E-cigarette smoke damages DNA and reduces repair activity in mouse lung, heart, and bladder as well as in human lung and bladder cells
- Proceedings of the National Academy of Sciences of the United States of America
- Published almost 2 years ago
E-cigarette smoke delivers stimulant nicotine as aerosol without tobacco or the burning process. It contains neither carcinogenic incomplete combustion byproducts nor tobacco nitrosamines, the nicotine nitrosation products. E-cigarettes are promoted as safe and have gained significant popularity. In this study, instead of detecting nitrosamines, we directly measured DNA damage induced by nitrosamines in different organs of E-cigarette smoke-exposed mice. We found mutagenic O6-methyldeoxyguanosines and γ-hydroxy-1,N2 -propano-deoxyguanosines in the lung, bladder, and heart. DNA-repair activity and repair proteins XPC and OGG1/2 are significantly reduced in the lung. We found that nicotine and its metabolite, nicotine-derived nitrosamine ketone, can induce the same effects and enhance mutational susceptibility and tumorigenic transformation of cultured human bronchial epithelial and urothelial cells. These results indicate that nicotine nitrosation occurs in vivo in mice and that E-cigarette smoke is carcinogenic to the murine lung and bladder and harmful to the murine heart. It is therefore possible that E-cigarette smoke may contribute to lung and bladder cancer, as well as heart disease, in humans.
Electronic cigarettes (e-cigarettes) are generally recognized as a safer alternative to combusted tobacco products, but there are conflicting claims about the degree to which these products warrant concern for the health of the vapers (e-cigarette users). This paper reviews available data on chemistry of aerosols and liquids of electronic cigarettes and compares modeled exposure of vapers with occupational safety standards.
Tobacco use is the leading cause of preventable disease and death in the United States, and cigarettes are the most commonly used tobacco product among U.S. adults (1,2). To assess progress toward achieving the Healthy People 2020 target of reducing the proportion of U.S. adults who smoke cigarettes to ≤12.0% (objective TU1.1),* CDC assessed the most recent national estimates of cigarette smoking prevalence among adults aged ≥18 years using data from the 2015 National Health Interview Survey (NHIS). The proportion of U.S. adults who smoke cigarettes declined from 20.9% in 2005 to 15.1% in 2015, and the proportion of daily smokers declined from 16.9% to 11.4%. However, disparities in cigarette smoking persist. In 2015, prevalence of cigarette smoking was higher among adults who were male; were aged 25-44 years; were American Indian/Alaska Native; had a General Education Development certificate (GED); lived below the federal poverty level; lived in the Midwest; were insured through Medicaid or were uninsured; had a disability/limitation; were lesbian, gay, or bisexual; or who had serious psychological distress. Proven population-based interventions, including tobacco price increases, comprehensive smoke-free laws, anti-tobacco mass media campaigns, and barrier-free access to tobacco cessation counseling and medications, are critical to reducing cigarette smoking and smoking-related disease and death among U.S. adults, particularly among subpopulations with the highest smoking prevalences (3).
Electronic cigarettes (e-cigarettes) may help cigarette smokers quit smoking, yet they may also facilitate cigarette smoking for never-smokers. We quantify the balance of health benefits and harms associated with e-cigarette use at the population level.
Although the association between psychotic illness and cigarette smoking is well known, the reasons are unclear why people with psychosis are more likely to smoke than are the general population. We aimed to test several hypotheses. First, that daily tobacco use is associated with an increased risk of psychotic illness in both case-control and prospective studies. Second, that smoking is associated with an earlier age at onset of psychotic illness. Finally, that an earlier age at initiation of smoking is associated with an increased risk of psychosis. We also aimed to derive an estimate of the prevalence of smoking in patients presenting with their first episode of psychosis.
BACKGROUND: The Tea Party, which gained prominence in the USA in 2009, advocates limited government and low taxes. Tea Party organisations, particularly Americans for Prosperity and FreedomWorks, oppose smoke-free laws and tobacco taxes. METHODS: We used the Legacy Tobacco Documents Library, the Wayback Machine, Google, LexisNexis, the Center for Media and Democracy and the Center for Responsive Politics (opensecrets.org) to examine the tobacco companies' connections to the Tea Party. RESULTS: Starting in the 1980s, tobacco companies worked to create the appearance of broad opposition to tobacco control policies by attempting to create a grassroots smokers' rights movement. Simultaneously, they funded and worked through third-party groups, such as Citizens for a Sound Economy, the predecessor of AFP and FreedomWorks, to accomplish their economic and political agenda. There has been continuity of some key players, strategies and messages from these groups to Tea Party organisations. As of 2012, the Tea Party was beginning to spread internationally. CONCLUSIONS: Rather than being a purely grassroots movement that spontaneously developed in 2009, the Tea Party has developed over time, in part through decades of work by the tobacco industry and other corporate interests. It is important for tobacco control advocates in the USA and internationally, to anticipate and counter Tea Party opposition to tobacco control policies and ensure that policymakers, the media and the public understand the longstanding connection between the tobacco industry, the Tea Party and its associated organisations.
The disease risks from cigarette smoking increased in the United States over most of the 20th century, first among male smokers and later among female smokers. Whether these risks have continued to increase during the past 20 years is unclear.
Background The Food and Drug Administration can set standards that reduce the nicotine content of cigarettes. Methods We conducted a double-blind, parallel, randomized clinical trial between June 2013 and July 2014 at 10 sites. Eligibility criteria included an age of 18 years or older, smoking of five or more cigarettes per day, and no current interest in quitting smoking. Participants were randomly assigned to smoke for 6 weeks either their usual brand of cigarettes or one of six types of investigational cigarettes, provided free. The investigational cigarettes had nicotine content ranging from 15.8 mg per gram of tobacco (typical of commercial brands) to 0.4 mg per gram. The primary outcome was the number of cigarettes smoked per day during week 6. Results A total of 840 participants underwent randomization, and 780 completed the 6-week study. During week 6, the average number of cigarettes smoked per day was lower for participants randomly assigned to cigarettes containing 2.4, 1.3, or 0.4 mg of nicotine per gram of tobacco (16.5, 16.3, and 14.9 cigarettes, respectively) than for participants randomly assigned to their usual brand or to cigarettes containing 15.8 mg per gram (22.2 and 21.3 cigarettes, respectively; P<0.001). Participants assigned to cigarettes with 5.2 mg per gram smoked an average of 20.8 cigarettes per day, which did not differ significantly from the average number among those who smoked control cigarettes. Cigarettes with lower nicotine content, as compared with control cigarettes, reduced exposure to and dependence on nicotine, as well as craving during abstinence from smoking, without significantly increasing the expired carbon monoxide level or total puff volume, suggesting minimal compensation. Adverse events were generally mild and similar among groups. Conclusions In this 6-week study, reduced-nicotine cigarettes versus standard-nicotine cigarettes reduced nicotine exposure and dependence and the number of cigarettes smoked. (Funded by the National Institute on Drug Abuse and the Food and Drug Administration Center for Tobacco Products; ClinicalTrials.gov number, NCT01681875 .).
Despite public awareness that tobacco secondhand smoke (SHS) is harmful, many people still assume that marijuana SHS is benign. Debates about whether smoke-free laws should include marijuana are becoming increasingly widespread as marijuana is legalized and the cannabis industry grows. Lack of evidence for marijuana SHS causing acute cardiovascular harm is frequently mistaken for evidence that it is harmless, despite chemical and physical similarity between marijuana and tobacco smoke. We investigated whether brief exposure to marijuana SHS causes acute vascular endothelial dysfunction.
To estimate how far changes in the prevalence of electronic cigarette (e-cigarette) use in England have been associated with changes in quit success, quit attempts, and use of licensed medication and behavioural support in quit attempts.