Concept: Tobacco smoking
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 3 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.
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 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.
- Proceedings of the National Academy of Sciences of the United States of America
- Published over 7 years ago
More than 5 million deaths a year are attributable to tobacco smoking, but attempts to help people either quit or reduce their smoking often fail, perhaps in part because the intention to quit activates brain networks related to craving. We recruited participants interested in general stress reduction and randomly assigned them to meditation training or a relaxation training control. Among smokers, 2 wk of meditation training (5 h in total) produced a significant reduction in smoking of 60%; no reduction was found in the relaxation control. Resting-state brain scans showed increased activity for the meditation group in the anterior cingulate and prefrontal cortex, brain areas related to self-control. These results suggest that brief meditation training improves self-control capacity and reduces smoking.
Dust and surfaces are important sources of lead and pesticide exposure in young children. The purpose of this pilot study was to investigate if third-hand smoke (THS) pollutants accumulate on the hands of children who live in environments where tobacco is used and if hand nicotine levels are associated with second-hand smoke (SHS), as measured by salivary cotinine.
Smoking is a major public health problem. As smokers age and die prematurely, the tobacco industry must continue to recruit new, young smokers. Survey data indicate that currently in the UK around 207 000 children aged 11-15 start smoking every year. We used local data on adult smoking rates to apportion national data on child smoking uptake to specific areas. The presentation of data for individual local authorities, which now have responsibility for public health, can be used to focus attention locally. For example, this analysis demonstrates that each day, 67 children, more than two classrooms full, start smoking in London.
Conspiracist ideation has been repeatedly implicated in the rejection of scientific propositions, although empirical evidence to date has been sparse. A recent study involving visitors to climate blogs found that conspiracist ideation was associated with the rejection of climate science and the rejection of other scientific propositions such as the link between lung cancer and smoking, and between HIV and AIDS (Lewandowsky et al., in press; LOG12 from here on). This article analyses the response of the climate blogosphere to the publication of LOG12. We identify and trace the hypotheses that emerged in response to LOG12 and that questioned the validity of the paper’s conclusions. Using established criteria to identify conspiracist ideation, we show that many of the hypotheses exhibited conspiratorial content and counterfactual thinking. For example, whereas hypotheses were initially narrowly focused on LOG12, some ultimately grew in scope to include actors beyond the authors of LOG12, such as university executives, a media organization, and the Australian government. The overall pattern of the blogosphere’s response to LOG12 illustrates the possible role of conspiracist ideation in the rejection of science, although alternative scholarly interpretations may be advanced in the future.