Abstract
BackgroundAirborne pollution, especially from diesel exhaust (DE), is known to have a negative effect on the central nervous system in exposed human populations. However, the consequences of gestational exposure to DE on the fetal brain remain poorly explored, with various effects depending on the conditions of exposure, as well as little information on early developmental stages. We investigated the short-term effects of indirect DE exposure throughout gestation on the developing brain using a rabbit model. We analyzed fetal olfactory tissues at the end of gestation and tested behaviors relevant to pups’ survival at birth.Pregnant dams were exposed by nose-only inhalation to either clean air or DE with a content of particles (DEP) adjusted to 1 mg/m3 by diluting engine exhaust, for 2 h/day, 5 days/week, from gestational day 3 (GD3) to day 27 (GD27). At GD28, fetal olfactory mucosa, olfactory bulbs and whole brains were collected for anatomical and neurochemical measurements. At postnatal day 2 (PND2), pups born from another group of exposed or control female were examined for their odor-guided behavior in response to the presentation of the rabbit mammary pheromone 2-methyl-3-butyn-2-ol (2MB2).ResultsAt GD28, nano-sized particles were observed in cilia and cytoplasm of the olfactory sensory neurons in the olfactory mucosa and in the cytoplasm of periglomerular cells in the olfactory bulbs of exposed fetuses. Moreover, cellular and axonal hypertrophies were observed throughout olfactory tissues. Concomitantly, fetal serotoninergic and dopaminergic systems were affected in the olfactory bulbs. Moreover, the neuromodulatory homeostasis was disturbed in a sex-dependent manner in olfactory tissues. At birth, the olfactory sensitivity to 2MB2 was reduced in exposed PND2 pups.ConclusionGestational exposure to DE alters olfactory tissues and affects monoaminergic neurotransmission in fetuses’ olfactory bulbs, resulting in an alteration of olfactory-based behaviors at birth. Considering the anatomical and functional continuum between the olfactory system and other brain structures, and due to the importance of monoamine neurotransmission in the plasticity of neural circuits, such alterations could participate to disturbances in higher integrative structures, with possible long-term neurobehavioral consequences.
Highlights
Airborne pollution, especially from diesel exhaust (DE), is known to have a negative effect on the central nervous system in exposed human populations
Transmission Electron microscopy (TEM) analysis Structural and ultrastructural changes in the olfactory mucosa (OM) Observations were made at different levels of the OM, from the apical part of the epithelium in contact with the mucus to the axon fascicles under the lamina propria (Fig. 1)
Chromatin was condensed and marginalized in the olfactory ensheating cells (OEC), as shown by the presence of dense patches of chromatin at the periphery of the nucleus, which was not observed in control samples (Fig. 1h compared to 1 g)
Summary
Especially from diesel exhaust (DE), is known to have a negative effect on the central nervous system in exposed human populations. Air pollution is a mixture of several components, among which particulate matter (PM) is believed to be the most widespread threat to human health and has been heavily implicated in various human diseases [1,2,3]. Among these components, diesel exhaust particles (DEP) represent a major source of PM-polluted air in urban environments (reviewed in [4, 5]). Gestational exposure to airborne pollution may affect fetal brain development during critical phases and might predispose the individual to neurodevelopmental and neurodegenerative diseases later in life [19]
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