Associations of Cadmium and Lead Exposure With Leukocyte Telomere Length: Findings From National Health and Nutrition Examination Survey, 1999–2002

↵*Correspondence to Dr. Ami R. Zota, Department of Environmental and Occupational Health, Milken Institute School of Public Health, The George Washington University, 950 New Hampshire Avenue NW, Suite 414, Washington, DC 20052 (e-mail: azota{at}gwu.edu).

Abbreviations: CDC, US Centers for Disease Control and Prevention; CI, confidence interval; LOD, limit of detection; LTL, leukocyte telomere length; NHANES, National Health and Nutrition Examination Survey; SES, socioeconomic status.

Received June 5, 2014.
Accepted September 22, 2014.

Abstract

Cadmium and lead are ubiquitous environmental contaminants that might increase risks of cardiovascular disease and other aging-related diseases, but their relationships with leukocyte telomere length (LTL), a marker of cellular aging, are poorly understood. In experimental studies, they have been shown to induce telomere shortening, but no epidemiologic study to date has examined their associations with LTL in the general population. We examined associations of blood lead and cadmium (n = 6,796) and urine cadmium (n = 2,093) levels with LTL among a nationally representative sample of US adults from the National Health and Nutrition Examination Survey (1999–2002). The study population geometric mean concentrations were 1.67 µg/dL (95% confidence interval (CI): 1.63, 1.70) for blood lead, 0.44 µg/L (95% CI: 0.42, 0.47) for blood cadmium, and 0.28 µg/L (95% CI: 0.27, 0.30) for urine cadmium. After adjustment for potential confounders, the highest (versus lowest) quartiles of blood and urine cadmium were associated with −5.54% (95% CI: −8.70, −2.37) and −4.50% (95% CI: −8.79, −0.20) shorter LTLs, respectively, with evidence of dose-response relationship (P for trend < 0.05). There was no association between blood lead concentration and LTL. These findings provide further evidence of physiological impacts of cadmium at environmental levels and might provide insight into biological pathways underlying cadmium toxicity and chronic disease risks.

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