Eberhard Greiser
University of Bremen
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Featured researches published by Eberhard Greiser.
International Journal of Cancer | 2000
Paul Brennan; Olivier Bogillot; Sylvaine Cordier; Eberhard Greiser; Walter Schill; Paolo Vineis; Gonzalo López-Abente; Anastasia Tzonou; Jenny Chang-Claude; Ulrich Bolm-Audorff; Karl-Heinz Jöckel; Francesco Donato; Consol Serra; Jorgen Wahrendorf; Martine Hours; Andrea t'Mannetje; Manolis Kogevinas; Paolo Boffetta
The primary risk factor for bladder cancer is cigarette smoking. Using a combined analysis of 11 case‐control studies, we have accurately measured the relationship between cigarette smoking and bladder cancer in men. Available smoking information on 2,600 male bladder cancer cases and 5,524 male controls included duration of smoking habit, number of cigarettes smoked per day and time since cessation of smoking habit for ex‐smokers. There was a linear increasing risk of bladder cancer with increasing duration of smoking, ranging from an odds ratio (OR) of 1.96 after 20 years of smoking (95% confidence interval [CI] 1.48–2.61) to 5.57 after 60 years (CI 4.18–7.44). A dose relationship was observed between number of cigarettes smoked per day and bladder cancer up to a threshold limit of 15–20 cigarettes per day, OR = 4.50 (CI 3.81–5.33), after which no increased risk was observed. An immediate decrease in risk of bladder cancer was observed for those who gave up smoking. This decrease was over 30% after 1–4 years, OR = 0.65 (0.53–0.79), and was over 60% after 25 years of cessation, OR = 0.37 (0.30–0.45). However, even after 25 years, the decrease in risk did not reach the level of the never‐smokers, OR = 0.20. (0.17–0.24). The proportion of bladder cancer cases attributable to ever‐smoking was 0.66 (0.61–0.70) for all men and 0.73 (0.66–0.79) for men younger than 60. These estimates are higher than previously calculated. Int. J. Cancer 86:289–294, 2000.
Cancer Causes & Control | 2003
Manolis Kogevinas; Andrea 't Mannetje; Sylvaine Cordier; Ulrich Ranft; Carlos A. González; Paolo Vineis; Jenny Chang-Claude; Elsebeth Lynge; Jürgen Wahrendorf; Anastasia Tzonou; Karl-Heinz Jöckel; Consol Serra; Stefano Porru; Martine Hours; Eberhard Greiser; Paolo Boffetta
Objectives: We examined which occupations and industries are currently at high risk for bladder cancer in men. Methods: We combined data from 11 case–control studies conducted between 1976–1996 in six European countries. The study comprised 3346 incident cases and 6840 controls, aged 30–79 years. Lifetime occupational and smoking histories were examined using common coding. Results: Odds ratios for eight a priori defined high-risk occupations were low, and with the exception of metal workers and machinists (OR = 1.16, 95% CI = 1.02–1.32), were not statistically significant. Higher risks were observed for specific categories of painters, metal, textile and electrical workers, for miners, transport operators, excavating-machine operators, and also for non-industrial workers such as concierges and janitors. Industries entailing a high risk included salt mining, manufacture of carpets, paints, plastics and industrial chemicals. An increased risk was found for exposure to PAHs (OR for highest exposure tertile = 1.23, 95% CI = 1.07–1.4). The risk attributable to occupation ranged from 4.2 to 7.4%, with an estimated 4.3% for exposure to PAHs. Conclusions: Metal workers, machinists, transport equipment operators and miners are among the major occupations contributing to occupational bladder cancer in men in Western Europe. In this population one in 10 to one in 20 cancers of the bladder can be attributed to occupation.
Cancer Causes & Control | 2001
Paul Brennan; Olivier Bogillot; Eberhard Greiser; Jenny Chang-Claude; Jürgen Wahrendorf; Sylvaine Cordier; Karl-Heinz Jöckel; Gonzalo López-Abente; Anastasia Tzonou; Paolo Vineis; Francesco Donato; Martine Hours; Consol Serra; Ulrich Bolm-Audorff; Walter Schill; Manolis Kogevinas; Paolo Boffetta
AbstractBackground: Using a combined analysis of 11 case–control studies from Europe, we have investigated the relationship between cigarette smoking and bladder cancer in women. Methods: Available smoking information on 685 female bladder cancer cases and 2416 female controls included duration of smoking habit, number of cigarettes smoked per day, and time since cessation of smoking habit for ex-smokers. Results: There was an increasing risk of bladder cancer with increasing duration of smoking, ranging from approximately a two-fold increased risk for a duration of less than 10 years (odds ratio (OR) = 1.9, 95% confidence interval (CI) 1.1–3.1) to over a four-fold increased risk for a duration of greater than 40 years (OR = 4.1, 95% CI 3.0–5.5). A dose–response relationship was observed between number of cigarettes smoked per day and bladder cancer up to a threshold limit of 15–20 cigarettes per day, OR = 3.8 (95% CI 2.7–5.4), after which no increased risk was observed. An immediate decrease in risk of bladder cancer was observed for those who gave up smoking. This decrease was over 30% in the immediate 1–4 years after cessation, OR = 0.68 (95% CI 0.38–1.2). However, even after 25 years the decrease in risk did not reach the level of the never-smokers, OR = 0.27 (95% CI 0.21–0.35). Conclusion: The proportion of bladder cancer cases among women attributable to ever smoking was 0.30, (0.25–0.35) and to current smoking was 0.18 (0.14–0.22). These attributable proportions are less than those observed among men, although they are likely to increase in the future as the smoking-related disease epidemic among women matures.
Cancer Causes & Control | 2000
Maria Sala; Sylvaine Cordier; Jenny Chang-Claude; Francesco Donato; Antonio Escolar-Pujolar; Francisco Fernandez; Carlos A. González; Eberhard Greiser; Karl-Heinz Jöckel; Elsebeth Lynge; Andrea 't Mannetje; Hermann Pohlabeln; Stefano Porru; Consol Serra; Anastasia Tzonou; Paolo Vineis; Jürgen Wahrendorf; Paolo Boffetta; Manolis Kogevinas
AbstractBackground: Coffee consumption has been associated with an excess bladder cancer risk, but results from epidemiological studies are inconsistent. This association has been long debated, in part due to the potential confounding by smoking. We examined the risk associated with coffee consumption in nonsmokers in a pooled analysis of ten European bladder cancer case–control studies. Methods: The pooled data set comprises 564 cases and 2929 hospital or population controls who had never smoked. They were enrolled in ten studies conducted in Denmark, Germany, Greece, France, Italy and Spain. Information on coffee consumption and occupation was re-coded following standard criteria. Unconditional logistic regression was applied adjusting for age, study center, occupation and gender. Results: Seventy-nine percent of the study population reported having drunk coffee, and 2.4% were heavy drinkers, reporting having drunk on average ten or more cups per day. There was no excess risk in ever coffee drinkers (OR = 1.0, 95% CI 0.8–1.3) compared to never drinkers. The risk did not increase monotonically with dose but a statistically significant excess risk was seen for subjects having drunk ten or more cups per day (OR = 1.8, 95% CI 1.0–3.3). This excess was seen in both men and women. There was no evidence of an association of the risk with duration or type of coffee consumption. The pooled results were not dependent on the findings of any specific study, but they depended on the type of controls with an overall excess risk observed only for studies using hospital controls. Conclusion: Nonsmokers who are heavy coffee drinkers may have a small excess risk of bladder cancer. Although these results cannot be attributed to confounding by smoking, the possibility of bias in control selection cannot be discarded. On the basis of these results, only a very small proportion of cancers of the bladder among nonsmokers could be attributed to coffee drinking.
Cancer Causes & Control | 2001
A. Pitard; Paul Brennan; Jacqueline Clavel; Eberhard Greiser; Gonzalo López-Abente; Jenny Chang-Claude; Jürgen Wahrendorf; Consol Serra; Manolis Kogevinas; Paolo Boffetta
AbstractObjective: Estimating the risk of bladder cancer from cigar and pipe smoking is complicated by a small number of non-cigarette smokers included in most relevant studies. Methods: We undertook a pooled analysis of the data on men from six published case–control studies from Denmark, France, Germany, and Spain, to assess the association between pipe and cigar smoking and bladder cancer, and to compare it with the risk from cigarette smoking. Complete history of tobacco smoking was ascertained separately for cigarettes, cigars, and pipe. Odds ratios (ORs) were estimated after adjusting for age, study, and employment in high-risk occupations. Results: The pooled data set comprised 2279 cases and 5268 controls, of whom 88 cases and 253 controls smoked only cigars or pipe. The OR for pure cigarette smoking was 3.5 (95% confidence interval [CI] 2.9–4.2), that for pure pipe smoking was 1.9 (95% CI 1.2–3.1) and that for pure cigar smoking was 2.3 (95% CI 1.6–3.5). The increase in the OR of bladder cancer that was observed with duration of smoking was non-significantly lower for cigars than for cigarettes. Conclusion: Our results suggest that smoking of cigars and pipe is carcinogenic to the urinary bladder, although the potency might be lower than for cigarettes.
Maturitas | 2010
Claudia M. Greiser; Eberhard Greiser; Martina Dören
OBJECTIVES Lung cancer rates increase among women in many regions of the world. To explore whether menopausal hormone therapy (MHT) plays a role. METHODS We conducted a systematic search of the literature and performed meta-analyses of cohort studies (C), case-control studies (CC), randomized controlled trials (RCTs), and cancer registry studies (CR) to analyse the impact of estrogen therapy (ET), estrogen/progestin therapy (EPT) and any hormone therapy (HT) on lung cancer risks. We explored associations between ever-use of therapies and risks, analysed annual changes of risk, and the impact of therapies on histological subtypes. We calculated summary odds ratios, relative risks, 95% confidence intervals (CI; fixed-effects model), and assessed heterogeneity across studies. Eighteen studies were eligible (9 CC, 4 C, 3 RCT, 2 CR). RESULTS We found a significant increase of risk - 76.2% - in non-smoking women with adenocarcinoma (CI 1.072-2.898) reporting ever-use of HT. Estrogen plus progestin therapy does not change the risk; however, the pooled analysis of 2 RCTs points at an increased risk (RR 1.359; CI 1.031-1.791). Our further results should be interpreted with caution as significances were found in analyses only when smoking and non-smoking women, various hormone regimens, or histological subtypes, respectively, were pooled. CONCLUSIONS Dedicated studies designed to more adequately delineate the role of MHT are necessary to substantiate whether use of MHT is a risk factor for this or other types of lung cancer.
BMC Cancer | 2012
Eberhard Greiser; Karin Halina Greiser; Wolfgang Ahrens; Rudolf Hagen; Roland Lazszig; Heinz Maier; Bernhard Schick; Hans Peter Zenner
BackgroundThere are few studies of the effects of nasal snuff and environmental factors on the risk of nasal cancer. This study aimed to investigate the impact of using nasal snuff and of other risk factors on the risk of nasal cancer in German men.MethodsA population-based case–control study was conducted in the German Federal States of Bavaria and Baden-Württemberg. Tumor registries and ear, nose and throat departments provided access to patients born in 1926 or later.ResultsTelephone interviews were conducted with 427 cases (mean age 62.1 years) and 2.401 population-based controls (mean age 60.8 years). Ever-use of nasal snuff was associated with an odds ratio (OR) for nasal cancer of 1.45 (95% confidence interval [CI] 0.88–2.38) in the total study population, whereas OR in smokers was 2.01 (95% CI 1.00-4.02) and in never smokers was 1.10 (95% CI 0.43–2.80). The OR in ever-smokers vs. never-smokers was 1.60 (95% CI 1.24–2.07), with an OR of 1.06 (95% CI 1.05–1.07) per pack-year smoked, and the risk was significantly decreased after quitting smoking. Exposure to hardwood dust for at least 1 year resulted in an OR of 2.33 (95% CI 1.40–3.91) in the total population, which was further increased in never-smokers (OR 4.89, 95% CI 1.92–12.49) in analyses stratified by smoking status. The OR for nasal cancer after exposure to organic solvents for at least 1 year was 1.53 (1.17–2.01). Ever-use of nasal sprays/nasal lavage for at least 1 month rendered an OR of 1.59 (1.04–2.44). The OR after use of insecticides in homes was 1.48 (95% CI 1.04–2.11).ConclusionsSmoking and exposure to hardwood dust were confirmed as risk factors for nasal carcinoma. There is evidence that exposure to organic solvents, and in-house use of insecticides could represent novel risk factors. Exposure to asbestos and use of nasal snuff were risk factors in smokers only.
Archive | 1986
Heiko Becher; Karl-Heinz Jöckel; Wolfgang Ahrens; Karsten Drescher; Eberhard Greiser; U. Maschewsky-Schneider; Jürgen Timm; Heinz-Erich Wichmann
Zum Nachweis eines Zusammenhanges zwischen Umweltfaktoren, wie z. B. der Luftverschmutzung und der Entstehung chronischer Erkrankungen, wie z. B. des Lungenkrebses, wird in der Epidemiologie haufig die Methodik der Fall-Kontroll-Studie angewendet. Sind diese Umweltrisiken einerseits klein und andererseits mit bekannten und gesicherten Risikofaktoren (wie z. B. dem Rauchen) assoziiert, so ergeben sich eine Reihe methodischer und inhaltlicher Probleme.
Archive | 1985
Karl-Heinz Jöckel; Eberhard Greiser; Wolfgang Ahrens; Heiko Becher; U. Maschewsky-Schneider; P. Metternich; Beate Molik; G. Schöneberg; Heinz-Erich Wichmann; Karsten Drescher; Jürgen Timm
For the question whether air pollution may cause lung cancer to a certain degree a preliminary epidemiologic study design will be described. Sample size estimates based on rather incomplete information and simple statistical models indicated that the study would involve a considerable number of cases and controls. We show that a pilot study is necessary, in order to clarify whether such a study is feasible or whether it goes beyond of what may be answered by an epidemiologic study.
American Journal of Public Health | 2010
Eberhard Greiser; Wolfgang Hoffmann
The explosion of depleted uranium ammunition generates ultrafine uranium dust particles that may pose health hazards, especially an increased risk for cancer, for people living in combat zones. Hagopian et al.1 claims a more than doubling of childhood leukemia incidence in Basrah governorate over a period of 15 years (1993–2007), based on data of a hospital-based tumor registry, speculating about possible effects of chemical warfare agents, benzene, and exposure to depleted uranium dust. In our opinion this claim is as yet unsubstantiated, because no reliable population figures are available for the whole period. Besides, a hospital-based tumor registry usually cannot provide complete population coverage and lacks at least one indispensable data source of population-based cancer registries: death certificates. One of us (E. G.) was part of a group of World Health Organization (WHO) temporary advisors visiting Baghdad in September 1995 on request from the Iraqi Ministry of Health to advise on problems of cancer control. At that instance proportionate incidence data were presented by scientists from the Iraqi National Cancer Registry indicating higher rates of childhood leukemia for the governorate of Basrah than for the rest of Iraq. Exposure to depleted uranium ammunition in and around Basrah was discussed as a possible cause. In a subsequent WHO mission in December of 1995 we analyzed the National Cancer Registry and abstracted from ledgers data on childhood leukemia for the whole of Iraq. No population figures were available, but we were provided with projections of population data for all Iraqi governorates. Based on these data no increase of childhood leukemia could be detected for the governorate of Basrah. In our report to the WHO we raised the suspicion of gross underreporting for all Iraqi governorates except for Baghdad (report available from the authors). A diverse group of children at Kingsmead Primary School pay close attention during a school assembly. Most of the children live on the Kingsmead Estate in Homerton, Hackney, UK, close to the site of the 2012 Summer Olympic Games. Photograph by Gideon Mendell. Printed with permission of Corbis. Supported by the German Academic Exchange Service (Deutscher Akademischer Austauschdienst (DAAD) 2005, 2006) and the Norwegian Foreign Office (2009) we conducted postgraduate courses on epidemiologic methods for scientists from Basrah and Baghdad in Amman, Jordan (February 2005); Greifswald, Germany (February 2006); and Istanbul, Turkey (July 2009) to enable our colleagues from Iraq to establish a population-based cancer registry in Basrah and to prepare a design for a case-control study on childhood leukemia. This endeavor is still under way.