Copenhagen Male Study, Epidemiological Research Unit, Clinic of Environmental and Occupational Medicine, Bispebjerg University Hospital, Bispebjerg Bakke 23, DK-2400 Copenhagen NV, Denmark. PS11@bbh.hosp.dk
Inflammation and genetic susceptibility influence the risk of lung cancer. Previous studies suggest that the inflammatory response may depend upon ABO phenotype. The hypothesis that the association with lung cancer mortality risk of lifestyle and occupational factors previously linked to inflammation would depend upon ABO phenotype was tested in a long-term follow-up of 3,346 male subjects aged 53-74 yrs. During a 16-yr period, 170 (5.1%) of the male subjects died due to lung cancer; 84 (5.9%) of phenotype O, 70 (4.9%) of phenotype A and 16 (3.2%) of phenotype B/AB. In addition to cumulative tobacco consumption, high salt intake long-term occupational dust exposure, high fat intake and consumption of alcohol were significantly predictive of lung cancer mortality for phenotype O subjects. After multivariable adjustment, the hazard ratios associated with the first three of these factors were 2.31, 2.08 and 1.67, respectively. Compared with abstainers, the hazard ratios for males drinking 1-10 wine drinks x week(-1) and males drinking >10 wine drinks x week(-1) were 1.65 and 2.02, respectively. Among phenotype A subjects, only cumulative tobacco consumption was associated with lung cancer mortality risk. The predictive role of inflammation-related risk factors for lung cancer mortality was significantly stronger among males of phenotype O than A.
Non insulin dependent diabetes mellitus (NIDDM) and essential hypertension (EH) are two of several manifestations of the insulin resistance syndrome. Although subjects with NIDDM and subjects with EH share a common defect in carbohydrate metabolism, only diabetics are advised to avoid sugar. We tested the theory that an adverse effect of diuretics treatment in men with EH with respect to risk of ischaemic heart disease (IHD) would depend on the intake of dietary sugar using sugar in hot beverages as a marker. The cohort consisted of 2,899 men from the Copenhagen Male Study aged 53-74 years (mean 63) who were without overt cardiovascular disease. Potential confounders were: age, alcohol,smoking, physical activity, body mass index, blood pressure, fasting lipids, cotinine, NIDDM,and social class. A total of 340 men took antihypertensives; 211 took diuretics (95% thiazides and related agents), and 129 used other antihypertensives. During 6 years, 179 men (6.2%) had a first IHD event. Among the 340 men taking antihypertensives, the incidence rate was 11%. Diuretics use was associated with a high risk of IHD in hypertensive men with a relatively high intake of dietary sugar; the cumulative incidence rate was 22%; in diuretics treated men with a low intake of sugar, the rate was 7%. After controlling for potential confounders, relative risk (95% ci.) was 3.1(1.3-7.6), p = 001. Among the 129 men who took other forms of antihypertensive drugs, the IHD incidence rate was 8%, and independent of the intake of sugar. The results indicate that the risk of IHD in hypertensives using diuretics is associated with intake of dietary sugar, which may explain at least some of the discouraging effects of antihypertensive agents on the reduction of risk of IHD.
OBJECTIVES: To test the hypothesis that long-term occupational exposure to airborne pollutants is a stronger risk factor for ischaemic heart disease (IHD) in men with blood type O than in men with other ABO phenotypes. DESIGN: Cross-sectional and prospective study taking into account potential confounders. SETTING: The Copenhagen Male Study. SUBJECTS: 3321 men aged 53-74 years. MAIN OUTCOME MEASURE: Lifetime prevalence of myocardial infarction and incidence of IHD in an 8-year follow-up among men without overt cardiovascular disease. RESULTS: Among men with phenotypes other than O no association was found between airborne pollutant exposure and IHD risk. Among men with blood type O (P = 1417, 42%), 4.7% had a history of myocardial infarction, as compared with 5.7% among men with other phenotypes (P = 1904, 58%). Long-term occupational exposure (> 5 years of exposure) to various airborne pollutants: soldering fumes, welding fumes and plastic fumes was associated with a significantly increased lifetime prevalence of myocardial infarction. Odds ratios (95% confidence limits) for these factors were 3.0 (1.6-5.8), P = 0.002, 2.1 (1.05-4.2), P = 0.05, and 8.3 (2.6-27.0), P = 0.003. In an 8-year follow-up a similar though weaker association was found with a significantly increased risk for those exposed long term to soldering fumes: 1.8 (1.0-3.2), P = 0.05. CONCLUSION: The finding of a quite strong interplay between airborne pollutants, ABO phenotypes, and risk of IHD, may open up new possibilities for clarifying the roles of the ABO blood group and air pollution as cardiovascular risk factors.
BACKGROUND: We have previously found a quite strong interplay between occupational airborne pollutants, ABO phenotypes, and risk of ischaemic heart disease (IHD), with long-term exposure being associated with a significantly increased risk among men with phenotype O, and not among men with other ABO phenotypes. We suggested that the biological pathway could be a stronger systemic inflammatory response in men with blood group O. Several inflammatory mediators likely to increase the risk of IHD have recently been linked also to obesity, suggesting that long-term exposure to airborne pollutants might play a role in the aetiology of obesity. Accordingly, we tested the hypothesis that long-term occupational exposure to airborne pollutants would be more strongly associated with obesity in men with phenotype O than in men with other ABO phenotypes. DESIGN: Cross-sectional exposure-response study taking into account potential confounders. SETTING: The Copenhagen Male Study. SUBJECTS: A total of 3290 men aged 53-74 y. MAIN OUTCOME MEASURE: Prevalence of obesity (BMI > or =30 (kg/m2)). RESULTS: Overall, no differences were found in the prevalence of obesity between men with the O phenotype (n=1399) and men with other phenotypes (n=1891), 8.6 and 9.0%. However, only among men with the O phenotype was long-term occupational exposure (at least 5 y of frequent exposure) to various respirable airborne pollutants: dust, asbestos, soldering fumes, welding fumes, organic solvents, fumes from lacquer, paint or varnish, toxic components, breath irritants, stench or strongly smelling products, and irritants (other than breath irritants or contagious components) associated with an increased prevalence of obesity. Statistically, the strongest univariate associations were found for asbestos exposure, welding fumes, and breath irritants. Odds ratios (95% confidence limits) for these factors were 3.7 (1.8-7.6), 2.7 (1.6-4.4), and 2.6 (1.5-4.4), respectively. This particular relationship of airborne exposures with obesity in men with phenotype O was supported in multivariate analysis including interaction terms and taking into account a number of potential confounders. In contrast, no gene-environment interactions with obesity were found with respect to ABO phenotypes and a number of nonrespirable exposures. CONCLUSION: The finding of a quite strong interplay between long-term exposure to airborne pollutants, ABO phenotypes, and risk of obesity may open up new possibilities for clarifying mechanisms underlying the global obesity epidemic.
OBJECTIVES: To investigate the interplay between use of alcohol, concentration of low density lipoprotein cholesterol, and risk of ischaemic heart disease. DESIGN: Prospective study with controlling for several relevant confounders, including concentrations of other lipid fractions. SETTING: Copenhagen male study, Denmark. SUBJECTS: 2826 men aged 53-74 years without overt ischaemic heart disease. MAIN OUTCOME MEASURE: Incidence of ischaemic heart disease during a six year follow up period. RESULTS: 172 men (6.1%) had a first ischaemic heart disease event. There was an overall inverse association between alcohol intake and risk of ischaemic heart disease. The association was highly dependent on concentration of low density lipoprotein cholesterol. In men with a high concentration (> or = 5.25 mmol/l) cumulative incidence rates of ischaemic heart disease were 16.4% for abstainers, 8.7% for those who drank 1-21 beverages a week, and 4.4% for those who drank 22 or more beverages a week. With abstainers as reference and after adjustment for confounders, corresponding relative risks (95% confidence interval) were 0.4 (0.2 to 1.0; P or = 3.63 mmol/l who abstained from drinking alcohol was 43% (10% to 64%). CONCLUSIONS: In middle aged and elderly men the inverse association between alcohol consumption and risk of ischaemic heart disease is highly dependent on the concentration of low density lipoprotein cholesterol. These results support the suggestion that use of alcohol may in part explain the French paradox.
Comment In: ACP J Club. 1996 Sep-Oct;125(2):51
Comment In: BMJ. 1996 Aug 10;313(7053):365-68760765
A high intake of saturated fat is associated with an increase in serum low density lipoprotein cholesterol (LDL) and an increase in risk of ischaemic heart disease (IHD). In some parts of France a high intake of fat is not associated with increased risk of IHD, an apparent discrepancy named the French paradox. It has been suggested, but never tested prospectively, that regular use of alcohol might explain this low risk. We investigated the interplay between use of alcohol, LDL and risk of IHD in a prospective study controlling for a number of relevant confounders including other lipid fraction, including 2,826 males aged 53-74 years without overt IHD. The incidence of IHD during a six year follow-up period was registered. One hundred and seventy-two men (6.1%) had a first IHD event. There was an overall inverse association between alcohol intake and risk of IHD. The association was highly dependent on LDL. In men with a high LDL (> or = 5.25 mmol/l), cumulative incidence rates of IHD were 16.4% for abstainers, 8.7% for those who drank 1-21 beverages/week and 4.4% for those who drank 22+. Using abstainers as reference, adjusted for confounders, corresponding relative risks (95% CI) were 0.4 (0.2-1.0), p or = 3.63 mmol/l who abstained from drinking alcohol was calculated; AR with 95% confidence limits was 43% (10-64%). To conclude, in middleaged and elderly men the inverse association between alcohol consumption and risk of IHD was highly dependent on the level of LDL. These results support the suggestion that alcohol intake may at least in part explain the French paradox.
In the Copenhagen Male Study we found an increased risk of ischaemic heart disease (IHD) in men with the Lewis phenotype Le(a-b-). This study investigated whether, within the group of Le(a-b-) men, any conventional risk factors modified their increased risk. Three thousand, three hundred and eighty-three men aged 53 to 75 years were examined in 1985/86 and their morbidity and mortality over the next four years recorded. Three hundred and forty-three men with cardiovascular diseases were excluded at baseline. Potential risk factors examined were: alcohol consumption, physical activity, tobacco smoking, serum cotinine, serum lipids, body mass index, blood pressure, hypertension, non-insulin dependent diabetes mellitus and social class. In eligible men with Le(a-b-), N = 280 (9.6%), alcohol was the only risk factor associated with risk of IHD. There was a significant inverse dose-effect relationship between alcohol consumption and risk. The age-adjusted p-values of trend tests were for risk of non-fatal + fatal IHD: p = 0.03; for risk of fatal IHD: p = 0.02. In eligible men with other phenotypes, N = 2,649 (90.4%) only a limited and non-significant negative association with alcohol. In Le(a-b-) men, a group genetically at increased risk of IHD, the risk was strongly and significantly negatively correlated with alcohol consumption.
In 1983 WHO, defined "The Sick Building Syndrome". Various conditions influence the indoor climate, among others the degassing of chemicals. An epidemic of sick building syndrome is described in a two year old office building. The symptoms appeared after exposure to toxic chemicals released by a stink bomb--a form of exposure not previously described in the literature. Gas chromatographic analysis of the content of the stink bomb revealed 22 different chemicals likely to be remains from an alcoholic fermentation process. Twenty-four employees were exposed. A questionnaire investigation of the employees revealed that seven had symptoms related to the exposure. A clinical investigation of those who claimed to have symptoms took place. Six of the seven patients were investigated. They all had toxic rhinitis with bleeding. Owing to an unsystematic procedure it took more than two months before the indoor climate was normalized. The toxic rhinitis and other symptoms gradually decreased over more than four months. In order to minimize potential health damage due to the sick building syndrome, we recommend that experts should be consulted within this particular field.