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

Abstract

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.

Prolonged Exposure to Traffic-related Particulate Matter Showed Distinct Molecular Mechanisms of Lung Injury in Rats

“…The whole-body exposure system and rat model was previously published in (16) to mimic the TRAP exposure in human. Brie y, ambient air was continuously sampled by an omnidirectional PM inlet located on the roof of the animal housing.…”

“…All the PM 1 exposure to rats were determined in the exposure system as reported previously (56,57). A tapered element oscillating microbalance (TEOM, Thermo Scienti c 1400a Mass concentrations were monitored using) was used to monitor particle mass concentration.…”

“…Several dysregulated proteins involved in mitochondria dysfunction, energy metabolism and ER stress were discovered as potential biomarkers for PM-induced organ damage. To exploit the impact of PM on organ injury, we have previously established the rat model with whole-body exposure system and reported the central neurotoxicity induced by sub-chronic or chronic exposure of tra c-related ne PM (PM 1 ), even though it was below the WHO air quality guideline (16). In this study, we aimed to investigate the effects of tra c-related PM 1 in lungs from the same rat model.…”

Alveolar Epithelial Inter-alpha-trypsin Inhibitor Heavy Chain 4 Deficiency Associated With Senescence-regulated Apoptosis by Particulate Air Pollution

“…Rats were whole-body exposed to (1) clean air in the Laboratory Animal Center of Taipei Medical University (as the control group), (2) high-e ciency particulate air (HEPA)-ltered tra crelated urban air (as the HEPA group), and (3) tra c-dominated urban PM 2.5 (as the PM 2.5 group) for 3 and 6 months. The whole-body exposure system to unconcentrated particulate pollution with a 2.5-μm particle size classi er for rodents was previously described [21,22]. Gaseous pollutants used for rat exposure were referenced from the nearest Yonghe EPA air quality monitoring station.…”

Avaliação dos efeitos da exposição pré e pós-natal à poluição atmosférica no sistema nervoso central de camundongos

“…Corroborando os dados, Shih et al, (2018) observaram aumento do volume do hipocampo e do cérebro total em camundongos com 6 meses de idade expostos durante 3 e 6 meses a partículas oriundas do tráfego veicular com tamanho aerodinâmico <1μm. Ainda, o estudo relatou aumento de 8isoprostano no córtex, cerebelo e hipocampo e, aumento de citocina inflamatória, IL-6, no hipocampo (Shih et al, 2018).…”