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Case-control investigation of occupational lead exposure and kidney cancer
  1. Catherine L Callahan1,
  2. Melissa C Friesen1,
  3. Sarah J Locke1,
  4. Pamela J Dopart1,
  5. Patricia A Stewart2,
  6. Kendra Schwartz3,
  7. Julie J Ruterbusch3,
  8. Barry I Graubard4,
  9. Wong-Ho Chow5,6,
  10. Nathaniel Rothman1,
  11. Jonathan N Hofmann1,
  12. Mark P Purdue1
  1. 1 Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology Genetics, National Cancer Institute, Bethesda, Maryland, USA
  2. 2 Stewart Exposure Assessments, LLC, Arlington, Texas, USA
  3. 3 Department of Family Medicine and Public Health Sciences, Karmanos Cancer Institute, Wayne State University, Detroit, Michigan, USA
  4. 4 Biostatistics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA
  5. 5 Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
  6. 6 The University of Texas, MD Anderson Cancer Center, Houston, Texas, USA
  1. Correspondence to Dr. Mark P Purdue, Occupational and Environmental Epidemiology, National Cancer Institute Division of Cancer Epidemiology and Genetics, Rockville, MD 20850, USA; purduem{at}mail.nih.gov

Abstract

Objectives Lead is a suspected carcinogen that has been inconsistently associated with kidney cancer. To clarify this relationship, we conducted an analysis of occupational lead exposure within a population-based study of kidney cancer using detailed exposure assessment methods.

Methods Study participants (1217 cases and 1235 controls), enrolled between 2002 and 2007, provided information on their occupational histories and, for selected lead-related occupations, answered questions regarding workplace tasks, and use of protective equipment. Industrial hygienists used this information to develop several estimates of occupational lead exposure, including probability, duration and cumulative exposure. Unconditional logistic regression was used to compute ORs and 95% CIs for different exposure metrics, with unexposed subjects serving as the reference group. Analyses were also conducted stratifying on several factors, including for subjects of European ancestry only, single nucleotide polymorphisms in ALAD (rs1805313, rs1800435, rs8177796, rs2761016), a gene involved in lead toxicokinetics.

Results In our study, cumulative occupational lead exposure was not associated with kidney cancer (OR 0.9, 95% CI 0.7 to 1.3 for highest quartile vs unexposed; ptrend=0.80). Other lead exposure metrics were similarly null. We observed no evidence of effect modification for the evaluated ALAD variants (subjects of European ancestry only, 662 cases and 561 controls) and most stratifying factors, although lead exposure was associated with increased risk among never smokers.

Conclusions The findings of this study do not offer clear support for an association between occupational lead exposure and kidney cancer.

  • kidney cancer
  • occupational lead exposure
  • cancer epidemiology
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Footnotes

  • Contributors KS, JJR, BIG, W-HC and NR contributed to the design, enrolment and/or data collection of the case-control study. PAS, MPP, MCF, CLC, PJD and SJL contributed to the exposure assessment. MPP, BIG, CLC and JNH conducted or advised on the creation of study complex sampling weights and/or statistical analysis for this project. MPP and CLC drafted the manuscript. All authors contributed to the writing of the manuscript.

  • Funding This research was supported by the Intramural Research Program of the NIH and the National Cancer Institute.

  • Competing interests PAS is employed by Stewart Exposure Assessments, LLC (Arlington, Virginia, USA). The remaining authors declare they have no actual or potential competing financial interests.

  • Ethics approval Institutional Review Boards at all participating institutions.

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

  • Patient consent for publication Not required.

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