Summary: New research finds that gestational exposure to ultrafine particulate (UFP) air pollution alters placental gene expression and is linked to reduced fetal and placental growth, particularly at lower exposure levels.
Source: Texas A&M
Air pollution is a major global health threat, contributing to millions of deaths annually and accounting for an estimated 20 percent of newborn fatalities worldwide, primarily through increased risks of preterm birth and low birth weight. Understanding how specific components of air pollution affect pregnancy and fetal development is essential for public health policy and maternal care.
Researchers at Texas A&M University, together with collaborators, investigated how exposure to ultrafine particles (UFPs)—airborne particulate matter smaller than 100 nanometers—affects placental biology and fetal outcomes in an experimental model. Their findings, published in Toxicological Sciences, identify dose- and sex-specific effects on placental morphology, fetal growth measures, and placental gene networks.
Led by doctoral candidate Jonathan Behlen and associate professor Natalie Johnson, the team exposed pregnant experimental animals to a realistic urban UFP mixture at two concentrations: a low dose below regulatory PM2.5 limits and a higher dose. Control animals breathed filtered air. The study evaluated fetal weight, crown-to-rump length, placental size and structure, and changes in placental gene expression using RNA sequencing to characterize transcriptional responses.
Particulate matter includes a range of particle sizes, with ultrafine particles (UFPs) being the smallest and increasingly implicated in adverse pregnancy outcomes. While epidemiological evidence links UFP exposure to negative maternal and fetal outcomes, mechanistic details have been scarce. This study addresses that gap by combining morphological assessments with transcriptomic profiling of placental tissue from male and female offspring.
Key results showed that the low-dose UFP group exhibited significant reductions in fetal crown-to-rump length and average placental weight in female offspring, along with trends toward lower fetal weight in both sexes. Placental morphology was altered in a dose- and sex-dependent manner: female decidual areas increased in both exposure groups, maternal lacunae mean areas were enlarged in low-dose females, and fetal blood vessel areas were larger in male placentas at both doses. These structural changes suggest disruptions to the maternal-fetal interface that could influence nutrient transfer and fetal growth.
On the molecular level, RNA sequencing revealed altered expression of genes involved in antioxidant responses, inflammation, and lipid metabolism. Notably, many transcriptional changes were more pronounced in the low-dose group than the high-dose group and were often greater in female placental tissue than in male tissue. The altered gene networks point to oxidative stress, inflammatory signaling, and disrupted lipid handling as potential pathways through which UFPs impact placental function and fetal development.
The researchers emphasize that the study examined mixed placental cell populations, so the observed transcriptional signatures reflect combined signals across cell types. They recommend future studies that apply single-cell or cell-type–specific approaches to pinpoint which placental cell populations drive the sex- and dose-specific responses. Additional mechanistic work will be needed to explain why female placentas and fetuses showed more pronounced transcriptional and morphological changes in some measures.
These findings align with broader evidence that fine and ultrafine particulate pollution negatively affect pregnancy and fetal development. By identifying specific gene networks and structural changes in the placenta, this work provides a foundation for follow-up studies aimed at clarifying mechanisms and informing interventions to reduce the harms of air pollution during pregnancy.
About this genetics and pollution research news
Author: Press Office
Source: Texas A&M
Contact: Press Office – Texas A&M
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Original Research: Closed access.
“Gestational Exposure to Ultrafine Particles Reveals Sex- and Dose-Specific Changes in Offspring Birth Outcomes, Placental Morphology, and Gene Networks” by Jonathan C. Behlen et al., Toxicological Sciences
Abstract
Gestational Exposure to Ultrafine Particles Reveals Sex- and Dose-Specific Changes in Offspring Birth Outcomes, Placental Morphology, and Gene Networks
Particulate matter exposure during pregnancy is linked to adverse developmental outcomes, but the biological mechanisms remain incompletely defined. This study examined the effects of diesel exhaust–derived ultrafine particles (UFPs) on placental and fetal development in a controlled experimental model. Time-mated C57Bl/6n mice received daily 6-hour exposures to UFPs at either a low dose (100 µg/m3) or a high dose (500 µg/m3), with filtered air as the control condition.
At gestational day 18.5, researchers measured fetal and placental phenotypes and performed RNA sequencing on placental tissue from male and female offspring. Female offspring in the low-dose exposure group showed significant decreases in average placental weight and crown-to-rump length. Placental morphology changed in a dose- and sex-specific manner: female decidua areas increased at both exposure levels, maternal lacunae expanded in low-dose females, and fetal blood vessel areas were larger in male placentas at both doses.
Transcriptomic analysis revealed disturbances in cellular functions related to lipid metabolism, with the greatest transcriptional disruption observed in the low-dose group and especially in female placental tissue. These results demonstrate that gestational UFP exposure produces measurable, sex-specific impacts on placental structure and gene networks, underscoring the vulnerability of offspring to ultrafine particle pollution and the importance of reducing maternal exposure to mitigate adverse outcomes.