The neurotoxicity induced by PM<sub>2.5</sub> might be strongly related to changes of the hippocampal tissue structure and neurotransmitter levels

Li, Qingzhao; Zheng, Jiali; Xu, Shuonan; Zhang, Jingshu; Cao, Yanhua; Zhen-long, Qin; Liu, Xiaoqin; Jiang, Chunyang

doi:10.1039/c8tx00093j

Cited by 27 publications

(14 citation statements)

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“…The neuronal damage in our PMB models were comparable to other in vitro models, [ 26 ] but more severe than in vivo chronic models. [ 27 ] First, we attributed the lower sensitivity toward PM2.5‐driven neuroinflammation to the heterogeneous populations of glial cells playing either proinflammatory or anti‐inflammatory roles depending on brain regions, [ 6 , 16 , 17 ] while our models could separate PM2.5‐involving proinflammatory immune cells from other populations. Second, inhaled particles can be removed by other immune cells in the respiratory system, such as alveolar macrophages and lung lymphatics, before reaching to the brain, [ 25 , 28 ] while our cellular models are a type of an acute model as we employed larger amounts of PM2.5 as described in the previous response.…”

Section: Discussionmentioning

confidence: 99%

An Air Particulate Pollutant Induces Neuroinflammation and Neurodegeneration in Human Brain Models

et al. 2021

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Fine particulate matter (PM2.5), a major component among air pollutants, highlights as a global health concern. Several epidemiological studies show the correlation between chronical PM2.5 exposure and incidents of neurological disorders including Alzheimer's disease. However, the mechanisms have not been well understood, partly due to the lack of model systems that reflect the physiologically relevant innate immunity in human brains. Here, PM2.5‐polluted human brain models (PMBs) are created in a 3D microfluidic platform reconstituting key aspects of human brain immunity under the PM2.5 exposure. PM2.5 penetration across a blood–brain barrier (BBB) model and accumulation in the brain tissue side of the model are first validated. Second, the PMB model shows that the BBB‐penetrating PM2.5 initiates astrogliosis, resulting in slight neuronal loss and microglial infiltration. Third, it is demonstrated that the infiltrating microglia obtain M1 phenotype induced by interleukin‐1β and interferon‐γ from neurons and reactive astrocytes under the PM2.5 exposure. Finally, it is observed that additional proinflammatory mediators and nitric oxide released from the M1 microglia exacerbate neuronal damages, such as synaptic impairment, phosphoric tau accumulation, and neuronal death. This study suggests that PM2.5 can be a potential environmental risk factor for dementia mediated by the detrimental neuroinflammation.

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Section: Discussionmentioning

confidence: 99%

An Air Particulate Pollutant Induces Neuroinflammation and Neurodegeneration in Human Brain Models

et al. 2021

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“…Offspring of mice exposed to PM 2.5 throughout gestation showed evidence of increased neuronal apoptosis, mitochondrial matrix swelling, and structural damage in the hippocampus of mouse pups following gestational exposure to PM. [66,97] Similarly to rodents exposed to PM postnatally, [59,97] gestationally-exposed offspring, tested at P30, demonstrated impaired spatial learning. [66] Increased ROS and NO production and decreased neurite outgrowth were observed in wild-type mouse hippocampal cultures treated with UFPM, altering NMDA receptor function and decreasing evoked post-synaptic currents of CA1 neurons.…”

Section: Mitochondrial Dysfunction Following Pm Exposurementioning

confidence: 99%

Early life exposure to air pollution impacts neuronal and glial cell function leading to impaired neurodevelopment

et al. 2021

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The World Health Organisation recently listed air pollution as the most significant threat to human health. Air pollution comprises particulate matter (PM), metals, black carbon and gases such as ozone (O 3 ), nitrogen dioxide (NO 2 ) and carbon monoxide (CO). In addition to respiratory and cardiovascular disease, PM exposure is linked with increased risk of neurodegeneration as well as neurodevelopmental impairments.Critically, studies suggest that PM crosses the placenta, making direct in utero exposure a reality. Rodent models reveal that neuroinflammation, neurotransmitter imbalance and oxidative stress are triggered following gestational/early life exposure to PM, and may be exacerbated by concomitant mitochondrial dysfunction. Gestational PM exposure (potentiated by mitochondrial impairment in the metabolically active neonatal brain) not only impacts neurodevelopment but may sensitise the brain to subsequent cognitive impairment. Having reviewed this field, we conclude that strategies are urgently required to reduce exposure to PM during this sensitive developmental period.

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“…The main crustal elementsaluminium (Al), calcium (Ca), iron (Fe), magnesium (Mg) and potassium (K)and also toxic elements from anthropogenic sourceszinc (Zn), copper (Cu), lead (Pb), nickel (Ni), arsenic (As), cadmium (Cd) and antimony (Sb)have been detected in the atmospheric PM2.5 and PM1 (diameter ≤ 1.0 µm) samples in Asian megacities [4] and large European cities [5,6,7]. Interestingly, Pb is the most common metal in the air, while Fe, Zn, Cu and Pb are the most abundant metals in PM2.5 [8].…”

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confidence: 99%

“…Interestingly, Pb is the most common metal in the air, while Fe, Zn, Cu and Pb are the most abundant metals in PM2.5 [8]. Some studies have identified Pb as the third most common metal behind Fe and Zn [3,5,9] or as the second most common metal in others surveys [4]. While the limit for airborne Pb determined by the World Health Organization (WHO) is 0.5 µg/m 3 , it is regularly exceeded in many cities around the world.…”

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confidence: 99%

A Clearance Period After Soluble Lead Nanoparticle Inhalation did not Ameliorate the Negative Effects on Target Tissues Due to Decreased Immune Response

Dumková

Smutná

Vrlíková

et al. 2020

Preprint

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Background: The inhalation of metal (including lead) nanoparticles poses a real health issue to people and animals living in polluted and/or industrial areas. In this study, we exposed mice to lead(II) nitrate nanoparticles [Pb(NO3)2 NPs], which represent a highly soluble form of lead, by inhalation. We aimed to uncover possible differences in the effects of lead exposure on individual target organs and to reveal potential variability in the clearance of lead from organs after inhalation of soluble and insoluble lead particles. Mice were exposed to Pb(NO3)2 NPs in whole-body inhalation chambers for up to 11 weeks. We examined (i) lead biodistribution in target organs using laser ablation and inductively coupled plasma mass spectrometry (LA-ICP-MS) and atomic absorption spectrometry (AAS), (ii) lead effect on histopathological changes and immune cells response in secondary target organs and (iii) the clearance ability of target organs (lung, liver, kidney, spleen, bone and blood). Results: After exposure to Pb(NO3)2 NPs, the lead concentration was the highest in femur at all designated time points with the exception of 3-day inhalation. In contrast to other organs, the ability to clear the lead from the femur was very low. In the lungs, Pb(NO3)2 NP inhalation induced serious structural changes; lung damage was present even after a 5-week clearance period despite the lead being almost completely eliminated from the lung tissue. Furthermore, in secondary target organs (kidney and liver), Pb(NO3)2 NPs induced several morphological defects, with alterations that remained visible after the clearance period even though the tissue lead concentrations decreased to minimal values. The numbers of lung and liver macrophages were significantly decreased after 11-week Pb(NO3)2 NP inhalation; conversely, abundance of alpha-smooth muscle actin (α-SMA)-positive cells, which are responsible for augmented collagen production, was increased in both tissues. Moreover, the expression of nuclear factor κB (NF-κB) and selected cytokines (tumour necrosis factor alpha [TNF-α], transforming growth factor beta 1 [TGFβ1], interleukin 6 [IL-6], IL-1α and IL-1β) displayed a tissue-specific response to lead exposure. Conclusions: Taken together, diminished inflammatory response in lung and liver after Pb(NO3)2 NPs inhalation was associated with prolonged negative effect of lead on tissues, as demonstrated by enhanced pathological changes in target organs, even after a 5-week clearance period that contrasts to the stronger effect observed previously after the clearance of insoluble lead nanoparticles.

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The neurotoxicity induced by PM_2.5 might be strongly related to changes of the hippocampal tissue structure and neurotransmitter levels

Abstract: Objective: The complex components of PM2.5 including metal elements transported through the blood brain barrier could induce nervous system damage.

Cited by 27 publications

References 38 publications

An Air Particulate Pollutant Induces Neuroinflammation and Neurodegeneration in Human Brain Models

An Air Particulate Pollutant Induces Neuroinflammation and Neurodegeneration in Human Brain Models

Early life exposure to air pollution impacts neuronal and glial cell function leading to impaired neurodevelopment

A Clearance Period After Soluble Lead Nanoparticle Inhalation did not Ameliorate the Negative Effects on Target Tissues Due to Decreased Immune Response

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The neurotoxicity induced by PM2.5 might be strongly related to changes of the hippocampal tissue structure and neurotransmitter levels

Abstract: Objective: The complex components of PM2.5 including metal elements transported through the blood brain barrier could induce nervous system damage.

Cited by 27 publications

References 38 publications

An Air Particulate Pollutant Induces Neuroinflammation and Neurodegeneration in Human Brain Models

An Air Particulate Pollutant Induces Neuroinflammation and Neurodegeneration in Human Brain Models

Early life exposure to air pollution impacts neuronal and glial cell function leading to impaired neurodevelopment

A Clearance Period After Soluble Lead Nanoparticle Inhalation did not Ameliorate the Negative Effects on Target Tissues Due to Decreased Immune Response

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The neurotoxicity induced by PM_2.5 might be strongly related to changes of the hippocampal tissue structure and neurotransmitter levels