106 resultados para NONSMOKERS


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The purpose of this study was to assess the effect of maternal pre-pregnancy weight status on the relationship between prenatal smoking and infant birth weight (IBW). Prenatal cigarette smoking and maternal weight exert opposing effects on IBW; smoking decreases birth weight while maternal pre-pregnancy weight is positively correlated with birth weight. As such, mutual effect modification may be sufficiently significant to alter the independent effects of these two birth weight correlates. Finding of such an effect has implications of prenatal smoking cessation education. Perception of risk is an important determinant of smoking cessation, and reduced or low birth weight (LBW) as a smoking-associated risk predominates prenatal smoking counseling and education. In a population such as the US, where obesity is becoming epidemic, particularly among minority and low-income groups, perception of risk may be lowered should increased maternal size attenuate the effect of smoking. Previous studies have not found a significant interaction effect of prenatal smoking and maternal pre-pregnancy weight on IBW; however, use of self-reported smoking status may have biased findings. Reliability of self-reported smoking status reported in the literature is variable, with deception rates ranging from a low of 5% to as high as 16%. This study, using data from a prenatal smoking cessation project, in which smoking status was validated by saliva cotinine, was an opportunity to assess effect modification of smoking and maternal weight using biochemically determined smoking status in lieu of self report. Stratified by saliva cotinine, 151 women from a prenatal smoking cessation cohort, who were 18 years and older and had full-term, singleton births, were included in this study. The effect of smoking in terms of mean birth weight across three levels of maternal pre-pregnancy weight was assessed by general linear modeling procedures, adjusting for other known correlates of IBW. Effect modification was marginally significant, p = .104, but only with control for differential effects among racial/ethnic groups. A smaller than planned sample of nonsmokers, or women who quit smoking during the pregnancy, prohibited rejection of the null hypothesis of no difference in the effect of smoking across levels of pre-pregnancy weight. ^

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Previous research supports the hypothesis that a "rich" diet (i.e., high in fat and low in fiber) increases the risk of colon cancer. Previous research also supports the hypothesis that physical inactivity increases the risk of colon cancer, perhaps because physical inactivity decreases gut motility, thereby increasing tee time that carcinogens are in contact with the intestinal mucosa. Habitual physical inactivity, combined with rich diet, ordinarily results in chronic energy imbalance and gain in weight, except when energy balance is modified by disease or factors such as cigarette smoking. Cigarette smokers typically stay lean because of effects of smoking on the resting metabolic rate as well as on efficiency of caloric intake and storage. Therefore, if physical inactivity and rich diet do increase the risk of colon cancer, then weight gain during young adulthood should be positively associated with incidence of colon cancer during later life, especially in nonsmokers.^ This hypothesis was investigated in a cohort of 2,059 randomly selected middle-aged men who were employed at the Western Electric Company in Chicago and were free of clinically diagnosed cancer at initial examination in 1958. Body mass index (BMI) in middle age was calculated from measured height and weight at the initial examination. BMI at age 20 was estimated from weight at age 20 as recalled at the initial examination and height as measured at the initial examination. Change in BMI between age 20 and middle age was estimated by subtracting the BMI at 20 from the BMI in middle age. Forty-nine incident cases of colon cancer were detected during 25 years (43,326 person-years) at risk. When stratified by level of change in BMI from age 20 to middle age ($\le$1.9, 2.0-3.9, 4.0-5.9, $\ge$6.0 kg/m$\sp2$), age-adjusted relative hazards of colon cancer in never-smokers were 1.00, 1.22, 2.31, and 5.01, respectively (p for trend = 0.008); corresponding values in ever-smokers were 1.00, 0.95, 0.77, and 0.87, These associations did not change appreciably after further adjustment for BMI at age 20, subscapular-triceps skinfold ratio, cigarette smoking, consumption of alcohol, energy, fat, and calcium.^ We also investigated the hypothesis that the risk of colon cancer was higher in men who were lean at age 20 and became fat by middle age (lean-to-fat) than in men who were fat at age 20 and stayed fat in middle-age (fat-to-fat). "Lean" was defined as BMI $<$24 kg/m$\sp2$ at age 20 and as BMI $<$27.0 kg/m$\sp2$ in middle age. Among never-smokers, in comparison to men who were lean at age 20 and in middle age (lean-to-lean), the age-adjusted relative hazard of colon cancer was 1.43 in the fat-to-fat group (95% confidence interval (CI) 0.37-5.52) and 3.36 in the lean-to-fat group (95% CI 1.21-9.37). This investigation provides new results on the magnitude of risk of colon cancer associated with weight gain during adulthood (from age 20 to middle age). This relation was obscured or underestimated in previous studies due to effect-modification by cigarette smoking. Finally, the result supports the idea that a life-style characterized by chronic energy imbalance during young adulthood increases risk of colon cancer. ^

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Smokers have a significantly higher risk for developing coronary and cerebrovascular disease than nonsmokers. Advanced glycation end products (AGEs) are reactive, cross-linking moieties that form from the reaction of reducing sugars and the amino groups of proteins, lipids, and nucleic acids. AGEs circulate in high concentrations in the plasma of patients with diabetes or renal insufficiency and have been linked to the accelerated vasculopathy seen in patients with these diseases. Because the curing of tobacco takes place under conditions that could lead to the formation of glycation products, we examined whether tobacco and tobacco smoke could generate these reactive species that would increase AGE formation in vivo. Our findings show that reactive glycation products are present in aqueous extracts of tobacco and in tobacco smoke in a form that can rapidly react with proteins to form AGEs. This reaction can be inhibited by aminoguanidine, a known inhibitor of AGE formation. We have named these glycation products “glycotoxins.” Like other known reducing sugars and reactive glycation products, glycotoxins form smoke, react with protein, exhibit a specific fluorescence when cross-linked to proteins, and are mutagenic. Glycotoxins are transferred to the serum proteins of human smokers. AGE-apolipoprotein B and serum AGE levels in cigarette smokers were significantly higher than those in nonsmokers. These results suggest that increased glycotoxin exposure may contribute to the increased incidence of atherosclerosis and high prevalence of cancer in smokers.

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The decrease with age of the adrenal-secreted dehydroepiandrosterone sulfate (DHEAS) in serum has suggested that it may be causally related to longevity. For the PAQUID [People (Personnes) Aged (Agées) About What (Quid, in Latin)] cohort of elderly subjects, we have previously reported higher DHEAS in men than in women, a decrease with age and, among men, a negative correlation between the DHEAS level and mortality at 2 and 4 years. Here, with an 8-year followup in 290 subjects, we show a global decrease of 2.3% per year for men and 3.9% per year for women. However, in approximately 30% of cases, there was an increase of DHEAS. We observed no relationship between the evolution of DHEAS level and functional, psychological, and mental status, possibly because of selection by death. In women, no association was found between mortality and DHEAS level. In men, the relative risk (RR) of death was higher for the lowest levels of DHEAS (RR = 1.9, P = 0.007), with RR = 6.5, P = 0.003 for those under 70 years old, a result indicating heterogeneity of the population. There was an effect of subjective health on mortality that disappeared after adjustment of DHEAS levels, suggesting its relation with these DHEAS levels. Death RR was much higher in smokers with a low DHEAS level than in nonsmokers with high DHEAS (RR = 6.7, P = 0.001). We submit that the involvement of DHEAS is possibly different according to gender, that association between low DHEAS level and mortality only for men under 70 years old possibly reflects heterogeneity of the population, and that DHEAS level is a reliable predictor of death in male smokers.

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Objetivo: Conocer los hábitos higiénicos en el colectivo de pacientes durante su estancia en el Hospital de la Magdalena de Castellón e identificar patologías causadas por posibles hábitos higiénicos bucodentales inadecuados. Metodología: Se trata de un estudio descriptivo transversal observacional basado en datos de registro e información de pacientes y cuidadores principales. Se seleccionó una muestra de 50 pacientes en el Hospital de la Magdalena de Castellón hospitalizados. Se realizó un examen odontológico a partir de datos recogidos en un registro diseñado para tal fin. Se usó el índice de LÖE y SILNESS y el índice VIGILD M. Para evaluar la satisfacción se utiliza el test GOHAI. El análisis de los datos se realiza con el programa estadístico R, en el cual saldrán los porcentajes de las patologías BD y hábitos de higiene diarios de los pacientes hospitalizados. Resultados: La edad media de los pacientes estudiados es de 68 años; la mayoría hombres (70%). Observamos en nuestro estudio que las mujeres no fuman y que sus hábitos higiénicos, patologías encontradas son mejores que en los hombres. Sin embargo un 100% de los pacientes estudiados necesitan atención bucodental. Conclusiones: En este estudio se observan problemas de higiene bucodental en los pacientes hospitalizados en un centro de larga estancia de Castellón.

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Many studies indicate that smoking is one of risk factors influencing the accumulation of visceral fat (VFA). The mechanism by which smoking contributes to the accumulation of visceral fat is not yet fully understood, but it is assumed that smoking increases the level of plasma cortisol, causes imbalance between male and female sex hormones in women, and decreases testosterone levels in men (Chiolero et al., 2008). The objection of this study was to evaluate the effect of smoking on the accumulation of VFA in the population of the Czech Republic. The research included 1,412 individuals of both genders divided into categories of smokers vs nonsmokers and physically active vs. physically inactive. VFA was measured by the device InBody 720 and information about physical activity and smoking was collected via a questionnaire. We supposed that smokers would have a higher percentage of VFA than non-smokers. The results showed that smokers had a higher amount of VFA, but the difference was not statistically significant. In contrast, statistically significant differences were found in the waist-to-hip ratio (WHR) and total % body fat. Physically active individuals had a much more favourable results than physically inactive individuals. Remarkably, the amount of VFA, WHR and % body fat tended to be smaller in smoking men than in non-smoking men, but higher in smoking women than in non-smoking women.

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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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In recognition of a central role of the kidney in long-term blood pressure control, we undertook an in-depth analysis of the relationship between blood pressure and kidney damage caused by environmental exposure to the common pollutants cadmium and lead. The subjects were 200 healthy Thais, 16 and 60 years of age (100 female non-smokers, 53 male non-smokers, and 47 male smokers). None of these subjects had been exposed to Cd or Pb in the workplace and their urinary Cd concentrations ranged from 0.4 to 37 nM, whereas their urinary Pb concentrations ranged from 0.1 to 30 nM. The prevalence of high blood pressure was 2%, 8% and 19%, respectively in subjects with low, average and high Cd-burden (linear trend chi(2) = 6.4, P = 0.01). Multiple regression analysis revealed a significant positive association between Cd-burden and blood pressure in male nonsmokers (adjusted beta = 0.31, P = 0.02) and an inverse association between blood pressure and urinary Pb excretion rate in male smokers (adjusted beta = -0.38, P = 0.005). Associations between Cd-burden and nephropathies were evidenced by increases in urinary excretion of beta 2-microglobutin (P = 0.02) and N-acetyl-beta-D-glucosaminidase (P = 0.005) in subjects with high Cd-burden, compared with the subjects with average Cd-burden. In addition, an association between Cd-related nephropathy and high blood pressure was evidenced by a 20% increase in the prevalence of high blood pressure in people with NAG-uria (linear trend chi(2) = 4.3, P = 0.04). Our present study provides first evidence for a possible link between renal tubular damage and dysfunction caused by environmental Cd exposure and increased risk of high blood pressure. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

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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.

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Background: Costs of tobacco-related disease can be useful evidence to support tobacco control. In Hong Kong we now have locally derived data on the risks of smoking, including passive smoking. Aim: To estimate the health-related costs of tobacco from both active and passive smoking. Methods: Using local data, we estimated active and passive smoking-attributable mortality, hospital admissions, outpatient, emergency and general practitioner visits for adults and children, use of nursing homes and domestic help, time lost from work due to illness and premature mortality in the productive years. Morbidity risk data were used where possible but otherwise estimates based on mortality risks were used. Utilisation was valued at unit costs or from survey data. Work time lost was valued at the median wage and an additional costing included a value of US$1.3 million for a life lost. Results: In the Hong Kong population of 6.5 million in 1998, the annual value of direct medical costs, long term care and productivity loss was US$532 million for active smoking and US$156 million for passive smoking; passive smoking accounted for 23% of the total costs. Adding the value of attributable lives lost brought the annual cost to US$9.4 billion. Conclusion: The health costs of tobacco use are high and represent a net loss to society. Passive smoking increases these costs by at least a quarter. This quantification of the costs of tobacco provides strong motivation for legislative action on smoke-free areas in the Asia Pacific Region and elsewhere.

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PURPOSE: Research on determinants of an individual's pattern of response, considered as a profile across time, for cohort studies with multiple waves is limited. In this prospective population-based pregnancy cohort, we investigated baseline characteristics of participants after partitioning them according to their history of response to different interview waves. METHODS: Data are from the Mater-University of Queensland Study of Pregnancy 1981 to 1983 cohort, Brisbane, Australia. Complete baseline information was collected for 7223 of 7535 eligible individuals (95.9%). Follow-up occurred at 6 months, 5 years, and 14 years. Response rates were 93.0%, 72.5%, and 71.8%. Participants were allowed to leave and reenter the study. Participants were categorized as always, intermittent, or never responders. Intermittent responders were categorized further as leavers (responded at least once before leaving the study) or returners (left the study before reentering). RESULTS: Participants who always responded were older, more educated, married, Caucasian, and nonsmokers and had higher incomes. Intermittent responders shared similar baseline characteristics. Relative risk for being an intermittent responder was located between risks for always or never responding. CONCLUSIONS: Participants who left and reentered the study had baseline characteristics similar to participants who responded at least once and then left the study.

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PURPOSE. To establish an alternative method, sequential and diameter response analysis (SDRA), to determine dynamic retinal vessel responses and their time course in serial stimulation compared with the established method of averaged diameter responses and standard static assessment. METHODS. SDRA focuses on individual time and diameter responses, taking into account the fluctuation in baseline diameter, providing improved insight into reaction patterns when compared with established methods as delivered by retinal vessel analyzer (RVA) software. SDRA patterns were developed with measurements from 78 healthy nonsmokers and subsequently validated in a group of 21 otherwise healthy smokers. Fundus photography and retinal vessel responses were assessed by RVA, intraocular pressure by contact tonometry, and blood pressure by sphygmomanometry. RESULTS. Compared with the RVA software method, SDRA demonstrated a marked difference in retinal vessel responses to flickering light (P 0.05). As a validation of that finding, SDRA showed a strong relation between baseline retinal vessel diameter and subsequent dilatory response in both healthy subjects and smokers (P 0.001). The RVA software was unable to detect this difference or to find a difference in retinal vessel arteriovenous ratio between smokers and nonsmokers (P 0.243). However, SDRA revealed that smokers’ vessels showed both an increased level of arterial baseline diameter fluctuation before flicker stimulation (P 0.005) and an increased stiffness of retinal arterioles (P 0.035) compared with those in nonsmokers. These differences were unrelated to intraocular pressure or systemic blood pressure. CONCLUSIONS. SDRA shows promise as a tool for the assessment of vessel physiology. Further studies are needed to explore its application in patients with vascular diseases.

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El presente estudio exploratorio evalúa la exposición al monóxido de carbono (CO), expresado en porcentaje de carboxihemoglobina (%COHb), entre los trabajadores de los centros de control vehicular (CRV) DANTON-Cuenca. Todos los trabajadores (n=55) de los CRVs de Capulispamba y Mayancela participaron en este estudio. El %COHb se determinó a partir de muestras de sangre tomadas al inicio y final de un día laboral de febrero, abril y julio de 2013. Los resultados muestran que el %COHb se incrementó del inicio al final de la jornada laboral en ambos CRVs tanto en el grupo de trabajadores que fuman y no fumadores (P<0.001). Entre los no fumadores (N=42), el %COHb al final de la jornada sobrepasó el valor límite biológico (VLB) para COHb (3.5%) únicamente en el CRV de Mayancela (4.12%, P<0.05). Entre los fumadores (N=13), los promedios de %COHb al final de la jornada sobrepasaron los VLB en ambos CRVs. Se concluye, que los trabajadores de los CRVs de Mayancela y aquellos que fuman presentan %COHb mayores al VLB.

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Tese (doutorado)—Universidade de Brasília, Faculdade de Ciências da Saúde, Programa de Pós-Graduação em Ciências da Saúde, 2015.

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BACKGROUND: Postprandial lipemia represents a risk factor for chronic diseases, including type 2 diabetes. Little is known about the effect of dietary fat on the plasma lipidome in the postprandial period. OBJECTIVE: The objective of this study was to assess the effect of dairy fat and soy oil on circulating postprandial lipids in men. METHODS: Men (40-60 y old, nonsmokers; n = 16) were randomly assigned in a crossover design to consume 2 breakfast meals of dairy-based or soy oil-based foods. The changes in the plasma lipidome during the 4-h postprandial period were analyzed with electrospray ionization tandem mass spectrometry and included 316 lipid species in 23 classes and subclasses, representing sphingolipids, phospholipids, glycerolipids, and sterols. RESULTS: Nonparametric Friedman tests showed significant changes in multiple plasma lipid classes, subclasses, and species in the postprandial period after both dairy and soy meals. No difference was found in triglyceridemia after each meal. However, 6 endogenous lipid classes increased after dairy but decreased after soy (P < 0.05), including ether-linked phospholipids and plasmalogens and sphingomyelin (not present in soy), dihexosylceramide, and GM3 ganglioside. Phosphatidylcholine and phosphatidylinositol were not affected by the soy meal but were significantly elevated after the dairy meal (8.3% and 16%, respectively; P < 0.05). CONCLUSIONS: The changes in postprandial plasma phospholipids in men relate to the diet composition and the relative size of the endogenous phospholipid pools. Despite similar lipemic responses as measured by changes in triglyceride concentrations, the differential responses to dairy and soy meals derived through lipidomic analysis of phospholipids suggest differences in the metabolism of soybean oil and dairy fat. The increased concentrations of plasmalogens, with potential antioxidant capacity, in the postprandial period after dairy but not soy meals may represent a further important difference in the response to these sources of fat. The trial was registered at www.anzctr.org.au as ACTRN12610000562077.