You Are What You Eat: Effects of Selenium and Environmental Toxins on Child Developmental Delays: A Case-Control Study in Taiwan

Abstract

This epidemiological study looked at the interactions between selenium, mercury, lead, and arsenic and their associations with developmental delays. This study was designed as an observational case-control study in which subjects were recruited based on their outcome, or disease, status, which in this case meant cases were children developmental delays and controls were children with normal neurodevelopment. Mercury, lead, and arsenic ingestion of varying degrees have been linked to neurodevelopmental problems, and selenium has been suggested as a potential buffer against mercury toxicity. Blood and urine samples were collected from cases (N=85) and controls (N=85) recruited at Shin Kong Wu Ho-Su Memorial Teaching Hospital between August 2010 and December 2014. All subject mothers were given a questionnaire about sociodemographic and health status for herself and her child. Blood selenium, mercury, and lead concentrations were measured using Inductively coupled plasma mass spectrometry (ICP-MS), and urinary arsenic species concentrations were measured using high-performance liquid chromatography with hydride generation atomic absorption spectrometry (HPLC/HG-AAS). The children’s and mother’s sociodemographic, health, and heavy metal concentrations were compared between cases and controls. Selenium, mercury, lead, and total arsenic all showed significant difference between cases and controls. All significant factors from were added into multivariate analysis to find direct association between the heavy metals and developmental delays. The models that included the most sociodemographic and health variables showed that selenium (Odds Ratio 1.01, 95% Confidence Interval 0.98-1.02) and corrected total arsenic (OR 1.01, 95% CI 0.98-1.03) were not significantly associated with developmental delays. Mercury (OR 1.30, 95% CI 1.05-1.84), Lead (OR 1.33, 95% CI 1.05-1.64), and total arsenic (OR 1.04, 95% CI 1.01-1.07) were directly associated with developmental delays. In logistic models, selenium and mercury were the only elements to shown an interaction. Selenium was significantly different between cases and controls but not significantly associated with decreasing developmental delays on its own. Mercury is significantly associated with increasing developmental delays on its own, but when selenium is present, the association disappears. This study is the first to look at these four metals in a human population, their correlations, and interactions in the context of developmental delays. We conclude: 1) selenium intake is important for normal brain activity and also for buffering the toxicity of mercury; 2) mercury has detrimental effects on neurodevelopment its own but can be prevented by the presence of selenium; 3) lead is associated with developmental delays at all levels of exposure; and 4) arsenic is potentially associated with developmental delays, but further research on the most accurate measure of arsenic concentration in human bodies is needed. Because this study was done on a human population and not in a lab or on animals, the findings can be used to develop policies to regulate environmental toxins, to determine levels of concerns, and to monitor of selenium intake.