Cadmium Poisoning

Cadmium is used for various industrial purposes, including plastic and battery manufacturing, smelting, pigment production, metal-plating, but also in the production of tobacco, suggesting that a wide range of workers are at risk of exposure [1] [2] [3] [4]. Cadmium poisoning can occur either by inhalation or ingestion and in both settings, poisoning may be acute or chronic, depending on the amount of cadmium introduced into the body and the rate of exposure [1] [2] [3] [5] [6]:

• Acute poisoning - Inhalation of cadmium-contaminated air causes profound damage to the respiratory system, and is primarily seen in the industrial setting [1] [2] [3]. Dyspnea, pulmonary edema, cyanosis, tachycardia, chest pain and pneumonitis develop within 4-24 hours after cadmium reaches the lungs and can be life-threatening without early recognition of the cause [1] [3]. Ingestion of large amounts of cadmium, on the other hand, occurs accidentally by eating food grown in cadmium-rich soil, or intentionally in suicidal purposes [3] [6]. As little as 10 mg is sufficient to cause severe erosion of the gastrointestinal (GI) tract, while > 100 mg is considered to be lethal [6]. Principal symptoms of acute poisoning after ingestion appear within 15-30 minutes and are abdominal pain, diarrhea, nausea, vomiting, but also muscle cramping, vertigo, bone pain, loss of consciousness, convulsions and even coma [1] [6].
• Chronic poisoning - Cadmium is known for its very long half-life in the human body (about 15-30 years), and is able to accumulate in the proximal renal tubules, the principal site of its reabsorption after glomerular filtration [1] [7]. Chronic exposure to this heavy metal results in its progressive deposition in the kidneys leading to chronic kidney disease [2], the most important long-term consequence of chronic cadmium poisoning. Because cadmium is found in cigarettes, tobacco smoking is a well-known risk factor for chronic poisoning, and urine levels of cadmium have shown to be substantially higher in this population compared to non-smokers [1] [2]. In addition to kidney damage and proteinuria, other known complications are hypertension, diabetes mellitus and diabetic nephropathy, anemia, osteomalacia, yellowing of teeth, and cardiovascular damage, while its carcinogenic potential is still being investigated [2] [3] [5] [7] [8] [9]. Moreover, the term Itai-Itai disease was designated to describe patients who suffer from frequent fractures, accelerated osteoporosis and bone-associated pain due to consumption of foods that were contaminated with high amounts of cadmium [1] [9].

The diagnosis of cadmium poisoning must be made promptly, especially if the overall condition of the patient suggests acute poisoning. A detailed patient history is vital in order to determine the potential source of symptoms - whether the patient was exposed to cadmium in the industrial setting (in the case of respiratory symptoms), or if "suspicious" food was eaten prior to the onset of complaints. After a thorough clinical examination to assess breathing, cardiac function and vital signs, an immediate laboratory workup comprised of serum electrolytes, renal function tests (blood urea nitrogen and creatinine), a complete blood count (CBC) and liver enzymes (alanine and aspartate aminotransferases, or ALT and AST, respectively) must be performed [3] [4]. If poisoning through inhalation is suspected, a chest X-ray, arterial blood gas (ABG) measurements, and oxygen saturation are also necessary. Regardless of the mode of exposure or severity of symptoms, cadmium can be detected in both serum and urine, and levels of > 5 μg/dL in serum will be present in the setting of acute poisoning [1] [3]. In addition to urine testing for cadmium (which will show >100 nmol/L and a markedly increased creatinine), levels of β2-microglobulin in urine will be markedly elevated in this patient population, whereas N-acetyl-α-D-glucosaminidase (NAG) and retinol-binding-protein (RBP) are also excreted in higher amounts in these patients. All three compounds are useful when cadmium is the presumed cause of symptoms, as their increased excretion occurs as a result of impaired proximal tubule reabsorption [1] [5] [9].

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