Alberto Ruano-Ravina1, Marco F Pereyra, Marta Tojo Castro, Mónica Pérez-Ríos, José Abal-Arca, Juan Miguel Barros-Dios. 1. *Department of Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, A Coruña; †CIBER de Epidemiología y Salud Pública, CIBERESP; ‡Service of Neumology, Clinic University Hospital; §Department of Physiology, School of Medicine-CIMUS-Instituto de Investigaciones Sanitarias, University of Santiago de Compostela, Santiago de Compostela, A Coruña, Spain; ‖Metabolic Research Laboratories, Department of Obstetrics and Gynaecology, University of Cambridge, Cambridge, United Kingdom; ¶Service of Neumology, Ourense Hospital Complex, Ourense; and #Service of Preventive Medicine, Clinic University Hospital Complex of Santiago de Compostela, A Coruña, Spain.
Abstract
INTRODUCTION: Radon exposure has been classified as the second cause of lung cancer, after tobacco, and the first in never smokers. GSTM1 and GSTT1 genes deletion increase the risk of lung cancer. We aim to know whether the risk of lung cancer because of residential radon is modulated by these genetic polymorphisms. METHODS: Hospital-based, case-control study where cases had confirmed lung cancer. Cases and controls did not have previous neoplasm and were older than 30. Controls attended hospital for noncomplex surgery. We analyzed the results for the whole sample and separately for never/light smokers and moderate/heavy smokers. RESULTS: Seven-hundred and ninety-two participants were analyzed. GSTM1 and GSTT1 deletion conferred an odds ratio (OR) of 1.38 (95% confidence interval [CI] 0.93-2.04) and 1.13 (95% CI 0.70-1.82), respectively. Individuals with GSTM1 present and residential radon concentrations higher than 148 Bq/m had an OR of 1.48 (95% CI 0.73-3.00), whereas those with GSTM1 deleted had an OR of 2.64 (95% CI 1.18-5.91) when compared with participants with GSTM1 present and radon concentrations below 50 Bq/m3. Similar results were observed for GSTT1 deletion. These results were basically the same for the moderate/heavy smokers' subgroup. CONCLUSIONS: The absence of GSTM1 and GSTT1 genes increases the risk of lung cancer because of radon exposure. These genes might modulate the carcinogenic pathway of alpha radiation. Further studies are warranted analyzing this association in never smokers.
INTRODUCTION: Radon exposure has been classified as the second cause of lung cancer, after tobacco, and the first in never smokers. GSTM1 and GSTT1 genes deletion increase the risk of lung cancer. We aim to know whether the risk of lung cancer because of residential radon is modulated by these genetic polymorphisms. METHODS: Hospital-based, case-control study where cases had confirmed lung cancer. Cases and controls did not have previous neoplasm and were older than 30. Controls attended hospital for noncomplex surgery. We analyzed the results for the whole sample and separately for never/light smokers and moderate/heavy smokers. RESULTS: Seven-hundred and ninety-two participants were analyzed. GSTM1 and GSTT1 deletion conferred an odds ratio (OR) of 1.38 (95% confidence interval [CI] 0.93-2.04) and 1.13 (95% CI 0.70-1.82), respectively. Individuals with GSTM1 present and residential radon concentrations higher than 148 Bq/m had an OR of 1.48 (95% CI 0.73-3.00), whereas those with GSTM1 deleted had an OR of 2.64 (95% CI 1.18-5.91) when compared with participants with GSTM1 present and radon concentrations below 50 Bq/m3. Similar results were observed for GSTT1 deletion. These results were basically the same for the moderate/heavy smokers' subgroup. CONCLUSIONS: The absence of GSTM1 and GSTT1 genes increases the risk of lung cancer because of radon exposure. These genes might modulate the carcinogenic pathway of alpha radiation. Further studies are warranted analyzing this association in never smokers.
Authors: Albert Rosenberger; Rayjean J Hung; David C Christiani; Neil E Caporaso; Geoffrey Liu; Stig E Bojesen; Loic Le Marchand; Ch A Haiman; Demetrios Albanes; Melinda C Aldrich; Adonina Tardon; G Fernández-Tardón; Gad Rennert; John K Field; B Kiemeney; Philip Lazarus; Aage Haugen; Shanbeh Zienolddiny; Stephen Lam; Matthew B Schabath; Angeline S Andrew; Hans Brunnsstöm; Gary E Goodman; Jennifer A Doherty; Chu Chen; M Dawn Teare; H-Erich Wichmann; Judith Manz; Angela Risch; Thomas R Muley; Mikael Johansson; Paul Brennan; Maria Teresa Landi; Christopher I Amos; Beate Pesch; Georg Johnen; Thomas Brüning; Heike Bickeböller; Maria Gomolka Journal: Int Arch Occup Environ Health Date: 2018-07-03 Impact factor: 3.015
Authors: Ruyi Huang; Yongyue Wei; Rayjean J Hung; Geoffrey Liu; Li Su; Ruyang Zhang; Xuchen Zong; Zuo-Feng Zhang; Hal Morgenstern; Irene Brüske; Joachim Heinrich; Yun-Chul Hong; Jin Hee Kim; Michele Cote; Angela Wenzlaff; Ann G Schwartz; Isabelle Stucker; John Mclaughlin; Michael W Marcus; Michael P A Davies; Triantafillos Liloglou; John K Field; Keitaro Matsuo; Matt Barnett; Mark Thornquist; Gary Goodman; Yi Wang; Size Chen; Ping Yang; Eric J Duell; Angeline S Andrew; Philip Lazarus; Joshua Muscat; Penella Woll; Janet Horsman; M Dawn Teare; Anath Flugelman; Gad Rennert; Yan Zhang; Hermann Brenner; Christa Stegmaier; Erik H F M van der Heijden; Katja Aben; Lambertus Kiemeney; Juan Barros-Dios; Monica Pérez-Ríos; Alberto Ruano-Ravina; Neil E Caporaso; Pier Alberto Bertazzi; Maria Teresa Landi; Juncheng Dai; Hongbing Hongbing Shen; Guillermo Fernandez-Tardon; Marta Rodriguez-Suarez; Adonina Tardon; David C Christiani Journal: EBioMedicine Date: 2015-11 Impact factor: 8.143
Authors: Erin C Peckham; Michael E Scheurer; Heather E Danysh; Joseph Lubega; Peter H Langlois; Philip J Lupo Journal: Int J Environ Res Public Health Date: 2015-09-25 Impact factor: 3.390