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Effect of Fine Particulate Matter (PM 2.5 ) on Rat Placenta Pathology and Perinatal Outcomes

View Article: PubMed Central - PubMed

ABSTRACT

Background: Fine particulate matter with aerodynamic diameters smaller than 2.5 μm (PM2.5) has been reported to cause adverse effects on human health. Evidence has shown the association between PM2.5 exposure and adverse perinatal outcomes, and the most common method is epidemiological investigation. We wished to investigate the impact of PM2.5 on placenta and prenatal outcomes and its related mechanisms in a rat model.

Material/methods: Pregnant rats were exposed to a low PM2.5 dose (15 mg/kg) with intratracheal instillation at pregnant day 10 and day 18, while the controls received an equivalent volume normal saline. All rats received cesarean section 24 h after the last intratracheal instillation and were sacrificed with anesthesia. Blood routine tests (BRT) and interleukin-6 (IL-6) were detected for analyzing inflammation and blood coagulation. Placenta tissue sections underwent pathologic examination, and the levels of homogenate glutathione peroxidase (GSH-Px) and methane dicarboxylic aldehyde (MDA) were determined for oxidative stress estimation.

Results: Increased absorbed blastocysts, and lower maternal weight gain and fetal weight were found in the PM2.5 exposure group compared to controls (p<0.05). Exposure to PM2.5 caused a significant increase of blood mononuclear cells (PBMC), platelets, and IL-6 levels (P<0.01). There were no differences in GSH-Px and MDA of placenta homogenate between the 2 groups (P>0.05). Placenta pathological examination demonstrated thrombus and chorioamnionitis in the PM2.5 exposure group.

Conclusions: PM2.5 exposure can result in placental pathological changes and adverse perinatal outcomes. The placental inflammation and hypercoagulability with vascular thrombosis may play important roles in placental impairment, but oxidative stress appears to be less important.

No MeSH data available.


Related in: MedlinePlus

Hematoxylin and eosin (HE) staining of placental tissue. (A, B) Non-exposed placental tissue did not shown abnormal pathological changes; (C–H) Placental tissues from PM2.5 exposure rats were described by: (C, D) placental infiltration of neutrophilic granulocytes involving amniotic membrane (E) thrombus (black triangle), (F) focal fibrinoid (black arrow), and (G) amnion with flat papillae and desquamated epithelial cells [=200×]. (H) Syncytiotrophoblast nodule (white arrow) observed from exposed placenta [=400×].
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f2-medscimonit-22-3274: Hematoxylin and eosin (HE) staining of placental tissue. (A, B) Non-exposed placental tissue did not shown abnormal pathological changes; (C–H) Placental tissues from PM2.5 exposure rats were described by: (C, D) placental infiltration of neutrophilic granulocytes involving amniotic membrane (E) thrombus (black triangle), (F) focal fibrinoid (black arrow), and (G) amnion with flat papillae and desquamated epithelial cells [=200×]. (H) Syncytiotrophoblast nodule (white arrow) observed from exposed placenta [=400×].

Mentions: All the exposed placentas demonstrated at least 1 abnormal pathological finding (Figure 2C–2H). Extensive neutrophilic granulocyte infiltration (87.50%) was the most common microscopic finding (Figure 2C, 2D), followed by placental thrombus (62.50%, Figure 2E), fibrin deposition (37.50%, Figure 2F) in fetal surface, and serious amnionitis (25.00%) with papillae loss and epithelial cell necrocytosis and shedding (Figure 2G). Syncytiotrophoblast cells hyperplasia was common and some specimens showed syncytiotrophoblast nodules (25.00%, Figure 2H).


Effect of Fine Particulate Matter (PM 2.5 ) on Rat Placenta Pathology and Perinatal Outcomes
Hematoxylin and eosin (HE) staining of placental tissue. (A, B) Non-exposed placental tissue did not shown abnormal pathological changes; (C–H) Placental tissues from PM2.5 exposure rats were described by: (C, D) placental infiltration of neutrophilic granulocytes involving amniotic membrane (E) thrombus (black triangle), (F) focal fibrinoid (black arrow), and (G) amnion with flat papillae and desquamated epithelial cells [=200×]. (H) Syncytiotrophoblast nodule (white arrow) observed from exposed placenta [=400×].
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Related In: Results  -  Collection

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f2-medscimonit-22-3274: Hematoxylin and eosin (HE) staining of placental tissue. (A, B) Non-exposed placental tissue did not shown abnormal pathological changes; (C–H) Placental tissues from PM2.5 exposure rats were described by: (C, D) placental infiltration of neutrophilic granulocytes involving amniotic membrane (E) thrombus (black triangle), (F) focal fibrinoid (black arrow), and (G) amnion with flat papillae and desquamated epithelial cells [=200×]. (H) Syncytiotrophoblast nodule (white arrow) observed from exposed placenta [=400×].
Mentions: All the exposed placentas demonstrated at least 1 abnormal pathological finding (Figure 2C–2H). Extensive neutrophilic granulocyte infiltration (87.50%) was the most common microscopic finding (Figure 2C, 2D), followed by placental thrombus (62.50%, Figure 2E), fibrin deposition (37.50%, Figure 2F) in fetal surface, and serious amnionitis (25.00%) with papillae loss and epithelial cell necrocytosis and shedding (Figure 2G). Syncytiotrophoblast cells hyperplasia was common and some specimens showed syncytiotrophoblast nodules (25.00%, Figure 2H).

View Article: PubMed Central - PubMed

ABSTRACT

Background: Fine particulate matter with aerodynamic diameters smaller than 2.5 μm (PM2.5) has been reported to cause adverse effects on human health. Evidence has shown the association between PM2.5 exposure and adverse perinatal outcomes, and the most common method is epidemiological investigation. We wished to investigate the impact of PM2.5 on placenta and prenatal outcomes and its related mechanisms in a rat model.

Material/methods: Pregnant rats were exposed to a low PM2.5 dose (15 mg/kg) with intratracheal instillation at pregnant day 10 and day 18, while the controls received an equivalent volume normal saline. All rats received cesarean section 24 h after the last intratracheal instillation and were sacrificed with anesthesia. Blood routine tests (BRT) and interleukin-6 (IL-6) were detected for analyzing inflammation and blood coagulation. Placenta tissue sections underwent pathologic examination, and the levels of homogenate glutathione peroxidase (GSH-Px) and methane dicarboxylic aldehyde (MDA) were determined for oxidative stress estimation.

Results: Increased absorbed blastocysts, and lower maternal weight gain and fetal weight were found in the PM2.5 exposure group compared to controls (p<0.05). Exposure to PM2.5 caused a significant increase of blood mononuclear cells (PBMC), platelets, and IL-6 levels (P<0.01). There were no differences in GSH-Px and MDA of placenta homogenate between the 2 groups (P>0.05). Placenta pathological examination demonstrated thrombus and chorioamnionitis in the PM2.5 exposure group.

Conclusions: PM2.5 exposure can result in placental pathological changes and adverse perinatal outcomes. The placental inflammation and hypercoagulability with vascular thrombosis may play important roles in placental impairment, but oxidative stress appears to be less important.

No MeSH data available.


Related in: MedlinePlus