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Effect acute

Acute indium poisonings are rare due to the low absorption of this metal from the gastrointestinal tract and moderate absorption from inhalation. However, in animal experiments indium toxicity is often related to the chemical form and route of exposure. Insoluble indium oxides were found to be more toxic to mice than ionic indium when expressed as lethality per quantity of [Pg.804]

A number of experiments have shown that indium compounds may cause reproductive toxicity in animals. Repetitive intratracheal instillation of indium arsenide (InAs) with doses of 1.3 mg kg caused a significant decrease in epididymal sperm counts in Wistar rats (Omura etal. 1996). Testicular toxicity of the radionuclide In was found in both adult and neonatal rats (Hoyes etal. 1995). Testicular and epididy- [Pg.805]

Experimental studies in tissue culture in vitro have also been performed for indium compounds. In vitro toxicity studies of InAs particles to hamster alveolar macrophages revealed slight damage to cells, but no necrotic or apoptotic changes and no cytostructural alterations were observed for 2, 4, 10, and 20 j,g doses (Okada etal. [Pg.806]

Indium chloride at concentrations above 500 j,M was found to inhibit gap junctional communication between rat primary hepatocytes (Guo etal. 1992). Inhibition of communication between cells may interfere with the rescue of damaged cells by healthy cells, hence weakening the buffering ability of hepatocytes during cell injury and hastening cell death. [Pg.806]

Together with arsenic, F has caused serious effects on livestock in the U.S. and other countries. The sources of the pollutant are mostly limited to [Pg.209]

The most sensitive ecosystems affected at Chernobyl were toe soil fauna and pine forest communities toe majority of toe terrestrial vertebrate communities were not adversely affected by released ionizing radiation. Pine forests seemed to be toe most sensitive ecosystem. One 400 ha stand of Pinus silvestris died and probably received a dose of 80-100 Gy. Other stands experienced heavy mortality of 10-12-year-old trees and as much as 95% necrotization of young shoots these pines received an estimated dose of 8-10 Gy. Abnormal top shoots developed in some Pinus, and these probably received 3-4 Gy. In contrast, leafed trees in toe Chernobyl Atomic Power Station zone, such as birch, oak, and aspen, survived undamaged, probably because they were about 10 times more radioresistant than pines. Extremely high radioresistance was documented in genetically adapted strains of toe filamentous fungus Alternaria alternata isolated from toe reactor of toe Chernobyl power plant other strains of this species are supersensitive to radiation. There was no increase in mutation rate of spiderwort (Arabidopsis thaliana), a radiosensitive plant, suggesting that toe dose rate was 0.05 Gy/h in toe Chernobyl locale. [Pg.699]

Populations of soil mites were reduced in toe Chernobyl area, but no population showed a catastrophic drop in numbers. By 1987, soil microfauna - even in toe most heavily contaminated plots - was comparable to controls. Flies (Drosophila spp.) collected at various distances from toe accident site and bred in toe laboratory had highest incidences of dominant lethal mutations (14.7%, estimated dose of 0.8 mGy/h) at sites nearest to toe accident and higher incidences than controls (4.2%). [Pg.699]

The most contaminated water body in toe Chernobyl emergency zone was toe Chernobyl cooling pond ecosystem, an area of about 30 km. On May 30, 1986, toe total amount of radioactivity in toe water of this system was estimated at 806 TBq and in sediments 5657 TBq. In water, I contributed about 31% of toe total radioactivity, Ba- La 25%, Zr- Nb 15%, Cs and Cs 11%, 4 Ce and Ce 10%, Ru and Ru 7%, and °Sr 1%. The distribution pattern in sediments was significantly different about 41% [Pg.699]

Fish populations seemed unaffected in July-August 1987, and no grossly deformed ini-viduals were found however, and Cs levels were elevated in young fish. The most heavily contaminated teleost in May 1987 was the carp Carassius carassius). But carp showed no evidence of mutagenesis, as judged by incidence of chromosomal aberrations in cells from the comeal epithelium of carp as far as 60 km from Chernobyl. [Pg.700]

In 1986, total radioactivity in muscle of birds near Chernobyl after the accident exceeded the temporarily permitted limits for human food consumption (598 Bq/kg FW) by about 100 times. In 1987, radionuclide concentrations in bird muscle had decreased by a factor of about 7 due, in part, to physical decay of short-lived isotopes. [Pg.700]


Interest ia the toxicity of aldehydes has focused primarily on specific compounds, particularly formaldehyde, acetaldehyde, and acroleia (13). Litde evidence exists to suggest that occupational levels of exposure to aldehydes would result ia mutations, although some aldehydes are clearly mutagenic ia some test systems. There are, however, acute effects of aldehydes. [Pg.473]

The short-term or acute effects of the P-agonists may be different from chronic effects. Acute Hpolysis and glycogenolysis are not observed beyond the first day or two of treatment. Exact mechanisms of action on Hpid metaboHsm may differ among species. Chronic effects of the P-agonists reduce circulating insulin concentrations ST treatment causes an opposite change. Whereas residue levels may be of concern with adrninistration of several of the P-agonists, such is not the case for ST or GRE. [Pg.414]

Acute effects of overexposure are as follows. Exposure to dust may cause mechanical irritation of the eye. PPS is essentially nonirritating to the skin, although freshly molded material may occasionally cause dermatitis. Inhalation of PPS dust may cause mechanical irritation to mucous membranes of nose, throat, and upper respiratory tract. [Pg.451]

NIOSH/MSHA-approved respiratory protection devices should be used. For skin protection, use of protective garments and gloves of Viton, Nitrile, or PVA constmction should be made. The acute effects of overexposure to styrene are shown in Table 6 (74). [Pg.487]

The principal mechanism of the hypotensive effect of diuretics (qv) is salt and fluid depletion, leading to reduction in blood volume (200,240). Acute effects lead to a decrease in cardiac output and an increase in total peripheral resistance. However, during chronic adrninistration, cardiac output and blood volume return toward normal and total peripheral resistance decreases to below pretreatment values. As a result, the blood pressure falls. The usual reduction in blood volume is about 5%. A certain degree of sustained blood volume contraction has to occur before the blood pressure decreases. The usual decrease in blood pressure achieved using a diuretic is about 20/10 mm Hg (2.7/1.3 kPa) (systoHc/diastoHc pressures. [Pg.142]

Diseased subjects Few covariates Vulnerable persons Cause-effect Acute effects only Hazards Public acceptance... [Pg.107]

Direct eye contact with liquid produces injury, generally transient, to the corneal epithelium. The liquid is mildly imtating to the skin due to the degreasing effect repeated contact may cause dermatitis. Ingestion of substantial quantities of liquid can damage the mucous membranes, and produce acute effects ranging from mild discomfort to profound anaesdiesia. [Pg.140]

In a cross-sectional study, exposure and effect are studied simultaneously. This approach contains an inherent problem because exposure must precede the effect. However, it can he used to investigate acute effects and also mild chronic effects (which do not force people to leave their jobs) if exposure has remained rather stable for a long time. When the prevalence of the effects studied are compared with the prevalence in other worker groups (controls or references) which correspond otherwise with the study group but are not exposed to the agent investigated, indicative evidence of possible causality may be obtained. For example, cross-sectional studies have been applied successfully to reveal the associations between mild neurotoxic effects and exposure to organic solvents. ... [Pg.242]

Acute toxicity Rats/mice 2 weeks Acute effects... [Pg.329]

After the use of a chemical becomes widespread, new deleterious effects on human health may be observed. In such situations, the occupational limit values will have to be modified. Usually the OELS tend to decrease when more information on the toxicity of a chemical is obtained. Knowledge of the specific features of various chemicals is thus extremely important for planning ventilation of industrial premises. It is important to be especially aware of those chemicals that may cause long-term effects without causing any acute effects. There are also compounds such as isocyanates that are extremely irritating at concentrations as low as 0.5 ppm. However, some workers may become sensitized to isothiocyanates at a concentration of 10 ppb, and therefore this has to be taken into consideration when planning the industrial ventilation. Thus, one has to plan against compounds that can cause serious health effects at concentrations at which their presence cannot be observed by the human senses, i.e., irritation or odor. [Pg.334]

Experimental studies with volunteers, especially for situations involving the acute effects of an identified adverse agent... [Pg.364]

However, there are substances for which an 8-hour OEL-TWA alone provides insufficient protection. In such cases the OEL-STEL is used in relation to a 15-minute period, unless otherwise specified, in order to prevent adverse health effects, immediate or delayed, due to peaks in exposure that cannot be ccmtrolled by the application of an 8-hour OEL-TWA. The OEL-STEL indicates a limit value above which exposure should not occur, and it is needed when there are recognized acute effects from a substance whose toxic effects are primarily of a chronic nature. [Pg.366]

Acute effects Symptoms of injury or other physical manifestations that follow an acute exposure. [Pg.1405]

The acute effects of very-short-term exposure to elevated... [Pg.271]

Psychostimulants. Table 3 Acute effects of psychostimulants and the brain regions that are mainly involved in these effects... [Pg.1042]

Acute effects Mainly involved brain region... [Pg.1042]

Matrila MJ, Aranko K, Seppala T Acute effects of huspirone and alcohol on psychomotor skills. J Clin Psychiatry 43 56-60, 1982 McMahon T, Andersen R, Merten P, et al Protein kinase C epsilon mediates upregu-lation ofN-type calcium channels by ethanol. Mol Pharmacol 37 33-58, 2000 Merry], Reynolds CM, Bailey], et al Prophylactic treatment of alcoholism by lithium carbonate. Lancet 2 481 82, 1976... [Pg.50]

Death after the use of MDMA or MDEA is rare but may occur because of induction of cardiac arrhythmias or as a consequence of risk-taking behavior. Following its acute effects, MDMA may produce symptoms such as anxiety, depression, and confusion, which, in some cases, continue for several weeks (Dowling et al. 1987). [Pg.231]

Taken for recreational use as an intoxicant, typical acute effects described by misusers are euphoria, relaxation, and increased sexuality (Galloway et al. 1997 Miotto et al. 2001). On the street, GHB is taken in capfuls or teaspoons of a salty/sour liquid, which because of variations in concentration, may range in dose from 0.5 to 5.0 g. Common side effects are nausea, headache, itching, and vomiting (Borgen et al. 2003). Doses of 10—20 mg/kg of GHB typically... [Pg.245]

Meredith TJ, Ruprah M, Liddle A, et al Diagnosis and treatment of acute poisoning with volatile substances. Hum Toxicol 8 277-286, 1989 Merry J, Zachariadis N Addiction to glue sniffing. Br Med J 5317 1448, 1962 Mihic SJ Acute effects of ethanol on GABAA and glycine receptor function. Neuro-chemint 35 115-123, 1999... [Pg.310]

Fazekas 1971) exposed by various routes. Because of a lack of toxicokinetic data, it cannot be assumed that the end points of methyl parathion toxicity would be quantitatively similar across all routes of exposure. The acute effects of dermal exposures to methyl parathion are not well characterized in humans or animals. Therefore, additional dermal studies are needed. [Pg.123]

The data in animals are insufficient to derive an acute inhalation MRL because serious effects were observed at the lowest dose tested (Hoechst 1983a). No acute oral MRL was derived for the same reason. The available toxicokinetic data are not adequate to predict the behavior of endosulfan across routes of exposure. However, the limited toxicity information available does indicate that similar effects are observed (i.e., death, neurotoxicity) in both animals and humans across all routes of exposure, but the concentrations that cause these effects may not be predictable for all routes. Most of the acute effects of endosulfan have been well characterized following exposure via the inhalation, oral, and dermal routes in experimental animals, and additional information on the acute effects of endosulfan does not appear necessary. However, further well conducted developmental studies may clarify whether this chemical causes adverse developmental effects. [Pg.190]

Janik F, Wolf HU. 1992. The Ca2-i-transport-atpase of human erythrocytes as an in vitro toxicity test system - acute effects of some chlorinated compounds. J Appl Toxicol 12(5) 351-358. [Pg.300]

Short-term exposure limits. These are concerned primarily with the avoidance of acute effects, or reducing the risk of the occurrence. [Pg.74]

Specific short-term exposure limits are listed by the HSE for those chemicals which pose a risk of acute effects from brief exposures. For other chemicals a recommended guideline for controlling short-term excursions is to restrict them to 3x long-term exposure limit averaged over a 10min period. [Pg.74]


See other pages where Effect acute is mentioned: [Pg.504]    [Pg.487]    [Pg.3]    [Pg.181]    [Pg.264]    [Pg.516]    [Pg.547]    [Pg.367]    [Pg.233]    [Pg.271]    [Pg.321]    [Pg.113]    [Pg.182]    [Pg.786]    [Pg.1234]    [Pg.731]    [Pg.172]    [Pg.46]    [Pg.229]    [Pg.233]    [Pg.245]    [Pg.3]   
See also in sourсe #XX -- [ Pg.5 ]

See also in sourсe #XX -- [ Pg.5 ]

See also in sourсe #XX -- [ Pg.254 ]




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Acute Effect on Food Consumption in Rats

Acute Effect on Milk Consumption in Mice

Acute Effects at High Doses

Acute Effects of Alcohol

Acute Effects of Caffeine

Acute Effects of Nicotine

Acute Effects on Animals

Acute Effects on Animals and Humans

Acute Effects on Humans

Acute Effects on Mammals (and Humans)

Acute Effects on Metabolic Blood Parameters in Conscious Dogs

Acute Effects on Metabolic Blood and Tissue Parameters

Acute Effects on Metabolic Blood and Tissue Parameters in Anesthetized Rats

Acute Effects on Metabolic Blood and Tissue Parameters in Conscious Rats

Acute Wolff—Chaikoff effect

Acute cardiac disease, effects

Acute cognitive effects, cannabi

Acute effects hazardous substances

Acute effects noise

Acute general effects

Acute health effects

Acute local effects

Acute radiation effect

Acute respiratory effects

Acute toxicity effects

Acute toxicity systemic effects

Alcohol acute effects

Alcohol consumption acute metabolic effects

Alcohol consumption acute systemic effects

Allergy acute health effects

Animals acute effects

Behavioral toxicity acute effects

Caffeine acute effects

Caffeine acute toxic effects

Cannabis acute cognitive effects

Central nervous system acute effects

Chemicals acute effects

Cholinesterase inhibitors acute effects

Copper acute effect

Drugs commonly used to treat acute extrapyramidal side effects

Effective Cell-Based Assays for Marked and Acute Cytotoxicity

Effectiveness of Currently Available Symptomatic Antitussives Against Acute Cough

Effects of acute exercise on the circulatory system

Fluoride acute effects

Hazards acute effects

Lipid acute effects

Lipopolysaccharides acute effects

Lithium acute effects

Marijuana acute effects

Nephrotoxicity acute effects

Nickel acute effect

Nicotine acute effects

Nicotine acute pharmacological effects

Occupational illnesses acute health effects

Poisoning acute effects

Protein acute exercise effects

Psychological effects acute

Stimulants acute effects

Sulfur mustard acute toxic effects

Treat Acute Extrapyramidal Side Effects

Trichothecene mycotoxins acute effects

Ultraviolet radiation acute effects

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