Hydrogen Chloride

CAS RN: 7647-01-0

Health Effects

0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) USES: Anhydrous hydrogen chloride is used in the production of pharmaceutical hydrochlorides and chlorine, rubber, as a gaseous flux for babbiting operations. It is also used in the leather tanning, electroplating, and food processing industries. Hydrogen chloride in aqueous solution (hydrochloric acid) has many commercial and industrial uses.
    • 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: Exposure is rare. Hydrogen chloride is typically available for industrial purposes.
    • D) WITH POISONING/EXPOSURE
      • 1) Hydrogen chloride exposure is unusual; limited data regarding specific human toxicity following hydrogen chloride exposure is available. The following effects could be expected to occur, based on exposure data of other acids.
      • 2) 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.
      • 3) 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.
        • 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.
      • 4) 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. The current NIOSH IMMEDIATELY DANGEROUS TO LIFE OR HEALTH (IDLH) air concentration for hydrogen chloride is 50 ppm. No significant effects have been seen with chronic exposure to low levels of gaseous hydrogen chloride.
      • 5) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent vision loss and in severe cases perforation.
      • 6) 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.
  • 0.2.1.2 CHRONIC EXPOSURE
    • A) Chronic or prolonged exposure may be associated with changes in pulmonary function, chronic bronchitis, dermatitis, erosion of dental enamel, conjunctivitis, and overt upper respiratory tract abnormalities. No significant effects have been seen from chronic exposure to low levels of gaseous hydrogen chloride. Symptoms may be delayed 1 or 2 days.
      • 1) Chronic exposure to the anhydrous form is unlikely because of its highly affinity for water.
      • 2) Because of its highly irritating and excellent warning properties, acute poisoning from hydrogen chloride occurs only rarely in controlled industrial environments except in accidental exposures. Poisoning can occur from inhalation, dermal, or oral exposure; it is a strong irritant of the eyes and skin. When heated to decomposition, hydrogen chloride emits toxic fumes of chloride.
      • 3) True systemic poisoning is highly unlikely because both hydronium ions and chloride ions are normal constituents of the body. However, the importance of hydrogen chloride as a strong poison should not be underestimated; the anhydrous gas can be fatal by the inhalation or dermal routes. Significant oral exposure is not likely because of its physical form.
    • B) Chronic or prolonged exposure may be associated with changes in pulmonary function, chronic bronchitis, dermatitis, erosion of dental enamel, conjunctivitis, and overt upper respiratory tract abnormalities. No significant effects have been seen from chronic exposure to low levels of gaseous hydrogen chloride. Symptoms may be delayed 1 or 2 days.
0.2.3 VITAL SIGNS
  • 0.2.3.1 ACUTE EXPOSURE
    • A) Shock, rapid breathing and pulse, circulatory collapse and other changes to pulse, blood pressure, and respiration may occur.
0.2.4 HEENT
  • 0.2.4.1 ACUTE EXPOSURE
    • A) Dental discoloration or erosion, bleeding gums, corneal necrosis, conjunctivitis, eye and nasal irritation, nasal ulceration, nose bleeds, throat irritation and ulceration have been observed.
0.2.5 CARDIOVASCULAR
  • 0.2.5.1 ACUTE EXPOSURE
    • A) Circulatory collapse and ischemic lesions may occur.
0.2.6 RESPIRATORY
  • 0.2.6.1 ACUTE EXPOSURE
    • A) Changes in breathing pattern, irritation, changes in pulmonary function, corrosion and edema of the respiratory tract, chronic bronchitis and noncardiogenic pulmonary edema have been observed.
0.2.8 GASTROINTESTINAL
  • 0.2.8.1 ACUTE EXPOSURE
    • A) Gastritis, burns, gastric hemorrhage, dilation, edema, necrosis, and strictures may occur.
0.2.9 HEPATIC
  • 0.2.9.1 ACUTE EXPOSURE
    • A) Ischemia and hepatotoxicity may be observed.
0.2.10 GENITOURINARY
  • 0.2.10.1 ACUTE EXPOSURE
    • A) Nephritis and renal failure may occur.
0.2.11 ACID-BASE
  • 0.2.11.1 ACUTE EXPOSURE
    • A) Hyperchloremic metabolic acidosis may occur.
0.2.12 FLUID-ELECTROLYTE
  • 0.2.12.2 CHRONIC EXPOSURE
    • A) Chlorosis may occur with prolonged or chronic exposure.
0.2.13 HEMATOLOGIC
  • 0.2.13.1 ACUTE EXPOSURE
    • A) Coagulopathy has been reported following an acute ingestion of hydrochloric acid.
  • 0.2.13.2 CHRONIC EXPOSURE
    • A) A diminished hemoglobin content developed in exposed animals.
0.2.14 DERMATOLOGIC
  • 0.2.14.1 ACUTE EXPOSURE
    • A) Burns, ulceration, scarring, blanching, and irritation may occur.
  • 0.2.14.2 CHRONIC EXPOSURE
    • A) Dermatitis may occur with prolonged or chronic exposure.
0.2.20 REPRODUCTIVE HAZARDS
  • A) Fetotoxicity, developmental abnormalities, and possible resistance to hydrogen chloride by inhalation during pregnancy have been noted.
  • B) At the time of this review, no data were available on the possible effects of hydrogen chloride exposure during lactation.
  • C) No information about possible male reproductive effects was found in available references at the time of this review.
0.2.21 CARCINOGENICITY
  • 0.2.21.1 IARC CATEGORY
    • A) IARC Carcinogenicity Ratings for CAS7647-01-0 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
      • 1) IARC Classification
        • a) Listed as: Hydrochloric acid
        • b) Carcinogen Rating: 3
      • 1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
  • 0.2.21.2 HUMAN OVERVIEW
    • A) There has been a lack of conclusive data regarding the carcinogenicity of this agent; however, carcinogenic effects may occur when this agent is in combination with other substances.
0.2.22 GENOTOXICITY
  • A) DNA repair, genotoxicity, sex chromosome loss and chromosome aberrations have been observed.
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