August 1952
I Hygiene Toxicity of sulfuric acid mist, and treatment of cyanide poisoning are subjects of recent reports
hlELLON INSTITUTE
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Industrial Hygiene column (June 1951) called attention to the lack of information on the physiological effects of sulfuric acid mist and to a report of animal toxicity studies. As evidence of the continued interest in this subject another report (1) has recently been published on the toxicity of sulfuric acid mist to guinea pigs. PREVIOUS
ToxZcftgof eulfurie aeZd miat This study was concerned with the effects of low concentrations of sulfuric acid mist; hence the guinea pig was chosen as the experimental animal, as previous investigations had shown it to be more susceptible than the mouse, rat, or rabbit. The sulfuric acid mist was generated by metering sulfuric acid a t a constant rate to a heated 500-ml. three-necked flask. The vapor was removed by passing dried filtered air through the Bask a t a rate of 1 liter per minute, which was mixed with a larger volume of dried filtered room air before entering the exposure chamber. The relative humidity in the exposure chamber was kept a t about 40 to 45%. Concentrations ranging from 8 to about 90 mg. per cubic meter were used, and the mean particle size was about 1 micron. This size is of the same general order of 0.75 micron reported for sulfuric acid particles collected from the atmosphere in Los Angeles. One of the statistically significant findings was the effect of age on the sensitivity of guinea pigs to the acid mist. The LD60 concentration of the sulfuric acid mist for an exposure of 8 hours was 50 mg. per cubic meter for guinea pigs a year and a half old and averaging over a kilogram in weight. The corresponding value for young guinea pigs 1to 2 monthsold andaveraging about 250 grams in weight, was 18 mg. No mortality was produced in the older animals when exposed for an 8-hour period to 20 mg. per cubic meter, whereas the corresponding value for the younger animals was 8 mg. August 1952
Autopsy findings on animals that died during exposure showed gross areas of hemorrhage in the lungs and in some instances the entire lungs were cherry red. The other organs appeared normal in the gross except the adrenal glands which frequently showed surface hemorrhage. Microscopic examination of tissue sections revealed hemorrhage and edema of the lungs. The adrenals and spleen showed some congestion, but the pathologic changes were not severe. Animals that survived exposure were kept under observation and sacrificed for pathological examination a t various periods up to 3 weeks. Very few of the animals that survived even an exposure that resulted in 50% or more mortality died spontaneously during the post-exposure observation period. Microscopic examination of lung tissues of the sacrificed animals showed evidence of severe damage as long as 3 weeks after termination of a single 8-hour exposure. However, in the other organs no severe pathological changes were observed. In another series of experiments, 1- to 2-month old guinea pigs were exposed for continuous periods up to 72 hours. No fatalities occurred in a concentration of 8 mg. per cubic meter for a continuous exposure of 72 hours. Further tests a t concentrations of 12 and 16 mg. per cubic meter showed that the mortality rate did not change significantly for exposure periods of 8, 24, 32, or 72 hours. However, a t higher concentration, the mortality increased with increase in exposure time. For example, a t 20 mg. per cubic meter the mortality was 50% a t 8 hours and BOYo a t 24 hours. Pathological changes in the lungs of animals that survived the exposure and were killed a t intervals up to 3 w e e k were similar to those observed in animals exposed for 8-hour periods. The results of these studies contribute significantly to a better understanding of the physiological action of sul-
furic acid mist. There appear to be two distinct types of toxic action: one causes respiratory difficulty and laryngeal spasm and the other, a deepseated lung injury. Mortality of the animals is associated with the laryngeal spasm response. The guinea pig is much more sensitive to the spasm-producing action of sulfuric acid mist than mice, rabbits, and rats, and this explains the guinea pig’s greater susceptibility. A concentration of 8 mg. per cubic meter of sulfuric acid mist did not produce spasm in the guinea pig, and no mortality occurred. At higher concentration, the spasm-producing action occurred and mortality increased. The laryngeal spasm effect is not related to the concentration+ime effect. For example, 40 mg. for 3 hours (120) produced 100% mortality, whereas 20 mg. for 8 hours (160) resulted in only 50% mortality. This emphasizes the significance of concentration in evaluating exposure to sulfuric acid mist. However, the hazard associated with exposure to the acid mist cannot be evaluated on the basis of mortality alone. The effects on the lungs are related to total dosage-for example, the lung damage was greater in animals exposed 72 hours, even though no mortality occurred, than in animals exposed 8 hours with a mortality of 5oy0,. Furthermore, although surviving animals seemed well, autopsy showed severe damage. Supplementing the animal studies, a report on the response of human subjects to inhalation of sulfuric acid mist was presented a t the recent meeting of the American Industrial Hygiene Association. The subjects inhaled sulfuric acid mist of an average particle size of 1 micron, in concentrations of 0.35 to 5 mg. per cubic meter through a face mask for 5 to 15 minutes. Changes indicative of shallower and a more (Continued on page 110 A ) rapid rate
INDUSTRIAL AND ENGINEERING CHEMISTRY
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ol iespiintion were produced by (*air centrations of 0.35 to 0.50 mg. psi. cubic meter even though concentiations as high as 1 mg. per cubic mefcr could riot be detected by most subjeds. This iiidicates that the response n a s due l o reflex protective mechanism sinve the concentration was below the detectable limit. AI1 subjects not,icd 3 mg. per cubic meter and in most caws ohjerted to 5 mg. per cubic inrter 11hich caiised coughing on deep inhalntion. At this high concentration there TI ere n i a r k ~ dchanges in respiration an(1 tlic nijnute volume was markedly ietluced. Trentment of cunnide peiNoning
T h e report by Geiger in 1932 oir t l i ~ methylene blue as an antidofc in cyaiiide poisoning stimulated incieased interest in the search for niow efl'ertive means of treating cyairitlc poisoirinp. The beneficial eff riiethylenc h l u ~are attributed t o tlip for~nation of methemoglobin whic~li colnbiires with the cyanide, thus pieventing it from reacting with the respirstory enzyme ferricytochrome oxidase ant1 inhibiting the normal uptake of oxygen by the tissues. Nethyleiie blue is not an efl'ecthc methemoglobin producer, hence attention was directed to other agents which readily pioduce methemoglobin. The results of these studies (2) indieatc clffectiveiiessof sodiumnitrite and sodiuni thiosulfate administered consecutively as well as amyl nitrite either alone or in conjmiction with sodium thiosulfatc. Cyanide is deoxidized in thp hotly mairrly by conversion t o t h i o c y a ~ r ~ t r . This conversion to thiocyanate is apparently enhanced b y the sodiuni thbosulfate, hence the use of this Rgwt in conjunction with the nitrites t l u t pi oducc methemoglobin. Kxperiineiits were conducted in a Irich (logs were injected subcutaneously with sodium cyanide which was promptly followed by the antidote. Amyl nitrite was given by inhalation by crusliiug n pearl of amyl nitrite in a towel and holding i t over the dog's nose. Sodium nitrite and sodium thiosulfate were sdministered intravenously. Sodium thiosulfate was administered dux ing the inhalation of the amyl nitrite but always after the administration of sodium nitritc. A comparison nf thc use of
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protect median lethal dose with various methods of treatment gave the following average results: thiosulfate alone increased the median lethal dose of cyanide by a factor of 3; amyl nitrite by a factor of 5 ; sodium nitrite by a factor of 5 ; amyl nitrite and sodium thiosulfate by a factor of 11; and sodium nitrite tand sodium thiosulfate by a factor of 18. These results indicate the effectiveness, particularly of the combination of nitrite and sodium thiosulfate, in the treatment of cyanide poisoning. The following procedure for treating cyanide poison was suggested : amyl nitrite pearls are broken, one a t a time, in a handkerchief and held over the patient's nose. m'hile this is being done 10 cc. of a 3% solution of sodium nitrite (0.3 gram) is taken into' onc syringe and 50 cc. of a 25% solution of sodium thiosulfate (12.5 grams) in another. Sodium nitrite is injected into the median cubital vein or substitute, followed by the sodium thiosulfate through the same needle. The inhalation of amyl nitrite is discontinued. Since speed is of the essence the amyl nitrite, which can be given by anyone, is administered first while the syringes are being prepared. If the poison has been taken internally, gastric lavage must be instituted. iilso if respiration has ceased, artificial respiration should be administered. In some cases marked improvement may be followed by reappearance of signs of poisoning. If this occurs the full doses of sodium nitrite and sodium thiosulfate should be repeated. The authors report the successful treatment of 16 cases by various physicians. To date, the method has been used in a total of 44 cases with 43 recoveries. The remarkable success in these cases leaves little doubt as to the effectiveness of this procedure. Therefore, the advisability of having available a kit with the essential articles for the emergency treatment of cyanide poisoning is obvious.
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(I) Amdur, M. O., et al., Arch. Ind. Hug.
Occupational Med., 5 , 318 (1952). K. K., and Rose, C. L.,J. ATU. Med. Assoc.. 149, 113 (1952).
( 2 ) Chen,
Correspondence concerning this column will be forwarded promptly if addrassed t o t h e author, % Editor, INDUSTRIAL AND ENQINEERINQ CHEM~ R T R Y 1155-16th , St.,N.W., Washington 6 , D. C.
August 1952
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INDUSTRIAL AND ENGINEERING CHEMISTRY
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