Industrial Agents


Hydrogen Fluoride

Hydrogen Fluoride
Hydrogen fluoride (HF, hydrofluoric acid) is a water soluble gas that is most commonly encountered as a solution. HF is encountered commonly in rust removers, oven cleaners, and automotive wheel cleaners. Commercial uses include glass etching, graffiti removal, and manufacture of semiconductors and certain fuels.

MECHANISM/TOXICITY

  • Absorbed through skin and mucous membranes → free fluoride ion avidly binds extracellular Ca++ and Mg+ → pain
  • Systemic hypocalcemia and hypomagnesemia may occur with ingestion or heavy dermal exposure.
  • Hyperkalemia may be delayed in onset due to cellular breakdown, acidosis and direct fluoride effects on K+ efflux.
  • HF is a weak acid and exposure to low-concentration (< 10%) solutions does not produce caustic injury.
  • High-concentration solutions can produce direct tissue injury similar to other strong acids.

SYMPTOMS/EXAM

  • There is a direct relationship between solution concentration and symptom
    onset.
    • Concentrated solutions produce symptoms earlier.
    • Onset can be delayed up to 24 hours after exposure to a dilute solution.
  • Dermal exposure to low concentrations:
    • Local pain, erythema, swelling, and a white-blue discoloration (especially
      subungual)
    • Pain “out of proportion” to skin findings
  • Oral ingestion or large dermal exposure to concentrated solutions:
    • Local pain of direct tissue injury
    • Systemic hypocalcemia → tetany, weakness, Chvostek’s sign, dysrhythmias, and sudden death.

DIAGNOSIS

  • Usually determined from the patient’s history and examination
  • ECG findings with severe hypocalcemia include prolonged QT interval and peaked T waves.
  • Direct measurement of total or ionized Ca++ confirms severe toxicity.

TREATMENT

  • Copious water irrigation for surface decontamination
  • Calcium Gluconate administration (to bind fluoride ions):
    • Topical paste
    • Subcutaneous and intradermal injections
    • Regional intraarterial infusion
    • Nebulized (for inhalation exposure)
  • Systemically ill patients should be monitored carefully and aggressively treated with intravenous calcium.
  • AVOID calcium chloride injection, which can cause skin necrosis.
Onset of symptoms from dermal exposure to low concentrations of HF may be delayed up to 24 hours

Calcium Gluconate paste, injection, and arterial infusions are key to treating ongoing pain and toxicity from dermal HF exposure.

Lead Toxicity

Lead
Lead is a heavy metal used extensively in commercial products and manufacturing processes. Adult lead exposure is primarily occupational (construction, mining, welding, smelting, manufacture of batteries, plastic and rubber, “moonshine”). Pediatric exposure usually results from accidental ingestion of lead-containing material, especially paint chips.

Most lead toxicity is due to chronic, low-level exposure. Acute toxicity from single exposures is rare.

MECHANISM/TOXICITY
  • Inhibits a wide variety of cellular enzymes
  • Directly damages peripheral nerves

SYMPTOMS/EXAM

  • Chronic lead toxicity produces subtle, insidious, and nonspecific symptoms, including headache, peripheral motor neuropathy, HTN, anemia, gout, and cognitive impairment.
  • Acute lead toxicity
    • Nausea/vomiting, abdominal pain
    • Ataxia
    • Encephalopathy and seizures

DIAGNOSIS

  • Diagnosis of lead toxicity requires a high index of suspicion.
  • Lead can be directly measured in whole blood.
  • Ingested lead-containing material is usually visible on X-ray.

TREATMENT

  • Remove the patient from the source of exposure.
  • Activated charcoal does not bind metals.
  • Whole-bowel irrigation is indicated in cases of lead ingestion with visible material on X-ray.
  • Antidote = BAL (British anti-lewisite, dimercaprol) and Ca-EDTA (calcium disodium ethylenediaminetetraacetic acid).
    • Use for the severely poisoned patient or level > 70 μG/dL
    • Both are parenteral chelating agents.
  • DMSA (2,3-dimercaptosuccinic acid, succimer) oral chelation therapy if no acute symptoms and level < 70 μG/dL
Indications for immediate IV chelation therapy (BAL and Ca-EDTA) in lead toxicity = level ≥70 ug/dL or the presence of symptoms.

Arsenic Toxicity

Arsenic
Arsenic-containing compounds are used in a wide variety of applications:
  • Pesticides, wood preservatives, metal alloys, chemical synthesis, and glass manufacturing
  • Arsenic trioxide is used as a chemotherapeutic agent for acute promyelocytic leukemia.

MECHANISM/TOXICITY

  • Inhibits multiple key enzymes in cellular oxidative metabolism
  • Arsine gas causes acute hemolysis by an unknown mechanism.

SYMPTOMS/EXAM

  • Chronic poisoning
    • Peripheral neuropathy, headache, ataxia, confusion
    • Diarrhea, constipation
    • Hyperpigmentation, Mees’ lines (transverse white lines on nails), alopecia, various rashes
    • Malaise, anorexia, fatigue
  • Acute poisoning
    • GI symptoms predominate: Violent gastroenteritis
    • Confusion, coma, seizures
    • Hypotension, tachycardia, prolonged QT interval, dysrhythmias
    • ARDS-like syndrome
  • Arsine gas poisoning
    • Findings consistent with acute hemolysis:
      • Hematuria, jaundice, renal failure
    • Abdominal pain, N/V
    • Hypotension, tachycardia, pulmonary edema

DIAGNOSIS

  • Suspect based on clinical presentation and possible exposure.
  • Blood or 24-hour urine arsenic levels
    • Levels may be elevated following consumption of seafood because of the presence of nontoxic, organic arsenic compounds.
  • Ingested arsenic-containing material is usually visible on X-ray.

TREATMENT

  • In chronic poisoning cases, identify and remove the source of arsenic exposure.
  • Whole-bowel irrigation: If radiopaque objects visible on X-ray
  • Antidote = BAL (British anti-lewisite, dimercaprol)
    • In cases of severe, acute toxicity
  • DMSA (2,3-dimercaptosuccinic acid, succimer)
    • In cases of chronic poisoning
  • Arsine gas toxicity does not usually require chelation.
Mee’s lines appear weeks to months after arsenic exposure

Acute arsenic exposure is characterized by violent gastroenteritis.

Mercury Toxicity

Mercury
Mercury is pervasive in industrial processes and commercial products. It is encountered in three forms:
  • Elemental mercury (quicksilver): Mercury-containing devices in workplace or home
  • Inorganic mercury salts: Disk batteries
  • Organic mercury: Occupational/agricultural exposure

Each form of mercury has differing toxicity. Elemental mercury primarily causes toxicity when inhaled, while the principal route of exposure for mercury salts and organic mercury is through GI absorption.

MECHANISM/TOXICITY

  • Inhibition of multiple cellular enzyme systems
  • Inhalation of elemental mercury may lead to severe pneumonitis.

SYMPTOMS/EXAM

  • Elemental mercury (quicksilver) inhalation: Rapid onset of shortness of breath, cough, chills, fever, respiratory distress
  • Acute ingestion of inorganic mercury: Corrosive gastroenteritis with shock (from massive fluid loss), renal failure, grayish discoloration of mucous membranes, metallic taste
  • Acute ingestion of organic mercury: Characterized by delayed (and permanent) neurotoxicity—ataxia, dysarthria, constricted visual fields
  • GI symptoms and dermatitis may occur acutely.

DIAGNOSIS

  • Based on presenting symptoms and history of exposure
  • Mercury can be measured in whole blood or urine.
  • Ingested mercury-containing material is usually visible on X-ray.

TREATMENT

  • Whole-bowel irrigation: If radiopaque objects visible on X-ray
  • Antidote = BAL (British anti-lewisite, dimercaprol) or DMSA (2,3-dimercaptosuccinic acid) for symptomatic patients
Elemental mercury (inhaled) → Respiratory distress.
Inorganic mercury (ingested) → Severe corrosive gastroenteritis.
Organic mercury (ingested) → Delayed neurotoxicity