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The Health Risk of Radon Gas

Radon is a class A known human carcinogen.
Alpha particles from the radon decay products can damage lung tissue.
Lung cancer is the main health effect from radon exposure.

How Does Radon Induce Cancer?
If inhaled, radon decay products (polonium-218 and polonium-214, solid form), unattached or attached to the surface of aerosols, dusts, and smoke particles, become deeply lodged or trapped in the lungs, where they can radiate and penetrate the cells of mucous membranes, bronchi, and other pulmonary tissues. The ionizing radiation energy affecting the bronchial epithelial cells is believed to initiate the process of carcinogenesis. Although radon-related lung cancers are mainly seen in the upper airways, radon increases the incidence of all histological types of lung cancer, including small cell carcinoma, adenocarcinoma, and squamous cell carcinoma. Lung cancer due to inhalation of radon decay products constitutes the only known risk associated with radon. In studies done on miners, variables such as age, duration of exposure, time since initiation of exposure and especially the use of tobacco have been found to influence individual risk. In fact, the use of tobacco multiplies the risk of radon-induced lung cancer enormously.

What is the Evidence?
More is known about the health risk of radon exposure to humans than about most other human carcinogens. This knowledge is based on extensive epidemiological studies of thousands of underground miners, carried out over more than fifty (50) years worldwide, including miners in the United States and Canada. In addition to the miner data, experimental exposures of animals confirm that radon and its decay products can cause lung cancer.

The research on lung cancer mortality in miners exposed to radon progeny is substantial and consistent. Studies of thousands of miners, some with follow-up periods of thirty (30) years and more, have been conducted in metal, fluorspar, shale, and uranium mines in the United States, Canada, Australia, China, and Europe. These studies have consistently shown an increase in lung cancer occurrence with exposure to radon decay products, despite differences in study populations and methodologies.

The miner studies produced some interesting findings.
At equal cumulative exposures, low exposures in the range of EPA's 4 pCi/L action level over longer periods produced greater lung cancer risk than high exposures over short periods.

Increased lung cancer risk with radon exposure has been observed even after controlling for, or in the absence of, other mine exposures such as asbestos, silica, diesel fumes, arsenic, chromium, nickel, and ore dust.

Increased lung cancer risk has been observed in miners at relatively low cumulative exposures in the range of EPA's 4 pCi/L action level (Sevc Kunz, Tomasik et al, Health Physics 54(1):27-46,1988; Mulles Wheeler et al, Proceedings of International Conference on Occupation Radiation Safety in Mining, Vol. 1, Canadian Nuclear Association; Radford and St. Clair Renard, New England Journal of Medicine310(23):1485-1494, 1984;Woodward, Roder et al, "Cancer Causes and Control" 2:213-220, 1991).

Nonsmoking miners exposed to radon have been observed to have an increased risk of lung cancer.

What About Smoking and Radon Exposure?
Some people ask whether the lung cancer deaths attributed to radon exposure actually may be the result of smoking. A 1989 study by researchers from the National Institute for Occupational Safety and Health, the Centers for Disease Control, the Harvard School of Public Health, and the University of California at Davis demonstrated a greatly incased lung cancer risk in nonsmoking uranium miners exposed to high radon concentrations: compared to typical non-smoking populations, these miners had nine (9) to twelve (12) times the risk of developing lung cancer (Roscoe et al, JAMA 262(5): 629-633, 1989).

Evidence from some of the epidemiological studies of underground miners, primarily U. S. uranium miners, indicates that radon exposure and smoking may have a synergistic relationship. Either smoking or radon exposure can independently increase the risk of lung cancer; however, exposure to both greatly enhances that risk.

Risk Chart

Continue to Other sources of Radiation Exposures.

FACT SHEET
Iowa Radon Lung Cancer Study (IRLCS)

Study Title: "Residential Radon Gas Exposure and Lung Cancer", American Journal of Epidemiology, June 2000
Authors: R. William Field, Daniel J. Steck, Brian J. Smith, et al
Study Population: Female Iowa residents, age 40-84 years, both non-smokers and ever smokers, who had lived in their current home for at least 20 consecutive years and completed year-long radon measurements. Included 413 lung cancer cases (86.4% ever smokers) and 614 controls (32.5% ever smokers).
Background: The Iowa radon lung cancer study had four major components: 1) rapid reporting of cases; 2) a mailed questionnaire followed by a face-to-face interview; 3) a comprehensive radon exposure assessment; and, 4) independent histopathologic review of lung cancer tissues.
The rapid case reporting allowed personal interviews with a high percentage (69%) of cases, providing much more accurate information than can be obtained by interviewing relatives. This study represents the most detailed attempt, to date, to reconstruct total individual radon exposure. Exposure reconstruction included on-site measurements of home radon with year-long tests on every level of the home, in current & historical bedrooms, and in 'in-home' work areas. These in-home measurements were linked with individual movements within the home. Outside exposure as well as exposures in other buildings were included in the reconstruction. The independent tissue review (performed on 96% of lung cancer tissues) provided a reliable classification of lung cancer cases.

Results: "The risk estimates obtained in this study suggest that cumulative [total] radon exposure in the residential environment is significantly associated with lung cancer risk." After adjusting for age, smoking, and education, and using categorical radon exposure levels, a 15 year exposure at levels equivalent to EPA's action level of 4 pCi/L yielded excess odds of 0.50 i.e., an increase in lung cancer risk of 50% (95%; confidence interval: 0.004, 1.81) for total cases and excess odds of 0.83 for cases with personal interviews i.e., an increase in lung cancer risk of 83% (95% confidence interval: 0.11, 3.34). The higher risk found for cases with personal interviews vs. the total cases most probably reflects the more accurate exposure assessment obtained from interviews with cases vs. interviews with relatives.
View of the Study: The Iowa study is exceptionally well designed and well executed. It adds to the body of knowledge which designates residential radon as the second leading cause of lung cancer. It supports EPA's position and the National Academy of Sciences' Institute of Medicine's 1999 report that radon exposure in homes is a public health problem. It confirms EPA's, the Center for Disease Control's, and the Surgeon General's positions that all homes should be tested for radon, and all homes testing over 4 pCi/L should be fixed. In terms of scientific advancements, the study breaks new ground in estimating total individual radon exposure.
LINKS: University of Iowa Center for Health Effects of Environmental Contamination Press Release.
Contains the Press Release; Abbreviated Findings; Study Methodology; Questions and Answers About the Study; and, Study Contact and Additional Radon Information.
Press Quotes:

To:  R. William Field, Ph.D.
College of Public Health, Department of Epidemiology
University of Iowa, Iowa City, Iowa


I wanted to commend you on your Iowa Radon Lung Cancer Study. I believe the methods you used to reduce the inherent random error associated with ascertaining long-term residential radon exposure are critical to validly assessing the lung cancer risk from this source. As you correctly point out the random error in estimating radon exposure has the potential to substantially underestimate the slope of the dose-response curve. Your estimates of risk are similar to my own in our study of lung cancer among Missouri women, where we used historic estimates of radon exposure from cumulative measures of radon progeny in glass. I believe that most studies published to date have been ineffective in reducing measurement error and their dose-response results have suffered from a bias toward the null. I look forward to the discussion your results will generate and urge you to complete the analysis of you radon progeny in glass measurements data. Along with your current manuscript, that data should help clarify the true nature of the dose-response curve between residential radon and lung cancer risk. Again congratulations on a job well done.
Signed:
    Michael Alavanja, Dr. P.H.
    Senior Investigator, Division of Cancer Epidemiology and Genetics,
    National Cancer Institute

"The Iowa Study is a significant addition to our already strong understanding of indoor radon and lung cancer. Its particular importance lies in the careful methodologic work done by the investigators on some nagging scientific issues--particularly the estimation of lifetime exposure to radon."

Signed:
    Dr. Jonathan Samet,
    Professor and Chairman, Department of Epidemiology, School of
    Hygiene and Public Health, Johns Hopkins University, Baltimore,
    Maryland.

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