Silica nanoparticles (SNPs) are widely used in many scientific and industrial fields despite the lack of proper evaluation of their potential toxicity. This study examined the effects of acute exposure to SNPs, either alone or in conjunction with ovalbumin (OVA), by studying the respiratory systems in exposed mouse models. Three types of SNPs were used: spherical SNPs (S-SNPs), mesoporous SNPs (M-SNPs), and PEGylated SNPs (P-SNPs). In the acute SNP exposure model performed, 6-week-old BALB/c female mice were intranasally inoculated with SNPs for 3 consecutive days. In the OVA/SNPs asthma model, the mice were sensitized two times via the peritoneal route with OVA. Additionally, the mice endured OVA with or without SNP challenges intranasally. Acute SNP exposure induced significant airway inflammation and airway hyper-responsiveness, particularly in the S-SNP group. In OVA/SNPs asthma models, OVA with SNP-treated group showed significant airway inflammation, more than those treated with only OVA and without SNPs. In these models, the P-SNP group induced lower levels of inflammation on airways than both the S-SNP or M-SNP groups. Interleukin (IL)-5, IL-13, IL-1β and interferon-γ levels correlated with airway inflammation in the tested models, without statistical significance. In the mouse models studied, increased airway inflammation was associated with acute SNPs exposure, whether exposed solely to SNPs or SNPs in conjunction with OVA. P-SNPs appear to be relatively safer for clinical use than S-SNPs and M-SNPs, as determined by lower observed toxicity and airway system inflammation.

Purpose: Lung injury from mechanical ventilation is one of the major pathogenetic factors of bronchopulmonary dysplasia. Permissive hypercapnia (PH) is one of the strategies for reducing lung injury. However, PH is frequently infeasible in very low birth weight infants (VLBWI) due to their immature renal compensation for respiratory acidosis. The purpose of this study was to identify time when metabolic compensation for hypercapnia begin to occur in VLBWIs. Methods: Data were retrospectively collected from 82 VLBWI who were admitted to Seoul National University Bundang Hospital from January 2011 to December 2012. The postnatal day when the difference between actual bicarbonate and expected bicarbonate levels became less than 2.0 mmol/L consistently for the first time under hypercapnea (>40 mmHg) was defined as the time when metabolic compensation for hypercapnea occurred. Results: Metabolic compensation for hypercapnea occurred on 9.1±3.9 postnatal day. The younger the gestational age (GA) was and the smaller the birth weight was, the later metabolic compensation for hypercapnea occurred. Late metabolic compensators (≥9 days) were significantly younger in GA (P=0.001), lighter at birth (P=0.041), intubated longer (P=0.002), and less frequently afflicted with respiratory distress syndrome (P=0.036) compared to early metabolic compensators (<9 days). However, logistic regression analysis revealed only young GA was associated with late metabolic compensation with marginal significance (P=0.068). Conclusion: Metabolic compensation for hypercapnea occurred 9 days after birth on average. PH strategy for reducing lung injury should be considered after renal metabolic compensation for hypercapnea occurs in VLBWI.