Abstract
Atmospheric pollution has major health effects on directly exposed subjects but intergenerational consequences are poorly characterized. We previously reported that diesel engine exhaust (DE) could lead to structural changes in the placenta of in utero exposed rabbits (first generation, F1). The effects of maternal exposure to DE were further studied on second-generation (F2) rabbits. Pregnant F0 females were exposed to filtered, diluted DE (1 mg/m3, median particle diameter: 69 nm) or clean filtered air (controls) for 2 h/day, 5 days/week by nose-only exposure during days 3–27 post-conception (dpc). Adult female offspring (F1) were mated to control males: F1 tissues and F2 foeto-placental units were collected at 28 dpc and placental structure and gene expression (microarray) analysed. Fatty acid profiles were determined in foetal and maternal plasma, maternal liver and placenta. In F1, compared to controls, hepatic neutral lipid contents were increased in exposed animals without change in the blood biochemistry. In F2, the placental lipid contents were higher, with higher monounsaturated fatty acids and reduced pro-inflammatory arachidonic acid (AA), without placental structural changes. Conversely, the proportion of anti-inflammatory n-3 polyunsaturated fatty acids in F2 plasma was increased while that of AA was decreased. Gene set enrichment analyses (GSEA) of F2 placenta transcriptomic data identified that the proteasome complex and ubiquitin pathways genes were over-represented and ion channel function and inflammation pathways genes were under-represented in exposed animals. These preliminary results demonstrate that diesel engine exhaust exposure and in utero indirect exposure should be considered as a programming factor within the context of the DOHaD (Developmental Origins of Health and Disease) with a probable intergenerational transmission.
Highlights
Atmospheric pollution has major health effects on directly exposed subjects but intergenerational consequences are poorly characterized
The ovarian reserve was reported to be decreased after maternal exposure to DE17. These results suggest that offspring gonads and gametes may be affected, possibly inducing second-generation effects, as described with other environmental factors[18,19]
Hereafter, cellular component (CC) refers to F2 foeto-placental units collected from F1 control (C) dams, and EC refers to F2 foeto-placental units collected from in utero-exposed F1 (E) dams, with no further exposure of these F1 females after birth until adulthood and during their own gestation
Summary
Atmospheric pollution has major health effects on directly exposed subjects but intergenerational consequences are poorly characterized. Gene set enrichment analyses (GSEA) of F2 placenta transcriptomic data identified that the proteasome complex and ubiquitin pathways genes were over-represented and ion channel function and inflammation pathways genes were under-represented in exposed animals These preliminary results demonstrate that diesel engine exhaust exposure and in utero indirect exposure should be considered as a programming factor within the context of the DOHaD (Developmental Origins of Health and Disease) with a probable intergenerational transmission. The ovarian reserve was reported to be decreased (reduced number of primary follicles) after maternal exposure to DE17 These results suggest that offspring gonads and gametes may be affected, possibly inducing second-generation effects, as described with other environmental factors[18,19]. One Brazilian study showed that in mice, continuous exposure to urban San Paulo pollution over 3 generations altered second generation female fertility and increased the incidence of foetal abortion, decreased foetal weight and altered placental structure in the third generation[8,9]
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