Pub Date : 1991-01-01DOI: 10.1080/15287399109531534
M. Gilbertson, R. Schneider
{"title":"International joint commission workshop on cause‐effect linkages: Preface","authors":"M. Gilbertson, R. Schneider","doi":"10.1080/15287399109531534","DOIUrl":"https://doi.org/10.1080/15287399109531534","url":null,"abstract":"","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91399023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1988-04-01DOI: 10.1016/0378-8741(88)90264-4
T. Klein, C. Newton, Herman Friedman
{"title":"Inhibition of natural killer cell function by marijuana components.","authors":"T. Klein, C. Newton, Herman Friedman","doi":"10.1016/0378-8741(88)90264-4","DOIUrl":"https://doi.org/10.1016/0378-8741(88)90264-4","url":null,"abstract":"","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1988-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78619882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1987-08-01DOI: 10.1080/15287398709531043
D.A.B.T. William M. Kluwe
{"title":"Effect of monochlorobenzene on rat liver reconsidered","authors":"D.A.B.T. William M. Kluwe","doi":"10.1080/15287398709531043","DOIUrl":"https://doi.org/10.1080/15287398709531043","url":null,"abstract":"","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1987-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85911145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1985-01-01DOI: 10.1080/15287398509530775
C. E. Becker
{"title":"In memoriam: Ronald Everett Talcott","authors":"C. E. Becker","doi":"10.1080/15287398509530775","DOIUrl":"https://doi.org/10.1080/15287398509530775","url":null,"abstract":"","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86777961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1984-01-01DOI: 10.1080/15287398409530596
P. Mccauley
{"title":"Dimethyltin dichloride (DMDC) studies: A retrospective response","authors":"P. Mccauley","doi":"10.1080/15287398409530596","DOIUrl":"https://doi.org/10.1080/15287398409530596","url":null,"abstract":"","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73569008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1984-01-01DOI: 10.1080/15287398409530493
Daniel B. Menzel
Ozone is one of the most toxic and ubiquitous air pollutants. This review focuses on the toxic effects of ozone in animals and on the similarities and disimilarities between the toxic effects in animals and humans. The molecular basis for the toxicity of ozone is discussed, based on the vigorous oxidizing properties of ozone. Despite the existence of anatomical differences between human, subhuman primate, and dog lungs versus common experimental rodent lungs, the anatomical lesion of ozone inhalation occurs at the functionally equivalent site of the junction between the conducting airway and the respiratory region. Ciliated cells of the upper airways and the type 1 cell of the centriacinar region are most affected. Type 2 cell proliferation is a hallmark of ozone toxicity. A wide variety of biochemical and physiological changes have been noted in several animal species and in humans. Considerable evidence for a free-radical-mediated or lipid peroxide-mediated toxicity is evident, especially in the induction of the glutathione peroxidase system and the protective effects of vitamins C and E. Ozone appears to be a weak mutagen and to produce chromosomal abnormalities. Defects in defense against airborne infection are present in animals, which are more susceptible to airborne infection after ozone exposure. Epidemiological studies, however, fail to detect increased respiratory infections in humans due to ozone. Despite the variety of toxic effects, few qualitative differences between species are apparent; rather, quantitative differences do occur. Ozone may thus be an ideal compound for quantitative extrapolation of toxicity from animals to humans.
{"title":"Ozone: an overview of its toxicity in man and animals.","authors":"Daniel B. Menzel","doi":"10.1080/15287398409530493","DOIUrl":"https://doi.org/10.1080/15287398409530493","url":null,"abstract":"Ozone is one of the most toxic and ubiquitous air pollutants. This review focuses on the toxic effects of ozone in animals and on the similarities and disimilarities between the toxic effects in animals and humans. The molecular basis for the toxicity of ozone is discussed, based on the vigorous oxidizing properties of ozone. Despite the existence of anatomical differences between human, subhuman primate, and dog lungs versus common experimental rodent lungs, the anatomical lesion of ozone inhalation occurs at the functionally equivalent site of the junction between the conducting airway and the respiratory region. Ciliated cells of the upper airways and the type 1 cell of the centriacinar region are most affected. Type 2 cell proliferation is a hallmark of ozone toxicity. A wide variety of biochemical and physiological changes have been noted in several animal species and in humans. Considerable evidence for a free-radical-mediated or lipid peroxide-mediated toxicity is evident, especially in the induction of the glutathione peroxidase system and the protective effects of vitamins C and E. Ozone appears to be a weak mutagen and to produce chromosomal abnormalities. Defects in defense against airborne infection are present in animals, which are more susceptible to airborne infection after ozone exposure. Epidemiological studies, however, fail to detect increased respiratory infections in humans due to ozone. Despite the variety of toxic effects, few qualitative differences between species are apparent; rather, quantitative differences do occur. Ozone may thus be an ideal compound for quantitative extrapolation of toxicity from animals to humans.","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85615258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1984-01-01DOI: 10.1080/15287398409530507
E. Goldstein
Animal models provide important information delineating the pathophysiologic lesions accounting for pollutant-induced enhancement in human susceptibility to bacterial infections. A review of studies which describe the ability of photochemical oxidants to induce these physiologic abnormalities is presented. It is concluded that: sufficient similarity exists between defense mechanisms in rodent and humans to permit use of the rodent as a surrogate; detection of pollutant-induced abnormalities in individual components of the pulmonary antibacterial system is a sensitive means of assessing potential toxicity; pollutant-induced abnormalities in individual components of the antibacterial defense systems results in diminished overall effectiveness of the system, and this in turn permits bacterial proliferation and the initiation of disease; at present these relationships are qualitative. Epidemiologic and human volunteer studies are needed to determine the likelihood of a specific pollutant exposure provoking bacterial proliferation and disease in humans.
{"title":"An assessment of animal models for testing the effect of photochemical oxidants on pulmonary susceptibility to bacterial infection.","authors":"E. Goldstein","doi":"10.1080/15287398409530507","DOIUrl":"https://doi.org/10.1080/15287398409530507","url":null,"abstract":"Animal models provide important information delineating the pathophysiologic lesions accounting for pollutant-induced enhancement in human susceptibility to bacterial infections. A review of studies which describe the ability of photochemical oxidants to induce these physiologic abnormalities is presented. It is concluded that: sufficient similarity exists between defense mechanisms in rodent and humans to permit use of the rodent as a surrogate; detection of pollutant-induced abnormalities in individual components of the pulmonary antibacterial system is a sensitive means of assessing potential toxicity; pollutant-induced abnormalities in individual components of the antibacterial defense systems results in diminished overall effectiveness of the system, and this in turn permits bacterial proliferation and the initiation of disease; at present these relationships are qualitative. Epidemiologic and human volunteer studies are needed to determine the likelihood of a specific pollutant exposure provoking bacterial proliferation and disease in humans.","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73507216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1984-01-01DOI: 10.1080/15287398409530594
J. R. Beall, A. Ulsamer
{"title":"Response to James E. Gibson","authors":"J. R. Beall, A. Ulsamer","doi":"10.1080/15287398409530594","DOIUrl":"https://doi.org/10.1080/15287398409530594","url":null,"abstract":"","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74141829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1983-07-01DOI: 10.1080/15287398309530402
W. Begell
{"title":"Publisher's page","authors":"W. Begell","doi":"10.1080/15287398309530402","DOIUrl":"https://doi.org/10.1080/15287398309530402","url":null,"abstract":"","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83009101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1983-02-01DOI: 10.1080/15287398309530332
J. Babish, J. Hotchkiss, T. Wachs, A. Vecchio, W. Gutenmann, D. Lisk
Aqueous extracts of four brands (eight types) of rubber nursing nipples purchased in the open market were analyzed for volatile N‐nitrosamines, diphenylamine, and mutagenic activity. N‐Nitrosodimethylamine, N‐nitrosodiethylamine, or N‐nitro‐sopiperidine were found in the aqueous extracts of the nipples and in the nipples themselves. All nipples analyzed contained one or more of the three volatile N‐nitrosamines. Diphenylamine was found to be continously released into aqueous extracts from most brands. Certain nipples produced a positive mutagenic response when incubated with Salmonella typhimurium (TA 100) in a modified liquid suspension test.
{"title":"N‐nitrosamines and mutagens in rubber nursing nipples","authors":"J. Babish, J. Hotchkiss, T. Wachs, A. Vecchio, W. Gutenmann, D. Lisk","doi":"10.1080/15287398309530332","DOIUrl":"https://doi.org/10.1080/15287398309530332","url":null,"abstract":"Aqueous extracts of four brands (eight types) of rubber nursing nipples purchased in the open market were analyzed for volatile N‐nitrosamines, diphenylamine, and mutagenic activity. N‐Nitrosodimethylamine, N‐nitrosodiethylamine, or N‐nitro‐sopiperidine were found in the aqueous extracts of the nipples and in the nipples themselves. All nipples analyzed contained one or more of the three volatile N‐nitrosamines. Diphenylamine was found to be continously released into aqueous extracts from most brands. Certain nipples produced a positive mutagenic response when incubated with Salmonella typhimurium (TA 100) in a modified liquid suspension test.","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88806391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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