Radon in homes and risk of lung cancer: collaborative analysis of individual data from 13 European case-control studies

BMJ 2005; 330 doi: http://dx.doi.org/10.1136/bmj.38308.477650.63 (Published 27 January 2005)
Cite this as: BMJ 2005;330:223

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Figures presented in the paper, Darby et al “Radon in homes and risk of lung cancer: collaborative analysis of individual data from 13 European case–control studies” BMJ, Jan 2005; 330: 223, show that:

- In the absence of radon, the absolute risks to non-smokers and to cigarette smokers would be 0.41% and 10.1% respectively by age 75. In other words, there is a 0.41% risk of lung cancer which has nothing to do with radon or tobacco smoke, and an additional 9.69% from smoking.

- The incremental risk to non-smokers from radon is about 0.06% per 100 Bq/m3 up to 800 Bq/m3.

- The incremental risk to smokers from radon is about 1.5% per 100 Bq/m3 up to 800 Bq/m3 (about 25 times greater than for non-smokers)

- Hence, at 100 Bq/m3 (which is about the mean value of radon concentration in this study), the risk to non-smokers from radon is 0.06% and the total risk to smokers from radon and smoking combined is 11.2% (about 190 times greater).

I therefore suggest that it is not appropriate to talk simply of a risk from radon in homes. The risk is from smoking, compounded by a synergistic effect of radon for smokers. Without smoking, the effect seems to be so small as to be insignificant.

The findings of Darby et al thus appear to demonstrate that it would be unreasonable to advise non-smokers that they need to modify their homes to protect themselves from exposure to domestic radon.

For smokers, the modification of their homes remains an option, of course, but they should at least be told that a more effective (and cheaper) way of avoiding the effect of radon is by not smoking.

Competing interests: None declared

Competing interests: None declared

Donald J Higson, Private

260 Glenmore Road, Paddington, NSW 2021, Australia

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In their article in the BMJ, originally published online 21December 2005 (DOi: 10.1136/bmj.38308.477.650.63) Darby et al make assumption of constant exposure pooling findings from a number of studies performed during a decade or longer. While they concomitantly assume a period of exposure between five or 30 years they allow for a temporal difference in findings collected between the 80s and 90s. The exposure assumptions lead to the problem that during the differential time for diagnosis there is a possibility of exposure due to new risk factors and substantial changes in exposure to radon. The assumption of constant and similar exposure would only work as scientific hypothesis if the researchers checked the health status of the involved subjects at the same time point.

The above comments are based on knowledge of comparative methods and the Authors make comparisons between various countries with considerable differences in life styles (in particular between males and females), policies on environmental protection as well different interventional politics in this aspect. This contributes even more to the necessity of subset analysis (separate analyses for males and females) and effect modifications in subsets. The constant exposure to the risk factor radon would probably be better explored using places of living during assumed exposure times as units of analysis with respect to local interventions reducing radioactivity. The reliance on studies with findings collected during a large period of time reduces the external validity of Darby et al.’s findings allowing for even larger discrepancies in life styles and protection interventions. Macro comparisons are an art, in particular between different subjects such as whole countries. The Authors do not mention contribution of asbestos at all in their discussion despite the recognised impact of asbestos on incidence of lung cancer.

Grazyna T Adamiak
Ph.D., Master of Health and Welfare, MA

Competing interests: None declared

Competing interests: None declared

Grazyna T Adamiak, PhD, Master of Health and Welfare, MA


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The paper by Darby et al.[1] provides compelling evidence that indoor radon is an important contributor to lung cancer risk. However, the derived estimate of radon-attributable lung cancers may be biased low.

From a pooling of the European residential case-control studies, the authors estimate an increase in lung cancer risk of 16% for each incremental 100 Bq/m3 of radon. Then based on an estimated average radon concentration of 59 Bq/m3 for 29 European countries, they estimate that radon may contribute to 9% of all lung cancers in those countries. It should be noted, however, that the relative risk per Bq/m3 was determined in each study for an exposure window 5-35 y before ascertainment of the disease. Typically, lung cancer cases will occur after age 55, so exposures received during childhood and young adulthood are not included. This would not be a problem if exposures occurring more than 35 y previously did not contribute appreciably to lung cancer risk. However, although the BEIR VI models do incorporate a fall-off in risk with time, the projected risk from childhood and young adult exposures are still about the same as for the population as a whole[2,3]. As a result, more than 30% of the radon contribution to the population risk would be unaccounted for by the case-control studies. Of course, this conclusion is based on model extrapolation; in reality, aside from very limited, and somewhat equivocal, data on Chinese tin miners[4], there is no direct information on risks from childhood exposures to radon.

It is also true that if radon levels prior to the 30-y measurement window were highly correlated with the estimated average levels during the window, the error would be reduced, since the measured average exposure rate would reflect the entire lifetime, rather than just 30 y. This is unlikely to be true in practice since individuals are unlikely to reside in the same houses during childhood and early adulthood as they live in for the 35 y prior to lung cancer incidence.


1. Darby S, Hill D, Auvinen A, Barros-Dios JM, Baysson H, Bochicchio F, et al. Radon in homes and risk of lung cancer: collaborative analysis of individual data from 13 European case-control studies. BMJ 2005; 330: 223-226.

2. National Research Council. Committee on health risks of exposure to radon (BEIR VI). Health effects of exposure to radon. Washington, DC: National Academy Press, 1999.

3. Pawel DJ, Puskin JS. The U.S. Environmental Protection Agency’s assessment of risks from indoor radon. Health Phys 2004; 87:68-74.

4. Xuan XZ, Lubin JH, Li JY, Li-Fen Y, Sheng LQ, Lan Y, et al. A cohort study in southern China of tin miners exposed to radon and radon decay products. Health Phys 1993; 64:120-131.

Competing interests: None declared

Competing interests: None declared

Jerome S. Puskin, Director, Center for Science and Risk Assessment, Radiation Protection Division

David J. Pawel

U.S. Environmental Protection Agency, Washington, DC 20460

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The BEIR VI report emphasised the need, that any risk assessment for indoor radon has to address the effect of radon on never-smokers and ever- smokers of tobacco, due to differing patterns of effect observed with radon exposed miners. Another reason to examine the influence of smoking and radon on indoor radon risk calculation might be a biological one. It is now well-known that the dose-response curves for certain radiogenic cancers are non-linear in the low dose range, that DNA damage can be repaired, and that cellular DNA is in a dynamic state in which damage is constantly occuring and being repaired. This capacity might have been weakened in smokers due to constant exposure to the cancerous tobacco smoke. In non-smokers this capacity is not weakened resulting in a lower risk for lung cancer due to radon. The dominant influence of smoking on the lung cancer risk in comparison to the weak influence from radon and the problem to control for the confounder smoking result in additional factors. Further details (http://www.precura.de/finalreport.html).

Competing interests: None declared

Competing interests: None declared

Karl Dr. Martin, Senior Scientist

Institute for Health Economics and Prevention, Auguststraße 2, D-16321 Bernau bei Berlin

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Professor Sarah Darby and other researchers have found that the risk from radon is larger for smokers. The smoke particles from side stream may act as carriers of the decay products of radon and will get deposited more efficiently in the lungs of smokers and non smokers.The particles from smoke stream which they inhale will be laced with polonium-218, lead- 214 and bismuth-214, besides traces of polonium-210 and lead-210 already present in tobacco smoke.The mechanism of tranport of these radionuclides in the lungs of smokers and non-smokers is likely to be different

Besides, smokers also receive considerable radiation dose from polonium-210 present in the main stream smoke.Thus the radiation dose to smokers will be significantly more than that to non-smokers.

Smoke particles from cigarettes are known to be of submicronic size; they reside in the atmosphere for a long time.Carbonaceous particles are reported to be negatively charged.Polonium-218, the decay product of radon are mostly formed as positive ions.They get readily attached to the smoke particles present in air.The unattached fraction of this isotope is very important in radon dosimetry.The contribution from attached and unattached fraction to lung dose will have to be evaluated separately. Possible reduction in the unattached fraction due to the presence of smoke particle may help to reduce dose to the lungs of smokers and non-smokers.

Whatever be the mechanism, the conclusions from this paper must inspire a few more smokers to quit their habit.

I am interested to see a critical comparison of the statistical treatment of the data in this paper with that in the paper titled "Test of the linear-no threshold theory of radiation carcinogenesis for inhaled radon decay products" Health Phys 1995 Feb;68(2):157-174] by Professor Bernard Cohen. This paper is quoted by all who believe in radiation hormesis

Professor Cohen claimed that cancer incidence decreased with increase in concentration of radon in residences.He documented the inverse relation based on data from over 1600 counties in USA containing 90 percent of US population. He claimed that he had grouped and calculated the data in more than 100 different ways, adjusting for every conceivable variable. Still he found that as the radon level in home increases the incidence of lung cancer falls!

Dr.K.S.Parthasarathy ksparth@vsnl.com

Competing interests: None declared

Competing interests: None declared

Parthasarathy K.S., DAE/BRNS Senior Scientist

Stategic Planning Group, Department of Atomic Energy, Mumbai

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