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Cigarette Smoking among Adolescents in Northwest Ohio: Correlates of Prevalence and Age at Onset  [PDF]
Sadik A. Khuder,James H. Price,Timothy Jordan,Saja S. Khuder,Kathi Silvestri
International Journal of Environmental Research and Public Health , 2008, DOI: 10.3390/ijerph5040278
Abstract: This study examined the prevalence and correlates of smoking initiation among adolescents. We have used data from adolescents (n=5,392) ages 10-18 who participated in the 2003 Tobacco Survey, a representative sample of adolescents in Northwest Ohio. A selfreport of cigarette smoking was obtained using a questionnaire administered in classrooms. Data were analyzed using weighted chi-square and multiple logistic regressions in SAS that accounted for the survey design. The prevalence rates for adolescents that ever tried smoking were 7.4% in elementary (grades 4-5); 17.7% in middle (grades 6-8), and 41.4% in high (grades 9-12) schools, respectively. The highest prevalence rate was among Hispanics. Having a close friend that smoked and a smoker at home correlated significantly with both initiation of smoking and smoking at an earlier age. Smoking was correlated with low academic achievement among adolescents in all grades. Students who reported smoking by parents or siblings were significantly more likely to start smoking at an earlier age, compared to other students living in a non-smoking home environment. Smoking prevention program should include components focused on adolescents’ home environment and should start as early as the 4th grade.
Genetic analyses of smoking initiation, persistence, quantity, and age-at-onset of regular cigarette use in Brazilian families: the Baependi Heart Study
Andréa RVR Horimoto, Camila M Oliveira, Suely R Giolo, Júlia P Soler, Mariza de Andrade, José E Krieger, Alexandre C Pereira
BMC Medical Genetics , 2012, DOI: 10.1186/1471-2350-13-9
Abstract: The data set consisted of 1,694 individuals enrolled in the Baependi Heart Study. The heritability and the heterogeneity in genetic and environmental variance components by gender were estimated from variance components approaches, using the SOLAR (Sequential Oligogenic Linkage Analysis Routines) computer package. The mixed-effects Cox model was used for the genetic analysis of the age-at onset of regular cigarette use.The heritability estimates were high (> 50%) for smoking initiation and were intermediate, ranging from 23.4 to 31.9%, for smoking persistence and quantity. Significant evidence for heterogeneity in variance components by gender was observed for smoking initiation and age-at-onset of regular cigarette use. Genetic factors play an important role in the interindividual variation of these phenotypes in females, while in males there is a predominant environmental component, which could be explained by greater social influences in the initiation of tobacco use.Significant heritabilities were observed in smoking phenotypes for both males and females from the Brazilian population. These data add to the literature and are concordant with the notion of significant biological determination in smoking behavior. Samples from the Baependi Heart Study may be valuable for the mapping of genetic loci that modulate this complex biological trait.Annually, tobacco smoking is responsible for 5.4 million deaths worldwide [1], with more than 200,000 occurring in Brazil alone. Although smoking prevalence is decreasing as a result of public policies for the prevention and control of the tobacco epidemic, approximately 15.1% of Brazilian adults continue to smoke, with prevalence higher among males (17.9%) than females (12.7%) [2].The natural history of addiction to nicotine can be characterized in stages. An individual first tries a puff or two, and eventually smokes a whole cigarette. Those who experience particular reinforcing biological or psycho-social influences will con
Early onset lung cancer, cigarette smoking and the SNP309 of the murine double minute-2 (MDM2) gene
Kirstin Mittelstrass, Wiebke Sauter, Albert Rosenberger, Thomas Illig, Maria Timofeeva, Norman Klopp, Hendrik Dienemann, Eckart Meese, Gerhard Sybrecht, Gabi Woelke, Mathias Cebulla, Maria Degen, Harald Morr, Peter Drings, Andreas Groeschel, Karsten Kreymborg, Karl Haeu?inger, Gerd Hoeffken, Christine Schmidt, Bettina Jilge, Wilhelm Schmidt, You-Dschun Ko, Dagmar Taeuscher, Jenny Chang-Claude, Heinz-Erich Wichmann, Heike Bickeboeller, Angela Risch
BMC Cancer , 2008, DOI: 10.1186/1471-2407-8-113
Abstract: We used 635 Caucasian patients diagnosed with lung cancer before 51 years of age and 1300 healthy gender and age frequency matched population Caucasian controls to investigate the association between the MDM2 SNP309 and the risk of developing early onset lung cancer. Conditional logistic models were applied to assess the genotype-phenotype association, adjusted for smoking.Compared to the GG genotype, the adjusted ORs for the TG and TT genotype were 0.9 (95% CI: 0.7–1.5) and 1.0 (95% CI: 0.7–1.5), respectively. Also no association was found for histological subtypes of lung cancer. The strength of this study is that within young cases the genetic component to develop lung cancer may be greater. Our results indicate that the MDM2 SNP309 is not significantly associated with lung carcinogenesis but point towards gender-specific differences.Human cells have developed a complex system to protect themselves from genotoxic damage where the p53 tumor suppressor gene plays an important role in protecting against such insults by serving as an integrator of the signals produced by DNA damage. The MDM2 protein inhibits p53 transactivation activity and promotes its export from the nucleus by binding to the transcriptional activation domain of p53 [1] and acts as an ubiquitin ligase upon p53 pushing fast degradation of the suppressor [2,3].Recently, a SNP (SNP309, G2580T) at the intronic p53-response promoter of MDM2 was identified and associated with altered Sp1 binding affinity and expression levels of MDM2 RNA and protein [4]. Contradictory results were reported regarding the MDM2 SNP309 association with lung cancer [5-8]. In addition the polymorphism was correlated with a decreased age at the time of lung cancer diagnosis in Li-Fraumeni syndrome and sporadic sarcoma patients [4]. Our study is the first report on a large German case-control study of young lung cancer patients (age of onset < 51 years) investigating the MDM2 SNP 309.The study population consists of 635 lung can
Cigarette Smoking and Dyspnea Perception
Rosi Elisabetta,Scano Giorgio
Tobacco Induced Diseases , 2004, DOI: 10.1186/1617-9625-2-3
Abstract: Cigarette smoking has been implicated as an important risk factor for the development of respiratory symptoms in adults. The relationship of dyspnea with cigarette smoking has been examined in smokers and ex-smokers and the beneficial effects of smoking cessation have been demonstrated. Recent studies reported that in subjects who smoke cigarettes the risk of developing respiratory symptoms is higher in a dose-dependent way. Environmental tobacco smoke heavily influences the incidence of respiratory symptoms in both adults and in children. Up to the present time, the mechanisms whereby cigarette smoking causes dyspnea perception remain to be defined. Abnormalities in sensory nerves might diminish the perception of bronchoconstriction in smokers. In this regard, it has been postulated that prolonged exposure to cigarette smoke may lead to chronic depletion of sensory nerve neurotransmitters. Eosinophil airway inflammation has been proposed as a determinant of breathlessness via mechanisms affecting either the mechanical pathways that control breathlessness or the afferent nerves involved in perception of dyspnea. An increased number of eosinophils in some smokers implies the possibility that smoking may trigger immunological or other reactions associated with eosinophilia. In conclusion, cigarette smoking is by far one of the greatest risk factors for most respiratory symptoms, including dyspnea. Smoking is associated with the development of symptoms in a dose-dependent way and eosinophilia and airway hyperresponsiveness (AHR) increase the risk of developing dyspnea.
Cigarette Smoking and Fertility
S. Soares
Reproductive Biology Insights , 2012,
Abstract: A strong body of evidence indicates that the negative effect of cigarette smoking on fertility comprises fairly every system involved in the reproductive process. The impact of cigarette smoking on ovarian reserve is clearly evidenced by younger age at menopause of smokers. Tobacco compounds’ impairment of the process of ovarian follicle maturation is expressed by worse in-vitro fertilization parameters in cycles performed on women with smoking habits. Also, uterine receptiveness and tubal function are significantly altered by the smoking habit. In men, cigarette smoking reduces sperm production, increases oxidative stress, and DNA damage. Spermatozoa from smokers have reduced fertilizing capacity, and embryos display lower implantation rates. Couples at reproductive age should be strongly discouraged to smoke.
Cigarette Smoking and Lung Cancer: Pediatric Roots  [PDF]
Norman Hymowitz
Lung Cancer International , 2012, DOI: 10.1155/2012/790841
Abstract: A vast array of data suggests that early age of smoking onset enhances the risk for development of lung cancer in adulthood. Initiation of smoking at a young age may influence the development of lung cancer because of its effect on duration of smoking. Early onset of smoking also may serve as an independent risk factor. It may increase the likelihood that smoking occurs during a critical period of development that enhances susceptibility to the adverse effects of cancer causing agents in cigarette smoke, thereby facilitating the initiation of the carcinogenic process. While evidence for the latter hypothesis derives from a variety of sources, definitive proof has proven elusive. Whether or not early age of smoking serves as an independent risk factor for lung carcinogenesis, the consensus of the public health community is that prevention of smoking onset at a young age and early cessation are keys to stemming the current lung cancer pandemic. Population approaches to tobacco prevention and control, such as measures contained in the World Health Organization Framework Convention Tobacco Control Treaty, offer the best opportunity, on the scale needed, to create a smoke-free world and bring an end to the pandemic of tobacco-related disease. 1. Introduction Cigarette smoking has been called a pediatric disease [1]. Worldwide, between 82,000 and 99,000 young people begin smoking every day, 80% of them from low-income countries [2]. If current trends continue, more than 200 million young people under the age of 20 will die prematurely from tobacco-related diseases. More immediate effects on child health include higher rates of cough, fatigue and shortness of breath, and shortness of breath on exertion than youth who do not smoke. Those who smoke also are more prone to allergies, respiratory and ear infections, enhanced risk of asthma, and impaired lung growth [2]. In addition to immediate effects of cigarette smoking, early age at initiation of smoking increases the risk of lung cancer [3] and cardiovascular disease [4] during their life time. Of the organ sites at which smoking is known to cause cancer, smoking-associated genotoxic effects have been found for oral nasal, esophagus, pharynx, lung, pancreas, myeloid organs, bladder/ureter, and uterine cervix [2]. In addition to permanent changes in DNA, the reversibility of cancer risk after smoking cessation implies a role for epigenetic factors in carcinogenesis [2]. Initiation of cigarette smoking in childhood and adolescence plays a role in the development of lung cancer by virtue of its contribution to
The effect of cigarette smoking on flexibility in Japanese  [PDF]
Kanae Oda, Nobuyuki Miyatake, Noriko Sakano, Takeshi Saito, Akihiko Katayama, Kenji Nishii, Takeyuki Numata
Health (Health) , 2012, DOI: 10.4236/health.2012.49089
Abstract: To investigate the link between cigarette smoking and flexibility in the Japanese population, we used data of 4234 men and 9169 women, aged 20-79 years, in this cross-sectional investigation study. Flexibility such as sit and reach were measured. In addition, habits of cigarette smoking and exercise were obtained by well-trained medical staff. The effect of cigarette smoking on flexibility was evaluated. A total of 1613 men (38.1%) and 995 women (10.9%) were having habits of cigarette smoking. Flexibility in men was decreased with aging and that in women increased with aging under 60’s. Flexibility in subjects with cigarette smoking was significantly lower than that in subjects without cigarette smoking even after adjusting for age and exercise habits in both sexes. Cigarette smoking might be modifiable factor of flexibility in the Japanese.
Cigarette Smoking in Iran
A Meysamie,R Ghaletaki,N Zhand,M Abbasi
Iranian Journal of Public Health , 2012,
Abstract: Background: Cigarette smoking is the largest preventable cause of death worldwide. No systematic review is available on the situation of the smoking in Iran, so we decided to provide an overview of the studies in the field of smoking in Iranian populations.Methods: Published Persian-language papers of all types until 2009 indexed in the IranMedex (http://www.iranmedex.com) and Magiran (http://www.magiran.com). Reports of World Health Organization were also searched and optionally employed. The studies concerning passive smoking or presenting the statistically insignificant side effects were excluded. Databases were searched using various combinations of the following terms: cigarette, smoking, smoking cessation, prevalence, history, side effects, and lung cancer by independent reviewers. All the 83 articles concerning the prevalence or side effects of the smoking habit in any Iranian population were selected. The prevalence rate of daily cigarette smoking and the 95% confidence interval as well as smoking health risk associated odds ratio (OR) were retrieved from the articles or calculated.Results: The reported prevalence rates of the included studies, the summary of smoking-related side effects and the ORs (95%CI) of smoking associated risks and the available data on smoking cessation in Iran have been shown in the article.Conclusion: Because of lack of certain data, special studies on local pattern of tobacco use in different districts, about the relationship between tobacco use and other diseases, especially non communicable diseases, and besides extension of smoking cessation strategies, studies on efficacy of these methods seems to be essential in this field.
Menthol and initiation of cigarette smoking
Rising Joshua,Wasson-Blader Kristina
Tobacco Induced Diseases , 2011, DOI: 10.1186/1617-9625-9-s1-s4
Abstract: The use of tobacco products would not continue without the initiation of their use by youth and adults. Since the vast majority of cigarette smokers begin smoking by age 25, understanding the role of menthol cigarettes in the initiation of smoking in youth (under the age of 18) and young adults (aged 18–25) is especially relevant. Data demonstrate that menthol cigarettes are disproportionately used by youth and young adults. This review seeks to examine what role, if any, menthol plays in the initiation of cigarette smoking. Overall, there is a paucity of data on this topic. The data that do exist suggests that youth who have smoked for less than 1 year are more likely to smoke menthol cigarettes than youth who have smoked for more than 1 year. A lack of data prevents further conclusions on the role of menthol cigarettes in the initiation of smoking.
Cigarette smoking and DNA methylation  [PDF]
Ken W. K. Lee,Zdenka Pausova
Frontiers in Genetics , 2013, DOI: 10.3389/fgene.2013.00132
Abstract: DNA methylation is the most studied epigenetic modification, capable of controlling gene expression in the contexts of normal traits or diseases. It is highly dynamic during early embryogenesis and remains relatively stable throughout life, and such patterns are intricately related to human development. DNA methylation is a quantitative trait determined by a complex interplay of genetic and environmental factors. Genetic variants at a specific locus can influence both regional and distant DNA methylation. The environment can have varying effects on DNA methylation depending on when the exposure occurs, such as during prenatal life or during adulthood. In particular, cigarette smoking in the context of both current smoking and prenatal exposure is a strong modifier of DNA methylation. Epigenome-wide association studies have uncovered candidate genes associated with cigarette smoking that have biologically relevant functions in the etiology of smoking-related diseases. As such, DNA methylation is a potential mechanistic link between current smoking and cancer, as well as prenatal cigarette-smoke exposure and the development of adult chronic diseases.
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