Academic journal article Environmental Health Perspectives

Association between Lead and Cadmium and Reproductive Hormones in Peripubertal U.S. Girls

Academic journal article Environmental Health Perspectives

Association between Lead and Cadmium and Reproductive Hormones in Peripubertal U.S. Girls

Article excerpt

BACKGROUND: Lead (Pb) and cadmium (Cd) are known reproductive toxicants thought to disrupt hormone production throughout sensitive developmental windows, although this has not been previously examined in nationally representative peripubertal children.

OBJECTIVES: We examined the association between blood Pb and urinary Cd concentrations and the reproductive hormones inhibin B and luteinizing hormone (LH) in girls 6-11 years of age who participated in the cross-sectional Third National Health and Nutrition Examination Survey (NHANES III) (1988-1994).

METHODS: Pb (micrograms per deciliter) was measured in whole blood, and Cd was measured in urine (nanograms per milliliter). Inhibin B (picograms per milliliter) and LH (milli-International units per milliliter) were measured in residual sera for 705 girls. Survey logistic regression was used to estimate associations with pubertal onset based on inhibin B concentration > 35 pg/mL or LH concentration < 0.4 mIU/mL, and multinomial logistic regression was used to estimate the association between Pb and increasing categories of hormone concentrations.

RESULTS: High Pb ([greater than or equal to] 5 [micro]g/dL) was inversely associated with inhibin B > 35 pg/mL [odds ratio (OR) = 0.26; 95% confidence interval (CI), 0.11-0.60; compared with Pb < 1 [micro]g/dL]. At 10 and 11 years of age, girls with low Pb (< 1 [micro]g/dL) had significantly higher inhibin B than did girls with moderate (1-4.99 [micro]g/dL) or high Pb ([greater than or equal to] 5 [micro]g/dL). In the subsample of 260 girls with levels of inhibin B above the level of detection and using survey regression modeling, inhibin B levels were lower among girls with both high Pb and high Cd ([beta] = -0.52; 95% CI, -0.09 to -1.04) than among girls with high Pb alone ([beta] = -0.35; 95% CI, -0.13 to -0.57), relative to girls with low Pb and low Cd.

CONCLUSIONS: Higher Pb was inversely associated with inhibin B, a marker of follicular development, and estimated effects suggestive of pubertal delays appeared to be stronger in the context of higher Cd concentrations. These data underscore the importance of Pb and Cd as reproductive toxicants for young girls.

KEY WORDS: heavy metals, inhibin B, luteinizing hormone, NHANES, puberty. Environ Health Perspect 118:1782-1787 (2010). doi:10.1289/ehp.1001943 [Online 30 July 2010]


The onset of puberty is a milestone marked by the appearance and development of secondary sexual characteristics and changes in behavior, growth, and reproductive capabilities. Changes in the timing of pubertal onset and/or progression have been associated with nutrition, obesity, and environmental contaminants, such as heavy metals and endocrine disruptors, supporting an environmental etiology to some degree (Buck Louis et al. 2008; Euling et al. 2008; Parent et al. 2005). Changes in the timing of onset and/or progression of puberty on a national scale have considerable public health and social implications for both boys and girls (Herman-Giddens 2006). Girls who mature relatively earlier are at increased risk of later obesity, diabetes, and reproductive-site cancers (Golub et al. 2008), and early-maturing girls and boys are reported to engage in more risky behaviors, such as cigarette smoking, substance use, and sexual activity (Dunbar et al. 2008; Hayatbakhsh et al. 2009). Relatively late-maturing girls, on the other hand, are at risk for diminished bone strength and fragility fractures later in life (Chevalley et al. 2009), whereas late-maturing boys may be at risk for victimization and depressive symptoms (Michaud et al. 2006). Assessment of environmental influences on the timing of puberty is thus important for health across the human life span, whether such influences are associated with advancements or delays in the onset of puberty.

However, few population-based data are available to characterize either environmental exposures or pubertal onset, contributing to our inability to identify environmental threats to human development across such sensitive windows. …

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