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DESCRIPTION
Cadmium is a metal used in a variety of occupations (by jewelers, painters, and welders) and industries (battery manufacturing, paint and glaze manufacturing, electroplating, mining, and smelting, among others).
TOXIC DOSE
- Death has occurred following ingestion of solutions containing more than 25 mg/L; recovery has been reported after ingestion of liquid containing 16 mg/L cadmium.
- Cadmium is an International Agency for Research on Cancer I carcinogen.
PATHOPHYSIOLOGY
- Ingestion of cadmium may cause marked local gastrointestinal irritation and hemorrhage, with only a small amount of systemic absorption.
- Inhalation primarily causes irritation of respiratory system (see SECTION IV, Cadmium Fume Fever chapter).
- Kidney and liver injury may develop from substantial exposure by either oral or inhalational routes.
- Toxic effects following exposure are typically mild, with death occurring rarely following acute cadmium pneumonitis or chronic renal failure.
EPIDEMIOLOGY
- Poisoning is uncommon.
- Approximately 500,000 workers in the United States may be exposed to cadmium on the job.
CAUSES
Accidental occupational exposure is most frequent.
RISK FACTORS
- Impaired renal function or poor renal perfusion (as in congestive heart failure).
- Tobacco smoking increases cadmium levels.
PREGNANCY
- Possible decreased birth weight has been reported.
- Cadmium crosses the placenta; however, teratogenic effects have not been observed in humans.
WORKPLACE STANDARDS
- ACGIH. TLV TWA is 0.01 mg/m3.
- OSHA. PEL: fume is 0.1 mg/m3; dust is 0.2 mg/m3.
- NIOSH. IDLH is 9 mg/m2.
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DIFFERENTIAL DIAGNOSIS
- Toxicologic causes of renal failure include heavy metals, radiographic contrast media, and analgesic papillary necrosis.
- Nontoxicologic causes of chronic renal disease include infection, diabetes, hypertension, and Fanconi syndrome.
SIGNS AND SYMPTOMS
- Acute poisoning reflects the pathway of exposure.
- Acute life-threatening pneumonitis results from inhalation of cadmium fumes.
- Acute gastrointestinal effects result from ingestion.
- Chronic exposure results in renal insufficiency.
Vital Signs
Tachycardia and hypotension may occur in severe cases.
Tachypnea and tachycardia may occur due to renal insufficiency.
HEENT
Chronic poisoning may result in yellow rings on the teeth; neck and facial edema, and salivation.
Dermatologic
Irritation may occur acutely.
Pulmonary
- Acute. Cadmium fume fever may occur.
- Chronic. Bronchitis, emphysema, or fibrosis may occur.
Cardiovascular
Development of hypertension during chronic exposure is a controversial topic; hypertension may be secondary to renal injury.
Gastrointestinal
- Acute. Salivation, vomiting, irritation of the mucosa, and increased bowel sounds and cramping may occur.
- Hemorrhagic gastroenteritis can occur in severe cases.
Hepatic
Liver enzyme elevation may occur.
Renal
- Acute. Flank pain and proximal tubular necrosis leading to acute tubular necrosis may occur in severe cases.
- Chronic. Proteinuria, aminoaciduria, glycosuria may occur.
Musculoskeletal
- Bone pain (Itai-Itai disease) and weakness may occur in chronic cases.
- Osteomalacia and osteoporosis may occur.
Neurologic
Headache, shivering, and nystagmus may occur.
PROCEDURES AND LABORATORY TESTS
Essential Tests
- Whole blood cadmium level
- Normal: 0.4 to 1 µg/L
- Smokers: 1 to 5 µg/L
- Toxicity: possible at >7 µg/L or serum cadmium >5 µg/L
- Level increases acutely; level does not reflect body burden until several months after acute exposure
- Urine cadmium level. Toxicity possible occurs at urine cadmium levels exceeding 3 µg/g creatinine.
- Serum electrolytes, BUN, creatinine, and urinalysis are advised for renal injury and volume changes after acute ingestion.
Recommended Tests
- Serum liver function tests for liver injury following serious acute ingestion
- Urine beta-2-microglobulin, retinol binding protein, lysozyme, or N-acetyl-glucosaminidase; possible elevation in subclinical renal injury
- ECG, serum acetaminophen, and aspirin levels in overdose setting to detect occult ingestion
- Chest radiograph in patients with chronic toxicity to assess pulmonary fibrosis, presence of cancer
- Bone films to reveal osteomalacia, fractures in chronic cases
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- Treatment should focus on general supportive care, and management of renal failure in advanced cases.
- Dose and time of exposure should be determined for all substances involved.
DIRECTING PATIENT COURSE
The health-care professional should call the poison control center when:
- Cadmium toxicity is suspected.
- Coingestant, drug interaction, or underlying disease presents an unusual problem.
The patient should be referred to a health-care facility when:
- Patient or caregiver seem unreliable.
- Toxic effects develop.
- Coingestant, drug interaction, or underlying disease presents an unusual problem.
Admission Considerations
Inpatient management is warranted for patients with gastrointestinal toxicity following acute ingestion or renal failure following chronic exposure.
DECONTAMINATION
Out of Hospital
- Following inhalation, the patient should be moved to fresh air.
- The patient should also be removed from further exposure, including cigarettes.
In Hospital
- Gastric emptying is usually not warranted because of the chronic inhalation nature of most exposures.
- Decontamination of the skin or eyes with water should be considered following dust exposure.
ANTIDOTES
- There is no specific antidote for cadmium poisoning.
- Ethylenediaminetetraacetic acid (CaNa2 EDTA) may increase urinary excretion if administered very soon after acute exposures; however, the role in humans is unclear (see SECTION III, EDTA chapter for dose), and consultation with a medical toxicologist is recommended.
- There is no evidence that chelation is effective in chronic cases.
ADJUNCTIVE TREATMENT
- Hypotension. The patient should be treated with isotonic fluid infusion, the Trendelenburg position, and, if needed, vasopressors. Dopamine is preferred, and norepinephrine is added for refractory hypotension.
- Hypertension should be treated if clinically indicated.
- Obstructive lung disease can be treated using inhaled bronchodilators and antiinflammatory agents.
- Osteomalacia and osteoporosis can be treated with calcium and vitamin D supplements to reduce bone pain.
- Reduced renal function. Nephrotoxic drugs should be avoided if possible.
- Hemodialysis is not useful unless needed for complications of renal failure (e.g., hyperkalemia).
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PATIENT MONITORING
- Acute. Electrolytes, volume status, and complete blood counts may be needed to guide supportive care.
- Chronic. Electrolytes, BUN, creatinine.
EXPECTED COURSE AND PROGNOSIS
- Acute exposures
- Poisoning may be life threatening.
- Toxicity peaks within the first 24 hours, but corrosive, renal, or hepatic injury may require weeks to resolve, or may become permanent.
- Chronic exposures
- Renal insufficiency may progress, despite removal from exposure.
- Pulmonary injury is irreversible.
- Cadmium is an IARC I carcinogen; lung cancer is possibly related to exposure.
DISCHARGE CRITERIA/INSTRUCTIONS
- From the emergency department. Patients may be discharged after acute exposure if adverse effects do not develop within 4 to 6 hours. Perform decontamination and psychiatric evaluation, if needed.
- From the hospital. Patients may be discharged after renal and pulmonary injury have stabilized.
PATIENT EDUCATION
Patients who smoke should be strongly warned of the additive effects of cadmium in cigarettes on episodes of cadmium poisoning.
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DIAGNOSISCareful occupational history is needed to detect cadmium toxicity.
TREATMENT
It is important to avoid nephrotoxic drugs and therapies that decrease renal function.
ICD-9-CM 985.5Toxic effect of other metals: cadmium and its compounds.
See Also: SECTION II, Hypotension chapter; SECTION III, EDTA chapter; and SECTION IV, Cadmium Fume Fever chapter.
RECOMMENDED READING
Barnhart S, Rosenstock L. Cadmium chemical pneumonitis. Chest 1984;86:789-791.
Garry VF, Pohlman BL, Wick MR, Garvy JS, Zeisler R. Chronic cadmium intoxication: tissue response in an occupationally exposed patient. Am J Indust Med 1986;10:153-161.
Nogawa K, Kobayashi, Honda R. A study of the relationship between cadmium concentration in urine and renal effects of cadmium. Environ Health Perspect 1979;28:161-168.
Roels HA, Lauwerys RR, Buchet JP, Bernard AM, Vos A. Health significance of cadmium induced renal dysfunction: a five year follow up. Br J Indust Med 1989;46:755-764.
Author: Scott D. Phillips
Reviewer: Richard C. Dart