p-Toluenesulfonic Acid

CAS RN: 104-15-4

Key Info

CLINICAL EFFECTS

0.2.1 SUMMARY OF EXPOSURE

0.2.1.1 ACUTE EXPOSURE
A) USES: Household uses include toilet, metal and drain cleaners, rust remover, in batteries, and as a primer for artificial nails.
Used in clandestine methamphetamine labs (ie, hydrochloric and sulfuric acid). Industrial uses include: metal refining, plumbing,
bleaching, engraving, plating, photography, disinfection, munitions, fertilizer manufacture, metal cleaning, and rust removal.
B) TOXICOLOGY: Acids cause coagulation necrosis. Hydrogen ions desiccate epithelial cells, causing edema, erythema, tissue sloughing
and necrosis, with formation of ulcers and eschars.
C) EPIDEMIOLOGY: Inadvertent ingestions occur with moderate frequency in children, and are less common than alkaline exposures.
Serious exposures are rare in the developed world (generally only seen with deliberate ingestions), largely because only low concentration
acids are 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 gastric outlet and esophageal. Some patients (particularly young children) may develop upper airway edema.
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.
Upper airway edema is common and often life threatening. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Other
rare complications include metabolic acidosis, hemolysis, renal failure, disseminated intravascular coagulation, elevated liver
enzymes, and cardiovascular collapse. Stricture formation (primarily gastric outlet and esophageal, less often oral) is likely
to develop long term. Esophageal carcinoma is another long term complication. Severe toxicity is generally limited to deliberate
ingestions in adults in the US, because acidic products available in the home are generally of low concentration.
a) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and
GI complications and mortality. Initial signs and symptoms may not reliably predict the extent of GI burns.
3) INHALATION EXPOSURE: Mild exposure may cause dyspnea, pleuritic chest pain, cough and bronchospasm. Severe inhalation may
cause upper airway edema and burns, hypoxia, stridor, pneumonitis, tracheobronchitis, and rarely acute lung injury or persistent
pulmonary function abnormalities. Pulmonary dysfunction similar to asthma has been reported.
4) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal
ischemia, permanent vision loss and in severe cases perforation.
5) DERMAL EXPOSURE: A minor exposure can cause irritation and partial thickness burns. More prolonged or a high concentration
exposure can cause full thickness burns. Complications may include cellulitis, sepsis, contractures, osteomyelitis, and systemic
toxicity.

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