Activation of the Stress Axis and Neurochemical Alterations in Specific Brain Areas by Concentrated Ambient Particle Exposure with Concomitant Allergic Airway Disease

Abstract

ObjectiveExposure to ambient particulate matter (PM) has been linked to respiratory diseases in people living in urban communities. The mechanism by which PM produces these diseases is not clear. We hypothesized that PM could act on the brain directly to stimulate the stress axis and predispose individuals to these diseases. The purpose of this study was to test if exposure to PM can affect brain areas involved in the regulation of neuroendocrine functions, especially the stress axis, and to study whether the presence of preexisting allergic airway disease aggravates the stress response.DesignAdult male rats (n = 8/group) with or without ovalbumin (OVA)-induced allergic airway disease were exposed to concentrated air particles containing PM with an aerodynamic diameter ≤ 2.5 μm (PM2.5) for 8 hr, generated from ambient air in an urban Grand Rapids, Michigan, community using a mobile air research laboratory (AirCARE 1). Control animals were exposed to normal air and were treated with saline.MeasurementsA day after PM2.5 exposure, animals were sacrificed and the brains were removed, frozen, and sectioned. The paraventricular nucleus (PVN) and other brain nuclei were micro-dissected, and the concentrations of aminergic neurotransmitters and their metabolites were measured using high-performance liquid chromatography with electrochemical detection. Serum corticosterone levels were measured using radioimmunoassay.ResultsA significant increase in the concentration (mean ± SE, pg/μg protein) of norepinephrine in the PVN was produced by exposure to concentrated ambient particles (CAPs) or OVA alone (12.45 ± 2.7 and 15.84 ± 2.8, respectively) or after sensitization with OVA (19.06 ± 3.8) compared with controls (7.98 ± 1.3; p < 0.05). Serum corticosterone (mean ± SE, ng/mL) was significantly elevated in the OVA + CAPs group (242.786 ± 33.315) and in the OVA-presensitized group (242.786 ± 33.315) compared with CAP exposure alone (114.55 ± 20.9). Exposure to CAPs (alone or in combination with OVA pretreatment) can activate the stress axis, and this could probably play a role in aggravating allergic airway disease.

Catecholamine levels in the brain of rats exposed by inhalation to benzalkonium chloride

“…Adrenaline concentrations, on the other hand, decreased. Growing DA and/or NA concentrations in the brain of animals subjected to stress is a reaction which has been observed by many authors [9,10,22]. In stressed animals, like in our study, a significant reduction of the DOPAC/DA and and mesencephalon of both BAC-exposed groups relative to control.…”

“…Glucocorticoids are important in the maintenance of functional and structural integrity of the brain. Therefore, increased blood glycocorticoid concentrations cause changes in the functional condition of the neurotransmission systems, and of the catecholaminergic systems in particular [8][9][10]. Data assessing BAC effects on central nervous system of experimental animals in inhalation exposure situations could not be located in the accessible literature.…”

Air pollution and daily emergency department visits for depression

“…It has become apparent that inhalation of particulate matter (PM) can have influence on the CNS. Recent work with experimental animals has provided evidence for neuropathological effects, including reduced dopaminergic neuron density in mice exposed to concentrated ambient particles (CAPs) [22], and changes in neurotransmitter levels in rats exposed by inhalation to CAPs [23]. There is some evidence from animal studies that inhaled particles, especially the ultrafine size fraction, may be able to distribute to the brain [24][25][26].…”

Prenatal exposure to zinc oxide particles alters monoaminergic neurotransmitter levels in the brain of mouse offspring

“…Previous studies indicated an association between chemical exposure in the environment and monoaminergic neurotransmitter regulation (Matsuda et al, 2010;Xia et al, 2011;Sirivelu et al, 2006). The monoaminergic system plays an important role in mental health, and its dysregulation leads to psychiatric dysfunction, such as behavioral depression, anxiety disorder, and Parkinsonism (Weiss et al, 1981;Elsworth and Roth, 1997;Morilak and Frazer, 2004).…”