Some 2,224 children given X-ray therapy for tinea capitis (ringworm of the scalp) have been followed for up to 50 years to determine cancer incidence, along with a control group of 1,380 tinea capitis patients given only topical medications. The study found a relative risk (RR) of 3.6 (95% confidence interval, 2.3-5.9) for basal cell skin cancer (BCC) of the head and neck among irradiated Caucasians (124 irradiated cases and 21 control cases), in response to a scalp dose of about 4.8 Gy. No melanomas of the head and neck have been seen, and only a few squamous cell carcinomas. About 40% of irradiated cases have had multiple BCCs, for a total of 328 BCCs. Although 25% of both the irradiated and control groups are African-American, only 3 skin cancers have been seen among them, all in the irradiated group, indicating the importance of susceptibility to UV radiation as a cofactor. Light complexion, severe sunburning and North European ancestry were predictive of BCC risk in the irradiated group, but chronic sun exposure was not. Children irradiated at young ages had the highest BCC risk. The RR for BCC risk is approximately constant with time since exposure, suggesting that risk will probably last for a lifetime.
A series of about 2200 children who received X-ray treatment for ringworm of the scalp (tinea capitis) during the 1940s and 1950s, and a comparable group of 1400 treated without X ray, have been followed by mail questionnaire for an average of 26 years since treatment to tabulate the incidence of skin cancer. The X-ray treatment consisted of 300-380 R to five overlapping fields on the scalp, to cause complete depilation. This delivered doses of 300-600 rad to various portions of the scalp, with lower doses to the skin of the face and neck. In the irradiated group, 41 persons have had one or more basal cell carcinomas of the scalp or face while only three have been diagnosed in controls. There was a high prevalence of multiple skin cancers in the irradiated group (80 lesions among 41 cases). The minimum latent period for radiation-induced skin cancers was long--about 20 years--and this may be attributable to the young age of the population. The skin cancer risk was particularly pronounced on the face, where there would be more UVR exposure in addition to X-ray exposure. Lightness of complexion proved to be an important factor in the skin cancer risk. In addition, skin cancers were found only among caucasians, even though 25% of the study population were blacks. These findings suggest that UVR exposure levels or sensitivity to such exposure interact with ionizing radiation exposure in defining skin cancer risk.
Test plants were grown within a chamber enriched with radon-222 in the atmosphere, in tobacco fields with different sources of phosphate-containing fertilizer, and in culture containing lead-210 in the nutrient solution. Harvested leaves were subjected to three curing conditions. The major portion of the lead-210 in the plant was probably absorbed through the roots. Airborne radon 222 and its daughters contributed much less to the plant's content of lead-210 and of polonium-210. The stage of leaf development and the methods used to cure the leaf affected the final amount of polonium-210 in tobacco leaf.
The objective of the study is to characterize the risk of tumors from radiation exposure to the head and neck. A cohort of 2,224 children given x-ray treatment and 1,380 given only topical medications for ringworm of the scalp (tinea capitis) during 1940-1959 have been followed up for a median of 39 y to determine tumor incidence. Follow-ups were by mail/telephone questionnaire, with 84-88% of the original cohort followed and with medical verification of diseases of interest. Sixteen intracranial tumors [7 brain cancers, 4 meningiomas, and 5 acoustic neuromas (vestibular schwannomas)] occurred in the x-irradiated group following an average brain dose of about 1.4 Gy, compared to 1 acoustic neuroma in the control group. The standardized incidence ratio (SIR) for brain cancer was 3.0 [95% confidence interval (CI): 1.3, 5.9]. Even though the dose to the thyroid gland was only about 60 mGy, 2 thyroid cancers were found in the irradiated group vs. none among controls, and 11 vs. 1 thyroid adenomas were found in the respective groups. Following an average dose of about 4 Gy to cranial marrow, 8 cases of leukemia (SIR = 3.2, CI: 1.5, 6.1) were observed in the irradiated group and 1 in the control group. There was also a suggestive excess of blood dyscrasias. There was no difference between the groups in the frequency of other cancers of the head and neck (excluding nonmelanoma skin cancer) or in total mortality.
Measurements of the environmental and metabolic behaviour of the naturally occurring radionuclides have provided necessary information on the behaviour of stable elements and have been useful analogues in the study of man-made radionuclides. Uranium has been studied primarily because of its role in the nuclear industry and its possible effects as a heavy metal in occupational exposure cases. There is abundant literature dealing with uranium studies in animals, and some literature on human studies with chronically ill patients. Relatively few data are available which document the uranium concentrations in humans under chronic, low level environmental conditions. Some recent bone measurements performed at the US Department of Energy, Environmental Measurements Laboratory are presented. For comparison, a summary of published information on uranium concentrations in blood, soft tissues and bones of humans is also presented. These data are selected to eliminate results from areas of known elevated natural radionuclide levels and occupational or controlled experimental exposure cases. From the measurements of the uranium concentration in bone from 12 countries, it is possible to derive a cumulative frequency distribution for the sampled populations.
The contribution of radon daughter exposure to excess lung cancer in underground miners is universally accepted. These miners received exposures from tens to thousands of WLM in a relatively few years. Although the miners were also exposed to other noxious agents in mines, the appearance of the excess lung cancer mortality in several types of mines and the increase with increasing exposure provide convincing evidence of the role of radon as the carcinogen. It is conceivable that exposures to radon at an average concentration of one to two pCi/liter, the levels for a majority of homes, might not produce excess lung cancers. This would require that a lifetime exposure at low concentrations produce a different response from that of a few years at higher levels for the miners. This is unlikely but not impossible. The current environmental epidemiology is of varying quality. The better studies may give some answers in a few years. These studies are more likely to establish an upper limit of risk than to provide an exposure-response model. Present risk estimates cannot be used accurately in estimating the overall lung cancer risk to the US population, since there are no good data on average exposure and exposure distribution. For example, the number of homes above the EPA guideline of four pCi/liter may range from two million to 10 million. An estimate of the actual radon exposure in the US may be forthcoming from a planned EPA survey, but these data will not be available for a few years. In the conservative tradition of radiation protection, indoor radon exposures in homes are estimated to produce a number of excess lung cancers in the population. One estimate by the NCRP is about 10,000 deaths per year in the US, for an average annual estimated exposure of 0.2 WLM (about one pCi/liter). The National Academy of Sciences (BEIR IV) estimates 13,000 deaths for the same exposure, and the EPA's estimate is 5,000 to 20,000.
An epidemiologic study of childhood leukemia in Denmark (2,400 cases; 6,697 controls) from 1968 to 1994 suggested a weak, but statistically significant, association of residential radon exposure and acute childhood lymphoblastic leukemia (ALL). The Danish study estimated a relative risk (RR) = 1.56 (95% CI, 1.05-2.30) for a cumulative exposure of 1,000 Bq m-3 y. For an exposure duration of 10 y their RR corresponds to a radon concentration of 100 Bq m-3. There are two dose pathways of interest where alpha particles could damage potential stem cells for ALL. One is the alpha dose to bone marrow, and two is the dose to bronchial mucosa where an abundance of circulating lymphocytes is found. Compared with an exposure of about 1 mSv y-1 from natural external background, radon and decay products contribute an additional 10 to 60% to the bone marrow equivalent dose. The other pathway for exposure of T (or B) lymphocytes is within the tracheobronchial epithelium (BE). Inhaled radon decay products deposit on the relatively small area of airway surfaces and deliver a significant dose to the nearby basal or mucous cells implicated in human lung cancer. Lymphocytes are co-located with basal cells and are half as abundant. Using a 10-y exposure to 100 Bq m-3, our dose estimates suggest that the equivalent dose to these lymphocytes could approach 1 Sv. The relatively high dose estimate to lymphocytes circulating through the BE, potential precursor cells for ALL, provides a dose pathway for an association.
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