Exposure to traffic-generated air pollutants mediates alterations in brain microvascular integrity in wildtype mice on a high-fat diet

Suwannasual, Usa; Lucero, JoAnn; McDonald, Jacob D.; Lund, Amie K.

doi:10.1016/j.envres.2017.10.029

Cited by 35 publications

(18 citation statements)

References 54 publications

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“…A breakdown of the BBB may result in alterations in the brain’s structures, such as cerebral edema and atrophy. A recent study found that 3-month-old C57BL/6 mice exposed to 100 μg/m 3 of vehicle emissions for 30 days exhibited increased BBB permeability and impaired BBB integrity [ 26 ]. Therefore, it is reasonable to hypothesize that chronic exposure to air pollution causes early brain pathologies, such as cerebral edema as observed in our study.…”

Section: Discussionmentioning

confidence: 99%

“…The difference from the current study could have been due to different expression levels between proteins and genes. Notably, one study observed that exposure to traffic-related air pollution altered the brain’s microvascular integrity in a high-fat diet animal model [ 26 ]. The authors suggested that particulate air pollution could cause BBB impairment, leading to local inflammation due to particles accumulating in the brain.…”

Section: Discussionmentioning

confidence: 99%

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Chronic pulmonary exposure to traffic-related fine particulate matter causes brain impairment in adult rats

et al. 2018

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BackgroundEffects of air pollution on neurotoxicity and behavioral alterations have been reported. The objective of this study was to investigate the pathophysiology caused by particulate matter (PM) in the brain. We examined the effects of traffic-related particulate matter with an aerodynamic diameter of < 1 μm (PM1), high-efficiency particulate air (HEPA)-filtered air, and clean air on the brain structure, behavioral changes, brainwaves, and bioreactivity of the brain (cortex, cerebellum, and hippocampus), olfactory bulb, and serum after 3 and 6 months of whole-body exposure in 6-month-old Sprague Dawley rats.ResultsThe rats were exposed to 16.3 ± 8.2 (4.7~ 68.8) μg/m3 of PM1 during the study period. An MRI analysis showed that whole-brain and hippocampal volumes increased with 3 and 6 months of PM1 exposure. A short-term memory deficiency occurred with 3 months of exposure to PM1 as determined by a novel object recognition (NOR) task, but there were no significant changes in motor functions. There were no changes in frequency bands or multiscale entropy of brainwaves. Exposure to 3 months of PM1 increased 8-isoporstance in the cortex, cerebellum, and hippocampus as well as hippocampal inflammation (interleukin (IL)-6), but not in the olfactory bulb. Systemic CCL11 (at 3 and 6 months) and IL-4 (at 6 months) increased after PM1 exposure. Light chain 3 (LC3) expression increased in the hippocampus after 6 months of exposure. Spongiosis and neuronal shrinkage were observed in the cortex, cerebellum, and hippocampus (neuronal shrinkage) after exposure to air pollution. Additionally, microabscesses were observed in the cortex after 6 months of PM1 exposure.ConclusionsOur study first observed cerebral edema and brain impairment in adult rats after chronic exposure to traffic-related air pollution.Electronic supplementary materialThe online version of this article (10.1186/s12989-018-0281-1) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chronic pulmonary exposure to traffic-related fine particulate matter causes brain impairment in adult rats

et al. 2018

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“…Cardiovascular diseases and metabolic syndrome are recognized as risk factors for the development of NGDs [ 24 , 25 ]. A previous study showed that exposure to traffic-related air pollution impaired the brain’s microvascular integrity in a high-fat diet animal model [ 26 ]. However, a paucity of evidence is available for neurotoxicity caused by PM 2.5 in hypertensive animals.…”

Section: Introductionmentioning

confidence: 99%

Neuropathology changed by 3- and 6-months low-level PM2.5 inhalation exposure in spontaneously hypertensive rats

et al. 2020

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Background Epidemiological evidence has linked fine particulate matter (PM2.5) to neurodegenerative diseases; however, the toxicological evidence remains unclear. The objective of this study was to investigate the effects of PM2.5 on neuropathophysiology in a hypertensive animal model. We examined behavioral alterations (Morris water maze), lipid peroxidation (malondialdehyde (MDA)), tau and autophagy expressions, neuron death, and caspase-3 levels after 3 and 6 months of whole-body exposure to urban PM2.5 in spontaneously hypertensive (SH) rats. Results SH rats were exposed to S-, K-, Si-, and Fe-dominated PM2.5 at 8.6 ± 2.5 and 10.8 ± 3.8 μg/m3 for 3 and 6 months, respectively. We observed no significant alterations in the escape latency, distance moved, mean area crossing, mean time spent, or mean swimming velocity after PM2.5 exposure. Notably, levels of MDA had significantly increased in the olfactory bulb, hippocampus, and cortex after 6 months of PM2.5 exposure (p < 0.05). We observed that 3 months of exposure to PM2.5 caused significantly higher expressions of t-tau and p-tau in the olfactory bulb (p < 0.05) but not in other brain regions. Beclin 1 was overexpressed in the hippocampus with 3 months of PM2.5 exposure, but significantly decreased in the cortex with 6 months exposure to PM2.5. Neuron numbers had decreased with caspase-3 activation in the cerebellum, hippocampus, and cortex after 6 months of PM2.5 exposure. Conclusions Chronic exposure to low-level PM2.5 could accelerate the development of neurodegenerative pathologies in subjects with hypertension.

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“…79 High-fat diet in a mouse model has also been shown to exacerbate changes in blood–brain barrier integrity after traffic-related motor vehicle exhaust exposures as evidenced by increased expression of oxidized low density lipoprotein signaling in the vasculature. 80 High-fat or high-carbohydrate/fructose diets in male and female Brown Norway rats, which are resistant to developing diet-induced obesity, showed increased body fat percentage relative to lean mass in males, 81 but when exposed to ozone, diet did not significantly exacerbate lung injury or inflammation. These studies imply that that diet-induced susceptibility differences are dependent on model selection and biological end point.…”

Section: Use Of Rodent Models Of Metabolic Alterations In Air Pollutimentioning

confidence: 98%

Susceptibility Variations in Air Pollution Health Effects: Incorporating Neuroendocrine Activation

Kodavanti

2019

Toxicol Pathol

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Diverse host factors/phenotypes may exacerbate or diminish biological responses induced by air pollutant exposure. We lack an understanding of biological indicators of environmental exposures that culminate in a physiological response versus those that lead to adversity. Variations in response phenotype might arise centrally and/or at the local tissue level. In addition to genetic differences, the current evidence supports the roles of preexisting cardiopulmonary diseases, diabetes, diet, adverse prenatal environments, neurobehavioral disorders, childhood infections, microbiome, sex, and psychosocial stressors in modifying the susceptibility to air pollutant exposures. Animal models of human diseases, obesity, nutritional inadequacies, and neurobehavioral conditions have been compared with healthy controls to understand the causes of variations in susceptibility. Although psychosocial stressors have been associated with increased susceptibility to air pollutant effects, the contribution of neuroendocrine stress pathways in mediating these effects is just emerging. The new findings of neuroendocrine activation leading to systemic metabolic and immunological effects of air pollutants, and the potential contribution to allostatic load, emphasize the consideration of these mechanisms into susceptibility. Variations in susceptibility to air pollution health effects are likely to underlie host genetic and physiological conditions in concert with disrupted neuroendocrine circuitry that alters physiological stability under the influence of stressors.

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Exposure to traffic-generated air pollutants mediates alterations in brain microvascular integrity in wildtype mice on a high-fat diet

Cited by 35 publications

References 54 publications

Chronic pulmonary exposure to traffic-related fine particulate matter causes brain impairment in adult rats

Chronic pulmonary exposure to traffic-related fine particulate matter causes brain impairment in adult rats

Neuropathology changed by 3- and 6-months low-level PM2.5 inhalation exposure in spontaneously hypertensive rats

Susceptibility Variations in Air Pollution Health Effects: Incorporating Neuroendocrine Activation

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