Radiation from tobacco smoke is one of the prime factors in causing lung cancer. The cancer usually begins at the bronchial branches called bifurcations by particles which collect and from hot spots with high radiation levels.
The smoker receives this type of radiation (called Alpha Radiation), from Tobacco smoke from the following sources:
In addition, smokers and non-smokers alike are exposed to alpha radiation from various radioactive decay products of the soil (mainly from phosphate fertilizers), the air, and natural indoor radon.
The cumulative alpha particle dose at the bifurcations of the lungs of smokers who die of lung cancer is 1600 rems, enough to cause cancer of nearby cells.
For over twenty years scientists have known that all types of tobacco contain radioactive Polonium-210 which emits alpha particles and radioactive Lead-210 which emits Beta particles and is a precursor of Polonium-210. But only recently has there been a degree of consensus about how tobacco becomes radioactive.
All soils contain radium, a radioactive element that decays into Lead-210 and Polonium-210. In addition, phosphate ore used to make fertilizers used on tobacco fields contains these isotopes in relatively high concentrations. While tobacco plants can absorb Lead-210 and Polonium-210 through their roots, relatively little enters this way.
Instead, radiation mainly enters tobacco through the leaves, which are coated with tiny hairs called trichomes, whose tips are coated with a sticky substance which collects dust. This airborne radioactive dust collects on the trichome tips, or heads, in concentrations of radioisotopes 10,000 times that of the overall leaf. almost all the radioactivity of tobacco comes from this air deposition process.
The soil and phosphate fertilizers are the source of the radioactive isotopes. When Radium-226, a component of soil and fertilizer, decays, it gives rise to Radon-222, a gas that escapes to the air. This radon decays into its daughters, (the scientific term for radioactive decay products of the original parent radon). These radon daughters have high electric charges that make them attach to dust particles. These dust particles, with the radon daughters attached, stick to the tips or heads of the hairs of tobacco leaves. During processing; the radiation is not removed from the tobacco.
Even in healthy lungs, the bifurcations where the bronchi branch are an obstacle to the clearing of mucus from the lungs. In a smoker's lungs, ciliary action to clear the lungs is reduced to about half of normal. (The cilia are the microscopic hair-like structures upon which mucus 'rides' in this process).
The average length of time during which the insoluble forms of Lead-210 and Polonium-210 remain at the bronchial bifurcations of smokers is 3 to 5 months. Coincidentally, the surface tissue of smokers' bronchi at the bifurcations is replaced by damaged, abnormal (metaplastic) tissue.
The alpha radiation emitted by Polonium-210 is ordinarily a non-penetrating form of radiation, one with a short path, but it is a very highly ionizing (harmful to basic cell structure) form of radiation and is concentrated at the damaged surface tissues of the lung bifurcations. Scientists have measured this alpha radiation at the bifurcations of smoker's lungs and calculated that it can do as much harm to these tissues as 300 chest X-rays per year would do to the skin of a person being X-rayed.
Whether radiation, chemicals or physical factors associated with smoking cause the damaged, abnormal (metaplastic) tissue found in all smokers' lungs is not clear.
However, the fact that these high doses of radiation are delivered to vulnerable tissue at the location where malignancy is most frequently observed argues strongly for alpha radiation playing the most important role in causing lung cancer.
Radium-226 is found in all soils, and is a significant source of radiation where concentrations are high. From the soil it decays to Radon-222, a gas that enters the surface air. The same radioactive decay diagram applies to this process of decay from natural indoor radon daughters. Radon enters buildings through construction materials or water service and levels can be high enough to require remedial action.
When there is little dust, the radon daughters mainly become attached to room surfaces, but when cigarette smoke is present, the radon daughters attach to smoke particles. Thus, the alpha radiation to a smoker's lungs from the natural radon daughters is increased because of smoking.
Radiation may play a role in the induction of cancer in passive smokers as well. In a historic 14-year study of 91,540 women in Japan, Hirayama demonstrated the direct ration between the amount of smoking in the household and the incidence of lung cancer among non-smoking wives of smokers. Other studies have also indicated that passive smoke may cause lung cancer.
The passive smoker is exposed to the same radioactive isotopes in the tobacco as the smoker. Moreover, the sidestream smoke contains 50 to 70 percent of the Polonium-210. In addition, the exposure of the passive smoker to naturally occurring radon daughters is increased in a smoky environment. Radon daughter exposure may account for 20 to 100 percent of lung cancer in non-smokers. There has been no autopsy study of radioactive isotope levels in non-smokers specifically to determine the effect of passive smoking, although medical scientists have found that there were high radioactive isotope levels in non-smoking individuals who died of lung cancer.
The soluble radioactive Polonium-210 that is produced at the burning temperature of cigarettes is cleared from the lungs at the expense of the rest of the body. It is carried by the circulation to every tissue and cell, causing early death from a body-wide spectrum of diseases reminiscent of the patterns afflicting early radiologists and others with long-term exposure to X-rays and other forms of radiation. Polonium-210 and other mutagens have been found in the blood and urine of smokers.
The number of deaths from cancer of all indirectly exposed tissues such as the stomach, intestines, and so on are 38 percent higher among smokers than among non-smokers, and the number of deaths from cardiovascular diseases are 58 percent higher among smokers than non-smokers.
The chart lists the ratio of observed death rate among smokers to the death rate among non-smokers.
|Cause of death||Observed/Expected Ratio|
|Cancer of directly exposed tissues (Mouth, pharynx, larynx, lung & bronchus, esophagus)||10.34|
|Cancer of indirectly exposed tissues (Stomach, intestines, rectum, liver & biliary passages, pancreas, prostate, kidney, bladder, brain, malignant lymphomas, leukemias, all other cancers)||1.38|
|All cardiovascular diseases (coronary heart disease, aortic aneurysm, cor pulmonale, all other cardiovascular)||1.58|
|Ulcer of stomach, small intestines||3.10|
|Cirrhosis of liver||2.69|
The numbers in the right-hand column show the ratio of deaths among smokers to that among non-smokers. A reading of "1.73" means a 73 percent increase in death among smokers. A reading of "14.83" means that the death rate among smokers is 14.83 times that among non-smokers or a 1,383 percent increase in death rate.
Appreciation is extended to: *VCH Publishers, Deerfield Beach, Florida and the authors, Drs. Thomas Winters and Joseph Di Franza, University of Massachusetts Medical Center, for their permission to use material from LUNG CANCER CAUSES AND PREVENTION, (Ed. Mizell and Correa, 1984), for much of the content of this publication.
*For the Section, "Effects of Smoking throughout the Body," we are indebted to material published by Dr. R.T. Ravenholt, Center for Disease Control, (Washington office) in the New England Journal of Medicine (307/5, p.312).
This information was compiled by Carol W. LaGrasse, P.E., a member of the Adirondack Branch Advisory Council, American Lung Association of New York State, in the interest of more fully informing the public and particularly smokers of the presence of radioactivity in cigarette smoke. It is hoped that this will become yet another contributing factor to assist them in quitting.
By Carol W. LaGrasse, P.E., member Adirondack Branch Advisory Council of the American Lung Association of N.Y. State 1986.
Originally presented by the American Lung Association of New York State.
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