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Variation in surfactant protein D (SP-D) is associated with lung function in tobacco smoke-induced chronic respiratory disease. We hypothesized that the same association exists in the general population and could be used to identify individuals sensitive to smoke-induced lung damage. The association between serum SP-D (sSP-D) and expiratory lung function was assessed in a cross-sectional design in a Danish twin population (n = 1,512, 18-72 yr old). The adjusted heritability estimates for expiratory lung function, associations between SP-D gene (SFTPD) single-nucleotide polymorphisms or haplotypes, and expiratory lung function were assessed using twin study methodology and mixed-effects models. Significant inverse associations were evident between sSP-D and the forced expiratory volume in 1 s and forced vital capacity in the presence of current tobacco smoking but not in nonsmokers. The two SFTPD single-nucleotide polymorphisms, rs1923536 and rs721917, and haplotypes, including these single-nucleotide polymorphisms or rs2243539, were inversely associated with expiratory lung function in interaction with smoking. In conclusion, SP-D is phenotypically and genetically associated with lung function measures in interaction with tobacco smoking. The obtained data suggest sSP-D as a candidate biomarker in risk assessments for subclinical tobacco smoke-induced lung damage. The data and derived conclusion warrant confirmation in a longitudinal population following chronic obstructive pulmonary disease initiation and development.

Introduction: COPD is a leading cause of death worldwide; however, prevalence estimates have varied considerably in previous studies. This study aimed to determine the prevalence and severity of COPD in Copenhagen using data from the 4th examination of The Copenhagen City Heart Study, to investigate the relationship between tobacco consumption and COPD, and to characterize the subjects with COPD with regard to BMI, dyspnoea, treatment with respiratory medication and co-morbidities., Methods: 6236 people participated. All non-asthmatic participants aged 35 years or older with adequate lung function data were included for the final prevalence analyses (n = 5,299). COPD staging was done according to the GOLD criteria., Results: The overall prevalence of COPD was 17.4%. The prevalence increased with age and was higher among males. 6.2% had mild COPD, 9.2% had moderate COPD, and 2.0% had severe or very severe COPD. Tobacco consumption was closely linked to both prevalence and disease severity. Subjects with COPD had lower mean Body Mass Index (BMI) and more frequently a BMI < 21 kg/m(2). Dyspnoea was correlated to lung function but a substantial number of participants with severe COPD experienced no dyspnoea. Only a minority of subjects with COPD received pulmonary medication. COPD was associated with cardiovascular disease and cancer., Conclusion: The prevalence of COPD in Denmark is among the highest in the world. It is closely correlated to smoking and age. It is accompanied by substantial co-morbidity and it is grossly under treated., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

Background: Smoking is associated with an accelerated loss of lung function and inhalation accelerates the decline further. Exhaled CO reflects the exposure of smoke to the lungs., Aim: To investigate whether self-reported inhalation and type of cigarette influenced the level of exhaled CO and whether CO could provide additional information to usual measures of smoking regarding prediction of present lung function and decline in lung function over an extended period of time., Method: Cigarette smokers from the Copenhagen City Heart Study with valid measures of lung function and exhaled CO; in total 3738 subjects, 2096 women and 1642 men., Results: Subjects not inhaling had slightly lower exhaled CO values than those inhaling, but substantially higher values than non-smokers (P<0.001). Smokers of plain cigarettes had slightly lower CO values than smokers of filter cigarettes (P<0.001). Increasing CO levels were correlated to a lower FEV(1)%pred and to an accelerated decline in lung function. However, in multiple linear regression analyses these correlations were not significant., Conclusion: Inhalation and type of cigarette affects exhaled CO levels. CO measures have no predictive value regarding neither present lung function nor decline in lung function with time in a population survey setting.

Background: Smokers are more prone to develop chronic obstructive pulmonary disease (COPD) than non-smokers, but this finding comes from studies spanning 10 years or less. The aim of this study was to determine the 25 year absolute risk of developing COPD in men and women from the general population., Methods: As part of the Copenhagen City Heart Study, 8045 men and women aged 30-60 years with normal lung function at baseline were followed for 25 years. Lung function measurements were collected and mortality from COPD during the 25 year observation period was analysed., Results: The percentage of men with normal lung function ranged from 96% of never smokers to 59% of continuous smokers; for women the proportions were 91% and 69%, respectively. The 25 year incidence of moderate and severe COPD was 20.7% and 3.6%, respectively, with no apparent difference between men and women. Smoking cessation, especially early in the follow up period, decreased the risk of developing COPD substantially compared with continuous smoking. During the follow up period there were 2912 deaths, 109 of which were from COPD. 92% of the COPD deaths occurred in subjects who were current smokers at the beginning of the follow up period., Conclusion: The absolute risk of developing COPD among continuous smokers is at least 25%, which is larger than was previously estimated.

Objective: To analyse the effects of smoking reduction and smoking cessation on incidence of myocardial infarction after adjustment for established cardiovascular risk factors., Design: Prospective cohort study with record linkage to mortality and hospital registers. The association of individual change in smoking with myocardial infarction was examined in Cox proportional hazard analyses with continuous heavy smokers (> or =5 cigarettes/day) as reference., Setting: Pooled data from three population studies conducted in Copenhagen, Denmark., Participants: 10 956 men and 8467 women with complete information on smoking habits at two examinations five to ten years apart were followed up from the second examination for a first hospital admission or death from myocardial infarction. Mean duration of follow up was 13.8 years., Main Results: A total of 643 participants who were heavy smokers at baseline reduced their daily tobacco consumption by at least 50% without quitting between first and second examination, and 1379 participants stopped smoking. During follow up 1658 men and 521 women experienced a fatal or non-fatal myocardial infarction. After adjustment for cardiovascular risk factors, people who stopped smoking had a decreased risk of myocardial infarction, hazard ratio 0.71 (95% confidence intervals 0.59 to 0.85). Smoking reduction was not associated with reduced risk of myocardial infarction, hazard ratio 1.15 (95% confidence intervals 0.94 to 1.40). These associations remained unchanged after controlling for baseline illness in different ways., Conclusions: Smoking cessation in healthy people reduces the risk of a subsequent myocardial infarction, whereas this study provides no evidence of benefit from reduction in the amount smoked.

The authors investigated the association between changes in smoking habits and mortality by pooling data from three large cohort studies conducted in Copenhagen, Denmark. The study included a total of 19,732 persons who had been examined between 1967 and 1988, with reexaminations at 5- to 10-year intervals and a mean follow-up of 15.5 years. Date of death and cause of death were obtained by record linkage with nationwide registers. By means of Cox proportional hazards models, heavy smokers (>or=15 cigarettes/day) who reduced their daily tobacco intake by at least 50% without quitting between the first two examinations and participants who quit smoking were compared with persons who continued to smoke heavily. After exclusion of deaths occurring in the first 2 years of follow-up, the authors found the following adjusted hazard ratios for subjects who reduced their smoking: for cardiovascular diseases, hazard ratio (HR) = 1.01 (95% confidence interval (CI): 0.76, 1.35); for respiratory diseases, HR = 1.20 (95% CI: 0.70, 2.07); for tobacco-related cancers, HR = 0.91 (95% CI: 0.63, 1.31); and for all-cause mortality, HR = 1.02 (95% CI: 0.89, 1.17). In subjects who stopped smoking, most estimates were significantly lower than the heavy smokers'. These results suggest that smoking reduction is not associated with a decrease in mortality from tobacco-related diseases. The data confirm that smoking cessation reduces mortality risk.

Because of a "healthy responder effect," secular trends in mortality based on cohort studies may be biased if based on responders only. Because responders are selected on the basis of their health at study entry, subjects just entering a study are not comparable with subjects who have been in the study for several years. The result may be an artificial increase in mortality, which impedes analyzing the effect of secular trends in risk factors on mortality. The objective of this paper is to suggest a solution by using data on nonresponders and applying a sensitivity analysis. We illustrate this solution with data on trends in smoking prevalence and all-cause mortality based on a large Danish cohort study with 19 years of complete follow-up on responders and nonresponders. Secular trends in mortality based on the whole sample vs responders only illustrated that results based on responders were biased. In a sensitivity analysis, the observed person-years of nonresponders were distributed among six categories of persons with respect to smoking behavior (never-smokers; ex-smokers; noninhaling current smokers; and current smokers of 1-14, 15-24, and > or =25 gm tobacco per day) according to preset assumptions regarding smoking habits. The observed deaths among nonresponders were then distributed on the six smoking categories according to relative risks derived from a Poisson regression analysis among responders. This procedure allowed us to study the effect of adjustment for smoking on the unbiased secular trend in mortality. By applying different assumptions regarding smoking habits among nonresponders, we explored the effect of the assumptions on the adjusted secular trend in mortality. We conclude that secular trends in mortality based on responders in a cohort study are likely to be biased. If complete follow-up on nonresponders is available, this method could prove useful in other cohort studies.

Objective: To compare risk of myocardial infarction associated with smoking in men and women, taking into consideration differences in smoking behaviour and a number of potential confounding variables., Design: Prospective cohort study with follow up of myocardial infarction., Setting: Pooled data from three population studies conducted in Copenhagen., Subjects: 11,472 women and 13,191 men followed for a mean of 12.3 years., Main Outcome Measures: First admission to hospital or death caused by myocardial infarction., Results: 1251 men and 512 women had a myocardial infarction during follow up. Compared with non-smokers, female current smokers had a relative risk of myocardial infarction of 2.24 (range 1.85-2.71) and male smokers 1.43 (1.26-1.62); ratio 1.57 (1.25-1.97). Relative risk of myocardial infarction increased with tobacco consumption in both men and women and was higher in inhalers than in non-inhalers. The risks associated with smoking, measured by both current and accumulated tobacco exposure, were consistently higher in women than in men and did not depend on age. This sex difference was not affected by adjustment for arterial blood pressure, total and high density lipoprotein cholesterol concentrations, triglyceride concentrations, diabetes, body mass index, height, alcohol intake, physical activity, and level of education., Conclusion: Women may be more sensitive than men to some of the harmful effects of smoking. Interactions between components of smoke and hormonal factors that may be involved in development of ischaemic heart disease should be examined further.

Background: Mortality from smoking-related diseases in women is increasing worldwide. Studies comparing hazards associated with smoking in women and men based on a sufficient number of heavy smokers of both genders are lacking., Methods: We used pooled data from three prospective population studies conducted in Copenhagen to compare total and cause-specific mortality in relation to smoking habits. A total of 30917 subjects, 44% women, with initial examinations between 1964 and 1992 were followed until 1994 for date and cause of death., Results: During follow up, 2900 women and 5744 men died. Smoking characteristics differed considerably with gender, particularly in the older subjects. Overall mortality rates in smokers were approximately twice those in people who never smoked. Positive associations with smoking in both men and women were confirmed for all-cause mortality as well as mortality from respiratory disease, vascular disease, lung cancer, and other tobacco-related cancers. Despite large gender differences in age at smoking debut, total and cause-specific relative mortality in smokers was similar in men and women. After excluding non-inhalers, relative risks associated with smoking for respiratory and vascular disease were higher for women than men whereas there were no gender differences in smoking related risk of cancers., Conclusions: The relative risks suggest that women may be more sensitive than men to some of the deleterious effects of smoking. However, because of lower baseline mortality rates in women, rate differences may be similar and results should be interpreted with caution.

Our aim was to compare risk of lung cancer associated with smoking by gender and histologic type. A total of 30,874 subjects, 44% women, from three prospective population-based studies with initial examinations between 1964 and 1992 were followed until 1994 through the National Cancer Registry. There were 867 cases of lung cancer, 203 among women and 664 among men. Rates among female and male never-smokers were similar, although confidence intervals around rates were wide. Rate ratios (RRs) increased with number of pack-years for both men and women to a maximum of approximately 20 in inhaling smokers with more than 60 pack-years of tobacco exposure. RRs did not differ much between men and women: adjusted for pack-years, age, and study population, the ratio between female and male smokers' RRs of developing lung cancer was 0.8 (95% confidence interval = 0.3-2.1). All histologic types were associated with smoking, with the largest RR seen for squamous cell carcinoma and anaplastic carcinoma. This prospective population-based study does not confirm previous reports from case-control studies of a higher relative risk in women than in men for lung cancer associated with smoking.

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.

Recent findings suggest that females may be more susceptible than males to the deleterious influence of tobacco smoking in developing chronic obstructive pulmonary disease (COPD). This paper studies the interaction of gender and smoking on development of COPD as assessed by lung function and hospital admission. A total of 13,897 subjects, born after 1920, from two population studies, 9,083 from the Copenhagen City Heart Study (CCHS) and 4,814 from the Glostrup Population Studies (GPS), were followed for 7-16 yrs. Data were linked with information on hospital admissions caused by COPD. Based on cross-sectional data, in the CCHS the estimated excess loss of forced expiratory volume in one second (FEV1) per pack-year of smoking was 7.4 mL in female smokers who inhaled and 6.3 mL in male smokers who inhaled. In the GPS, the corresponding excess loss of FEV1 was 10.5 and 8.4 mL in females and males, respectively. Two hundred and eighteen subjects in the CCHS and 23 in the GPS were hospitalized during follow-up. Risk associated with pack-years was higher in females than in males (relative risks (RRs) for 1-20, 20-40 and >40 pack-years were 7.0 (3.5-14.1), 9.8 (4.9-19.6) and 23.3 (10.7-50.9) in females, and 3.2 (1.1-9.1), 5.7 (2.2-14.3) and 8.4 (3.3-21.6) in males) but the interaction term gender x pack-years did not reach significance (p=0.08). Results were similar in the GPS. After adjusting for smoking in more detail, females in both cohorts had an increased risk of hospitalization for COPD compared to males with a RR of 1.5 (1.2-2.1) in the CCHS and 3.6 (1.4-9.0) in the GPS. This was not likely to be caused by a generally increased rate of hospital admission for females. Results were similar when including deaths from COPD as endpoint. In two independent population samples, smoking had greater impact on the lung function of females than males, and after adjusting for smoking females subsequently suffered a higher risk of being admitted to hospital for COPD. Results suggest that adverse effects of smoking on lung function may be greater in females than in males.

Data from a cross-sectional study of 1045 men comprising a random population sample (768 men) and a sample of cement workers (277 men) were analyzed in order to examine the effects of smoking and occupation on forced expiratory volume in one second (FEV1). The continuous FEV1 variable and five dichotomous FEV1 variables based on % of predicted were analyzed. Differences between the "relative importance" of smoking and occupation were found to depend on the choice of the FEV1 variable. The effects of occupation compared with the effects of smoking varied considerably with different FEV1 variables, continuous or dichotomized at different cut-off levels. We conclude that comparison of surveys utilizing different FEV1 variables must be made with caution.

A group of 1404 middle-aged men from Aalborg who were examined in 1974 with interview and lung function tests were re-examined in 1985 using a postal questionnaire. Of the 1404 men, 1045 could be classified into well-defined occupational categories using information up to 1974. Of these men, 791 were alive at the time of the questionnaire survey. Questions on lung symptoms, occupation and smoking habits since the 1974 study were included in the follow-up survey; the response rate was 88%. Age and main occupation until 1974 were significantly related to the development of severe breathlessness from 1974 to 1985. After controlling for age, both cement workers and blue collar workers were considerably more likely to develop severe breathlessness than white collar workers: odds ratios (ORs) 2.51 (95% confidence interval 1.04-6.7) and 2.35 (1.02-5.42), respectively. Although weakened, these relationships remained after further controlling for forced expiratory volume in one second (FEV1) in 1974. Present smoking habit was an important determinant for the presence of cough, both in men with and without cough in 1974, yielding ORs of approximately 3 when comparing with lifetime nonsmokers. Cement workers tended to have cough in 1985 more frequently than white collar workers, OR = 2.09 (0.89-4.89) for men without cough in 1974 and OR = 2.60 (1.04-6.51) for men with cough in 1974.

Deals with a study which described differences in smoking characteristics between Danish men and women. Methodology; Results; Discussion.