Clinical Information

The toxicity of cadmium resembles the other heavy metals (arsenic, mercury and lead) in that it attacks the kidney; renal dysfunction with proteinuria with slow onset (over a period of years) is the typical presentation. Measurable changes in proximal tubule function, such as decreased clearance of para-aminohippuric acid, also occur over a period of years and precede overt renal failure.

Breathing the fumes of cadmium vapors leads to nasal epithelial deterioration and pulmonary congestion resembling chronic emphysema.

For nonsmokers, the primary source of cadmium exposure is from the food supply. In general, leafy vegetables such as lettuce and spinach, potatoes and grains, peanuts, soybeans, and sunflower seeds contain high levels of cadmium. For smokers, the most common source of cadmium exposure is tobacco smoke, which has been implicated as the primary sources of the metal leading to reproductive toxicity in both males and females.

Chronic exposure to cadmium causes accumulated renal damage. The excretion of cadmium is proportional to creatinine except when renal damage has occurred. Renal damage due to cadmium exposure can be detected by increased cadmium excretion relative to creatinine.

The Occupational Safety and Health Administration (OSHA) mandated (Fed Reg 57:42,102-142,463, September 1992) that all monitoring of employees exposed to cadmium in the workplace should be done using the measurement of urine cadmium and creatinine, expressing the results of mcg of cadmium per gram of creatinine.