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Archives of Environmental Health: An International Journal Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/vzeh20
Respiratory Cancer and Occupational Exposure to Arsenicals a
Steven Samuels & Cynthia Howarth a
b
Department of Biostatistics
b
Department of Epidemiology , International Health University of Washington , Seattle Published online: 02 May 2013.
To cite this article: Steven Samuels & Cynthia Howarth (1975) Respiratory Cancer and Occupational Exposure to Arsenicals, Archives of Environmental Health: An International Journal, 30:8, 423-423, DOI: 10.1080/00039896.1975.10666739 To link to this article: http://dx.doi.org/10.1080/00039896.1975.10666739
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http://www.tandfonline.com/page/terms-and-conditions
Lette rs to the Edito r
Downloaded by [JAMES COOK UNIVERSITY] at 03:45 16 March 2015
Hexach lorophe ne in Mice
To the Editor .-In respect to the article, "Hexac hloroph ene in Mice," that appeare d in the Januar y issue of the ARCHIVES (30:32-35, 1975) there certain ly seems to be a discrep ancy in some of the materia l as correla ted with the tables. The table on page 34 finds that there were 29 tumors in 50 control animals and yet only 15 tumors out of 50 animals that had been treated with 50% hexachlorophene. The two treated groups also had fewer tumors than the control group. The author states "the number and distribu tion of the tumors did not, however, differ from that of the untreat ed controls ." That is incompatible with that table. One could conclude the reverse , that is, that a 50% concen tration of hexachlorophene cut the tumor inciden ce in half, as measur ed against the control group. Could the author advise this reader as to the veracit y of the table? WILLIAM E. NEELD Jr, MD Medical Division E.I. du Pont de Nemou rs & Co Deepw ater, NJ Respira tory Cal1HCer and Occupa tional Exposur@ to Arsenic als
To the Editor .-The article by Ott et al, "Respir atory Cancer and Occupational Exposu re to Arsenic als," that appeare d in the Novem ber issue of the ARCHIVES (29:250-255, 1974) claims that there is a dose-response relation betwee n an index of arsenic exposur e and the ratio of observe d-to-ex pected respira tory cancer deaths among Dow Compa ny employees. This finding is subject to criticism on three counts. First of all, the estimat es of expected number s of deaths, based on estimat ed Proport ional Mortali ty Ratio (PMR), are unreliab le. The estimating equatio n left 43% of the observed variabi lity in PMR among control s unexpla ined. Simulta neous 90% confidence interva ls for PMR among the exposed would probabl y be consist ent with the hypothe sis of no dose-response relation ship. Second, both exposed and control study groups are badly biased samArch Environ Health IVol 30, Aug 1975
tobacco smoke is a major source of injury for smoker s is clearly false!,5 The fact that N0 2 is not an import ant compon ent of fresh tobacco smoke should be recognized, and the allegation of N0 2 -based damagi ng effects rejected . RICHARD J. HICKEY, PHD RICHARD C. CLELLAND, PHD DAVID E. BOYCE, PHD EVELYN J. BOWERS Philade lphia
pIes of the actual populat ion of employees. Both groups excluded men who had left the compan y prior to retiremen t. One can easily imagin e situatio ns where no dose-response relation ship existed in the total populat ion, but where differen tial biases among the control and exposed groups have ind.uced a relation ship in the study populat ion. Finally , althoug h the produc t-lead arsenic -is pentava lent, trivalen t arsenic is used in the first stages of the manufa cture (M.G. Ott, written communica tion). Is it possible that the trivalen t arsenic as well as pentavalent could have been present in the environ ment of the exposed workers ? It is import ant to comple tely eliminate the possibi lity of exposur e to arsenic trioxide before the pentav alent form can be comple tely evaluat ed. STEVEN SAMUELS Depart ment of Biostat istics CYNTHIA HOWARTH Depart ment of Epidem iology and Interna tional Health Univer sity of Washin gton Seattle
1. Public Health Service: Smoking and Health, publication No. 1103. Wasbington, DC, US Government Printing Office, 1964, p 60. 2. Abelson PH: A damaging source of air pollution, editorial. Science 158:1527, 1967. 3. Goldstein E: Evaluation of the role of nitrogen dioxide in the development of respiratory diseases in man, in National Academy of Sciences-National Research Council: Proceedings of
the Conference on Health Effects of Air Pollutants, serial No. 93-15. Washington, DC, US Government Printing Office, 1973, pp 407-439. 4. Norman V, Keith CH: Nitrogen oxides in tobacco smoke. Nature 205:915-916, 1965. 5. Hoffman D, Wynder EL: Chamber development and aerosol dispersion, in Hanna MG Jr, Nettesheim P, and Gilbert JR (eds): Inhalation Carcinogenesis. Oak Ridge, Tenn, US Atomic Energy Commission, 1970, pp 173-189.
Nitroge n Oxides , Tobacc o Smoke , @.ilnd Chroni c Diseas e
In Reply. -I can refer Dr. Hickey et al to the text as follows:
To the Editor .-In the Octobe r issue of the ARCHIVES (29:203-210, 1974), Freeman et aI, in their discussion of pulmonary disease and its relation to exposur e to nitroge n dioxide (N0 2 ) and ozone, claim that " . . . . injury from tobacco smoke would be due largely to its relative ly high concentration of N0 2 ." Asserti ons that N0 2 is an import ant compon ent of tobacco smoke 2 • 3 are incomp atible with observed data!,5 Althou gh atmosp heric NO oxidizes slowly to N0 2 , fresh tobacco smoketo which smoker s are directly exposed- contain s nitric oxide (NO), but little or no NO,!·5 But NO and N0 are quite differen t, just as are carbon monoxide (CO) and carbon dioxide (C0 Accordingly, the physiological effects of N0 2 cannot be equated with effects of NO nor of fresh tobacco smoke. While N0 2 is not harmle ss to humans, the claim that N0 2 in fresh
The positive epidemiologic correlation between cigarett e smoking and the prevalence of chronic obstruct ive pulmona ry disease led us to investig ate the possible etiologic role of nitrogen oxides (NO x ), invariable components of tobacco smoke (p 203). Should these prelimin ary observations be applied hypothetically to man, the population in which emphyse ma would be likely to emerge would consist largely of smokers who unwittin gly inhale the high concentrations of oxides of nitrogen in tobacco smoke (p 209).
2
2 ),
Their objectio n is to the phrase in the subjunc tive tense in the summa ry implying that if any of the oxides of nitrogen were to be found at fault, it would be the dioxide of nitroge n. It may be of interes t that the oxides of nitroge n, when inhaled , are almost entirely retaine d. In view of the inevita ble presenc e of oxygen in the respira tory apparat us, it is most unlikely that the large amount of NO could escape oxidati on to N0 2 to some Letters
to the Editor
423
Archives of Environmental Health: An International Journal Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/vzeh20
Respiratory Cancer and Occupational Exposure to Arsenicals a
Steven Samuels & Cynthia Howarth a
b
Department of Biostatistics
b
Department of Epidemiology , International Health University of Washington , Seattle Published online: 02 May 2013.
To cite this article: Steven Samuels & Cynthia Howarth (1975) Respiratory Cancer and Occupational Exposure to Arsenicals, Archives of Environmental Health: An International Journal, 30:8, 423-423, DOI: 10.1080/00039896.1975.10666739 To link to this article: http://dx.doi.org/10.1080/00039896.1975.10666739
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http://www.tandfonline.com/page/terms-and-conditions
Lette rs to the Edito r
Downloaded by [JAMES COOK UNIVERSITY] at 03:45 16 March 2015
Hexach lorophe ne in Mice
To the Editor .-In respect to the article, "Hexac hloroph ene in Mice," that appeare d in the Januar y issue of the ARCHIVES (30:32-35, 1975) there certain ly seems to be a discrep ancy in some of the materia l as correla ted with the tables. The table on page 34 finds that there were 29 tumors in 50 control animals and yet only 15 tumors out of 50 animals that had been treated with 50% hexachlorophene. The two treated groups also had fewer tumors than the control group. The author states "the number and distribu tion of the tumors did not, however, differ from that of the untreat ed controls ." That is incompatible with that table. One could conclude the reverse , that is, that a 50% concen tration of hexachlorophene cut the tumor inciden ce in half, as measur ed against the control group. Could the author advise this reader as to the veracit y of the table? WILLIAM E. NEELD Jr, MD Medical Division E.I. du Pont de Nemou rs & Co Deepw ater, NJ Respira tory Cal1HCer and Occupa tional Exposur@ to Arsenic als
To the Editor .-The article by Ott et al, "Respir atory Cancer and Occupational Exposu re to Arsenic als," that appeare d in the Novem ber issue of the ARCHIVES (29:250-255, 1974) claims that there is a dose-response relation betwee n an index of arsenic exposur e and the ratio of observe d-to-ex pected respira tory cancer deaths among Dow Compa ny employees. This finding is subject to criticism on three counts. First of all, the estimat es of expected number s of deaths, based on estimat ed Proport ional Mortali ty Ratio (PMR), are unreliab le. The estimating equatio n left 43% of the observed variabi lity in PMR among control s unexpla ined. Simulta neous 90% confidence interva ls for PMR among the exposed would probabl y be consist ent with the hypothe sis of no dose-response relation ship. Second, both exposed and control study groups are badly biased samArch Environ Health IVol 30, Aug 1975
tobacco smoke is a major source of injury for smoker s is clearly false!,5 The fact that N0 2 is not an import ant compon ent of fresh tobacco smoke should be recognized, and the allegation of N0 2 -based damagi ng effects rejected . RICHARD J. HICKEY, PHD RICHARD C. CLELLAND, PHD DAVID E. BOYCE, PHD EVELYN J. BOWERS Philade lphia
pIes of the actual populat ion of employees. Both groups excluded men who had left the compan y prior to retiremen t. One can easily imagin e situatio ns where no dose-response relation ship existed in the total populat ion, but where differen tial biases among the control and exposed groups have ind.uced a relation ship in the study populat ion. Finally , althoug h the produc t-lead arsenic -is pentava lent, trivalen t arsenic is used in the first stages of the manufa cture (M.G. Ott, written communica tion). Is it possible that the trivalen t arsenic as well as pentavalent could have been present in the environ ment of the exposed workers ? It is import ant to comple tely eliminate the possibi lity of exposur e to arsenic trioxide before the pentav alent form can be comple tely evaluat ed. STEVEN SAMUELS Depart ment of Biostat istics CYNTHIA HOWARTH Depart ment of Epidem iology and Interna tional Health Univer sity of Washin gton Seattle
1. Public Health Service: Smoking and Health, publication No. 1103. Wasbington, DC, US Government Printing Office, 1964, p 60. 2. Abelson PH: A damaging source of air pollution, editorial. Science 158:1527, 1967. 3. Goldstein E: Evaluation of the role of nitrogen dioxide in the development of respiratory diseases in man, in National Academy of Sciences-National Research Council: Proceedings of
the Conference on Health Effects of Air Pollutants, serial No. 93-15. Washington, DC, US Government Printing Office, 1973, pp 407-439. 4. Norman V, Keith CH: Nitrogen oxides in tobacco smoke. Nature 205:915-916, 1965. 5. Hoffman D, Wynder EL: Chamber development and aerosol dispersion, in Hanna MG Jr, Nettesheim P, and Gilbert JR (eds): Inhalation Carcinogenesis. Oak Ridge, Tenn, US Atomic Energy Commission, 1970, pp 173-189.
Nitroge n Oxides , Tobacc o Smoke , @.ilnd Chroni c Diseas e
In Reply. -I can refer Dr. Hickey et al to the text as follows:
To the Editor .-In the Octobe r issue of the ARCHIVES (29:203-210, 1974), Freeman et aI, in their discussion of pulmonary disease and its relation to exposur e to nitroge n dioxide (N0 2 ) and ozone, claim that " . . . . injury from tobacco smoke would be due largely to its relative ly high concentration of N0 2 ." Asserti ons that N0 2 is an import ant compon ent of tobacco smoke 2 • 3 are incomp atible with observed data!,5 Althou gh atmosp heric NO oxidizes slowly to N0 2 , fresh tobacco smoketo which smoker s are directly exposed- contain s nitric oxide (NO), but little or no NO,!·5 But NO and N0 are quite differen t, just as are carbon monoxide (CO) and carbon dioxide (C0 Accordingly, the physiological effects of N0 2 cannot be equated with effects of NO nor of fresh tobacco smoke. While N0 2 is not harmle ss to humans, the claim that N0 2 in fresh
The positive epidemiologic correlation between cigarett e smoking and the prevalence of chronic obstruct ive pulmona ry disease led us to investig ate the possible etiologic role of nitrogen oxides (NO x ), invariable components of tobacco smoke (p 203). Should these prelimin ary observations be applied hypothetically to man, the population in which emphyse ma would be likely to emerge would consist largely of smokers who unwittin gly inhale the high concentrations of oxides of nitrogen in tobacco smoke (p 209).
2
2 ),
Their objectio n is to the phrase in the subjunc tive tense in the summa ry implying that if any of the oxides of nitrogen were to be found at fault, it would be the dioxide of nitroge n. It may be of interes t that the oxides of nitroge n, when inhaled , are almost entirely retaine d. In view of the inevita ble presenc e of oxygen in the respira tory apparat us, it is most unlikely that the large amount of NO could escape oxidati on to N0 2 to some Letters
to the Editor
423
