Home Research Feeds Sex-specific effects of PM<sub>2.5</sub> maternal exposure on offspring's serum lipoproteins and gut microbiota

Sex-specific effects of PM<sub>2.5</sub> maternal exposure on offspring's serum lipoproteins and gut microbiotaOriginal paper

Researched by:

  • Karen Pendergrass

Last Updated: 2026-07-04

Karen Pendergrass
Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.

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Location
China
Sample Site
Colon
Species
Mus musculus

What was studied?

This study examined whether maternal exposure to fine particulate matter (PM2.5) during gestation and lactation affects serum lipoprotein levels and gut microbiota composition in offspring. Pregnant mice received PM2.5 by intratracheal instillation, and offspring were assessed at multiple postnatal timepoints. Serum lipoproteins were measured on postnatal day 35, while gut microbiota were profiled by 16S rDNA sequencing of colon contents on postnatal days 3, 10, 21, and 35. The design allowed comparison of sex-specific effects of maternal PM2.5 exposure on metabolic and microbial outcomes in offspring.

Who was studied?

The subjects were male and female mouse pups born to dams exposed to PM2.5 during pregnancy and lactation, compared against pups from an unexposed control group. Offspring were evaluated at several postnatal ages (days 3, 10, 21, and 35) to track developmental changes in gut microbiota. The abstract does not specify the exact number of animals per group. This was an animal (mouse) model study rather than a human cohort.

What were the most important findings?

Male offspring from PM2.5-exposed dams had significantly higher serum triglyceride concentrations than controls, while female offspring showed no significant lipoprotein differences. On postnatal day 35, PM2.5-exposed male offspring showed enrichment of Bacteroides, Desulfovibrio, and Anaerotruncus, whereas control males had more Streptococcus. Desulfovibrio, a sulfate-reducing bacterium associated with hydrogen sulfide production, was specifically enriched in the exposed male group. In female offspring, Clostridium XI was enriched in controls rather than the exposed group, and Bacteroides abundance correlated positively with serum triglyceride concentration.

What are the greatest implications of this study?

The findings suggest that maternal PM2.5 exposure produces sex-specific, long-term effects on offspring metabolism and gut microbiota, with male offspring appearing more vulnerable to lipid disturbances. The enrichment of Desulfovibrio, a sulfate-reducing, hydrogen sulfide-producing genus, alongside Bacteroides in exposed males raises questions about links between air pollution exposure, sulfur-metabolizing gut bacteria, and triglyceride regulation. These results imply that prenatal air pollution exposure could programmatically shape gut microbial communities and metabolic risk in a sex-dependent manner. Further work would be needed to clarify the mechanistic role of these bacterial shifts in the observed lipid changes.

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