Radon and lung cancer: Assessing and mitigating the risk

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Risk in miners

As early as in the 16th century, metal miners in central Europe were noted to have a high rate of death from respiratory disease. Radon was discovered in 1900, and in the 20th century lung cancer was linked to high levels of radon detected in uranium mines.

Several small studies of underground miners exposed to high concentrations of radon consistently demonstrated an increased risk of lung cancer.

The Committee on the Biological Effects of Ionizing Radiation (BEIR VI 1999) reviewed 11 major cohort studies of miners. The studies included more than 60,000 miners in Europe, North America, Asia, and Australia, of whom 2,600 died of lung cancer. Lung cancer rates increased linearly with cumulative radon exposure, and the estimated average increase in the lung cancer death rate per WLM in the combined studies was 0.44% (95% confidence interval [CI] 0.20–1.00%). The percentage increase in the lung cancer death rate per WLM varied with time since exposure, with the highest increase in risk during the 5 to 14 years after exposure.4,17 Furthermore, the increase in risk was higher in younger miners, who were exposed to a relatively low radon concentration.

Risk in the general population

The magnitude of the risk in miners led to concern about radon exposure as a cause of lung cancer in the general population. Statistical models were generated that suggested a causal link between radon exposure and lung cancer. Although extrapolation of the results from miners caused controversy, the BEIR VI estimation of risk was validated by studies in the general population.7,20–23

Since the 1980s, several small case-control studies with limited power examined the relationship between indoor radon and lung cancer in the general population. In these studies, individuals who had developed lung cancer were compared with controls who had not developed the disease but who otherwise represented the population from which the cases of lung cancer came.

To improve the statistical power, the investigators of the major studies in Europe, North America, and China pooled the results in separate analyses (Table 2).7,20–23 The average radon concentration to which each individual had been exposed over the previous decades was estimated by measuring the radon concentration at their present and previous homes. On the basis of information from the uranium miners, these studies assumed that the period of exposure was the 30 years ending 5 years before the diagnosis or at death from lung cancer.

The results provided convincing evidence that radon exposure is a cause of lung cancer in the general population and substantiated the extrapolation from the studies of miners. Further, the results of all three pooled analyses were consistent with a linear dose-response relationship with no threshold, suggesting an increased risk of lung cancer even with a radon level below 4 pCi/L (200 Bq/m3), which is the concentration at which mitigation actions are recommended in many countries.17

The North American pooled analysis included 3,662 cases and 4,966 controls from seven studies in the United States and Canada. When data from all studies were combined, the risk of lung cancer was found to increase by 11% per 100-Bq/m3 (about 2.7-pCi/L) increase in measured radon concentration (95% CI 0%–28%). The estimated increase in lung cancer was independent of age, sex, or smoking history.7,20

The Chinese pooled data22 demonstrated a 13% (95% CI 1%–36%) increased risk per 100 Bq/m3.

In the European study, the risk of lung cancer increased by 8% per 100 Bq/m3 (95% CI 3%–16%). The European investigators repeated the analysis, taking into account the random year-to-year variability in measured radon concentration, finding the final estimated risk was an increase of 16% per 100 Bq/m3 using long-term average concentration.21

The combined estimate21,24 from the three pooling studies based on measured radon concentration is an increased risk of lung cancer of 10% per 100 Bq/m3.

Synergistic risk with smoking

Radon exposure was independently associated with lung cancer, and the relationship with cigarette smoking is believed to be synergistic. The radon progeny particles attach themselves to smoke and dust and are then deposited in the bronchial epithelium.25

In the pool of European case-control studies, the cancer risk for current smokers of 15 to 24 cigarettes per day relative to that in never-smokers was 25.8 (95% CI 21–31). Assuming that in the same analysis the lung cancer risk increased by 16% per 100 Bq/m3 of usual radon concentration regardless of smoking status, the cumulative absolute risk by age 75 would be 0.67% in those who never smoked and 16% in smokers at usual radon levels of 400 Bq/m3 (11 pCi/L).21

Rates of all lung cancer subtypes increased

Radon exposure is not associated with a specific histologic subtype of lung cancer. It has been speculated that the incidence of the small-cell subtype might be slightly increased because radon tends to deposit in the more central bronchial carinae.20,21 However, all subtypes have been described in association with radon, the most common being adenocarcinoma and squamous cell carcinoma.26–28


The US Surgeon General and the EPA recommend that all homes be tested.18 Short-term tests should be used first, keeping in mind that diurnal and seasonal variations may occur.

The World Health Organization has proposed a reference level of 100 Bq/m3 (2.7 pCi/L) to minimize health hazards from indoor radon exposure.17 If this level cannot be reached under the country-specific conditions, the chosen reference level should not exceed 300 Bq/m3 (8 pCi/L).

In the United States, if the result of home testing is higher than 4 pCi/L, a follow-up measurement should be done using a different short-term test or a long-term test. If the follow-up result confirms a level of more than 4 pCi/L, mitigating actions are recommended. The goal is to reduce the indoor radon level as much as possible—down to zero or at least comparable to outdoor levels (national average 0.4 pCi/L).18

A variety of radon mitigation strategies have been used, with different rates of efficacy (Table 3). The optimal strategy depends on the likely source or cause, construction characteristics, soil, and climate.29Table 4 lists resources for the general public about testing and mitigation measures.

How beneficial is radon mitigation?

Although it is logical to try to reduce the indoor radon concentration, there is no strong evidence yet that this intervention decreases the incidence of lung cancer in the general population.

Using the BEIR VI risk model, Méndez et al30 estimated a 21% reduction in the annual radon-related lung cancer mortality rate by 2100 if all households were compliant with government recommendations (mitigation actions at levels of 4 pCi/L) and assuming that the percentage of cigarette smokers remained constant.

On the other hand, if the number of smokers continues to decline, the benefits from radon mitigation may be less. The expected benefit from mitigation in this scenario is a reduction of 12% in annual radon-related deaths by the year 2100.30 However, it will be challenging to determine whether the expected decline in the incidence of lung cancer and lung cancer deaths is truly attributable to mitigation measures.

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