Dataset Information

Maternal exposure to diluted diesel engine exhaust alters placental function and induces intergenerational effects in rabbits.

ABSTRACT: Airborne pollution is a rising concern in urban areas. Epidemiological studies in humans and animal experiments using rodent models indicate that gestational exposure to airborne pollution, in particular diesel engine exhaust (DE), reduces birth weight, but effects depend on exposure duration, gestational window and nanoparticle (NP) concentration. Our aim was to evaluate the effects of gestational exposure to diluted DE on feto-placental development in a rabbit model. Pregnant females were exposed to diluted (1 mg/m(3)), filtered DE (NP diameter???69 nm) or clean air (controls) for 2 h/day, 5 days/week by nose-only exposure (total exposure: 20 days in a 31-day gestation).DE exposure induced early signs of growth retardation at mid gestation with decreased head length (p?=?0.04) and umbilical pulse (p?=?0.018). Near term, fetal head length (p?=?0.029) and plasma insulin and IGF1 concentrations (p?=?0.05 and p?=?0.019) were reduced. Placental function was also affected, with reduced placental efficiency (fetal/placental weight) (p?=?0.049), decreased placental blood flow (p?=?0.009) and fetal vessel volume (p?=?0.002). Non-aggregated and "fingerprint" NP were observed at various locations, in maternal blood space, in trophoblastic cells and in the fetal blood, demonstrating transplacental transfer. Adult female offspring were bred with control males. Although fetoplacental biometry was not affected near term, second generation fetal metabolism was modified by grand-dam exposure with decreased plasma cholesterol (p?=?0.008) and increased triglyceride concentrations (p?=?0.015).Repeated daily gestational exposure to DE at levels close to urban pollution can affect feto-placental development in the first and second generation.

SUBMITTER: Valentino SA

PROVIDER: S-EPMC4962477 | biostudies-literature | 2016 Jul

REPOSITORIES: biostudies-literature

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Maternal exposure to diluted diesel engine exhaust alters placental function and induces intergenerational effects in rabbits.

Valentino Sarah A SA Tarrade Anne A Aioun Josiane J Mourier Eve E Richard Christophe C Dahirel Michèle M Rousseau-Ralliard Delphine D Fournier Natalie N Aubrière Marie-Christine MC Lallemand Marie-Sylvie MS Camous Sylvaine S Guinot Marine M Charlier Madia M Aujean Etienne E Al Adhami Hala H Fokkens Paul H PH Agier Lydiane L Boere John A JA Cassee Flemming R FR Slama Rémy R Chavatte-Palmer Pascale P

Particle and fibre toxicology 20160726 1

<h4>Background</h4>Airborne pollution is a rising concern in urban areas. Epidemiological studies in humans and animal experiments using rodent models indicate that gestational exposure to airborne pollution, in particular diesel engine exhaust (DE), reduces birth weight, but effects depend on exposure duration, gestational window and nanoparticle (NP) concentration. Our aim was to evaluate the effects of gestational exposure to diluted DE on feto-placental development in a rabbit model. Pregnan ...[more]

PMID: 27460165

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Project description:BackgroundDiesel engine exhaust (DEE) exposure causes lung cancer, but the molecular mechanisms by which this occurs are not well understood.ObjectivesTo assess transcriptomic alterations in nasal epithelium of DEE-exposed factory workers to better understand the cellular and molecular effects of DEE.MethodsNasal epithelial brushings were obtained from 41 diesel engine factory workers exposed to relatively high levels of DEE (17.2-105.4 μg/m3), and 38 unexposed workers from factories without DEE exposure. mRNA was profiled for gene expression using Affymetrix microarrays. Linear modeling was used to identify differentially expressed genes associated with DEE exposure and interaction effects with current smoking status. Pathway enrichment among differentially expressed genes was assessed using EnrichR. Gene Set Enrichment Analysis (GSEA) was used to compare gene expression patterns between datasets.Results225 genes had expression associated with DEE exposure after adjusting for smoking status (FDR q < 0.25) and were enriched for genes in pathways related to oxidative stress response, cell cycle pathways such as MAPK/ERK, protein modification, and transmembrane transport. Genes up-regulated in DEE-exposed individuals were enriched among the genes most up-regulated by cigarette smoking in a previously reported bronchial airway smoking dataset. We also found that the DEE signature was enriched among the genes most altered in two previous studies of the effects of acute DEE on PBMC gene expression. An exposure-response relationship was demonstrated between air levels of elemental carbon and the first principal component of the DEE signature.ConclusionsA gene expression signature was identified for workers occupationally exposed to DEE that was altered in an exposure-dependent manner and had some overlap with the effects of smoking and the effects of acute DEE exposure. This is the first study of gene expression in nasal epithelial cells of workers heavily exposed to DEE and provides new insights into the molecular alterations that occur with DEE exposure.

Project description:Epidemiological studies have reported an increased risk of cardiopulmonary and lung cancer mortality associated with increasing exposure to air pollution. Ambient particulate matter consists of primary particles emitted directly from diesel engine vehicles and secondary organic aerosols (SOAs) are formed by oxidative reaction of the ultrafine particle components of diesel exhaust (DE) in the atmosphere. However, little is known about the relationship between exposure to SOA and central nervous system functions. Recently, we have reported that an acute single intranasal instillation of SOA may induce inflammatory response in lung, but not in brain of adult mice. To clarify the whole body exposure effects of SOA on central nervous system functions, we first created inhalation chambers for diesel exhaust origin secondary organic aerosols (DE-SOAs) produced by oxidation of diesel exhaust particles caused by adding ozone. Male BALB/c mice were exposed to clean air (control), DE and DE-SOA in inhalation chambers for one or three months (5 h/day, 5 days/week) and were examined for memory function using a novel object recognition test and for memory function-related gene expressions in the hippocampus by real-time RT-PCR. Moreover, female mice exposed to DE-SOA for one month were mated and maternal behaviors and the related gene expressions in the hypothalamus examined. Novel object recognition ability and N-methyl-D-aspartate (NMDA) receptor expression in the hippocampus were affected in male mice exposed to DE-SOA. Furthermore, a tendency to decrease maternal performance and significantly decreased expression levels of estrogen receptor (ER)-α, and oxytocin receptor were found in DE-SOA exposed dams compared with the control. This is the first study of this type and our results suggest that the constituents of DE-SOA may be associated with memory function and maternal performance based on the impaired gene expressions in the hippocampus and hypothalamus, respectively.

Dataset Information

Maternal exposure to diluted diesel engine exhaust alters placental function and induces intergenerational effects in rabbits.

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Maternal exposure to diluted diesel engine exhaust alters placental function and induces intergenerational effects in rabbits.

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