Acute poisoning

Poisoning may be characterized by inebriation, muscular incoordination, blurred vision, impaired reaction time, excitement due to loss of inhibitions, impairment of consciousness, coma, tachycardia, and slow respiration. A blood alcohol level of 80 mg/dl can produce recognizable features of drunkenness a level above 300 mg/dl is life threatening. In children, severe hypoglycemia and convulsions may also occur. 

Acute poisoning is treated with gastric aspiration and lavage combined with intensive supportive therapy, including thorough assessment of the patient plus measures to prevent respiratory failure. In cases of very severe poisoning, peritoneal dialysis or hemodialysis may be necessary. 

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The hver of sharks and other oily fishes sometimes accumulate toxic levels of vitamin A, and cases of acute poisoning have been reported both among Eskimos and the Japanese. 

In addition to the CIR process the cosmetic industry has instituted a second, important, self-regulatory procedure the voluntary reporting of adverse reactions, which is intended to provide data on the type and incidence of adverse reactions noted by consumers or by their medical advisors. This reporting procedure creates early awareness of problems handled outside hospital emergency facilities or centers for acute poisoning. 

Inhalation is the most common means by which ethers enter the body. The effects of various ethers may include narcosis, irritation of the nose, throat, and mucous membranes, and chronic or acute poisoning. In general, ethers are central nervous system depressants, eg, ethyl ether and vinyl ether are used as general anesthetics. 

Emetogenic drugs may be of value in treating cases of acute poisoning but usually nausea and vomiting induced by a drag are unwanted effects occurring in addition to its therapeutic action. 

Cadmium, 5, 925-1022 acute poisoning, 5,1000 binding to metallothioneins, 6, 673 chronic poisoning, 5, 1000 gravimetry, 1,532 masking, 1,538 metallothioneins, 5,1021 poisoning... 

Compounds containing mercury, particularly its organic compounds, are acutely poisonous. Mercury vapor is an insidious poison because its effect is cumulative. Frequent exposure to low levels of mercury vapor can allow mercury to accumulate in the body. The effects include impaired neurological function, hearing loss, and other ailments. 

The purpose of this study was to compare hepatotoxic effects of monobromo-benzene, 3 dibromobenzene isomers, hexabromobenzene and tetrabromobisphenol A with special attention paid to the dynamics of changes of selected indicators of liver necrosis during acute poisoning. 

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... 

Lukaszewicz-Hussain A, Moniuszko-Jakoniuk J, Pawlowska D. 1985. Blood glucose and insulin concentration in rats subjected to physical exercise in acute poisoning with parathion-methyl. Pol J Pharmacol Pharm 37 647-651. 

Vandekar M, Reiner E, Svetlicic, et al. 1965. Value of ED50 testing in assessing hazards of acute poisoning by carbamates and organophosphates. Br J Ind Med 22 317-320. 

Hematological Effects. Leukocytosis and decreased platelet counts were reported in a group of subjects shortly after they ingested an unknown amount of endosulfan (Blanco-Coronado et al. 1992). One subject from that study, who eventually died, had prolonged partial thromboplastin time and prothrombin time with thrombocytopenia, and decreased fibrinogen two days after being admitted to the hospital. Elevated white cell count was also observed in an additional case of fatal acute poisoning with... 

Metabolic Effects. Severe metabolic acidosis with high anion gap and hyperglycemia was reported in humans after acute poisoning with endosulfan (Blanco-Coronado et al. 1992 Lo et al. 1995). In five of the six cases reported by Blanco-Coronado et al. (1992), the metabolic acidosis was corrected with gastric lavage with activated charcoal and intravenous sodium bicarbonate and diazepam. No further information regarding metabolic effects in humans after exposure to endosulfan was located. 

Similarly, convulsive seizures and a sustained epileptic state persisted after stomach contents were pumped and activated charcoal and anticonvulsive medication were administered in a 43-year-old man who ingested approximately 260 mg/kg endosulfan (Boereboom et al. 1998). At 4 days after exposure, the man was pronounced brain dead, and autopsy revealed cerebral hernia from massive cerebral edema. Eight additional accidental and/or intentional cases of acute poisoning with endosulfan resulting in adverse neurological effects have been reported in more recent studies, six by Blanco-Coronado et al. (1992), one by Lo et al. (1995), and one by Pradhan et al. (1997) two out of the eight resulted in death. Tonic-clonic convulsions were seen in the Blanco-Coronado et al. (1992) cases, whereas Lo et al. (1995) reported the development of muscle fasciculations and episodes of convulsions in their case. In the case reported by Pradhan et al. (1997), the patient had consumed about 75 mL of hquid endosulfan (35% w/v). In this case, in addition to tonic-clonic seizures and myoclonic jerks, the patient developed... 

Acute poisoning of humans by freshwater cyanobacteria as occurs with paralytic shellfish poisoning, while reported, has never been confirmed. Humans are probably just as susceptible as pets, livestock, or wildlife but people naturally avoid contact with heavy waterblooms of cyanobacteria. In addition, there are no known vectors, like shellfish, to concentrate toxins from cyanobacteria into the human food chain. Susceptibility of humans to cyanobacteria toxins is supported mostly by indirect evidence. In many of these cases, however, if a more thorough epidemiological study had been possible these cases probably would have shown direct evidence for toxicity. 

Assessment of whether a chemical has the potential to cause adverse effects in humans arises usually from direct observation of an effect in animals or humans, such as the acute poisoning episodes that have occurred when potatoes contain high levels of glycoalkaloids. Epidemiological studies have also been used to infer a possible relationship between intake of a particular type of food, or constituent of that food, and the potential to cause an adverse effect. Such observations led to the characterisation of the aflatoxins as human carcinogens. However, natural toxic substances that occur in plant foods have often been identified through observations in animals, particularly farm animals. It was observations of adverse effects in farm animals that led to the further characterisation of the phytoestrogens and the mycotoxins. In other instances, the concern arises from the chemical similarity to other known toxins. 

Yet, except for specific cases of acute poisoning (2,10, 11), and thus mostly of liver damage, there appears to be no reliably documented evidence that there are any cases of human cancer which can be unambiguously associated with an antecedent exposure to nitrosamines In the Western world (12). 

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