Calcium Hydroxide

CAS RN: 1305-62-0

Key Info

CLINICAL EFFECTS

0.2.1 SUMMARY OF EXPOSURE

0.2.1.1 ACUTE EXPOSURE
A) USES: Used as drain openers, household cleaners (oven, bathroom), hair relaxers, dishwasher soap, and in automobile air bags.
In industry used as cleaners, in cement, and as chemical precursors.
B) TOXICOLOGY: 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.
C) EPIDEMIOLOGY: Exposure is common. Serious effects are rare in the developed world (generally only seen in adults with deliberate
ingestion), largely because mostly low concentration corrosives are present in products available in the home. Serious effects
are more common in developing countries.
D) WITH POISONING/EXPOSURE
1) MILD TO MODERATE ORAL TOXICITY: Patients with mild ingestions may only develop irritation or grade I (superficial hyperemia
and edema) burns of the oropharynx, esophagus or stomach; acute or chronic complications are unlikely. Patients with moderate
toxicity may develop grade II burns (superficial blisters, erosions and ulcerations) are at risk for subsequent stricture formation,
particularly esophageal. Some patients (particularly young children) may develop upper airway edema.
a) Alkaline corrosive ingestion may produce burns to the oropharynx, upper airway, esophagus and occasionally stomach. Spontaneous
vomiting may occur. The absence of visible oral burns does NOT reliably exclude the presence of esophageal burns. The presence
of stridor, vomiting, drooling, and abdominal pain are associated with serious esophageal injury in most cases.
b) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and
GI complications and mortality.
2) 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. Severe toxicity is generally limited to deliberate ingestions in adults in the US, because alkaline products
available in the home are generally of low concentration.
3) INHALATION EXPOSURE: Mild exposure may cause cough and bronchospasm. Severe inhalation may cause upper airway edema and burns,
stridor, and rarely acute lung injury.
4) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal
ischemia, permanent visual loss and in severe cases perforation.
5) 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.

FIRE FIGHTING PROCEDURES

Skin: Remove contaminated clothes. Rinse skin with plenty of water or shower. Refer for medical attention .
Inhalation: Fresh air, rest. Refer for medical attention.
In case of fire in the surroundings, use appropriate extinguishing media.
Eye: First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.
Ingestion: Rinse mouth. Do NOT induce vomiting. Give nothing to drink. Refer for medical attention.


REACTIVITIES & INCOMPATIBILITIES

Phosphorus boiled with alkaline hydroxides yields mixed phosphines which may ignite spontaneously in air.
When chlorinated phenols are heated for analytical purposes with calcium hydroxide-potassium nitrate mixtures, chlorinated benzodioxins
analogous to the extremely toxic tetrachlorodibenzodioxin may be formed.
The self-heating and decomposition of /1,3,5-trinitrohexahydro-1,3,5-triazine, calcium hydroxide and water/ was studied ... in
a sealed capsule and in a larger scale furnace test. A rapid exothermic decomposition reaction can be initiated at 100 deg C or
below, and may lead to spontaneous ignition and then deflagration or detonation.
Maleic anhydride, phosphorus, nitroethane, nitromethane, nitroparaffins, nitropropane [Note: Attacks some metals].
/Calcium Hydroxide/ will dissolve in water and react with carbonate ions or CO2 in water to form calcium carbonate.
Decomposes on heating. This produces calcium oxide. The solution in water is a medium strong base. Reacts violently with acids.
Attacks many metals in the presence of water. This produces flammable/explosive gas
/Calcium hydroxide/ may react violently with acids, maleic anhydride, nitromethane, nitroethane, nitropropane, nitroparaffins
and phosphorus.
Alkali and other alkaline earth cmpds such as potassium, lithium, calcium, barium and magnesium cmpds, as well as amines and other
nitrogen cmpds will cause explosive decomposition of maleic anhydride.
The nitroparaffins, in the presence of water, form salts with inorganic bases. The dry salts are explosive.
Violent reaction with maleic anhydride, nitroethane, nitromethane, nitroparaffins, nitropropane, phosphorus. Reaction with polychlorinated
phenols + potassium nitrate forms extremely toxic products.

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