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Associations of low-level urine cadmium with kidney function in lead workers
  1. Virginia M Weaver1,2,
  2. Nam-Soo Kim3,
  3. Bernard G Jaar2,4,
  4. Brian S Schwartz1,2,4,
  5. Patrick J Parsons5,6,
  6. Amy J Steuerwald5,6,
  7. Andrew C Todd7,
  8. David Simon8,
  9. Byung-Kook Lee3
  1. 1Division of Occupational and Environmental Health, Department of Environmental Health Sciences, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA
  2. 2Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
  3. 3Institute of Industrial Medicine, Soonchunhyang University, Asan, South Korea
  4. 4Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA
  5. 5Laboratory of Inorganic and Nuclear Chemistry, Wadsworth Center, New York State Department of Health, Albany, New York, USA
  6. 6Department of Environmental Health Sciences, School of Public Health, The University at Albany, Albany, New York, USA
  7. 7Department of Community and Preventive Medicine, Mount Sinai School of Medicine, New York, New York, USA
  8. 8Biostatistical Consulting, Cincinnati, Ohio, USA
  1. Correspondence to Virginia M Weaver, Division of Occupational and Environmental Health, Johns Hopkins University Bloomberg School of Public Health, 615 N. Wolfe St., Rm. 7041, Baltimore, MD 21205, USA; vweaver{at}


Objectives Low-level cadmium exposure, resulting in, for example, urinary cadmium <2.0 μg/g creatinine, is widespread; recent data suggest nephrotoxicity even at these low levels. Few studies have examined the impact of low-level cadmium exposure in workers who are occupationally exposed to other nephrotoxicants such as lead.

Methods We evaluated associations of urine cadmium, a measure of cumulative dose, with four glomerular filtration measures and N-acetyl-β-D-glucosaminidase (NAG) in lead workers. Recent and cumulative lead doses were assessed via blood and tibia lead, respectively.

Results In 712 lead workers, mean (SD) blood and tibia lead values, urine cadmium values and estimated glomerular filtration rate (eGFR) using the Modification of Diet in Renal Disease equation were 23.1 (14.1) μg/dl, 26.6 (28.9) μg Pb/g bone mineral, 1.15 (0.66) μg/g creatinine and 97.4 (19.2) ml/min/1.73 m2, respectively. After adjustment for age, sex, body mass index, urine creatinine, smoking, alcohol, education, annual income, diastolic blood pressure, current or former lead worker job status, new or returning study participant, and blood and tibia lead, higher ln-urine cadmium was associated with higher calculated creatinine clearance, eGFR (β=8.7 ml/min/1.73 m2; 95% CI 5.4 to 12.1) and ln-NAG but lower serum creatinine.

Conclusions Potential explanations for these results include a normal physiological response in which urine cadmium levels reflect renal filtration, the impact of adjustment for urine dilution with creatinine in models of kidney outcomes, and cadmium-related hyperfiltration.

  • Cadmium
  • kidney function
  • lead exposure
  • urine creatinine
  • biomonitoring
  • toxicology
  • metals

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  • Funding This research was supported by NIEHS grant 2 ES007198 (Dr Weaver) and KRF-2000-00545 (Dr Lee) from the Korea Research Foundation.

  • Competing interests None.

  • Ethics approval This study was conducted with the approval of the Institutional Review Boards at the Soonchunhyang University School of Medicine and the Johns Hopkins University Bloomberg School of Public Health.

  • Provenance and peer review Not commissioned; externally peer reviewed.