摘要:

Results of two recent prospective incidence studies have suggested that certain subgroups ot men with diabetes mellitus may be protected from developing prostate cancer. Two earlier studies, however, concluded that diabetes increased the risk of mortality from prostate cancer. With hundreds of thousands of male respondents, the 1959–1972 Cancer Prevention Study provided a unique opportunity to explore whether men with diabetes were more likely to develop prostate cancer during a 13-year follow-up period than were men without diabetes. After adjusting for factors associated with prostate cancer in previous studies, we found little association between diabetes at baseline and prostate cancer incidence [incidence density ratio (IDR) = 1.05; 95% confidence interval (CD = 0.81–1.36]. Men who had diabetes mellitus for 5 or more years, however, had a higher incidence of prostate cancer than did men without diabetes (IDR = 1.56; 95% CI = 1.02–2.38). Among all study participants who were diagnosed with prostate cancer, men with diabetes were only slightly more likely to die from prostate cancer than were men without diabetes (IDR = 1.11; 95% CI = 0.76–1.62). (Epidemiology 1999;10:313–318)

ISSN:1044-3983    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Small effects of environmental tobacco smoke exposure on lung function have been demonstrated in many studies of children, but fewer studies have examined adults in this respect. We examined these relations in a 7-year longitudinal study of 1,623 British adults, age 18–73 years, who were nonsmokers throughout. Outcome was measured by forced expiratory volume in 1 second (FEV1) adjusted for sex, age, and height. Exposure was assessed by asking subjects whether they lived with a smoker (at both the initial and the follow-up studies) and by salivary cotinine measurements (follow-up study only). Cross-sectionally, subjects exposed at home showed tiny FEV1deficits at both studies of −4 ml [95% confidence limits (CL) = −31, 23] and −5 ml (95% CL = −32, 22), respectively. Cotinine adjusted for potential confounders showed a stronger association with FEV1, with the highest quintile showing a −105-ml deficit (95% CL = −174, −37) in comparison with the lowest. Longitudinally, no clear relation was apparent between change in FEV1and average exposure or change in exposure. These results indicate that environmental tobacco smoke is associated with small deficits in adult lung function, consistent with our meta-analysis estimate of a 2.7% deficit in exposed nonsmoking adults. The relations seen with cotinine but not with household exposure may reflect the importance of exposure outside the home. (Epidemiology 1999;10:319–326)

ISSN:1044-3983    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

The etiology of Parkinson's disease has been enigmatic to clinicians, epidemiologists, and basic scientists since the clinical syndrome was first described in 1817. Mendelian inheritance probably accounts for a small proportion of Parkinson's disease. Apart from an increasing risk with age, the most consistent epidemiologic observation has been an inverse relation with cigarette smoking. Neither selective survival of nonsmokers nor behavioral characteristics of smokers can explain this seemingly protective association. Interest in environmental exposures, particularly pesticides, metals, and industrial solvents, heightened substantially following the discovery of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a street drug contaminant, as a cause of human parkinsonism. Epidemiologic and toxicologic research has since been guided to a great extent, although not exclusively, by mechanisms of MPTP toxicity. Efforts to characterize gene/environment interactions have also intensified in recent years. In this review, we evaluate recent evidence concerning the etiology of Parkinson's disease, with emphasis on environmental and lifestyle exposures and their potential interactions with genetic susceptibility traits. The most challenging aspects of epidemiologic research into Parkinson's disease causation include methodologic difficulties surrounding case definition, completeness of case ascertainment, selection of appropriate controls in case-control studies, and assessment of environmental exposures. We conclude with recommendations for future research directions. (Epidemiology 1999; 10:327–336)

ISSN:1044-3983    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Data to assess the benefits and risks of hepatitis B vaccine for the general population of U.S. children are sparse. This study addressed the problem of external validity found in previous studies of high risk populations by evaluating the benefit of hepatitis B vaccination for the general population of American children. We calculated the risk of liver problems among hepatitis B vaccinated and non-hepatitis B vaccinated children using logistic regression. Hepatitis B vaccinated children had an unadjusted odds ratio of 2.94 and age-adjusted odds ratio of 2.35 for liver problems compared with non-hepatitis B vaccinated children in the 1993 National Health Interview Survey. Hepatitis B vaccinated children had an unadjusted odds ratio of 2.57 and age-adjusted odds ratio of 1.53 for liver problems compared with non-hepatitis B vaccinated children in the 1994 National Health Interview Survey dataset. (Epidemiology 1999;10:337–339)

ISSN:1044-3983    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:1044-3983    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:1044-3983    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:1044-3983    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:1044-3983    

出版商:OVID    

年代:1999

数据来源: OVID