Tobacco Radioactivity and Cancer in Smokers

Our plain-English summary of Tobacco Radioactivity and Cancer in Smokers, by E.A. Martell (1975).

The study

• Author: E.A. Martell
• Published: American Scientist, Volume 63, July-August 1975
• Type of article: Journal article
• Our copy: from Johns-Manville's own medical library. The article is still under copyright, so we describe it here rather than post it.

In plain English

This 1975 article was a theoretical discussion with partial review of earlier work, not a study of people. The author proposed that lead-210, concentrated in a few insoluble cigarette smoke particles, and the polonium-210 that builds up in them over time may cause cancer in smokers. Most inhaled polonium-210, the author wrote, is on soluble particles and should clear fairly quickly. The author also suggested a role in early atherosclerosis. The article described how radon decay products may collect on tobacco leaf hairs and listed lead-210 levels in tobacco and smoke. The author estimated that tissue around each insoluble particle receives alpha radiation 100 to 10,000 times the natural level. A worked example gave a tumor risk about 1,000 times higher than the same activity spread evenly through the lung. Asbestos appeared once: the author wrote that asbestos and other fibrous dusts may enhance tumor risks from inhaled insoluble radioactive particles. The author called the risk formula highly oversimplified. Comparisons of lung, lymph node and arterial tissue from deceased smokers and nonsmokers were still in progress.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Theoretical article with a partial review of earlier studies and some laboratory measurements of radioactivity in tobacco and smoke; no human study population
• Who was studied: No human subjects were studied. Measurements listed in Table 1 concerned air (at the NCAR Mesa Laboratory roof, Boulder, Colorado), North Carolina flue-cured and Kentucky burley tobacco, tobacco trichomes, and smoke condensate from 1R1 and Players cigarettes.
• Exposure: Alpha radiation from lead-210 concentrated in a small number of insoluble cigarette smoke particles, and from its decay products (bismuth-210, polonium-210), which build up in those particles over time. The author wrote that most inhaled polonium-210 is on soluble smoke particles that clear fairly quickly. The author linked the lead-210 to radon and radium in tobacco soils and phosphate fertilizers. Asbestos was mentioned only as a possible enhancing factor; no asbestos exposure was studied.
• Main results:
  • In the surviving text, after about one month of extraction with a lung-fluid simulant, about 90 percent of the undissolved residue consisted of spherical particles or distorted spheres of about 0.1 to 5.0 micrometers. The sample tested is cut off in the text.
  • By the author's estimate, the small volume of tissue around each insoluble smoke particle or particle cluster receives alpha interaction rates between 100 and 10,000 times the natural level.
  • In a theoretical example, 10 pCi of alpha activity held in insoluble particles was calculated to give a tumor risk about 1,000 times higher than 10 pCi of dissolved activity spread uniformly in the lung.
  • The author wrote that certain chemicals, as well as asbestos and other fibrous dusts, may play a significant role in enhancing tumor risks from inhaled insoluble radioactive particles.
• The authors' conclusion: The author concluded that insoluble alpha-emitting particles of relatively low activity appear to be very effective carcinogenic agents. The author suggested they may be the principal agent of cancer in smokers, and that suspected chemical carcinogens in tobacco smoke are wrongly blamed.
• Limitations the authors state:
  • The author stated that the risk formula is highly oversimplified and that the real situation will be much more complicated.
  • The author stated that the alpha-radiation dose distribution in smokers' lungs is complex and requires experimental evaluation.
  • The author noted that conflicting earlier findings on polonium-210 at bronchial sites had not been resolved.
  • The author stated that alpha-radioactivity accumulation in arterial tissue had not been studied. Measurements in deceased smokers and nonsmokers were described as still in progress, with no results reported.

Browse return to medical research.