SOURCES:
Found in food such as shellfish, leafy vegetables, rice, cereals, cocoa butter, dried seaweed, and legumes. Also present in nickel cadmium batteries, cigarette smoke (including second-hand smoke), insecticides, fertilizer, motor oil, emissions and exhaust. Drinking water, air, and occupational exposures are also seen.
NUTRIENT INTERACTIONS:
Iron deficiency is associated with higher cadmium burden and absorption of cadmium may increase during very early stages of iron deficiency. Zinc deficiency is associated with an increase in Cadmium, as a result of the antagonistic relationship between the elements.
Dietary cadmium inhibits GI absorption of calcium and interferes with calcium and vitamin D metabolism. Low dietary calcium stimulates synthesis of calcium- binding protein which enhances Cadmium absorption.
References:
- Yedjou CG, Patlolla AK, Sutton DJ. Heavy Metals Toxicity and the Environment Paul B Tchounwou. Published in final edited form as: EXS. 2012;3:133-164.
- Kordas K, Loonnerdal B, Stoltzfus RJ. Interactions between Nutrition and Environmental Exposures: Effects on Health Outcomes in Women and Children. J Nutr. 2007;137(12):2794-2797.
- Afridi HI, Kazi TG, Kazi NG, et al. Evaluation of cadmium, lead, nickel and zinc status in biological samples of smokers and nonsmokers hypertensive patients. J Hum Hypertens. 2010;24(1):34-43.
- ATSDR. Cadmium Toxicity Clinical Assessment - Laboratory Tests. Environmental Health and Medicine Education 2008; https://www.atsdr.cdc.gov/csem/csem.asp?csem=6&po=15 2020.
- Lauwerys R, Buchet J, Roels H. The relationship between cadmium exposure or body burden and the concentration of cadmium in blood and urine in man. Int Arch Occup Environ health. 1976;36(4):275-285.
- Adams SV, Newcomb PA. Cadmium blood and urine concentrations as measures of exposure: NHANES 1999-2010. J Expo Sci Environ Epidemiol. 2014;24(2):163-170.
- Goyer RA. Toxic and essential metal interactions. Ann Rev Nutr. 1997;17(1):37-50.
What does it mean if your CADMIUM result is too high?
PHYSIOLOGIC EFFECTS:
Cadmium accumulates in the liver and kidneys and has a long half-life (17-30 years). The renal and skeletal systems are the main targets of Cadmium toxicity. Urinary cadmium reflects integrated exposure over time and body burden. Urinary levels do not rise significantly after acute exposure. Elevated blood cadmium levels confirm recent acute exposure.
CLINICAL SIGNIFICANCE:
Renal tubular toxicity, decreased bone density with increased bone turnover and fractures.
Chronic inhalation exposure is associated with emphysema. Acute oral ingestion leads to abdominal pain, nausea, vomiting, muscle cramps, and GI tract erosions.
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