Markers of early renal changes induced by industrial pollutants. III. Application to workers exposed to cadmium.

Roels, Harry; Bernard, Alfred; Cárdenas, A. de Pablo; Buchet, Jean‐Pierre; Lauwerys, Robert; Hotter, Georgina; Ramis, Isabel; Mutti, Antonio; Franchini, I; Bundschuh, I

doi:10.1136/oem.50.1.37

Cited by 42 publications

(45 citation statements)

References 23 publications

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“…Elevations in enzymes primarily of renal tubular origin, such as N-acetyl-β-Dglucosaminidase (NAG) and alanine aminopeptidase (AAP), have been observed at occupational cadmium exposures of 3.7-6.3 µg urinary cadmium/g creatinine (2,4,7). Increases in these enzymes have been associated with chemical-induced renal tubular damage (8,9) Most studies of cadmium-induced renal effects using these and other biomarkers have been conducted among individuals with occupational or high environmental exposures (4,7,(10)(11)(12)(13)(14)(15)(16). Results of a national health survey indicate that the geometric mean value (and 95th percentile) for urinary cadmium among the U.S. general population age 6 years or older is approximately 0.27 (1.48) µg/g creatinine (17), but little information is available on renal effects that may occur in people with urinary cadmium levels < 2 µg/g.…”

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confidence: 99%

Effects of exposure to low levels of environmental cadmium on renal biomarkers.

Noonan

Sarasua

Campagna

et al. 2002

Environ Health Perspect

148

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We conducted a study among residents of a small community contaminated with heavy metals from a defunct zinc smelter and residents from a comparison community to determine whether biologic measures of cadmium exposure were associated with biomarkers of early kidney damage. Creatinine-adjusted urinary cadmium levels did not differ between the smelter and comparison communities; thus we combined individuals from both communities (n = 361) for further analyses. The overall mean urinary cadmium level was low, 0.26 microg/g creatinine, similar to reference values observed in the U.S. general population. For children ages 6-17 years, urinary concentration of N-acetyl-beta-D-glucosaminidase (NAG), alanine aminopeptidase (AAP), and albumin were positively associated with urinary cadmium, but these associations did not remain statistically significant after adjusting for urinary creatinine and other potential confounders. For adults ages 18 or older, urinary concentration of NAG, AAP, and albumin were positively associated with urinary cadmium. The associations with NAG and AAP but not with albumin remained statistically significant after adjusting for creatinine and other potential confounders. We found a positive dose-effect relationship between levels of creatinine-adjusted urinary cadmium and NAG and AAP activity, and statistically significant differences in mean activity for these two enzymes between the highest (> or =1.0 microg cadmium/g creatinine) and the lowest (< or =0.25 microg cadmium/g creatinine) exposure groups. The findings of this study indicate that biologic measures of cadmium exposure at levels below 2.0 microg/g creatinine may produce measurable changes in kidney biomarkers.

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confidence: 99%

Effects of exposure to low levels of environmental cadmium on renal biomarkers.

Noonan

Sarasua

Campagna

et al. 2002

Environ Health Perspect

148

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“…This indicates that both B-Cd and U-Cd are valid as indicators of long-term environmental exposure of the general population to cadmium. Several studies have supported this assumption and the close correlation between B-Cd and U-Cd in such circumstances (Liu et al 2001;Moon et al 1999;Roels et al 1993). In fact, many years after an exposure, B-Cd is likely better than U-Cd as an indicator of previous exposure because if tubular damage has occurred, U-Cd measurements may be difficult to interpret (Börjesson et al 2001;Ikeda et al 1999;Järup et al 2000).…”

Section: Case Discussionmentioning

confidence: 77%

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

Wittman¹,

Hu²

2002

Environ Health Perspect

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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.

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“…Through the use of biomarkers of damage to various parts of the nephron, a pattern of damage is emerging that is consistently observed now both in U.S. and European studies of men occupationally exposed to cadmium (4)(5)(6)(7)(8)(9)(10) The lowest observed effect is indicated by a significant prevalence of abnormal 6-keto-prostaglandin Fla (6-keto-PGFi,a) and sialic acid levels in urine at an approximate urine cadmium concentration of 2.4 nmol Cd/mmol creatinine (2.4 pg Cd/g creatinine) (10). Proteins such as albumin and transferrin originate in the plasma and are filtered to a limited degree through the glomerulus, and the protein that is filtered is primarily reabsorbed by the tubules.…”

Section: Thresholds Of Effects: Cadmiummentioning

confidence: 99%

“…Some of these candidate markers are beginning to be examined in human studies. Excretion of fibronectin has been examined in relation to exposure to three heavy metals (cadmium, lead, and mercury), with no significant changes in excretion seen in the exposed groups (7)(8)(9).…”

Section: Potential New Biomarkersmentioning

confidence: 99%

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New Approaches for Detecting Thresholds of Human Nephrotoxicity Using Cadmium as an Example

Mueller¹,

Price²,

Finn³

1998

Environmental Health Perspectives

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Damage to the kidneys is one of the primary toxic actions of metals. Nephrotoxic substances not only cause renal disease directly, but they can also destroy renal reserve capacity, potentially placing those people with additional risk factors, such as diabetes, hypertension, cardiovascular disease, and genetic predispositions, at greater risk. To detect nephrotoxicity in people at a stage where intervention can be effective, sensitive methods are needed. One of the major advantages of using sensitive biomarkers of renal damage is that people who may be particularly susceptible to renal damage can be identified early, at a reversible stage of damage, and the progression to end-stage renal disease may be halted or delayed. Various categories of tets can be used to detect effects of nephrotoxic subsances on the kidney. Through the use of biomarkers of damage to various parts of the nephron, U.S. and European studies have both shown a similar pattern of damage among men occupationally exposed to-cadmium. These studies indicate various thresholds of renal effects, which researchers suggest represent a cascade ofprogressively severe damage to the kidney. Research into new biomarkers of damage caused by exposure to nephrotoxic substances centers around mechanisms of cell death, induding necrosis and apoptosis; mechanisms of cell growth, regeneration, and proliferation, induding factors that control cell cle, influence gene expression, and modulate nudeic acid synthesis; and genetic factors that increase susceptibility to renal disease. Examples of types of candidate biomarkers indude cytokines, lipid mediators, growth factors, transcription factors and protooncogenes, extracellular matrix components (collagen, glycoproteins, and proteoglycans), and cell adhesion molecules. Research into new categories of biomarkers may provide additional insights into the mechanisms of damage caused by nephrotoxins.

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Markers of early renal changes induced by industrial pollutants. III. Application to workers exposed to cadmium.

Cited by 42 publications

References 23 publications

Effects of exposure to low levels of environmental cadmium on renal biomarkers.

Effects of exposure to low levels of environmental cadmium on renal biomarkers.

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

New Approaches for Detecting Thresholds of Human Nephrotoxicity Using Cadmium as an Example

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