Chromium toxicity

Background

• Blue white metal
• Essential in glucose and fat metabolism
• The predominant forms are trivalent (Cr³⁺) and hexavalent (Cr⁶⁺)
• Cr⁶⁺ is a carcinogen
• Uses
  • Chrome platting
  • Component of making stainless steel
  • Used to make cement
  • Welding
  • Joint arthroplasty
  • Coronary artery stents
  • Tanned leather products

Toxicokinetics

Form	Toxicity	Absorption	Distribution	Elimination
Cr3+	Rarely develops toxicity	Limited oral absorption with 98% recovered in feces		Urinary excretion
Cr6+	Main cause of toxicity Oxidative agent producing oxidative DNA damage	Modestly absorbed 10% orally 50-85% inhalational	50% total body burden is localized to the kidney and liver With additional stores in bone marrow, lymph nodes, spleen, and testes	Cr6+ is rapidly converted to Cr3+ in the blood

Clinical Features

Acute

• Similar to corrosive metal ingestions
• Gastrointestinal bleeding
• Vomiting
• Bowel perforation
• Intravascular hemolysis with DIC
• Acute tubular necrosis and Renal failure
• Metabolic acidosis
• Hyperkalemia
• Acute lung injury
• Skin inflammation and ulcerations
  • Dermal chromic acid (H₂CrO₄) can lead to systemic toxicity with as little as 10% BSA

Chronic

• Most are occupational inhalation exposures
• Chrome holes
  • Nasal septal perforation
  • Skin ulcerations
• Chronic cough
• Dyspnea and bronchospasm
• Anaphylactoid-like reactions
• Pneumoconicosis
• Increase risk of lung cancer
  • Small cell lung cancer, however all types are associated with Cr⁶⁺ exposure
• Contact dermatitis and Type IV hypersensitivity reaction

Background

Heavy metal toxicity results from exposure to metals like lead, mercury, arsenic, or cadmium, which interfere with cellular function. Exposure may occur occupationally, environmentally, through ingestion, or from alternative medicines. Chronic toxicity can present insidiously, while acute toxicity may mimic sepsis or encephalopathy. Diagnosis is often delayed due to nonspecific symptoms.

Clinical Features

Symptoms depend on the metal and exposure duration but may include:

Neurologic: Peripheral neuropathy, confusion, tremor, encephalopathy

GI: Abdominal pain, nausea, vomiting, diarrhea, anorexia

Heme: Anemia (especially microcytic or hemolytic), basophilic stippling (lead)

Renal: Tubular dysfunction, proteinuria, Fanconi syndrome

Dermatologic: Mees’ lines (arsenic), hyperpigmentation, hair loss

Others: Fatigue, weight loss, hypertension (cadmium), immunosuppression

Differential Diagnosis

Sepsis or systemic inflammatory response

Drug toxicity or overdose

Metabolic disorders (e.g., porphyria, uremia)

Psychiatric illness (if symptoms are vague or bizarre)

Neurologic diseases (e.g., Guillain-Barré, MS, Parkinson’s)

Vitamin deficiencies (e.g., B12, thiamine)

Evaluation

Workup

History: Occupational exposures, home remedies, hobbies (e.g., jewelry making, battery recycling), diet, water source, imported goods

Labs:

• CBC, CMP, urinalysis
• Blood lead level, serum/urine arsenic, mercury, or cadmium (based on suspicion)
• Urine heavy metal screen (note: spot testing may require creatinine correction)

Imaging: Abdominal X-ray (radiopaque material in GI tract, especially with lead)

EKG: Evaluate for QT prolongation or arrhythmias in severe cases

Diagnosis

Confirmed by elevated blood or urine levels of the specific metal in the context of clinical findings. Hair and nail testing are unreliable for acute toxicity. Interpret results with toxicologist input if possible.

Management

Remove the source of exposure (e.g., occupational control, GI decontamination if recent ingestion)

Supportive care: IV fluids, seizure control, electrolyte repletion

Chelation therapy (in consultation with toxicology or Poison Control):

Lead: EDTA, dimercaprol (BAL), succimer

Mercury/arsenic: Dimercaprol or DMSA

Cadmium: No effective chelation—focus on supportive care

Notify local public health authorities if exposure source is environmental or occupational

Disposition

Admit if symptomatic, unstable, or requiring chelation

Discharge may be appropriate for asymptomatic patients with low-level exposure and outpatient follow-up

Arrange toxicology or environmental medicine follow-up for source control and serial testing

See Also

• Aluminum toxicity
• Antimony toxicity
• Arsenic toxicity
• Barium toxicity
• Bismuth toxicity
• Cadmium toxicity
• Chromium toxicity
• Cobalt toxicity
• Copper toxicity
• Gold toxicity
• Iron toxicity
• Lead toxicity
• Lithium toxicity
• Manganese toxicity
• Mercury toxicity
• Nickel toxicity
• Phosphorus toxicity
• Platinum toxicity
• Selenium toxicity
• Silver toxicity
• Thallium toxicity
• Tin toxicity
• Zinc toxicity

Evaluation

• BMP
• LFTs
• CBC
• CPK
• EKG
• If toxicity present add coagulation factors

Chromium levels

Baseline levels have varied over the past 50 years by 5000-fold, additionally it is difficult to establish standard reference range, use caution when interpreting these levels; phlebotomy needles and blood containers for storage can contain chromium

• Whole blood: 20-30 μg/L (380-580 nmol/L)
• Serum: 0.05-2.86 μg/L (1-56 nmol/L)
• Urine: < 1μg/g creatinine (<19.2 nmol/g creatinine)
  • Can reflect acute absorption of chromium over the past 1-2 days, however wide variation in metabolism and total body burden

Management

• Decontamination
  • Activated charcoal not indicated
  • Consider NG lavage if Cr⁶⁺ ingestion and presenting within 1-2 hours without signs of vomiting
  • Consider oral N-acetylcysteine
    • Shown to increases renal elimination of chromium in rats
• Supportive care
• Chelation
  • Not effective in reducing chromium levels
• Dialysis
  • Not effective in those with normal renal function
  • Consider in those on chronic dialysis

Disposition

• Acute toxicity likely requires intensive care unit
• Consult Toxicology or poison control

See Also

• Toxicology (main)
• Heavy Metals

References

• Bird, S. Chromium. In: Goldfrank's Toxicologic Emergencies. 9th Ed. New York: McGraw-Hill; 2011: 1243-1247