Article

Cadmium Exposure and Neurodevelopmental Outcomes in U.S. Children

Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA.
Environmental Health Perspectives (Impact Factor: 7.03). 01/2012; 120(5):758-63. DOI: 10.1289/ehp.1104152
Source: PubMed

ABSTRACT Low-level environmental cadmium exposure in children may be associated with adverse neurodevelopmental outcomes.
Our aim was to evaluate associations between urinary cadmium concentration and reported learning disability (LD), special education utilization, and attention deficit hyperactivity disorder (ADHD) in U.S. children using National Health and Nutrition Examination Survey (NHANES) data.
We analyzed data from a subset of participants in NHANES (1999-2004) who were 6-15 years of age and had spot urine samples analyzed for cadmium. Outcomes were assessed by parent or proxy-respondent report. We fit multivariable-adjusted logistic regression models to estimate associations between urinary cadmium and the outcomes.
When we compared children in the highest quartile of urinary cadmium with those in the lowest quartile, odds ratios adjusted for several potential confounders were 3.21 [95% confidence interval (CI): 1.43, 7.17] for LD, 3.00 (95% CI: 1.12, 8.01) for special education, and 0.67 (95% CI: 0.28, 1.61) for ADHD. There were no significant interactions with sex, but associations with LD and special education were somewhat stronger in males, and the trend in the ADHD analysis was only evident among those with blood lead levels above the median.
These findings suggest that children who have higher urinary cadmium concentrations may have increased risk of both LD and special education. Importantly, we observed these associations at exposure levels that were previously considered to be without adverse effects, and these levels are common among U.S. children.

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    • "The median U-Cd levels found in the urine of our volunteers are far lower than 1 μgCd/g creatinine, the European Food Safety Authority threshold value for protection against kidney damage, thereby suggesting the lack of an important exposure source of this metal (EFSA, 2009). However, a reduction in Cd exposure is still relevant as adverse effects have been reported for the kidney and on bone and neurodevelopmental deficits at U-Cd cr concentrations as low as 1 μgCd/g creatinine (Järup and Åkesson, 2009, Ciesielski et al., 2012). Even at lower concentrations (o0.50 μg/g creatinine) Cd has been reported to be associated with hypertension and cardiovascular disease (Tellez–Plaza et al., 2012b), breast cancer incidence (McElroy et al., 2006) and mortality (Menke et al., 2009; Adams et al., 2012). "
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    • "Cd is suspected to cause several other adverse health effects in humans, also at exposure levels found in the general population; however, results have not been consistent or causality had not been definitely demonstrated. Examples include neurodevelopmental effects (Cao et al. 2009; Ciesielski et al. 2012; Kippler et al. 2012a, 2012b), diabetes (Afridi et al. 2008; Barregard et al. 2013; Schwartz et al. 2003), and cardiovascular disease or mortality (Agarwal et al. 2011; Bao et al. 2009; Fagerberg et al. 2012, 2013; Li et al. 2011; Menke et al. 2009; Messner et al. 2009; Nakagawa et al. 2006; Nawrot et al. 2008; Nishijo et al. 2006; Peters et al. 2010; Tellez-Plaza et al. 2012b, 2013). "
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