892 resultados para CIGARETTE SMOKING
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Background. This cross-sectional study was designed to evaluate the role of cigarette smoking and high-risk HPV types as risk factors of CIN 2 and 3 in young, sexually active Brazilian women. Materials and method. A series of 100 consecutive women with abnormal Pap smears were recruited, subjected to colposcopy, punch biopsy, and questionnaire for their social, sexual and reproductive factors. Of these, 77 women between 20 and 35 years of age (median 26.5 years) with biopsy-confirmed CIN 1 or CIN 2 and 3, were enrolled in this study. Representative samples from the exocervix and endocervix were obtained for HPV testing with the Hybrid Capture HPV-DNA assay, including the probes for the oncogenic HPV types (16, 18, 31, 33, 35, 45, 51, 52 and 56). Results. The overall rate of CIN 2 and 3 was 23/77 (29.8%). The women with CIN 1, 2 and 3 did not differ from each other with regard to their age, race, schooling, marital status, life-time number of sexual partners, age at first intercourse, use of oral contraceptives, or parity. However, current cigarette smoking was strongly associated with CIN 2 and 3 (p < 0,001), and among smokers, the risk of high-grade CIN increased in parallel with the time of exposure (years of smoking) p = 0.07), HPV-DNA of the oncogenic types was detected in 43 (56%) women, the risk of being HPV DNA-positive was significantly higher in CIN 2 and 3 as compared with CIN 1 (p = 0.037). Importantly, the prevalence of high-risk HPV types was significantly higher in cigarette smokers than in non-smokers (p = 0.046). Conclusions. The results indicate that the severity of CIN lesions was clearly related to two fundamental risk factors: 1) high-risk HPV types, and 2) current cigarette smoking. These two risk factors were closely interrelated in that the high-risk HPV types were significantly more frequent in current smokers than in non-smokers, suggesting the possibility of a synergistic action between these two risk factors in cervical carcinogenesis.
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Solitary keratoacanthoma (KA) is a common benign epithelial tumor of the skin characterized by rapid growth and a tendency toward spontaneous regression. The exact etiology and classification of KA are a matter of debate. Smokers also seem to be more affected than persons who never smoke. The objective of this study was to evaluate the association between solitary KA and smoking habit. A case-control study involving 78 patients diagnosed with KA and 199 controls from the related community was performed to evaluate the association between cigarette smoking and KA. A higher smoking prevalence was noted in cases (69.2 %) than controls (21.6 %) and the odds ratio adjusted for sex and age was 9.1 (95 % CI 4.9 to 17.1, p< 0.01). The mean tumoral diameter at surgery and the site of involvement was not statistically related to smoking. These findings suggest that cigarette smoking is associated with the development of KA. © 2006 Dermatology Online Journal.
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Background: Smoking impairs mucociliary clearance and increases respiratory infection frequency and severity in subjects with and without smoking-related chronic lung diseases. Objective: This study evaluated the effects of smoking intensity on mucociliary clearance in active smokers. Methods: Seventy-five active smokers were grouped into light (1-10 cigarettes/day; n = 14), moderate (11-20 cigarettes/day; n = 34) and heavy smokers (≥21 cigarettes/day; n = 27) before starting a smoking cessation programme. Smoking behaviour, nicotine dependence, pulmonary function, carbon monoxide in exhaled air (exCO), carboxyhaemoglobin (COHb) and mucociliary clearance measured by the saccharin transit time (STT) test were all evaluated. An age-matched non-smoker group (n = 24) was assessed using the same tests. Results: Moderate (49 ± 7 years) and heavy smokers (46 ± 8 years) had higher STT (p = 0.0001), exCO (p < 0.0001) and COHb (p < 0.0001) levels compared with light smokers (51 ± 15 years) and non-smokers (50 ± 11 years). A positive correlation was observed between STT and exCO (r = 0.4; p < 0.0001), STT and cigarettes/day (r = 0.3, p = 0.02) and exCO and cigarettes/day (r = 0.3, p < 0.01). Conclusion: Smoking impairs mucociliary clearance and is associated with cigarette smoking intensity. Copyright © 2013 S. Karger AG, Basel.
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Many persons in the U.S. gain weight during young adulthood, and the prevalence of obesity has been increasing among young adults. Although obesity and physical inactivity are generally recognized as risk factors for coronary heart disease (CHD), the magnitude of their effect on risk may have been seriously underestimated due to failure to adequately handle the problem of cigarette smoking. Since cigarette smoking causes weight loss, physically inactive cigarette smokers may remain relatively lean because they smoke cigarettes. We hypothesize cigarette smoking modifies the association between weight gain during young adulthood and risk of coronary heart disease during middle age, and that the true effect of weight gain during young adulthood on risk of CHD can be assessed only in persons who have not smoked cigarettes. Specifically, we hypothesize that weight gain during young adulthood is positively associated with risk of CHD during middle-age in nonsmokers but that the association is much smaller or absent entirely among cigarette smokers. The purpose of this study was to test this hypothesis. The population for analysis was comprised of 1,934 middle-aged, employed men whose average age at the baseline examination was 48.7 years. Information collected at the baseline examinations in 1958 and 1959 included recalled weight at age 20, present weight, height, smoking status, and other CHD risk factors. To decrease the effect of intraindividual variation, the mean values of the 1958 and 1959 baseline examinations were used in analyses. Change in body mass index ($\Delta$BMI) during young adulthood was the primary exposure variable and was measured as BMI at baseline (kg/m$\sp2)$ minus BMI at age 20 (kg/m$\sp2).$ Proportional hazards regression analysis was used to generate relative risks of CHD mortality by category of $\Delta$BMI and cigarette smoking status after adjustment for age, family history of CVD, major organ system disease, BMI at age 20, and number of cigarettes smoked per day. Adjustment was not performed for systolic blood pressure or total serum cholesterol as these were regarded as intervening variables. Vital status was known for all men on the 25th anniversary of their baseline examinations. 705 deaths (including 319 CHD deaths) occurred over 40,136 person-years of experience. $\Delta$BMI was positively associated with risk of CHD mortality in never-smokers, but not in ever-smokers (p for interaction = 0.067). For never-smokers with $\Delta$BMI of stable, low gain, moderate gain, and high gain, adjusted relative risks were 1.00, 1.62, 1.61, and 2.78, respectively (p for trend = 0.010). For ever-smokers, with $\Delta$BMI of stable, low gain, moderate gain, and high gain, adjusted relative risks were 1.00, 0.74, 1.07, and 1.06, respectively (p for trend = 0.422). These results support the research hypothesis that cigarette smoking modifies the association between weight gain and CHD mortality. Current estimates of the magnitude of effect of obesity and physical inactivity on risk of coronary mortality may have been seriously underestimated due to inadequate handling of cigarette smoking. ^
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This study investigates the relationship between cigarette smoking and adolescents in Ecuador, South America. Using the Social Learning Theory as a basis, the cross-sectional survey focuses attention on such social influences as the smoking habits of family members and peers as well as, the role of cigarette advertisements. Actual use prevalence, access to cigarettes and knowledge and attitudes about smoking are also obtained.^ The survey was conducted in both urban and rural areas, with 50 schools in 40 different communities participating. Two thousand four hundred and fifty-seven adolescents aged 9 to 15 years completed a self-administered questionnaire. This part of the study was conducted in collaboration with the international health organization Amigos de las Americas (AMIGOS). Staff assigned to the AMIGOS Ecuador projects worked with local health and education officials to implement the cross-sectional survey in the field.^ The key informant survey and subsequent policy review were designed to illuminate the social, cultural and institutional environment for anti-smoking activities and interventions in Ecuador. Key individuals involved with this issue on both national and local levels were interviewed. A review of past legislative efforts and present anti-smoking laws was also conducted.^ The current smoking prevalence among the study population was 8.6 percent. Findings from the cross-sectional survey revealed significant positive associations between the smoking habits of siblings and peers and the smoking behavior of the adolescents surveyed. Significant age and gender differences were also found in association with several different variables.^ The policy review found an unfavorable environment for anti-smoking efforts. Several factors contribute to this including, most importantly, lack of funding and lack of public support. The present anti-smoking law is often vague and lacks important provisions, such as a prohibition on selling tobacco products to minors.^ Together, the two surveys provide comprehensive information for the purpose of designing smoking prevention interventions. Using the results from the two surveys, recommendations for intervention are proposed. ^
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The digestive tract is colonized from birth by a bacterial population called the microbiota which influences the development of the immune system. Modifications in its composition are associated with problems such as obesity or inflammatory bowel diseases. Antibiotics are known to influence the intestinal microbiota but other environmental factors such as cigarette smoking also seem to have an impact on its composition. This influence might partly explain weight gain which is observed after smoking cessation. Indeed there is a modification of the gut microbiota which becomes similar to that of obese people with a microbiotical profile which is more efficient to extract calories from ingested food. These new findings open new fields of diagnostic and therapeutic approaches through the regulation of the microbiota.
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Little is known about the effects of smoking on inflammatory bowel diseases (IBD). However the co-occurrence of smoking and IBD often happens in ambulatory care. Smokers have a doubled risk of developing a Crohn's disease with a more active disease course. After quitting, a decrease in risk can be observed after only one year. An inverse relationship is found between smoking and ulcerative colitis. Smoking seems protective for the development of the disease and its course is less active among smokers. Smoking cessation transitorily increases the risk of developing ulcerative colitis. Nevertheless, continuing smoking cannot be justified among those patients given the risks of long-term extra-digestive effects. It is thus important to counsel all smokers with an IBD to quit smoking.
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The magnitude of the interaction between cigarette smoking, radiation therapy, and primary lung cancer after breast cancer remains unresolved. This case control study further examines the main and joint effects of cigarette smoking and radiation therapy (XRT) among breast cancer patients who subsequently developed primary lung cancer, at The University of Texas M. D. Anderson Cancer Center (MDACC) in Houston, Texas. Cases (n = 280) were women diagnosed with primary lung cancer between 1955 and 1970, between 30–89 years of age, who had a prior history of breast cancer, and were U.S. residents. Controls (n = 300) were randomly selected from 37,000 breast cancer patients at MDACC and frequency matched to cases on age at diagnosis (in 5-year strata), ethnicity, year of breast cancer diagnosis (in 5-year strata), and had survived at least as long as the time interval for lung cancer diagnosis in the cases. Stratified analysis and unconditional logistic regression modeling were used to calculate the main and joint effects of cigarette smoking and radiation treatment on lung cancer risk. Medical record review yielded smoking information on 93% of cases and 84% of controls, and among cases 45% received XRT versus 44% of controls. Smoking increased the odds of lung cancer in women who did not receive XRT (OR = 6.0, 95%CI, 3.5–10.1) whereas XRT was not associated with increased odds (OR = 0.5, 95%CI, 0.2–1.1) in women who did not smoke. Overall the odds ratio for both XRT and smoking together compared with neither exposure was 9.00 (9 5% CI, 5.1–15.9). Similarly, when stratifying on laterality of the lung cancer in relation to the breast cancer, and when the time interval between breast and lung cancers was >10 years, there was an increased odds for both smoking and XRT together for lung cancers on the same side as the breast cancer (ipsilateral) (OR = 11.5, 95% CI, 4.9–27.8) and lung cancers on the opposite side of the breast cancer (contralateral) (OR= 9.6, 95% CI, 2.9–0.9). After 20 years the odds for the ipsilateral lung were even more pronounced (OR = 19.2, 95% CI, 4.2–88.4) compared to the contralateral lung (OR = 2.6, 95% CI, 0.2–2.1). In conclusion, smoking was a significant independent risk factor for lung cancer after breast cancer. Moreover, a greater than multiplicative effect was observed with smoking and XRT combined being especially evident after 10 years for both the ipsilateral and contralateral lung and after 20 years for the ipsilateral lung. ^
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Our national focus and emphasis on the promotion of healthy behavior choices regarding tobacco and other drugs continues to target adolescents. Multiple studies have shown that adolescence is the optimum period for the prevention of substance use initiation as life-long patterns of health behaviors are established during this critical developmental stage. Tobacco use is associated with an increase in morbid and mortal health conditions of which prevalence increases throughout the lifespan. Attention to the antecedents of preventable health conditions aims to modify the risks and identify health promotion factors. Modifying antecedent factors for tobacco initiation in youth and identifying protective factors for successful smoking cessation has major public health implications across the lifespan. Of foremost interest are those risk factors and resultant behaviors that predict a youth's probability of initiating cigarette use and their cessation of cigarette use. Specifically, this dissertation supports previous results identifying intervention variables on the initiation/cessation continuum model especially with the established predictors of smoking (decisional balance and susceptibility) and with more recently identified predictors of smoking (nicotine dependence and withdrawal symptoms) in current and former smokers in a sample of high school students in Austin and Houston, Texas. These results offer insight for the development of appropriate intervention program strategies for our youth. ^
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Previous research has shown an association between mental health status and cigarette smoking. This study examined four specific mental health predictors and the outcome variable any smoking, defined as smoking one or more cigarettes in the past 30 days. The population included active duty military members serving in the United States Army, Air Force, Navy and Marine Corps. The data was collected during the 2005 Department of Defense Survey of Health Related Behaviors Among Active Duty Military Personnel, a component of the Defense Lifestyle Assessment Program. The sample size included 13,603 subjects. This cross sectional prevalence study consisted of descriptive statistics, univariate analysis, and multivariate logistic regression analysis of the four mental health predictors and the any smoking outcome variable. Multivariate adjustment showed an association between the four mental health predictors and any smoking. This association is consistent with previous literature and can help guide public health officials in the development of smoking prevention and cessation programs.^
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Epidemiologic and biochemical evidence suggest that smoking is an independent risk factor for cervical neoplasia; however, only two studies have adjusted by the potential confounding effect of human papillomavirus (HPV). To determine the association between self-reported current cigarette smoking and cervical intraepithelial neoplasia (CIN), we conducted a case-control study that controlled for HPV infection and other reported risk factors. The medical records of all new patients referred to the University of Texas M. D. Anderson Cancer Center (UTMDACC) Colposcopy Clinic were reviewed. The study population (n = 564) consisted of all white, black, and Hispanic non-pregnant women who were residents of Texas, and had no history of treatment for cervical neoplasia. Cases (n = 313) included women diagnosed at the UTMDACC with CIN; while controls (n = 251) included those patients diagnosed at the colposcopy clinic as non-CIN (negative 47%, inflammation or atypia 25%, and koilocytosis 27%). Diagnosis was based on a colposcopically directed biopsy in 95% of the subjects, and all subjects were tested for HPV by dot blot hybridization. The crude odds ratio for cigarette smoking and CIN was 1.37 (95% CI 0.97-1.95); however, after adjusting for HPV, age, education, race, number of sexual partners, and age at first sexual intercourse, the odds ratio decreased to 0.91 (95% CI 0.61-1.41). A higher crude odds ratio was observed with CIN 3 (OR = 1.75, 95% CI 1.08-2.83), but this effect also disappeared after adjustment (OR = 1.06, 95% CI 0.57-1.96). Similar results were observed when controlling only for HPV: OR = 1.11 (95% CI 0.77-1.59) for CIN combined and 1.25 (95% CI 0.76-2.08) for CIN 3. These findings suggest that cigarette smoking is not an independent risk factor for CIN in this population, and that HPV may be an important confounding factor for this association. ^