Ammonia exposure

The NIOSH web site states that deaths occur as a result of ammonia exposures between 5,000 and 10,000 ppm over a 30-min period. Compare the result to the results from the probit equation (Table 2-5). 

Exposure to and inhalation of concentrations of 2500-6500ppm, as might result from accidents with liquid anhydrous ammonia, cause severe corneal irritation, dyspnea, bron-chospasm, chest pain, and pulmonary edema that may be fatal. Upper airway obstruction due to laryngeal/pharyngeal edema and desquamation of mucous membranes may occur early in the course and require endotracheal intubation or tracheostomy. " Case reports have documented chronic airway hyperreactivity and asthma, with associated obstructive pulmonary function changes after massive ammonia exposures. ... 

YadavJS and KaushikVK Genotoxic effect of ammonia exposure on workers in a fertilizer factory. IndJ Exp Biol 35(5) 487-492, 1997... 

Fig. 28. Effect of pelleting technique on the spectra of Alon-C exposed to ammonia (A) Alon-C, (B) Alon-C after ammonia exposure, (C) ammonia-exposed Alon-C in a KBr disk.

Dichloro-5,6-dicyano-1,4-benzoquinone (2%) in benzene Purple-blue spots changing to orange upon ammonia exposure 119... 

Gibbs Yellow turning to brown upon ammonia exposure 168... 

Figure 3. ID NMR imaging and saturation-recovery spectra for powdered toluic acid during the first few minutes of ammonia exposure.

We can estimate the extent of conversion from 4-bromobenzoic acid to ammonium 4-bromobenzoate of portions of the crystal by using the contour plots shown in Figures 4 and 5 and by making corrections for saturation effects. Before ammonia exposure, most areas of the crystal had an intensity, relative to the ferrocene marker, of about 30 % (41 % after correction for saturation of 4-bromobenzoic acid) while after ammonia exposure the more reacted portions of the crystal have an intensity of 50 % (28 % after correction for saturation of ferrocene and ammonium 4-bromobenzoate). The extent of conversion is then given by... 

Figure 6. The total conversion of toluic acid into ammonium toluate is shown here as a function of ammonia exposure time.

Henderson and Haggard (1943) reviewed the early data on ammonia exposure in humans, primarily that of Hurry and Zemick (1931) and Lehmann (1886), and reported responses to various concentrations of ammonia as listed in Table 2-2. 

There are no known specific biomarkers for exposure to ammonia. Plasma concentrations cannot serve this purpose, as relatively large amounts of ammonia are produced endogenously. Previously discussed studies (Schaerdel et al. 1983 Silverman et al. 1949) have demonstrated that inhalation of relatively high concentrations of ammonia do not significantly alter blood or urinary ammonia. Biomarkers of effect from ammonia exposure are limited to resultant tissue injuries from contact with the irritant gas. Unfortunately, the lesions are nonspecific and are consistent with exposure to other irritant gasses and caustic compounds. 

The primary immediate effect of ammonia exposure is burns to the skin, eyes, and respiratory tract. Ammonia dissolves in tissue water and forms ammonium hydroxide that breaks down cellular proteins, saponifies cell membrane lipids resulting in cell disruption and death, and initiates an inflammatory response that further damages surrounding tissues. 

Ammonia has an odor threshold ranging from 1 to 5 ppm. Exposures between 20 and 25 ppm can cause complaints and discomfort in some workers unaccustomed to ammonia exposure but have little effect on pulmonary function or odor sensitivity. Concentrations of 100 ppm caused definite irritation of the respiratory tract and eyes, and exposures at 250 ppm ammonia are bearable for 30-60 min. Severe irritation of the respiratory tract, skin, and eyes has been observed following ammonia exposures ranging from 400 to 700 ppm. Exposure to 2500-4500 ppm ammonia can be fatal within 30 min. Immediate fatalities appear to be the result of airway obstruction, particularly laryngeal edema and glottic spasm, while infections and other secondary complications appear to be the cause of fatality among those who survive for several days to weeks. 

Wood and Coleman (1995) assessed the behavioral response to formaldehyde exposure in male Swiss mice. Eight mice were trained to terminate exposure to noxious gases, using 1,000 ppm ammonia. All animals learned to terminate 100% of the ammonia exposures. After mice consistently terminated... 

Dermal exposures to liquid ammonia or concentrated solutions and/or ammonia gas are frequently occupationally related and produce cutaneous bums, blisters, and lesions of varying degrees of severity. Bums can be severe enough to require skin grafting, and loss of the epidermal layer increases body fluid loss and incidence of infection. While most ammonia exposures are occupational, household products containing ammonia can also cause dermal injury. Several cases of young children (2-3 years old) who bit into ammonia pellets/capsules and sustained oral and esophageal lesions have been reported in the literature. 

Other oeeupational studies also evaluated the effects of ammonia exposure and pulmonary function. Firefighters who reported exposure to ammonia while working had a rate of decline of FEV of 1.7 times that of nonexposed firefighters over a period of 6-10 years (Tepper et al. 1991). 

The primary and most immediate effect of ammonia exposure is bums to the skin, eyes, and respiratory tract. The topical damage caused by ammonia is probably due mainly to its alkaline properties. Its high water solubility allows it to dissolve in moisture on the mucous membranes, skin, and eyes, forming ammonium hydroxide, which causes liquefaction necrosis of the tissues (Jarudi and Golden 1973). Specifically, ammonium hydroxide causes saponification of cell membrane lipids, resulting in cell disruption and death. Additionally, it breaks down cell stmctural proteins, extracts water from the cells, and initiates an inflammatory response, which further damages the surrounding tissues (Amshel et al. 

Chronic-Duration Exposure and Cancer. Several studies have examined the relationship between chronic exposure to ammonia and respiratory effects. Studies of farmers working in enclosed livestock facilities provide evidence that ammonia may contribute to transient respiratory distress (Choudat et al. 1994 Cormier et al. 2000 Donham et al. 1995, 2000 Heederik et al. 1990, 1991 Melbostad and Eduard 2001 Reynolds et al. 1996 Vogelzang et al. 1997, 2000) however, co-exposure to total dust, respirable dust, carbon dioxide, total endotoxins, respirable endotoxins, fungi, bacteria, and/or molds complicates the interpretation of these studies. A study of workers at a fertilizer production facility found an association between respiratory effects and ammonia exposure (Ballal et al. 1998). Another study did not find respiratory effects (Holness et al. 1989). Animal studies examining the chronic toxicity of inhaled ammonia were not identified. The human data were considered adequate for derivation of an inhalation MRL (Holness et al. 1989). No chronic-duration oral or dermal data were located. Studies by these routes of exposure would provide useful information on the identification of target organs especially after low-dose exposure. 

A third study evaluated S04 and exposure to 24 children (ages were not provided) living in Uniontown, Pennsylvania (Suh et al. 1992). This study did not focus on ammonia exposure per se, but on other airborne contaminant concentrations in aerosols found outdoors, indoors, and by personal monitors. It sought to determine how personal exposures to these aerosols correlated with indoor and outdoor concentrations. Ammonia concentrations were measured in order to assess their potential for neutralizing found in aerosols. Ammonia was found to be in highest concentrations near the children (detected by the personal monitors), followed by indoor concentrations, and were minimal outdoors. It was proposed that a large proportion of the found in indoor aerosols are neutralized by NH3, and thus would lower the children s exposure to acid aerosols. The authors noted that more research is needed to fully model the influence of factors, including NH3, on indoor acid aerosol exposure. 

Mitz SV, Giesy JP. 1985. Sewage effluent biomonitoring. II. Biochemical indicators of ammonia exposure in channel catfish. Ecotoxicol Environ Saf 10 40-52. 

Tuskes PM, Tilton MA, Graff RM. 1988. Ammonia exposures of blue-line printers in Houston, Texas. ApplIndHyg 3 155-157. 

Yang GY, Tominack RL, Deng JF. 1987. An industrial mass ammonia exposure. Vet Hum Toxicol 29 476-477. 

The as-prepared PPY and PAN complexes can be undoped electrochemically or chemically. The interactions between ammonia and PPY have been reported to result in both reversible and irreversible charges in the electrical conductivity [111]. At low concentrations of ammonia, the conductivity change is almost completely reversible upon removal of the gas. At high concentrations of ammonia, the irreversible changes are significant, and after seven days of wet ammonia exposure the irreversibility is complete. It was not even possible to increase the conductivity in such a film by electrochemical oxidation or immersion in aqueous HCl for 30 minutes. The XPS measurements indicated... 

Interaction of polythiophene containing BF4 counter-ions with atmospheric oxygen is reversible and somewhat similar to what has been observed in PPY(BF4) on ammonia exposure [45] as evident from... 

Sample PCa5P3 had no peaks around 25° and 32°in 2 theta, attributable to apatite though denoted as Ca-P, while samples PCa5P3 A80 clearly showed those peaks after 1 h exposure. Thus, the ammonia exposure was found critical for the calcium phosphate deposition. 

The range of effects of ammonia exposure to humans can be divided into three groups ... 

A person caught in a large spill should stay indoors with doors and windows closed and ventilation shut down. Only in circumstances where there is little alternative or where success is sure should one run away from the cloud. In any case, respiratory breathing apparatus is recommended. The most serious injuries often occur within a couple of hundred meters from the spill source. Most risks from ammonia exposure are accidental or occupational. 

Epidemiological studies with respect to ammonia exposures are still inadequate. Since the aquatic ecosystems are the most sensitive to high ammonia concentrations, long-term monitoring of ammonia is needed in underground sewage systems and outfalls. Effects of other chemical species in the presence of ammonia should also be studied. 

Eye contact The eyes must be flooded immediately with copious quantities of clean water. Speed is essential. In isolated areas, water in a squeeze bottle, which can be carried in the pocket, is helpful for emergency irrigation purposes. Eye fountains should be used, but if they are not available, water may be poured over the eyes. In any case, the eyelids must be held open and irrigation must continue for at least 30 minutes. The patient must receive prompt attention from a physician, preferably an ophthalmologist. Persons subject to ammonia exposure should not wear contact lenses. 

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