Underground miners
We started this section by telling about the health risks associated with radon exposures in underground mines. As early as around 1500, lung disease was found in two regions of Germany and Czechoslo- vakia, Schneeberg and Joachimsthal, among miners. The miners developed a deadly disease, called
"Bergkrankheit". Between 1876 and 1938, 60 to 80% of all miners died from the disease which, on average, lasted 25 years. Certain regions of the mines were known as "death pits," where all workers got sick. As a result, lung cancer in miners was recognized as an occupational disease.
The atmosphere in underground mines contain several carcinogenic compounds like arsenic and silica dust, diesel exhaust from mining machinery, and radon and its decay products. Furthermore, the majority of the miners were smokers – and we can note that there are no marked differences in the cell type of primary lung cancer resulting from radon exposure in underground miners compared to cancers resulting from cigarette smoking.
We intend to discuss cancer and radiation in a later chapter – after we have presented some of the main topics in radiation biology.
However, it seems reasonable – at this point – to discuss some of the models used with regard to radon and lung cancer.
The radon concentration in the mines could be very large. Thus, measurements published in 1924 confirmed that the air in the mines contained high concentrations of radon gas, the highest more than 18,000 picocuires per liter – or 666 000 Bq/m3. It would therefore be of interest to arrive at the expo- sure rate and accumulated lung doses – or effective radon doses for those who worked for years in the mines. All the dosimetry is carried out in recent years.
The unit used for exposure was called "Working Level" - abbreviated to WL. The definition of WL is:
1 WL = 1.3 . 105 MeV of radon daughters
In the more usual units 1 WL = 3700 Bq/m3 for equilibrium between radon and its progeny. The work- ers in those days worked 40 hours per week or 170 hours per month. This gives a new unit; WLM (Working Level Month) – which is the exposure of 1 WL in 170 hours. With regard to effective dose – the calculations give: 1 WLM is approximately 4.5 mSv.
Several retrospective cohort studies have been made and some conclusions can be drawn. An excess number of lung cancers have been found – even for nonsmokers. No excess lung cancers are observed for doses below 100 WLM (about 450 mSv). The risk increases with dose – up to the largest found for the Colorado Plateau miners (up to 7.4 Sv). However, wether the dose-effct curve is linear is dif- ficult to ascertain.
Another point that should be mentioned is that the old German data seem to indicate that the risk was at a maximum in the period 15 – 24 years after exposure – indicating a latency period of that length.
Radon in homes
We know that exposure to large radon doses can give lung cancer. Unfortunately, this type of lung cancer can not be distinguished from the type induced by smoking. Since the smoking has an effect on the bronchial cilia, it is reasonable to assume that the radon doses to smokers are larger than that for non-smokers.
Formation of cancer by radiation in the low dose range (below 100 mSv) can not be confirmed by epidemiology. ICRP therefore use models to give the risk. The model used – and still in use – is the so called "Linear no Threshold hypothesis" (LNT). This theory originate from the old target theory that a small amount of radiation can give a "hit" (e.g. a damage to the DNA that can initiate a cancer).
Doubling this dose will give two hits – and a linear dose-effect curve is the result.
If this model is correct, an experimental value at a high dose would give the risk. Furthermore, the collective dose conception can be applied. ICRP have used the uranium worker data for lung cancer and also the Hiroshima bomb data to arrive at a risk factor. Using the LNT-model the consensus is that the risk of eventual fatal cancer is 0.05 per Sv.
This model therefore suggest that radon in homes is responsible for about 20 000 lung cancer per year in USA (between 6 000 and 30 000 according to United States Environmental Protection Agency – EPA). For Norway the same model result in about 400 lung cancers per year.
The data based on the LNT theory have resulted in a fear for radon in the homes. In USA limits have been introduced. The level in schools and public buildings should be below 4 pCi per liter (148 Bq/
m3. In Norway the level should be below 200 Bq/m3.
The opposite view
The majority of radiation biologists seem to agree that the mechanisms for radiation induced cancer does not follow a LNT model. The main points for cancer development is as follows.
Normal cells are constantly exposed to potentially toxic agents. These agents derive from oxidative metabolism, from micro nutrient deficiencies, and various toxic compounds from the environment as well as radiation. About 1 million oxidative DNA damages of various kinds have been estimated to occur in vivo per mammalian cell per day from nonradiation sources. Most of the damages are ef- ficiently repaired. Yet repair is not fully effective and leaves some DNA damage to persist and cause mutations in some DNA regions, perhaps 1 mutation/cell/day. These DNA damages, even if eventu- ally partly removed, accumulate and are held to be largely responsible for spontaneous carcinogenesis and aging.
The DNA repair begin almost immediately after the damage has occurred. Thus, different base chang- es are repaired from about 10 minutes to 1 hour. Single strand breaks are usually repaired with a half time of less than 10 minutes, whereas the repair half times for double strand breaks are longer than 30 minutes. Damage removal by interphase death, or apoptosis, is readily seen within hours after ir- radiation.
Illustration of the primary step for Radon and lung cancer
Track of an
a-particle
The above illustration by Per Einar Arnstad gives an idea of the first steps with regard to radon ir- radiation. The a-particle creates a track with dense ionizations (high LET) which may give "clustered damage" to the DNA of the bronchial cells. The damage may add the cell to the pool of "damaged cells". If the damage is not repaired or if the cell is not killed by apoptosis – the possibility exists for
During the latter years we have learned a lot of the repair mechanisms and in particular about apopto- sis (programmed cell death) which remove damaged cells – and consequently seems to be a major av- enue to remove oncogenic transformed cells. We know that small amounts of radiation (doses below 100 – 200 mGy) will initiate both repair and apoptosis. Consequently, radiation itself may remove damaged and dangerous cells. If the radiation-induced reduction of spontaneous cancer outweighs the incidence of radiation-induced cancer, the net dose–effect curve will show what is called a “hormetic effect”. If cancer reduction at low doses equals the corresponding induction, a threshold would result.
At higher doses, above approximately 200 mGy, cellular damage increasingly outweighs low-dose–
induced protection.
Conclusion; The LNT dose effect curve can not be used for radiation induced cancers.
Some attempts have been made to explore the relation between the radon level in homes and the appearance of lung cancer. The most extensive studies have been made in USA. Bernhard L. Cohen published in 1995 and later in 2000 "radon and cancer" data from 1729 US counties including 90 % of the US population. He studied the relation between lung cancer deaths and the average radon level in the homes – and the main results are given by the figure below.
Theoretical LNT model
Radon in Bq m–3
Lung cancer death (relative units)
The figure shows the main results of Bernhard L. Cohens investigations from 1995 and 2000 (Health Physics 68 (2), 157 – 174 (1995)). Data points from group of counties with almost the same radon level have been grouped together. The data from 2000 include more recent cancer data. Furthermore, data for Florida and California have been deleted because deaths there are frequently due to retirees who received their radon doses elsewhere. The results are like those shown above.
Cohens data have been discussed and a lot of critical arguments can be raised. The data are com- pletely opposite to the LNT-hypothesis.
Other data from Finland have been presented, which show no correlation between the appearance of lung cancer and radon in Finnish homes. All the Finnish results can be explained by smoking – and the changes in the smoking habits.
We shall leave the field here – but intend to embark on a more extensive discussion when we have presented the main mechanisms in radiation biology.