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ACUTE EXPOSURE INFORMATION

  1. USES: Benzotrichloride is used as a raw material in synthetic dyes, as an intermediate in the synthesis of ethyl benzoate and benzenyl groups, and in the production of benzotrifluoride, which is an important additive in herbicide, pharmaceutical, and antimicrobial agents. This compound is also used in the production of hydroxybenzophenone ultra-violet stabilizers which are used to prevent discoloration of plastics.
  1. TOXICOLOGY: Acids cause coagulation necrosis. Hydrogen ions desiccate epithelial cells, causing edema, erythema, tissue sloughing and necrosis, with formation of ulcers and eschars. Benzotrichloride is a possible human carcinogen and may be associated with lung tumors from occupational exposure.
  1. EPIDEMIOLOGY: Exposure is rare. Benzotrichloride is typically available for industrial purposes.
  1. In experimental animals, signs and symptoms of exposure have included slowed respiration; hyperemia of extremities; motor automatism; twitching of peripheral muscles; leukopenia; mild anemia; decreased renal function; and mild histological changes in the liver, kidney, and thyroid.
  1. WITH POISONING/EXPOSURE
    1. Benzotrichloride exposure is unusual; limited data regarding specific toxicity following exposure is available. The following effects could be expected to occur, based on exposure data of other acids.
    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. Exposure to large doses may cause CNS depression.
    1. 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.
      1. 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.
    1. 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. Exposure to large doses may cause CNS depression.
    1. OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent vision loss and in severe cases perforation.
    1. 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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