Longitudinal assessment of prenatal phthalate exposure on serum and cord thyroid hormones homeostasis during pregnancy - Tainan birth cohort study (TBCS)

Han Bin Huang, Pao Lin Kuo, Jung Wei Chang, Jouni J.K. Jaakkola, Kai Wei Liao, Po Chin Huang

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

An increasing number of studies have revealed that phthalate exposure alters thyroid hormone homeostasis in the general population, but there is insufficient evidence of the effect of longitudinal maternal phthalate exposure on maternal and fetal thyroid hormones during pregnancy. We longitudinally assessed the effect of prenatal phthalate exposure in pregnant women on umbilical cord and maternal thyroid hormones at three trimesters during pregnancy. We recruited 98 pregnant women and collected urine and blood samples at three trimesters in an obstetrics clinic in Southern Taiwan from 2013 to 2014. We analyzed the concentrations of 11 urinary phthalate metabolites, including monoethylhexyl phthalate, mono-(2-ethyl-5-oxo-hexyl) phthalate (MEOHP), mono-(2-ethyl-5-hydroxyhexyl) phthalate, mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP), mono-n-butyl phthalate, monoisobutyl phthalate (MiBP), monoethyl phthalate (MEP), using online liquid chromatography–tandem mass spectrometry. The cord and maternal serum levels of thyroxine (T4), free T4, triiodothyronine (T3), thyroid-stimulating hormone (TSH), and thyroxine-binding globulin were measured using an electrochemiluminescence immunoassay. A mixed-model analysis was utilized to assess the effect of longitudinal phthalate exposure on thyroid hormones and adjusted for significant covariates. We found that urinary MiBP (β = − 0.065, 95% confidence interval (CI): − 0.124, − 0.005), and MEOHP (β = − 0.083, 95% CI: − 0.157, − 0.009) were significantly negatively associated with serum TSH. Urinary MECPP was inversely related to serum T3 (β = − 0.027, 95% CI: − 0.047, − 0.006). Urinary MEP (β = 0.014, 95% CI: − 0.001, 0.028) and MiBP (β = 0.033, 95% CI: 0.018, 0.049) were positively related to free T4. We found that cord serum T3 (β = 0.067, 95% CI: 0.003, 0.131) and free T4 (β = 0.031, 95% CI: 0.001, 0.062) levels had significant positive associations with maternal ΣDBPm levels at the second trimester. We concluded that different phthalates exposure windows during gestation may alter cord and serum thyroid hormone homoeostasis.

Original languageEnglish
Pages (from-to)1058-1065
Number of pages8
JournalScience of the Total Environment
Volume619-620
DOIs
Publication statusPublished - Apr 1 2018
Externally publishedYes

Fingerprint

phthalate
homeostasis
Thyroid Hormones
pregnancy
hormone
serum
confidence interval
Thyrotropin
Obstetrics
Metabolites
exposure
phthalic acid
Thyroxine-Binding Globulin
Mass spectrometry
Blood
Triiodothyronine
Thyroxine
Liquids
immunoassay

Keywords

  • Cord blood
  • Phthalate metabolites
  • Pregnant women
  • Taiwanese
  • Thyroid hormones
  • Urine

ASJC Scopus subject areas

  • Environmental Engineering
  • Environmental Chemistry
  • Waste Management and Disposal
  • Pollution

Cite this

Longitudinal assessment of prenatal phthalate exposure on serum and cord thyroid hormones homeostasis during pregnancy - Tainan birth cohort study (TBCS). / Huang, Han Bin; Kuo, Pao Lin; Chang, Jung Wei; Jaakkola, Jouni J.K.; Liao, Kai Wei; Huang, Po Chin.

In: Science of the Total Environment, Vol. 619-620, 01.04.2018, p. 1058-1065.

Research output: Contribution to journalArticle

Huang, Han Bin ; Kuo, Pao Lin ; Chang, Jung Wei ; Jaakkola, Jouni J.K. ; Liao, Kai Wei ; Huang, Po Chin. / Longitudinal assessment of prenatal phthalate exposure on serum and cord thyroid hormones homeostasis during pregnancy - Tainan birth cohort study (TBCS). In: Science of the Total Environment. 2018 ; Vol. 619-620. pp. 1058-1065.
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abstract = "An increasing number of studies have revealed that phthalate exposure alters thyroid hormone homeostasis in the general population, but there is insufficient evidence of the effect of longitudinal maternal phthalate exposure on maternal and fetal thyroid hormones during pregnancy. We longitudinally assessed the effect of prenatal phthalate exposure in pregnant women on umbilical cord and maternal thyroid hormones at three trimesters during pregnancy. We recruited 98 pregnant women and collected urine and blood samples at three trimesters in an obstetrics clinic in Southern Taiwan from 2013 to 2014. We analyzed the concentrations of 11 urinary phthalate metabolites, including monoethylhexyl phthalate, mono-(2-ethyl-5-oxo-hexyl) phthalate (MEOHP), mono-(2-ethyl-5-hydroxyhexyl) phthalate, mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP), mono-n-butyl phthalate, monoisobutyl phthalate (MiBP), monoethyl phthalate (MEP), using online liquid chromatography–tandem mass spectrometry. The cord and maternal serum levels of thyroxine (T4), free T4, triiodothyronine (T3), thyroid-stimulating hormone (TSH), and thyroxine-binding globulin were measured using an electrochemiluminescence immunoassay. A mixed-model analysis was utilized to assess the effect of longitudinal phthalate exposure on thyroid hormones and adjusted for significant covariates. We found that urinary MiBP (β = − 0.065, 95{\%} confidence interval (CI): − 0.124, − 0.005), and MEOHP (β = − 0.083, 95{\%} CI: − 0.157, − 0.009) were significantly negatively associated with serum TSH. Urinary MECPP was inversely related to serum T3 (β = − 0.027, 95{\%} CI: − 0.047, − 0.006). Urinary MEP (β = 0.014, 95{\%} CI: − 0.001, 0.028) and MiBP (β = 0.033, 95{\%} CI: 0.018, 0.049) were positively related to free T4. We found that cord serum T3 (β = 0.067, 95{\%} CI: 0.003, 0.131) and free T4 (β = 0.031, 95{\%} CI: 0.001, 0.062) levels had significant positive associations with maternal ΣDBPm levels at the second trimester. We concluded that different phthalates exposure windows during gestation may alter cord and serum thyroid hormone homoeostasis.",
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AU - Jaakkola, Jouni J.K.

AU - Liao, Kai Wei

AU - Huang, Po Chin

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N2 - An increasing number of studies have revealed that phthalate exposure alters thyroid hormone homeostasis in the general population, but there is insufficient evidence of the effect of longitudinal maternal phthalate exposure on maternal and fetal thyroid hormones during pregnancy. We longitudinally assessed the effect of prenatal phthalate exposure in pregnant women on umbilical cord and maternal thyroid hormones at three trimesters during pregnancy. We recruited 98 pregnant women and collected urine and blood samples at three trimesters in an obstetrics clinic in Southern Taiwan from 2013 to 2014. We analyzed the concentrations of 11 urinary phthalate metabolites, including monoethylhexyl phthalate, mono-(2-ethyl-5-oxo-hexyl) phthalate (MEOHP), mono-(2-ethyl-5-hydroxyhexyl) phthalate, mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP), mono-n-butyl phthalate, monoisobutyl phthalate (MiBP), monoethyl phthalate (MEP), using online liquid chromatography–tandem mass spectrometry. The cord and maternal serum levels of thyroxine (T4), free T4, triiodothyronine (T3), thyroid-stimulating hormone (TSH), and thyroxine-binding globulin were measured using an electrochemiluminescence immunoassay. A mixed-model analysis was utilized to assess the effect of longitudinal phthalate exposure on thyroid hormones and adjusted for significant covariates. We found that urinary MiBP (β = − 0.065, 95% confidence interval (CI): − 0.124, − 0.005), and MEOHP (β = − 0.083, 95% CI: − 0.157, − 0.009) were significantly negatively associated with serum TSH. Urinary MECPP was inversely related to serum T3 (β = − 0.027, 95% CI: − 0.047, − 0.006). Urinary MEP (β = 0.014, 95% CI: − 0.001, 0.028) and MiBP (β = 0.033, 95% CI: 0.018, 0.049) were positively related to free T4. We found that cord serum T3 (β = 0.067, 95% CI: 0.003, 0.131) and free T4 (β = 0.031, 95% CI: 0.001, 0.062) levels had significant positive associations with maternal ΣDBPm levels at the second trimester. We concluded that different phthalates exposure windows during gestation may alter cord and serum thyroid hormone homoeostasis.

AB - An increasing number of studies have revealed that phthalate exposure alters thyroid hormone homeostasis in the general population, but there is insufficient evidence of the effect of longitudinal maternal phthalate exposure on maternal and fetal thyroid hormones during pregnancy. We longitudinally assessed the effect of prenatal phthalate exposure in pregnant women on umbilical cord and maternal thyroid hormones at three trimesters during pregnancy. We recruited 98 pregnant women and collected urine and blood samples at three trimesters in an obstetrics clinic in Southern Taiwan from 2013 to 2014. We analyzed the concentrations of 11 urinary phthalate metabolites, including monoethylhexyl phthalate, mono-(2-ethyl-5-oxo-hexyl) phthalate (MEOHP), mono-(2-ethyl-5-hydroxyhexyl) phthalate, mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP), mono-n-butyl phthalate, monoisobutyl phthalate (MiBP), monoethyl phthalate (MEP), using online liquid chromatography–tandem mass spectrometry. The cord and maternal serum levels of thyroxine (T4), free T4, triiodothyronine (T3), thyroid-stimulating hormone (TSH), and thyroxine-binding globulin were measured using an electrochemiluminescence immunoassay. A mixed-model analysis was utilized to assess the effect of longitudinal phthalate exposure on thyroid hormones and adjusted for significant covariates. We found that urinary MiBP (β = − 0.065, 95% confidence interval (CI): − 0.124, − 0.005), and MEOHP (β = − 0.083, 95% CI: − 0.157, − 0.009) were significantly negatively associated with serum TSH. Urinary MECPP was inversely related to serum T3 (β = − 0.027, 95% CI: − 0.047, − 0.006). Urinary MEP (β = 0.014, 95% CI: − 0.001, 0.028) and MiBP (β = 0.033, 95% CI: 0.018, 0.049) were positively related to free T4. We found that cord serum T3 (β = 0.067, 95% CI: 0.003, 0.131) and free T4 (β = 0.031, 95% CI: 0.001, 0.062) levels had significant positive associations with maternal ΣDBPm levels at the second trimester. We concluded that different phthalates exposure windows during gestation may alter cord and serum thyroid hormone homoeostasis.

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