Copper hydroxide nanoparticles provide protection against toxic oxygen radicals in cigarette smoke

Chemists at Johannes Gutenberg University Mainz (JGU) have developed a technique that reduces the toxic effects of commercially available cigarettes. In spite of the fact that the World Health Organization (WHO) estimates that some 6 million people die every year as a consequence of tobacco consumption, the number of smokers around the world is on the rise. The number of tobacco-related deaths is equivalent to the fatality rate that would occur if a passenger plane were to crash every hour. According to figures published by the German Federal Statistical Office, the tobacco industry generated a turnover of around EUR 20.5 billion in 2016 through the sale of cigarettes in Germany alone.

Quantitative study of aldehyde content in electronic cigarettes

(—Electronic cigarettes have had their share of both detractors and advocates since they hit the market in 2004. Many people believe that they are healthier than cigarettes, but others say that the effects of e-cigarette vapors are largely unknown. Medical organizations have generally taken a cautious approach and do not specifically recommend e-cigarettes for stopping smoking or as a healthier alternative to smoking.

How to measure potentially damaging free radicals in cigarette smoke

Smoking cigarettes can lead to illness and death. Free radicals, which are atoms or groups of atoms with unpaired electrons, in inhaled smoke are thought to be partly responsible for making smokers sick. Now researchers report in ACS’ journal Chemical Research in Toxicology a method for measuring free radicals in cigarette smoke that could help improve our understanding of the relationship between these substances and health.

Novel Methodologies and the Need for Big Data in Nicotine and Tobacco Genetics Research

<span class=”paragraphSection”>Tobacco use is a complex polygenic disorder and continues to be the leading cause of preventable death worldwide.<sup><a href=”#CIT0001″ class=”reflinks”>1–3</a></sup> The present issue highlights seven original investigations that address some of the complexities and gaps in the state of the science with innovative methods.</span>

A Genetic Epidemiological Mega Analysis of Smoking Initiation in Adolescents

<span class=”paragraphSection”><div class=”boxTitle”>Abstract</div><div class=”boxTitle”>Introduction:</div>Previous studies in adolescents were not adequately powered to accurately disentangle genetic and environmental influences on smoking initiation (SI) across adolescence.<div class=”boxTitle”>Methods:</div>Mega-analysis of pooled genetically informative data on SI was performed, with structural equation modeling, to test equality of prevalence and correlations across cultural backgrounds, and to estimate the significance and effect size of genetic and environmental effects according to the classical twin study, in adolescent male and female twins from same-sex and opposite-sex twin pairs (<span style=”font-style:italic;”>N</span> = 19 313 pairs) between ages 10 and 19, with 76 358 longitudinal assessments between 1983 and 2007, from 11 population-based twin samples from the United States, Europe, and Australia.<div class=”boxTitle”>Results:</div>Although prevalences differed between samples, twin correlations did not, suggesting similar etiology of SI across developed countries. The estimate of additive genetic contributions to liability of SI increased from approximately 15% to 45% from ages 13 to 19. Correspondingly, shared environmental factors accounted for a substantial proportion of variance in liability to SI at age 13 (70%) and gradually less by age 19 (40%).<div class=”boxTitle”>Conclusions:</div>Both additive genetic and shared environmental factors significantly contribute to variance in SI throughout adolescence. The present study, the largest genetic epidemiological study on SI to date, found consistent results across 11 studies for the etiology of SI. Environmental factors, especially those shared by siblings in a family, primarily influence SI variance in early adolescence, while an increasing role of genetic factors is seen at later ages, which has important implications for prevention strategies.<div class=”boxTitle”>Implications:</div>This is the first study to find evidence of genetic factors in liability to SI at ages as young as 12. It also shows the strongest evidence to date for decay of effects of the shared environment from early adolescence to young adulthood. We found remarkable consistency of twin correlations across studies reflecting similar etiology of liability to initiate smoking across different cultures and time periods. Thus familial factors strongly contribute to individual differences in who starts to smoke with a gradual increase in the impact of genetic factors and a corresponding decrease in that of the shared environment.</span>