RESUMO
Background: Indoor and outdoor air pollution levels are associated with poor asthma outcomes in children. However, few studies have evaluated whether breathing zone pollutant levels associate with asthma outcomes. Objective: Determine breathing zone exposure levels of NO 2 , O 3 , total PM 10 and PM 10 constituents among children with exacerbation-prone asthma, and examine correspondence with in-home and community measurements and associations with outcomes. Methods: We assessed children's personal breathing zone exposures using wearable monitors. Personal exposures were compared to in-home and community measurements and tested for association with lung function, asthma control, and asthma exacerbations. Results: 81 children completed 219 monitoring sessions. Correlations between personal and community levels of PM 10 , NO 2 , and O 3 were poor, whereas personal PM 10 and NO 2 levels correlated with in-home measurements. However, in-home monitoring underdetected brown carbon (Personal:79%, Home:36.8%) and ETS (Personal:83.7%, Home:4.1%) personal exposures, and detected black carbon in participants without these personal exposures (Personal: 26.5%, Home: 96%). Personal exposures were not associated with lung function or asthma control. Children experiencing an asthma exacerbation within 60 days of personal exposure monitoring had 1.98, 2.21 and 2.04 times higher brown carbon (p<0.001), ETS (p=0.007), and endotoxin (p=0.012), respectively. These outcomes were not associated with community or in-home exposure levels. Conclusions: Monitoring pollutant levels in the breathing zone is essential to understand how exposures influence asthma outcomes, as agreement between personal and in-home monitors is limited. Inhaled exposure to PM 10 constituents modifies asthma exacerbation risk, suggesting efforts to limit these exposures among high-risk children may decrease their asthma burden. CLINICAL IMPLICATIONS: In-home and community monitoring of environmental pollutants may underestimate personal exposures. Levels of inhaled exposure to PM 10 constituents appear to strongly influence asthma exacerbation risk. Therefore, efforts should be made to mitigate these exposures. CAPSULE SUMMARY: Leveraging wearable, breathing-zone monitors, we show exposures to inhaled pollutants are poorly proxied by in-home and community monitors, among children with exacerbation-prone asthma. Inhaled exposure to multiple PM 10 constituents is associated with asthma exacerbation risk.
RESUMO
The WAVE/SCAR complex promotes actin nucleation through the Arp2/3 complex, in response to Rac signaling. We show that loss of WVE-1/GEX-1, the only C. elegans WAVE/SCAR homolog, by genetic mutation or by RNAi, has the same phenotype as loss of GEX-2/Sra1/p140/PIR121, GEX-3/NAP1/HEM2/KETTE, or ABI-1/ABI, the three other components of the C. elegans WAVE/SCAR complex. We find that the entire WAVE/SCAR complex promotes actin-dependent events at different times and in different tissues during development. During C. elegans embryogenesis loss of CED-10/Rac1, WAVE/SCAR complex components, or Arp2/3 blocks epidermal cell migrations despite correct epidermal cell differentiation. 4D movies show that this failure occurs due to decreased membrane dynamics in specific epidermal cells. Unlike myoblasts in Drosophila, epidermal cell fusions in C. elegans can occur in the absence of WAVE/SCAR or Arp2/3. Instead we find that subcellular enrichment of F-actin in epithelial tissues requires the Rac-WAVE/SCAR-Arp2/3 pathway. Intriguingly, we find that at the same stage of development both F-actin and WAVE/SCAR proteins are enriched apically in one epithelial tissue and basolaterally in another. We propose that temporally and spatially regulated actin nucleation by the Rac-WAVE/SCAR-Arp2/3 pathway is required for epithelial cell organization and movements during morphogenesis.