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Objective: Allergic rhinitis (AR) is an immunoglobulin E (IgE)-mediated inflammatory disorder of the nasal mucosa, and the impact of ozone on AR is gaining increasing attention. Although NOD-like receptor thermal protein domain associated protein 3 (NLRP3) plays a crucial role in the pathogenesis of AR, its regulatory mechanisms in ozone-induced exacerbation remain unclear. Therefore, we explored the impact of ozone inhalation on inflammation in AR and investigated the regulatory mechanisms involving NLRP3. Methods: Fifty female Sprague–Dawley rats were selected and divided into five groups: normal control (NC), normal with ozone exposure (NE), AR model, AR with ozone exposure (ARE), and ARE treated with the NLRP3 inhibitor MCC950 (ARE+MCC950). Behavioral changes were observed in the rats, and the expression of NLRP3, active-caspase 1, and GSDMD-N was detected by western blotting. The expression levels of interleukin (IL)− 4, IL-5, IL-13, IL-1β, and ovalbumin-specific IgE (OVA-sIgE) in nasal lavage fluid as well as IL-6 in the serum were measured by ELISA. The expression and distribution of NLRP3 and IL-1β in nasal mucosal tissue were detected by immunohistochemistry, and pathological changes and eosinophilic infiltration in nasal mucosal tissue were observed by hematoxylin and eosin (HE) staining. The effects of ozone exposure on inflammation in the nasal mucosal tissue of rats with AR and the relationship between NLRP3 and inflammation were analyzed. Results: Upregulation of NLRP3 was observed in the AR rat model, and ozone further aggravated the expression of NLRP3 in the nasal mucosal tissue. Compared to the AR, NC, and NE groups, NLRP3 inflammasomes were activated in the ARE group, and the expression levels of related indexes active-caspase 1 and GSDMD-N were significantly increased; the expression levels of Th2 inflammatory factors IL-4, IL-5, IL-13, and OVA-sIgE were increased, and inflammatory factors such as IL-1β and IL-6 expression was also significantly increased. HE staining revealed that ozone aggravated damage to the nasal mucosal tissue in AR. Compared with the ARE group, the expression of NLRP3 inflammasomes was downregulated, sneezing and scratching symptoms were reduced, inflammatory indicators in nasal lavage fluid were decreased, and nasal mucosal tissue damage was alleviated in rats in the ARE+MCC950 group. Conclusion: Ozone exposure significantly increased the inflammatory response in an animal model of AR. MCC950 can selectively inhibit the expression of NLRP3, inhibit the activity of inflammasomes, and reduce nasal mucosal inflammation by regulating the NLRP3-caspase-1-IL-1β pathway.

Objective and design: An experimental rat allergic rhinitis(AR) model was made to explore the effect of different concentrations of ozone exposure and evaluate the roles of nuclear factor erythroid 2-related factor 2(Nrf2) and oxidative stress in ozone exposure. Method: Sprague-Dawley rats were sensitized with ovalbumin (OVA). Three groups of AR rats were exposed respectively to different concentrations of ozone for 2 h on 6 weeks. Nasal symptoms and OVA- specific Ig E in the serum were evaluated. The pathological changes in the nasal mucosa were examined. Malondialdehyde (MDA) level and activity of superoxide dismutase(SOD) and glutathione peroxidase (GSH-Px,GPX) in the nasal mucosa tissue were measured through a spectrophotometry-based method. Nrf2、Kelch-1ike ECH- associated protein-l (Keap1) proteins was measured by western blotting. GPX1、GPX2 mRNA were detected by quantitative real time-PCR(qRT-PCR). Results: Our results showed that ozone exposure induced a significant increase of the number of sneezes, nasal rubs, amount of nasal secretion and OVA-sIgE in the serum of AR model. Ozone effected oxidative stress in different concentration. The content of MDA in AREH group was significantly higher than AR groups. The activities of SOD and GSH-Px in nasal mucosa showed different trends in different concentration groups. The activities of SOD and GSH-Px in AREL and AREM groups were higher than AR group, but decreased at AREH group. The nucleoprotein level of Nrf2 in AREL and AREM groups was higher than AR groups. However, in AREH group, it was significantly decreased, compared with AREL and AREM groups. GPX1 and GPX2 mRNA levels in nasal mucosa showed the same trend in different exposure groups. Conclusions: Different concentrations of ozone inhalation causes changes of the expression of Nrf2 nuclear protein and its target genes in nasal mucosa of AR. High concentration ozone breaks the redox balance and aggravates oxidative damage in AR. This study suggests that inhibiting oxidative stress might be a solution for ozone-elicited detrimental effects on AR.

To investigate composition characteristics and assess occupational health risks and odor pollution of volatile organic compounds (VOCs) from industrial activities in the Yangtze River Delta (YRD) region, China, one-year field measurements of VOCs were conducted simultaneously at an iron and steel industrial park (ISP), one chemical industrial park (CMP) and one petrochemical industrial park (PCP) from September, 2018 to August, 2019. The concentrations of VOCs were 80.2 ± 67.9 ppbv, 28.1 ± 27.2 ppbv and 144 ± 378 ppbv for ISP, CMP and PCP, respectively. Aromatics, alkanes and alkenes were the major components of VOCs at ISP, CMP and PCP, respectively. Moreover, the toluene to benzene ratios were 0.330 ± 0.302, 4.31 ± 6.48 and 1.84 ± 3.34, which generally showed the characteristics of combustion source for ISP, industrial activities for CMP and petrochemical industry for PCP, respectively. The hazard index values were 0.752 ± 0.438, 0.108 ± 0.248 and 0.090 ± 0.260 at ISP, CMP and PCP, which were generally lower than threshold limit value, suggesting a low noncarcinogenic risk for workers. Meanwhile, the 95th percentile LCR values of VOCs were 8.76 × 10−5, 1.15 × 10−5 and 1.00 × 10−5 at ISP, CMP and PCP, respectively, which were also under acceptable risk level, indicating a low carcinogenic risk. Benzene and 1,3-butadiene were main harmful substances for both noncarcinogenic and carcinogenic risks of VOCs. The odor levels of VOCs were 2.12 ± 4.21, 12.5 ± 28.7 and 1.01 ± 7.84 at ISP, CMP and PCP, respectively. Aromatics for ISP and sulfide compounds for CMP and PCP were primary pollutants for odor pollution. This work could improve the understanding of risk levels and odor characteristics of VOCs and benefit policy development on alleviating odor complaints and health risks for workers in YRD region, China.