Registration Dossier
Registration Dossier
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EC number: 203-819-3 | CAS number: 110-96-3
Endpoint summary
Administrative data
Description of key information
Alkaline corrosives cause liquefaction necrosis. They saponify the fats in the cell membrane, destroying the cell and allowing deep penetration into mucosal tissue. In gastrointestinal tissue an initial inflammatory phase may be followed by tissue necrosis (sometimes resulting in perforation), then granulation and finally stricture formation.
Key value for chemical safety assessment
Acute toxicity: via oral route
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- LD50
- Value:
- 258 mg/kg bw
Acute toxicity: via inhalation route
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- LC50
Acute toxicity: via dermal route
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- LD50
- Value:
- 1 001 mg/kg bw
Additional information
sources: RTECS, HSDB, SIDS
Justification for classification or non-classification
SEVERE ORAL TOXICITY: May develop deep burns and necrosis of the gastrointestinal mucosa. Complications often include perforation (esophageal, gastric, rarely duodenal), fistula formation (tracheoesophageal, aortoesophageal), and gastrointestinal bleeding. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Stricture formation (esophageal, less often oral or gastric) is likely to develop long term. Esophageal carcinoma is another long term complication. Upper airway edema is common and often life threatening.
INHALATION EXPOSURE: Mild exposure may cause cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, stridor, and rarely acute lung injury.
DERMAL EXPOSURE: Mild exposure causes irritation and partial thickness burns. Metabolic acidosis may develop in patients with severe burns or shock. Prolonged exposure or high concentration products can cause full thickness burns.
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