Ozone Chemistry on Greasy Glass Surfaces Affects the Levels of Volatile Organic Compounds in Indoor Environments.

The chemistry of ozone (O3) on indoor surfaces leads to secondary pollution, aggravating the air quality in indoor environments. Here, we assess the heterogeneous chemistry of gaseous O3 with glass plates after being 1 month in two different kitchens where Chinese and Western styles of cooking were applied, respectively. The uptake coefficients of O3 on the authentic glass plates were measured in the dark and under UV light irradiation typical for indoor environments (320 nm < λ < 400 nm) at different relative humidities. The gas-phase product compounds formed upon reactions of O3 with the glass plates were evaluated in real time by a proton-transfer-reaction quadrupole-interface time-of-flight mass spectrometer. We observed typical aldehydes formed by the O3 reactions with the unsaturated fatty acid constituents of cooking oils. The formation of decanal, 6-methyl-5-hepten-2-one (6-MHO), and 4-oxopentanal (4-OPA) was also observed. The employed dynamic mass balance model shows that the estimated mixing ratios of hexanal, octanal, nonanal, decanal, undecanal, 6-MHO, and 4-OPA due to O3 chemistry with authentic grime-coated kitchen glass surfaces are higher in the kitchen where Chinese food was cooked compared to that where Western food was cooked. These results show that O3 chemistry on greasy glass surfaces leads to enhanced VOC levels in indoor environments.

Causal associations between pediatric asthma and united airways disease: a two-sample Mendelian randomization analysis.

Background: Prior observational research has indicated a potential link between pediatric asthma and united airways disease (UAD). However, these findings could be subject to confounding factors and reverse causation. Therefore, our study utilizes Mendelian randomization (MR) method to further investigate the causal relationship between pediatric asthma and UAD. Methods: We conducted a comprehensive two-sample Mendelian randomization (MR) analysis to investigate the association between pediatric asthma and seven groups of UAD, including chronic sinusitis, chronic rhinitis, nasopharyngitis and pharyngitis, chronic diseases of tonsils and adenoids, chronic laryngitis and laryngotracheitis, chronic bronchitis, bronchiectasis, chronic obstructive pulmonary disease (COPD). The present study employed a range of methods for two-sample MR analysis, including inverse variance weighted (IVW), MR-Egger regression, Simple mode, weighted median, and weighted models. The conclusion of the MR analysis primarily relies on the IVW results, while other analytical methods are utilized as supplementary evidence to ensure result robustness in this MR analysis. And sensitivity analyses were conducted, including heterogeneity test, horizontal pleiotropy test, MR-PRESSO test, and leave-one-out analysis to validate the results. Results: The results of the MR analysis indicate significant causal effects of pediatric asthma on chronic rhinitis, nasopharyngitis and pharyngitis (IVW: OR = 1.15, 95%CI: 1.05-1.26, p-value = 0.003), chronic diseases of tonsils and adenoids (IVW: OR = 1.07, 95%CI: 1.00-1.15, p-value = 0.038), chronic bronchitis (IVW: OR = 1.51, 95%CI: 1.42-1.62, p-value <0.001), bronchiectasis (IVW: OR = 1.51, 95%CI: (1.30-1.75), p-value <0.001), and COPD (IVW: OR = 1.43, 95%CI: 1.34-1.51, p-value <0.001). However, no significant causal association was observed between pediatric asthma and chronic sinusitis (IVW: OR = 1.00, 95%CI: 1.00-1.00, p-value = 0.085), chronic laryngitis and laryngotracheitis (IVW: OR = 1.05, 95%CI: 0.90-1.21, p-value = 0.558). Conclusion: Our findings support a potential causal relationship between pediatric asthma and UAD, suggesting that pediatric asthma may be a potential risk factor for various UAD.