Biomedical subjects
J E Huff
Publications and source records attributed to J E Huff.
Clinical toxicology of mercury.
Based on an extensive literature search, general principles of mercury toxicity are outlined with respect to human individuals and populations. For the metal itself, as well as for its most important inorganic and organic compounds, the review discussed behavior in the body, characteristic clinical pictures, assessment of threshold levels, and evaluation as potential environmental hazards. Particular emphasis is placed on those diagnostic signs and symptoms which furnish early warning signals, permitting detection and elimination of overexposures.
Trichloroethylene. I. An overview.
Trichloroethylene (TCE) has been an industrial chemical of some importance for the past 50 years. First synthesized by Fischer in 1864, TCE has enjoyed considerable industrial usage as a degreaser and limited medical use as an inhalation anesthetic and analgesic. This TCE overview provides a narrative survey of the reference literature. Highlights include history, nomenclature, physical and chemical properties, manufacture, analysis, uses, metabolism, toxicology, carcinogenic potential, exposure routes, recommended standards, and conclusions. Chemically, TCE is a colorless, highly volatile liquid of molecular formula C2HCl3. Autoxidation of the unstable compound yields acidic products. Stabilizers are added to retard decomposition. TCE's multitude of industrial uses center around its highly effective fat-solvent properties. Metabolically, TCE is transformed in the liver to trichloroacetic acid, trichloroethanol, and trichloroethanol glucuronide; these breakdown products are excreted through the kidneys. Most toxic responses occur as a result of industrial exposures. TCE affects principally the central nervous system (CNS). Short exposures result in subjective symptoms such as headache, nausea, and incoordination. Longer exposures may result in CNS depression, hepatorenal failure, and increased cardiac output. Cases of sudden death following TCE exposure are generally attributed to ventricular fibrillation. Current interest in TCE has focused on recent experimental data that implicate TCE as a cause of hepatocellular carcinoma in mice. No epidemiological data are available that demonstrate a similar action in humans. The overall population may be exposed to TCE through household cleaning fluids, decaffeinated coffee, and some spice extracts. The NIOSH recommended standard for TCE is 100 ppm as a time-weighted average for an 8-hr day, with a maximum allowable peak concentration of 150 ppm for 10 min.
Selected case histories and epidemiologic examples of human mercury poisoning.
To illustrate the various clinical pictures resulting from toxic effects of mercury and its compounds, highlighted literature excerpts have been prepared and arranged in a logical sequence. Particular emphasis is placed upon early diagnosis and prevention of epidemic outbreaks involving intoxication through organomercurials.
Occurrence, physiologic effects, and toxicity of heavy metals--arsenic, cadmium, lead, mercury, and zinc--in marine biota: an annotated literature collection.
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Health effects of vinyl chloride monomer: an annotated literature collection.
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Hematologic changes in mice during and after exposure to severe hypobaric hypoxia.
Exposing mice to an atmospheric pressure of 300 mm Hg for 16 d caused a variety of hematologic effects. Hematocrit increased rapidly in the first 8 d of exposure and slowly in the second 8 d. Reticulocyte counts rose above normal, peaked on Day 8, and then fell rapidly toward the control level. Macrocytic erythrocytes, formed during exposure, remained macrocytic after the termination of exposure and after the loss of their reticulum. The posthypoxic mice proved sensitive for erythropoietin bioassay. Mice injected with normal dog serum showed a significantly higher incorporation of 59Fe than control mice injected with physiologic saline. A reduction of the duration of exposure to 10 d resulted in only a slight decrease in the sensitivity of the mouse bioassay system. However, a 16-d exposure at a pressure of 360 mm Hg resulted in considerably less sensitive bioassay animals.
Contraceptives available by prescription.
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A health view of asbestos: an annotated literature collection--1960-1974.
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Contraception--a choice of methods. O-T-C contraceptives.
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Contraception--a choice of methods. Family planning. A general overview and new directions in fertility control.
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Chlorinated dibenzodioxins and dibenzofurans.
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New evidence on the old problems of trichloroethylene.
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Effect of acute and chronic stress on amobarbital metabolism in the rat.
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Protective agents modifying biological effects of radiation. A selective review.
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A review of the genetic toxicology of chlorinated dibenzo-p-dioxins.
Information from both published and unpublished sources considered relevant to the understanding of the genetic toxicology of chlorinated dibenzo-p-dioxins is summarized in this review. Interest in writing this paper was stimulated by the fact that this class of compounds, particularly 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), has gained notoriety as an extreme environmental and industrial hazard. The potential for human exposure occurs in the work place when dioxins are formed during the synthesis of a number of commercially important compounds such as 2,4,5-trichlorophenoxyacetic acid, hexachlorophene, and pentachlorophenol. Environmental contamination may result from manufacturing processes and from dioxin contaminants in marketed products. Research on dioxins as potential mutagens was initiated because of their structural similarity to acridines, a class of known intercalating agents. To date, only 4 dioxin compounds have been evaluated for mutagenicity: the di-, tetra-, and octa-chlorinated derivatives and the unsubstituted dibenzo-p-dioxin. Since only a few of the many possible structural forms of dioxins have been tested, no definite conclusions can be made about their potential mutagenicity. Furthermore, the positive mutagenicity and cytological effects reported thus far with the few dioxin isomers examined seems to depend on the position of chlorine substitution. The most active form of the molecule is the 2,3,7,8-derivative (TCDD). Data available for assessing the mutagenic potential of TCDD are conflicting and scarce. Differences in testing results reported in these studies could be attributed to solubility problems with the test chemical, treatment protocols, purity of test samples, or toxicity. Because there are conflicting data, additional experiments are needed before the mutagenic potential of TCDD and other dioxins can be determined. Studies exploring the promoting effect of dioxins on the mutagenicity of other compounds are also recommended because experiments have shown TCDD to be an extremely active liver enzyme inducing agent that enhances the mutagenicity of certain polycyclic hydrocarbons such as 3-methylcholanthrene in vitro. The importance of discerning the hazards to human health from dioxin compounds became apparent after an accidental release of TCDD from a chemical plant contaminated the Seveso, Italy area in July 1976. This accident revealed that insufficient data were available to properly evaluate the long-term health risks posed by dioxin compounds. Several research projects were therefore initiated after the Seveso incident; it is hoped that many of the questions concerning the mutagenicity of TCDD and possibly of other dioxin congeners will be answered as a result of this work.
No evidence of carcinogenicity of D-mannitol and propyl gallate in F344 rats or B6C3F1 mice.
Chronic toxicity and carcinogenicity studies were conducted on D-mannitol and propyl gallate in F344 rats and B6C3F1 mice. Groups of 50 rats and 50 mice of each sex were maintained on diets containing either 0, 2.5 or 5.0% D-mannitol or 0, 0.6 or 1.2% propyl gallate for 103 wk. D-Mannitol had no effect on survival or mean body weight of rats and mice, and feed consumption was approximately the same in control and treated groups in each species. Gastric fundal gland dilation occurred at a higher incidence in treated female rats than in controls. A mild nephrosis characterized by focal vacuolization of the renal tubular epithelium was observed in an increased incidence in treated mice. No significant increase in tumour incidence was observed in any of the treated groups in comparison with the corresponding controls. Survival of rats and mice given propyl gallate was similar to that of the controls. Mean body weights were lower in chemically exposed animals, and more so for females. Male rats exposed to propyl gallate showed an increased incidence of hepatic cytoplasmic vacuolization and suppurative inflammation of the prostate gland. Tumours of the preputial gland, islet-cell tumours of the pancreas, and phaeochromocytoma of the adrenal gland occurred at a significantly (P less than 0.05) higher incidence in the low-dose male rats. Malignant lymphoma occurred with a positive trend in male mice (control 1/50, low dose 3/49 and high dose 8/50), and the incidence in the high-dose group was significantly (P less than 0.05) higher than in the control group. However, since the incidence in the control group was much less than the historical control rate (36/398 or 9%) in this laboratory, this apparent increase was not considered to be related to propyl gallate administration. Under the conditions of these studies, neither D-mannitol nor propyl gallate was considered to be carcinogenic to F344 rats or B6C3F1 mice of either sex.