Genetic susceptibility, residential radon, and lung cancer in a radon prone area.
BACKGROUND
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.
*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.
Alberto
A
Ruano-Ravina
Marco F
MF
Pereyra
Marta Tojo
MT
Castro
Mónica
M
Pérez-Ríos
José
J
Abal-Arca
Juan Miguel
JM
Barros-Dios
D000368:Aged; D000396:Air Pollutants, Radioactive / Q000633:toxicity*; D016902:Air Pollution, Indoor / Q000009:adverse effects*; D016022:Case-Control Studies; D004851:Epoxide Hydrolases / Q000235:genetics; D005260:Female; D020022:Genetic Predisposition to Disease / Q000453:epidemiology; D005838:Genotype; D005982:Glutathione Transferase / Q000235:genetics; D006801:Humans; D008175:Lung Neoplasms / Q000453:epidemiology / Q000209:etiology* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009381:Neoplasms, Radiation-Induced / Q000453:epidemiology / Q000209:etiology* / Q000235:genetics; D020641:Polymorphism, Single Nucleotide; D011829:Radiation Dosage; D011886:Radon / Q000633:toxicity*; D012307:Risk Factors; D017384:Sequence Deletion; D012907:Smoking / Q000009:adverse effects / Q000453:epidemiology
D000396:Air Pollutants, Radioactive; D004851:Epoxide Hydrolases; D005982:Glutathione Transferase; D011886:Radon; C412602:glutathione S-transferase Mu 2; C522330:EPHX1 protein, human