Kurt Straif

Publications of Kurt Straif

• Second primary malignancies among women with uterine sarcoma.

  Authors: Riitta Koivisto-Korander, Ghislaine Scélo, Gilles Ferro, Lene Mellemkjaer, Kari Hemminki, Elisabete Weiderpass, Sharon Tamaro, Vera Pompe-Kirn, Elizabeth Tracey, David H Brewster, Erich V Kliewer, Jon M Tonita, Chia Kee-Seng, Jon G Jonasson, Carmen Martos, Paul Brennan, Kurt Straif, Eero Pukkala

  Gynecologic oncology. 04/2012;

  OBJECTIVE: Uterine sarcomas (US) are rare malignancies with unclear aetiology. Studies on uterine sarcomas in the setting of second primary malignant tumours can provide clues to aetiology andOBJECTIVE: Uterine sarcomas (US) are rare malignancies with unclear aetiology. Studies on uterine sarcomas in the setting of second primary malignant tumours can provide clues to aetiology and identify side effects of different treatments. METHODS: A cohort of 8,606 cases of US was extracted from the data from 13 cancer registries and followed for second primary cancers within the period 1943-2000. Standardized incidence ratios (SIRs) were calculated, and Poisson regression analyses were performed. RESULTS: There were 499 cancer cases observed after a first diagnosis of US (SIR 1.26, 95%CI 1.16-1.38). SIRs were elevated for cancers of the mouth and pharynx (2.16, 95%CI 1.15-3.69), colorectum (1.60, 95%CI 1.28-1.98), lung (1.73, 95%CI 1.27-2.29), breast (1.25, 95%CI 1.05-1.49), urinary bladder (1.74, 95%CI 1.02-2.79), kidney (2.00, 95%CI 1. 24-3.06), thyroid gland (2.74, 95%CI 1.42-4.79), and soft tissue sarcoma (5.23, 95%CI 2.51-9.62). The risk of breast cancer increased along with increasing age of US diagnosis (p trend 0.040). The risk of kidney cancer increased along with decreasing age of US diagnosis (p trend 0.004) and short time since the US diagnosis (p trend 0.018). CONCLUSIONS: Our study demonstrated increased risk of certain cancers following of a diagnosis of US. The elevated risk for breast cancer may indicate shared hormonal aetiology, while the increased risk of colorectal and bladder cancers after US may be caused by radiation therapy of US. The clustering of smoking-related cancers after US is worth exploring in the future.

• Carcinogenicity of malaria and of some polyomaviruses.

  Authors: Véronique Bouvard, Robert A Baan, Yann Grosse, Béatrice Lauby-Secretan, Fatiha El Ghissassi, Lamia Benbrahim-Tallaa, Neela Guha, Kurt Straif

  The lancet oncology. 04/2012; 13(4):339-40.

• Development of an exposure measurement database on five lung carcinogens (ExpoSYN) for quantitative retrospective occupational exposure assessment.

  Authors: Susan Peters, Roel Vermeulen, Ann Olsson, Rainer Van Gelder, Benjamin Kendzia, Raymond Vincent, Barbara Savary, Nick Williams, Torill Woldbæk, Jérôme Lavoué, Domenico Cavallo, Andrea Cattaneo, Dario Mirabelli, Nils Plato, Dirk Dahmann, Joelle Fevotte, Beate Pesch, Thomas Brüning, Kurt Straif, Hans Kromhout

  The Annals of occupational hygiene. 01/2012; 56(1):70-9.

  SYNERGY is a large pooled analysis of case-control studies on the joint effects of occupational carcinogens and smoking in the development of lung cancer. A quantitative job-exposure matrix (JEM)SYNERGY is a large pooled analysis of case-control studies on the joint effects of occupational carcinogens and smoking in the development of lung cancer. A quantitative job-exposure matrix (JEM) will be developed to assign exposures to five major lung carcinogens [asbestos, chromium, nickel, polycyclic aromatic hydrocarbons (PAH), and respirable crystalline silica (RCS)]. We assembled an exposure database, called ExpoSYN, to enable such a quantitative exposure assessment. Existing exposure databases were identified and European and Canadian research institutes were approached to identify pertinent exposure measurement data. Results of individual air measurements were entered anonymized according to a standardized protocol. The ExpoSYN database currently includes 356 551 measurements from 19 countries. In total, 140 666 personal and 215 885 stationary data points were available. Measurements were distributed over the five agents as follows: RCS (42%), asbestos (20%), chromium (16%), nickel (15%), and PAH (7%). The measurement data cover the time period from 1951 to present. However, only a small portion of measurements (1.4%) were performed prior to 1975. The major contributing countries for personal measurements were Germany (32%), UK (22%), France (14%), and Norway and Canada (both 11%). ExpoSYN is a unique occupational exposure database with measurements from 18 European countries and Canada covering a time period of >50 years. This database will be used to develop a country-, job-, and time period-specific quantitative JEM. This JEM will enable data-driven quantitative exposure assessment in a multinational pooled analysis of community-based lung cancer case-control studies.

• Preventable exposures associated with human cancers.

  Authors: Vincent James Cogliano, Robert Baan, Kurt Straif, Yann Grosse, Béatrice Lauby-Secretan, Fatiha El Ghissassi, Véronique Bouvard, Lamia Benbrahim-Tallaa, Neela Guha, Crystal Freeman, Laurent Galichet, Christopher P Wild

  Journal of the National Cancer Institute. 12/2011; 103(24):1827-39.

  Information on the causes of cancer at specific sites is important to cancer control planners, cancer researchers, cancer patients, and the general public. The International Agency for Research onInformation on the causes of cancer at specific sites is important to cancer control planners, cancer researchers, cancer patients, and the general public. The International Agency for Research on Cancer (IARC) Monograph series, which has classified human carcinogens for more than 40 years, recently completed a review to provide up-to-date information on the cancer sites associated with more than 100 carcinogenic agents. Based on IARC's review, we listed the cancer sites associated with each agent and then rearranged this information to list the known and suspected causes of cancer at each site. We also summarized the rationale for classifications that were based on mechanistic data. This information, based on the forthcoming IARC Monographs Volume 100, offers insights into the current state-of-the-science of carcinogen identification. Use of mechanistic data to identify carcinogens is increasing, and epidemiological research is identifying additional carcinogens and cancer sites or confirming carcinogenic potential under conditions of lower exposure. Nevertheless, some common human cancers still have few (or no) identified causal agents.

• Bitumens and bitumen emissions, and some heterocyclic polycyclic aromatic hydrocarbons.

  Authors: Beatrice Lauby-Secretan, Robert Baan, Yann Grosse, Fatiha El Ghissassi, Véronique Bouvard, Lamia Benbrahim-Tallaa, Neela Guha, Laurent Galichet, Kurt Straif

  The lancet oncology. 12/2011; 12(13):1190-1.

• Cigarette smoking and lung cancer-relative risk estimates for the major histological types from a pooled analysis of case-control studies.

  Authors: Beate Pesch, Benjamin Kendzia, Per Gustavsson, Karl-Heinz Jöckel, Georg Johnen, Hermann Pohlabeln, Ann Olsson, Wolfgang Ahrens, Isabelle Mercedes Gross, Irene Brüske [......] Eleonora Fabianova, Rodica Stanescu Dumitru, Vladimir Bencko, Lenka Foretova, Vladimir Janout, Charles M Rudin, Paul Brennan, Paolo Boffetta, Kurt Straif, Thomas Brüning

  International journal of cancer. Journal international du cancer. 11/2011;

  Lung cancer is mainly caused by smoking, but the quantitative relations between smoking and histologic subtypes of lung cancer remain inconclusive. By using one of the largest lung cancer datasetsLung cancer is mainly caused by smoking, but the quantitative relations between smoking and histologic subtypes of lung cancer remain inconclusive. By using one of the largest lung cancer datasets ever assembled, we explored the impact of smoking on risks of the major cell types of lung cancer. This pooled analysis included 13,169 cases and 16,010 controls from Europe and Canada. Studies with population controls comprised 66.5% of the subjects. Adenocarcinoma (AdCa) was the most prevalent subtype in never smokers and in women. Squamous cell carcinoma (SqCC) predominated in male smokers. Age-adjusted odds ratios (ORs) were estimated with logistic regression. ORs were elevated for all metrics of exposure to cigarette smoke and were higher for SqCC and small cell lung cancer (SCLC) than for AdCa. Current male smokers with an average daily dose of >30 cigarettes had ORs of 103.5 (95% confidence interval (CI): 74.8-143.2) for SqCC, 111.3 (95% CI: 69.8-177.5) for SCLC and 21.9 (95% CI: 16.6-29.0) for AdCa. In women, the corresponding ORs were 62.7 (95% CI: 31.5-124.6), 108.6 (95% CI: 50.7-232.8) and 16.8 (95% CI: 9.2-30.6), respectively. Although ORs started to decline soon after quitting, they did not fully return to the baseline risk of never smokers even 35 years after cessation. The major result that smoking exerted a steeper risk gradient on SqCC and SCLC than on AdCa is in line with previous population data and biological understanding of lung cancer development.

• Modelling of occupational respirable crystalline silica exposure for quantitative exposure assessment in community-based case-control studies.

  Authors: Susan Peters, Roel Vermeulen, Lützen Portengen, Ann Olsson, Benjamin Kendzia, Raymond Vincent, Barbara Savary, Jérôme Lavoué, Domenico Cavallo, Andrea Cattaneo, Dario Mirabelli, Nils Plato, Joelle Fevotte, Beate Pesch, Thomas Brüning, Kurt Straif, Hans Kromhout

  Journal of environmental monitoring : JEM. 11/2011; 13(11):3262-8.

  We describe an empirical model for exposure to respirable crystalline silica (RCS) to create a quantitative job-exposure matrix (JEM) for community-based studies. Personal measurements of exposure toWe describe an empirical model for exposure to respirable crystalline silica (RCS) to create a quantitative job-exposure matrix (JEM) for community-based studies. Personal measurements of exposure to RCS from Europe and Canada were obtained for exposure modelling. A mixed-effects model was elaborated, with region/country and job titles as random effect terms. The fixed effect terms included year of measurement, measurement strategy (representative or worst-case), sampling duration (minutes) and a priori exposure intensity rating for each job from an independently developed JEM (none, low, high). 23,640 personal RCS exposure measurements, covering a time period from 1976 to 2009, were available for modelling. The model indicated an overall downward time trend in RCS exposure levels of -6% per year. Exposure levels were higher in the UK and Canada, and lower in Northern Europe and Germany. Worst-case sampling was associated with higher reported exposure levels and an increase in sampling duration was associated with lower reported exposure levels. Highest predicted RCS exposure levels in the reference year (1998) were for chimney bricklayers (geometric mean 0.11 mg m(-3)), monument carvers and other stone cutters and carvers (0.10 mg m(-3)). The resulting model enables us to predict time-, job-, and region/country-specific exposure levels of RCS. These predictions will be used in the SYNERGY study, an ongoing pooled multinational community-based case-control study on lung cancer.

• The role of alcohol dehydrogenase genes in head and neck cancers: a systematic review and meta-analysis of ADH1B and ADH1C.

  Authors: Jeffrey S Chang, Kurt Straif, Neela Guha

  Mutagenesis. 10/2011;

  Alcohol drinking is a major risk factor for head and neck cancer (HNC). This risk may be modified by alcohol dehydrogenase (ADH) genes, particularly ADH1B and ADH1C, that oxidise ethanol to itsAlcohol drinking is a major risk factor for head and neck cancer (HNC). This risk may be modified by alcohol dehydrogenase (ADH) genes, particularly ADH1B and ADH1C, that oxidise ethanol to its carcinogenic metabolite, acetaldehyde. A meta-analysis was conducted to assess the association between ADH1B and ADH1C and HNC risk. Twenty-nine studies from 28 articles identified from a literature search were included. Summary odds ratios (meta-ORs) were generated using random effect models. A reduced risk for HNC was associated with carrying the ADH1B*2 and ADH1C*1 alleles that confer faster metabolism of ethanol to acetaldehyde [meta-OR ADH1B, 0.50; 95% confidence interval (CI): 0.37-0.68, 13 studies; meta-OR ADH1C, 0.87; 95% CI: 0.76-0.99, 22 studies]. ADH1B*2 and ADH1C*1 alleles appear to be protective for HNC, possibly due to: (i) decreasing the opportunity for oral microflora to produce acetaldehyde locally from a prolonged systemic circulation of ethanol, (ii) preventing ethanol from acting as a solvent for other carcinogens, and (iii) decreasing the amount of ethanol a person consumes since a consequent peak in systemic acetaldehyde could cause discomfort. These results underscore the importance of ADH1B and ADH1C in the association between alcohol consumption and the risk for HNC.

• Occupational exposure to organic dust increases lung cancer risk in the general population.

  Authors: Susan Peters, Hans Kromhout, Ann C Olsson, Heinz-Erich Wichmann, Irene Brüske, Dario Consonni, Maria Teresa Landi, Neil Caporaso, Jack Siemiatycki, Lorenzo Richiardi [......] Vladimir Janout, Isabelle Stücker, Rodica Stanescu Dumitru, Simone Benhamou, Bas Bueno-de-Mesquita, Benjamin Kendzia, Beate Pesch, Kurt Straif, Thomas Brüning, Roel Vermeulen

  Thorax. 08/2011; 67(2):111-6.

  Organic dust is a complex mixture of particulate matter from microbial, plant or animal origin. Occupations with exposure to animal products have been associated with an increased lung cancer risk,Organic dust is a complex mixture of particulate matter from microbial, plant or animal origin. Occupations with exposure to animal products have been associated with an increased lung cancer risk, while exposure to microbial components (eg, endotoxin) has been associated with a decreased risk. To date there has not been a comprehensive evaluation of the possible association between occupational organic dust exposure (and its specific constituents) and lung cancer risk in the general population. The SYNERGY project has pooled information on lifetime working and smoking from 13 300 lung cancer cases and 16 273 controls from 11 case-control studies conducted in Europe and Canada. A newly developed general population job-exposure matrix (assigning no, low or high exposure to organic dust, endotoxin, and contact with animals or fresh animal products) was applied to determine level of exposure. ORs for lung cancer were estimated by logistic regression, adjusted for age, sex, study, cigarette pack-years, time since quitting smoking, and ever employment in occupations with established lung cancer risk. Occupational organic dust exposure was associated with increased lung cancer risk. The second to the fourth quartile of cumulative exposure showed significant risk estimates ranging from 1.12 to 1.24 in a dose-dependent manner (p<0.001). This association remained in the highest quartile after restricting analyses to subjects without chronic obstructive pulmonary disease or asthma. No association was observed between lung cancer and exposure to endotoxin or contact with animals or animal products. Occupational exposure to organic dust was associated with increased lung cancer risk in this large pooled case-control study.

• Lung cancer risk in painters: a meta-analysis.

  Authors: Neela Guha, Franco Merletti, Nelson Kyle Steenland, Andrea Altieri, Vincent Cogliano, Kurt Straif

  Ciência & saúde coletiva. 08/2011; 16(8):3613-32.

  We conducted a meta-analysis to quantitatively compare the association between occupation as a painter and the incidence or mortality from lung cancer. PubMed and the reference lists of pertinentWe conducted a meta-analysis to quantitatively compare the association between occupation as a painter and the incidence or mortality from lung cancer. PubMed and the reference lists of pertinent publications were searched and reviewed. For the meta-analysis, we used data from 47 independent cohort, record linkage, and case-control studies (from a total of 74 reports), including > 11,000 incident cases or deaths from lung cancer among painters. Three authors independently abstracted data and assessed study quality. The summary relative risk (meta-RR, random effects) for lung cancer in painters was 1.35 [95% confidence interval (CI), 1.29-1.41; 47 studies] and 1.35 (95% CI, 1.21-1.51; 27 studies) after controlling for smoking. The relative risk was higher in never-smokers (meta-RR = 2.00; 95% CI, 1.09-3.67; 3 studies) and persisted when restricted to studies that adjusted for other occupational exposures (meta-RR = 1.57; 95% CI, 1.21-2.04; 5 studies). These results support the conclusion that occupational exposures in painters are causally associated with the risk of lung cancer.

• Carcinogenicity of radiofrequency electromagnetic fields.

  Authors: Robert Baan, Yann Grosse, Béatrice Lauby-Secretan, Fatiha El Ghissassi, Véronique Bouvard, Lamia Benbrahim-Tallaa, Neela Guha, Farhad Islami, Laurent Galichet, Kurt Straif

  The lancet oncology. 07/2011; 12(7):624-6.

• AGRICOH: a consortium of agricultural cohorts.

  Authors: Maria E Leon, Laura E Beane Freeman, Jeroen Douwes, Jane A Hoppin, Hans Kromhout, Pierre Lebailly, Karl-Christian Nordby, Marc Schenker, Joachim Schüz, Stephen C Waring [......] John McLaughlin, James A Merchant, Punam Pahwa, Torben Sigsgaard, Leslie Stayner, Catharina Wesseling, Keun-Young Yoo, Shelia H Zahm, Kurt Straif, Aaron Blair

  International journal of environmental research and public health. 05/2011; 8(5):1341-57.

  AGRICOH is a recently formed consortium of agricultural cohort studies involving 22 cohorts from nine countries in five continents: South Africa (1), Canada (3), Costa Rica (2), USA (6), Republic ofAGRICOH is a recently formed consortium of agricultural cohort studies involving 22 cohorts from nine countries in five continents: South Africa (1), Canada (3), Costa Rica (2), USA (6), Republic of Korea (1), New Zealand (2), Denmark (1), France (3) and Norway (3). The aim of AGRICOH, initiated by the US National Cancer Institute (NCI) and coordinated by the International Agency for Research on Cancer (IARC), is to promote and sustain collaboration and pooling of data to investigate the association between a wide range of agricultural exposures and a wide range of health outcomes, with a particular focus on associations that cannot easily be addressed in individual studies because of rare exposures (e.g., use of infrequently applied chemicals) or relatively rare outcomes (e.g., certain types of cancer, neurologic and auto-immune diseases). To facilitate future projects the need for data harmonization of selected variables is required and is underway. Altogether, AGRICOH provides excellent opportunities for studying cancer, respiratory, neurologic, and auto-immune diseases as well as reproductive and allergic disorders, injuries and overall mortality in association with a wide array of exposures, prominent among these the application of pesticides.

• Carcinogenicity of chemicals in industrial and consumer products, food contaminants and flavourings, and water chlorination byproducts.

  Authors: Yann Grosse, Robert Baan, Béatrice Secretan-Lauby, Fatiha El Ghissassi, Véronique Bouvard, Lamia Benbrahim-Tallaa, Neela Guha, Farhad Islami, Laurent Galichet, Kurt Straif

  The lancet oncology. 04/2011; 12(4):328-9.

• Exposure to environmental tobacco smoke in childhood and incidence of cancer in adulthood in never smokers in the European Prospective Investigation into Cancer and Nutrition.

  Authors: Shu-Chun Chuang, Valentina Gallo, Dominique Michaud, Kim Overvad, Anne Tjønneland, Francoise Clavel-Chapelon, Isabelle Romieu, Kurt Straif, Domenico Palli, Valeria Pala, Rosario Tumino, Carlotta Sacerdote, Salvatore Panico, Petra H Peeters, Eiliv Lund, Inger Torhild Gram, Jonas Manjer, Signe Borgquist, Elio Riboli, Paolo Vineis

  Cancer causes & control : CCC. 03/2011; 22(3):487-94.

  The association between childhood environmental tobacco smoke (ETS) exposure and adult cancer risk is controversial; we examined this relationship in never smokers within the European ProspectiveThe association between childhood environmental tobacco smoke (ETS) exposure and adult cancer risk is controversial; we examined this relationship in never smokers within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Over an average of 10 years, 8,372 cases of cancer were diagnosed in 112,430 never smokers in EPIC. Childhood ETS was self-reported by participants at baseline, along with other lifestyle factors. Hazard ratios (HR) for ETS exposure in childhood and their 95% confidence intervals (CI) were estimated by Cox proportional hazards models stratified by age, sex, and study center and adjusted for education, alcohol drinking, body mass index, physical activity, non-alcoholic energy intake, fruit and vegetable intake, and adulthood ETS exposure. Models were further adjusted for reproductive factors for female cancers, for meat intake for digestive system cancers, and for diabetes status for pancreatic cancer. No association was observed between childhood ETS exposure and overall cancer risks (HR = 0.97, 95% CI = 0.92-1.02), and for selected sites. The only exception was pancreatic cancer, as previously reported by Vrieling et al., among those who had been exposed daily in childhood (overall HR = 2.09, 95% CI = 1.14-3.84). In conclusion, childhood ETS exposure might not be a major risk factor for common cancers in adulthood.

• Prediagnostic circulating parathyroid hormone concentration and colorectal cancer in the European Prospective Investigation into Cancer and Nutrition cohort.

  Authors: Veronika Fedirko, Elio Riboli, H Bas Bueno-de-Mesquita, Sabina Rinaldi, Tobias Pischon, Teresa Norat, Eugène H J M Jansen, Fränzel J B van Duijnhoven, Anne Tjønneland, Anja Olsen [......] Richard Palmqvist, Göran Hallmans, Timothy J Key, Konstantinos K Tsilidis, Kay-Tee Khaw, Isabelle Romieu, Kurt Straif, Petra A Wark, Dora Romaguera, Mazda Jenab

  Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. 03/2011; 20(5):767-78.

  Parathyroid hormone (PTH) has been proposed to play a promoting role in carcinogenesis. However, no epidemiologic studies have yet directly investigated its role in colorectal cancer (CRC). AParathyroid hormone (PTH) has been proposed to play a promoting role in carcinogenesis. However, no epidemiologic studies have yet directly investigated its role in colorectal cancer (CRC). A case-control study nested within the European Prospective Investigation into Cancer and Nutrition cohort was conducted with 1,214 incident, sporadic CRC cases matched to 1,214 controls. Circulating prediagnostic PTH and 25-hydroxy vitamin D [25(OH)D] concentrations were measured by enzyme-linked immunosorbent assays. Detailed dietary and lifestyle questionnaire data were collected at baseline. Multivariable conditional logistic regression was used to estimate the incidence rate ratio (RR) with 95% confidence intervals (95% CI) for the association between circulating PTH and CRC risk. In multivariate analyses [including adjustment for 25(OH)D concentration] with a priori defined cutoff points, high levels of serum PTH (≥65 ng/L) compared with medium PTH levels of 30-65 ng/L were associated with increased CRC risk (RR = 1.41, 95% CI: 1.03-1.93). In analyses by sex, the CRC risk was 1.77 (95% CI: 1.14-2.75) and 1.15 (95% CI: 0.73-1.84) in men and women, respectively (P(heterogeneity) = 0.01). In subgroup analyses by anatomical subsite, the risk for colon cancer was RR = 1.56, 95% CI: 1.03-2.34, and for rectal cancer RR = 1.20, 95% CI: 0.72-2.01 (P(heterogeneity) = 0.21). Effect modification by various risk factors was examined. The results of this study suggest that high serum PTH levels may be associated with incident, sporadic CRC in Western European populations, and in particular among men. To our knowledge, this is the first study on PTH and CRC. The role of PTH in carcinogenesis needs to be further investigated.

• Updating IARC's carcinogenicity assessment of benzene.

  Authors: Vincent James Cogliano, Robert Baan, Kurt Straif

  American journal of industrial medicine. 02/2011; 54(2):165-7.

• Comparison of exposure assessment methods for occupational carcinogens in a multi-centre lung cancer case-control study.

  Authors: Susan Peters, Roel Vermeulen, Adrian Cassidy, Andrea 't Mannetje, Martie van Tongeren, Paolo Boffetta, Kurt Straif, Hans Kromhout

  Occupational and environmental medicine. 02/2011; 68(2):148-53.

  Retrospective exposure assessment remains a problematic aspect of population-based case-control studies. Different methods have been developed, including case-by-case expert assessment andRetrospective exposure assessment remains a problematic aspect of population-based case-control studies. Different methods have been developed, including case-by-case expert assessment and job-exposure matrices (JEM). The present analyses compare exposure prevalence and risk estimates derived by different exposure assessment methods. In the context of a case-control study conducted in seven European countries, exposure was estimated for asbestos, diesel motor emissions (DME) and crystalline silica, using three different assessment methods. First, experts assigned exposures to all reported jobs on a case-by-case basis. Second, a population-specific JEM (PSJEM) was developed using the expert assessments of controls only, and re-applied to all study subjects. Third, an independent general population JEM (GPJEM) was created by occupational exposure experts not involved in the original study, and applied to study subjects. Results from these methods were compared. There was poor to fair agreement in assigned exposure between expert assessment and the GPJEM (kappas: asbestos 0.17; DME 0.48; silica 0.38). Exposure prevalence was significantly heterogeneous (p<0.01) between countries for all three agents and assessment methods. For asbestos and DME, significant country heterogeneity in risk estimates was observed when using expert assessment. When applying the GPJEM, the heterogeneity in risk estimates for asbestos and, to some extent, silica diminished. It has been previously advocated that the expert assessment approach to assign exposures based on detailed questionnaire responses provides more accurate exposure estimates than JEM-based results. However, current results demonstrated little, if any, advantage of case-by-case assessment when compared to a JEM approach.

• Alcohol drinking and esophageal squamous cell carcinoma with focus on light-drinkers and never-smokers: a systematic review and meta-analysis.

  Authors: Farhad Islami, Veronika Fedirko, Irene Tramacere, Vincenzo Bagnardi, Mazda Jenab, Lorenza Scotti, Matteo Rota, Giovanni Corrao, Werner Garavello, Joachim Schüz, Kurt Straif, Eva Negri, Paolo Boffetta, Carlo La Vecchia

  International journal of cancer. Journal international du cancer. 12/2010; 129(10):2473-84.

  Quantification of the association between alcohol drinking and risk of esophageal squamous cell carcinoma (ESCC) is an open issue, particularly among light alcohol drinkers, never-smokers, and AsianQuantification of the association between alcohol drinking and risk of esophageal squamous cell carcinoma (ESCC) is an open issue, particularly among light alcohol drinkers, never-smokers, and Asian populations, in which some high-risk polymorphisms in alcohol metabolizing genes are more prevalent. To address these issues, we conducted a systematic review and meta-analysis using 40 case-control and 13 cohort studies that reported on the risk associated with alcohol drinking for at least three levels of consumption. In studies adjusted for age, sex, and tobacco smoking, the relative risk (RR) and 95% confidence interval (CI) for the association between light alcohol drinking (≤ 12.5 g/d) and risk of ESCC was 1.38 (1.14-1.67). The association was slightly stronger in Asian countries than in other populations. The adjusted RRs (95% CIs) were 2.62 (2.07-3.31) for moderate drinking (>12.5-<50 g/d) and 5.54 (3.92-7.28) for high alcohol intake (≥50 g/d); the RRs were slightly higher in non-Asian populations. In prospective studies, the RR (95% CI) was 1.35 (0.92-1.98) for light, 2.15 (1.55-2.98) for moderate, and 3.35 (2.06-5.46) for high alcohol intakes; light drinking showed an association with ESCC in Asia (five studies) but not in other regions (three studies). Among never-smokers (nine studies), the RR (95% CI) was 0.74 (0.47-1.16) for light, 1.54 (1.09-2.17) for moderate, and 3.09 (1.75-5.46) for high intakes. This meta-analysis further corroborates the association of moderate and high alcohol intake with risk of ESCC and provides risk estimates based on multiple prospective studies. Light alcohol intake appears to be associated to ESCC mainly in studies in Asia, which suggests a possible role of genetic susceptibility factors.

• Effectiveness of tax and price policies in tobacco control.

  Authors: Frank J Chaloupka, Kurt Straif, Maria E Leon

  Tobacco control. 11/2010; 20(3):235-8.

  Over 20 experts on economics, epidemiology, public policy and tobacco control were asked by the International Agency for Research on Cancer (IARC) to evaluate the strength of the available evidenceOver 20 experts on economics, epidemiology, public policy and tobacco control were asked by the International Agency for Research on Cancer (IARC) to evaluate the strength of the available evidence on the effects of tax and price policies to prevent and reduce tobacco use. Draft papers presenting and assessing the evidence on the following topics were developed by the experts in an 8-month period prior to the meeting: tobacco industry pricing strategies and tax related lobbying; tax, price and aggregate demand for tobacco; tax, price and adult tobacco use, use among young people and use among the poor; tax avoidance and tax evasion; and the economic and health impact of tobacco taxation. Subsequently, papers were peer reviewed, revised and resubmitted for final discussion at a 6-day meeting at IARC in Lyon, France, where a consensus evaluation of 18 concluding statements using the pre-established criteria of the IARC Cancer Prevention Handbooks took place. Studies published (or accepted for publication) in the openly available scientific literature were the main source of evidence for the review and evaluation; other types of publications were included when appropriate. In support of 12 of the 18 conclusions, the experts agreed that there was sufficient evidence of effectiveness of increased tobacco excise taxes and prices in reducing overall tobacco consumption and prevalence of tobacco use and improvement of public health, including by preventing initiation and uptake among young people, promoting cessation among current users and lowering consumption among those who continue to use. For the remaining six concluding statements the evidence was strong (four statements) or limited (two statements). The evidence presented and assessed in IARC Handbook volume 14 documents the effectiveness of tax and price policies in the control of tobacco use and improvement of public health.

• Alcohol drinking and laryngeal cancer: overall and dose-risk relation--a systematic review and meta-analysis.

  Authors: Farhad Islami, Irene Tramacere, Matteo Rota, Vincenzo Bagnardi, Veronika Fedirko, Lorenza Scotti, Werner Garavello, Mazda Jenab, Giovanni Corrao, Kurt Straif, Eva Negri, Paolo Boffetta, Carlo La Vecchia

  Oral oncology. 11/2010; 46(11):802-10.

  Alcohol drinking is a known risk factor for laryngeal cancer. However, little information is available on the risk associated with light alcohol drinking. To address this issue, we conducted aAlcohol drinking is a known risk factor for laryngeal cancer. However, little information is available on the risk associated with light alcohol drinking. To address this issue, we conducted a meta-analysis using two methods: (i) random-effects models with reconstruction of alcohol consumption categories and calculation of risk estimates associated with predefined consumption levels using Hamling method and (ii) random-effects meta-regression models. The PubMed database was searched for all case-control or cohort studies published in the English language on the association between alcohol consumption and risk of laryngeal cancer. Forty studies (38 case-control, 2 cohort) reporting on at least three levels of consumption were included. Overall, alcohol drinking versus non-drinking was associated with an approximately 2-fold increase in risk of laryngeal cancer (RR=1.90; 95% CI: 1.59-2.28). While light alcohol drinking (≥1 drink/day) did not show any significant association with risk of laryngeal cancer (12 studies. RR=0.88; 95% CI: 0.71-1.08), moderate drinking (>1 to <4drinks/day) was associated with a 1.5-fold increase in risk (35 studies. RR=1.47; 95% CI: 1.25-1.72) and heavy drinking (⩾4drinks/day) was associated with a 2.5-fold increased risk (33 studies. RR=2.62; 95% CI: 2.13-3.23). Subgroup analyses for studies that adjusted for main potential confounding factors (age, sex, and tobacco use) and several further subgroup analyses showed similar results, which suggest the robustness of the results.