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National Research Council (US) Committee on Toxicology. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2. Washington (DC): National Academies Press (US); 1984.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2.

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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


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.


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).


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

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.


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.

TABLE 11. Summary of Data on Toxicity of NaOH in Animals.


Summary of Data on Toxicity of NaOH in Animals.


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.


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.

10-min EEL4 mg/m32 mg/m3
30-min EEL4 mg/m32 mg/m3
60-min EEL2 mg/m32 mg/m3


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Bookshelf ID: NBK208293


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