Related Experiment Video
Updated: Aug 28, 2025
A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
Mediation Effects of Placental Inflammatory Transcriptional Biomarkers on the Sex-Dependent Associations between
Jian Qing Wang1, Zhi Juan Li2, Hui Gao3
1Department of Maternal, Child and Adolescent Health, School of Public Health, Anhui Medical University, Hefei 230032, Anhui, China;MOE Key Laboratory of Population Health across Life Cycle, Hefei 230032, Anhui, China;NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Hefei 230032, Anhui, China;Anhui Provincial Key Laboratory of Population Health and Aristogenics, Anhui Medical University, Hefei 230032, Anhui, China;The Fourth Affiliated Hospital, Anhui Medical University, Hefei 230022, Anhui, China.
Insights
Prenatal exposure to certain phthalates increases infant allergic rhinitis (AR) risk in males, with placental HO-1 acting as a mediator. This highlights the placenta's role in maternal exposure-induced childhood diseases.
Area of Science:
- Environmental Health
- Pediatrics
- Immunology
Background:
- Prenatal phthalate exposure is linked to infant allergic rhinitis (AR), but findings are inconsistent.
- Placental inflammatory factors may influence this association, particularly in a sex-dependent manner.
Purpose of the Study:
- To investigate the role of placental inflammatory biomarkers in the relationship between maternal phthalate exposure and infant AR.
- To examine sex-specific associations between prenatal phthalate exposure and infant AR.
Main Methods:
- A population-based cohort study included 2,348 pregnant women and their offspring at 36 months.
- Infant AR was assessed via questionnaire; placental inflammatory factor mRNAs were measured using quantitative PCR.
- Multivariable logistic regression and mediation analysis were employed.
Main Results:
- Maternal exposure to MEHP and MEHHP was associated with increased infant AR risk in males, but not females.
- Increased placental HO-1 and IL-4 expression correlated with AR in male infants.
- Placental HO-1 was identified as a partial mediator between MEHHP exposure and infant AR.
Conclusions:
- Maternal phthalate metabolites (MEHHP, MEOHP) significantly associate with infant AR in males.
- The placenta, specifically HO-1, acts as a mediator in phthalate-induced AR risk.
- Further research into the placenta's role in mediating maternal exposure effects on child health is warranted.
Objective:
Prenatal phthalate exposure has been associated with placental inflammatory factors and infant allergic rhinitis (AR). However, the results are inconclusive. We designed a population-based cohort study to examine the effects of placental inflammatory biomarkers on the sex-dependent associations between maternal phthalate exposure and infant AR.
Methods:
A total of 2,348 pregnant women from Ma'anshan, Anhui Province, China, who were screened before antenatal visits and met the inclusion criteria, were included in the present study. We assessed AR in their offspring aged 36 months with a questionnaire. Quantitative PCR was performed to measure placental inflammatory factor mRNAs. The independent samples t-test and multivariable logistic regression were used to determine the associations between infant AR and maternal phthalates.
Results:
Childhood AR may be related to education and family monthly income ( P = 0.01). The phthalate metabolites, mono (2-ethylhexyl) phthalate (MEHP), mono (2-ethyl-5-hydroxyl) phthalate (MEHHP), in pregnant women were associated with a significantly increased risk for infant AR in males [ P < 0.05; odds ratio ( OR): 1.285; 95% confidence interval ( CI): 1.037-1.591, and OR: 1.232, 95% CI: 1.008-1.507, respectively], but not females. Additionally, irritably-increased expression levels of HO-1 and IL-4 were associated with AR in male infants ( OR: 1.175; 95% CI: 1.038-1.329 and OR: 1.181; 95% CI: 1.056-1.322, respectively). The association between maternal urinary MEHHP and placental HO-1 was marginally significant according to mediation analysis.
Conclusion:
The associations of maternal MEHHP and MEOHP levels with fetal AR in males were significant. Placental HO-1 was a fractional mediator in the associations between MEHHP and AR. Thus, the placenta should be further investigated as a potential mediator of maternal exposure-induced disease risk in children.
More Related Videos
05:31Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels
Published on: August 7, 2017
11:44A Primary Human Trophoblast Model to Study the Effect of Inflammation Associated with Maternal Obesity on Regulation of Autophagy in the Placenta
Published on: September 27, 2017