Epidemiological studies have established an association between air pollution particulate matter exposure (PM2.5) and neurocognitive decline. Experimental data suggest that microglia play an essential role in air pollution PM-induced neuroinflammation and oxidative stress. This study examined the effect of nano-sized particulate matter (nPM) on complement C5 deposition and microglial activation in the corpus callosum of mice (C57BL/6J males). nPM was collected in an urban Los Angeles region impacted by traffic emissions. Mice were exposed to 10 weeks of re-aerosolized nPM or filtered air for a cumulative 150 hours. nPM-exposed mice exhibited reactive microglia and 2-fold increased local deposition of complement C5/ C5α proteins and complement component C5a receptor 1 (CD88) in the corpus callosum. However, serum C5 levels did not differ between nPM and filtered air cohorts. These findings demonstrate white matter C5 deposition and microglial activation secondary to nPM exposure. The C5 upregulation appears to be localized to the brain.
Background:
Exposure to ambient air pollution particulate matter (PM) is associated with increased risk of dementia and accelerated cognitive loss. Vascular contributions to cognitive impairment are well recognized. Chronic cerebral hypoperfusion (CCH) promotes neuroinflammation and blood–brain barrier weakening, which may augment neurotoxic effects of PM.
Objectives:
This study examined interactions of nanoscale particulate matter (nPM; fine particulate matter with aerodynamic diameter
) and CCH secondary to bilateral carotid artery stenosis (BCAS) in a murine model to produce white matter injury. Based on other air pollution interactions, we predicted synergies of nPM with BCAS.
Methods:
nPM was collected using a particle sampler near a Los Angeles, California, freeway. Mice were exposed to 10 wk of reaerosolized nPM or filtered air (FA) for 150 h. CCH was induced by BCAS surgery. Mice (C57BL/6J males) were randomized to four exposure paradigms:
a
) FA,
b
) nPM,
c
)
, and
d
)
. Behavioral outcomes, white matter injury, glial cell activation, inflammation, and oxidative stress were assessed.
Results:
The joint
group exhibited synergistic effects on white matter injury (2.3× the additive nPM and
scores) with greater loss of corpus callosum volume on T2 magnetic resonance imaging (MRI) (30% smaller than FA group). Histochemical analyses suggested potential microglial-specific inflammatory responses with synergistic effects on corpus callosum C5 immunofluorescent density and whole brain nitrate concentrations (2.1× and 3.9× the additive nPM and
effects, respectively) in the joint exposure group. Transcriptomic responses (RNA-Seq) showed greater impact of
than individual additive effects, consistent with changes in proinflammatory pathways. Although nPM exposure alone did not alter working memory, the
cohort demonstrated impaired working memory when compared to the
group.
Discussion:
Our data suggest that nPM and CCH contribute to white matter injury in a synergistic manner in a mouse model. Adverse neurological effects may be aggravated in a susceptible population exposed to air pollution.
https://doi.org/10.1289/EHP8792
This article describes the introduction of abdominal massage techniques by a community team as part of a total bowel management programme for people with learning disabilities. A trust-wide audit of prescribed laxative use by this client group raised concerns, and led to a more systematic approach to managing constipation in people with learning disabilities. An education programme for carers proved to be successful. Some reported that adopting abdominal massage provided further opportunity to develop the therapeutic relationship.
Fine and ultra-fine particulate matter (PM) are major constituents of urban air pollution and recognized risk factors for cardiovascular diseases. This review examined the effects of PM exposure on vascular tissue. Specific mechanisms by which PM affects the vasculature include inflammation, oxidative stress, actions on vascular tone and vasomotor responses, as well as atherosclerotic plaque formation. Further, there appears to be a greater PM exposure effect on susceptible individuals with pre-existing cardiovascular conditions.
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