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 and welding and in nickel-cadmium batteries. 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 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).
Inhalation. The ACGIH-recommended threshold limit value (TLV-TWA) for air exposure to Cd dusts and fumes is 0.01 (inhalable fraction) to 0.002 (respirable dusts) mg/m3 as an 8-hour time-weighted average. Exposure to 5 mg/m3 inhaled for 8 hours may be lethal. The level considered immediately dangerous to life or health (IDLH) for Cd dusts or fumes is 9 mg of Cd per cubic meter.
Ingestion. Cd salts in solutions at concentrations greater than 15 mg/L may induce vomiting. The lethal oral dose ranges upward from 150 mg.
Water. The US Environmental Protection Agency has established a safe limit of 0.005 mg/L in drinking water.
Direct contact may cause local skin or eye irritation. There are no data on dermal absorption of Cd in humans.
Acute inhalation may cause cough, dyspnea, headache, fever, and, if severe, chemical pneumonitis and noncardiogenic pulmonary edema within 12–36 hours after exposure.
Chronic inhalation may result in bronchitis, emphysema, and fibrosis. Chronic inhalation at high levels is associated with lung cancer (IARC 2000).
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.
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).
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.
Other useful laboratory studies include CBC, electrolytes, glucose, BUN, creatinine, arterial blood gases ...