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1. |
Coral bleaching: A potential biomarker of environmental stress |
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Journal of Toxicology and Environmental Health,
Volume 50,
Issue 6,
1997,
Page 529-552
WilliamJ. Meehan,
GaryK. Ostrander,
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摘要:
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.
ISSN:0098-4108
DOI:10.1080/15287399709532053
出版商:Taylor & Francis Group
年代:1997
数据来源: Taylor
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2. |
Amorphous silica: A review of health effects from inhalation exposure with particular reference to cancer |
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Journal of Toxicology and Environmental Health,
Volume 50,
Issue 6,
1997,
Page 553-566
JosephK. McLaughlin,
Wong‐Ho Chow,
LeonardS. Levy,
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摘要:
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.
ISSN:0098-4108
DOI:10.1080/15287399709532054
出版商:Taylor & Francis Group
年代:1997
数据来源: Taylor
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3. |
Reassessment of the carcinogenicity of polychlorinated biphenyls (PCBS) |
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Journal of Toxicology and Environmental Health,
Volume 50,
Issue 6,
1997,
Page 567-579
MaryAlice Smith,
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摘要:
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 ah, 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)−1with 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 (mglkgld)−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.
ISSN:0098-4108
DOI:10.1080/15287399709532055
出版商:Taylor & Francis Group
年代:1997
数据来源: Taylor
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4. |
Biological monitoring of exposure to chlorpyrifos‐methyl by assay of urinary alkylphosphates and 3,5,6‐trichloro‐2‐pyridinol |
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Journal of Toxicology and Environmental Health,
Volume 50,
Issue 6,
1997,
Page 581-594
Cristina Aprea,
Gianfranco Sciarra,
Pietro Sartorelli,
Emilio Sartorelli,
Fabio Strambi,
GiuseppeA. Farina,
Alessandro Fattorini,
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摘要:
The results of biological monitoring by assay of urinary 3,5,6‐trichloro‐2‐pyridinol and alkyl‐phosphates (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 V‐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 + 2 75.4 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.
ISSN:0098-4108
DOI:10.1080/15287399709532056
出版商:Taylor & Francis Group
年代:1997
数据来源: Taylor
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5. |
Characterization of methemoglobinemia induced by 3,5‐xylidine in rats |
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Journal of Toxicology and Environmental Health,
Volume 50,
Issue 6,
1997,
Page 595-604
Sylvia Shardonofsky,
Kannan Krishnan,
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摘要:
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.
ISSN:0098-4108
DOI:10.1080/15287399709532057
出版商:Taylor & Francis Group
年代:1997
数据来源: Taylor
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6. |
Lymphocyte proliferative response and tissue distribution of methylmercury sulfide and chloride in exposed rats |
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Journal of Toxicology and Environmental Health,
Volume 50,
Issue 6,
1997,
Page 605-616
HectorG. Ortega,
Manuel Lopez,
JohnE. Salvaggio,
Robert Reimers,
Chen Hsiao‐Lin,
JamesE. Bollinger,
William George,
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摘要:
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 μg/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 MeHgCI. Results indicated that exposure to methylmercury significantly enhanced lymphocyte responsiveness in most of the exposed groups at the low concentration of 5 μg/L, with the highest proliferative response (fourfold increase) in the MeHgCl group. At 500 μg/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.
ISSN:0098-4108
DOI:10.1080/15287399709532058
出版商:Taylor & Francis Group
年代:1997
数据来源: Taylor
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7. |
Book reviews |
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Journal of Toxicology and Environmental Health,
Volume 50,
Issue 6,
1997,
Page 617-620
RamP. Gupta,
JamesJ. Corcoran,
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摘要:
INTRODUCTION TO BIOCHEMICAL TOXICOLOGYEdited byE. HodgsonandP. E. LeviAppleton and Lange, Connecticut, 1994, xiv‐588 pp., $62.95
ISSN:0098-4108
DOI:10.1080/15287399709532059
出版商:Taylor & Francis Group
年代:1997
数据来源: Taylor
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8. |
Editorial board |
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Journal of Toxicology and Environmental Health,
Volume 50,
Issue 6,
1997,
Page -
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ISSN:0098-4108
DOI:10.1080/15287399709532052
出版商:Taylor & Francis Group
年代:1997
数据来源: Taylor
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