Neonila Szeszenia-Dabrowska

Publications (97)371.65 Total impact

• Article: Previous lung diseases and lung cancer risk: a pooled analysis from the international lung cancer consortium.

  Darren R Brenner, Paolo Boffetta, Eric J Duell, Heike Bickeböller, Albert Rosenberger, Valerie McCormack, Joshua E Muscat, Ping Yang, H-Erich Wichmann, Irene Brueske-Hohlfeld, [......], Geoffrey Liu, John Wiencke, Monica Neri, Donatella Ugolini, Angeline S Andrew, Qing Lan, Wei Hu, Irene Orlow, Bernard J Park, Rayjean J Hung
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  ABSTRACT: To clarify the role of previous lung diseases (chronic bronchitis, emphysema, pneumonia, and tuberculosis) in the development of lung cancer, the authors conducted a pooled analysis of studies in the International Lung Cancer Consortium. Seventeen studies including 24,607 cases and 81,829 controls (noncases), mainly conducted in Europe and North America, were included (1984-2011). Using self-reported data on previous diagnoses of lung diseases, the authors derived study-specific effect estimates by means of logistic regression models or Cox proportional hazards models adjusted for age, sex, and cumulative tobacco smoking. Estimates were pooled using random-effects models. Analyses stratified by smoking status and histology were also conducted. A history of emphysema conferred a 2.44-fold increased risk of lung cancer (95% confidence interval (CI): 1.64, 3.62 (16 studies)). A history of chronic bronchitis conferred a relative risk of 1.47 (95% CI: 1.29, 1.68 (13 studies)). Tuberculosis (relative risk = 1.48, 95% CI: 1.17, 1.87 (16 studies)) and pneumonia (relative risk = 1.57, 95% CI: 1.22, 2.01 (12 studies)) were also associated with lung cancer risk. Among never smokers, elevated risks were observed for emphysema, pneumonia, and tuberculosis. These results suggest that previous lung diseases influence lung cancer risk independently of tobacco use and that these diseases are important for assessing individual risk.
  American journal of epidemiology 09/2012; 176(7):573-85. · 5.59 Impact Factor
• Article: Increased risk of lung cancer in individuals with a family history of the disease: a pooled analysis from the International Lung Cancer Consortium.

  Michele L Coté, Mei Liu, Stefano Bonassi, Monica Neri, Ann G Schwartz, David C Christiani, Margaret R Spitz, Joshua E Muscat, Gad Rennert, Katja K Aben, [......], Donatella Ugolini, Henricus F M van der Heijden, Erich Wichmann, John K Wiencke, Penella J Woll, Ping Yang, David Zaridze, Zuo-Feng Zhang, Carol J Etzel, Rayjean J Hung
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  ABSTRACT: Familial aggregation of lung cancer exists after accounting for cigarette smoking. However, the extent to which family history affects risk by smoking status, histology, relative type and ethnicity is not well described. This pooled analysis included 24 case-control studies in the International Lung Cancer Consortium. Each study collected age of onset/interview, gender, race/ethnicity, cigarette smoking, histology and first-degree family history of lung cancer. Data from 24,380 lung cancer cases and 23,305 healthy controls were analysed. Unconditional logistic regression models and generalised estimating equations were used to estimate odds ratios and 95% confidence intervals. Individuals with a first-degree relative with lung cancer had a 1.51-fold increase in the risk of lung cancer, after adjustment for smoking and other potential confounders (95% CI: 1.39, 1.63). The association was strongest for those with a family history in a sibling, after adjustment (odds ratios (OR) = 1.82, 95% CI: 1.62, 2.05). No modifying effect by histologic type was found. Never smokers showed a lower association with positive familial history of lung cancer (OR = 1.25, 95% CI: 1.03, 1.52), slightly stronger for those with an affected sibling (OR = 1.44, 95% CI: 1.07, 1.93), after adjustment. The occurrence of lung cancer among never smokers and similar magnitudes of the effect of family history on lung cancer risk across histological types suggests familial aggregation of lung cancer is independent of those risks associated with cigarette smoking. While the role of genetic variation in the aetiology of lung cancer remains to be fully characterised, family history assessment is immediately available and those with a positive history represent a higher risk group.
  European journal of cancer (Oxford, England: 1990) 03/2012; 48(13):1957-68. · 4.12 Impact Factor
• Article: Welding and lung cancer in Central and Eastern Europe and the United Kingdom.

  Andrea 't Mannetje, Paul Brennan, David Zaridze, Neonila Szeszenia-Dabrowska, Peter Rudnai, Jolanta Lissowska, Eleonóra Fabiánová, Adrian Cassidy, Dana Mates, Vladimir Bencko, Lenka Foretova, Vladimir Janout, Joelle Fevotte, Tony Fletcher, Paolo Boffetta
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  ABSTRACT: Occupation as a welder has been associated with a 25%-40% increase in lung cancer risk. This study aims to elucidate to what extent confounding by smoking and asbestos drives this association and to evaluate the role of welding-related exposures such as chromium. The study included 2,197 male incident lung cancer cases and 2,295 controls from Romania, Hungary, Poland, Russia, Slovakia, the Czech Republic, and the United Kingdom from 1998 to 2001. Information on risk factors was collected through face-to-face interviews. Experts assessed exposure to 70 agents, and risk estimates were adjusted for smoking and occupational exposures. Occupation as a welder/flame cutter (prevalence controls: 3.7%) was associated with an odds ratio of 1.36 (95% confidence interval (CI): 1.00, 1.86) after adjustment for smoking and occupational exposures including asbestos. An odds ratio of 1.18 (95% CI: 1.01, 1.38) was found for welding fumes (prevalence controls: 22.8%), increasing to 1.38 for more than 25 exposure years (95% CI: 1.09, 1.75). A duration-response association was also observed for mild steel welding without chromium exposure. In this population, occupational exposure to welding fumes accounted for approximately 4% of lung cancer cases, to which both stainless and mild steel welding contributed equally. Given that welding remains a common task for many workers, exposure to welding fumes represents an important risk factor for lung cancer.
  American journal of epidemiology 02/2012; 175(7):706-14. · 5.59 Impact Factor
• Source

  Available from: Lee E Moore

  Article: Xenobiotic metabolizing gene variants and renal cell cancer: a multicenter study.

  Julia E Heck, Lee E Moore, Yuan-Chin A Lee, James D McKay, Rayjean J Hung, Sara Karami, Valérie Gaborieau, Neonila Szeszenia-Dabrowska, David G Zaridze, Anush Mukeriya, Dana Mates, Lenka Foretova, Vladimir Janout, Helena Kollárová, Vladimir Bencko, Nathaniel Rothman, Paul Brennan, Wong-Ho Chow, Paolo Boffetta
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  ABSTRACT: Background: The countries of Central and Eastern Europe have among the highest worldwide rates of renal cell cancer (RCC). Few studies have examined whether genetic variation in xenobiotic metabolic pathway genes may modify risk for this cancer. Methods: The Central and Eastern Europe Renal Cell Cancer study was a hospital-based case-control study conducted between 1998 and 2003 across seven centers in Central and Eastern Europe. Detailed data were collected from 874 cases and 2053 controls on demographics, work history, and occupational exposure to chemical agents. Genes [cytochrome P-450 family, N-acetyltransferases, NAD(P)H:quinone oxidoreductase I (NQO1), microsomal epoxide hydrolase (mEH), catechol-O-methyltransferase (COMT), uridine diphosphate-glucuronosyltransferase (UGT)] were selected for the present analysis based on their putative role in xenobiotic metabolism. Haplotypes were calculated using fastPhase. Odds ratios and 95% confidence intervals were estimated by unconditional logistic regression adjusted for country of residence, age, sex, smoking, alcohol intake, obesity, and hypertension. Results: We observed an increased risk of RCC with one SNP. After adjustment for multiple comparisons it did not remain significant. Neither NAT1 nor NAT2 slow acetylation was associated with disease. Conclusion: We observed no association between this pathway and renal cell cancer.
  Frontiers in oncology. 01/2012; 2:16.
• Article: Asthma and lung cancer risk: a systematic investigation by the International Lung Cancer Consortium.

  Albert Rosenberger, Heike Bickeböller, Valerie McCormack, Darren R Brenner, Eric J Duell, Anne Tjønneland, Soren Friis, Joshua E Muscat, Ping Yang, H-Erich Wichmann, [......], Loic LeMarchand, Monica Neri, Stefano Bonassi, Angeline S Andrew, Qing Lan, Wei Hu, Irene Orlow, Bernard J Park, Paolo Boffetta, Rayjean J Hung
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  ABSTRACT: Asthma has been hypothesized to be associated with lung cancer (LC) risk. We conducted a pooled analysis of 16 studies in the International Lung Cancer Consortium (ILCCO) to quantitatively assess this association and compared the results with 36 previously published studies. In total, information from 585 444 individuals was used. Study-specific measures were combined using random effects models. A meta-regression and subgroup meta-analyses were performed to identify sources of heterogeneity. The overall LC relative risk (RR) associated with asthma was 1.28 [95% confidence intervals (CIs) = 1.16-1.41] but with large heterogeneity (I(2) = 73%, P < 0.001) between studies. Among ILCCO studies, an increased risk was found for squamous cell (RR = 1.69, 95%, CI = 1.26-2.26) and for small-cell carcinoma (RR = 1.71, 95% CI = 0.99-2.95) but was weaker for adenocarcinoma (RR = 1.09, 95% CI = 0.88-1.36). The increased LC risk was strongest in the 2 years after asthma diagnosis (RR = 2.13, 95% CI = 1.09-4.17) but subjects diagnosed with asthma over 10 years prior had no or little increased LC risk (RR = 1.10, 95% CI = 0.94-1.30). Because the increased incidence of LC was chiefly observed in small cell and squamous cell lung carcinomas, primarily within 2 years of asthma diagnosis and because the association was weak among never smokers, we conclude that the association may not reflect a causal effect of asthma on the risk of LC.
  Carcinogenesis 12/2011; 33(3):587-97. · 5.70 Impact Factor
• Source

  Available from: Beate Pesch

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

  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
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  ABSTRACT: 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 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.
  International Journal of Cancer 11/2011; 131(5):1210-9. · 5.44 Impact Factor
• Article: Lung cancer risk attributable to occupational exposures in a multicenter case-control study in Central and Eastern Europe.

  Ann C Olsson, Per Gustavsson, David Zaridze, Anush Mukeriya, Neonila Szeszenia-Dabrowska, Peter Rudnai, Jolanta Lissowska, Eleonora Fabianova, Dana Mates, Vladimir Bencko, Lenka Foretova, Vladimir Janout, Joelle Fevotte, Andrea 't Mannetje, Tony Fletcher, Paul Brennan, Paolo Boffetta
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  ABSTRACT: To estimate the lung cancer risk attributable to occupational lung carcinogens. Information was collected through interviews from 2624 newly diagnosed lung cancer cases and 2690 frequency-matched controls in Central and Eastern Europe. Industrial hygiene experts evaluated exposure to 70 occupational agents. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using unconditional logistic regression and attributable fractions (AF) by Miettinen's formula. Exposure to at least one occupational lung carcinogen resulted in an AF of 7.9% in men and 1.4% in women. Metals and silica contributed the most to the AF. The AF was highest for squamous cell carcinoma among men (11.4%) and for small cell carcinoma among women (7.1%); the effect of occupational lung carcinogens was stronger overall among current smokers. This estimation of the AF of occupational lung carcinogens is comparable to that estimated in other European studies, and cannot alone explain the high lung cancer rates in Central and Eastern Europe.
  Journal of occupational and environmental medicine / American College of Occupational and Environmental Medicine 11/2011; 53(11):1262-7. · 1.88 Impact Factor
• Article: Occupational exposure to metal compounds and lung cancer. Results from a multi-center case-control study in Central/Eastern Europe and UK.

  Andrea 't Mannetje, Vladimir Bencko, Paul Brennan, David Zaridze, Neonila Szeszenia-Dabrowska, Peter Rudnai, Jolanta Lissowska, Eleonóra Fabiánová, Adrian Cassidy, Dana Mates, Lenka Foretova, Vladimir Janout, Joelle Fevotte, Tony Fletcher, Paolo Boffetta
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  ABSTRACT: To study the association between occupational exposure to metals including chromium, cadmium, nickel, and arsenic compounds, within a population-based study design, while adjusting for confounding factors. A population-based lung cancer case-control study in Central/Eastern Europe and UK was conducted in 1998-2003, including 2,853 cases and 3,104 controls. Exposure to 70 occupational agents was assessed by local expert-teams for all subjects. Odds ratios (OR) for exposure to dust and fumes/mist of chromium, nickel, cadmium, arsenic, as well as inorganic pigment dust and inorganic acid mist, were adjusting for smoking, age, center, sex, and exposure to other occupational agents including the metals under study. Exposure to arsenic (prevalence = 1.4%) was associated with an increased lung cancer risk ((OR) 1.65, 95% confidence interval (95% CI):1.05-2.58). For chromium dust (prevalence = 4.8%, OR: 1.25, 95% CI: 0.95-1.65), a linear upward trend for duration and cumulative exposure was observed. A weak association was observed for exposure to cadmium fumes (prevalence = 1.8%, OR: 1.19, 95% CI: 0.77-1.82), which was strongest for the highest category of cumulative exposure (OR: 2.04, 95% CI: 1.07-3.90). No increased risk was observed for inorganic acid mist, inorganic pigment dust, or nickel, after adjustment for other metals. An independent effect of nickel cannot be excluded, due to its collinearity with chromium exposure. Occupational exposure to metals is an important risk factor for lung cancer. Although the strongest risk was observed for arsenic, exposure to chromium dust was most important in terms of attributable risk due to its high prevalence.
  Cancer Causes and Control 09/2011; 22(12):1669-80. · 2.88 Impact Factor
• Source

  Available from: José Eluf-Neto

  Article: Genome-wide association study of HPV seropositivity.

  Dan Chen, James D McKay, Gary Clifford, Valérie Gaborieau, Amélie Chabrier, Tim Waterboer, David Zaridze, Jolanta Lissowska, Peter Rudnai, Eleonora Fabianova, [......], Victor Wünsch-Filho, José Eluf-Neto, Leticia Fernández Garrote, Elena Matos, Diana Zelenika, Anne Boland, Paolo Boffetta, Michael Pawlita, Mark Lathrop, Paul Brennan
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  ABSTRACT: High-risk α mucosal types of human papillomavirus (HPV) cause anogenital and oropharyngeal cancers, whereas β cutaneous HPV types (e.g. HPV8) have been implicated in non-melanoma skin cancer. Although antibodies against the capsid protein L1 of HPV are considered as markers of cumulative exposure, not all infected persons seroconvert. To identify common genetic variants that influence HPV seroconversion, we performed a two-stage genome-wide association study. Genome-wide genotyping of 316 015 single nucleotide polymorphisms was carried out using the Illumina HumanHap300 BeadChip in 4811 subjects from a central European case-control study of lung, head and neck and kidney cancer that had serology data available on 13 HPV types. Only one association met genome-wide significance criteria, namely that between HPV8 seropositivity and rs9357152 [odds ratio (OR) = 1.37, 95% confidence interval (CI) = 1.24-1.50 for the minor allele G; P=1.2 × 10(-10)], a common genetic variant (minor allele frequency=0.33) located within the major histocompatibility complex (MHC) II region at 6p21.32. This association was subsequently replicated in an independent set of 2344 subjects from a Latin American case-control study of head and neck cancer (OR=1.35, 95% CI=1.18-1.56, P=2.2 × 10(-5)), yielding P=1.3 × 10(-14) in the combined analysis (P-heterogeneity=0.87). No heterogeneity was noted by cancer status (controls/lung cancer cases/head and neck cancer cases/kidney cancer cases). This study provides a proof of principle that genetic variation plays a role in antibody reactivity to HPV infection.
  Human Molecular Genetics 09/2011; 20(23):4714-23. · 7.64 Impact Factor
• Article: Occupational exposure to organic dust increases lung cancer risk in the general population.

  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
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  ABSTRACT: 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.
  Thorax 08/2011; 67(2):111-6. · 6.84 Impact Factor
• Article: Correction: A Genome-Wide Association Study of Upper Aerodigestive Tract Cancers Conducted within the INHANCE Consortium.

  James D McKay, Therese Truong, Valerie Gaborieau, Amelie Chabrier, Shu-Chun Chuang, Graham Byrnes, David Zaridze, Oxana Shangina, Neonila Szeszenia-Dabrowska, Jolanta Lissowska, [......], Doris Lechner, Hélène Blanché, Ivo G Gut, Pilar Galan, Simon Heath, Mia Hashibe, Richard B Hayes, Paolo Boffetta, Mark Lathrop, Paul Brennan
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  ABSTRACT: [This corrects the article on p. e1001333 in vol. 7.].
  PLoS Genetics 04/2011; 7(4). · 8.69 Impact Factor
• Source

  Available from: José Eluf-Neto

  Article: A genome-wide association study of upper aerodigestive tract cancers conducted within the INHANCE consortium.

  James D McKay, Therese Truong, Valerie Gaborieau, Amelie Chabrier, Shu-Chun Chuang, Graham Byrnes, David Zaridze, Oxana Shangina, Neonila Szeszenia-Dabrowska, Jolanta Lissowska, [......], Doris Lechner, Hélène Blanché, Ivo G Gut, Pilar Galan, Simon Heath, Mia Hashibe, Richard B Hayes, Paolo Boffetta, Mark Lathrop, Paul Brennan
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  ABSTRACT: Genome-wide association studies (GWAS) have been successful in identifying common genetic variation involved in susceptibility to etiologically complex disease. We conducted a GWAS to identify common genetic variation involved in susceptibility to upper aero-digestive tract (UADT) cancers. Genome-wide genotyping was carried out using the Illumina HumanHap300 beadchips in 2,091 UADT cancer cases and 3,513 controls from two large European multi-centre UADT cancer studies, as well as 4,821 generic controls. The 19 top-ranked variants were investigated further in an additional 6,514 UADT cancer cases and 7,892 controls of European descent from an additional 13 UADT cancer studies participating in the INHANCE consortium. Five common variants presented evidence for significant association in the combined analysis (p ≤ 5 × 10⁻⁷). Two novel variants were identified, a 4q21 variant (rs1494961, p = 1×10⁻⁸) located near DNA repair related genes HEL308 and FAM175A (or Abraxas) and a 12q24 variant (rs4767364, p =2 × 10⁻⁸) located in an extended linkage disequilibrium region that contains multiple genes including the aldehyde dehydrogenase 2 (ALDH2) gene. Three remaining variants are located in the ADH gene cluster and were identified previously in a candidate gene study involving some of these samples. The association between these three variants and UADT cancers was independently replicated in 5,092 UADT cancer cases and 6,794 controls non-overlapping samples presented here (rs1573496-ADH7, p = 5 × 10⁻⁸); rs1229984-ADH1B, p = 7 × 10⁻⁹; and rs698-ADH1C, p = 0.02). These results implicate two variants at 4q21 and 12q24 and further highlight three ADH variants in UADT cancer susceptibility.
  PLoS Genetics 03/2011; 7(3):e1001333. · 8.69 Impact Factor
• Article: Renal cancer risk and occupational exposure to polycyclic aromatic hydrocarbons and plastics.

  Sara Karami, Paolo Boffetta, Paul Brennan, Patricia A Stewart, David Zaridze, Vsevolod Matveev, Vladimir Janout, Helena Kollarova, Vladimir Bencko, Marie Navratilova, Neonila Szeszenia-Dabrowska, Dana Mates, Jan P Gromiec, Roman Sobotka, Wong-Ho Chow, Nathaniel Rothman, Lee E Moore
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  ABSTRACT: To investigate whether occupational exposure to polycyclic aromatic hydrocarbons and certain plastic monomers increased renal cell carcinoma (RCC) risk. Unconditional logistic regression was used to calculate RCC risk in relation to exposure. No association between RCC risk and having ever been occupationally exposed to any polycyclic aromatic hydrocarbons or plastics was observed. Duration of exposure and average exposure also showed no association with risk. Suggestive positive associations between RCC risk and cumulative exposure to styrene (P-trend = 0.02) and acrylonitrile (P-trend = 0.06) were found. Cumulative exposure to petroleum/gasoline engine emissions was inversely associated with risk (P-trend = 0.02). Results indicate a possible association between occupational styrene and acrylonitrile exposure and RCC risk. Additional studies are needed to replicate findings, as this is the first time these associations have been reported and they may be due to chance.
  Journal of occupational and environmental medicine / American College of Occupational and Environmental Medicine 02/2011; 53(2):218-23. · 1.88 Impact Factor
• Article: [Occupational diseases in Poland, 2010].

  Urszula Wilczyńska, Neonila Szeszenia-Dabrowska, Wojciech Sobala, Danuta Drozdz
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  ABSTRACT: The aim of the paper was to present basic statistical data on occupational diseases diagnosed in 2010. The work was based on the data compiled from "Occupational Disease Reporting Forms" received by the Central Register of Occupational Diseases in 2010. The data comprised information on nosologic units, gender and age of patients, and duration of occupational exposure to harmful agents responsible for the development of specified pathologies. These data were further classified by sectors of the national economy and voivodeships. The incidence was specified in terms of the number of cases in relation to paid employees or to employed persons. The number of occupational diseases diagnosed in 2010 accounted for 2933 cases. The incidence rate was 28.3 cases per 100 000 paid employees. The highest incidence rates were noted for pneumoconioses (7.6/100,000), infectious and parasitic diseases (7/100 000), hearing loss (3.2/100,000) and chronic voice disorders (3.1/100,000). As many as 77% of patients affected by occupational diseases had been exposed to harmful agents for longer than 20 years. In industrial sectors of the national economy, the highest incidence rate was noted in mining and quarrying (368.2/100,000). Taking into account geographic distribution of occupational diseases, the highest incidence was recorded in the Silesian and the lowest in the Mazovian voivodeships (79.7 and 9.7 cases per 100 000 employed persons, respectively). A decrease of 213 (6.8%) cases of occupational diseases and a decrease of 5.4% in their incidence rate over previous year were noted. The greatest drop in the number of cases was noted in chronic voice disorders (of 302 cases--48.5%) and the greatest rise in pneumonioses (of 156 cases--24.6%).
  Medycyna pracy 01/2011; 62(4):347-57. · 0.30 Impact Factor
• Source

  Available from: Lee E Moore

  Article: Comprehensive evaluation of one-carbon metabolism pathway gene variants and renal cell cancer risk.

  Todd M Gibson, Paul Brennan, Summer Han, Sara Karami, David Zaridze, Vladimir Janout, Helen Kollarova, Vladimir Bencko, Marie Navratilova, Neonila Szeszenia-Dabrowska, [......], Ruth M Pfeiffer, Rachael Z Stolzenberg-Solomon, Susan T Mayne, Meredith Yeager, Stephen Chanock, Nat Rothman, Wong-Ho Chow, Philip S Rosenberg, Paolo Boffetta, Lee E Moore
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  ABSTRACT: Folate and one-carbon metabolism are linked to cancer risk through their integral role in DNA synthesis and methylation. Variation in one-carbon metabolism genes, particularly MTHFR, has been associated with risk of a number of cancers in epidemiologic studies, but little is known regarding renal cancer. Tag single nucleotide polymorphisms (SNPs) selected to produce high genomic coverage of 13 gene regions of one-carbon metabolism (ALDH1L1, BHMT, CBS, FOLR1, MTHFR, MTR, MTRR, SHMT1, SLC19A1, TYMS) and the closely associated glutathione synthesis pathway (CTH, GGH, GSS) were genotyped for 777 renal cell carcinoma (RCC) cases and 1,035 controls in the Central and Eastern European Renal Cancer case-control study. Associations of individual SNPs (n = 163) with RCC risk were calculated using unconditional logistic regression adjusted for age, sex and study center. Minimum p-value permutation (Min-P) tests were used to identify gene regions associated with risk, and haplotypes were evaluated within these genes. The strongest associations with RCC risk were observed for SLC19A1 (P(min-P) = 0.03) and MTHFR (P(min-P) = 0.13). A haplotype consisting of four SNPs in SLC19A1 (rs12483553, rs2838950, rs2838951, and rs17004785) was associated with a 37% increased risk (p = 0.02), and exploratory stratified analysis suggested the association was only significant among those in the lowest tertile of vegetable intake. To our knowledge, this is the first study to comprehensively examine variation in one-carbon metabolism genes in relation to RCC risk. We identified a novel association with SLC19A1, which is important for transport of folate into cells. Replication in other populations is required to confirm these findings.
  PLoS ONE 01/2011; 6(10):e26165. · 4.09 Impact Factor
• Source

  Available from: Linda M Liao

  Article: LINE-1 methylation levels in leukocyte DNA and risk of renal cell cancer.

  Linda M Liao, Paul Brennan, Dana M van Bemmel, David Zaridze, Vsevolod Matveev, Vladimir Janout, Hellena Kollarova, Vladimir Bencko, Marie Navratilova, Neonila Szeszenia-Dabrowska, Dana Mates, Nathaniel Rothman, Paolo Boffetta, Wong-Ho Chow, Lee E Moore
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  ABSTRACT: Leukocyte global DNA methylation levels are currently being considered as biomarkers of cancer susceptibility and have been associated with risk of several cancers. In this study, we aimed to examine the association between long interspersed nuclear elements (LINE-1) methylation levels, as a biomarker of global DNA methylation in blood cell DNA, and renal cell cancer risk. LINE-1 methylation of bisulfite-converted genomic DNA isolated from leukocytes was quantified by pyrosequencing measured in triplicate, and averaged across 4 CpG sites. A total of 328 RCC cases and 654 controls frequency-matched(2∶1) on age(±5years), sex and study center, from a large case-control study conducted in Central and Eastern Europe were evaluated. LINE-1 methylation levels were significantly higher in RCC cases with a median of 81.97% (interquartile range[IQR]: 80.84-83.47) compared to 81.67% (IQR: 80.35-83.03) among controls (p = 0.003, Wilcoxon). Compared to the lowest LINE-1 methylation quartile(Q1), the adjusted ORs for increasing methylation quartiles were as follows: OR(Q2) = 1.84(1.20-2.81), OR(Q3) = 1.72(1.11-2.65) and OR(Q4) = 2.06(1.34-3.17), with a p-trend = 0.004. The association was stronger among current smokers (p-trend<0.001) than former or never smokers (p-interaction = 0.03). To eliminate the possibility of selection bias among controls, the relationship between LINE-1 methylation and smoking was evaluated and confirmed in a case-only analysis, as well. Higher levels of LINE-1 methylation appear to be positively associated with RCC risk, particularly among current smokers. Further investigations using both post- and pre-diagnostic genomic DNA is warranted to confirm findings and will be necessary to determine whether the observed differences occur prior to, or as a result of carcinogenesis.
  PLoS ONE 01/2011; 6(11):e27361. · 4.09 Impact Factor
• Source

  Available from: Nikolay Chekanov

  Article: Genome-wide association study of renal cell carcinoma identifies two susceptibility loci on 2p21 and 11q13.3.

  Mark P Purdue, Mattias Johansson, Diana Zelenika, Jorge R Toro, Ghislaine Scelo, Lee E Moore, Egor Prokhortchouk, Xifeng Wu, Lambertus A Kiemeney, Valerie Gaborieau, [......], Gilles Thomas, Zhaoming Wang, Meredith Yeager, Joseph F Fraumeni, Konstantin G Skryabin, James D McKay, Nathaniel Rothman, Stephen J Chanock, Mark Lathrop, Paul Brennan
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  ABSTRACT: We conducted a two-stage genome-wide association study of renal cell carcinoma (RCC) in 3,772 affected individuals (cases) and 8,505 controls of European background from 11 studies and followed up 6 SNPs in 3 replication studies of 2,198 cases and 4,918 controls. Two loci on the regions of 2p21 and 11q13.3 were associated with RCC susceptibility below genome-wide significance. Two correlated variants (r² = 0.99 in controls), rs11894252 (P = 1.8 × 10⁻⁸) and rs7579899 (P = 2.3 × 10⁻⁹), map to EPAS1 on 2p21, which encodes hypoxia-inducible-factor-2 alpha, a transcription factor previously implicated in RCC. The second locus, rs7105934, at 11q13.3, contains no characterized genes (P = 7.8 × 10⁻¹⁴). In addition, we observed a promising association on 12q24.31 for rs4765623, which maps to SCARB1, the scavenger receptor class B, member 1 gene (P = 2.6 × 10⁻⁸). Our study reports previously unidentified genomic regions associated with RCC risk that may lead to new etiological insights.
  Nature Genetics 01/2011; 43(1):60-5. · 35.53 Impact Factor
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  Available from: Karina Braga Ribeiro

  Article: Low human papillomavirus prevalence in head and neck cancer: results from two large case-control studies in high-incidence regions.

  Karina Braga Ribeiro, José Eduardo Levi, Michael Pawlita, Sérgio Koifman, Elena Matos, José Eluf-Neto, Victor Wunsch-Filho, Maria Paula Curado, Oxana Shangina, David Zaridze, [......], Ana Menezes, Vladimir Bencko, Dana Mates, Letícia Fernandez, Eleonora Fabianova, Tarik Gheit, Massimo Tommasino, Paolo Boffetta, Paul Brennan, Tim Waterboer
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  ABSTRACT: Recent studies support an important role for human papillomavirus (HPV) in a subgroup of head and neck squamous cell carcinomas (HNSCC). We have evaluated the HPV deoxyribonucleic acid (DNA) prevalence as well as the association between serological response to HPV infection and HNSCC in two distinct populations from Central Europe (CE) and Latin America (LA). Cases (n = 2214) and controls (n = 3319) were recruited from 1998 to 2003, using a similar protocol including questionnaire and blood sample collection. Tumour DNA from 196 fresh tissue biopsies was analysed for multiple HPV types followed by an HPV type-specific polymerase chain reaction (PCR) protocol towards the E7 gene from HPV 16. Using multiplex serology, serum samples were analysed for antibodies to 17 HPV types. Statistical analysis included the estimation of adjusted odds ratios (ORs) and the respective 95% confidence intervals (CIs). HPV16 E7 DNA prevalence among cases was 3.1% (6/196), including 4.4% in the oropharynx (3/68), 3.8% in the hypopharynx/larynx (3/78) and 0% among 50 cases of oral cavity carcinomas. Positivity for both HPV16 E6 and E7 antibodies was associated with a very high risk of oropharyngeal cancer (OR = 179, 95% CI 35.8-899) and hypopharyngeal/laryngeal cancer (OR = 14.9, 95% CI 2.92-76.1). A very low prevalence of HPV DNA and serum antibodies was observed among cases in both CE and LA. The proportion of head and neck cancer caused by HPV may vary substantially between different geographical regions and studies that are designed to evaluate the impact of HPV vaccination on HNSCC need to consider this heterogeneity.
  International Journal of Epidemiology 01/2011; 40(2):489-502. · 6.41 Impact Factor
• Article: [Implementation of the Amiantus project involving prophylactic medical examinations of the former employees of asbestos processing plants].

  Zuzanna Szubert, Bozenna Stankiewicz-Choroszucha, Magdalena Wrońska-Sobolewska, Elzbieta Cwynar, Joanna Dobrowolska, Regina Wróbel, Małgorzata Ratka, Jacek Jakubowski, Iwona Skórska-Ciszewska, Renata Turbańska, Urszula Gazda, Mieczysław Sova, Halina Pawłowska-Koziełł, Ewa Latala-Łoś, Ewa Komorowska, Wojciech Sobala, Beata Swiatkowska, Neonila Szeszenia-Dabrowska
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  ABSTRACT: Based on a 11-year implementation of the Amiantus Project, this paper reports the results of prophylactic medical examinations of the former workers of asbestos processing plants. The Project involving employees of 28 former asbestos plants was started by the Ministry of Health in 2000 under the Act on the ban of all products containing asbestos. Preventive examinations, continued in 13 centers of occupational medicine throughout the whole territory of Poland, have been coordinated by the Nofer Institute of Occupational Medicine in Lodz (NIOM). During the examinations, a specific Examination Form is filled-in by a physician. The Form is then sent to NIOM for monitoring health effects in the population covered by the Project. The results obtained by analyzing the lung radiological images are recorded in the Examination Form according to the ILO 1980 classification of pneumoconiosis. The diagnosis of the asbestos-related pathologies is based on the Helsinki criteria. During the years 2000-2010, altogether 6,853 people were involved in the Project, and they were subjected to a total of 18,955 preventive examinations. Asbestosis was diagnosed in 1475 people, representing 21% of all respondents, lung cancer in 68 and mesothelioma in 40 people. Pleural radiographic changes were observed in 3027 (44%) patients, pulmonary parenchymal opacities in 4086 (60%) patients. The analysis showed that the asbestos-related pathologies were most frequent in the group of former employees of asbestos-cement plants. This group was also characterized by an age-, tenure-, and latency-related increasing trend in the prevalence of silicosis and the frequency of radiographic lesions in the lungs of those subjects. The continuation of the examinations of former workers of asbestos processing industry has improved the detection of pathologies associated with exposure to asbestos and enabled undertaking an appropriate preventive action. The growing percentage of poorer radiography results reflects the progressive development of pathological processes in the respiratory system of people occupationally exposed to asbestos dust in the past.
  Medycyna pracy 01/2011; 62(5):465-72. · 0.30 Impact Factor
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  Available from: PubMed Central

  Article: In-home coal and wood use and lung cancer risk: a pooled analysis of the International Lung Cancer Consortium.

  H Dean Hosgood, Paolo Boffetta, Sander Greenland, Yuan-Chin Amy Lee, John McLaughlin, Adeline Seow, Eric J Duell, Angeline S Andrew, David Zaridze, Neonila Szeszenia-Dabrowska, [......], Eleonóra Fabiánová, Dana Mates, Vladimir Bencko, Lenka Foretova, Vladimir Janout, Hal Morgenstern, Nathaniel Rothman, Rayjean J Hung, Paul Brennan, Qing Lan
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  ABSTRACT: Domestic fuel combustion from cooking and heating is an important public health issue because roughly 3 billion people are exposed worldwide. Recently, the International Agency for Research on Cancer classified indoor emissions from household coal combustion as a human carcinogen (group 1) and from biomass fuel (primarily wood) as a probable human carcinogen (group 2A). We pooled seven studies from the International Lung Cancer Consortium (5,105 cases and 6,535 controls) to provide further epidemiological evaluation of the association between in-home solid-fuel use, particularly wood, and lung cancer risk. Using questionnaire data, we classified subjects as predominant solid-fuel users (e.g., coal, wood) or nonsolid-fuel users (e.g., oil, gas, electricity). Unconditional logistic regression was used to estimate the odds ratios (ORs) and to compute 95% confidence intervals (CIs), adjusting for age, sex, education, smoking status, race/ethnicity, and study center. Compared with nonsolid-fuel users, predominant coal users (OR = 1.64; 95% CI, 1.49-1.81), particularly coal users in Asia (OR = 4.93; 95% CI, 3.73-6.52), and predominant wood users in North American and European countries (OR = 1.21; 95% CI, 1.06-1.38) experienced higher risk of lung cancer. The results were similar in never-smoking women and other subgroups. Our results are consistent with previous observations pertaining to in-home coal use and lung cancer risk, support the hypothesis of a carcinogenic potential of in-home wood use, and point to the need for more detailed study of factors affecting these associations.
  Environmental Health Perspectives 12/2010; 118(12):1743-7. · 7.04 Impact Factor