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SODIUM HYDROXIDE

BACKGROUND INFORMATION

PHYSICAL AND CHEMICAL PROPERTIES

Chemical formula:

NaOH

Molecular weight:

40.01

Synonyms:

White caustic, caustic soda, soda lye, lye

CAS number:

1310–73–2

Melting point:

318. 4°C

Boiling point:

1390°C

Specific gravity:

2.13

Solubility:

Soluble in water, ethanol and glycerol; insoluble in acetone and ether

General characteristics:

White deliquescent solid

OCCURRENCE AND USE

Sodium hydroxide is widely used in the manufacture of soaps, paper, rayon, cellophane, mercerized cotton, aluminum, and many chemicals. It is also used in petroleum refining, degreasing, etching, zinc extraction, tin plating, oxide coating, and food processing (for peeling fruits and vegetables). In concentrated form, it is used as a drain cleaner. Sodium hydroxide has been used in the management of pleural effusions.

SUMMARY OF TOXICITY INFORMATION

Sodium hydroxide toxicity depends on the concentration of the sodium hydroxide solution and the duration of its contact with tissue. The chemical acts locally, exerting a strong corrosive action whose mechanism is not known, and causes almost Immediate degeneration of the tissue, which can result in rapid absorption of sodium hydroxide into the circulating system and distribution with the body water. It dissociates completely in water, blood, and cytoplasm and is not metabolized.

Because toxicity of sodium hydroxide is determined primarily by concentration of the hydroxyl ion, the total alkalinity is reduced when sodium carbonate (Na2CO3) forms. Therefore, measurement of sodium ion concentration is not always an accurate indication of alkalinity and toxic potential (Cooper et al., 1979).

EFFECTS ON HUMANS

Humans can be exposed during the manufacture of sodium hydroxide and in the handling of sodium hydroxide as a solid or concentrated solution.



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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 SODIUM HYDROXIDE BACKGROUND INFORMATION PHYSICAL AND CHEMICAL PROPERTIES Chemical formula: NaOH Molecular weight: 40.01 Synonyms: White caustic, caustic soda, soda lye, lye CAS number: 1310–73–2 Melting point: 318. 4°C Boiling point: 1390°C Specific gravity: 2.13 Solubility: Soluble in water, ethanol and glycerol; insoluble in acetone and ether General characteristics: White deliquescent solid OCCURRENCE AND USE Sodium hydroxide is widely used in the manufacture of soaps, paper, rayon, cellophane, mercerized cotton, aluminum, and many chemicals. It is also used in petroleum refining, degreasing, etching, zinc extraction, tin plating, oxide coating, and food processing (for peeling fruits and vegetables). In concentrated form, it is used as a drain cleaner. Sodium hydroxide has been used in the management of pleural effusions. SUMMARY OF TOXICITY INFORMATION Sodium hydroxide toxicity depends on the concentration of the sodium hydroxide solution and the duration of its contact with tissue. The chemical acts locally, exerting a strong corrosive action whose mechanism is not known, and causes almost Immediate degeneration of the tissue, which can result in rapid absorption of sodium hydroxide into the circulating system and distribution with the body water. It dissociates completely in water, blood, and cytoplasm and is not metabolized. Because toxicity of sodium hydroxide is determined primarily by concentration of the hydroxyl ion, the total alkalinity is reduced when sodium carbonate (Na2CO3) forms. Therefore, measurement of sodium ion concentration is not always an accurate indication of alkalinity and toxic potential (Cooper et al., 1979). EFFECTS ON HUMANS Humans can be exposed during the manufacture of sodium hydroxide and in the handling of sodium hydroxide as a solid or concentrated solution.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Sodium hydroxide is corrosive to all body tissues; concentrated vapors cause serious damage to the eyes and respiratory system. Ingestion of sodium hydroxide, which occurs frequently in children, can cause severe necrosis, with stricture of the esophagus and death. Contact with the skin can result in dermatitis, loss of hair, and necrosis due to irritation. Skin types vary in sensitivity to caustic irritation. Airborne mists of sodium hydroxide around degreasing vats (at 200°F) containing Seco 75 or Tysol 810 (concentrated sodium hydroxide solutions combined with chelating and wetting agents) were associated with irritation of the upper respiratory tract in workers exposed to sodium hydroxide at 0.01–0.7 mg/m3 (mean, 0.1–0.15 mg/m3). The work area also contained vapors of Stoddard solvent, ENSIS 254 oil, Zyglo, and Magna-flux solutions (Stoddard solvent air concentrations were 13–780 mg/m3) and, at vat-cleaning time, sulfuric acid at 0.1–0.6 mg/m3 (Hervin and Cohen, 1974). The effect of these chelating agents and solvents on sodium hydroxide toxicity is not known. Ott et al. (1977) assessed mortality rates among chemical-plant employees exposed chronically to caustic dust. Records of acute exposures (unknown concentrations) indicated that the caustic materials in the plant had caused mild to severe responses (irritation, erythema, and “objective damage to organs”) in skin, eyes, and the respiratory system. No indication of purity was given, but it was noted that sodium chloride and sodium carbonate were known to be included in the caustic exposures; workers known to be exposed to arsenicals or asbestos, as well as caustic, were excluded from the study. According to the results of a study that measured total alkalinity of air samples in the workplace, sodium hydroxide concentrations of up to 6.7 mg/m3 in one area of the plant correlated well with subjective response data that indicated increasing respiratory irritation with increasing alkali concentration; in a second area of the plant, where sodium hydroxide content was up to 7.7 mg/m3, the correlation was poor. No explanation for the poor correlation could be found. Sodium hydroxide estimated to be as high as 2 mg/m3 (TWA) did appear to cause nasal and skin irritation, especially in plant areas with high temperatures. No correction factor for temperature effects on sodium hydroxide toxicity is available, but it is expected that increased temperatures would increase toxicity. Controlled exposures to sodium hydroxide solutions have been limited to dermal application, usually to the forearms of volunteers. Malten and Spruit (1966) placed 0.12% (0.03 M) or 0.27% (0.0675 M) solutions of sodium hydroxide in cups fixed to the forearms of human volunteers. Erythema was produced within 0.5 h by the stronger solution and within 1 h by the more dilute preparation (see also Spruit and Malten, 1968). Marzulli and Maibach (1975) applied sodium hydroxide solutions to the backs of human subjects in occluded patches renewed daily for 21 d. The lowest concentration studied (0.05%, 0.0125 M) produced no erythema, a 0.5% (0.125 M) solution was mildly irritating, and solutions of 4% or 5% were severely irritating. Similar results were observed in rabbits.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 EFFECTS ON ANIMALS Many toxicologic evaluations of sodium hydroxide have been carried out in animals; the studies have focused on eyes, skin, and lungs as targets. These investigations are summarized in Table 11. INHALATION EXPOSURE LIMITS The current ACGIH (1983) ceiling limit for sodium hydroxide is 2 mg/m3 (TWA); this concentration is also used by NIOSH. Exposure ceilings in West Germany, Finland and Yugoslavia are 2 mg/m3. The concentration appears to be based on an undocumented comment by Patty (1949) that 2 mg/m3 is thought to cause noticeable, but not excessive, respiratory irritation. COMMITTEE RECOMMENDATIONS Few inhalation studies to evaluate the toxicity of sodium hydroxide have been reported. The one detailed analysis of workers in a degreasing plant exposed to heated caustic vapor indicated that aerosols containing an average of 0.1 mg/m3 were reversibly irritating to the upper respiratory tract (Hervin and Cohen, 1974); the workers in that study were also exposed to detergent and organic solvents, so evaluation of the toxicity of sodium hydroxide alone is difficult. Sodium hydroxide at 2 mg/m3 (TWA) appeared to cause nasal and skin irritation, especially at high temperatures. Because increased temperature increases toxicity, the Committee concludes that a 1-h exposure to sodium hydroxide at 2 mg/m3 would probably produce no more than a reversible mild irritation of eyes, skin, and respiratory system. The Committee’s previous recommendations for sodium hydroxide exposure limits were made in 1965 on the basis of an undocumented statement that 6.0 mg/m3 produced intolerable respiratory discomfort; the 1965 recommendation was for 10- and 30-min EELs of 4 mg/m3 and a 60-min EEL of 2 mg/m3. Little new information on the toxicity of sodium hydroxide by inhalation is available; experimental-animal studies have concentrated on topical application to eyes and skin, and extrapolation from such studies to human inhalation is difficult. On the basis of the report on workers in a degreasing plant (Hervin and Cohen, 1974), an EEL above 2 mg/m3 may produce much nasal and skin discomfort, especially at high temperature, but no available inhalation report provides a basis on which to establish an EEL for sodium hydroxide with confidence. The present Committee’s recommended EELs for sodium hydroxide and the limits proposed in 1965 are shown below.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2   1965 1984 10-min EEL 4 mg/m3 2 mg/m3 30-min EEL 4 mg/m3 2 mg/m3 60-min EEL 2 mg/m3 2 mg/m3

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 TABLE 11 Summary of Data on Toxicity of NaOH in Animals Species Route Dose Duration of Exposure Effects Reference Rat Skin 50% 1 min, no wash 1 min, HAC wash 1 min, H2O wash Edema, sloughing Edema, sloughing Edema, limited sloughing Davidson, 1927 Mouse Skin 50% Immediate rinse 30 min, rinse 1 h, rinse 2 h, rinse No wash No burn, no dead Burn, 1/5 dead Burn, 2/5 dead Burn, 4/5 dead Burn, 5/7 dead Bromberg et al., 1965 Rat Eye 40% NGa Necrosis, death Cosgrove and Hubbard, 1928 Rabbit Eye 20% 10 s Necrosis Hubbard, 1937; Hubbard, 1938 Rabbit Eye 0.2% 3 min Necrosis Hughes, 1946 Rabbit Eye pH 11 pH 12 15 min 15 min Slight injury Necrosis Grant and Kern, 1955 Rabbit Eye 2% 30 s Necrosis Brown, 1971; Brown and Weller, 1970; Brown et al., 1969a,b,c; 1970 Rabbit Eye 0.5%b 2.0%b 8.0%b Not specified Not specified Not specified Intraocular pressure up Intraocular pressure up Intraocular pressure up Chiang et al., 1971

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Species Route Dose Duration of Exposure Effects Reference Rabbit Eye 2% H2O rinse, 1 min H2O rinse, 4 min Corneal perforations Corneal perforations Geeraets et al., 1966 Rabbit Eye 4%c 1 s 2 s No injury Corneal swelling Shapiro, 1956 Rat Inhalation 40% soln.d 2.5 moe Degeneration of pulmonary tissue, undefined “tumors” Dluhos et al., 1969 Rat Inhalation 40% soln. aerosolf 1 mo Death Vyskocil et al., 1966     20% soln. aerosolf 1 mo Degeneration of pulmonary tissue       10% soln. aerosolf 1 mo Little change in pulmonary tissue       5% soln. aerosolf 1 mo Little change in pulmonary tissue   a 0.5 ml applied, b In impregnated paper. c Aerosol; 80% of particles under 1 μm in diameter, d 30 min twice a day for 2.5 mo with 10-d rest after third week. e Aerosol included quartz dust at 10 g/m3. f Twice a week.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 REFERENCES American Conference of Governmental Industrial Hygienists. 1983. TLVs(R): Threshold Limit Values for Chemical Substances and Physical Agents in the Work Environment with Intended Changes for 1983–1984. Cincinnati, Ohio: American Conference of Governmental Industrial Hygienists. 93 p. Bromberg, B.E., Song, I.C., and Walden, R.H. 1965. Hydrotherapy of chemical burns. Plast. Reconstr. Surg. 35:85–95. Brown, S.I. 1971. Treatment of the alkali-burned cornea. Sight Sav. Rev. 41:83–88. [Ind. Medicus 13:1052, 1972] Brown, S.I., and Weller, C.A. 1970. Collagenase inhibitors in prevention of ulcers of alkali-burned cornea. Arch. Ophthalmol. 83:352–353. Brown, S.I., Akiya, S., and Weller, C.A. 1969a. Prevention of the ulcers of the alkali-burned cornea—Preliminary studies with collagenase inhibitors. Arch. Ophthalmol. 82:95–97. Brown, S.I., Wassermann, H.E., and Dunn, M.W. 1969b. Alkali-burns of the cornea. Arch. Ophthalmol. 82:91–94. Brown, S.I., Weller, C.A., and Akiya, S. 1970. Pathogenesis of ulcers of the alkali-burned cornea. Arch. Ophthalmol. 83:205–208. Brown, S.I., Weller, C.A., and Wassermann, H.E. 1969c. Collagenolytic activity of alkali-burned corneas. Arch. Ophthalmol. 81:370–373. Chiang, T.S., Moorman, L.R., and Thomas, R.P. 1971. Ocular hypertensive response following acid and alkali burns in rabbits. Invest. Ophthalmol. 10:270–273. Cooper, D.W., Underbill, D.W., and Ellenbecker, M.J. 1979. A critique of the U.S. standard for industrial exposure to sodium hydroxide aerosols. Am. Ind. Hyg. Assoc. J. 40:365–371. Cosgrove, K.W., and Hubbard, W.B. 1928. Acid and alkali burns of the eye—An experimental study. Ann. Surg. 87:89–94. Davidson, E.C. 1927. The treatment of acid and alkali burns—An experimental study. Ann. Surg. 85:481–489. Dluhos, M., Sklensky, B., and Vyskocil, J. 1969. Effect of aerosol inhalation of soda hydroxide on the respiratory tract of rats. Vnitr. Lek. 15:38–42. [CA 70:80666e, 1969]

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Geeraets, W.J., Aaron, S.D., and Guerry, D., III. 1966. Alkali burns of the cornea and neutral ammonium tartrate—An in vitro and in vivo study. Guildcraft 40:13–16. Grant, W.M., and Kern, H.L. 1955. Action of alkalies on the corneal stroma. Arch. Ophthalmol. 54:931–939. Hervin, R.L., and Cohen, S.R. 1974. Health hazard evaluation/toxicity determination report 72–97–135, Chicago and North Western Railway, Oelwein, Iowa. Rockville, Maryland: National Institute for Occupational Safety and Health. 18 p. [NIOHS-TR-HHE 72–97–135 and PB-146 442] Hubbard, W.B. 1937. Treatment of caustic burns of the eye. Arch. Ophthalmol. 18:263–266. Hubbard, W.B. 1938. Caustic burns of the eye. Arch. Ophthalmol. 19:968–975. Hughes, W.F., Jr. 1946. Alkali burns of the eye. II. Clinical and pathologic course. Arch. Ophthalmol. 36:189–214. Malten, K.E., and Spruit, D. 1966. Injury to the skin by alkali and its regeneration. Dermatologica 132:124–130. Marzulli, F.N., and Maibach, H.I. 1975. The rabbit as a model for evaluating skin irritants: A comparison of results obtained on animals and man using repeated skin exposures. Food Cosmet. Toxicol. 13:533–540. Ott, M.G., Gordon, H.L., and Schneider, E.J. 1977. Mortality among employees chronically exposed to caustic dust. J. Occup. Med. 19:813–816. Patty, F.A. 1949. Sodium hydroxide. In: Patty, F.A., ed. Industrial Hygiene and Toxicology, Vol. II. New York: Interscience Publ. p. 560–561. Shapiro, H. 1956. Swelling and dissolution of the rabbit cornea in alkali. Am. J. Ophthalmol. 42:292–298. Spruit, D., and Malten, K.E. 1968. Estimation of the injury of human skin by alkaline liquids. Berufs-Dermatosen 16:11–24. [Ind. Medicus 9:8578, 1968] Vyskocil, J., Tuma, J., and Dluhos, M. 1966. Effect of aerosol inhalations of sodium hydroxide on the elimination of quartz dust from lungs of rats. Scr. Med. Fac. Med. Univ. Brun. Purkynianae 39:25–29. [Chem. Abs. 65:4519d, 1966]