Associations of Cadmium and Lead Exposure With Leukocyte Telomere Length: Findings From National Health and Nutrition Examination Survey, 1999–2002
Author(s) -
Ami R. Zota,
Belinda L. Needham,
Elizabeth H. Blackburn,
Jue Lin,
Sung Kyun Park,
David H. Rehkopf,
Elissa S. Epel
Publication year - 2014
Publication title -
american journal of epidemiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.33
H-Index - 256
eISSN - 1476-6256
pISSN - 0002-9262
DOI - 10.1093/aje/kwu293
Subject(s) - national health and nutrition examination survey , cadmium , medicine , urine , confounding , quartile , physiology , population , cadmium exposure , confidence interval , telomere , environmental health , toxicity , biology , chemistry , genetics , dna , organic chemistry
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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