Department of Occupational & Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology; Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Department of Occupational & Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology; Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Chest. 2023 Jun;163(6):1395-1409. doi: 10.1016/j.chest.2022.12.004. Epub 2022 Dec 14.
Toxicologic studies have reported propylene oxide (PO) exposure may harm the respiratory system, but the association between PO exposure and lung function and potential mechanism remains unclear.
What is the association between PO exposure and lung function and potential mediating mechanism?
Urinary PO metabolite [N-Acetyl-S-(2-hydroxypropyl)-L-cysteine (2HPMA)] as PO internal exposure biomarker and lung function were measured for 3,692 community residents at baseline and repeated at 3-year follow up. Cross-sectional and longitudinal associations between urinary 2HPMA and lung function were assessed by linear mixed model. Urinary 8-hydroxy-deoxyguanosine, urinary 8-iso-prostaglandin-F2α, and plasma protein carbonyls as biomarkers of oxidative DNA damage, lipid peroxidation, and protein carbonylation, respectively, were measured for all participants to explore their potential roles in 2HPMA-associated lung function decline by mediation analysis.
After adjustment for potential covariates, each threefold increase in urinary 2HPMA was cross sectionally associated with a 26.18 mL (95% CI, -50.55 to -1.81) and a 21.83 mL (95% CI, -42.71 to -0.95) decrease in FVC and FEV, respectively, at baseline (all P < .05). After 3 years of follow up, 2HPMA was observed to be longitudinally associated with FEV/FVC decline. No significant interaction effect of smoking or passive smoking was observed (P > .05), and the associations between 2HPMA and lung function indexes were persistent among participants who were not smoking and those who were not passive smoking in both baseline and follow-up evaluations. We observed urinary 8-hydroxy-deoxyguanosine partially mediated the associations of 2HPMA with FVC (mediation proportion, 5.48%) and FEV (mediation proportion, 6.81%), and plasma protein carbonyl partially mediated the association between 2HPMA and FEV (mediation proportion, 3.44%).
PO exposure was associated with lung function decline among community residents, and oxidative DNA damage and protein carbonylation partially mediated PO exposure-associated lung function decline. Further attention on respiratory damage caused by PO exposure is warranted.
毒理学研究报告称，环氧丙烷（PO）暴露可能会损害呼吸系统，但 PO 暴露与肺功能的关联及其潜在机制仍不清楚。
PO 暴露与肺功能的关联以及潜在的介导机制是什么？
在基线和 3 年随访时，对 3692 名社区居民测量尿中 PO 代谢物[N-乙酰-S-(2-羟丙基)-L-半胱氨酸（2HPMA）]作为 PO 内暴露生物标志物和肺功能。通过线性混合模型评估尿 2HPMA 与肺功能的横断面和纵向关联。对所有参与者测量尿 8-羟基脱氧鸟苷、尿 8-异前列腺素 F2α 和血浆蛋白羰基作为氧化 DNA 损伤、脂质过氧化和蛋白质羰基化的生物标志物，通过中介分析探索它们在 2HPMA 相关肺功能下降中的潜在作用。
在调整了潜在的混杂因素后，尿 2HPMA 每增加三倍，与 FVC 分别下降 26.18 毫升（95%置信区间，-50.55 至-1.81）和 FEV 下降 21.83 毫升（95%置信区间，-42.71 至-0.95）相关，均具有统计学意义（均 P <.05）。在 3 年的随访中，观察到 2HPMA 与 FEV/FVC 下降呈纵向相关。吸烟或被动吸烟的交互作用无统计学意义（P >.05），并且在基线和随访评估中，不吸烟和不被动吸烟的参与者中，2HPMA 与肺功能指标的关联均持续存在。我们发现尿 8-羟基脱氧鸟苷部分介导了 2HPMA 与 FVC（中介比例，5.48%）和 FEV（中介比例，6.81%）的关联，而血浆蛋白羰基部分介导了 2HPMA 与 FEV（中介比例，3.44%）的关联。
PO 暴露与社区居民的肺功能下降有关，氧化 DNA 损伤和蛋白质羰基部分介导了 PO 暴露与肺功能下降的关联。需要进一步关注 PO 暴露引起的呼吸损伤。
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