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Acute Inhalatory mass ammonia intoxication with fatal course
Exp. Pathol. 1989; 37: 291-295
Poster
VEB Gustav Fischer Verlag lena
Acute inhalatory mass ammonia intoxication with fatal course By 1. R. WEISER and T. MACKENROTH Department of Internal Medicine, Medical University of Lubeck, D-2400 Lubeck, FRG
Address for correspondence: Dr. 1. R. WEISER, Department of Internal Medicine; Medical University of Lubeck, Ratzeburger Allee 160, D-2400 Lubeck, FRG Keywords: ammonia gas, intoxication; industrial accident; plate refrigeration apparatus; shock freezing equipment; injuries, ammonia gas-induced
Introduction Ammonia is a dangerous irritant gas which is primarily used industrially. Ammonia gas has a greater depth effect than other aqueous alkalis because it penetrates easily into the cell in the undissociated form as a lipid-soluble substance and leads to cell edema there after dissociation with water. Destruction of the airways occurs after brief inhalation of highly concentrated ammonia vapors. An industrial mass accident is to be reported on in which 8 workers were affected. This was caused by a sudden efflux of ammonia from a broken pipe situated above them (see table 1). After hospitalisation one of the intensive-care patients suffered cardio-respiratory arrest of 1 to 3 min. Cutaneous lesions showed third degree burns over about 20 % of the body surface. He was -treated with epinephrine, atropine, NaHC0 3 , prednisolone (800 mg/d) , dexamethasone (l mg/kg/ d) and later cephalosporine without success. After 13 days he died from therapy-resistant bronchopneumonia with collagen breakdown. The pathologic status showed signs of glottis edema and toxic edema of the lung. The other intensive-care patients, who had second degree burns over 10% of his body, was given 3 I of Oz and 7 I of acetic acid by insufflation through the endotracheal tube. X-rays showed prominent pulmonary vascular markings, no traces of which could be detected in later X-ray controls. Continuous control of blood gas analysis showed a decrease down to 60 % pOz (torr) after 8 h (see table 2). Emergency shower facilities should be available wherever ammonia is handled. Persons who come in contact with ammonia should shower immediately. Eyes sprayed with ammonia should be immediately irrigated with high quantities of water for a minimum of 15 min. The present paper once more points out the risk entailed in work with plate refrigeration apparatus for quick freezing and demands especially strict accident prevention regulations and the informing of employees.
Technical and chemical data Ammonia is a colorless gas with an intensive pungent smell (smell of ammonium chloride) and can be liquified under hyperbaric conditions. In the form of ammonium compounds, ammonia is a very important fertilizer. Ammonia is used industrially to manufacture acids, aliphatic and aromatic amines, acid amines, nitric acid, nitrates and for neutralization of acids. In the liquified form, it is used in compression and absorpation refrigeration plants. 19*
Exp. Pathol. 37 (1989) 1-4
291
Table 1. Clinical and anamnestic data of ammonia-intoxication. clinical and anamnestic data of ammonia - intoxication
. ,.~/ voo/'I'c>7~
Ilge sex /~7..,."Y~~
No.
1
23
d'
f2f
(21
f2f
121
140/80 f2f ~
2
20
~ 0
0
0
90
120170
3
24
cf' f2f
~
0
96
140/80 0
4
19
~ 0
0
+
102 150/80 0
5
20 ~ ~
+
0
6
21
~
7
35
++ f2f
f2f
f2f
~
flJ ++ flJ
f2f
flf
0
multiple small area burn
+ + +
(21
0
+
bullerfly erythema
+ + +
f2f
~
120
140/80 0 f2f
bullerlly erythema
+
~
+
0
~
+ + 0
80
120/80
+
0
(21
0
0
~
0
f2f
d' + f2f f2f
88
130/95
+
0
second degree burn
+
l+ +
edema of the lung
~
Pat. Iransfered
8
..\o.. /'I'o/e.. .'/~~ ,.s-"'/i
to spec;al clinic
+
f2f 0
120 140/80
small area burn
+ +
+ + + ++
third degree
+ 0
~
burn
eaem'l of lefhal the lung
after
tldays
Table 2. Decrease of blood gas by acute ammonia inhalation.
decrease of blood gas by acute ammonia inhalation pat.: P. K., 35J. r1
% Pa02
120
100~
so 60 40~
,
,
(Torr)
,
I
r------------I---l------~
,29.5 30;:8 38,1 - o~- - - -~ -
3t 0
j
nas~'
I ""
admission to
t -
38.4
'
31,1
%PoC02 I
T - :- - J - - - --
I
0
tube .7/ acetic acid J,
I
i-; -
31.9 34.2'
,
"
o _ _ ;./"
0-1/1_ : 111-0
0:
' :I I
Intubation
inten~/"e car~ unit i , , 00 16" 19" 22" 24 2" /. day
I
I
I
: '
"
,
~", I
I
13"" /l day
VI tra~sferable , I
I
S"" l//. day
Function of the freezing equipment (Froster) for shock freezing of fruits The Froster has 10 chambers which are liquid-filled with fruits. After 20 min, these are frozen through and are stacked as 50 kg ice blocks on pallets in the cold-storage depot. The refrigeration plant is an ammonia plant, i.e. the system is filled with 100 % ammonia. In the operational circulation of the refrigeration plant, ammonia is both liquid and gaseous. Depending on 292
Exp. Pathol. 37 (1989) 1-4
Type S4A. The valve in its closed position, with the solenoid coil de-energized and the plunger-needle and main port plug in the seated position. is shown in Figure 3. Electrical ener$tization of the solenoid coil forms a magnetic field, pulling up the plunger which strikes the needle, lifting it off its seat. Upward
S4A EXTERNAL EQUALIZER CONNECTION(S4AE CRY)
MAIN PORT
PLUG
motion of the needle permits entrance of the fluid from the valve inlet M through Port N and down through the pilot port to the top of the power piston. This forces the piston downward and pushes the main port plug open, thereby permitting flow of the refrigerant through the valve. The closing spring meanwhile is held in a compressed position. De-energization of the solenoid coil permits the springassisted needle to drop back into its seat, stopping the flow through the pilot port. Bleed-off, through the bleed hole in the piston, decreases the pressure above the piston and allows the closing spring to force the main port plug upward into Ii closed position to stop the flow. The pressure difference across the valve, acting upon the area of the valve seat, plus the force of the closing spring, holds the main port plug in a tightly closed position.
Fig.1. Froster Type S4A. (Reproduced from Bulletin 30-04B, 1978, Refrigerating Specialities Comp., Broadview, Illinois 60153, USA).
Exp. Pathol. 37 (1989) 1-4
293
the aggregate state of the ammonia, the pressure in the system reaches 9-13 bar. The safety valve of the plant is set to 16 bar. In the freezing process, when liquid ammonia is injected into the refrigeration chambers, the pressure reaches 2- 3 bar. In thawing out, when heated gas at a temperature of about 89°C flows in, the pressure reaches 9-13 bar. This process, carried out for brief incipient thawing of the Froster surfaces in order to be able to detach the blocks from the chamber easily ,only takes about 3 min. At the time of the accident, the Froster was in thaw operation. The temperature at the Froster changes from about - 35°C to + 25 °C within a process of freezing to thawing (about 2 Y2 h).
General first aid measures Persons subject to danger from ammonia must be informed on the health hazards and on first aid measures.
Respiratory organs Fresh air, possibly oxygen inhalation instrument. In arrest ofcirculation and breathing: institution of resuscitation measures. The emergency ambulance must be informed immediately.
Eyes Flush burned eyes with lots of water. Further opthalmological treatment is required immediately.
Skin After exposure of the skin to liquid ammonia, the affected person should take off his clothes immediately and flush the skin with lots ofwater. In skin burns amounting to more than 5 % ofthe skin area, the patient must be admitted to a hospital with a special burns unit.
Results and Discussion Ammonia (NH 3 ) is a toxically acting inhalative noxa. In agreement with the literature, acute inhalatory ammonia intoxications with a lethal course are rarely reported. 8 workers were injured by fracture of the cast body of an ammonia refrigeration plant (see fig. I). One worker who was directly below the outflowing ammonia gas died 13 days later, and a further worker who was 2 m away required intensive medical treatment owing to 10% bums. 6 further workers without noteworthy negative effects were hospitalized for further surveillance after first aid. The 21-year-old patient who was in greatest danger was transported immediately by heliocopterto a special burns clinic. Clinical findings upon arrival, he suffered cardio-respiratory arrest 1 to 3 min and received adrenalin, atropine and sodium bicarbonate parenterally. Third degree burns were present on up to 20 % of the body surface. There was also conjunctivitis and bums of the oral mucosa with swelling of the epiglottis, so that an endotracheal tube was inserted. The patient showed significant radiological evidence of edema of the lung and bronchial inflammation. On the 4th day, chest radiograms showed infiltrates in the left lower lobes and right middle lobes. Penicillin treatment was commenced. 2 days later, the respiratory secretions were thick and yellow-green in color, and cultures demonstrated Staphylococcus aureus and Hemophilus injluenzae. The body temperature was still over 39°C. Switching the antibiotic to cephalosporin did not result in any improvement. After the 13th day, the patient died of a therapy-resistant bronchopneumonia after toxic pulmonary edema and severe skin burns. The histological findings showed a massive, hemorrhagic pulmonary edema as well as smaller regions of emphysema of the lungs, edema of the epiglottis and glottis. The other patient who received intensive medical care was given 31 of O2 and 71 of acetic acid by insufflation via the tube for neutralization. In this case, the X-ray merely revealed more pronounced pulmonary vessels, which could not longer be demonstrated in a later check-up. Continuous monitoring of blood gases showed a fall in the course to 60 % p02 (torr) after 8 h (see table 2). The main clinical problem of severe acute ammonia intoxication (more than 3,000 ppm NH3 ) consists in the destruction of airways, followed by skin burns. The predominant effect on the 294
Exp. Pathol. 37 (1989) 1-4
respiratory organs can lead to potentially fatal conditions owing to swelling of the larynx and pulmonary edema. These dangerous symptoms may frequently occur already after 20min, but also even hours later. Liquified ammonia, concentrated aqueous ammonia solutions as well as gaseous ammonia at high concentrations have a severe burning action on the skin, mucosae and eyes. Liquified ammonia can cause congelation on contact with the skin. Intensive medical care ist always necessary in the above injuries. Preventive measures must include worker education and limitation of human exposure by control environmental and human factors.
References BIRKEN, G. A., FABRI, P. J., CAREY, L. c.: Acute ammonia intoxication complicating multiple trauma. J. Trauma 1981; 21: 820-822. BURNS, T. R., MACE, M. L., GREENBERG, S. D., JACHIMCZYK, J. A.: Ultrastructure of acute ammonia toxicity in human lung. Am. J. Forensic. Med. Pathol. 1985; 6: 204-210. BUTTERWORTH, R. F., GIGUERE, J. F., MICHAUD, J., LAVOIE, J., LAYRARGUES, G. P.: Ammonia: key factor in the pathogenesis of hepatic encephalopathy. Neurochem. Pathol. 1987; 6: 1-12. DONG, J. M., ZHAO, 1. R.: Effects of acute ammonia intoxication on cerebral amino acids metabolism in rats. Acta Pharmacol. Sin. 1984;5: 14-17. DONHAM, K. J., KNAPP, L. W., MONSON, R., GUSTAFSON, U.: Acute toxic exposure to gases form liquid manure. J. Occup. Med. 1982; 24: 142-145. EBERSTALLER, E.: Massenunfall durch Ammoniakausbruch an einem Plattengefrierapparat. Berufsgenossenschaft 1965; 77: 468-470. HATTON, D. V., LEACH, C. S.: Collagen breakdown and ammonia inhalation. Arch. Environmental Health 1979; 2: 83-87. KANE, L. E., BARROW, C. S., ALAIRE, Y.: A short-term test to predict acceptable levels of exposure to airborne ~ensory irritants. Am. Ind. Hyg. Assoc. J. 1979; 40: 207-229. KENNEDY, G. L. jr.: Dermal toxicity of ammonium perfluorooctanoate. Toxicol. Appl. Pharmacol. 1985; 81: 348-355. - HALL, G. T., BRITELLI, M. R., BARNES, J. R., CHEN, H. C.: Inhalation toxicity of ammonium perfluorooctanoate. Food Chern. Toxicol. 1986; 24: 1325- 1329. KOSTER, I. W., LETTINGA, G.: Anaerobic digestion at extreme ammonia concentrations. BioI. Waste 1988,25: 51-59. LIN, S., RAABE, W.: Ammonia intoxication: effects on cerebral cortex and spinal cord. J. Neurochem. 1985; 44: 1252-1258. PERNOT, C., et al.: L'intoxication aigue professionnelle par la gaz ammoniac. Arch. Mal. Professionelles 1972; 33: 5-12. SHAHID, A., QURESHI, H., ZUBEN, S. J.: Ammonia intoxication in hepatic coma. J. Pak. Med. Assoc. 1984; 34 9-12. SZAM, J., VINCE, E., SZENTER, J.: Zur Pathogenese des Ammoniumchlorid-Lungenodems. Z. Inn. Med. 1971; 26: 371-381. STAAK, M., KRAEMER, R., RAFF, G.: Irritant gas poisoning: clinical and pharmacological findings. Med. Welt 1979; 30 (40): 1457-1459. STRASSBURGER, K. V., ZELLNER, P., THIESS, A. M.: Lungenfunktionsdiagnostik bei Ammoniak-Intoxikationen. Dtsch. Ges. Arbcitsmed. 1979; 19: 381-391. THIES, A. M.: Gewerbliche Vergiftungen mit Reizgasen. Arztl. Praxis 1969; 91: 5074-5081. WHITE, E. S.: A case of near fatal ammonia gas poisoning. J. Occupation. Med. 1971; 13: 549- 550.
Exp. Pathol. 37 (1989) 1-4
295
Poster
VEB Gustav Fischer Verlag lena
Acute inhalatory mass ammonia intoxication with fatal course By 1. R. WEISER and T. MACKENROTH Department of Internal Medicine, Medical University of Lubeck, D-2400 Lubeck, FRG
Address for correspondence: Dr. 1. R. WEISER, Department of Internal Medicine; Medical University of Lubeck, Ratzeburger Allee 160, D-2400 Lubeck, FRG Keywords: ammonia gas, intoxication; industrial accident; plate refrigeration apparatus; shock freezing equipment; injuries, ammonia gas-induced
Introduction Ammonia is a dangerous irritant gas which is primarily used industrially. Ammonia gas has a greater depth effect than other aqueous alkalis because it penetrates easily into the cell in the undissociated form as a lipid-soluble substance and leads to cell edema there after dissociation with water. Destruction of the airways occurs after brief inhalation of highly concentrated ammonia vapors. An industrial mass accident is to be reported on in which 8 workers were affected. This was caused by a sudden efflux of ammonia from a broken pipe situated above them (see table 1). After hospitalisation one of the intensive-care patients suffered cardio-respiratory arrest of 1 to 3 min. Cutaneous lesions showed third degree burns over about 20 % of the body surface. He was -treated with epinephrine, atropine, NaHC0 3 , prednisolone (800 mg/d) , dexamethasone (l mg/kg/ d) and later cephalosporine without success. After 13 days he died from therapy-resistant bronchopneumonia with collagen breakdown. The pathologic status showed signs of glottis edema and toxic edema of the lung. The other intensive-care patients, who had second degree burns over 10% of his body, was given 3 I of Oz and 7 I of acetic acid by insufflation through the endotracheal tube. X-rays showed prominent pulmonary vascular markings, no traces of which could be detected in later X-ray controls. Continuous control of blood gas analysis showed a decrease down to 60 % pOz (torr) after 8 h (see table 2). Emergency shower facilities should be available wherever ammonia is handled. Persons who come in contact with ammonia should shower immediately. Eyes sprayed with ammonia should be immediately irrigated with high quantities of water for a minimum of 15 min. The present paper once more points out the risk entailed in work with plate refrigeration apparatus for quick freezing and demands especially strict accident prevention regulations and the informing of employees.
Technical and chemical data Ammonia is a colorless gas with an intensive pungent smell (smell of ammonium chloride) and can be liquified under hyperbaric conditions. In the form of ammonium compounds, ammonia is a very important fertilizer. Ammonia is used industrially to manufacture acids, aliphatic and aromatic amines, acid amines, nitric acid, nitrates and for neutralization of acids. In the liquified form, it is used in compression and absorpation refrigeration plants. 19*
Exp. Pathol. 37 (1989) 1-4
291
Table 1. Clinical and anamnestic data of ammonia-intoxication. clinical and anamnestic data of ammonia - intoxication
. ,.~/ voo/'I'c>7~
Ilge sex /~7..,."Y~~
No.
1
23
d'
f2f
(21
f2f
121
140/80 f2f ~
2
20
~ 0
0
0
90
120170
3
24
cf' f2f
~
0
96
140/80 0
4
19
~ 0
0
+
102 150/80 0
5
20 ~ ~
+
0
6
21
~
7
35
++ f2f
f2f
f2f
~
flJ ++ flJ
f2f
flf
0
multiple small area burn
+ + +
(21
0
+
bullerfly erythema
+ + +
f2f
~
120
140/80 0 f2f
bullerlly erythema
+
~
+
0
~
+ + 0
80
120/80
+
0
(21
0
0
~
0
f2f
d' + f2f f2f
88
130/95
+
0
second degree burn
+
l+ +
edema of the lung
~
Pat. Iransfered
8
..\o.. /'I'o/e.. .'/~~ ,.s-"'/i
to spec;al clinic
+
f2f 0
120 140/80
small area burn
+ +
+ + + ++
third degree
+ 0
~
burn
eaem'l of lefhal the lung
after
tldays
Table 2. Decrease of blood gas by acute ammonia inhalation.
decrease of blood gas by acute ammonia inhalation pat.: P. K., 35J. r1
% Pa02
120
100~
so 60 40~
,
,
(Torr)
,
I
r------------I---l------~
,29.5 30;:8 38,1 - o~- - - -~ -
3t 0
j
nas~'
I ""
admission to
t -
38.4
'
31,1
%PoC02 I
T - :- - J - - - --
I
0
tube .7/ acetic acid J,
I
i-; -
31.9 34.2'
,
"
o _ _ ;./"
0-1/1_ : 111-0
0:
' :I I
Intubation
inten~/"e car~ unit i , , 00 16" 19" 22" 24 2" /. day
I
I
I
: '
"
,
~", I
I
13"" /l day
VI tra~sferable , I
I
S"" l//. day
Function of the freezing equipment (Froster) for shock freezing of fruits The Froster has 10 chambers which are liquid-filled with fruits. After 20 min, these are frozen through and are stacked as 50 kg ice blocks on pallets in the cold-storage depot. The refrigeration plant is an ammonia plant, i.e. the system is filled with 100 % ammonia. In the operational circulation of the refrigeration plant, ammonia is both liquid and gaseous. Depending on 292
Exp. Pathol. 37 (1989) 1-4
Type S4A. The valve in its closed position, with the solenoid coil de-energized and the plunger-needle and main port plug in the seated position. is shown in Figure 3. Electrical ener$tization of the solenoid coil forms a magnetic field, pulling up the plunger which strikes the needle, lifting it off its seat. Upward
S4A EXTERNAL EQUALIZER CONNECTION(S4AE CRY)
MAIN PORT
PLUG
motion of the needle permits entrance of the fluid from the valve inlet M through Port N and down through the pilot port to the top of the power piston. This forces the piston downward and pushes the main port plug open, thereby permitting flow of the refrigerant through the valve. The closing spring meanwhile is held in a compressed position. De-energization of the solenoid coil permits the springassisted needle to drop back into its seat, stopping the flow through the pilot port. Bleed-off, through the bleed hole in the piston, decreases the pressure above the piston and allows the closing spring to force the main port plug upward into Ii closed position to stop the flow. The pressure difference across the valve, acting upon the area of the valve seat, plus the force of the closing spring, holds the main port plug in a tightly closed position.
Fig.1. Froster Type S4A. (Reproduced from Bulletin 30-04B, 1978, Refrigerating Specialities Comp., Broadview, Illinois 60153, USA).
Exp. Pathol. 37 (1989) 1-4
293
the aggregate state of the ammonia, the pressure in the system reaches 9-13 bar. The safety valve of the plant is set to 16 bar. In the freezing process, when liquid ammonia is injected into the refrigeration chambers, the pressure reaches 2- 3 bar. In thawing out, when heated gas at a temperature of about 89°C flows in, the pressure reaches 9-13 bar. This process, carried out for brief incipient thawing of the Froster surfaces in order to be able to detach the blocks from the chamber easily ,only takes about 3 min. At the time of the accident, the Froster was in thaw operation. The temperature at the Froster changes from about - 35°C to + 25 °C within a process of freezing to thawing (about 2 Y2 h).
General first aid measures Persons subject to danger from ammonia must be informed on the health hazards and on first aid measures.
Respiratory organs Fresh air, possibly oxygen inhalation instrument. In arrest ofcirculation and breathing: institution of resuscitation measures. The emergency ambulance must be informed immediately.
Eyes Flush burned eyes with lots of water. Further opthalmological treatment is required immediately.
Skin After exposure of the skin to liquid ammonia, the affected person should take off his clothes immediately and flush the skin with lots ofwater. In skin burns amounting to more than 5 % ofthe skin area, the patient must be admitted to a hospital with a special burns unit.
Results and Discussion Ammonia (NH 3 ) is a toxically acting inhalative noxa. In agreement with the literature, acute inhalatory ammonia intoxications with a lethal course are rarely reported. 8 workers were injured by fracture of the cast body of an ammonia refrigeration plant (see fig. I). One worker who was directly below the outflowing ammonia gas died 13 days later, and a further worker who was 2 m away required intensive medical treatment owing to 10% bums. 6 further workers without noteworthy negative effects were hospitalized for further surveillance after first aid. The 21-year-old patient who was in greatest danger was transported immediately by heliocopterto a special burns clinic. Clinical findings upon arrival, he suffered cardio-respiratory arrest 1 to 3 min and received adrenalin, atropine and sodium bicarbonate parenterally. Third degree burns were present on up to 20 % of the body surface. There was also conjunctivitis and bums of the oral mucosa with swelling of the epiglottis, so that an endotracheal tube was inserted. The patient showed significant radiological evidence of edema of the lung and bronchial inflammation. On the 4th day, chest radiograms showed infiltrates in the left lower lobes and right middle lobes. Penicillin treatment was commenced. 2 days later, the respiratory secretions were thick and yellow-green in color, and cultures demonstrated Staphylococcus aureus and Hemophilus injluenzae. The body temperature was still over 39°C. Switching the antibiotic to cephalosporin did not result in any improvement. After the 13th day, the patient died of a therapy-resistant bronchopneumonia after toxic pulmonary edema and severe skin burns. The histological findings showed a massive, hemorrhagic pulmonary edema as well as smaller regions of emphysema of the lungs, edema of the epiglottis and glottis. The other patient who received intensive medical care was given 31 of O2 and 71 of acetic acid by insufflation via the tube for neutralization. In this case, the X-ray merely revealed more pronounced pulmonary vessels, which could not longer be demonstrated in a later check-up. Continuous monitoring of blood gases showed a fall in the course to 60 % p02 (torr) after 8 h (see table 2). The main clinical problem of severe acute ammonia intoxication (more than 3,000 ppm NH3 ) consists in the destruction of airways, followed by skin burns. The predominant effect on the 294
Exp. Pathol. 37 (1989) 1-4
respiratory organs can lead to potentially fatal conditions owing to swelling of the larynx and pulmonary edema. These dangerous symptoms may frequently occur already after 20min, but also even hours later. Liquified ammonia, concentrated aqueous ammonia solutions as well as gaseous ammonia at high concentrations have a severe burning action on the skin, mucosae and eyes. Liquified ammonia can cause congelation on contact with the skin. Intensive medical care ist always necessary in the above injuries. Preventive measures must include worker education and limitation of human exposure by control environmental and human factors.
References BIRKEN, G. A., FABRI, P. J., CAREY, L. c.: Acute ammonia intoxication complicating multiple trauma. J. Trauma 1981; 21: 820-822. BURNS, T. R., MACE, M. L., GREENBERG, S. D., JACHIMCZYK, J. A.: Ultrastructure of acute ammonia toxicity in human lung. Am. J. Forensic. Med. Pathol. 1985; 6: 204-210. BUTTERWORTH, R. F., GIGUERE, J. F., MICHAUD, J., LAVOIE, J., LAYRARGUES, G. P.: Ammonia: key factor in the pathogenesis of hepatic encephalopathy. Neurochem. Pathol. 1987; 6: 1-12. DONG, J. M., ZHAO, 1. R.: Effects of acute ammonia intoxication on cerebral amino acids metabolism in rats. Acta Pharmacol. Sin. 1984;5: 14-17. DONHAM, K. J., KNAPP, L. W., MONSON, R., GUSTAFSON, U.: Acute toxic exposure to gases form liquid manure. J. Occup. Med. 1982; 24: 142-145. EBERSTALLER, E.: Massenunfall durch Ammoniakausbruch an einem Plattengefrierapparat. Berufsgenossenschaft 1965; 77: 468-470. HATTON, D. V., LEACH, C. S.: Collagen breakdown and ammonia inhalation. Arch. Environmental Health 1979; 2: 83-87. KANE, L. E., BARROW, C. S., ALAIRE, Y.: A short-term test to predict acceptable levels of exposure to airborne ~ensory irritants. Am. Ind. Hyg. Assoc. J. 1979; 40: 207-229. KENNEDY, G. L. jr.: Dermal toxicity of ammonium perfluorooctanoate. Toxicol. Appl. Pharmacol. 1985; 81: 348-355. - HALL, G. T., BRITELLI, M. R., BARNES, J. R., CHEN, H. C.: Inhalation toxicity of ammonium perfluorooctanoate. Food Chern. Toxicol. 1986; 24: 1325- 1329. KOSTER, I. W., LETTINGA, G.: Anaerobic digestion at extreme ammonia concentrations. BioI. Waste 1988,25: 51-59. LIN, S., RAABE, W.: Ammonia intoxication: effects on cerebral cortex and spinal cord. J. Neurochem. 1985; 44: 1252-1258. PERNOT, C., et al.: L'intoxication aigue professionnelle par la gaz ammoniac. Arch. Mal. Professionelles 1972; 33: 5-12. SHAHID, A., QURESHI, H., ZUBEN, S. J.: Ammonia intoxication in hepatic coma. J. Pak. Med. Assoc. 1984; 34 9-12. SZAM, J., VINCE, E., SZENTER, J.: Zur Pathogenese des Ammoniumchlorid-Lungenodems. Z. Inn. Med. 1971; 26: 371-381. STAAK, M., KRAEMER, R., RAFF, G.: Irritant gas poisoning: clinical and pharmacological findings. Med. Welt 1979; 30 (40): 1457-1459. STRASSBURGER, K. V., ZELLNER, P., THIESS, A. M.: Lungenfunktionsdiagnostik bei Ammoniak-Intoxikationen. Dtsch. Ges. Arbcitsmed. 1979; 19: 381-391. THIES, A. M.: Gewerbliche Vergiftungen mit Reizgasen. Arztl. Praxis 1969; 91: 5074-5081. WHITE, E. S.: A case of near fatal ammonia gas poisoning. J. Occupation. Med. 1971; 13: 549- 550.
Exp. Pathol. 37 (1989) 1-4
295