Underground miners exposed to high levels of radon have an excess risk of lung cancer. Residential exposure to radon is at much lower levels, and the risk of lung cancer with residential exposure is less clear. We conducted a systematic analysis of pooled data from all North American residential radon studies.
The pooling project included original data from 7 North American case–control studies, all of which used long-term α-track detectors to assess residential radon concentrations. A total of 3662 cases and 4966 controls were retained for the analysis. We used conditional likelihood regression to estimate the excess risk of lung cancer.
Odds ratios (ORs) for lung cancer increased with residential radon concentration. The estimated OR after exposure to radon at a concentration of 100 Bq/m3 in the exposure time window 5 to 30 years before the index date was 1.11 (95% confidence interval = 1.00–1.28). This estimate is compatible with the estimate of 1.12 (1.02–1.25) predicted by downward extrapolation of the miner data. There was no evidence of heterogeneity of radon effects across studies. There was no apparent heterogeneity in the association by sex, educational level, type of respondent (proxy or self), or cigarette smoking, although there was some evidence of a decreasing radon-associated lung cancer risk with age. Analyses restricted to subsets of the data with presumed more accurate radon dosimetry resulted in increased estimates of risk.
These results provide direct evidence of an association between residential radon and lung cancer risk, a finding predicted using miner data and consistent with results from animal and in vitro studies.
Supplemental Digital Content is Available in the Text.
From the*McLaughlin Centre for Population Health Risk Assessment, University of Ottawa, Ottawa, Ontario, Canada; the †Biostatistics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD; the ‡Healthy Environments and Consumer Safety Branch, Health Canada, Ottawa, Ontario, Canada; the §Occupational Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Washington, DC; the ∥Centre of Excellence for Children and Adolescents with Special Needs, Lakehead University, Thunder Bay, Ontario, Canada; the Departments of ¶Epidemiology and **Occupational and Environmental Health, College of Public Health, University of Iowa, Iowa City, Iowa; ††Cancer Epidemiology, Department of Health and Senior Services, Trenton, New Jersey; the ‡‡Radiation Protection Bureau, Health Protection Branch, Health Canada, Ottawa, Ontario, Canada; the§§Department of Family and Preventive Medicine, University of Utah, Salt Lake City, Utah; the ∥∥Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina; the ¶¶Department of Physics, St. John's University, Collegeville, Minnesota; the ***School of Medicine, Yale University, New Haven, Connecticut; and the †††Biostatistics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina.
Submitted 14 October 2004; final version accepted 19 November 2004.
Salary support for R. W. Field, C. Lynch, and D. Steck provided in part by grant no. R01 CA85942 from US NCI and grant no. P30 ES05695 from U.S. NIEHS. Research supported by grants from Canadian Institutes of Health Research and Natural Sciences and Engineering Research Council of Canada. Additional support provided by Health Canada and the U.S. Department of Energy.
Supplemental material for this article is available with the online version of the Journal at www.epidem.com.
Correspondence: Daniel Krewski, McLaughlin Centre for Population Health Risk Assessment, Institute of Population Health, University of Ottawa, One Stewart Street, Room 320, Ottawa, Ontario, Canada K1N 6N5. E-mail: email@example.com.