Abstract

PDS 74: Pregnancy outcomes, Exhibition Hall (PDS), Ground floor, August 26, 2019, 1:30 PM - 3:00 PM Background: Prenatal exposure to persistent organic pollutants (POPs) can interfere with thyroid hormone (TH) homeostasis, resulting in disorders in fetal and postnatal development [1]. Here we aim to develop a method for TH determination in placenta and examine the associations of THs with POPs. Methods: Liquid chromatography with quadrupole time-of-flight mass spectrometry (LC-Q-TOF-MS) method was developed for the quantification of thyroxine (T4), 3,3’,5-triiodothyronine (T3), and 3,3’,5’-triiodothyronine (rT3), 3,3’-diiodo-L-thyronine (T2), 3,5-diiodo-L-thyronine (rT2), 3-iodo-L-thyronine (T1) and 3-iodothyronamine (T1AM) in placenta [2]. Fifty-eight placenta samples were collected from a Danish birth cohort study. The levels of THs and a wide variety of POPs, including polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs), organotin chemicals (OTCs), organochlorine pesticides (OCPs) were measured. The associations between placental THs and various POPs were analyzed using multiple linear regression [3]. Results: The LC-Q-TOF-MS method developed here showed high sensitivity and selectivity. T4, T3, rT3, and T2 were measured in human placenta. Five PBDEs, 35 PCBs, 14 PCDD/Fs, 3 OTCs, 25 OCPs were also quantified. Some significant associations were observed here: a) T4 was inversely associated with BDEs 99, 100, ΣPBDE, and 2378-TCDD, and positively associated with 1234678-HpCDF; b) T3 was positively associated with 2378-TCDF and 12378-PeCDF; c) rT3 was positively associated with PCB 81, 12378-PeCDF and 234678-HxCDF, and inversely associated with tributyltin (TBT), ΣOTC, and methoxychlor (MOC). Conclusion: This study shows that POP exposures were associated with TH levels in placenta, which leads to the concerns of environmental exposure on the proper development of the fetus and children. The method here allows a comprehensive evaluation of TH homeostasis in research of environmental exposures.

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