Abstract

OPS 39: Metals and biomarkers, Room 411, Floor 4, August 26, 2019, 1:30 PM - 3:00 PM Background/Aim: Metals and trace elements may affect thyroid homeostasis, but the role of prenatal exposure is unclear. We evaluated the association of pregnancy exposure to mixtures of trace elements with maternal and child thyroid function in 800 mother-child pairs from the RHEA pregnancy cohort in Crete, Greece. Methods: Concentrations of 11 essential and non-essential trace elements were determined in first trimester maternal urine using inductively coupled plasma mass spectrometry. Thyroid hormones (thyroid stimulating hormone (TSH), free T(4), and free T(3)) were measured in serum samples collected from mothers (1st trimester) and their children at 4 years of age. Associations of each element and mixtures with thyroid hormone levels were assessed using linear regression and Bayesian Kernel Machine Regression (BKMR), respectively. Results: In BKMR analysis, higher total urinary element concentration was associated with lower maternal TSH and higher FT3 levels, while there was no association with FT4. Results from BKMR were in line with findings from linear models, with negative associations of urinary copper (adj. b=-49.7 %, 95%CI: -65.6, -26.5), selenium (b=-51.2 %, 95%CI: -66.8, -28.1) and cadmium (b=-23.1 %, 95%CI: -38.1, -4.5) with maternal TSH levels. Exposure to urinary copper was positively associated with maternal FT3 levels (b= 0.6 pg/mL, 95%CI: 0.2, 1.0). Cobalt was associated with lower maternal FT4 levels (b=-0.05 ng/dL, 95%CI: -0.1, -0.01) while copper (b=0.1 ng/dL, 95%CI: 0.02, 0.2), zinc (b=0.1 ng/dL, 95%CI: 0.02, 0.1), selenium (b=0.1 ng/dL, 95%CI: 0.1, 0.2) and cadmium (b=0.1 ng/dL, 95%CI: 0.02, 0.11) were associated with higher maternal FT4 levels. We observed no interactions between the different elements. No associations were observed with child thyroid hormones. Conclusions: The present results suggest that exposure to metals and trace elements at exposure levels relevant for the general population, can alter maternal thyroid homeostasis.

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