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Published on: June 2, 2023
Perinatal exposure to di-(2-ethylhexyl) phthalate leads to restricted growth and delayed lung maturation in newborn
Shang-Qin Chen1, Jin-Ni Chen, Xiao-Hong Cai
1Department of Pediatrics, Yuying Children's Hospital of Wenzhou Medical College, Wenzhou, China.
Insights
Perinatal exposure to di-(2-ethylhexyl) phthalate (DEHP) caused significant growth restriction and delayed lung maturation in newborn rats. These effects were dose-dependent and persisted at postnatal day 21.
Area of Science:
- Environmental Health
- Toxicology
- Developmental Biology
Background:
- Pregnant women and infants are highly exposed to di-(2-ethylhexyl) phthalate (DEHP), a common plasticizer.
- Understanding DEHP's impact on vulnerable populations is crucial for public health.
Purpose of the Study:
- To investigate the effects of perinatal di-(2-ethylhexyl) phthalate (DEHP) exposure on rat growth and lung maturation.
- To determine the role of 11beta-hydroxysteroid dehydrogenase type 1 gene (Hsd11b1) regulation in DEHP's lung maturation effects.
Main Methods:
- Pregnant Sprague-Dawley rats received varying oral doses of DEHP from gestational day 12 to postnatal day 21.
- Rat pups were assessed for body weight, lung histology, interstitial tissue proportion, and gene expression (Hsd11b1, Sftpa1, Sftpb) at postnatal days 1 and 21.
Main Results:
- DEHP exposure resulted in dose-dependent intrauterine and postnatal growth restriction.
- High-dose DEHP exposure impaired lung gas-exchange space, indicated by increased interstitial tissue, but did not alter Hsd11b1, Sftpa1, or Sftpb gene expression at postnatal day 1.
- Lung histology changes persisted at postnatal day 21, showing some improvement despite ongoing DEHP exposure.
Conclusions:
- Perinatal di-(2-ethylhexyl) phthalate (DEHP) exposure induces significant growth restriction in newborn rats.
- DEHP exposure delays lung maturation, evidenced by impaired lung development, though specific gene expressions related to lung maturation were not significantly altered at postnatal day 1.
Background:
Pregnant women and infants have significant exposures to the most commonly used plasticizer di-(2-ethylhexyl) phthalate (DEHP).
Objectives:
This study was designed to evaluate the effects of DEHP exposure on growth and lung maturation in rats and determine if DEHP regulation of 11beta-hydroxysteroid dehydrogenase type 1 gene (Hsd11b1) expression in the lung tissue plays a role in its effects on lung maturation.
Method:
Pregnant Sprague-Dawley rats were treated from gestational day 12 to postnatal day (PND) 21 with DEHP orally at dosages of 0, 10, 100 or 750 mg/kg/day, respectively (n=8 for each group). Two rat pups (one male and one female) from each litter were sacrificed at PND 1 and 21. Body weight was measured and the lung was processed for histology and calculation of lung interstitial tissue proportion as well as real-time PCR determination of the expressions of Hsd11b1, surfactant associated protein-A1 gene (Sftpa1) and B gene (Sftpb).
Results:
The perinatal DEHP exposure led to a dose dependent intrauterine and postnatal growth restriction (P<0.001). High dose DEHP (750 mg/kg/day) exposure led to decreased gas-exchange space as evidenced by increased lung interstitial tissue proportion (P<0.001), but did not cause significant changes in Hsd11b1, Sftpa1 or Sftpb gene expression in the rat lung at PND 1. The DEHP-induced change in lung histology remained significant at PND 21 with improvement despite continual exposure to DEHP.
Conclusion:
Perinatal DEHP exposure leads to growth restriction and delayed lung maturation in newborn rats.
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