{"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":"22 1","pages":"536-538"},"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}
{"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":"36 1","pages":"5-6"},"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}
{"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":"14 1","pages":"473-474"},"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}
{"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":"120 1","pages":"183-204"},"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}
{"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":"129 1","pages":"415-21"},"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}
{"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":"1 1","pages":"468-470"},"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}
{"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":"37 1","pages":"3-3"},"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}
J. Babish, J. Hotchkiss, T. Wachs, A. Vecchio, W. Gutenmann, D. Lisk
{"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":"72 1","pages":"167-177"},"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}
{"title":"Effects of pretreatment with skf‐525a, n‐methyl‐2‐thioimidazole, sodium phenobarbital, or 3‐methylcholanthrene on ethylenethiourea‐induced teratogenicity in hamsters","authors":"K. S. Khera, C. Whalen, F. Iverson","doi":"10.1080/15287398309530342","DOIUrl":"https://doi.org/10.1080/15287398309530342","url":null,"abstract":"Teratogenicity of ethylenethiourea (ETU) was studied in the hamster to define the organ most vulnerable to its teratogenic action. A single intragastric dose of 600, 1200, 1800 or 2400 mg ETU/kg was given in 1.5% aqueous gelatin on d 11 of pregnancy. None of these dose levels produced any apparent maternal toxicity. However, fetal toxicity was apparent in the form of deaths, reduced body weight at the 2400 mg/kg dose, and dose‐related incidences of hydrocephalus, hypoplastic cerebellum, cleft palate, delayed calvarial ossification, and ectrodactyly. The ventricular system of the brain and the cerebellum were among the most sensitive sites for malformations. Effects of metabolic modifiers on the teratogenicity of ETU were studied in separate experiments. Doses of ETU were administered by gastric intubation on d 11 of pregnancy either immediately after an intragastric dose of 200 or 400 mg N‐methyl‐2‐thioimidazole/kg, or 1 h after an ip 40‐mg/kg dose of SKF‐525A. The SKF‐525A pretreatment significantly incr...","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":"9 1","pages":"287-300"},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82587211","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}
{"title":"Pathology of lethal and sublethal exposure of fathead minnows, pimephales promelas, to cadmium: A model for aquatic toxicity assessment","authors":"P. Stromberg, J. Ferrante, S. D. Carter","doi":"10.1080/15287398309530339","DOIUrl":"https://doi.org/10.1080/15287398309530339","url":null,"abstract":"Seventy‐six fathead minnows were exposed to 12 ppm cadmium for 96‐ h and examined histologically at 1‐wk intervals for 30 d. Thirteen fish (17.1%) died during the exposure period. Lesions associated with acute cadmium toxicity were epithelial necrosis of the skin, oral cavity, gills, olfactory organs, kidney, urinary bladder, ureters, gastrointestinal tract, and hemopoietic organ. The lesions were most severe in fish which died. Survivors had similar but less severe and less extensive lesions. Residual minimal to mild multifocal necrosis was observed In gastrointestinal, branchial epithelium and and hemopoietic tissue up to 29 d postexposure. Radiotracer studies in 50 fish using 115Cd demonstrated a rapid uptake and two phase elimination of cadmium by the fish. Rapid elimination of cadmium occurred within 7 wk and was correlated with lesions in the urinary epithelium. Slow phase elimination occurred for at least 3 wk and was correlated with persistant minimal necrosis in several tissues.","PeriodicalId":17418,"journal":{"name":"Journal of Toxicology and Environmental Health, Part A","volume":"23 1","pages":"247-259"},"PeriodicalIF":0.0,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83622547","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}