Case-control study of childhood acute lymphoblastic leukemia and residential radon exposure.

BACKGROUND: Several ecologic analyses have shown significant positive associations between mean indoor radon concentrations and risk of leukemia at all ages (acute myeloid leukemia and chronic lymphocytic leukemia) and for children (all leukemia, acute myeloid leukemia, and acute lymphoblastic leukemia [ALL]). As part of an age-matched, case-control study of childhood ALL in the United States, we investigated the association between the incidence of ALL in children under age 15 years and indoor radon exposure. METHODS: Radon detectors were placed in current and previous homes of subjects where they resided for 6 months or longer. Children were included in analyses if radon measurements covered 70% or more of the 5-year period prior to diagnosis for case subjects (or from birth for case subjects under age 5 years) and the corresponding reference dates for control subjects. Radon levels could be estimated for 97% of the exposure period for the eligible 505 case subjects and 443 control subjects. RESULTS: Mean radon concentration was lower for case subjects (65.4 becquerels per cubic meter [Bqm(-3)]) than for control subjects (79.1 Bqm(-3)). For categories less than 37, 37-73, 74-147, and 148 or more Bqm(-3) of radon exposure, relative risks based on matched case-control pairs were 1.00, 1.22, 0.82, and 1.02, respectively, and were similar to results from an unmatched analysis. There was no association between ALL and radon exposure within subgroups defined by categories of age, income, birth order, birth weight, sex, type of residence, magnetic field exposure, parental age at the subject's birth, parental occupation, or parental smoking habits. CONCLUSIONS: In contrast to prior ecologic studies, the results from this analytic study provide no evidence for an association between indoor radon exposure and childhood ALL.

Adjusting lung cancer risks for temporal and spatial variations in radon concentration in dwellings in Gansu Province, China.

Our recent study in Gansu Province, China reported an increasing risk of lung cancer with increasing residential radon concentration that was consistent with previous pooled analyses and with meta-analyses of other residential studies (Wang et al., Am. J. Epidemiol. 155, 554-564, 2002). Dosimetry used current radon measurements (1-year track-etch detectors) in homes to characterize concentrations for the previous 30 years, resulting in uncertainties in exposure and possibly reduced estimates of disease risk. We conducted a 3-year substudy in 55 houses to model the temporal and spatial variability in radon levels and to adjust estimates of radon risk. Temporal variation represented the single largest source of uncertainty, suggesting the usefulness of multi-year measurements to assess this variation; however, substantial residual variation remained unexplained. The uncertainty adjustment increased estimates of the excess odds ratio by 50-100%, suggesting that residential radon studies using similar dosimetry may also underestimate radon effects. These results have important implications for risk assessment.

Radon measurements in underground dwellings from two prefectures in China.

Radon, an established lung carcinogen, remains the single most important environmental radiation exposure. Yet, an excess of lung cancer from breathing radon in homes has not been consistently demonstrated in studies conducted to date. To address several major problems that have hindered previous studies of lung cancer and radon in homes, we have embarked upon a lung cancer case-control study in Gansu Province, China, where a substantial proportion of the population live in underground dwellings. In this paper, we report on results of a pilot study in which radon measurements were made for 3 days in the summer in 40 homes under normal occupancy conditions using short-term E-PERM detectors and for 6 months from February through August in 49 homes using long-term alpha-track detectors. Useable E-PERM data were obtained from 38 homes and useable alpha-track data from 47 homes. For both types of detectors, measurements were approximately log-normally distributed. Arithmetic and geometric means were 233 and 185 Bq m-3 (range 74-1,590 Bq m-3) for E-PERM measurements and 165 and 158 Bq m-3 (range 74-592 Bq m-3) for alpha-track measurements, respectively; 68% of E-PERM measured homes and 55% of alpha-track measured homes exceeded 148 Bq m-3. Alpha-track measurements made at the entry, middle, and rear areas of the underground dwellings did not differ significantly (arithmetic means of 168, 162, and 165 Bq m-3 with standard deviations 63, 73, and 48, respectively), which suggests that air circulation may be minimal. The underground dwellings measured in the pilot study had high radon levels and the underground dwellers may provide an excellent population for studying indoor radon and risk of lung cancer.

The use of epidemiology, scientific data, and regulatory authority to determine risk factors in cancers of some organs of the digestive system. 6. Pancreatic cancer.

The etiology of pancreatic cancer remains elusive. It predominates in males and in certain ethnic populations (i.e., Polynesians and blacks). Primarily a disease of aging, it is rare in individuals under 40. Genetics is believed to play a very small part if any. While diabetics have higher than expected incidence and mortality rates, several recent studies have indicated that in most cases the diabetes is an early sign of pancreatic cancer rather than a predisposing condition. Other conditions have been infrequently reported in association with pancreatic cancer. None of them have shown a definitive associative pattern and are believed to represent coincidental occurrences. Migrant studies of Japanese immigrants implicate some type of environmental etiology, since pancreatic cancer rates increase dramatically within one to two generations. Studies on atom bomb survivors have demonstrated no link between a single intense dose of radiation and subsequent development of this disease. Workers exposed to low-level radiation have shown an increase in pancreatic cancer, but this result may reflect methodologic problems. Many chemicals have been shown to cause pancreatic cancer in animals, and chemists exhibit higher pancreatic cancer rates than expected. However, the human cases have not been traced to any specific chemical. Many other occupations besides chemistry have shown increased pancreatic cancer rates, but the common factor in these occupations is not obvious. Studies analyzing the relationship of alcohol consumption to pancreatic cancer yield conflicting results. This may be explained if the observed effects are due to a confounder, such as cigarette smoking; to an ingredient other than alcohol contained in alcoholic beverages, such as nitrosamines; or to the immunosuppressive effects of chronic excessive alcohol consumption. Smoking is the risk factor showing the most definitive and consistent results. There is little doubt that it plays an etiologic role, and it probably accounts for the higher incidence of the disease in males. Most other research does not support MacMahon's reported association between coffee drinking and pancreatic cancer. Recent studies have indicated a generally increased fluid intake in pancreatic cancer patients due to a disease-induced disturbance in glucose tolerance function. Such increased fluid intake would tend to manifest itself in the most popular beverage of the country (i.e., coffee in the United States and tea in the United Kingdom). Animal studies have indicated a link between pancreatic cancer and high fat and/or high protein diets as well as raw soybean consumption.(ABSTRACT TRUNCATED AT 400 WORDS)

The validity of determining pancreatic cancer incidence in the United States by the use of mortality data.

To test the validity of using pancreatic cancer mortality as an indicator of incidence, mortality data for 1969-1971 were compared to incidence data for those areas covered by the Third National Cancer Survey, which was conducted during the same time period. Good correlation was found for whites but not for blacks. Small numbers of black study subjects in the Third National Cancer Survey probably influenced the incidence data for blacks. Pancreatic cancer mortality and incidence data for U.S. whites appear to be fairly accurate indicators of each other. The same cannot be said for the corresponding data for blacks. The pancreatic cancer mortality data from 1970 to 1978 for whites in the United States were analyzed to determine the current trend of the disease. In contrast to previously increasing rates, the age-adjusted rates for white females were determined to have leveled off, while the age-adjusted rates for white males appear to have started to decline slightly.