Toxicology – Cadmium Poisoning

Source

Cadmium exposure is usually occupational and may occur during:

• Welding
• Soldering
• Electroplating
• Mining and smelting of zinc, copper, or lead

Other possible sources include nickel–cadmium batteries, ceramic pigments and glazes, and some metal-containing consumer products.

Typical Presentation

A worker exposed to cadmium fumes may initially develop a flu-like illness several hours later, with fever, chills, muscle aches, and dry cough. Despite an initially mild examination, severe lung injury can develop later.

Clinical Features

Inhaled cadmium is particularly dangerous because it can cause delayed pulmonary toxicity.

Acute inhalation may lead to:

• Fever and chills
• Myalgia
• Dry cough
• Shortness of breath
• Chemical pneumonitis
• Pulmonary edema
• Acute respiratory distress syndrome (ARDS)
• Respiratory failure

The early flu-like syndrome is sometimes called the “cadmium blues.”

Acute ingestion may cause severe gastrointestinal irritation and injury.

Chronic Toxicity

Long-term exposure may cause:

• Renal tubular dysfunction
• Bone disease, including osteomalacia
• Neurologic abnormalities
• Increased cancer risk

Mechanism of Action

Cadmium is a toxic metal that binds to cellular proteins and interferes with normal enzyme and cellular functions. It also promotes oxidative injury.

The protein metallothionein can bind cadmium and reduce its immediate toxicity, but cadmium–metallothionein complexes can accumulate in the kidneys and contribute to chronic renal injury.

Management

Treatment is primarily supportive:

• Immediate removal from exposure
• Respiratory support as needed
• Monitoring for delayed pulmonary edema and ARDS
• Renal and electrolyte monitoring

There is no well-established chelation therapy for cadmium poisoning, and some chelators may worsen toxicity. Management should involve a medical toxicologist or poison center.

Key Points

• Inhalation of cadmium fumes can cause delayed, severe lung injury.
• Early symptoms may resemble metal fume fever but can progress to respiratory failure.
• Chronic exposure primarily damages the kidneys and bones.
• BAL (dimercaprol) is generally avoided because it may increase renal toxicity.
• Significant suspected exposure warrants careful observation because pulmonary deterioration may be delayed.