Physiological effects of ammonia

For data concerning the physiological effects of ammonia, protective equipment, and first aid measures, see CGA G-2, Anhydrous Ammonia, and the monograph on ammonia in Part III. [10]... 

Ammonia compounds are a primary chemical component of many reconstituted tobaccos. The importance of ammoniation in the development of the characteristic flavor popularized by Marlboro has been widely pubhcized (Bates et al. 1999 Freedman 1995 Hurt and Robertson 1998). The chemical impact of ammoniation is complex and appears to influence the form and delivery of nicotine in a variety of interconnected ways (see BW Fig. 4) (Johnson 1989). Ammoniated reconstituted tobacco has a characteristic mild sensory profile, and features a number of important compounds created through the reaction between ammonia and sugars (J.R. Reynolds 1980 Wells and Kendrick 1995). Addition of ammonia as a strong base leads to increased smoke pH, which corresponds with increased levels of free nicotine in smoke (Hurt and Robertson 1998). Thus, a 1982 position paper from RJR observed that ... ammonia in smoke is one of the major pH controlling components and that ... studies of the effect of ammonia on smoke composition showed... an increase in physiological satisfaction with increasing ammonia content (Bemasek and Nystrom 1982). 

Ammonia is a strong local irritant which also has a corrosive effect on the eyes and the membranes of the pulmonary system. Vapor concentrations of 10,000 ppm are mildly irritating to the skin, whereas 30,000 ppm may cause bums. The physiological effects from inhalation are described in Table 16. Prolonged, intentional exposure to high levels of ammonia is unlikely because its characteristic odor can be detected at levels as low as 1 —5 ppm (94). The real danger occurs when escape is impossible, or the exposure victim has lost consciousness. 

Cohen and Grisolia then concentrated on the first step in the reaction, obtaining citrulline from ornithine. The reaction appeared to depend on oxygen, a requirement traced to the need for high concentrations of ATP. Physiologically the formation of urea occurs at very low levels of ammonia, which is extremely toxic as it is also lipid soluble and enters cells very easily. Cells are not very effectively buffered against OH. ... 

Some toxic effects are reversible. Everyone has been exposed to some agent, household ammonia for example, that produces irritation to the skin or eyes. Exposure ends and, sometimes perhaps with a delay, the irritation ends. Some readers have no doubt been poisoned on occasion by the ingestion of too much alcohol. The effects here also reverse. The time necessary for reversal can vary greatly depending upon the severity of the intoxication and certain physiological features of the person intoxicated. But most people also realize that chronic alcohol abuse can lead to a serious liver disorder, cirrhosis, which may not reverse even if alcohol intake ceases. This type of effect is irreversible or only very slowly reversible. It is important in making a toxicological evaluation to understand whether effects are reversible or irreversible, because one is obviously much more serious than the other. 

Amines are the particular products of putrefaction. None of the AF tested utilized amines (putrescine, ethylenediamine) as the sole source of nitrogen in culture (Table 4.1), although some amines (ethylenediamine, trimethyl-amine) are as effective as urea in the field (Sagara 1975,1992). This would show that AF do not directly utilize amines but utilize them only after decomposition to ammonia. Thus, the word postputrefaction in the term PPF may seem inappropriate from the fungal physiological point of view (Yamanaka 2002), but this word indicates the characteristic feature of cadaver and fecal decomposition. It also describes the major cause for growth of the AF in nature. 

Alkylation often causes very poisonous compounds to lose this effect e.g., the nitriles (RCN) and isonitriles (R—N=C) are poisonous only when HCN is split off. The action of alkyl radicals can be masked or inhibited by the presence of other radicals this is illustrated by the behavior of methyl-, dimethyl-, and trimethylamine, which react like ammonia but have no narcotic effect. In this conduct, these amines follow Schmiede-berg s preceding rule and are less toxic than ammonia. The physiological action of alcohols and ethers is ascribed to the nature of the alkyl groups. For the ethers, single or mixed, the effect is due to the presence of the alkyls, each of which acts independently f the other. 

Fig. 9.3 Effect of liver failure on inter-organ trafficking of ammonia. Under normal physiological conditions, ammonia produced by the gut is removed by the liver as urea (periportal hepatocytes) or glutamine (perivenous hepatocytes). Increased ammonia synthesis by the kidney is offset by increased urinary ammonia excretion. In liver failure, skeletal muscle becomes the major route for ammonia detoxification as a result of a post-translational increase of glutamine synthetase. Unlike muscle, the brain does not adapt to liver failure by induction or glutamine synthetase...

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