Short-term and repeated exposure to particulate matter sizes from Imperial Valley, California to induce inflammation and asthmatic-like symptoms in mice.

Imperial Valley, California has become increasingly hot, dry, and polluted over the past decade. Particulate matter (PM) levels are amongst the highest in this State, associated with significantly higher asthma prevalence among children in the region compared to national and state averages. The present study was performed to test the hypothesis that Imperial Valley PM by size and chemical composition might possess allergenic properties following introduction into murine lungs without prior sensitization to a known allergen with size fraction as a determining factor. In acute exposure experiments, BALB/c male mice were administered a single 50-µl oropharyngeal aspiration of nanopure water (H2O; control) or a stock 1 µg/µl PM solution. In sub-acute exposure experiments, male and female mice were treated with a total of six 16.6-µl intranasal instillations of H2O or stock PM solution over the course of 14 days. In all experiments, pulmonary function tests were performed 24 hr after the final instillation followed by necropsies for the collection of biological samples. Inflammatory responses measured via cellularity in histopathological tissue sections as well as significant, marked influxes of eosinophils and lymphocytes were noted in the bronchoalveolar lavage fluid in mice administered PM compared to control. Allergic responses, including airway hyperresponsiveness and significantly increased expression of IL-1ß, were found in male mice exposed to either PM2.5 or ultrafine (PMUF). A combination of all three size fractions of PM from Imperial Valley initiated atopic and asthmatic-like symptoms in the lungs of mice in the absence of additional allergen or preexisting condition.

Repeated Iron-Soot Exposure and Nose-to-brain Transport of Inhaled Ultrafine Particles.

Particulate exposure has been implicated in the development of a number of neurological maladies such as multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's disease, and idiopathic Parkinson's disease. Only a few studies have focused on the olfactory pathway as a portal through which combustion-generated particles may enter the brain. The primary objective of this study was to define the deposition, uptake, and transport of inhaled ultrafine iron-soot particles in the nasal cavities of mice to determine whether combustion-generated nanoparticles reach the olfactory bulb via the olfactory epithelium and nerve fascicles. Adult female C57B6 mice were exposed to iron-soot combustion particles at a concentration of 200 µg/m3, which included 40 µg/m3 of iron oxide nanoparticles. Mice were exposed for 6 hr/day, 5 days/week for 5 consecutive weeks (25 total exposure days). Our findings visually demonstrate that inhaled ultrafine iron-soot reached the brain via the olfactory nerves and was associated with indicators of neural inflammation.