Environmental Microcystin Exposure Increases Liver Injury Risk Induced by Hepatitis B Virus Combined with Aflatoxin: A Cross-Sectional Study in Southwest China
Environmental Microcystin Exposure Increases Liver Injury Risk Induced by Hepatitis B Virus Combined with Aflatoxin: A Cross-Sectional Study in Southwest China
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环境微囊藻毒素暴露会增加乙型肝炎病毒与黄曲霉毒素联合引起的肝损伤风险：中国西南地区的一项横断面研究
DOI：
10.1021/acs.est.6b05404
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发表时间：
2017-06-06
影响因子：
11.4
通讯作者：
Shu, Weiqun
中科院分区：
文献类型：
--
作者：
Liu, Wenyi;Wang, Lingqiao;Shu, Weiqun
热带和潮湿地区同时存在三种肝脏危害，两种已证实的乙型肝炎病毒（HBV）和黄曲霉毒素（AFB），以及一种在人群中很少研究的微囊藻毒素（MC）；然而，在同一人群中没有流行病学数据表明其风险。我们对两个农村城镇的5493名成年人进行了基于社区的横断面调查，在检测HBsAg和HBV DNA滴度、测定AFB1和MC-LR的估计每日摄入量（EDIs）以及检测血清AST和ALT作为肝损伤标志物后，统计分析了这三个因素的比较和联合效应。我们观察到HBsAg（+）率为7.6%，AFB1暴露水平相对较高（平均EDIAFB1 = 471.30 ng/d）， MC-LR暴露水平相对较低（平均EDIMC-LR = 228.25 ng/d）。与未暴露于HBV的受试者相比，异常AST （2.42, 95%CI = 1.69-3.45）和ALT （2.87, 95%CI = 1.91-4.29）的or值升高，但单独或联合暴露于AFB1和MC-LR的受试者的or值未升高（EDIs >=平均值）。同时，校正混杂因素后，暴露于HBV、HBV&AFB1（或HBV&MC-LR）、HBV&AFB1& mc - lr后，AST和ALT均值及异常AST和ALT的or值依次升高，特别是在HBV DNA可检测组（AST: or = 11.38, 95%CI = 3.91-33.17; ALT: or = 17.09, 95%CI = 5.36-54.53）。值得注意的是，HBV暴露组与HBV& afb1和HBV& mc - lr暴露组相比，AST和ALT异常的or值无显著差异，但HBV& afb1和HBV& mc - lr暴露组的or值显著高于HBV& afb1和HBV& mc - lr暴露组（P = 0.029和P = 0.037）。我们的研究表明，微囊藻毒素可能会增加HBV和黄曲霉毒素联合暴露引起的肝损伤的风险。然而，考虑到毒素检测和EDIs评价的不确定性，需要更多的流行病学数据来确定微囊藻毒素日益增加的毒性作用。
Three liver hazards, two confirmed-hepatitis B virus (HBV) and aflatoxin (AFB), and one rarely studied in populations-microcystin (MC), simultaneously exist in tropical and humid areas; however, there are no epidemiological data on their risks in the same population. We conducted a community-based cross-sectional survey among 5493 adults in two rural towns and statistically analyzed the comparative and combinative effects of the three factors after detecting HBsAg and HBV DNA titers, determining estimated daily intakes (EDIs) of AFB1 and MC-LR and testing serum AST and ALT as liver injury markers for each participant. We observed a HBsAg(+) rate of 7.6%, a relatively high AFB1 exposure level (mean EDIAFB1 = 471.30 ng/d), and a relatively low MC-LR exposure level (mean EDIMC-LR = 228.25 ng/d). ORs for abnormal AST (2.42, 95%CI = 1.69-3.45) and ALT (2.87, 95%CI = 1.91-4.29) increased in HBV infections compared with HBV-unexposed participants but did not increase in participants with separate or combined exposure to AFB1 and MC-LR (EDIs >= mean). Meanwhile, after adjustment for confounding factors, means of AST and ALT and ORs of abnormal AST and ALT were successively elevated after exposure to HBV, HBV&AFB1 (or HBV&MC-LR), and HBV&AFB1&MC-LR, especially in the group with detectable HBV DNA (AST: OR = 11.38, 95%CI = 3.91-33.17; ALT: OR = 17.09, 95%CI = 5.36-54.53). Notably, ORs for abnormal AST and ALT in the HBV exposed group were not significantly different from those in HBV&AFB1 or in the HBV&MC-LR exposed group but were significantly higher in the HBV&AFB1&MC-LR exposed group (P = 0.029 and P = 0.037, respectively). Our study indicated that microcystin may have the potential to increase the risk of liver injury induced by combined exposure to HBV and aflatoxin. However, in consideration of the uncertainties in the detection of the toxins and evaluation of the EDIs, more epidemiological data are expected to determine the increasing toxic effects of microcystins.