Cadmium exposure and nephropathy in a 28-year-old female metals worker.

Abstract

A 28-year-old female presented for evaluation of left flank pain and polyuria after having been exposed to cadmium in the jewelry manufacturing industry for approximately 3 years. This patient possessed both elevated 24-hr urinary β 2 -microglobulin and elevated blood cadmium levels. Approximately 6 months after initial presentation, the patient resigned from her job due to shortness of breath, chest pain, and anxiety. Exposure to cadmium in the jewelry industry is a significant source of occupational cadmium exposure. Other occupational sources include the manufacture of nickel-cadmium batteries, metal plating, zinc and lead refining, smelting of cadmium and lead, and production of plastics. Cadmium is also an environmental pollutant that accumulates in leafy vegetables and plants, including tobacco. Major toxicities anticipated from cadmium exposure involve the renal, pulmonary, and, to a lesser extent, gastrointestinal systems. These include the development of renal proximal tubular dysfunction, glomerular damage with progressive renal disease, and respiratory symptoms including pneumonitis and emphysema. Low-level cadmium exposure has also been associated with increased urinary calcium excretion and direct bone toxicity, effects that recent research suggests may result in the development of osteoporosis. The body burden of cadmium, over half of which may reside in the kidneys, is most often measured through the use of urinary cadmium levels. Blood cadmium measurements generally reflect current or recent exposure and are especially useful in cases with a short exposure period and only minimal accumulation of cadmium in the kidneys. Both β 2 -microglobulin and α 1 -microglobulin serve as organ-specific, early-effect biomarkers of tubular proteinuria and thus play a role in identifying early signs of cadmium-induced renal damage in those with potential exposures. In addition to ensuring workplace compliance with Occupational Safety and Health Administration-mandated monitoring and screening measures, it is prudent for those with cadmium exposure to maintain adequate intake of both iron and calcium, appropriate measures even in the absence of exposure.

Internal exposure to pollutants measured in blood and urine of Flemish adolescents in function of area of residence

“…Heavy metals (cadmium and lead) were determined in whole blood by the VUB. Cadmium levels in blood are generally regarded as a reflection of current exposure but cadmium levels in blood are also an estimate of the accumulated body burden of cadmium, many years after exposure (Wittman and Howard, 2002). Polychlorinated biphenyls (PCB 138,PCB 153 and PCB 180) and chlorinated pesticides (p,p 0 -dichlorodiphenyldichloroethylene (DDE) and hexachlorobenzene (HCB)) were analysed in serum by VITO and Toxicology Centre-UA.…”

Acute and subchronic co-administrations to cadmium, diazinon and selenium induce apparent osteoporotic symptoms in adult male rats

“…Moreover, exposure to low levels of Cd has also been associated with increased urinary calcium (Ca) excretion and subsequent skeletal demineralization, i.e. effects that may accelerate bone loss and increase bone fragility (Wittman & Hu 2002;Jin et al 2004). The results by Galicka et al (2004) also demonstrate the direct toxic impact of Cd on bone collagen content in rats.…”

Cadmium exposure: Health hazards of silver cottage industry in developing countries

“…The body burden of cadmium, over half of which may reside in kidneys, is usually measured by a urinary estimation of cadmium levels. Both ss2-microglobulin and alpha1-microglobulin serve as organ specific, early effect biomarkers of tubular proteinuria and thus play a role in early detection of nephrotoxicity [7].…”