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In the present study the possibility of using nicotine in house dust as an index of environmental tobacco smoke (ETS) exposure was evaluated in an environmental investigation of 23 children with asthma. A standardized procedure for house dust sampling of nicotine with a filter holder connected to a vacuum cleaner, for a defined time and area was developed (F-nicotine). Also, house dust sampling was carried out from the vacuum cleaner bags of the homes (VC-nicotine). There was a larger variation in VC-nicotine (13–655, median 66 μg/g) compared with F-nicotine (15–393 median 156 μg/g). There were statistically significant associations between an inquiry data based ETS exposure index on the one hand, and urinary cotinine concentrations in children (U-cotinine), F-nicotine and VC-nicotine of their homes, on the other. The strong correlation between U-cotinine and F-nicotine ( rs = 0.93; P < 0.0001) indicates that the new standardized house dust sampling method should be useful in ETS exposure assessment. However, further validation by a larger sample size with repeated measurements in the same homes is needed. Environmental tobacco smoke (ETS) exposure assessment is important in indoor air quality (IAQ) investigations. A developed standardized sampling method for the determination of nicotine in house dust was evaluated. The strong correlation between urinary concentrations of cotinine (U-cotinine; an excellent biomarker of ETS exposure) in children and the house dust concentrations of nicotine indoors at home, indicate that it might be useful in ETS exposure assessment. [ABSTRACT FROM AUTHOR]

Background: Although the J-shaped relation between alcohol intake and mortality has been reproduced in many large cohort studies, the question of whether the effects of beer, wine, and spirits differ remains controversial.Objective: To examine the relation between intake of different types of alcohol and death from all causes, coronary heart disease, and cancer.Design: Pooled cohort studies in which intake of beer, wine, and spirits; smoking status; educational level; physical activity; and body mass index were assessed at baseline.Setting: Copenhagen, Denmark.Participants: 13 064 men and 11 459 women 20 to 98 years of age.Measurements: Number of deaths and time to death from all causes, coronary heart disease, and cancer during follow-up.Results: During 257 859 person-years of follow-up, 4833 participants died. J-shaped relations were found between total alcohol intake and mortality at various levels of wine intake. Compared with nondrinkers, light drinkers who avoided wine had a relative risk for death from all causes of 0.90 (95% CI, 0.82 to 0.99) and those who drank wine had a relative risk of 0.66 (CI, 0. 55 to 0.77). Heavy drinkers who avoided wine were at higher risk for death from all causes than were heavy drinkers who included wine in their alcohol intake. Wine drinkers had significantly lower mortality from both coronary heart disease and cancer than did non-wine drinkers (P = 0.007 and P = 0.004, respectively).Conclusion: Wine intake may have a beneficial effect on all-cause mortality that is additive to that of alcohol. This effect may be attributable to a reduction in death from both coronary heart disease and cancer. [ABSTRACT FROM AUTHOR]

Background: In the Copenhagen Male Study men with the Lewis blood group phenotype Le(a+b-), non-secretors of ABH antigen, and men with the O or the A phenotype in the ABO blood group have been found to have a significantly higher lifetime prevalence of peptic ulcer than others. We investigated the importance of the association of these genetic markers, life-style factors, and social class with lifetime risk of peptic ulcer, testing specifically the hypothesis that the strength of the association of risk factors with peptic ulcer depends on genetic susceptibility. Methods: Three thousand three hundred and forty-six white men 55-74 years old were included for study. From a questionnaire validated during an interview information was obtained about life-style factors and peptic ulcer history (gastric or duodenal). Potential non-genetic risk factors examined were smoking history, alcohol consumption, physical activity level, consumption of tea and coffee, and use of sugar in tea or coffee. Results: Three hundred and eighty-four men (11.5%) had a history of peptic ulcer; 120 (3.6%) had had an operation due to peptic ulcer. Non-genetic peptic ulcer risk factors identified were ever having been a smoker, use of sugar in tea or coffee, abstention from tea consumption, and low social class. On the basis of these and the genetic factors, it was possible to identify a low-risk group (n = 142) with a lifetime prevalence of 4.2%, several intermediate-risk groups, and a high-risk group (n = 55) with a prevalence of 29%; the odds ratio with 95% confidence limits (OR) was 9.3 (3.4-25.3). Corresponding values with regard to operation were 1.4% and 20.0%; OR = 17.5 (3.7-82.0). Several significant interactions were found; for example, the use of sugar was associated with peptic ulcer risk only when interacting with genetic risk groups. Conclusions: Considering the role of Helicobacter pylori, it is interesting that the factors identified in this study were able to identify groups with extremely different lifetime risks. This finding and also the finding of strong interactions between genetic and life-style factors and between genetic factors and social class for the risk of peptic ulcer may have both public-health and clinical implications. [ABSTRACT FROM AUTHOR]

Background: Two recent much cited publications have raised the concern that risk associated with cigarette smoking has so far been underestimated. In this study we wish to determine whether excess all-cause mortality associated with smoking has increased during the last 20-30 years in a study population representative of the general Danish population and whether any such changes relate to changes in smoking behaviour.Methods: Pooled data from three prospective population studies conducted in Copenhagen with detailed information on smoking habits. A total of 31,194 subjects, 17,669 males and 13,525 females, initially examined between 1964 and 1992 with examinations repeated at intervals from 1-10 years, were followed until 1995 for all-cause mortality. Relative mortality risk in smokers versus never-smokers was calculated within periods of five calendar years and compared throughout the study period.Results: Male smokers' exposure did not change during the study period whereas female smokers' exposure to tobacco increased in terms of age at smoking onset, quantity smoked and depth of inhalation. During follow-up 5744 males and 2900 females died. In males, death rate ratios (comparing continuous smokers with never-smokers) did not change in the study period. In females, ratios increased from 1964-1978 to 1979-1994 by a factor of 1.3 (95% confidence interval 1.0-1.8).Conclusions: In agreement with the observed changes in smoking habits, excess mortality in male smokers did not increase whereas excess mortality in female smokers increased slightly. [ABSTRACT FROM AUTHOR]

Objective: Large social inequalities exist in risk of ischaemic heart disease (IHD) in Western populations; inequalities which are only little accounted for by established risk factors. We wished to find out if some newly identified cardiovascular risk factors in concert with established factors might contribute further to the explanation.Design and Setting: A 6-year follow-up in the Copenhagen Male Study.Subjects: Some 2974 males aged 53-75 years (mean 63) without overt cardiovascular disease were included in the study. Potential confounders included were: alcohol, physical activity, smoking, serum lipids, serum cotinine, serum selenium, lifetime occupational exposure to soldering fumes and organic solvents, body mass index, blood pressure, hypertension, use of sugar in hot beverages, use of diuretics, and Lewis phenotypes.Main Outcome Measures: During the 6-year follow-up period (1985/1986-1991), 184 men (6.2%) had a first IHD event. Compared to higher social classes (classes I, II and III), lower classes (classes IV and V) had a significantly (P < 0.05) increased risk of IHD; age-adjusted relative risk (RR) with 95% confidence limits was 1.44 (1.1-1.9), P = 0.02. After multivariate adjustment for age, blood pressure, serum lipids, physical activity, and smoking, the RR dropped to 1.38 (1.0-1.9), P = 0.05. Some newly identified risk factors were significantly associated with increased risk of IHD as well as with low social class: a low serum selenium concentration, a low level of leisure time physical activity in midlife, long-term exposure to soldering fumes, and abstention from or a low consumption of wine and strong spirits. After adjustment for these factors also, the RR dropped to 1.12 (P = 0.54).Conclusions: The results of this study suggest that potentially modifiable risk factors associated with lifestyle and working environment are strong mediators of social inequalities in risk of ischaemic heart disease. [ABSTRACT FROM AUTHOR]

Objective: Misclassification of smokers as non-smokers may bias estimates of the excess morbidity and mortality associated with smoking. The issue has been given little, if any, attention in prospective epidemiological studies. This study examined characteristics of potentially misclassified smokers with respect to mortality, morbidity, and risk factors.Method: A prospective study (within The Copenhagen Male Study, Denmark) used serum cotinine as an objective marker of use of tobacco. A serum concentration of 100 ng/ml was regarded as a relevant threshold for active smoking. In all, 3270 males aged 53-74 years who reported their previous and current tobacco habits, including the use of chew tobacco and snuff, were included. Incidence of all causes of mortality (ACM) during 9 years and death due to ischaemic heart disease (IHD) during 8 years of follow-up were the main outcome measures.Results: Overall cumulative incidence rates of ACM and IHD were 19.1% and 4.3%, respectively. Of 1405 men who reported being non-tobacco users, i.e. no current smoking and no use of chewing tobacco or snuff, 1377 had levels < 100 ng/ml, 28 men (2%) had levels equal to or above this threshold value and were considered potentially misclassified smokers. They had significantly higher mortality rates, 35.7% versus 14.7%, P < 0.001, than other self-reported non-tobacco users, and a slightly higher prevalence of tobacco-related cancer, and a highly significant higher prevalence of myocardial infarction, P < 0.001. Compared to non-tobacco users with low cotinine, age-adjusted relative risks (95% CI) were 2.4 (1.3-4.5), P < 0.01, for ACM, and 5.3 (95% CI : 2.1-13.4), P < 0.001, for IHD.Conclusions: Potentially misclassified smokers deviated strongly from other non-smokers with respect to mortality and morbidity. The importance of this reporting bias when estimating the risk associated with active or passive smoking is discussed. [ABSTRACT FROM AUTHOR]