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Long-term Smoking (long-term + smoking)
Selected AbstractsA prospective study of tobacco and alcohol use as risk factors for pharyngeal carcinomas in Singapore ChineseCANCER, Issue 6 2007Jeppe T. Friborg MD Abstract BACKGROUND Nasopharyngeal carcinoma (NPC) is a rare disease in most populations; however, in areas of Southeast Asia and North Africa and in the Arctic, undifferentiated NPC is the most frequent pharyngeal malignancy. Although smoking and alcohol have been established firmly as synergistic risk factors for other pharyngeal carcinomas, previous studies on the association between these risk factors and NPC have not been consistent. Therefore, the authors analyzed this relation in a cohort of Singapore Chinese, which is a population with a high incidence of NPC. METHODS From 1993 to 1998, a population-based cohort of 61,320 Singapore Chinese ages 45 years to 74 years who were free of cancer completed a comprehensive interview on living conditions and dietary and lifestyle factors. By linkage to Singapore population-based registries, the cohort was followed through 2005, and cancer occurrence was determined. The relative risk of NPC and other oropharyngeal carcinomas in the cohort was investigated by using a Cox proportional hazards model. RESULTS In total, 173 NPCs and 75 other oropharyngeal carcinomas were observed during 601,879 person-years of follow-up. Smoking for >40 years was associated with a doubled risk of NPC (relative risk, 2.0; 95% confidence interval, 1.2,3.3), whereas smoking intensity, age at smoking initiation, and alcohol consumption were not associated with NPC risk. In contrast, smoking duration, smoking intensity, age at smoking initiation, and alcohol consumption all were associated with an increased risk of other oropharyngeal carcinoma (P for trend, <.0001). CONCLUSIONS Smoking and alcohol influenced the risk of NPC and other oropharyngeal carcinomas differently in a high-incidence NPC population. Long-term smoking was a risk factor for NPC, but alcohol consumption was not. Cancer 2007. © 2007 American Cancer Society. [source] Alterations of plasma antioxidants and mitochondrial DNA mutation in hair follicles of smokersENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 3 2002Chin-San Liu Abstract The effects of long-term smoking on mitochondrial DNA (mtDNA) deletions in hair follicles were investigated in subjects with different antioxidant capacity. Twenty-two male smokers with a smoking index of greater than 5 pack-years and without any known systemic diseases were recruited for this study. Forty healthy nonsmoking males were included as controls. We found that the concentrations of ascorbate and ,-tocopherol and the activities of glutathione S -transferase (GST) and glutathione peroxidase in blood plasma were significantly decreased in smokers. The levels of glutathione and protein thiols in whole blood and the incidence of a 4,977 bp deletion of mtDNA (dmtDNA) in hair follicles were significantly increased in smokers. A significantly higher incidence of the 4,977 bp dmtDNA was found in smokers with plasma GST activity less than 5.66 U/l (OR = 7.2, P = 0.020). Using multiple covariate ANOVA and logistic regression, we found that age and low plasma GST activity were the only two risk factors for the 4,977 bp dmtDNA. These results suggest that smoking depletes antioxidants and causes mtDNA deletions and that plasma GST may play an important role in the preservation of the mitochondrial genome in tissue cells of smokers. Environ. Mol. Mutagen. 40:168,174, 2002. © 2002 Wiley-Liss, Inc. [source] Cigarette smoking and periodontal disease among 32-year-olds: a prospective study of a representative birth cohortJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 10 2007W. Murray Thomson Abstract Background: Smoking is recognized as the primary behavioural risk factor for periodontal attachment loss (AL), but confirmatory data from prospective cohort studies are scarce. Aim: To quantify the association between cigarette smoking patterns and AL by age 32. Methods: Periodontal examinations were conducted at ages 26 and 32 in a longstanding prospective study of a birth cohort born in Dunedin (New Zealand) in 1972/1973. Longitudinal categorization of smoking exposure was undertaken using data collected at ages 15, 18, 21, 26 and 32. Results: Complete data were available for 810 individuals of whom 48.9% had ever smoked (31.5% were current smokers). Compared with never-smokers, long-term smokers (and other age-32 smokers) had very high odds ratios (ORs of 7.1 and 5.7, respectively) for having 1 +sites with 5 +mm AL, and were more likely to be incident cases after age 26 (ORs of 5.2 and 3.2, respectively). Two-thirds of new cases after age 26 were attributable to smoking. There were no significant differences in periodontal health between never-smokers and those who had quit smoking after age 26. Conclusions: Current and long-term smoking in young adults is detrimental to periodontal health, but smoking cessation may be associated with a relatively rapid improvement in the periodontium. [source] Effects of 4 months of smoking in mice with ovalbumin-induced airway inflammationCLINICAL & EXPERIMENTAL ALLERGY, Issue 12 2007B. N. Melgert Summary Background The effects of smoking on asthma pathogenesis are complex and not well studied. We have shown recently that 3 weeks of smoking attenuates ovalbumin (OVA)-induced airway inflammation in mice and that 4,6 months of smoking induces emphysema in mice without airway inflammation. Effects of combined long-term smoking and OVA exposure have not been investigated so far. Objective To study whether long-term smoking affects progression of allergic airway inflammation and/or enhances the development of emphysema in mice. Methods Mice were sensitized to OVA and challenged with saline or OVA aerosols for 6 months. From 2 months onwards, mice were also exposed to air or smoke. Lung tissue was analysed for extent of inflammation, emphysema, remodelling and for cytokine levels, and serum for OVA-specific IgE levels. Results Chronic OVA exposure of 6 months resulted in a T helper type 2 (Th2)-type inflammation with increased levels of IL-4, IL-5, IL-6 and infiltration of eosinophils, CD4+ T cells, macrophages and plasma cells. Smoking induced a Th17-type of airway inflammation, characterized by neutrophils, macrophages, B cells and increased levels of IL-17, IL-6, granulocyte-macrophage colony-stimulating factor, granulocyte colony-stimulating factor and monocyte chemoattractant protein-1. Concomittant smoking and OVA exposure resulted in inflammation similar to OVA exposure alone. OVA exposure increased IgE levels compared with saline exposure, and smoking did not further increase these levels. Conclusion We did not find evidence for increased inflammation, IgE levels or emphysema in mice with allergic airway inflammation after 4 months of smoking compared with non-smoking. However, a 4-month exposure to smoke alone did enhance neutrophilic airway inflammation characterized by high pulmonary IL-17 levels. A Th2 inflammatory environment due to OVA exposure may be one explanation as to why no further detrimental effects of smoking on allergic airway inflammation were found. [source] | ||||||||||