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ZINC CHLORIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Zinc chloride and zinc chloride fume are irritants to the respiratory tract, skin and eyes. Ingested zinc chloride is caustic.

Specific Substances

    1) Zinci Chloridum
    2) Zincum Chloratum
    3) Zinc Dichloride
    4) Molecular Formula: ZnCl(2)
    5) CAS 7646-85-7
    6) ZINC CHLORIDE FUME
    1.2.1) MOLECULAR FORMULA
    1) Cl2-Zn
    2) ZnCl2

Available Forms Sources

    A) FORMS
    1) White granules, crystals or crystalline powder (Sax & Lewis, 1987).
    B) SOURCES
    1) Zinc chloride is the primary constituent of fumes from smoke ammunition bombs (hexite) (Hjortso et al, 1988) and soldering flux (Proctor et al, 1989). Zinc chloride (13%) is also found in a moss killer solution called Moss-Killer by Lilly Miller (Hedtke et al, 1989).
    C) USES
    1) Zinc chloride is used in the manufacture of agricultural chemicals, pharmaceuticals, dry cells, synthetic fabrics, in organic synthesis, and gilding (ITI, 1985). It is also used in disinfectants, wood preservatives, fireproofing materials, moss killers, and soldering fluxes (Knapp et al, 1994).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) WITH POISONING/EXPOSURE
    1) INHALATION - Zinc chloride and fumes are pulmonary irritants. Laryngeal, tracheal, and bronchial mucosal edema and ulceration; interstitial fibrosis; alveolar obliteration; interstitial edema; and bronchiolitis obliterans have been associated with inhalation of zinc chloride smoke.
    2) INGESTION - Zinc chloride is caustic or irritating, depending on the concentration ingested. May cause nausea, vomiting, epigastric pain, burns, hematemesis, or diarrhea. CNS depression and renal damage are possible.
    3) EYE OR SKIN CONTACT may result in mild, moderate, or severe irritation and burns, depending on the concentration and duration of exposure.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Patients may develop considerable respiratory irritation, cough, dyspnea, and/or cyanosis after inhalation exposure. Hypertension developed in one pediatric case after ingesting liquid soldering flux containing zinc chloride and ammonium chloride.
    0.2.5) CARDIOVASCULAR
    A) WITH POISONING/EXPOSURE
    1) Premature atrial beats were reported in an infant 3 hours after ingesting a zinc chloride solution.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Effects of zinc chloride fume or smoke inhalation may range from mild cough, chest pain, and shortness of breath, to pneumonia, cyanosis and potentially fatal pulmonary edema. Chronic inhalation of soldering fume containing zinc chloride may cause asthma.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Lethargy and confusion have been seen after hyperzincemia caused by zinc chloride ingestion.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, hematemesis, burns, gastric strictures, abdominal pain, and elevated amylase levels have occurred in cases of ingestion.
    0.2.9) HEPATIC
    A) WITH POISONING/EXPOSURE
    1) Elevated hepatic enzyme activities have been reported following ingestion of zinc chloride solutions.
    0.2.10) GENITOURINARY
    A) WITH POISONING/EXPOSURE
    1) Renal failure, hematuria and albuminuria can occur after ingestion.
    0.2.11) ACID-BASE
    A) WITH POISONING/EXPOSURE
    1) Metabolic acidosis has been reported in a pediatric case after ingesting liquid soldering flux containing zinc chloride and ammonium chloride.
    0.2.12) FLUID-ELECTROLYTE
    A) WITH POISONING/EXPOSURE
    1) Hypercalcemia, hypocalcemia, hypomagnesemia, and hypophosphatemia have been reported following ingestion of zinc chloride solutions.
    0.2.13) HEMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Anemia may develop secondary to gastrointestinal blood loss following ingestion of zinc chloride. Leukocytosis has been reported.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Zinc chloride causes acute skin irritation. Occupational dermatitis has been reported in workers exposed to zinc chloride. Severe exposures may result in ulcerations of fingers and hands.
    0.2.16) ENDOCRINE
    A) WITH POISONING/EXPOSURE
    1) Hyperglycemia has been reported occasionally following ingestion of zinc chloride solutions.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) When it is unknown if zinc chloride is the cause of pulmonary irritation/edema, a urine zinc level may aid in the determination.
    B) Monitor complete blood count, electrolytes, amylase, renal and liver function tests after zinc chloride ingestion.
    C) If respiratory tract irritation is present, pulse oximetry, chest radiographs, arterial blood gases, should be monitored as indicated. Pulmonary function tests may be useful. Tests that may be useful in differential diagnosis include sputum gram stain, white count differential, arterial blood gases, and electrocardiogram.
    D) Serial chest x-rays may be useful in determining the extent of and progression of injury after inhalation exposures.
    E) Upper gastrointestinal endoscopy should be performed to assess the damage in the GI tract in patients who become symptomatic following zinc chloride ingestion.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Do not induce vomiting. Do not perform gastric lavage. Zinc chloride is highly corrosive. Spontaneous vomiting usually occurs.
    B) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    C) Chelation therapy has been instituted to decrease or minimize the effects of hyperzincemia. Several chelators have been used in symptomatic patients. Chelators have never been shown to increase zinc elimination or affect outcome.
    1) NAC - Intravenous and nebulized acetylcysteine was used to increase the urinary excretion of zinc in two cases.
    2) CALCIUM EDTA
    a) In one pediatric case, a dose of 150 milligrams of calcium disodium edetate was dissolved in 75 milliliters of 1:5 normal saline and used to normalize an elevated serum zinc level.
    b) 15 milligrams per kilogram were used in a 13-month-old who ingested a zinc chloride solution.
    3) BAL/CALCIUM EDTA - In a 16-month-old boy who swallowed soldering flux, chelation with calcium EDTA and BAL starting 75 hours postingestion was ineffective in enhancing zinc clearance. BAL (12 milligrams/kilogram) and calcium EDTA (1 gram/square meter) were given daily divided into 4 doses for 5 days.
    D) FLUID REPLACEMENT - Replace fluids lost with 5% dextrose in saline, treat metabolic acidosis and hypocalcemic tetany if present.
    E) PAIN - Relieve pain by parenteral opiates.
    F) ANURIA - Observe for and provide symptomatic and supportive care in patients who develop anuria and liver damage.
    G) GASTRIC COMPLICATIONS - Observe carefully for gastric perforations and late complications such as pyloric stenosis.
    0.4.3) INHALATION EXPOSURE
    A) Inhalation exposures should be monitored for possible severe pulmonary irritation resulting in bronchopneumonia, acute lung injury, or pneumothorax.
    B) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    C) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    B) The efficacy and safety of edetate disodium have not been demonstrated in the treatment of zinc chloride eye (exposure) injury. However, zinc chloride eye injury has been treated by edetate disodium.
    1) The eye should first be irrigated with water as quickly as possible, then irrigated with 1.7% (or 0.5 molar) edetate disodium solution for 15 minutes. Unless treatment is started within 2 minutes, it may be ineffective.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) Minimum lethal human exposure is unknown.

Clinical Effects

Summary Of Exposure

    A) WITH POISONING/EXPOSURE
    1) INHALATION - Zinc chloride and fumes are pulmonary irritants. Laryngeal, tracheal, and bronchial mucosal edema and ulceration; interstitial fibrosis; alveolar obliteration; interstitial edema; and bronchiolitis obliterans have been associated with inhalation of zinc chloride smoke.
    2) INGESTION - Zinc chloride is caustic or irritating, depending on the concentration ingested. May cause nausea, vomiting, epigastric pain, burns, hematemesis, or diarrhea. CNS depression and renal damage are possible.
    3) EYE OR SKIN CONTACT may result in mild, moderate, or severe irritation and burns, depending on the concentration and duration of exposure.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Patients may develop considerable respiratory irritation, cough, dyspnea, and/or cyanosis after inhalation exposure. Hypertension developed in one pediatric case after ingesting liquid soldering flux containing zinc chloride and ammonium chloride.
    3.3.2) RESPIRATIONS
    A) WITH POISONING/EXPOSURE
    1) Severe dyspnea may occur, or a delayed ARDS may develop. Cough, copious sputum, and cyanosis may also be present.
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) CASE REPORT - Significant hypertension developed in a 16-month-old following ingestion of liquid zinc chloride/ammonium chloride soldering flux (McKinney et al, 1994).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CORNEAL BURNS/OPACIFICATION -
    a) The accidental splash contact of one drop of a 50% solution caused immediate severe pain which persisted despite aqueous irrigation. Examination showed burns of the corneal epithelium and later corneal vascularization (Grant, 1986). Opacification and vascularization of the cornea persisted for many weeks.
    b) May produce conjunctivitis or keratitis (corneal burns) (Evans, 1945).
    c) IRRITATION: Severe irritation of the eyes developed in a 21-year-old man with Down syndrome after inhalational exposure to zinc chloride and hexachloroethane from a smoke bomb (Gil et al, 2008).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Nasal irritation may occur with fume inhalation (ITI, 1985).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) Zinc chloride produces local corrosive effects. Hoarseness, esophagitis, erosive pharyngitis and oropharyngeal burns have resulted from ingestion of zinc chloride solutions (Mendelsohn et al, 1997; Chobanian, 1981; Potter, 1981; McKinney et al, 1994).
    2) The oral mucosa and throat may be without evidence of corrosive or irritant effects despite ingestion of amounts great enough to cause systemic effects (Knapp et al, 1994).
    3) CASE REPORT - Laryngeal or tracheal edema and ulceration may occur (Matarese & Matthews, 1986). A 13-month-old male presented to a health care facility with an erythematous uvula following an accidental ingestion of 30 mL of a moss killer containing 13% zinc chloride (Hedtke et al, 1989).
    4) DYSPHAGIA -
    a) CASE REPORT - Dysphagia and profuse drooling were present in an infant who suffered severe oropharyngeal burns following ingestion of soldering flux (McKinney et al, 1994).
    b) Zinc chloride fume inhalation can result in sore throat and hoarseness (ITI, 1985; Proctor et al, 1989).

Cardiovascular

    3.5.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Premature atrial beats were reported in an infant 3 hours after ingesting a zinc chloride solution.
    3.5.2) CLINICAL EFFECTS
    A) ATRIAL ARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Premature atrial beats were reported in a 13-month-old approximately 3 hours after an accidental ingestion of 30 mL of a 13% solution (Hedtke et al, 1989).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Effects of zinc chloride fume or smoke inhalation may range from mild cough, chest pain, and shortness of breath, to pneumonia, cyanosis and potentially fatal pulmonary edema. Chronic inhalation of soldering fume containing zinc chloride may cause asthma.
    3.6.2) CLINICAL EFFECTS
    A) EDEMA OF LARYNX
    1) WITH POISONING/EXPOSURE
    a) Glottis edema (ITI, 1985), laryngeal or tracheal edema and ulceration may be present following ingestion (Matarese & Matthews, 1986).
    B) DISORDER OF RESPIRATORY SYSTEM
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Rales and rhonchi were present in a 16-month-old who had ingested a soldering flux and who had extensive oropharyngeal burns (McKinney et al, 1994).
    b) Zinc chloride inhalation (generally of fume or smoke) can result in mild to severe cough, chest pain, stridor, retrosternal pain, copious sputum, shortness of breath, cyanosis, pneumonia, and potentially fatal, delayed pulmonary edema (Evans, 1945; ITI, 1985; Proctor et al, 1989).
    C) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Pulmonary edema was the cause of death within a few hours in cases reported by Evans (1945). Others in this group developed bronchopneumonia. Those who recovered did so one to six weeks after the initial exposure.
    D) PNEUMOTHORAX
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Pneumothorax and subpleural emphysematous blebs were present after acute inhalation of zinc chloride. The patient gradually recovered over a period of several months but chest X-rays still showed emphysematous blebs (Matarese & Matthews, 1986).
    E) RESPIRATORY DISTRESS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORTS - Two soldiers developed fatal adult respiratory distress syndrome (ARDS) over 2 weeks following an exposure of 1 to 2 minutes duration to hexite (zinc chloride) from a smoke bomb (Hjortso et al, 1988).
    1) Acute injury was mild and the patients were doing well clinically for 10 days before ARDS developed (Homma et al, 1992). The cause of the delay is uncertain. The patients had been given steroids prophylactically. Plasma zinc concentrations were elevated.
    b) CASE REPORT - A 49-year-old man began developing signs of ARDS after intentionally ingesting 360 mL of liquid soldering flux that contained 25% zinc chloride (43.1 grams). His peak serum zinc level was 2,430 mcg/dL. The serum zinc level decreased and the patient stabilized following combined administration of chelating agents and continuous hemodialysis; however, he died approximately 1 month post-ingestion due to complications associated with gastric perforation(Mendelsohn et al, 1997).
    c) CASE REPORT: A 23-year-old man developed acute respiratory distress syndrome after inhalational exposure to zinc chloride from a smoke grenade for 10 to 15 minutes. Initially, he presented with a sore throat, dry cough, and chest pain. He later developed dyspnea, fever, and a productive cough after admission. A chest radiograph revealed bilateral consolidations, subcutaneous emphysema, pneumomediastinum, and pneumothorax. On day 4, he was severely hypoxemic despite mechanical ventilation and bilateral tube thoracostomy. He was treated with high-dose corticosteroids and extracorporeal life support (ECLS) and his symptoms improved. ECLS was discontinued on day 6 and systemic corticosteroids dose was gradually tapered. Despite continued intensive supportive therapy, his condition deteriorated on day 16. Once again, his symptoms improved gradually following treatment with corticosteroids and ECLS. He gradually recovered and was discharged on day 176 (Chian et al, 2010).
    d) CASE REPORT: A 21-year-old man with Down syndrome developed acute respiratory distress syndrome after inhalational exposure to zinc chloride and hexachloroethane from a smoke bomb during a fire simulation at a school. Initially, he presented with marked agitation, nausea, strong irritation of the eyes, tachypnea, cyanosis, wheezing, and normal heart sound. A chest radiograph showed a mixed interstitial-alveolar infiltrate in bases of both lung fields. His condition deteriorated and 5 days after presentation, muscular respiratory fatigue developed with temperature above 39 degrees C, severe hypoxemia with hypercapnia, hypotension, and oliguria. At this time, he developed a general impairment and a chest x-ray revealed typical interstitial-alveolar bilateral condensation. Despite supportive therapy, he developed shock, right pneumothorax with bronchopulmonary shunt, and severe respiratory and renal failure with oliguria. He died 9 days later of multiorgan failure. Postmortem examination revealed severe damage to the mucous membranes of tracheobronchial and upper respiratory tracts, as well as congestion and edema of lungs, liver, and kidneys. Microscopic findings of lungs showed blood vessel congestion, hemorrhagic areas, intraalveolar and interstitial edema, and intraalveolar fibrosis (Gil et al, 2008).
    F) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES - Three soldiers wearing ill-fitting gas masks were exposed to a zinc chloride smoke bomb for 1 to 2 minutes. They developed immediate severe coughing and dyspnea. Improvement to near normal was occurred over the next 12 months, but exertional dyspnea persisted (Hjortso et al, 1988).
    b) Laryngeal, tracheal, and bronchial mucosal edema and ulceration have been reported after exposure to zinc chloride smoke (Matarese & Matthews, 1986).
    G) BRONCHOSPASM
    1) WITH POISONING/EXPOSURE
    a) Occupational asthma was reported in workers who used corrosive soldering fluxes containing zinc chloride and ammonium chloride. The diagnosis was determined using work related deterioration in daily peak expiratory flow rate and positive responses in bronchial provocation tests (Weir et al, 1989).
    1) Symptoms of cough, chest tightness, and wheeze developed after 12 to 18 months of exposure with the onset of symptoms occurring several hours after arriving at work and progressed during working hours. In general, the patients were symptom free on weekends and periods of time away from work setting.
    2) Decrease in FEV1 caused by the flux was partially accounted for upon challenge testing with ammonium chloride alone in one patient, and zinc chloride alone did not provoke bronchoconstriction (Weir et al, 1989).
    b) Bronchial asthma has been precipitated by zinc chloride exposure (Lange & Kirk, 1986).
    H) FIBROSIS OF LUNG
    1) WITH POISONING/EXPOSURE
    a) Interstitial fibrosis, alveolar obliteration, interstitial edema, and bronchiolitis obliterans have been associated with inhalation of zinc chloride smoke (Matarese & Matthews, 1986; Knaan et al, 1970; Schenker et al, 1981).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PULMONARY EDEMA
    a) RATS given 2.5 mg/kg of zinc chloride intratracheally developed pulmonary edema, alveolitis, and some fibrosis at a later stage. The periphery of the lung was generally spared. Oxygen administration did not affect the development or progression of the pathological changes (Brown et al, 1990).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Lethargy and confusion have been seen after hyperzincemia caused by zinc chloride ingestion.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Lethargy and confusion have been reported from hyperzincemia caused by zinc chloride ingestion (Chobanian, 1981).
    b) CASE REPORT - A 13-month-old male became increasingly lethargic and somnolent at 3 hours following an accidental ingestion of 30 mL of a moss killer solution containing 13% zinc chloride (Hedtke et al, 1989).
    c) CASE REPORT - A 16-month-old boy who ingested an unknown amount of soldering flux (22.5 percent ZnCl) presented with depression and lethargy (McKinney et al, 1994) 1995).
    d) CASE REPORT - A 23-month-old was responsive only to vigorous sternal rub had significantly depressed deep tendon reflexes 2 hours after ingesting about two mouthfuls of a solder flux compound (Knapp et al, 1994).
    e) CASE REPORT - A 21-month-old boy was brought to the ED shortly after an accidental ingestion of a zinc chloride solution. Pronounced lethargy was the major presenting symptom. Neurologic examination was normal otherwise. Intramuscular dimercaprol (BAL) (4 mg/kg) was given. Improvement in mental status occurred rapidly following chelator therapy (De Groote et al, 1998).
    B) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache can occur after inhalation exposure (ITI, 1985).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, hematemesis, burns, gastric strictures, abdominal pain, and elevated amylase levels have occurred in cases of ingestion.
    3.8.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Significant gastric burns, with or without oral or esophageal injury, may occur following the ingestion of solutions of zinc chloride or soldering flux containing zinc chloride. Corrosive pharyngeal lesions may occur (De Groote et al, 1998; Michels et al, 1998).
    b) CASE REPORT - A large superficial mucosal burn to the greater curvature of the stomach was detected by endoscopic examination in a 13-month-old on the day of accidental ingestion of a 13% solution (Hedtke et al, 1989).
    c) CASE REPORT - Severe first, second, and third degree burns were present from the vocal cords down to the gastric antrum in a boy who swallowed an unknown amount of soldering flux with a pH of 2 (McKinney et al, 1994).
    d) CASE REPORT - Following the accidental ingestion of soldering flux (10 to 30% ZnCl), a 42-year-old male presented to the ED 2 weeks later with vomiting, hematemesis, abdominal pain and melena. A 20-25 cm fundal gastric ulcer of the greater curvature was revealed on endoscopy. Hypertrophic gastritis surrounded the ulcer (Michels et al, 1998).
    B) GASTROINTESTINAL COMPLICATION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 39-year-old man presented with abdominal pain and vomiting after ingesting 30 mL of soldering fluid containing 30% to 60% zinc chloride and 10% ammonium chloride (pH 3.9) in a suicide attempt. All laboratory results were normal, except for hyperamylasemia (240 mg/L). Initially, he developed a candidal infection of the oral cavity requiring nystatin and fluconazole therapy, but his recovery was complicated with aspiration pneumonia. On day 21, he complained of worsening dysphagia and vomiting. An esophagogastroduodenoscopy revealed widespread inflammation and ulceration, and stenosis of the pylorus. After a gastric stricture was identified, he underwent successful laparoscopic Roux-en-y gastrojejunostomy. He recovered gradually and was discharged 9 days after surgery (Tayyem et al, 2009).
    C) STENOSIS OF STOMACH
    1) WITH POISONING/EXPOSURE
    a) Gastric stricture has been reported after ingestion of zinc chloride (Chew et al, 1986). Esophagitis and erosive pharyngitis have also been reported after ingestion of a zinc chloride solution (Chobanian, 1981; Potter, 1981).
    b) CASE REPORT - A 16-month-old boy developed gastric outlet obstruction requiring antrectomy from antral scarring after ingesting zinc chloride (McKinney et al, 1994).
    D) GASTROENTERITIS
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, hematemesis, and abdominal pain have occurred following ingestion of a zinc chloride solution (Mendelsohn et al, 1997; Potter, 1981; Chobanian, 1981; Hedtke et al, 1989; Knapp et al, 1994). In one case vomiting and hematemesis, lasting for several days occurred following the ingestion soldering flux, containing 10 to 30% zinc chloride (Michels et al, 1998).
    b) ZINC CHLORIDE (CASE REPORT): Nausea developed in a 21-year-old man following inhalational exposure to zinc chloride and hexachloroethane from a smoke bomb. He developed acute respiratory distress syndrome and died 9 days later of multiorgan failure (Gil et al, 2008).
    E) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Bloody diarrhea, melena, and hematochezia may be present after ingestion (Mendelsohn et al, 1997; ITI, 1985; Michels et al, 1998).
    F) SERUM AMYLASE RAISED
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Elevated amylase levels were reported in a pediatric case of soldering flux ingestion (McKinney et al, 1995). Five months after the ingestion, the child developed pancreatic exocrine insufficiency.
    b) CASE REPORT - Hyperamylasemia developed in one individual following zinc chloride solution ingestion (Chobanian, 1981). The laboratory results were suggestive of acute pancreatitis, but the relationship was never conclusively proved.
    c) CASE REPORT - A 13-month-old male developed hyperamylasemia (120 Units/L) on the day following an accidental ingestion of 30 mL of a moss killer solution containing 13% zinc chloride (Hedtke et al, 1989).
    d) CASE REPORT - Hyperamylasemia occurred in a 49-year-old man who intentionally ingested 360 mL of a liquid soldering flux that contained 25% zinc chloride (43.1 grams). His maximum serum amylase level was 174 international units/liter (Mendelsohn et al, 1997).

Hepatic

    3.9.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Elevated hepatic enzyme activities have been reported following ingestion of zinc chloride solutions.
    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A 13-month-old male developed an elevated alkaline phosphatase (288 Units/L) following an accidental ingestion of 30 mL of a moss killer solution containing 13% zinc chloride (Hedtke et al, 1989).
    b) CASE REPORT - A 16-month-old child developed elevated alkaline phosphatase (527 Units/L) after ingesting zinc chloride/ammonium chloride soldering flux (McKinney et al, 1994).
    c) CASE REPORT - SGOT (AST) and SGPT (ALT) activities were significantly elevated in a 16-month-old following ingestion of a soldering flux (McKinney et al, 1994).

Genitourinary

    3.10.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Renal failure, hematuria and albuminuria can occur after ingestion.
    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Renal failure and oliguria have been reported in humans (Mendelsohn et al, 1997; Csata et al, 1968; Hedtke et al, 1989) and animals (Fazzari & Catini, 1966) exposed to zinc chloride.
    b) CASE REPORT: A 21-year-old man with Down syndrome presented with severe respiratory symptoms after exposure to zinc chloride and hexachloroethane from a smoke bomb during a fire simulation at a school. Despite supportive therapy, his condition deteriorated and he developed shock, hypotension, right pneumothorax with bronchopulmonary shunt, and severe respiratory and renal failure with oliguria, and increased BUN, creatinine and potassium levels. He died 9 days later of multiorgan failure. Postmortem examination revealed severe damage to the mucous membranes of tracheobronchial and upper respiratory tracts, as well as congestion and edema of lungs, liver, and kidneys (Gil et al, 2008).
    B) OLIGURIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Oliguria was reported in a 13-month-old male following an ingestion of 30 mL of a moss killer solution containing 13% zinc chloride (Hedtke et al, 1989).
    C) BLOOD IN URINE
    1) WITH POISONING/EXPOSURE
    a) Albuminemia and hematuria may be present (ITI, 1985). Microhematuria which was not associated with renal dysfunction was reported after a child ingested a zinc chloride solution (Chobanian, 1981).

Acid-Base

    3.11.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Metabolic acidosis has been reported in a pediatric case after ingesting liquid soldering flux containing zinc chloride and ammonium chloride.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Metabolic acidosis developed in a 16-month-old following ingestion of a soldering flux which resulted in severe burns to the oropharyngeal area and stomach (McKinney et al, 1994).
    b) CASE REPORT - A 49-year-old man developed severe metabolic acidosis (pH 7.06, PaCO2 27 mmHg, and PaO2 122 mmHg on 50% FiO2, anion gap 23) after intentionally ingesting 360 mL of a liquid soldering flux that contained 25% zinc chloride (43.1 grams). Clinically, the patient stabilized following combined administration of chelating agents and continuous hemodialysis; however, he died approximately 1 month post-ingestion due to complications associated with gastric perforation(Mendelsohn et al, 1997).

Hematologic

    3.13.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Anemia may develop secondary to gastrointestinal blood loss following ingestion of zinc chloride. Leukocytosis has been reported.
    3.13.2) CLINICAL EFFECTS
    A) ANEMIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A 16-month old boy developed esophageal and gastric burns after ingesting zinc chloride (McKinney et al, 1994). Hemoglobin dropped from 14 grams/deciliter to 8.4 grams/deciliter and a few fragmented red cells were noted on peripheral smear.
    b) CASE REPORT - Anemia (Hct 18.1%; Hgb 6.7 g/dL) was reported in a 42-year-old male 2 weeks after the accidental ingestion of soldering flux (10-30% ZnCl). Severe anemia was secondary to persistent GI bleeding from gastric ulceration (Michels et al, 1998).
    B) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A leukocytosis of 16,000 cells/mm(3), with a normal differential leukocyte count, was reported in a 22-month-old boy following an accidental ingestion of a zinc chloride solution (De Groote et al, 1998).

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Zinc chloride causes acute skin irritation. Occupational dermatitis has been reported in workers exposed to zinc chloride. Severe exposures may result in ulcerations of fingers and hands.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Zinc chloride fume can cause dermal irritation (US DHHS, 1981).
    B) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Occupational dermatitis has been reported in workers exposed to zinc chloride (Belostotskaia & Reizina, 1969). Severe exposures may result in ulcerations of fingers and hands (ITI, 1985; Stokinger, 1963).

Endocrine

    3.16.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hyperglycemia has been reported occasionally following ingestion of zinc chloride solutions.
    3.16.2) CLINICAL EFFECTS
    A) HYPERGLYCEMIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Hyperglycemia was reported in a 13-month-old male following an accidental ingestion of 30 mL of a moss killer solution containing 13% zinc chloride (Hedtke et al, 1989). Hyperglycemia of 176 mg/dL was reported in a 21-month-old boy following the accidental ingestion of a zinc chloride solution (De Groote et al, 1998).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) ANIMAL STUDIES
    1) Zinc chloride caused birth defects in mice when injected into the peritoneal cavity (Chang, 1977), but was not teratogenic in hamsters when administered intravenously (Ferm & Carpenter, 1977). Zinc chloride prevented birth defects (Garcia & Lee, 1981) and male sterility (Gunn, 1961) in rats exposed to cadmium by preventing its uptake. It also prevented birth defects in mice exposed to acetazolamide (Brown, 1983)
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.5) FERTILITY
    A) DECREASED FERTILITY MALE
    1) Zinc chloride inhibited the motility of human sperm in vitro (Rosado, 1970).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7646-85-7 (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) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    B) CARCINOMA
    1) Two embryonal carcinomas were found 10 weeks after injection of zinc chloride into the testes of Syrian hamsters. The injection caused about a 25% necrosis of the testes (Guthrie & Guthrie, 1974).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) When it is unknown if zinc chloride is the cause of pulmonary irritation/edema, a urine zinc level may aid in the determination.
    B) Monitor complete blood count, electrolytes, amylase, renal and liver function tests after zinc chloride ingestion.
    C) If respiratory tract irritation is present, pulse oximetry, chest radiographs, arterial blood gases, should be monitored as indicated. Pulmonary function tests may be useful. Tests that may be useful in differential diagnosis include sputum gram stain, white count differential, arterial blood gases, and electrocardiogram.
    D) Serial chest x-rays may be useful in determining the extent of and progression of injury after inhalation exposures.
    E) Upper gastrointestinal endoscopy should be performed to assess the damage in the GI tract in patients who become symptomatic following zinc chloride ingestion.
    4.1.2) SERUM/BLOOD
    A) HEMATOLOGIC
    1) Follow complete blood count after zinc chloride ingestion.
    B) BLOOD/SERUM CHEMISTRY
    1) Monitor amylase, electrolytes, renal and liver functions, and zinc levels after zinc chloride ingestion.
    4.1.3) URINE
    A) URINALYSIS
    1) Monitor urinalysis and urine output.
    B) URINARY LEVELS
    1) When it is unknown if zinc chloride is the cause of pulmonary irritation/edema, a urine zinc may aid in the determination (Proctor & Hughes, 1978).
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Upper gastrointestinal endoscopy should be performed to assess the damage in the GI tract in patients who become symptomatic following zinc chloride ingestion.
    2) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present pulse oximetry, chest radiographs, arterial blood gases should be obtained as indicated.
    3) OTHER
    a) Tests that may be useful in differential diagnosis include sputum gram stain, differential white count, arterial blood gases, and electrocardiogram (Proctor & Hughes, 1978).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Serial chest X-rays may be useful in determining the extent or progression of injury after inhalation exposures (Proctor & Hughes, 1978).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) When it is unknown if zinc chloride is the cause of pulmonary irritation/edema, a urine zinc level may aid in the determination.
    B) Monitor complete blood count, electrolytes, amylase, renal and liver function tests after zinc chloride ingestion.
    C) If respiratory tract irritation is present, pulse oximetry, chest radiographs, arterial blood gases, should be monitored as indicated. Pulmonary function tests may be useful. Tests that may be useful in differential diagnosis include sputum gram stain, white count differential, arterial blood gases, and electrocardiogram.
    D) Serial chest x-rays may be useful in determining the extent of and progression of injury after inhalation exposures.
    E) Upper gastrointestinal endoscopy should be performed to assess the damage in the GI tract in patients who become symptomatic following zinc chloride ingestion.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Zinc chloride is highly corrosive and emesis or activated charcoal should generally be avoided following ingestion.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Zinc chloride is highly corrosive and emesis or gastric lavage should be avoided following oral ingestion.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    C) ACTIVATED CHARCOAL
    1) It is unknown if activated charcoal is useful in adsorbing zinc chloride. The use of activated charcoal should not delay dilution or other therapy. Use may obscure and make more difficult observing irritant/caustic damage done by the zinc chloride. Consider use with multiple item ingestions.
    2) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    3) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    4) May obscure and make more difficult for endoscopist looking for irritation/caustic damage done by the zinc chloride.
    D) NASOGASTRIC TUBE
    1) INDICATIONS: Consider insertion of a small, flexible nasogastric tube to aspirate gastric contents after large, recent ingestion of caustics. The risk of worsening mucosal injury (including perforation) must be weighed against the potential benefit.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric emptying.
    b) AIRWAY PROTECTION: Alert patients - place in Trendelenburg and left lateral decubitus position, with suction available. Obtunded or unconscious patients - cuffed endotracheal intubation. COMPLICATIONS:
    1) Complications of gastric aspiration may include: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach (Vale, 1997). Combative patients may be at greater risk for complications.
    6.5.3) TREATMENT
    A) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    B) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Replace fluids lost with crystalloids; treat metabolic acidosis and hypocalcemia tetany if present.
    C) SUPPORT
    1) Relieve pain by parenteral opiates.
    2) Observe for gastric perforations and late complications such as pyloric stenosis.
    D) MONITORING OF PATIENT
    1) Observe for and provide symptomatic and supportive care to patients with anuria and liver damage.
    E) ENDOSCOPIC PROCEDURE
    1) The following recommendations are extrapolated from experience with ingestions of acids and/or alkaline corrosives.
    2) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
    3) INDICATIONS: Most studies associating the presence or absence of gastrointestinal burns with signs and symptoms after caustic ingestion have involved primarily alkaline ingestions. Because acid ingestion may cause severe gastric injury with fewer associated initial signs and symptoms, endoscopic evaluation is recommended in any patient with a definite history of ingestion of a strong acid, even if asymptomatic.
    4) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
    a) REFERENCES: Gaudreault et al, 1983; Symbas et al, 1983; Crain et al, 1984; (Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992; Nuutinen et al, 1994)
    5) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
    a) Advancing across the cricopharynx under direct vision
    b) Gently advancing with minimal air insufflation
    c) Never retroverting or retroflexing the endoscope
    d) Using a pediatric flexible endoscope
    e) Using extreme caution in advancing beyond burn lesion areas
    f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).
    6) GRADING
    a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding and perforation is related to the severity of the initial burn (Zargar et al, 1991):
    b) Grade 0 - Normal examination
    c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
    d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
    e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
    f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding may occur.
    g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.
    7) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    F) SUCRALFATE
    1) Sucralfate may be useful in relieving symptomatology from acid induced injury. Efficacy in accelerating healing or preventing complications has not been proven. Famotidine, omeprazole and sucralfate were administered in one case of gastric ulcer due to soldering flux ingestion. Improvement was seen by the fourth day of therapy and the patient was discharged (Michels et al, 1998).
    G) CORTICOSTEROID
    1) The use of steroids for the treatment of caustic ingestion is controversial. The following recommendations are extrapolated from experience with ingestions of acids and/or alkaline corrosives.
    2) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
    3) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
    4) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
    5) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
    6) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
    7) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
    8) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
    9) STUDIES
    a) ANIMAL
    1) Some animal studies have suggested that corticosteroid therapy may reduce the incidence of stricture formation after severe alkaline corrosive injury (Haller & Bachman, 1964; Saedi et al, 1973a).
    2) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
    3) Other studies have shown no evidence of reduced stricture formation in steroid treated animals (Reyes et al, 1974). An increased rate of esophageal perforation related to steroid treatment has been found in animal studies (Knox et al, 1967).
    b) HUMAN
    1) Most human studies have been retrospective and/or uncontrolled and generally involve small numbers of patients with documented second or third degree mucosal injury. No study has proven a reduced incidence of stricture formation from steroid use in human caustic ingestions (Haller et al, 1971; Hawkins et al, 1980; Yarington & Heatly, 1963; Adam & Brick, 1982).
    2) META ANALYSIS
    a) Howell et al (1992), analyzed reports concerning 361 patients with corrosive esophageal injury published in the English language literature since 1956 (10 retrospective and 3 prospective studies). No patients with first degree burns developed strictures. Of 228 patients with second or third degree burns treated with corticosteroids and antibiotics, 54 (24%) developed strictures. Of 25 patients with similar burn severity treated without steroids or antibiotics, 13 (52%) developed strictures (Howell et al, 1992).
    b) Another meta-analysis of 10 studies found that in patients with second degree esophageal burns from caustics, the overall rate of stricture formation was 14.8% in patients who received corticosteroids compared with 36% in patients who did not receive corticosteroids (LoVecchio et al, 1996).
    c) Another study combined results of 10 papers evaluating therapy for corrosive esophageal injury in humans published between January 1991 and June 2004. There were a total of 572 patients, all patients received corticosteroids in 6 studies, in 2 studies no patients received steroids, and in 2 studies, treatment with and without corticosteroids was compared. Of 109 patients with grade 2 esophageal burns who were treated with corticosteroids, 15 (13.8%) developed strictures, compared with 2 of 32 (6.3%) patients with second degree burns who did not receive steroids (Pelclova & Navratil, 2005).
    3) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
    4) Ferguson et al (1989) retrospectively compared 10 patients who did not receive antibiotics or steroids with 31 patients who received both antibiotics and steroids in a study of caustic ingestion and found no difference in the incidence of esophageal stricture between the two groups (Ferguson et al, 1989).
    5) A randomized, controlled, prospective clinical trial involving 60 children with lye or acid induced esophageal injury did not find an effect of corticosteroids on the incidence of stricture formation (Anderson et al, 1990).
    a) These 60 children were among 131 patients who were managed and followed-up for ingestion of caustic material from 1971 through 1988; 88% of them were between 1 and 3 years old (Anderson et al, 1990).
    b) All patients underwent rigid esophagoscopy after being randomized to receive either no steroids or a course consisting initially of intravenous prednisolone (2 milligrams/kilogram per day) followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks prior to tapering and discontinuation (Anderson et al, 1990).
    c) Six (19%), 15 (48%), and 10 (32%) of those in the treatment group had first, second and third degree esophageal burns, respectively. In contrast, 13 (45%), 5 (17%), and 11 (38%) of the control group had the same levels of injury (Anderson et al, 1990).
    d) Ten (32%) of those receiving steroids and 11 (38%) of the control group developed strictures. Four (13%) of those receiving steroids and 7 (24%) of the control group required esophageal replacement. All but 1 of the 21 children who developed strictures had severe circumferential burns on initial esophagoscopy (Anderson et al, 1990).
    e) Because of the small numbers of patients in this study, it lacked the power to reliably detect meaningful differences in outcome between the treatment groups (Anderson et al, 1990).
    6) ADVERSE EFFECTS
    a) The use of corticosteroids in the treatment of caustic ingestion in humans has been associated with gastric perforation (Cleveland et al, 1963) and fatal pulmonary embolism (Aceto et al, 1970).
    H) SURGICAL PROCEDURE
    1) In severe cases of gastrointestinal necrosis or perforation, emergent surgical consultation should be obtained. The need for gastric resection or laparotomy in the stable patient is controversial (Chodak & Passaro, 1978; Dilawari et al, 1984).
    2) LAPAROTOMY/LAPAROSCOPY - Early laparotomy or laparoscopy should be considered in patients with endoscopic evidence of severe esophageal or gastric burns after acid ingestion to evaluate for the presence of transmural gastric or esophageal necrosis (Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993). Emergent laparotomy should be strongly considered in any patient with hypotension, altered mental status, or acidemia (Hovarth et al, 1991).
    a) STUDY - In a retrospective study of patients with extensive transmural gastroesophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (endoscopy, steroids, antibiotics, and repeated evaluation for the occurrence of esophagogastric necrosis and perforation) died, while all 3 patients treated with early laparotomy and immediate esophagogastric resection survived (Estrera et al, 1986).
    b) Wu & Lai (1993) reported the results of emergency surgical resection of the alimentary tract in 28 patients who had extensive corrosive injuries due to the ingestion of acids or other caustics. Operative mortality was most frequently associated with sepsis. Non-fatal bleeding, infections, biliary or bronchial fistulas were other noted complications. Morbidity and mortality were related to the severity of the damage and the extent of surgery required.
    1) Immediate postoperative management included antibiotics, extensive respiratory care, tracheobronchial toilet, maintenance of fluid, electrolyte and acid-base balance, and jejunostomy feeding or total parenteral nutrition.
    I) CHELATION THERAPY
    1) NAC - Intravenous and nebulized acetylcysteine was used to increase the urinary excretion of zinc in two cases.
    2) CALCIUM EDTA
    a) In one pediatric case, a dose of 150 milligrams of calcium disodium edetate was dissolved in 75 milliliters of 1:5 normal saline and used to normalize an elevated serum zinc level.
    b) CASE REPORT - A 13-month-old male was given calcium disodium EDTA 180 milligrams (15 milligrams/kilogram) intravenously following accidental ingestion of 30 milliliters of a moss killer solution containing 13 percent zinc chloride.
    1) Serum zinc concentration decreased from 1,020 micrograms/deciliter prior to chelation to 145 micrograms/deciliter after chelation. A dramatic improvement in mental status was also noted (Hedtke et al, 1989).
    3) BAL/CALCIUM EDTA
    a) In a 16-month-old boy who swallowed soldering flux, chelation with calcium EDTA and BAL starting 75 hours postingestion was NOT effective in enhancing zinc clearance (McKinney et al, 1994). Blood zinc levels had declined from 1199 to 160 micrograms/deciliter prior to chelation and decreased only from 160 to 87 micrograms/deciliter after chelation. BAL (3 milligrams/kilogram every 6 hours) and calcium EDTA (1 gram/square meter) were given daily divided into 4 doses for 5 days.
    b) A 49-year-old man presented with abdominal pain, hoarseness, and intermittent hematemesis after intentionally ingesting 360 milliliters of liquid soldering flux containing 25% zinc chloride (43.1 grams). Thirty-six hours post-ingestion and after repeated hemodialysis sessions, the patient's serum zinc level peaked at 2,430 micrograms/deciliter. Combined administration of BAL-EDTA and continuous hemodialysis reduced his serum zinc level, within 6 days, to 193 micrograms/deciliter. Clinically, the patient stabilized, but died on day 33 due to complications associated with gastric perforation (Mendelsohn et al, 1997).
    4) BAL - Dimercaprol (BAL) was administered intramuscularly (4 mg/kg) to a 21-month-old boy following ingestion of an unknown quantity of zinc chloride solution. Within 30 minutes of the chelator, dramatic improvement in his mental status was observed. Zinc serum levels prior to BAL were reported to be 1014 mcg/dL. Twenty-four hours after the ingestion, levels decreased to 203 mcg/dL (De Groote et al, 1998). Zinc clearance during or before chelation was not determined.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    8) ACUTE RESPIRATORY DISTRESS SYNDROME: A 23-year-old man developed acute respiratory distress syndrome after inhalational exposure to zinc chloride from a smoke grenade for 10 to 15 minutes. Initially, he presented with a sore throat, dry cough, and chest pain. He later developed dyspnea, fever, and a productive cough after admission. A chest radiograph revealed bilateral consolidations, subcutaneous emphysema, pneumomediastinum, and pneumothorax. On day 4, he was severely hypoxemic despite mechanical ventilation and bilateral tube thoracostomy. He was treated with high-dose corticosteroids (hydrocortisone and methylprednisolone) and extracorporeal life support (ECLS) and his symptoms improved. ECLS was discontinued on day 6 and systemic corticosteroids dose was gradually tapered. Despite continued intensive supportive therapy, his condition deteriorated on day 16. Once again, his symptoms improved gradually following treatment with corticosteroids and ECLS. He gradually recovered and was discharged on day 176 (Chian et al, 2010).
    B) CORTICOSTEROID
    1) In two patients exposed to zinc chloride from a smoke bomb, steroids were given prophylactically. There were no symptoms for 10 days, but the patients eventually developed pulmonary vascular lesions and adult respiratory distress syndrome (ARDS). The steroids may have delayed but not prevented the development of ARDS.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) EDETATE DISODIUM
    1) The efficacy and safety of edetate disodium in the treatment of zinc chloride eye (exposure) injury have yet to be demonstrated. However, zinc chloride eye injury has been treated by edetate disodium.
    a) The eye should first be irrigated with water as quickly as possible, then irrigated with 1.7% (or 0.5 molar) edetate disodium solution for 15 minutes (Johnstone et al, 1973).
    b) Unless treatment is started within 2 minutes, it may be ineffective.
    c) Edetate disodium itself is toxic to the corneal stroma, so only the minimum amount necessary should be used. Avoid over-application.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) BURN
    1) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    2) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    3) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    4) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) HEMODIALYSIS
    1) A 49-year-old man presented with abdominal pain, hoarseness, and intermittent hematemesis after intentionally ingesting 360 milliliters of liquid soldering flux containing 25% zinc chloride (43.1 grams). Despite repeated hemodialysis sessions, the patient's serum zinc level peaked at 2,430 micrograms/deciliter; however, combined administration of BAL-EDTA and continuous hemodialysis reduced his serum zinc level, within 6 days, to 193 micrograms/deciliter. Clinically, the patient stabilized, but died on day 33 due to complications associated with gastric perforation (Mendelsohn et al, 1997).

Abstracts

Case Reports

    A) INFANT
    1) A 13-month-old child accidentally ingested 30 mL of a moss killer solution containing 13 percent zinc chloride.
    a) The child developed spontaneous vomiting, erythematous uvula, lethargy, somnolence, frequent premature atrial beats, hyperglycemia, elevated alkaline phosphatase, oliguria, hyperamylasemia, and a large superficial burn to the greater curvature of the stomach.
    b) He was treated with intravenous fluids and 15 milligrams/kilogram of calcium disodium EDTA. His mental status improved dramatically and he was discharged after a day of additional observation (Hedtke et al, 1989).
    2) Severe burns, metabolic acidosis, lethargy, hypertension, hepatic damage, and hyperamylasemia were seen in a 16-month-old boy who ingested liquid soldering flux containing zinc chloride and ammonium chloride. Chelation therapy with dimercaprol and EDTA did not increase urinary excretion of zinc. Recovery was apparently complete after an antrectomy necessitated by scarring (McKinney et al, 1994).
    B) ADULT
    1) Two soldiers were exposed for a short time to high concentrations of zinc chloride in a smoke bomb. Initially they were asymptomatic, but were given steroids prophylactically. After 10 days, they both unexpectedly developed severe respiratory distress syndrome with pulmonary hypertension (Homma et al, 1992).
    a) Mechanical ventilation was required at the 12th day postexposure in one and the 15th day postexposure in the other. Despite supportive care, one died on day 25, the other on day 32.
    b) The lungs showed extensive interstitial and intra-alveolar space fibrosis. The blood vessels showed significant lumen reduction by contracture. Microvessels showed obliteration and widespread occlusion by endothelial cell proliferation and clots. There was no evidence of infection.
    c) The reason for the delay until symptom onset is unknown. It may have been that the steroids given prophylactically delayed, but did not prevent the injury.
    d) Nebulized acetylcysteine was used to increase plasma zinc excretion and worked for a short time. L-3,4 dehydroproline was given to arrest collagen deposition in the lungs (Hjorts et al, 1988).
    2) A firefighter was exposed to a high, unknown concentration of zinc chloride from a smoke generator. He arrived at the hospital with complaints of nausea, chest tightness, and sore throat. Initial improvement was seen, followed by substernal soreness, fever, cyanosis, tachypnea, and eventually coma.
    a) Auscultation indicated clear lung fields, although chest x-rays showed diffuse pulmonary infiltrates. The patient died 18 days post exposure. Autopsy showed active fibroblastic proliferation and cor pulmonale (Milliken et al, 1963).
    C) PEDIATRIC
    1) A 13-month-old child accidentally ingested 30 milliliters of a moss killer solution containing 13% zinc chloride and developed spontaneous vomiting, erythematous uvula, lethargy, somnolence, frequent premature atrial beats, hyperglycemia, elevated alkaline phosphatase, oliguria, hyperamylasemia, and a large superficial burn to the greater curvature of the stomach. He was treated with intravenous fluids and 15 milligrams/kilogram of calcium disodium EDTA. His mental status improved dramatically and he was discharged after a day of additional observation (Hedtke et al, 1989a).

Range Of Toxicity

Summary

    A) Minimum lethal human exposure is unknown.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    B) ROUTE OF EXPOSURE
    1) Deaths were reported after inhalation of high concentrations of zinc chloride smoke of unknown origin (Evans, 1945; Milliken et al, 1963).
    2) Workplace exposure to zinc chloride fume concentrations of 50 milligrams per cubic meter or greater are believed to be immediately dangerous to life or health (NIOSH , 1994).
    3) Exposure to 50,000 milligrams per cubic meter or greater have caused severe respiratory tract effects and may cause fatal shock or pulmonary edema (Karlsson, 1988).
    4) ORAL - A 49-year-old man developed severe metabolic acidosis, electrolyte abnormalities, hematemesis, hematochezia, renal failure and ARDS after intentionally ingesting 360 mL of a liquid soldering flux that contained 25% zinc chloride (43.1 grams). Clinically, the patient stabilized following combined administration of chelating agents and continuous hemodialysis; however, he died approximately 1 month post-ingestion due to complications associated with gastric perforation (Mendelsohn et al, 1997).

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) INGESTION
    a) PEDIATRIC - A 13-month-old accidentally ingested 30 milliliters of a moss killer solution containing 68% zinc chloride.
    1) The child developed spontaneous vomiting, erythematous uvula, lethargy, somnolence, frequent premature atrial beats, hyperglycemia, elevated alkaline phosphatase, oliguria, hyperamylasemia, and a large superficial burn to the greater curvature of the stomach.
    2) He was treated with intravenous fluids and 15 milligrams/kilogram of calcium disodium EDTA. His mental status improved dramatically and he was discharged after a day of additional observation (Hedtke et al, 1989).
    b) ADULT - A 39-year-old man presented with abdominal pain and vomiting after ingesting 30 mL of soldering fluid containing 30% to 60% zinc chloride and 10% ammonium chloride (pH 3.9) in a suicide attempt. All laboratory results were normal, except for hyperamylasemia (240 mg/L). Initially, he developed a candidal infection of the oral cavity requiring nystatin and fluconazole therapy, but his recovery was complicated with aspiration pneumonia. On day 21, he complained of worsening dysphagia and vomiting. An esophagogastroduodenoscopy revealed widespread inflammation and ulceration, and stenosis of the pylorus. After a gastric stricture was identified, he underwent successful laparoscopic Roux-en-y gastrojejunostomy. He recovered gradually and was discharged 9 days after surgery (Tayyem et al, 2009).
    2) INHALATION
    a) TCLo (INHL) HUMAN - 4800 milligrams per meter squared

Serum Plasma Blood Concentrations

    7.5.1) THERAPEUTIC CONCENTRATIONS
    A) THERAPEUTIC CONCENTRATION LEVELS
    1) GENERAL
    a) NORMAL THERAPEUTIC ZINC LEVELS IN BLOOD - 68 to 136 mcg percent
    b) Normal range for serum zinc is reported to be 80 to 130 micrograms/deciliter (De Groote et al, 1998).
    c) NORMAL LEVELS IN CSF - 0.02 to 0.06 mg/kg/liter.
    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) The serum zinc concentration was 1,420 micrograms/deciliter at one hour postingestion in a 13-month-old who ingested 30 milliliters of a 13 percent solution (Hedtke et al, 1989).
    b) Serum zinc was reported to be 1014 micrograms/deciliter approximately 4 hours following an accidental ingestion of an unknown amount of zinc chloride solution (De Groote et al, 1998).
    c) A serum zinc level of 2,430 micrograms/deciliter was reported in a 49-year-old man, 36 hours following intentional ingestion of 360 milliliters of liquid soldering flux containing 25% zinc chloride (43.1 grams), and after repeated hemodialysis (Mendelsohn et al, 1997).

Workplace Standards

    A) ACGIH TLV Values for CAS7646-85-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Zinc chloride fume
    a) TLV:
    1) TLV-TWA: 1 mg/m(3)
    2) TLV-STEL: 2 mg/m(3)
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): LRT and URT irr
    d) Molecular Weight: 136.29
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS7646-85-7 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Zinc chloride fume
    2) REL:
    a) TWA: 1 mg/m(3)
    b) STEL: 2 mg/m(3)
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 50 mg/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7646-85-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Zinc chloride fume
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (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): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Zinc chloride fume
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7646-85-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Zinc chloride fume
    2) Table Z-1 for Zinc chloride fume:
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 1
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) TCLo- (INHALATION)HUMAN:
    1) 4800 mg/m(2)

Pharmacology Toxicology

Toxicologic Mechanism

    A) Zinc is an irritant/caustic, depending on the concentration and duration of exposure.

Physicochemical

Physical Characteristics

    A) Odorless (JEF Reynolds , 1992)
    B) Zinc chloride is a white, odorless, deliquescent, crystalline powder or granule (JEF Reynolds , 1992).

Ph

    A) 4.6-5.5 (approximately 10% solution in water) (JEF Reynolds , 1992)
    B) 1.5-2.5 (USP injection) (JEF Reynolds , 1992)

Molecular Weight

    A) 136.3

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