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Radon, secondhand smoke, glutathione-S-transferase M1 and lung cancer among women

Matthew R Bonner1, William P Bennett, Wenying Xiong

  • 1Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, US Department of Health and Human Services, Rockville, MD, USA. mrbonner@buffalo.edu

Insights

Glutathione-S-transferase M1 (GSTM1) null individuals show increased lung cancer risk with high radon exposure. Secondhand smoke also elevates risk in never-smokers with this genetic profile.

Area of Science:

  • Environmental Health
  • Genetics
  • Oncology

Background:

  • Oxidative stress from tobacco smoke and radiation is linked to lung cancer.
  • Glutathione-S-transferase M1 (GSTM1) null homozygotes may have reduced capacity to neutralize reactive oxygen species (ROS).

Purpose of the Study:

  • To investigate the interaction between GSTM1 genotype and exposure to radon and secondhand smoke (SHS) in lung cancer risk.

Main Methods:

  • A case-only study design utilizing archival tissue samples from 270 lung cancer cases.
  • GSTM1 genotyping, radon concentration measurement, and SHS exposure assessment via questionnaires and interviews.
  • Unconditional logistic regression analysis to calculate interaction odds ratios (OR).

Main Results:

  • High radon concentrations (>121 Bq m(-3)) showed a >3-fold increased interaction OR for GSTM1 null homozygotes (OR=3.41).
  • A significant linear trend (p=0.03) was observed for radon interaction with GSTM1 genotype.
  • Elevated interaction OR (OR=2.28) for SHS and GSTM1 was found among never-smokers.

Conclusions:

  • This study provides evidence for a significant interaction between GSTM1 genotype and radon exposure in lung cancer risk.
  • Findings suggest that radon and SHS may promote lung cancer via shared pathways, particularly in individuals with the GSTM1 null genotype.

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