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.