Cadmium

Optimal result: 0 – 0.9 µg/g creatinine

Urinary cadmium (Cd) provides an indication of recent or ongoing exposure to the toxic metal, and endogenous detoxification to a lesser extent. Most of absorbed Cd is retained in the liver and kidneys for many years. A small portion of assimilated Cd body leaves slowly in urine and bile/feces. Absorption, systemic transport and cellular uptake of Cd are mediated by metal transporters that the body uses for the essential elements iron, zinc and calcium.

Urinary cadmium (Cd) provides an indication of recent or ongoing exposure to the toxic metal, and endogenous detoxification to a lesser extent. Most of absorbed Cd is retained in the liver and kidneys for many years. A small portion of assimilated Cd body leaves slowly in urine and bile/feces. Absorption, systemic transport and cellular uptake of Cd are mediated by metal transporters that the body uses for the essential elements iron, zinc and calcium.

For nonsmokers the primary source of Cd exposure is food. Cd is found in varying amounts in foods; from very low for fruits to high in some shellfish (oysters, anchovies) and organ meats. Root vegetables tend to have higher Cd content than other vegetables. Refined carbohydrates have very little zinc in relation to the Cd; zinc competes with Cd for absorption from the gut. Tobacco leaves accumulate high levels of cadmium, and Cd absorption across the lungs is very efficient. Urban particulate air pollution/dust (diesel smoke, tire wear) is a significant source of Cd exposure. Other sources of Cd include: human biosolids, tires, pigments and paints, plastics, and batteries (Ni-Cd). The majority of Cd-containing batteries are improperly disposed of and contribute to environmental exposure.

Excessive exposure to Cd may be symptomatically associated with fatigue, weight loss, osteomalacia, and lumbar pain. Chronic exposure to Cd may adversely affect the kidneys, lungs, testes, arterial walls, and bones. Chronic Cd excess may lead to hypertension, coronary and peripheral vascular disease, macular degeneration, kidney disease, obesity-independent diabetes, and microcytic, hypochromic anemia and functional zinc deficiency. Cd is known to damage the kidneys, especially the proximal tubular cells that actively reabsorb Cd along with zinc, glucose and amino acids. Cd is pro-inflammatory and pro-oxidative.

Urinary or serum beta-2-microglobulin is considered to be the best test for assessment of Cd-associated functional damage to the kidneys. Urine amino acid wasting may also be considered. Chelation may acutely increase urinary excretion of Cd.

Cadmium
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