&lt;i&gt;In utero&lt;/i&gt; exposure to diesel exhaust particles induces anxiogenic effects on male offspring via chronic activation of serotonergic neuron in dorsal raphe nucleus

Yokota, Satoshi; Oshio, Shigeru; Takeda, Ken

doi:10.2131/jts.41.583

Cited by 11 publications

(8 citation statements)

References 65 publications

(83 reference statements)

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“…In mice, exposure to fine particles in utero and during the period corresponding to the third trimester of pregnancy in human beings was linked to structural changes in white matter. Other studies of in utero exposure in mice showed delayed cognitive development, increased anxiety and disrupted methylation of genes related to neurogenesis . In human beings, the available evidence on the effect of in utero exposure to air pollution on foetal and early brain structure and function is very scarce.…”

Section: Are Children More Vulnerable?mentioning

confidence: 99%

“…We propose to focus research on pre-natal life ( Table 1) because, as elaborated above, it can be considered as a critical window of exposure and provide a great opportunity for prevention and there have been reports on transgenerational brain effects in mice. 14,[25][26][27] Disruptions in the embryological process during pre-natal period could impair or make more fragile the brain for the rest of the life. 19 Moreover, pregnancy offers the opportunity of a more feasible and valid assessment of the cumulative exposure.…”

Section: Recommendations For the Future Research?mentioning

confidence: 99%

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Pre‐natal brain development as a target for urban air pollution

Sunyer

Dadvand

2019

Basic Clin Pharma Tox

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Air pollution is the main urban‐related environmental hazard and one of the major contributors to the global burden of disease based on its cardiovascular‐respiratory impacts. In children, exposure to urban air pollution is associated, among others, with decelerated neurodevelopment early in life and increased risk of neurodevelopmental problems such as attention‐deficit hyperactivity disorder, autism spectrum disorders, academic failure and the start of Alzheimer's pathogenesis. However, the evidence of the effects of air pollution on brain development is still inadequate, mainly due to the limitations in (a) characterizing brain development (most studies were based on subjective tools such as questionnaires or neuropsychological tests) and (b) air pollution exposure (most studies only used residential levels based on geographical modelling and also overlooking the variation in the mixture of air pollutants as well as the composition and hence toxicity of particulate pollutants in different settings), (c) the lack of studies during the most vulnerable stages of brain development (foetal and early life (first two years post‐natally)) and (d) the lack of structural and functional imaging data underlying these effects. In mice, in utero exposure to fine particles was linked to structural brain changes and there is a need to establish the generalizability of these findings in human beings. Though scarce, current evidence in children supports the importance of the pre‐natal period as a susceptible window of exposure. Two studies in schoolchildren found that pre‐natal air pollution exposure might damage brain structure while exposure during childhood was not linked to any structural alteration. Another study showed that children with higher traffic‐related air pollution at school had lower functional integration in key brain networks, but no changes in brain structure, possibly partly because of the time window of air pollution exposure (in utero versus childhood exposure). A key development is to discover the windows of greatest sensitivity of structural brain changes to air pollution exposure by incorporating the recent advances in non‐invasive imaging to characterize natal and post‐natal brain development and exploring whether and to what extend placental dysfunction could mediate such an association. Studying pre‐natal life is important because effects at this time are of a potentially irreversible nature and because the largest preventive opportunities occur during these periods.

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Section: Are Children More Vulnerable?mentioning

confidence: 99%

Section: Recommendations For the Future Research?mentioning

confidence: 99%

Pre‐natal brain development as a target for urban air pollution

Sunyer

Dadvand

2019

Basic Clin Pharma Tox

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“…Within the existing literature, one study indicated that prenatal exposure to DEPs via subcutaneous injections of DEP suspensions leads to serotonergic neuronal activation of the dorsal raphe nucleus eventually resulting in an increased anxiety-like behavior in male offspring (Yokota et al, 2016). In a SVEE model in rats, whole-body exposures to gaseous constituents of exhaust, namely, CO 2 , CO, and NO 2 , resulted in elevated anxiety-like and depression-like behaviors and memory deficits in exposed rats (Salvi et al, 2017).…”

Section: Psychological Impact Of Vehicle Exhaust Emissionsmentioning

confidence: 99%

Neurobehavioral Consequences of Traffic-Related Air Pollution

Salvi

Salim

2019

Front. Neurosci.

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Traffic-related air pollution (TRAP) is a major contributor to global air pollution. The World Health Organization (WHO) has reported that air pollution due to gasoline and diesel emissions from internal combustion engines of automobiles, trucks, locomotives, and ships leads to 800,000 premature deaths annually due to pulmonary, cardiovascular, and neurological complications. It has been observed that individuals living and working in areas of heavy vehicle traffic have high susceptibility to anxiety, depression, and cognitive deficits. Information regarding the mechanisms that potentially lead to detrimental mental health effects of TRAP is gradually increasing. Several studies have suggested that TRAP is associated with adverse effects in the central nervous system (CNS), primarily due to increase in oxidative stress and neuroinflammation. Animal studies have provided further useful insights on the deleterious effects of vehicle exhaust emissions (VEEs). The mechanistic basis for these effects is unclear, although gasoline and diesel exhaust-induced neurotoxicity seems the most plausible cause. Several important points emerge from these studies. First, TRAP leads to neurotoxicity. Second, TRAP alters neurobehavioral function. Exactly how that happens remains unclear. This review article will discuss current state of the literature on this subject and potential leads that have surfaced from the preclinical work.

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“…Interestingly, imbalances in the monoaminergic systems related to various neurocognitive disorders have also been noticed. Studies performed by Yokota et al in mice [41–43] pointed out that maternal exposure to DE leads to perturbations of the offspring’s dopaminergic, noradrenergic and serotoninergic systems in specific brain regions that could be related to motor coordination and impulsive behavior disturbances. Nevertheless, some incongruence remains as another study has revealed contradictory monoaminergic changes [44], possibly based on different mixtures or routes used for exposure.…”

Section: Introductionmentioning

confidence: 99%

“…Animal research has confirmed and expanded the observed findings in humans, and has shown that the fetal stage is a critical period of vulnerability. Nevertheless, the effects on the CNS of a gestational exposure to air pollution at such a critical period for its anatomic and functional development remain questioned and have been poorly investigated in controlled conditions mimicking indirect human exposure and in early postnatal stages [39–43]. Moreover, how the neuroanatomical continuum between brain and olfactory tissues is impacted by DE exposure remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Repeated gestational exposure to diesel engine exhaust affects the fetal olfactory system and alters olfactory-based behavior in rabbit offspring

et al. 2019

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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.

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<i>In utero</i> exposure to diesel exhaust particles induces anxiogenic effects on male offspring via chronic activation of serotonergic neuron in dorsal raphe nucleus

Cited by 11 publications

References 65 publications

Pre‐natal brain development as a target for urban air pollution

Pre‐natal brain development as a target for urban air pollution

Neurobehavioral Consequences of Traffic-Related Air Pollution

Repeated gestational exposure to diesel engine exhaust affects the fetal olfactory system and alters olfactory-based behavior in rabbit offspring

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