The big idea: polonium, radon and cigarettes

Between 9¹ and 14%² of deaths from lung cancer in smokers are presently attributed to the effects of low levels of the radioactive gas radon in houses. The highly carcinogenic alpha-particles (radiation) from radon have a major synergistic effect with the chemical carcinogens in cigarette smoke, increasing the lifetime risk of lung cancer by a factor of 8.3² to 25¹ compared with never-smokers. Radon and its radioactive daughter products, one of which is polonium-210 (Po-210), arise from the radioactive decay of uranium, which is ubiquitous in the soil. Low levels of Po-210, which emits the same kind of alpha-radiation as radon, contaminate tobacco.³ Po-210 is relatively long-lived fallout from the decay of radon in the atmosphere close to tobacco plants. This in turn comes from the decay of uranium-contaminated calcium phosphate fertilizer used on tobacco fields. Sub-microscopic particles of Po-210 in the air are trapped on sticky hairs on the leaves of tobacco plants. These hairs are very hydrophobic, and once trapped the radioactivity does not wash off in the rain. Other crops are not affected. Owing to the recognition of the carcinogenicity of low levels of radon in smokers, it appears possible that low levels of Po-210 in cigarettes could be responsible for some lung cancers currently attributed to radon. This is of significance because steps could be taken to moderate uranium contamination of tobacco fields and reduce Po-210 levels in cigarette smoke.

Over 40 years ago quantitative analysis suggested that sufficient Po-210 was present in cigarettes and cigarette smoke to be a possible cause of some lung cancers.³ The suspicion attached to Po-210 appeared to be supported by animal studies.⁴ Additionally, Po-210 was found to be concentrated in the mucosa at the bronchial bifurcations of a group of smokers who had consumed an average of 1.5 packs of cigarettes per day over 30 years.⁵ Little et al.⁵ calculated that the levels of Po-210 at bronchial bifurcations could deliver a potentially carcinogenic dose of radiation at these sites, but these represent only a tiny fraction of the entire epithelium. However, bronchial bifurcations are sites of predilection for bronchial carcinoma. The very low levels of Po-210 in the majority of the mucosa seemed unremarkable at that time, but may now be regarded as being of possible significance. Overwhelming evidence for chemical carcinogenesis led to it becoming the preferred theory for the origin of lung cancer, and the radiation carcinogenesis hypothesis was discarded. However, we should re-evaluate whether low-level alpha-radiation to the lung from Po-210 from cigarettes might still be sufficient to account for some of the lung cancer currently attributed to radon.

When the radiation dose from Po-210 to the part of the bronchial mucosa of the lungs of smokers, other than at bronchial bifurcations, is calculated from the data of Little et al.⁵ and compared with the radiation dose which would be received over 25 years from the average household radon concentration in England,⁶ the radiation dose from Po-210 appears, surprisingly, to exceed that from radon by a factor of nearly two. At lower-than-average household radon levels the proportion arising from Po-210 would be higher, and vice versa. Radford and Hunt³ concluded that the bronchial epithelium of a deceased smoker would have received a minimum radiation dose from Po-210 of seven times background, so a factor of almost two does not seem implausible. One might reasonably be tempted to impute to Po-210 much of the excess carcinogenicity attributed to radon at average levels in smokers. This estimate is very approximate, and it discounts any carcinogenic risk from any high levels of radiation from Po-210 at bronchial bifurcations. There is arguably a case for performing a more formal assessment of whether there could be sufficient radiation from Po-210 in cigarette smoke to be an important contributor to lung cancer.

Lung cancer is by far the largest single cause of cancer mortality in the UK, only slightly exceeded by the mortality from bowel, breast and prostate cancers combined. If a significant number of lung cancer deaths are actually due to Po-210, in addition to radon, one might consider that the currently recommended level for radon remediation in houses (the level above which active steps to reduce radon concentrations are desirable) might have been set higher than would otherwise be required. Above the currently recommended remediation level, however, 70% or more of the radiation dose to the bronchial mucosa would still come from radon rather than Po-210. There would therefore be very little case for raising the recommended radon remediation level. To the contrary, regardless of any effects from Po-210, consideration should be given to lowering the recommended radon remediation level for the houses of smokers. About 90% of lung cancer cases are thought to arise below the current remediation level, and over 100,000 houses in the UK are believed to have unacceptable radon levels.

Smoking has another interaction with radon of importance to passive, as well as active, smokers. Smoking increases the number of particles in the air of a room by several orders of magnitude.⁷ The short-lived radioactive decay products of radon – from which most of the radiation dose, loosely and conventionally attributed to ‘radon’, actually arises – are submicroscopic electrically charged solids. These become attached to the smoke particles,⁷ some of which are so small that they may remain suspended almost indefinitely. Particles are available for inhalation by non-smokers and smokers alike. There is debate about how much of this airborne radioactivity is actually deposited in the lungs because the calculations are complex and contain factors that are variable or not precisely known. It should not be overlooked that passive smokers, in whom the incidence of lung cancer is increased, also inhale synergistic chemical carcinogens from tobacco smoke along with radioactivity. The best advice would be for smokers to cease smoking, but otherwise to reduce the risk to themselves and others by smoking outside where suspended radioactivity would not be re-inhaled, or inhaled by passive smokers.

Uranium has a very long half-life and will accumulate in the soil with repeated applications of fertilizer. As a result, modern cigarettes may contain higher levels of Po-210 than those measured 40 years ago.³ Measurements of Po-210 in the cigarettes of today are needed. Additional measurements of Po-210 in autopsy specimens of smokers and controls are also required to better understand the levels and distribution of Po-210 in the bronchial tree. Smokers are killed by alpha-radiation, whatever its origin. Arguably, a significant part of this mortality is a result of Po-210 in tobacco. Technology to reduce Po-210 in cigarette smoke was available in 1967⁸ and presumably could be improved. Now may be the time to apply it.

Footnotes

DECLARATIONS —

Competing interests None declared

Funding Not applicable

Ethical approval Not applicable

Guarantor MJT

Contributorship MJT is the sole contributor