Guangdong Provincial Engineering Technology Research Center for Drug and Food Biological Resources Processing and Comprehensive Utilization, School of Life Sciences, South China Normal University, Guangzhou, 510631, China.
Guangzhou Women and Children's Medical Center, Guangzhou, 510120, China.
Environ Pollut. 2020 Nov;266(Pt 2):115220. doi: 10.1016/j.envpol.2020.115220. Epub 2020 Jul 18.
As previous studies found that the direct associations between urinary polycyclic aromatic hydrocarbon (PAH), benzene and toluene (BT) metabolites and the decreased lung function were not conclusive, we further investigated relationship of oxidative damage and airway inflammation induced by PAHs and BTs exposure with lung function. A total of 262 children diagnosed with asthma and 72 heathy children were recruited. Results showed that asthmatic children had higher levels of PAHs and BTs exposure, as well as Malonaldehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) compared with healthy children. Furthermore, binary logistic regression showed that each unit increases in level of urinary 2-&3-hydroxyfluorene (2-&3-OHF), 2-hydroxyphenanthrene (2-OHPhe), 1-hydroxyphenanthrene (1-OHP) and S-phenylmercapturic acid (S-PMA) were significantly associated with an elevated risk of asthma in children with odds ratios of 1.5, 2.3, 1.7 and 1.4, respectively, suggesting that PAHs and BTs exposure could increase the risk of asthma for children. Neither PAH nor BT metabolite could comprehensively indicate the decreased lung function as only 2-&3-OHF and 1-OHP were significantly and negatively correlated with forced vital capacity (FVC). Moreover, levels of most individual PAH and BT metabolite were significantly correlated to MDA and 8-OHdG. Further hierarchical regression analysis indicated that MDA and 8-OHdG levels did not show significant effects on the decreased lung function, suggesting that they are not the suitable biomarkers to indirectly indicate the altered lung function induced by PAHs and BTs. Urinary 2-OHPhe and 1-&9-hydroxyphenanthrene (1-&9-OHPhe) were significantly correlated with fractional exhaled nitric oxide (FeNO). Moreover, FeNO significantly contributed to decreased lung function and explained 7.7% of variance in ratio of forced expiratory volume in 1 s (FEV) and FVC (FEV/FVC%). Hence, FeNO, rather than oxidative damage indicators or any urinary PAH and BT metabolite, is more sensitive to indirectly reflect the decreased lung function induced by PAHs and BTs exposure for asthmatic children.
先前的研究发现,尿液中多环芳烃(PAH)、苯和甲苯(BT)代谢物与肺功能下降之间的直接关联并不明确,因此我们进一步研究了 PAH 和 BT 暴露引起的氧化损伤和气道炎症与肺功能之间的关系。共招募了 262 名被诊断为哮喘的儿童和 72 名健康儿童。结果显示,与健康儿童相比,哮喘儿童的 PAH 和 BT 暴露水平以及丙二醛(MDA)和 8-羟基-2'-脱氧鸟苷(8-OHdG)水平更高。此外,二元逻辑回归显示,尿液中 2-和 3-羟基芴(2-和 3-OHF)、2-羟基菲(2-OHPhe)、1-羟基菲(1-OHP)和 S-苯巯基尿酸(S-PMA)水平每增加一个单位,儿童患哮喘的风险分别增加 1.5 倍、2.3 倍、1.7 倍和 1.4 倍,这表明 PAH 和 BT 暴露会增加儿童患哮喘的风险。PAH 和 BT 代谢物都不能全面说明肺功能下降,因为只有 2-和 3-OHF 和 1-OHP 与用力肺活量(FVC)呈显著负相关。此外,大多数个体 PAH 和 BT 代谢物的水平与 MDA 和 8-OHdG 显著相关。进一步的分层回归分析表明,MDA 和 8-OHdG 水平对肺功能下降没有显著影响,这表明它们不是间接指示 PAH 和 BT 引起的肺功能改变的合适生物标志物。尿液中 2-OHPhe 和 1-和 9-羟基菲(1-和 9-OHPhe)与呼出气一氧化氮(FeNO)显著相关。此外,FeNO 显著导致肺功能下降,解释了 1 秒用力呼气量(FEV)和 FVC(FEV/FVC%)的 7.7%的变异性。因此,FeNO 比氧化损伤指标或任何尿液 PAH 和 BT 代谢物更敏感,能够更灵敏地间接反映 PAH 和 BT 暴露引起的哮喘儿童肺功能下降。