The association between traffic-related air pollution and obstructive sleep apnea: A systematic review.

Recent evidence suggests that air pollution exposure may be a contributing risk factor for obstructive sleep apnea (OSA), however, current evidence is conflicting. This systematic review aims to determine the association between air pollution and OSA in the general population, and examine for potential effect modification by seasonality, temperature and humidity. Five full-text articles were included in the review out of 905 articles found by systematically searching PubMed, Embase and Scopus databases. The included studies were limited to OSA in adults that were conducted in middle to high-income countries. The results highlight heterogeneity in the diagnostic criteria for OSA and method used to assess air pollution exposure. There is some evidence to support a relationship between air pollution exposure and OSA. However, the duration of exposure to different air pollutants including particulate matter (PM2.5 and PM10) and nitric oxides (NO2) in relation to OSA varied across different seasons, temperatures, and countries. This variability of the pollutants across studies warrants a more robust study design using time-series analysis with multiple follow-ups to strengthen the evidence for this relationship before considering its implications.

Inflammation in Traumatic Brain Injury: Roles for Toxic A1 Astrocytes and Microglial-Astrocytic Crosstalk.

Traumatic brain injury triggers neuroinflammation that may contribute to progressive neurodegeneration. We investigated patterns of recruitment of astrocytes and microglia to inflammation after brain trauma by firstly characterising expression profiles over time of marker genes following TBI, and secondly by monitoring glial morphologies reflecting inflammatory responses in a rat model of traumatic brain injury (i.e. the lateral fluid percussion injury). Gene expression profiles revealed early elevation of expression of astrocytic marker glial fibrillary acidic protein relative to microglial marker allograft inflammatory factor 1 (also known as ionized calcium-binding adapter molecule 1). Adult rat brains collected at day 7 after injury were processed for immunohistochemistry with allograft inflammatory factor 1, glial fibrillary acidic protein and complement C3 (marker of bad/disruptive astrocytic A1 phenotype). Astrocytes positive for glial fibrillary acidic protein and complement C3 were significant increased in the injured cortex and displayed more complex patterns of arbourisation with significantly increased bifurcations. Our observations suggested that traumatic brain injury changed the phenotype of microglia from a ramified appearance with long, thin, highly branched processes to a swollen amoeboid shape in the injured cortex. These findings suggest differential glial activation with astrocytes likely undergoing strategic changes in morphology and function. Whilst a detailed analysis is needed of temporal patterns of glial activation, ours is the first evidence of a role for the bad/disruptive astrocytic A1 phenotype in an open head model of traumatic brain injury.