Tin toxicity
Background
- True tin toxicity is rare, as tin is poorly absorbed in the GI tract (<5%)
- Inorganic tin does not cross blood-brain barrier
- Information on effects of toxicity based primarily on animal/in vitro studies and extrapolation from other heavy metals
Clinical Features
- Inhalation of tin chloride may cause irritation of mucous membranes
- Occupational exposure to tin oxide has be reported to be associated with a benign pneumoconiosis, stannosis
- Not associated with fibrosis or loss of pulmonary function
- Eating canned food from unlacquered tin cans may cause mild GI upset due to irritation from unabsorbed tin
Differential Diagnosis
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
Management
- Stop exposure
- Decontaminate if topical exposure
- Role of chelation not established