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Introduction

Cadmium (Cd) is found in sulfide ores, along with zinc and lead. Exposure is common during the mining and smelting of zinc, copper, and lead. The metallic form of Cd is used in electroplating because of its anticorrosive properties, the metallic salts are used as pigments and stabilizers in plastics, and Cd alloys are used in soldering, welding, nickel-cadmium batteries, and photovoltaic cells. Cd solder in water pipes and Cd pigments in pottery can be sources of contamination of water and acidic foods.

Mechanism of Toxicity

Inhaled Cd is at least 60 times more toxic than the ingested form. Fumes and dust may cause delayed chemical pneumonitis and resultant pulmonary edema and hemorrhage. Ingested Cd, at very high levels, is a GI tract irritant. Once absorbed, Cd is bound to metallothionein and filtered by the kidney, where renal tubule damage may occur. Cd is a known human carcinogen (IARC Group 1).

Toxic Dose

  1. Inhalation. The ACGIH-recommended threshold limit value (TLV) for air exposure to Cd dusts and fumes is 0.01 (total dusts) to 0.002 (respirable dusts) mg/m3 as an 8-hour time-weighted average (TWA). The OSHA permissible exposure limit (PEL) is 0.005 mg Cd/m3 TWA. The level considered immediately dangerous to life or health (IDLH) for Cd dusts or fumes is 9 mg/m3.
  2. Ingestion. The emetic threshold of Cd salts in water is estimated to be 15 mg/L. The lethal oral dose is estimated to be 20 mg Cd/kg.
  3. Water. The US Environmental Protection Agency has established a safe limit of 0.005 mg/L in drinking water.

Clinical Presentation

  1. Direct contact may cause local skin or eye irritation. There is no data on dermal and ocular absorption of Cd in humans.
  2. Acute inhalation may cause cough, dyspnea, headache, fever, and, if severe, chemical pneumonitis and noncardiogenic pulmonary edema within 12-36 hours after exposure.
  3. Chronic inhalation may result in bronchitis, emphysema, and fibrosis. Chronic inhalation at high levels is associated with lung cancer (IARC 2000).
  4. Acute ingestion of Cd salts causes nausea, vomiting, abdominal cramps, and diarrhea, sometimes bloody, within minutes after exposure. Deaths after oral ingestion result from shock or acute renal failure.
  5. Chronic ingestion has been associated with kidney damage and skeletal system effects. Environmental contamination of food and water in Japan's Jinzu River basin in the 1950s resulted in an endemic painful disease called itai-itai (“ouch-ouch”).

Diagnosis

Is based on a history of exposure and the presence of respiratory complaints (after inhalation) or gastroenteritis (after acute ingestion).

  1. Specific levels. Whole-blood Cd levels may confirm recent exposure; normal levels, in unexposed nonsmokers, are less than 1 mcg/L. Very little Cd is excreted in the urine until binding of Cd in the kidney is exceeded or renal damage occurs. Urine Cd values are normally less than 1 mcg/g of creatinine. Measures of tubular microproteinuria (beta2-microglobulin, retinol-binding protein, albumin, and metallothionein) are used to monitor the early and toxic effects of Cd on the kidney.
  2. Other useful laboratory studies include CBC, electrolytes, glucose, BUN, creatinine, arterial blood gases or oximetry, and chest radiography.

Treatment

  1. Emergency and supportive measures
    1. Inhalation. Monitor arterial blood gases and obtain chest radiograph. Observe for at least 6-8 hours and treat wheezing and pulmonary edema if they occur. After significant exposure, it may be necessary to observe for 1-2 days for delayed-onset noncardiogenic pulmonary edema.
    2. Ingestion. Treat fluid loss caused by gastroenteritis with IV crystalloid fluids.
  2. Specific drugs and antidotes. There is no evidence that chelation therapy is effective, although various chelating agents have been used following acute overexposure. BAL, penicillamine, and EDTA are contraindicated owing to the increased risk for renal damage.
  3. Decontamination
    1. Inhalation. Remove the victim from exposure and give supplemental oxygen if available.
    2. Ingestion. Perform gastric lavage after significant ingestion. The effectiveness of activated charcoal is unknown.
    3. Skin and eyes. Remove contaminated clothing and wash exposed skin with water. Irrigate exposed eyes with copious amounts of tepid water or saline.
  4. Enhanced elimination. There is no role for dialysis, hemoperfusion, or repeat-dose charcoal.