study design and findings. The authors mention: “In conclusion, E-cig exposure results in immunomodulatory effects that are similar to those observed after exposure to cigarette smoke. Since bacterial and viral exacerbations are major drivers of COPD disease progression, this study raises a concern that COPD patients who switch from cigarettes to E-cigs may not observe substantial improvement in their disease progression”. This is irrelevant because they did not assess switching from tobacco to e-cigarette use. That would need a group of mice to be exposed to tobacco cigarettes, and then randomly select half of the mice to switch to e-cigarettes while the others will continue to be exposed to tobacco cigarettes. They did not do that. Moreover, they did not even include a group of mice exposed to tobacco cigarettes as a comparison. I am sure we would have seen some impressive differences. Thus, the information provided by this study is limited and irrelevant to the conclusion presented. It seems that researchers have yet to realize that e-cigarettes are marketed as smoking substitutes. Studying healthy non-smoking populations (humans or animals) to evaluate the effects of e-cigarette exposure is of limited value.
Furthermore, I have serious doubts about the findings of free radicals in e-cigarette vapor. Studies evaluating cigarette smokehave confirmed that the free radicals are derived from catechol (in the gas phase of the smoke) and from hydroquinone (in the particulate matter of the smoke). Recently, we assessed 21 e-liquids for the presence of phenols, including catechol and hydroquinone. Hydroquinone was not found in any of the liquids, while catechol was present in only 2 e-liquids, at minute quantities (the study is currently under review for publication).
The only conclusions that can be drawn from this study is that e-cigarettes should only be used by smokers as a smoking substitute and that they are by far less harmful than tobacco cigarettes (based on emitting 150 times less radicals). Any other conclusions about the probable effects of e-cigarette use on COPD patients are totally irrelevant.
http://www.ecigarette-research.com/research/index.php/whats-new/whatsnew-2015/192-ecig-mice
