Ammonia respiratory toxicity

Dodd, K.T., and D.R.Gross. 1980. Ammonia inhalation toxicity in cats a study of acute and chronic respiratory dysfunction. Arch. Environ. Health 35(1) 6-14. 

Manufacture, Shipment, and Analysis. In the United States, sodium and potassium thiocyanates are made by adding caustic soda or potash to ammonium thiocyanate, followed by evaporation of the ammonia and water. The products are sold either as 50—55 wt % aqueous solutions, in the case of sodium thiocyanate, or as the crystalline soHds with one grade containing 5 wt % water and a higher assay grade containing a maximum of 2 wt % water. In Europe, the thiocyanates may be made by direct sulfurization of the corresponding cyanide. The acute LD q (rat, oral) of sodium thiocyanate is 764 mg/kg, accompanied by convulsions and respiratory failure LD q (mouse, oral) is 362 mg/kg. The lowest pubhshed toxic dose for potassium thiocyanate is 80—428 mg/kg, with hallucinations, convulsions, or muscular weakness. The acute LD q (rat, oral) for potassium thiocyanate is 854 mg/kg, with convulsions and respiratory failure. 

Toxic or potentially toxic agents may be inhaled into the respiratory tract where they may cause localized effects such as irritation (e.g., ammonia, chlorine gas), inflammation, necrosis, and cancer. Chemicals may also be absorbed by the lungs into the circulatory system, thereby leading to systemic toxicity (e.g., CO, lead). 

Recent observations have shown a direct relation between the pH of the blood and the depth of hepatic coma (VI). They are interpreted as evidence that the intracellular ammonia is increased in alkalosis because it is un-ionized ammonia and not ammonium ion which readily diffuses into cells. This finding may be a result of the central action of ammonium on the respiratory mechanism (F7), rather than the primary cause of the coma. In this sense it would seriously enhance the coma and set up a cycle which would be lethal. However this may be, there is no mechanism presented for the actual toxic effect of ammonia per se, and the data, except for the internal inconsistencies noted in a previous part of this discussion, would be compatible with the ketoglutarate depletion hypothesis. 

EOA s are corrosive and will attack some plastics and rubbers. They are a moderate fire hazard. MEA and TEA are clear, viscous liquids with a mild ammonia-like odor. EOA s absorb water and carbon dioxide from air. DEA is crystalline or a viscous liquid. All are soluble in water and ethanol. Vapor is irritating to the eyes, skin and respiratory tract and depression of the central nervous system can occur. It can also be absorbed by the skin in toxic amounts12. 

The subcommittee reviewed data that came primarily from human experimental studies and from toxicity studies in various animal species. The evaluation focused on inhalation exposure studies that measured respiratory irritation and tolerance to odor. Human case studies, accident reports, and epidemiologic studies of industrial exposures were extensive but of limited use to the subcommittee because they lack quantitative exposure measurements. Controlled human experiments were most important to the subcommittee for establishing the SEALs for ammonia. There appears to be a broad range of sensitivity to ammonia s pungent odor and in irritation caused by exposures to low concentrations... 

Some studies indicate that ammonia can increase susceptibility to pathogens (Anderson et al. 1964 Broderson et al. 1976 Schoeb et al. 1982 Targowski et al. 1984) and could affect behavior (Tepper et al. 1985). There are no animal toxicity studies specifically on dermal exposure to ammonia gas, but most of the inhalation studies outlined in Table 2-8 involved whole body exposures. Those studies report bums and irritation of the skin, eyes, and mucous membranes of the upper respiratory system. In general, the severity of the damage is related to the concentration and duration of exposure. 

Ethylene oxide is a colorless gas with an aromatic odor. The threshold limit for the odor is 700 ppm. The OSHA specification for worker exposure is 10 ppm. The toxicity of ethylene oxide is similar to that of ammonia. It causes conjunctival and respiratory irritation, dizziness, headaches, and vomiting. It is known to be mutagenic and may be carcinogenic. By-products include ethylene glycol (bp, 198.9°C) and ethylene chlorhydrin (bp, 128.4°C). Pure ethylene oxide is flammable and explosive. It is generally mixed... 

The toxicity of hypochlorite arises from its corrosive activity on skin and mucous membranes. Corrosive burns may occur immediately upon exposure to concentrated bleach products. Most of this corrosiveness stems from the oxidizing potency of the hypochlorite itself, a capacity that is measured in terms of available chlorine . The alkalinity of some preparations may contribute substantially to the tissue injury and mucosal erosion. Sodium hypochlorite when combined with an acid or ammonia may produce chlorine or chloramine gas, respectively. An inhalation exposure to these gases may result in irritation to mucous membranes and the respiratory tract, which may manifest itself as a chemically induced pneumonitis. 

Chloramines are toxic to the respiratory system, with asthma and chronic bronchitis resulting from repeated exposures. 11,12 In an exposure event I investigated, a woman poured a mixture of ammonia and bleach into a toilet bowl. She experienced respiratory failure and eventually died when she inhaled the resultant fumes. 

Not all mixtures that are toxic to the respiratory system are mixtures of lipophiles and hydrophiles. In some instances, irritant chemicals react to produce more toxic species. Chloramine-induced pneumonitis from the mixing of household ammonia and bleach is an example of this phenomenon. 100 101 Household ammonia cleaner is usually a 5-10% aqueous solution of ammonia. Household bleach is generally a 5.25% solution of sodium hypochlorite. At these concentrations, these chemicals alone act as respiratory irritants. When mixed together, however, they react to form monochloroamine, dichloroamine, and trichloroamine as shown in Fig. 17.1. Chloramines are far more toxic than either hypochlorite or ammonia and are capable of producing inflammation and edema of the respiratory system. Case 14 is an example of the toxicity of chloramines. 

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