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The objective of the study was to assess the relationship between exposure to selected solvents and the risk of bladder cancer. This study is based on the Nordic Occupational Cancer (NOCCA) database and comprises 113,343 cases of bladder cancer diagnosed in Finland, Iceland, Norway and Sweden between 1961 and 2005 and 566,715 population controls matched according to country, sex and birth year. Census‐based occupational titles of the cases and controls were linked with the job exposure matrix created by the NOCCA project to estimate quantitative cumulative occupational exposures. A conditional logistic regression model was used to estimate hazard ratios (HRs) and their 95% confidence intervals (95% CI). Increased risks were observed for trichloroethylene (HR 1.23, 95% CI 1.12–1.40), toluene (HR 1.20, 95% CI 1.00–1.38), benzene (HR 1.16, 95% CI 1.04–1.31), aromatic hydrocarbon solvents (HR 1.10, 95% CI 0.94–1.30) and aliphatic and alicyclic hydrocarbon solvents (HR 1.08, 95% CI 1.00–1.23) at high exposure level versus no exposure. The highest excess for perchloroethylene was observed at medium exposure level (HR 1.12, 95% CI 1.02–1.23). The study provides evidence of an association of occupational exposure to trichloroethylene, perchloroethylene, aromatic hydrocarbon solvents, benzene and toluene and the risk of bladder cancer.  相似文献   
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Neoplastic diseases in families of breast cancer patients.   总被引:4,自引:1,他引:4       下载免费PDF全文
OBJECTIVE--To investigate whether the risk of cancer at all sites, and at individual sites other than breast, prostate, ovaries, and endometrium, is increased among relatives of breast cancer patients compared with the general population. DESIGN--A cohort of family members of breast cancer patients was established. The probands were chosen by year of birth or time of diagnosis. Any influence of knowledge of the cancer experience of the relatives has been avoided. The risk estimates are based on expected numbers computed from age and time specific incidence rates for the Icelandic population. SETTING--Iceland. SUBJECTS--The population of Iceland. MAIN OUTCOME MEASURES--Relative risks by degree of relatedness and age of proband. RESULTS--The relative risk of cancer at all sites is raised for males and females. This is more than expected based on the known familial risk of breast cancer, prostate, and ovarian cancer. The excess risk of breast, prostate, and ovarian cancer is confirmed, but not that of cancer of the endometrium. The risk of cancer of the pancreas in both sexes and the stomach and kidneys in females is significantly raised. No evidence was found for decreased risk for any cancer type. CONCLUSIONS--The risk of cancer at all sites in relatives of breast cancer patients is increased. In addition to the risk of breast, prostate, and ovarian cancer, the risk of pancreas cancer and cancer of the stomach and kidneys in females is raised, but the last mentioned observations need further confirmation.  相似文献   
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Metabolic syndrome is associated with several cancers, but evidence for aggressive prostate cancer is sparse. We prospectively investigated the influence of metabolic syndrome and its components on risk of total prostate cancer and measures of aggressive disease in a cohort of Icelandic men. Men in the Reykjavik Study (n = 9,097, enrolled 1967–1987) were followed for incident (n = 1,084 total; n = 378 advanced; n = 148 high‐grade) and fatal (n = 340) prostate cancer until 2014. Cox regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for (1) measured metabolic factors at cohort entry (body mass index (BMI), blood pressure, triglycerides, fasting blood glucose) and (2) a metabolic syndrome score (range 0–4) combining the risk factors: BMI ≥30 kg/m2; systolic blood pressure (SBP) ≥130 or diastolic blood pressure (DBP) ≥85 mm Hg or taking antihypertensives; triglycerides ≥150 mg/dl; fasting blood glucose ≥100 mg/dl or self‐reported type 2 diabetes. Hypertension and type 2 diabetes were associated with a higher risk of total, advanced, high‐grade, and fatal prostate cancer, independent of BMI. Neither BMI nor triglycerides were associated with prostate cancer risk. Higher metabolic syndrome score (3–4 vs 0) was associated with a higher risk of fatal prostate cancer (HR 1.55; 95% CI: 0.89, 2.69; p trend = 0.08), although this finding was not statistically significant. Our findings suggest a positive association between midlife hypertension and diabetes and risk of total and aggressive prostate cancer. Further, metabolic syndrome as a combination of factors was associated with an increased risk of fatal prostate cancer.  相似文献   
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Studies on the relationship between unemployment and body weight show a positive relationship between Body Mass Index (BMI) and unemployment at the individual level, while aggregate unemployment is negatively related to a population’s average BMI. The aim of this study was to examine the relationship between job loss and changes in body weight following the Icelandic economic collapse of 2008. The analysis relies on a health and lifestyle survey “Heilsa og líðan”, carried out by The Public Health Institute of Iceland in the years 2007 and 2009. The sample is a stratified random sample of 9,807 Icelanders between the ages of 18 and 79, with a net response rate of 42.1 % for individuals responding in both waves. A linear regression model was used when estimating the relationship between job loss following the economic collapse and changes in body weight. Family income and mental health were explored as mediators. Point estimates indicated that both men and women gain less weight in the event of a job loss relative to those who retained their employment. The coefficients of job loss were only statistically significant for females, but not in the male population. The results from all three models were inconsistent with results from other studies where job loss has been found to increase body weight. However, body weight has been shown to be procyclical, and the fact that the data used were gathered during a severe economic downturn might separate these results from earlier findings.  相似文献   
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Familial risk of lung carcinoma in the Icelandic population   总被引:2,自引:0,他引:2  
Context  The dominant role of tobacco smoke as a causative factor in lung carcinoma is well established; however, an inherited predisposition may also be an important factor in the susceptibility to lung carcinoma. Objective  To investigate the contribution of genetic factors to the risk of developing lung carcinoma in the Icelandic population. Design, Setting, and Participants  Risk ratios (RRs) of lung carcinoma for first-, second-, and third-degree relatives of patients with lung carcinoma were estimated by linking records from the Icelandic Cancer Registry (ICR) of all 2756 patients diagnosed with lung carcinoma within the Icelandic population from January 1, 1955, to February 28, 2002, with an extensive genealogical database containing all living Icelanders and most of their ancestors since the settlement of Iceland. The RR for smoking was similarly estimated using a random population-based cohort of 10 541 smokers from the Reykjavik Heart Study who had smoked for more than 10 years. Of these smokers, 562 developed lung cancer based on the patients with lung cancer list from the ICR. Main Outcome Measures  Estimation of RRs of close and distant relatives of patients with lung carcinoma and comparison with RRs for close and distant relatives of smokers. Results  A familial factor for lung carcinoma was shown to extend beyond the nuclear family, as evidenced by significantly increased RR for first-degree relatives (for parents: RR, 2.69; 95% confidence interval [CI], 2.20-3.23; for siblings: RR, 2.02; 95% CI, 1.77-2.23; and for children: RR, 1.96; 95% CI, 1.53-2.39), second-degree relatives (for uncles/aunts: RR, 1.34; 95% CI, 1.15-1.49; and for nephews/nieces: RR, 1.28; 95% CI, 1.10-1.43), and third-degree relatives (for cousins: RR, 1.14; 95% CI, 1.05-1.22) of patients with lung carcinoma. This effect was stronger for relatives of patients with early-onset disease (age at onset 60 years) (for parents: RR, 3.48; 95% CI, 1.83-8.21; for siblings: RR, 3.30; 95% CI, 2.19-4.58; and for children: RR, 2.84; 95% CI, 1.34-7.21). The hypothesis that this increased risk is solely due to the effects of smoking was rejected for all relationships, except cousins and spouses, with a single-sided test of the RRs for lung carcinoma vs RRs for smoking. Conclusions  These results underscore the importance of genetic predisposition in the development of lung carcinoma, with its strongest effect in patients with early-onset disease. However, tobacco smoke plays a dominant role in the pathogenesis of this disease, even among those individuals who are genetically predisposed to lung carcinoma.   相似文献   
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