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

https://arctichealth.org/en/permalink/ahliterature129910
Source
Int J Cancer. 2012 Sep 1;131(5):1210-9
Publication Type
Article
Date
Sep-1-2012
Author
Beate Pesch
Benjamin Kendzia
Per Gustavsson
Karl-Heinz Jöckel
Georg Johnen
Hermann Pohlabeln
Ann Olsson
Wolfgang Ahrens
Isabelle Mercedes Gross
Irene Brüske
Heinz-Erich Wichmann
Franco Merletti
Lorenzo Richiardi
Lorenzo Simonato
Cristina Fortes
Jack Siemiatycki
Marie-Elise Parent
Dario Consonni
Maria Teresa Landi
Neil Caporaso
David Zaridze
Adrian Cassidy
Neonila Szeszenia-Dabrowska
Peter Rudnai
Jolanta Lissowska
Isabelle Stücker
Eleonora Fabianova
Rodica Stanescu Dumitru
Vladimir Bencko
Lenka Foretova
Vladimir Janout
Charles M Rudin
Paul Brennan
Paolo Boffetta
Kurt Straif
Thomas Brüning
Author Affiliation
Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of Ruhr Universität Bochum (IPA), Bochum, Germany. pesch@ipa-dguv.de
Source
Int J Cancer. 2012 Sep 1;131(5):1210-9
Date
Sep-1-2012
Language
English
Publication Type
Article
Keywords
Adenocarcinoma - epidemiology - etiology - pathology
Adolescent
Adult
Canada - epidemiology
Carcinoma, Squamous Cell - epidemiology - etiology - pathology
Case-Control Studies
Child
Europe - epidemiology
Female
Humans
Lung Neoplasms - epidemiology - etiology - pathology
Male
Middle Aged
Neoplasm Staging
Prevalence
Prognosis
Risk
Small Cell Lung Carcinoma - epidemiology - etiology - pathology
Smoking - adverse effects
Young Adult
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.
Notes
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PubMed ID
22052329 View in PubMed
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Exposure to diesel motor exhaust and lung cancer risk in a pooled analysis from case-control studies in Europe and Canada.

https://arctichealth.org/en/permalink/ahliterature139682
Source
Am J Respir Crit Care Med. 2011 Apr 1;183(7):941-8
Publication Type
Article
Date
Apr-1-2011
Author
Ann C Olsson
Per Gustavsson
Hans Kromhout
Susan Peters
Roel Vermeulen
Irene Brüske
Beate Pesch
Jack Siemiatycki
Javier Pintos
Thomas Brüning
Adrian Cassidy
Heinz-Erich Wichmann
Dario Consonni
Maria Teresa Landi
Neil Caporaso
Nils Plato
Franco Merletti
Dario Mirabelli
Lorenzo Richiardi
Karl-Heinz Jöckel
Wolfgang Ahrens
Hermann Pohlabeln
Jolanta Lissowska
Neonila Szeszenia-Dabrowska
David Zaridze
Isabelle Stücker
Simone Benhamou
Vladimir Bencko
Lenka Foretova
Vladimir Janout
Peter Rudnai
Eleonora Fabianova
Rodica Stanescu Dumitru
Isabelle M Gross
Benjamin Kendzia
Francesco Forastiere
Bas Bueno-de-Mesquita
Paul Brennan
Paolo Boffetta
Kurt Straif
Author Affiliation
International Agency for Research on Cancer, Lyon, France.
Source
Am J Respir Crit Care Med. 2011 Apr 1;183(7):941-8
Date
Apr-1-2011
Language
English
Publication Type
Article
Keywords
Adult
Age Distribution
Aged
Canada - epidemiology
Carcinogens - toxicity
Case-Control Studies
Confidence Intervals
Europe - epidemiology
Female
Humans
Incidence
Logistic Models
Lung Neoplasms - chemically induced - epidemiology - physiopathology
Male
Middle Aged
Occupational Exposure - adverse effects - statistics & numerical data
Occupational Health
Odds Ratio
Reference Values
Risk assessment
Severity of Illness Index
Sex Distribution
Smoking - adverse effects
Survival Analysis
Time Factors
Vehicle Emissions - toxicity
Abstract
Diesel motor exhaust is classified by the International Agency for Research on Cancer as probably carcinogenic to humans. The epidemiologic evidence is evaluated as limited because most studies lack adequate control for potential confounders and only a few studies have reported on exposure-response relationships.
Investigate lung cancer risk associated with occupational exposure to diesel motor exhaust, while controlling for potential confounders.
The SYNERGY project pooled information on lifetime work histories and tobacco smoking from 13,304 cases and 16,282 controls from 11 case-control studies conducted in Europe and Canada. A general population job exposure matrix based on ISCO-68 occupational codes, assigning no, low, or high exposure to diesel motor exhaust, was applied to determine level of exposure.
Odds ratios of lung cancer and 95% confidence intervals were estimated by unconditional logistic regression, adjusted for age, sex, study, ever-employment in an occupation with established lung cancer risk, cigarette pack-years, and time-since-quitting smoking. Cumulative diesel exposure was associated with an increased lung cancer risk highest quartile versus unexposed (odds ratio 1.31; 95% confidence interval, 1.19-1.43), and a significant exposure-response relationship (P value
Notes
Comment In: Am J Respir Crit Care Med. 2011 Sep 1;184(5):619; author reply 619-2021885639
Comment In: Am J Respir Crit Care Med. 2011 Apr 1;183(7):843-421471076
Comment In: Am J Respir Crit Care Med. 2012 Jan 1;185(1):104-6; author reply 106-722210791
Comment In: Am J Respir Crit Care Med. 2012 Jan 1;185(1):104; author reply 106-722210790
PubMed ID
21037020 View in PubMed
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Hierarchical modeling identifies novel lung cancer susceptibility variants in inflammation pathways among 10,140 cases and 11,012 controls.

https://arctichealth.org/en/permalink/ahliterature116704
Source
Hum Genet. 2013 May;132(5):579-89
Publication Type
Article
Date
May-2013
Author
Darren R Brenner
Paul Brennan
Paolo Boffetta
Christopher I Amos
Margaret R Spitz
Chu Chen
Gary Goodman
Joachim Heinrich
Heike Bickeböller
Albert Rosenberger
Angela Risch
Thomas Muley
John R McLaughlin
Simone Benhamou
Christine Bouchardy
Juan Pablo Lewinger
John S Witte
Gary Chen
Shelley Bull
Rayjean J Hung
Author Affiliation
International Agency for Research on Cancer, Lyon, France. brenner.darren@gmail.com
Source
Hum Genet. 2013 May;132(5):579-89
Date
May-2013
Language
English
Publication Type
Article
Keywords
Alleles
Canada - epidemiology
Case-Control Studies
Europe - epidemiology
European Continental Ancestry Group - genetics
Female
Gene Frequency
Genetic Predisposition to Disease
Genetic Variation - genetics
Genome-Wide Association Study
Genotype
Humans
Inflammation - genetics
Likelihood Functions
Lung Neoplasms - epidemiology - genetics
Male
Middle Aged
Models, Statistical
Polymorphism, Single Nucleotide - genetics
Risk
United States - epidemiology
Abstract
Recent evidence suggests that inflammation plays a pivotal role in the development of lung cancer. In this study, we used a two-stage approach to investigate associations between genetic variants in inflammation pathways and lung cancer risk based on genome-wide association study (GWAS) data. A total of 7,650 sequence variants from 720 genes relevant to inflammation pathways were identified using keyword and pathway searches from Gene Cards and Gene Ontology databases. In Stage 1, six GWAS datasets from the International Lung Cancer Consortium were pooled (4,441 cases and 5,094 controls of European ancestry), and a hierarchical modeling (HM) approach was used to incorporate prior information for each of the variants into the analysis. The prior matrix was constructed using (1) role of genes in the inflammation and immune pathways; (2) physical properties of the variants including the location of the variants, their conservation scores and amino acid coding; (3) LD with other functional variants and (4) measures of heterogeneity across the studies. HM affected the priority ranking of variants particularly among those having low prior weights, imprecise estimates and/or heterogeneity across studies. In Stage 2, we used an independent NCI lung cancer GWAS study (5,699 cases and 5,818 controls) for in silico replication. We identified one novel variant at the level corrected for multiple comparisons (rs2741354 in EPHX2 at 8q21.1 with p value = 7.4 × 10(-6)), and confirmed the associations between TERT (rs2736100) and the HLA region and lung cancer risk. HM allows for prior knowledge such as from bioinformatic sources to be incorporated into the analysis systematically, and it represents a complementary analytical approach to the conventional GWAS analysis.
Notes
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PubMed ID
23370545 View in PubMed
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Occupational exposure to organic dust increases lung cancer risk in the general population.

https://arctichealth.org/en/permalink/ahliterature131973
Source
Thorax. 2012 Feb;67(2):111-6
Publication Type
Article
Date
Feb-2012
Author
Susan Peters
Hans Kromhout
Ann C Olsson
Heinz-Erich Wichmann
Irene Brüske
Dario Consonni
Maria Teresa Landi
Neil Caporaso
Jack Siemiatycki
Lorenzo Richiardi
Dario Mirabelli
Lorenzo Simonato
Per Gustavsson
Nils Plato
Karl-Heinz Jöckel
Wolfgang Ahrens
Hermann Pohlabeln
Paolo Boffetta
Paul Brennan
David Zaridze
Adrian Cassidy
Jolanta Lissowska
Neonila Szeszenia-Dabrowska
Peter Rudnai
Eleonora Fabianova
Francesco Forastiere
Vladimir Bencko
Lenka Foretova
Vladimir Janout
Isabelle Stücker
Rodica Stanescu Dumitru
Simone Benhamou
Bas Bueno-de-Mesquita
Benjamin Kendzia
Beate Pesch
Kurt Straif
Thomas Brüning
Roel Vermeulen
Author Affiliation
Environmental Epidemiology Division, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands. s.peters@uu.nl
Source
Thorax. 2012 Feb;67(2):111-6
Date
Feb-2012
Language
English
Publication Type
Article
Keywords
Adult
Aged
Canada - epidemiology
Case-Control Studies
Dust - analysis
Europe - epidemiology
Female
Humans
Lung Neoplasms - epidemiology - etiology
Male
Middle Aged
Occupational Diseases - epidemiology - etiology
Occupational Exposure - adverse effects - analysis
Smoking - adverse effects - epidemiology
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
PubMed ID
21856697 View in PubMed
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