Journal of toxicology and environmental health最新文献

{"title":"Comparative toxicity of polychlorinated biphenyls to Japanese quail (Coturnix c. japonica) and American kestrels (Falco sparverius).","authors":"J E Elliott,&nbsp;S W Kennedy,&nbsp;A Lorenzen","doi":"10.1080/00984109708984011","DOIUrl":"https://doi.org/10.1080/00984109708984011","url":null,"abstract":"<p><p>Polychlorinated biphenyls (PCBs) and related halogenated hydrocarbons bioaccumulate to high concentrations in top predators, such as raptorial birds, yet little is known of PCB toxicity to such species. This study explored several aspects of both the acute and chronic response of American kestrels (Falco sparverius) to three purified PCB congeners and a commercial mixture, Aroclor 1254, and compared the response to that of the Japanese quail (Coturnix c. japonica), a more studied species known to be PCB sensitive. In one experiment, adult female birds were given single oral doses of either Aroclor 1254, 3,3',4,4'-TCB (PCB 77, IUPAC nomenclature), 3,3',4,4',5-PCB (PCB 126) or 2,2',4,4',5,5'-HCB (PCB 153) and sacrificed after 5 d. In kestrels, neither the pure compounds nor the mixture affected hepatic or renal porphyrin levels. There was slight but significant hepatic and renal ethoxyresorufin O-deethylase (EROD) induction in birds dosed with PCBs 77 and 126. A cytochrome P-4501A (CYP1A) cross-reactive protein was detected in liver and kidney of kestrels given PCBs 77 and 126, but not in Aroclor 1254-dosed birds. In quail, an acute dose of Aroclor 1254 caused significant liver weight increases, hepatic and renal EROD and aminopyrine n-demethylase (APND) induction, and dose-related hepatic and renal porphyria. Quail treated with PCB 126 developed hepatic and renal porphyria; EROD and APND were also induced. Administration of PCB 77 caused only slight induction of hepatic EROD activity. PCB 153 caused some hepatic and renal porphyria and induced EROD to the same degree as PCB 126. A hepatic CYP1A cross-reactive protein was induced about 200-fold in all individual quail that exhibited significant EROD induction and was also induced in kidney of 1 quail given Aroclor 1254. A second experiment examined chronic exposure to Aroclor 1254 by feeding adult females of both species a daily dose of 7 mg/kg/d for 4-, 8-, and 12-wk periods. There were no effects on hepatic porphyrins in kestrels. APND and aldrin epoxidase (AE) were induced; EROD was not induced, although a hepatic CYP1A-like protein was detected in 1 kestrel dosed for 12 wk. Chronic exposure of quail to Aroclor 1254 caused highly significant increases in mean hepatic porphyrin levels and in activity of EROD, APND, and 4-chlorobiphenyl hydroxylase; a CYP1A-like protein was also induced about 200-fold. In both studies, Aroclor 1254 residues accumulated in tissues of both species, but there was no significant relationship between residue levels and effects. In conclusion, adult American kestrels were relatively insensitive to the effects of PCBs, from both acute and chronic exposure, on hepatic and renal porphyrin levels. Although concentrations of a CYP1A-like protein were increased in some kestrels given PCBs, EROD activity was only marginally increased, suggesting that catalytic activity of this protein differed among the two species.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 1","pages":"57-75"},"PeriodicalIF":0.0,"publicationDate":"1997-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20114923","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":"Effect of furazolidone on sister-chromatid exchanges, cell proliferation kinetics, and mitotic index in vivo and in vitro.","authors":"E Madrigal-Bujaidar,&nbsp;J C Ibañez,&nbsp;M Cassani,&nbsp;G Chamorro","doi":"10.1080/00984109708984013","DOIUrl":"https://doi.org/10.1080/00984109708984013","url":null,"abstract":"<p><p>Furazolidone is an antimicrobial compound used in human and veterinary medicine. The aim of this investigation was to determine its genotoxic capacity in vitro and in vivo. We used the human lymphocyte culture system to detect the effect of 2.0, 4.0, 6.0, 8.0, or 10.0 micrograms/ml, and the mouse bone marrow assay to determine the effect of 8.6, 30.0, or 75.0 mg/kg furazolidone. In both systems we determined the frequency of sister-chromatid exchanges (SCE), the cell proliferation kinetics (CPK), and the mitotic index (MI). The in vitro results showed a significant SCE increase starting from the second dose tested and a CPK and MI decrease starting from the third dose. The in vivo results showed a SCE increase with the two high doses tested, but no significant modification was found in the CPK and MI with the three doses tested in the experiment.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 1","pages":"89-96"},"PeriodicalIF":0.0,"publicationDate":"1997-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20114836","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":"High blood cadmium levels are not associated with consumption of traditional food among the Inuit of Nunavik.","authors":"M Rey,&nbsp;F Turcotte,&nbsp;C Lapointe,&nbsp;E Dewailly","doi":"10.1080/00984109708984007","DOIUrl":"https://doi.org/10.1080/00984109708984007","url":null,"abstract":"<p><p>High levels of cadmium in the liver and kidneys of caribous and sea mammals of the Canadian Arctic have led to recommendations to remove such offal from the traditional diet. Blood cadmium levels have been found to be very high in samples of Inuit volunteers, hence the hypothesis that the Inuit might be exposed to cadmium through their diet. This survey of a population-based random sample of Nunavik residents (n = 518) confirms that blood cadmium of Inuit is indeed very high by comparison to published reports. Blood cadmium levels are closely associated with the current smoking status and are independent of dietary patterns among nonsmokers. Plasma omega-3 fatty acids concentrations have been used to assess the reliability of the dietary information collected by questionnaires and to test for any association of blood cadmium with the consumption of sea mammals. Blood cadmium levels are not related to the reported consumption of sea mammals. Blood cadmium levels are very high among smokers and are associated with levels of exposure to tobacco. Among nonsmoking Inuit, blood cadmium levels are comparable with those reported in nonsmokers elsewhere in the world. In reference to international standards, blood cadmium concentrations are high enough among the Inuit to warrant energetic public health interventions.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 1","pages":"5-14"},"PeriodicalIF":0.0,"publicationDate":"1997-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20114919","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":"Restriction of cadmium transfer to eggs from laying hens exposed to cadmium.","authors":"S Sato,&nbsp;M Okabe,&nbsp;T Emoto,&nbsp;M Kurasaki,&nbsp;Y Kojima","doi":"10.1080/00984109708984008","DOIUrl":"https://doi.org/10.1080/00984109708984008","url":null,"abstract":"<p><p>The transfer of Cd to eggs of white Leghorn laying hens has been shown to be restricted. After Cd was injected ip into laying hens, the Cd concentrations in the blood, livers, ovaries, and eggs were measured. Although the Cd concentrations in the maternal blood and livers increased remarkably at certain levels of administrations, the Cd concentration in the yolks of eggs was not significantly increased, and was less than 0.04 microgram/g wet weight. After egg production stopped in the highest injected group (7.5 mg Cd/kg), Cd in the yolks of eggs had an accumulated range of 0.02-0.03 microgram/g wet weight. This was despite the high Cd accumulation in the liver. Furthermore, the Cd concentration in the follicle walls of the ovary increased and was 13- to 52-fold higher than in the follicle yolks. An additional experiment was conducted in order to estimate whether hatching success is affected by the Cd in the laid eggs of Cd-injected laying hens. The ratio of hatching success in the 0.3 or 1.2 micrograms Cd/egg-injected groups was similar to that in the saline-injected group, indicating that a small amount of Cd in the eggs might exert no marked influence on the hatching success. In conclusion, Cd transfer from laying hen to eggs was restricted after the maternal bird was exposed to Cd. Furthermore, Cd accumulates in the follicle walls of ovary. These results suggest that the follicle walls might play a role in protecting the follicle yolks against Cd toxicity.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"51 1","pages":"15-22"},"PeriodicalIF":0.0,"publicationDate":"1997-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00984109708984008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20114920","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":"Reassessment of the carcinogenicity of polychlorinated biphenyls (PCBs).","authors":"M A Smith","doi":"10.1080/15287399709532055","DOIUrl":"https://doi.org/10.1080/15287399709532055","url":null,"abstract":"<p><p>The current policy for regulating polychlorinated biphenyls (PCBs) is based on one chronic bioassay that examined the carcinogenicity of a 60% chlorinated PCB (Norback & Weltman, 1985). All studies originally considered by the U.S. Environmental Protection Agency (EPA) for use in calculating a cancer slope factor (CSF) for PCBs were reevaluated and new CSFs calculated based on the results of a pathology reassessment (Moore et al., 1994). When studies of 60% chlorine PCBs from 3 different laboratories were compared, there was no scientific basis for selecting only 1 data set for deriving CSF estimates. Using a geometric mean to calculate a CSF based on all studies of PCBs with 60% chlorine replaces the current value of 7.7 (mg/kg/d)(-1) with a value of 1.9 (mg/kg/d)(-1). CSFs for PCBs containing less than 60% chlorine (54% and 42%) were less than 1.0 (mg/kg/d)(-1). Using a toxic equivalency factor (TEF) approach similar to that of 2,3,7,8-tetrachlorodibenzo-p-dioxin shows no correlation between toxic equivalent dose and CSFs, indicating that use of TEFs is not predictive of cancer potency for PCBs. Based on these findings, PCB cancer risk assessment policy would more closely reflect scientific data if (1) separate risk assessments were developed for each major PCB formulation and (2) all appropriate data were used when calculating cancer potency for PCB mixtures of 60% chlorine.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 6","pages":"567-79"},"PeriodicalIF":0.0,"publicationDate":"1997-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15287399709532055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40874476","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":"Coral bleaching: a potential biomarker of environmental stress.","authors":"W J Meehan,&nbsp;G K Ostrander","doi":"10.1080/15287399709532053","DOIUrl":"https://doi.org/10.1080/15287399709532053","url":null,"abstract":"<p><p>Coral bleaching refers to the loss of symbiotic algae by host corals, or to the loss of pigmentation by the algae themselves, causing corals to appear white or \"bleached.\" Some corals may regain algae or pigmentation and survive, but when bleaching is severe the host coral dies. Coral bleaching events have increased dramatically in the last two decades, and coral reefs throughout the world have been extensively degraded as a result. This article reviews coral bleaching for investigators working in the field of toxicology and environmental health, a group of scientists not normally exposed to this issue. Several environmental stressors have been correlated with bleaching, including fluctuations in sea surface temperatures and salinity, increased sedimentation, increased solar radiation, and contaminants such as oil and herbicides. Molecular mechanisms of bleaching are only beginning to be investigated and are thus far poorly understood. Toxicologists have the potential to make significant contributions toward understanding anthropogenic aspects of coral bleaching and elucidating molecular mechanisms of this important environmental problem.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 6","pages":"529-52"},"PeriodicalIF":0.0,"publicationDate":"1997-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15287399709532053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40874474","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":"Lymphocyte proliferative response and tissue distribution of methylmercury sulfide and chloride in exposed rats.","authors":"H G Ortega,&nbsp;M Lopez,&nbsp;J E Salvaggio,&nbsp;R Reimers,&nbsp;C Hsiao-Lin,&nbsp;J E Bollinger,&nbsp;W George","doi":"10.1080/15287399709532058","DOIUrl":"https://doi.org/10.1080/15287399709532058","url":null,"abstract":"<p><p>The immunotoxic effects and tissue distribution of different forms of methylmercury compounds were studied in rats. Methylmercury sulfide or methylmercury chloride was fed to rats at concentrations of 5 or 500 microg/L in drinking water for 8 wk. T-cell lymphocyte proliferative response to phytohemagglutinin (PHA) and determination of tissue distribution of mercury by gas chromatography using electron capture were assayed. Four different forms of mercury compounds were employed: MeHgS-, (MeHg)2S, (MeHg)3S+, and MeHgCl. Results indicated that exposure to methylmercury significantly enhanced lymphocyte responsiveness in most of the exposed groups at the low concentration of 5 microg/L, with the highest proliferative response (fourfold increase) in the MeHgCl group. At 500 microg/L, a significant decrease in the lymphocyte proliferative response was observed in the (MeHg)3S+ and MeHgCl groups; conversely, the MeHgS(-)- and (MeHg)2S-exposed animals had a modest increase of the lymphocyte proliferative response. The largest concentrations of all four mercury forms were detected in the kidney and spleen. The levels of mercury found in kidney, spleen, liver, brain, and testis were lower in the MeHgCl group than in those exposed to (MeHg)2S and (MeHg)3S+. These data indicate that the organ distribution of mercury and immune alteration may vary according to the chemical structure of the compound. This observation may have important implications in humans potentially exposed to low levels of methylmercury present in the environment, since the immune system plays an important regulatory role in the host-defense mechanisms.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 6","pages":"605-16"},"PeriodicalIF":0.0,"publicationDate":"1997-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15287399709532058","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40874339","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":"Characterization of methemoglobinemia induced by 3,5-xylidine in rats.","authors":"S Shardonofsky,&nbsp;K Krishnan","doi":"10.1080/15287399709532057","DOIUrl":"https://doi.org/10.1080/15287399709532057","url":null,"abstract":"<p><p>The objective of this study was to characterize the dose effect and kinetics of methemoglobinemia in rats following oral or intravenous administration of 3,5-xylidine (XYL). The first set of experiments involved the intravenous administration of 0.06, 0.12, 0.24, 0.48, or 0.60 mmol XYL/kg to groups of 3 rats each and the serial sampling of blood from the tail vein of individual animals for the determination of methemoglobin levels. An additional series of experiments involved the oral administration of 0.24, 0.48, 0.72, 0.96, 1.2, 1.8, 2.4, or 4.8 mmol XYL/kg and the serial sampling of blood for the determination of methemoglobin levels. The results showed a dose-dependent induction of methemoglobinemia by XYL in the rat, for both routes of administration. The maximal percent methemoglobin observed in the treated animals was 28.90 +/- 0.34% and 32.67 +/- 2.14% for the intravenous (0.6 mmol/kg) and oral (4.8 mmol/kg) routes, respectively. The dose levels of 0.06 mmol/kg (iv) and 0.96 mmol/kg (po) were the no-observable-adverse-effect levels with respect to XYL-induced methemoglobinemia in the rat. The dose-effect information on XYL-induced methemoglobinemia obtained in this study may be useful for the characterization of noncarcinogenic risks of acute human exposure to this chemical.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 6","pages":"595-604"},"PeriodicalIF":0.0,"publicationDate":"1997-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15287399709532057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40874338","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":"Amorphous silica: a review of health effects from inhalation exposure with particular reference to cancer.","authors":"J K McLaughlin,&nbsp;W H Chow,&nbsp;L S Levy","doi":"10.1080/15287399709532054","DOIUrl":"https://doi.org/10.1080/15287399709532054","url":null,"abstract":"<p><p>Silicas and silicates are some of the most abundant compounds found naturally in the earth's crust. Excessive exposure to crystalline silicas can cause serious lung disease such as silicosis and has been associated with lung cancer in some studies, but the potential health effects of amorphous silicas (silicon dioxide without crystalline structure) have not been well studied. Results from animal studies of amorphous silicas, unlike those seen with crystalline silicas, have suggested limited and largely reversible cytotoxic and possibly fibrogenic effects associated with some forms, but data on cancer outcomes are scanty and for the most part negative. Epidemiologic investigations to date for any potential cancer risk are not informative because the effects of crystalline and amorphous silicas have not been separated. Any future epidemiologic study should attempt to clarify the health effects of amorphous silicas from those of crystalline silicas, particularly with regard to any potential for carcinogenicity.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 6","pages":"553-66"},"PeriodicalIF":0.0,"publicationDate":"1997-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15287399709532054","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40874475","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":"Biological monitoring of exposure to chlorpyrifos-methyl by assay of urinary alkylphosphates and 3,5,6-trichloro-2-pyridinol.","authors":"C Aprea,&nbsp;G Sciarra,&nbsp;P Sartorelli,&nbsp;E Sartorelli,&nbsp;F Strambi,&nbsp;G A Farina,&nbsp;A Fattorini","doi":"10.1080/15287399709532056","DOIUrl":"https://doi.org/10.1080/15287399709532056","url":null,"abstract":"<p><p>The results of biological monitoring by assay of urinary 3,5,6-trichloro-2-pyridinol and alkylphosphates (DMP, DMTP) in groups of 9 and 2 workers exposed to chlorpyrifos-methyl during vine spraying and manual leaf thinning 5-11 d after spraying, respectively, are reported. The results are compared with those of a control group of 46 subjects not occupationally exposed to organophosphate insecticides. Significantly higher urinary excretion of metabolites (Mann-Whitney U-test) was found in both groups than in controls. Levels of 3,5,6-trichloro-2-pyridinol (mean +/- SD) were 15.9 + 10.6 nmol/g creatinine (n = 33) for controls, 92.4 + 162.5 nmol/g creatinine (n = 20) for manual workers, and 675.5 + 1110.8 nmol/g creatinine (n = 48) for workers spraying and mixing the insecticide. Levels of DMP (mean +/- SD) were 63.8 + 100.1 nmol/g creatinine (n = 42), 123.0 + 79.0 nmol/g creatinine (n = 20), and 577.2 + 1003.2 nmol/g creatinine (n = 61), respectively, for the same 3 groups. Levels of DMTP (mean +/- SD) were 153.4 + 164.4 nmol/g creatinine (n = 43), 489.3 + 288.3 nmol/g creatinine (n = 20), and 297.6 + 215.4 nmol/g creatinine (n = 61), respectively, for the same 3 groups. Good correlations were found between urinary excretion of 3,5,6-trichloro-2-pyridinol and DMP (r = .776 for manual workers; r = .775 for workers mixing and spraying the insecticide) or DMTP (r = .558 and r = .746, respectively for the same 2 groups). The peak of excretion of the three metabolites was found in urine samples collected the night after the spraying or leaf thinning operations.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 6","pages":"581-94"},"PeriodicalIF":0.0,"publicationDate":"1997-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15287399709532056","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40874337","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}