Prenatal Exposure to Organophosphate Flame Retardants and the Risk of Low Birth Weight: A Nested Case-Control Study in China

Luo, Dan; Liu, Wenyu; Tao, Ye; Wang, Limei; Yu, Meng; Hu, Li-Sheng; Zhou, Aifen; Covaci, Adrian; Xia, Wei; Li, Yuanyuan; Xu, Shunqing; Mei, Surong

doi:10.1021/acs.est.9b06026

Cited by 75 publications

(55 citation statements)

References 61 publications

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“…These ndings are consistent with several other epidemiologic studies that indicate a potential link between OPE exposure and altered fetal growth (22,23). For example, a recent prospective case-control study of low birth weight (n = 339) based in China reported that the odds of low birth weight in women with the highest tertile of urinary DPhP was 4.62 (95% CI: 1.72, 12.40) times that observed in the lowest tertile (22). Notably, concentrations of DPhP and BDCPP were higher in our cohort (DPhP median = 0.74 ng/mL, BDCPP median = 0.67 ng/mL) compared to the Chinese cohort (DPhP median = 0.05 ng/mL, BDCPP median = 0.05 ng/mL) (22).…”

Section: Discussionsupporting

confidence: 92%

“…We observed that levels of urinary DPhP as well as the mixture of OPE metabolites were associated with reduced odds of LGA births although there was no association with SGA. These ndings are consistent with several other epidemiologic studies that indicate a potential link between OPE exposure and altered fetal growth (22,23). For example, a recent prospective case-control study of low birth weight (n = 339) based in China reported that the odds of low birth weight in women with the highest tertile of urinary DPhP was 4.62 (95% CI: 1.72, 12.40) times that observed in the lowest tertile (22).…”

Section: Discussionsupporting

confidence: 90%

“…DPhP and BDCPP) were detected in maternal urine frequently enough for analysis. This is in part due to the analytical method used to quantify OPE metabolites, which was less sensitive for some metabolites relative to recent studies on this topic (22,55,56). While this has limited our ability to examine associations between OPEs and fetal growth, it is worth pointing out that DPhP and BDCPP are two of the most frequently detected OPE metabolites in the general population (83).…”

Section: Discussionmentioning

confidence: 99%

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Prenatal exposure to consumer product chemical mixtures and size for gestational age at delivery

Bommarito

Welch

Keil

et al. 2021

Preprint

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Background: While fetal growth is a tightly regulated process, it is sensitive to environmental exposures that occur during pregnancy. Many commonly used consumer products contain chemicals that can disturb processes underlying fetal growth. However, mixtures of these chemicals have been minimally examined. We investigated associations between prenatal exposure to 33 consumer product chemicals (nine organophosphate ester flame retardant [OPE] metabolites, 12 phthalate metabolites, and 12 phenols) and the odds of small- or large-for-gestational age (SGA and LGA) births.Methods: This case-control study was comprised of SGA (N = 31), LGA (N = 28), and appropriate for gestational age control (N = 31) births selected from the larger LIFECODES cohort. Biomarkers of exposure to consumer product chemicals were quantified in maternal urine collected from up to three study visits during pregnancy. In a single-pollutant approach, odds ratios (OR) and 95% confidence intervals (CI) of SGA and LGA associated with an interquartile range (IQR)-increase in exposure biomarkers were estimated using multinomial logistic regression. In a multi-pollutant approach, quantile g-computation was used to jointly estimate the OR (95% CI) of SGA and LGA per simultaneous one quartile-change in all biomarkers belonging to each chemical class. Results: Among the 33 biomarkers analyzed, 20 were detected in at least 50% of the participants. After adjusting for potential confounders, we observed reduced odds of LGA in association with higher urinary concentrations of several exposure biomarkers. For example, an IQR-increase in the OPE metabolite, diphenyl phosphate, was associated with lower odds of LGA births (OR: 0.40 [95% CI: 0.18, 0.87]). Using quantile g-computation, we estimated lower odds of an LGA birth for higher OPE metabolite concentrations (OR: 0.49 [95% CI: 0.27, 0.89]) and phthalate metabolite concentrations (OR: 0.23 [95% CI: 0.07, 0.73]). Associations between consumer product chemicals and SGA were largely null. Conclusions: Joint exposure to OPEs and phthalates was associated with lower odds of delivering LGA. Associations with LGA could indicate a specific impact of these exposures on the high end of the birth weight spectrum. Future work to understand this nuance in the associations between consumer product chemical mixtures and fetal growth is warranted.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Prenatal exposure to consumer product chemical mixtures and size for gestational age at delivery

Bommarito

Welch

Keil

et al. 2021

Preprint

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“…We observed that levels of urinary DPhP as well as the mixture of OPE metabolites were associated with reduced odds of LGA births (i.e., lower birth weight) although there was no association with SGA. These ndings are consistent with two other epidemiologic studies that indicate a potential link between OPE exposure and altered fetal growth (17,18). For example, a recent prospective case-control study of low birth weight (n = 339) based in China reported that the odds of low birth weight in women with the highest tertile of urinary DPhP was 4.62 (95% CI: 1.72, 12.40) times that observed in the lowest tertile (17).…”

Section: Discussionsupporting

confidence: 90%

“…Nevertheless, the literature linking consumer product chemicals with altered fetal growth is highly inconsistent (1). These inconsistencies may be the result of differences in study design (17,18), timing and frequency of exposure assessment (19)(20)(21), and the metrics used to monitor and de ne fetal growth outcomes (22)(23)(24). In addition to these considerations, pregnant women are exposed to highly complex mixtures of consumer product chemicals (25,26).…”

Section: Introductionmentioning

confidence: 99%

Prenatal exposure to consumer product chemical mixtures and size for gestational age at delivery

Bommarito

Welch

Keil

et al. 2020

Preprint

View full text Add to dashboard Cite

Background While fetal growth is a tightly regulated process, it is sensitive to environmental exposures that occur during pregnancy. Many commonly used consumer products contain chemicals that can disturb processes underlying fetal growth. However, mixtures of these chemicals have been minimally examined. We investigated associations between prenatal exposure to 33 consumer product chemicals (nine organophosphate ester flame retardant [OPE] metabolites, 12 phthalate metabolites, and 12 phenols) and the odds of small- or large-for-gestational age (SGA and LGA) births. Methods This case-control study was comprised of SGA (N = 31), LGA (N = 28), and appropriate for gestational age control (N = 31) births selected from the larger LIFECODES cohort. Biomarkers of exposure to consumer product chemicals were quantified in maternal urine collected from up to three study visits during pregnancy. In a single-pollutant approach, odds ratios (OR) and 95% confidence intervals (CI) of SGA and LGA associated with an interquartile range (IQR)-increase in exposure biomarkers were estimated using multinomial logistic regression. In a multi-pollutant approach, quantile g-computation was used to jointly estimate the OR (95% CI) of SGA and LGA per simultaneous one quartile-change in all biomarkers belonging to each chemical class. Results Among the 33 biomarkers analyzed, 20 were detected in at least 50% of the participants. After adjusting for potential confounders, we observed reduced odds of LGA in association with higher urinary concentrations of several exposure biomarkers. For example, an IQR-increase in the OPE metabolite, diphenyl phosphate, was associated with lower odds of LGA births (OR: 0.40 [95% CI: 0.18, 0.87]). Using quantile g-computation, we estimated lower odds of an LGA birth for lower OPE metabolites (OR: 0.49 [95% CI: 0.27, 0.89]) and phthalate metabolites (OR: 0.23 [95% CI: 0.07, 0.73]). Associations between consumer product chemicals and SGA were largely null. Conclusions Joint exposure to OPEs and phthalates was associated with lower odds of delivering LGA. Associations with LGA could indicate a specific impact of these exposures on the high end of the birth weight spectrum. Future work to understand this nuance in the associations between consumer product chemical mixtures and fetal growth is warranted.

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Triphenyl phosphate interferes with the synthesis of steroid hormones through the PPARγ/CD36 pathway in human trophoblast JEG‐3 cells

Chen,

Liu,

Wang

et al. 2024

Environmental Toxicology

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Triphenyl phosphate (TPhP), a chemical commonly found in human placenta and breast milk, has been shown to disturb the endocrine system. Our previous study confirmed that TPhP could accumulate in the placenta and interference with placental lipid metabolism and steroid hormone synthesis, as well as induce endoplasmic reticulum (ER) stress through PPARγ in human placental trophoblast JEG‐3 cells. However, the molecular mechanism underlying this disruption remains unknown. Our study aimed to identify the role of the PPARγ/CD36 pathway in TPhP‐induced steroid hormone disruption. We found that TPhP increased lipid accumulation, total cholesterol, low‐ and high‐density protein cholesterol, progesterone, estradiol, glucocorticoid, and aldosterone levels, and genes related to steroid hormones synthesis, including 3βHSD1, 17βHSD1, CYP11A, CYP19, and CYP21. These effects were largely blocked by co‐exposure with either a PPARγ antagonist GW9662 or knockdown of CD36 using siRNA (siCD36). Furthermore, an ER stress inhibitor 4‐PBA attenuated the effect of TPhP on progesterone and glucocorticoid levels, and siCD36 reduced ER stress‐related protein levels induced by TPhP, including BiP, PERK, and CHOP. These findings suggest that ER stress may also play a role in the disruption of steroid hormone synthesis by TPhP. As our study has shed light on the PPARγ/CD36 pathway's involvement in the disturbance of steroid hormone biosynthesis by TPhP in the JEG‐3 cells, further investigations of the potential impacts on the placental function and following birth outcome are warranted.

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Prenatal Exposure to Organophosphate Flame Retardants and the Risk of Low Birth Weight: A Nested Case-Control Study in China

Cited by 75 publications

References 61 publications

Prenatal exposure to consumer product chemical mixtures and size for gestational age at delivery

Prenatal exposure to consumer product chemical mixtures and size for gestational age at delivery

Prenatal exposure to consumer product chemical mixtures and size for gestational age at delivery

Triphenyl phosphate interferes with the synthesis of steroid hormones through the PPARγ/CD36 pathway in human trophoblast JEG‐3 cells

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