Household air pollution and chronic hypoxia in the placenta of pregnant Nigerian women: A randomized controlled ethanol Cookstove intervention

Dutta, Anindita; Khramtsova, Galina; Brito, Katherine; Alexander, Donee; Mueller, Ariel; Chinthala, Sireesha; Adu, Damilola; Ibigbami, Tope; Olamijulo, John; Odetunde, Abayomi; Adigun, Kehinde; Pruitt, Liese C.C.; Hurley, Ian; Olopade, Olufunmilayo I.; Ojengbede, Oladosu; Rana, Sarosh; Olopade, Christopher O.

doi:10.1016/j.scitotenv.2017.11.091

Cited by 27 publications

(15 citation statements)

References 52 publications

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“…Air pollution has already been linked to placental transcriptome changes (74), placental DNA methylation (75) and a reduced placenta weight (76). Further, women exposed to high levels of air pollution from cooking with solid fuels have shown chronic placental hypoxia (77) and fetal thrombotic vasculopathy (78). Adding to this body of knowledge, our data suggest that exposure to PM2.5 in vitro has the potential to induce cellular toxicity as well as hormone dysregulation, oxidative damage, inflammatory response, and interference with mitochondria in first trimester placental cells (HTR-8 cells).…”

Section: Discussionmentioning

confidence: 66%

Urban PM2.5 Induces Cellular Toxicity, Hormone Dysregulation, Oxidative Damage, Inflammation, and Mitochondrial Interference in the HRT8 Trophoblast Cell Line

et al. 2020

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Objective: Epidemiological studies have found air pollution to be a driver of adverse pregnancy outcomes, including gestational diabetes, low term birth weight and preeclampsia. It is unknown what biological mechanisms are involved in this process. A first trimester trophoblast cell line (HTR-8/SVneo) was exposed to various concentrations of PM2.5 (PM2.5) in order to elucidate the effect of urban particulate matter (PM) of size <2.5 µm on placental function. Methods: PM2.5 were collected at a site representative of urban traffic and dispersed in cell media by indirect and direct sonication. The HTR-8 cells were grown under standard conditions. Cellular uptake was studied after 24 and 48 h of exposure by transmission electron microscopy (TEM). The secretion of human chorionic gonadotropin (hCG), progesterone, and Interleukin-6 (IL-6) was measured by ELISA. Changes in membrane integrity and H 2 O 2 production were analyzed using the CellTox TM Green Cytotoxicity and ROSGlo TM assays. Protease activity was evaluated by MitoTox TM assay. Mitochondrial function was assessed through high resolution respirometry in an Oroboros O2k-FluoRespirometer, and mitochondrial content was quantified by citrate synthase activity. Results: TEM analysis depicted PM2.5 cellular uptake and localization of the PM2.5 to the mitochondria after 24 h. The cells showed aggregated cytoskeleton and generalized necrotic appearance, such as chromatin condensation, organelle swelling and signs of lost membrane integrity. The mitochondria displayed vacuolization and disruption of cristae morphology. At 48 h exposure, a significant drop in hCG secretion and a significant increase in progesterone secretion and IL-6 production occurred. At 48 h exposure, a five-fold increase in protease activity and a significant alteration of H 2 O 2 production was observed. The HTR-8 cells exhibited evidence of increased cytotoxicity with increasing exposure time and dose of PM2.5. No significant difference in mitochondrial respiration or mitochondrial mass could be demonstrated. Nääv et al. Urban PM2.5 Toxic to Trophoblast Cells Conclusion: Following exposure to air pollution, intracellular accumulation of PM may contribute to the placental dysfunction associated with pregnancy outcomes, such as preeclampsia and intrauterine growth restriction, through their direct and indirect effects on trophoblast protein secretion, hormone regulation, inflammatory response, and mitochondrial interference.

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Section: Discussionmentioning

confidence: 66%

Urban PM2.5 Induces Cellular Toxicity, Hormone Dysregulation, Oxidative Damage, Inflammation, and Mitochondrial Interference in the HRT8 Trophoblast Cell Line

et al. 2020

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“…IL-6, IL-1b) into the human circulation following exposure to PM has been demonstrated [17]. Changes in placental functions including altered gene expression and increases in markers of oxidative stress [28, 29], mitochondrial dysfunction and altered methylation profiles [30–32], and endothelial and villi pathology [21] have been reported following inhalation of PM during human pregnancy. More recently, Qin and colleagues found that exposure to high levels of urban PM2.5 (particles ≤ 2.5 μm) induced cell-cycle arrest, inhibited migration and invasion of extravillous trophoblast cells [33].…”

Section: Introductionmentioning

confidence: 99%

Exposure of trophoblast cells to fine particulate matter air pollution leads to growth inhibition, inflammation and ER stress

et al. 2019

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Ambient air pollution is considered a major environmental health threat to pregnant women. Our previous work has shown an association between exposure to airborne particulate matter (PM) and an increased risk of developing pre-eclamspia. It is now recognized that many pregnancy complications are due to underlying placental dysfunction, and this tissue plays a pivotal role in pre-eclamspia. Recent studies have shown that PM can enter the circulation and reach the human placenta but the effects of PM on human placental function are still largely unknown. In this work we investigated the effects of airborne PM on trophoblast cells. Human, first trimester trophoblast cells (HTR-8/SV) were exposed to urban pollution particles (Malmö PM2.5; Prague PM10) for up to seven days in vitro and were analysed for uptake, levels of hCGβ and IL-6 secretion and proteomic analysis. HTR-8/SVneo cells rapidly endocytose PM within 30 min of exposure and particles accumulate in the cell in perinuclear vesicles. High doses of Prague and Malmö PM (500–5000 ng/ml) significantly decreased hCGβ secretion and increased IL-6 secretion after 48 h exposure. Exposure to PM (50 ng/ml) for 48h or seven days led to reduced cellular growth and altered protein expression. The differentially expressed proteins are involved in networks that regulate cellular processes such as inflammation, endoplasmic reticulum stress, cellular survival and molecular transport pathways. Our studies suggest that trophoblast cells exposed to low levels of urban PM respond with reduced growth, oxidative stress, inflammation and endoplasmic reticulum stress after taking up the particles by endocytosis. Many of the dysfunctional cellular processes ascribed to the differentially expressed proteins in this study, are similar to those described in PE, suggesting that low levels of urban PM may disrupt cellular processes in trophoblast cells. Many of the differentially expressed proteins identified in this study are involved in inflammation and may be potential biomarkers for PE.

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“…Exposure to pollutant cooking fuel is associated with LBW [15]. Exposure to household air pollution (HAP) is associated with placental function (placental inflammation, placental hypoxia and thrombotic placental lesions) [44,45]. Exposure to these fuels affects placental function.…”

Section: Social and Demographic Factors (Table 2)mentioning

confidence: 99%

Interactions between the Physical and Social Environments with Adverse Pregnancy Events Related to Placental Disorders—A Scoping Review

Dube

Nyapwere

Magee

et al. 2020

IJERPH

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Background: Due to different social and physical environments across Africa, understanding how these environments differ in interacting with placental disorders will play an important role in developing effective interventions. Methods: A scoping review was conducted, to identify current knowledge on interactions between the physical and social environment and the incidence of placental disease in Africa. Results: Heavy metals were said to be harmful when environmental concentrations are beyond critical limits. Education level, maternal age, attendance of antenatal care and parity were the most investigated social determinants. Conclusions: More evidence is needed to determine the relationships between the environment and placental function in Africa. The results show that understanding the nature of the relationship between social determinants of health (SDH) and placental health outcomes plays a pivotal role in understanding the risk in the heterogenous communities in Africa.

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Household air pollution and chronic hypoxia in the placenta of pregnant Nigerian women: A randomized controlled ethanol Cookstove intervention

Cited by 27 publications

References 52 publications

Urban PM2.5 Induces Cellular Toxicity, Hormone Dysregulation, Oxidative Damage, Inflammation, and Mitochondrial Interference in the HRT8 Trophoblast Cell Line

Urban PM2.5 Induces Cellular Toxicity, Hormone Dysregulation, Oxidative Damage, Inflammation, and Mitochondrial Interference in the HRT8 Trophoblast Cell Line

Exposure of trophoblast cells to fine particulate matter air pollution leads to growth inhibition, inflammation and ER stress

Interactions between the Physical and Social Environments with Adverse Pregnancy Events Related to Placental Disorders—A Scoping Review

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