Disease relevance of Tobacco Smoke Pollution

• Adjustment was made for age; gestation; parity; cigarette smoking; passive smoking at home and at work; indoor domestic pets; family history of asthma, atopic eczema, and allergic rhinitis; family income; education; mite allergen level in house dust; changes in diet in the previous month; season when data were collected; and body mass index [1].
• To test whether postnatal nicotine exposure could contribute to the increased neuronal expression of apoptotic markers that we have previously observed in SIDS infants, as well as including study of gender influences, we developed a piglet model to mimic passive smoking in the early postnatal period [2].
• Associations between smoking, passive smoking, GSTM-1, NAT2, and rectal cancer [3].
• STUDY OBJECTIVE--To explore the relationship between self reported environmental tobacco smoke exposure (or passive smoking), the serum cotinine concentration, and evidence of respiratory or coronary disease in men and women who have never smoked [4].
• In those aged 10 to 17 years, heartburn reported by the children was associated with reported cigarette use (odds ratio, 6.5; 95% confidence interval, 2-21); no other complaint was associated with cigarette, alcohol, or caffeine consumption or passive smoking exposure [5].

Psychiatry related information on Tobacco Smoke Pollution

• Logistic regression analysis showed a significant positive association of smoking cessation with low caffeine consumption in pregnancy, many years in school, no exposure to passive smoking outside the home, and previous attempts to stop smoking [6].

High impact information on Tobacco Smoke Pollution

• Effects of environmental tobacco smoke on urinary cotinine excretion in nonsmokers. Evidence for passive smoking [7].
• RESULTS: Heart rate and blood pressure responses to adenosine triphosphate infusion were not affected by passive smoking exposure in either group [8].
• OBJECTIVE--To introduce a series of papers discussing previously undocumented tobacco industry activities regarding strategies to avoid products liability litigation, understand nicotine addiction, and manipulate both internal and external scientific research on the effects of both active and passive smoking [9].
• Passive smoking and uptake of carbon monoxide in flight attendants [10].
• Gene-by-environment interaction for passive smoking and glutathione S-transferase M1 [11]?

Chemical compound and disease context of Tobacco Smoke Pollution

• Four groups of rabbits were investigated: control (C), passive smoking of three cigarettes twice daily/30 minutes (S), control + captopril (7.5 mg/kg body weight twice daily) (Cap), and smoking + captopril (SCap) as in group 2 and 3 [12].
• There is a strong need to analyze passive smoking more than two decades before diagnosis as a confounding variable in all studies of other risk factors for breast cancer such as alcohol, dietary fat, and endogenous or exogenous estrogen [13].

Biological context of Tobacco Smoke Pollution

• Relationships of active and passive smoking to total IgE in adults of the Epidemiological Study of the Genetics and Environment of Asthma, Bronchial Hyperresponsiveness, and Atopy (EGEA) [14].
• CONCLUSION: Passive smoking in children is associated with a reduction in the cosinor mean and an increase in the amplitude of the normal circadian rhythm of airway calibre [15].
• There was a positive correlation between the prevalence of wheezing as well as allergic rhinitis and the indicators of traffic density, controlling for age, sex, nationality, passive smoking, active smoking, parental history of asthma, and so on [16].
• The data do not favor the premise that measuring urinary hydroxyproline excretion is an accurate method of investigating a lung-damaging effect of smoking, passive smoking, or air pollution [17].
• Biological monitoring of exposure to cadmium, a human carcinogen, as a result of active and passive smoking [18].

Anatomical context of Tobacco Smoke Pollution

• In both cases and controls PAH-DNA adducts in leukocytes measured by an enzyme-linked immunosorbent assay were not significantly related to age, sex, ethnicity, amount of cigarette smoking, passive smoking, dietary charcoal, or caffeine consumption [19].
• The technique of monitoring cotinine concentrations in body fluids as a means of measuring nicotine intake during passive smoking has been evaluated in two studies, both of which used intravenous infusion to stimulate nicotine intake [20].
• Toll-like receptor 2-positive and Toll-like receptor 4-positive cells in adenoids of children exposed to passive smoking [21].
• Infants exposed to passive smoking and to smoke via breast milk had N/C ratios in the range of 3.0 to 42 (median 12) and C/C ratios in the range of 225 to 870 (median 550) [22].
• These results indicate that the change in thyroid function as evaluated by serum TG concentrations observed at birth can persist at least for 1 year if the exposure to passive smoking from both parents is continued [23].

Associations of Tobacco Smoke Pollution with chemical compounds

• Serum thiocyanate in passive smoking [24].
• Previous studies have demonstrated an association of decreased HDL cholesterol with passive smoking in children but have not adjusted for potential confounding factors [25].
• Effects of passive smoking on theophylline clearance [26].
• Vitamin C prevents the acute atherogenic effects of passive smoking [27].
• OBJECTIVE: Our objective was to assess the relation between household exposure to passive smoking and serum concentrations of retinol, tocopherols, and carotenoids [28].

Gene context of Tobacco Smoke Pollution

• This study was developed to investigate the genetic influence of the whole deletion-allele of CYP2A6 on active and passive smoking behavior [29].
• Lung cancer and passive smoking [30].
• Information on passive smoking, respiratory symptoms, asthma, and allergic rhinitis was gathered through a structured interview [31].
• High density lipoprotein (HDL) cholesterol was lower in passive smoking children (p less than 0.05); the HDL2 subfraction was reduced in passive smoking boys, while the HDL3 subfraction was reduced in passive smoking girls [32].
• Exposure to passive smoking was also related to an increased risk of readmission with COPD after adjustment for clinical factors (1.63, 95% CI 1.04 to 2.57) but did not remain in the final model [33].

Analytical, diagnostic and therapeutic context of Tobacco Smoke Pollution

• Adjustment was made for potential confounding by gender, parental atopy, parental education, number of older siblings, day care outside the home and passive smoking [34].
• Properly selected McAb offer distinct advantages over conventional antisera in nonisotopic immunoassays and RIAs for cotinine as a biochemical marker of active or passive smoking [35].
• Because cotinine urinalysis is a noninvasive and reliable method for the determination of passive smoking, it can be used for that purpose [36].
• This cohort study investigated postnatal serum malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) levels in 14 active-smoking, 14 passive-smoking, and 15 non-smoking mothers and their newborns on day 7 post-partum [37].

References