64 resultados para cigarette smoking

em University of Queensland eSpace - Australia


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Objective: To examine the relationship between self-reported tobacco smoking and urinary cotinine concentrations in the setting of a remote Aboriginal community. Methods: In a remote Northern Territory (NT) Aboriginal community the relationship between self-reported tobacco smoking and urinary cotinine concentrations was examined as part of a cross-sectional survey of cardiovascular risk factors. Current tobacco smoking was assessed as part of a questionnaire. The concentration of cotinine and cotinine/creatinine ratio (CCR) in a spot urine sample were used as a biochemical marker of nicotine exposure. Results: A total of 237 people took part in the survey, although completed questionnaires and urine results were available for 184 people. Current tobacco smoking was reported by 161 (69 [95% Cl 63 to 75]%) people, with higher rates among males (84/104, 81 [95% Cl 72 to 88]%) than females (77/129, 60 [95% Cl 51 to 68]%, p

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The influence of cigarette smoking, body iron store status and gender on cadmium (Cd) body burden was examined in a group of 197 healthy Thais with overall mean age of 30.5 year (19-47 year). The lowest, geometric mean, and the highest urinary Cd excretion rate was 0.04, 0.46 and 3.84 mug/g creatinine, respectively. The prevalence of low iron stores (serum ferritin

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Effects of cigarette smoking and exposure to dietary cadmium (Cd) and lead (Pb) on urinary biomarkers of renal function and phenotypic variability of cytochrome P450 2A6 (CYP2A6) were investigated in a group of 96 healthy Thai men with mean age of 36.7 year (19-57 years). In non-smokers, Cd burden increased with age (r = 0.47, P < 0.001). In current smokers, Cd burden increased with both age (r = 0.45, P = 0.01) and number of cigarettes smoked per day (r = 0.32, P = 0.05). Cd-linked renal tubular dysfunction was seen in both smokers and non-smokers, but Pb-linked glomerular dysfunction was seen in smokers only, possibly due to more recent exposure to high levels of Cd and Pb, as reflected by 30-50% higher serum Cd and Pb levels in smokers than non-smokers (P < 0.05). Exposure to dietary Cd and Pb appeared to be associated with mild tubular dysfunction whereas dietary exposure plus cigarette smoking was associated with tubular plus glomerular dysfunction. Hepatic CYP2A6 activity in non-smokers showed a positive association with Cd burden (adjusted P = 0.38, P = 0.006), but it showed an inverse correlation with Pb (adjusted beta = -0.29, P = 0.003), suggesting opposing effects of Cd and Pb on hepatic CYP2A6 phenotype. In contrast, CYP2A6 activity in current smokers did not correlate with Cd or Pb, but it showed a positive correlation with serum ferritin levels (r = 0.45, P = 0.01). These finding suggest that Pb concentrations in the liver probably were too low to inhibit hepatic synthesis of heme and CYP2A6 and that the concurrent induction of hepatic CYP2A6 and ferritin was probably due to cigarette smoke constituents other than the Cd and Pb. (C) 2004 Elsevier Ireland Ltd. All rights reserved.

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This paper briefly explains why it would be unwise to use genetic and neurobiological knowledge to prevent cigarette smoking and tobacco-related disease. However implausible these uses may seem to those who are well informed about the genetics of tobacco use or tobacco-control policy, it is the preventive uses of genetic information and nicotine vaccines that most excite the interest of the media and the public. The major challenges that these approaches face need to be widely understood if we are to prevent these superfi cially attractive but controversial uses from undermining effective control policies and the development of better methods of helping smokers to quit.

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Background Non-random mating affects population variation for substance use and dependence. Developmentally, mate selection leading to positive spousal correlations for genetic similarity may result in increased risk for substance use and misuse in offspring. Mate selection varies by cohort and thus, assortative mating in one generation may produce marked changes in rates of substance use in the next. We aim to clarify the mechanisms contributing to spousal similarity for cigarette smoking and alcohol consumption. Methods Using data from female twins and their male spouses, we fit univariate and bivariate twin models to examine the contribution of primary assortative mating and reciprocal marital interaction to spousal resemblance for regular cigarette smoking and nicotine dependence, and for regular alcohol use and alcohol dependence. Results We found that assortative mating significantly influenced regular smoking, regular alcohol use, nicotine dependence and alcohol dependence. The bivariate models for cigarette smoking and alcohol consumption also highlighted the importance of primary assortative mating on all stages of cigarette smoking and alcohol consumption, with additional evidence for assortative mating across the two stages of alcohol consumption. Conclusions Women who regularly used, and subsequently were dependent on cigarettes or alcohol were more likely to marry men with similar behaviors. After mate selection had occurred, one partner's cigarette or alcohol involvement did not significantly modify the other partner's involvement with these psychoactive substances.

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This study explored influences on adoption, maintenance and cessation of smoking among young women as they experienced life transitions: leaving home, gaining employment or attending college/university, marriage and parenthood. Standardized, open-ended telephone interviews were conducted with 80 women (including never smokers, continuing smokers, recent adopters and quitters) aged 24-29 years, recruited from participants in the Australian Longitudinal Study on Women's Health. The social context of smoking (socializing with other smokers, drinking alcohol and going to pubs and clubs) was perceived to be a predominant influence on smoking from the time young women left home until they settled into a committed relationship or started their own family. Stress was identified as an important factor as they experienced lifestyle changes. An increased sensitivity to the negative aspects of smoking after turning 21 was reported, and around the mid-20s the women became concerned about the addictive nature of cigarettes. Motherhood was seen to carry increased responsibilities to protect children from passive smoking and there was a perceived importance of positive role modelling to protect children from becoming smokers themselves. This study highlights the need for public health campaigns to address the social role that smoking plays in young women's lives, and the perceived use of cigarettes for stress relief. Life changes such as settling down with a partner and the contemplation of motherhood provide opportunities for targeted interventions to promote quitting.

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Background: Describe the recent evolution of cigarette smoking habits by gender in Geneva, where incidence rates of lung cancer have been declining in men but increasing in women. Methods: Continuous cross-sectional surveillance of the general adult ( 35 - 74 yrs) population of Geneva, Switzerland for 11 years ( 1993 - 2003) using a locally-validated smoking questionnaire, yielding a representative random sample of 12,271 individuals ( 6,164 men, 6,107 women). Results: In both genders, prevalence of current cigarette smoking was stable over the 11-year period, at about one third of men and one quarter of women, even though smoking began at an earlier age in more recent years. Older men were more likely to be former smokers than older women. Younger men, but not women, tended to quit smoking at an earlier age. Conclusion: This continuous ( 1993 - 2003) risk factor surveillance system, unique in Europe, shows stable prevalence of smoking in both genders. However, sharp contrasts in age-specific prevalence of never and former smoking and of ages at smoking initiation indicate that smoking continues a long-term decline in men but has still not reached its peak in women.

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Smoking rate is disproportionately high among patients with schizophrenia, resulting in significant morbidity and mortality. However, cigarette smoking has been reported to have beneficial effects on negative symptoms, extrapyramidal symptoms, cognitive functioning and mood symptoms. Therefore, smoking cessation may worsen disability in schizophrenia. The association between smoking and these key clinical parameters was examined. Additionally, severity of smoking across four different antipsychotic treatment groups was explored. One hundred and forty-six patients with schizophrenia were assessed for smoking using expired carbon monoxide and smoking history. They were administered the Positive and Negative Symptom Scale, The Extrapyramidal Symptom Rating Scale, the Barnes Akathisia Rating Scale, Reitans Trail-making Test (A and B) and General Health Questionnaire-28. There was no difference in the chlorpromazine equivalent dose of any of the medications studied. Atypical agents were associated with significantly lower levels of smoking when compared with typical medications. There was no difference in smoking severity between the individual atypical medications examined. Similarly, there were no significant differences between smoking and non-smoking groups with regard to Positive and Negative Symptom Scale, Extrapyramidal Symptom Rating Scale, Trail-making Test and General Health Questionnaire-28. However, there was a significant difference between these groups with the smoking group demonstrating less akathisia. Smoking is not associated with positive, negative cognitive and mood symptoms in schizophrenia. Smoking is associated with lower levels of antipsychotic induced akathisia. Clinicians should not be discouraged from helping patients stop smoking for fear of worsening symptoms. However, akathisia may emerge upon cessation of smoking. Switching patients from typical to atypical antipsychotics may assist patients with schizophrenia to give up smoking.

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Current opinion contends that complex interactions between genetic and environmental factors play a role in the etiology of Parkinson's disease (PD). Cigarette smoking is thought to reduce risk of PD, and emerging evidence suggests that genetic factors may modulate smoking's effect. We used a case-only design, an approach not previously used to study gene-environment interactions in PD, specifically to study interactions between glutathione-S-transferase (GST) gene polymorphisms and smoking in relation to PD. Four-hundred PD cases (age at onset: 60.0 +/- 10.7 years) were genotyped for common polymorphisms in GSTM1, PI, T1 and Z1 using well-established methods. Smoking exposure data were collected in face-to-face interviews. The independence of the studied GST genotypes and smoking exposure was confirmed by studying 402 healthy, aged individuals. No differences were observed in the distributions of GSTM1, T1 or Z1 polymorphisms between ever-smoked and never-smoked PD cases using logistic regression (all P > 0.43). However, GSTP1 *C haplotypes were over-represented among PD cases who ever smoked (odds ratio for interaction (ORi) = 2.00 (95% Cl: 1.11-3.60, P = 0.03)). Analysis revealed that ORi between smoking and the GSTP1-114Val carrier status increased with increasing smoking dose (P = 0.02 for trend). These data suggest that one or more GSTP1 polymorphisms may interact with cigarette smoking to influence the risk for PD. (C) 2004 Elsevier Ireland Ltd. All rights reserved.

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Cadmium is a cumulative nephrotoxicant that is absorbed into the body from dietary sources and cigarette smoking. The levels of Cd in organs such as liver and kidney cortex increase with age because of the lack of an active biochemical process for its elimination coupled with renal reabsorption. Recent research has provided evidence linking Cd-related kidney dysfunction and decreases in bone mineral density in nonoccupationally exposed populations who showed no signs of nutritional deficiency. This challenges the previous view that the concurrent kidney and bone damage seen in Japanese itai-itai disease patients was the result of Cd toxicity in combination with nutritional deficiencies, notably, of zinc and calcium. Further, such Cd-linked bone and kidney toxicities were observed in people whose dietary Cd intakes were well within the provisional tolerable weekly intake (PTWI) set by the Joint Food and Agriculture Organization/World Health Organization Expert Committee on Food Additives of 1 mug/kg body weight/day or 70 mug/day. This evidence points to the much-needed revision of the current PTWI for Cd. Also, evidence for the carcinogenic risk of chronic Cd exposure is accumulating and Cd effects on reproductive outcomes have begun to emerge.

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This study investigated smoking behaviour among Indigenous youth. A sample of schools (n = 12) in north Queensland with large proportions of Indigenous students was selected. Details about the prevalence of smoking behaviour in both Indigenous and non-Indigenous students ( n = 883) were gathered. Data were also collected on the cultural, social, and psychological factors associated with cigarette smoking for Indigenous and non-Indigenous students. This survey indicated smoking rates for Indigenous and non-Indigenous students were 24% and 30%, respectively. The study found similarities between both groups regarding where they obtained their cigarettes ( friends) and their reasons for not smoking ( their parents and health). Results of this survey challenge the belief that Indigenous youth are significantly different in their smoking patterns and behaviours compared to non-Indigenous secondary school students in rural regions. It indicated the potential importance of school communities in promoting non-smoking behaviours among Indigenous students even in the face of strong normative pressures from elsewhere in the community. This survey can be used to monitor smoking prevalence among Indigenous secondary students in north Queensland, help guide the development of culturally appropriate school curriculum resources and contribute to the overall evaluation of smoking prevention and smoking cessation programs which are developed for Indigenous secondary school students.

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Although smoking is widely recognized as a major cause of cancer, there is little information on how it contributes to the global and regional burden of cancers in combination with other risk factors that affect background cancer mortality patterns. We used data from the American Cancer Society's Cancer Prevention Study II (CPS-II) and the WHO and IARC cancer mortality databases to estimate deaths from 8 clusters of site-specific cancers caused by smoking, for 14 epidemiologic subregions of the world, by age and sex. We used lung cancer mortality as an indirect marker for accumulated smoking hazard. CPS-II hazards were adjusted for important covariates. In the year 2000, an estimated 1.42 (95% CI 1.27-1.57) million cancer deaths in the world, 21% of total global cancer deaths, were caused by smoking. Of these, 1.18 million deaths were among men and 0.24 million among women; 625,000 (95% CI 485,000-749,000) smoking-caused cancer deaths occurred in the developing world and 794,000 (95% CI 749,000-840,000) in industrialized regions. Lung cancer accounted for 60% of smoking-attributable cancer mortality, followed by cancers of the upper aerodigestive tract (20%). Based on available data, more than one in every 5 cancer deaths in the world in the year 2000 were caused by smoking, making it possibly the single largest preventable cause of cancer mortality. There was significant variability across regions in the role of smoking as a cause of the different site-specific cancers. This variability illustrates the importance of coupling research and surveillance of smoking with that for other risk factors for more effective cancer prevention. (C) 2005 Wiley-Liss, Inc.

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Background and Purpose - The cause of subarachnoid hemorrhage ( SAH) is poorly understood and there are few large cohort studies of risk factors for SAH. We investigated the risk of SAH mortality and morbidity associated with common cardiovascular risk factors in the Asia-Pacific region and examined whether the strengths of these associations were different in Asian and Australasian ( predominantly white) populations. Methods - Cohort studies were identified from Internet electronic databases, searches of proceedings of meetings, and personal communication. Hazard ratios (HRs) for systolic blood pressure (SBP), current smoking, total serum cholesterol, body mass index (BMI), and alcohol drinking were calculated from Cox models that were stratified by sex and cohort and adjusted for age at risk. Results - Individual participant data from 26 prospective cohort studies ( total number of participants 306 620) that reported incident cases of SAH ( fatal and/or nonfatal) were available for analysis. During the median follow-up period of 8.2 years, a total of 236 incident cases of SAH were observed. Current smoking (HR, 2.4; 95% CI, 1.8 to 3.4) and SBP > 140 mm Hg ( HR, 2.0; 95% CI, 1.5 to 2.7) were significant and independent risk factors for SAH. Attributable risks of SAH associated with current smoking and elevated SBP ( similar to 140 mm Hg) were 29% and 19%, respectively. There were no significant associations between the risk of SAH and cholesterol, BMI, or drinking alcohol. The strength of the associations of the common cardiovascular risk factors with the risk of SAH did not differ much between Asian and Australasian regions. Conclusions - Cigarette smoking and SBP are the most important risk factors for SAH in the Asia-Pacific region.

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Background. Adolescents' intentions to smoke are generally regarded as a valid and reliable predictor of subsequent smoking. This association is largely based on research with adults and needs a more detailed analysis for adolescents. Methods. Data on intentions and smoking status were collected as part of a longitudinal, birth-cohort study when the study members were 9, 11, 13, 15, 18, and 21 years of age. Results. The results showed that intention to smoke only had an important predictive power in the subgroup of previous nonsmokers. Among those already smoking (on a monthly basis or greater), previous level of smoking was a more important predictor of future behavior than intention to smoke. In addition, the effect of positive intention to smoke was nonlinear over age and had the greatest effect at age 15. Conclusion. The results indicated that in adolescence, measurement of intentions to smoke or not smoke cannot be assumed to be a general predictor of behavior at a later age for all groups of adolescents. (C) 2004 The Institute For Cancer Prevention and Elsevier Inc. All rights reserved.