OBJECTIVE--To investigate long term mortality among women who smoked during pregnancy and those who stopped smoking. DESIGN--A follow up of a geographically defined cohort from 1966 through to 1993. SUBJECTS--11,994 women in northern Finland expected to deliver in 1966, comprising 96% of all women giving birth in the area during that year. Smoking habits were recorded during pregnancy but not later. MAIN OUTCOME MEASURE--Mortality by cause (571 deaths). RESULTS--The mortality ratio adjusted for age, place of residence, years of education and marital status was 2.3 (95% confidence interval 1.8 to 2.8) for the women who smoked during pregnancy and 1.6 (1.1 to 2.2) for those who stopped smoking before the second month of pregnancy, both compared with non-smokers. Among the smokers the relative mortality was higher for typical diseases related to tobacco intake, such as respiratory and oesophageal cancer and diseases of the cardiovascular and digestive organs and also for accidents and suicides. CONCLUSION--The risk of premature death seems to be higher in women who smoke during pregnancy than in other women who smoke. This may be explained either by the low proportion of those who stop later and the high proportion of heavy smokers or by other characteristics of these subjects that increase the risk.
A cohort of some 11,000 men born 1891-1920 and employed for at least one month in the chrysotile mines and mills of Quebec, was established in 1966 and has been followed ever since. Of the 5351 men surviving into 1976, only 16 could not be traced; 2508 were still alive in 1989, and 2827 had died; by the end of 1992 a further 698 were known to have died, giving an overall mortality of almost 80%. This paper presents the results of analysis of mortality for the period 1976 to 1988 inclusive, obtained by the subject-years method, with Quebec mortality for reference. In many respects the standardised mortality ratios (SMRs) 20 years or more after first employment were similar to those for the period 1951-75--namely, all causes 1.07 (1951-75, 1.09); heart disease 1.02 (1.04); cerebrovascular disease 1.06 (1.07); external causes 1.17 (1.17). The SMR for lung cancer, however, rose from 1.25 to 1.39 and deaths from mesothelioma increased from eight (10 before review) to 25; deaths from respiratory tuberculosis fell from 57 to five. Among men whose exposure by age 55 was at least 300 million particles per cubic foot x years (mpcf.y), the SMR (all causes) was elevated in the two main mining regions, Asbestos and Thetford Mines, and for the small factory in Asbestos; so were the SMRs for lung cancer, ischaemic heart disease, cerebrovascular disease, and respiratory disease other than pneumoconiosis. Except for lung cancer, however, there was little convincing evidence of gradients over four classes of exposure, divided at 30, 100, and 300 mpcf.y. Over seven narrower categories of exposure up to 300 mpcf.y the SMR for lung cancer fluctuated around 1.27 with no indication of trend, but increased steeply above that level. Mortality form pneumoconiosis was strongly related to exposure, and the trend for mesothelioma was not dissimilar. Mortality generally was related systematically to cigarette smoking habit, recorded in life from 99% of survivors into 1976; smokers of 20 or more cigarettes a day had the highest SMRs not only for lung cancer but also for all causes, cancer of the stomach, pancreas, and larynx, and ischaemic heart disease. For lung cancer SMRs increased fivefold with smoking, but the increase with dust exposure was comparatively slight for non-smokers, lower again for ex-smokers, and negligible for smokers of at least 20 cigarettes a day; thus the asbestos-smoking interaction was less than multiplicative. Of the 33 deaths from mesothelioma in the cohort to date, 28 were in miners and millers and five were in employees of a small asbestos products factory where commercial amphiboles had also been used. Preliminary analysis also suggest that the risk of mesothelioma was higher in the mines and mills at Thetford Mines than in those at Asbestos. More detailed studies of these differences and of exposure-response relations for lung cancer are under way.
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INTRODUCTION: Respiratory symptoms are among the main reasons why patients make contact with healthcare professionals and they are associated with several diseases. OBJECTIVE: The aim of this study was to investigate the relationship between respiratory symptoms reported at one time and 30 years cause-specific mortality and incidence of lung cancer in an urban Norwegian population. MATERIALS AND METHODS: A total of 19 998 men and women, aged 15-70 years, were in 1972 selected from the general population of Oslo. They received a postal respiratory questionnaire (response rate 89%). All were followed for 30 years for end-point mortality and for lung cancer. The association between respiratory symptoms, given as a symptom load, and end point of interest were investigated separately for men and women by multivariable analyses, with adjustment for age, occupational exposure to air pollution and smoking habits. RESULTS: A total of 6710 individuals died during follow-up. Obstructive lung diseases (OLDs) and pneumonia accounted for 250 and 293 of the total deaths, respectively. Ischaemic heart disease (IHD) accounted for 1572; stroke accounted for 653 of all deaths. Lung cancer developed in 352 persons during follow-up. The adjusted hazard ratio for mortality from OLD and pneumonia, IHD and stroke increased in a dose-response manner with symptom score, more strongly for OLD and IHD than for pneumonia and stroke. CONCLUSIONS: Respiratory symptoms were positively associated with mortality from OLD, pneumonia, IHD and stroke, and incidence of lung cancer. This association was significant for mortality from OLD and IHD.
To examine the relative size of the effects of fitness and fatness on mortality in Russian men, and to make comparison to US men.
Prospective closed cohort.
1359 Russian men and 1716 US men aged 40-59 y at baseline (1972-1977) who were enrolled in the Lipids Research Clinics Study.
Fitness was assessed using a treadmill test and fatness was assessed as body mass index (BMI) calculated from measured height and weight. Hazard ratios were calculated using proportional hazard models that included covariates for age, education, smoking, alcohol intake and dietary keys score. All-cause and cardiovascular disease (CVD) mortality were assessed through 1995.
In Russian men, fitness was associated with all-cause and CVD mortality, but fatness was not. For mortality from all causes, compared to the fit-not fat, the adjusted hazard ratios were 0.87 (95% CI: 0.55, 1.37) among the fit-fat, 1.86 (95% CI: 1.31, 2.62) among the unfit-not fat and 1.68 (95% CI: 1.06, 2.68) among the unfit-fat. Among US men, the same hazard ratios were 1.40 (95% CI: 1.07, 1.83), 1.41 (95% CI: 1.12, 1.77) and 1.54 (95% CI: 1.24, 2.06), respectively. There were no statistically significant interactions between fitness and fatness in either group of men for all-cause or CVD mortality.
The effects of fitness on mortality may be more robust across populations than are the effects of fatness.
Although a clear risk of mortality is associated with obesity, the risk of mortality associated with overweight is equivocal. The objective of this study is to estimate the relationship between BMI and all-cause mortality in a nationally representative sample of Canadian adults. A sample of 11,326 respondents aged >or=25 in the 1994/1995 National Population Health Survey (Canada) was studied using Cox proportional hazards models. A significant increased risk of mortality over the 12 years of follow-up was observed for underweight (BMI 35; RR = 1.36, P 0.05). Our results are similar to those from other recent studies, confirming that underweight and obesity class II+ are clear risk factors for mortality, and showing that when compared to the acceptable BMI category, overweight appears to be protective against mortality. Obesity class I was not associated with an increased risk of mortality.
OBJECTIVES: It is well known that pulmonary function is associated with all-cause and cardiovascular (CV) death. Less is known about the association between respiratory symptoms and mortality and whether such an association is independent of physical fitness. In this study, we assessed the association of breathlessness and productive cough with CV and all-cause mortality over 26 years. DESIGN: Prospective occupational cohort study. SETTING AND SUBJECTS: In 1972-75, 1999 apparently healthy men aged 40-59 years were recruited to the study from five companies in Oslo, Norway. At study entry clinical, physiological and biochemical parameters including respiratory symptoms, spirometry, and an objective assessment of physical fitness were measured in all subjects, of whom 1,623 had acceptable spirometry. The data was analysed using Cox proportional hazards analysis, adjusting for age, lung function, physical fitness, and other possible confounders, with mortality until 2000. RESULTS: After 26 years (range 25-27), 615 men (38%) had died, of whom 308 (50%) from CV deaths. In multivariable proportional hazards models, 'having phlegm winter mornings' [hazard ratio (HR) 1.30, P = 0.01], 'breathlessness when hurrying/walking uphill' (HR 1.43, P = 0.005) and combinations of the two symptoms remained significant predictors of all-cause mortality. None of six respiratory symptoms were significant predictors of CV mortality in multivariable models. CONCLUSIONS: Phlegm, breathlessness and combinations of them were associated with all-cause mortality, even after adjusting for physical fitness, known CV and other risk factors such as smoking, and lung function. The finding of an association also after adjustment for physical fitness is new. In contrast, none of the six respiratory symptoms individually or in combination were associated with CV mortality in multivariable analysis.
We describe the mortality currently attributable to smoking in the European Union (EU), and the change that would result if all EU countries had the smoking prevalence of Sweden. Almost 500,000 smoking-attributable deaths occur annually among men in the EU; about 200,000 would be avoided at Swedish smoking rates. In contrast, only 1100 deaths would be avoided if EU women smoked at Swedish rates. The low smoking-related mortality among Swedish men probably is due to their use of snus (Swedish smokeless tobacco).
Cardiovascular diseases (CVDs) have been related to low birth weight, suggesting the foetal environment may program future risk. Alternatively, common genetic factors for both low birth weight and CVD could explain such associations. We investigated associations between offspring birth weight and paternal and maternal cardiovascular mortality and offspring birth weight and cardiovascular mortality among all four grandparents, and further assessed the mediating role of maternal smoking during pregnancy.
All births from 1967 to 2008 that could be linked to parents and grandparents comprised the population (n = 1,004,255). The mortality follow-up among parents was from 1970 to 2008 and among grandparents from 1960 to 2008. The association of grandparental mortality with maternal smoking during pregnancy was analysed in a subpopulation of those born after 1997 (n = 345,624). Per quintile higher in birth weight was related to 0.82 (0.75-0.89) hazard ratio from coronary heart disease in mothers and 0.94 (0.92-0.97) in fathers. For stroke, these were 0.85 (0.78-0.92) and 0.94 (0.89-1.00), respectively. In grandparents for cardiovascular causes, the effects were 0.95 (0.93-0.96) (maternal grandmother), 0.97 (0.96-0.98) (maternal grandfather), 0.96 (0.94-0.98) (paternal grandmother), and 0.98 (0.98-1.00) (paternal grandfather). Adjusting for maternal smoking in pregnancy in the subpopulation accounted for much of the effect on grandparental cardiovascular mortality in all categories of birth weight. For grandparental diabetes mortality, U-shaped associations were seen with grandchild birth weight for the maternal grandmother and inverse associations for all other grandparents.
Associations between CVD mortality in all four grandparents and grandchild birth weight exist, and while genetic and environmental factors may contribute to these, it appears that there is an important role for maternal smoking during pregnancy (and associated paternal smoking) in generating these associations. For diabetes, however, it appears that intrauterine environmental influences and genetic factors contribute to the transgenerational associations.
Comment In: Eur Heart J. 2013 Nov;34(44):3398-923103662