CORRESPONDENCE Indoor Radon and Lung Cancer in China
1722
A third problem, common to all current epidemiologic investigations of residential radon, is the uncertain relationship between currently measured levels and lifetime exposure doses. This uncertainty, even when using year-long alpha-track measurements, creates a bias to underestimate the effect of radon due to potential misclassification of exposure. It is interesting, despite all of these problems (low exposure levels, a further dosimetric reduction of exposure due to dust, exposure to other lung carcinogens, and uncertainty in estimating historic exposure), that a slight upward trend for small cell carcinoma of the lung was nonetheless linked with increasing dose. As the authors point out, it is this histologic form of lung cancer that has been disproportionately increased in other radon studies (2-4). The importance of this finding must be adequately stressed. Although the authors recognize some of the noted limitations of this study, additional caution must be applied. It would be inappropriate to suggest, on the basis of this study, that indoor-radon lung cancer risk has been overestimated. Further, readers must be advised that this study provides no justification for raising the remedial action level of 4 pCi/L suggested by the Environmental Protection Agency. The press is closely following and reporting on radon investigations and cautionstoavoid overinterpretation of the data are incumbent upon scientists in the field.
MARK J. UPFAL*
Occupational Medicine Wayne State University School ofMedicine Detroit, Mich G. ALEX JOHNSON
American Lung Association of Southeast Michigan Southfield, Mich A. P. JACOBSON
Radon Resource and Training Center PEGGY A. BRADY
University of Michigan School of Public Health Ann Arbor, Mich JOHN A. CAMPBELL
Wayne State University School of Medicine Detroit, Mich
References (1) Burr W J , X U Z Y , B O I C E J D J R , E T AL: Indoor radon and lung cancer in China. J Natl Cancer Inst 82:1025-1030, 1990 (2) SAMET JM: Radon and lung canceT. J Natl Cancer Inst 81:745-757, 1989 (i) DAMBER L, LARSSON LG: Combined effects of
mining and smoking in the causation of lung carcinoma. A case-control study in northern Sweden. Acta Radiol 21:305-30, 1982 (4) GOTTLIEB LS, HUSEN LA: Lungcanceramong
Navajo uranium miners. Chest 81:449-452, 1982
Response The correspondence by Upfal et al. raises the question of whether our case-control study (7) could evaluate, with any precision, the risks of lung cancer associated with indoorradonin Shenyang, China. Particular concern is expressed that the dustiness of homes in Shenyang may have influenced radiation dosetolung tissue. Although this issue could not be directly evaluted, it seems likely there was substantial variation in tissue exposure among the women studied because the differences in home air radon levels were so great. The median radon levels were 7.6 times greater in the high versus low exposure groups. Further, even dustier condi-
*Correspondence to: Mark 1 Upfal, M.D., MPH, Division of Occupational and Environmental Medicine, UHC-4J, Wayne Stale University School of Medicine, 4201 S t Antoine, Detroit, MI 48201.
Journal of the National Cancer Institute
Downloaded from http://jnci.oxfordjournals.org/ at New York University on May 30, 2015
Wereadwith great interest the recent paper by Blot et al. (7). Their study was an elegant technical application of a case-control design to an important question of the relationship between residential radon exposure and lung cancer. The case-control design is certainly appropriate for investigating this relationship. However, there are several important problems that would preclude the detection of radon-induced lung cancer in this population. First, the choice of a population with "exceptionally high rates of lung cancer," but without exceptionally high radon levels (mean, 2.3 pCi/h; 20% of levels exceed 4 pCi/L), is curious. Qearly, one would not expect many of the excess lung cancers in this population to be attributed to radon. In fact, one would anticipate, a priori, that the effect due to radon would most likely be obscured. The high levels of other indoor air pollutants, particularly benzo[a]pyrene at levels 70 times higher than in the U.S., would provide a biologically plausible alternative hypothesis for the excess malignancies. As the authors state, "confounding by other risk factors may have hindered detection of increased risks among women exposed to high radon levels." Certainly, the excess malignancies due to such risk factors would dilute the ability to detect radon-induced malignancies, unless there was a significant positive interactive factor. Second, the consistently high, indoor dust levels will have significantly reduced the exposure dose of the respiratory epithelium to alpha radiation. The unattached fraction of radon daughters will decrease in this setting, lowering the dose of radiation to the respiratory tract for any given exposure level measured by alpha-track. The number ofradon-inducedlung cancers for a given ambient exposure level could be significantly reduced by this
effect. The authors state that they attempted to adjust for this effect by comparing lung cancer rates at high and low indoor air pollution levels. However, uncertainties relating to this adjustment render it meaningless because (a) even the lower air pollution categories were dusty by western standards, (b) as dust levels increase, there is an increase in exposure to other carcinogens, which would be expected to cause an increase in non-radon-induced lung cancers, tending to offset any decrease in radon-induced lung cancers associated with increasing dust levels, and (c) there is inadequate information about dust particle size distribution to predict therelativedosimetric effect of the authors' categories of dust exposure.
1722
A third problem, common to all current epidemiologic investigations of residential radon, is the uncertain relationship between currently measured levels and lifetime exposure doses. This uncertainty, even when using year-long alpha-track measurements, creates a bias to underestimate the effect of radon due to potential misclassification of exposure. It is interesting, despite all of these problems (low exposure levels, a further dosimetric reduction of exposure due to dust, exposure to other lung carcinogens, and uncertainty in estimating historic exposure), that a slight upward trend for small cell carcinoma of the lung was nonetheless linked with increasing dose. As the authors point out, it is this histologic form of lung cancer that has been disproportionately increased in other radon studies (2-4). The importance of this finding must be adequately stressed. Although the authors recognize some of the noted limitations of this study, additional caution must be applied. It would be inappropriate to suggest, on the basis of this study, that indoor-radon lung cancer risk has been overestimated. Further, readers must be advised that this study provides no justification for raising the remedial action level of 4 pCi/L suggested by the Environmental Protection Agency. The press is closely following and reporting on radon investigations and cautionstoavoid overinterpretation of the data are incumbent upon scientists in the field.
MARK J. UPFAL*
Occupational Medicine Wayne State University School ofMedicine Detroit, Mich G. ALEX JOHNSON
American Lung Association of Southeast Michigan Southfield, Mich A. P. JACOBSON
Radon Resource and Training Center PEGGY A. BRADY
University of Michigan School of Public Health Ann Arbor, Mich JOHN A. CAMPBELL
Wayne State University School of Medicine Detroit, Mich
References (1) Burr W J , X U Z Y , B O I C E J D J R , E T AL: Indoor radon and lung cancer in China. J Natl Cancer Inst 82:1025-1030, 1990 (2) SAMET JM: Radon and lung canceT. J Natl Cancer Inst 81:745-757, 1989 (i) DAMBER L, LARSSON LG: Combined effects of
mining and smoking in the causation of lung carcinoma. A case-control study in northern Sweden. Acta Radiol 21:305-30, 1982 (4) GOTTLIEB LS, HUSEN LA: Lungcanceramong
Navajo uranium miners. Chest 81:449-452, 1982
Response The correspondence by Upfal et al. raises the question of whether our case-control study (7) could evaluate, with any precision, the risks of lung cancer associated with indoorradonin Shenyang, China. Particular concern is expressed that the dustiness of homes in Shenyang may have influenced radiation dosetolung tissue. Although this issue could not be directly evaluted, it seems likely there was substantial variation in tissue exposure among the women studied because the differences in home air radon levels were so great. The median radon levels were 7.6 times greater in the high versus low exposure groups. Further, even dustier condi-
*Correspondence to: Mark 1 Upfal, M.D., MPH, Division of Occupational and Environmental Medicine, UHC-4J, Wayne Stale University School of Medicine, 4201 S t Antoine, Detroit, MI 48201.
Journal of the National Cancer Institute
Downloaded from http://jnci.oxfordjournals.org/ at New York University on May 30, 2015
Wereadwith great interest the recent paper by Blot et al. (7). Their study was an elegant technical application of a case-control design to an important question of the relationship between residential radon exposure and lung cancer. The case-control design is certainly appropriate for investigating this relationship. However, there are several important problems that would preclude the detection of radon-induced lung cancer in this population. First, the choice of a population with "exceptionally high rates of lung cancer," but without exceptionally high radon levels (mean, 2.3 pCi/h; 20% of levels exceed 4 pCi/L), is curious. Qearly, one would not expect many of the excess lung cancers in this population to be attributed to radon. In fact, one would anticipate, a priori, that the effect due to radon would most likely be obscured. The high levels of other indoor air pollutants, particularly benzo[a]pyrene at levels 70 times higher than in the U.S., would provide a biologically plausible alternative hypothesis for the excess malignancies. As the authors state, "confounding by other risk factors may have hindered detection of increased risks among women exposed to high radon levels." Certainly, the excess malignancies due to such risk factors would dilute the ability to detect radon-induced malignancies, unless there was a significant positive interactive factor. Second, the consistently high, indoor dust levels will have significantly reduced the exposure dose of the respiratory epithelium to alpha radiation. The unattached fraction of radon daughters will decrease in this setting, lowering the dose of radiation to the respiratory tract for any given exposure level measured by alpha-track. The number ofradon-inducedlung cancers for a given ambient exposure level could be significantly reduced by this
effect. The authors state that they attempted to adjust for this effect by comparing lung cancer rates at high and low indoor air pollution levels. However, uncertainties relating to this adjustment render it meaningless because (a) even the lower air pollution categories were dusty by western standards, (b) as dust levels increase, there is an increase in exposure to other carcinogens, which would be expected to cause an increase in non-radon-induced lung cancers, tending to offset any decrease in radon-induced lung cancers associated with increasing dust levels, and (c) there is inadequate information about dust particle size distribution to predict therelativedosimetric effect of the authors' categories of dust exposure.
