Nervous system toxicity respiratory failure

Phenols are carcinogenic [39-42] and mutagenic thus affect the central nervous system. Long term contact to phenol may even paralyze the body and damage liver, kidneys [41] and heart [43]. Phenol and its vapour are corrosive to the eyes, skin and respiratory tract [44], Renal failure and pulmonary toxicity has been reported with overdose of 89% injectable phenol solution [45]. According to Central Pollution Control Board (CPCB) the discharge limit of phenol in inland water should be lower than 1 mg/1 [46],... 

Inhaled nickel is at least 100 times more toxic than ingested nickel because it is more readily absorbed from the lungs than from the gastrointestinal tract, and death is more often the result of respiratory failure than of nervous system effects. For example, oral ingestion of 0.05 mg Ni/kg BW and inhalation at 0.005 Ni/m3 are equally effective threshold doses in rats (USPHS 1977). 

Ethanol Multiple effects on neurotransmitter receptors, ion channels, and signaling pathways Antidote in methanol and ethylene glycol poisoning Zero-order metabolism duration depends on dose Toxicity Acutely, CNS depression and respiratory failure chronically, damage to many systems, including liver, pancreas, GI tract, and central and peripheral nervous systems Interactions Induces CYP2E1 Increased conversion of acetaminophen to toxic metabolite... 

The most probable cause of a submarine sinking is flooding caused by an event that breaches the outer hull. The force required would have to be substantial. Potential causes include surface collision, grounding, external explosion, and catastrophic failure of a hull valve. It is likely that such an event also would start a fire within the submarine. The immediate concern for the crew is the release of toxic gases that are produced as the combustion products of on-board fires (U.S. Navy 1998). Human exposure to these gases can lead to adverse health effects, particularly respiratory and central nervous system effects, and even... 

SAFETY PROFILE Moderately toxic to humans by ingestion. Poison experimentally by subcutaneous route. Moderately toxic by intraperitoneal and intravenous routes. Mildly toxic by inhalation. Human systemic effects by inhalation olfactory changes. Mutation data reported. A severe eye and moderate skin irritant. Ethyl ether is not corrosive or dangerously reactive. It must not be considered safe for individuals to inhale or ingest. It is a depressant of the central nervous system and is capable of producing intoxication, drowsiness, smpor, and unconsciousness. Death due to respiratory failure may result from severe and continued exposure. 

High blood levels after topical application or injection of anesthetics may potentially cause systemic reactions. Toxic effects may appear in the central nervous system (CNS), cardiovascular system, or respiratory system. CNS toxicity appears initially as stimulation and may manifest itself clinically as nervousness, tremors, or convulsions. CNS depression, observed clinically as loss of consciousness and depression of respiration, usually follows. The earliest signs of cardiovascular involvement are hypertension, tachycardia, and, occasionally, cardiac arrhythmias. Late cardiovascular signs are hypotension, absent pulse, and weak or absent heartbeat. The effects on the cardiovascular system can develop either simultaneously with CNS depression or alone. If allowed to continue, such cardiac depression and resultant peripheral vasodilation are followed by secondary respiratory failure. 

The literature on the toxicity of benzene in humans is extensive. The acute effects of benzene exposure generally differ markedly from the chronic effects. Acute exposure to high doses of benzene in air (at concentrations in excess of 3000 ppm) causes symptoms typical of organic solvent intoxication. Symptoms may progress from excitation, euphoria, headache, and vertigo, in mild cases, to central nervous system depression, confusion, seizures, coma, and death from respiratory failure in severe cases. The rate of recovery depends on the initial exposure time and concentration, but, following severe intoxication, the symptoms may persist for weeks. 

Human Bromoform was used in the late nineteenth and early twentieth centuries as a sedative to children suffering from whooping cough and several deaths due to overdoses have been reported. Hence, its use was discontinued. The principal causes for death were severe central nervous system depression and respiratory failure. No studies are available for shortterm bromoform toxicity in humans. 

Ethylene glycol and glycoaldehyde have an intoxicating effect on the central nervous system that can lead to ataxia, sedation, coma, and respiratory arrest. The metabolic acidosis reported in toxicity is due to the acidic metabolites, especially glycolic acid. Ethylene glycol itself may result in a large osmolar gap. Oxalic acid may combine with calcium to form calcium oxylate crystals. The precipitation of these crystals in tissue may result in renal failure and hypocalcemia. 

Regardless of their subclassification, all of these compounds have the identical mechanism of action, which is inhibition of acetylcholinesterase at nerve junctions where the molecule acetylcholine is the neuotransmitter. Most acute signs of toxicity are expressed as uncontrollable activity of the nervous system, which clinically is presented as salivation, lacrimation, urination, defecation, and dyspnea. After lethal doses, death results from failure of the respiratory system. Variations in the specific nerves affected, in how the body metabolizes the individual chemical, in where the chemical enters the body, and in the route of administration employed will change the specific clinical presentation seen for an individual exposure scenario. 

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