Objective:To systematically evaluate the relationship between arsenic exposure and pulmonary ventilation dysfunction, so as to provide a basis for clarifying the mechanism of lung function injury caused by arsenic exposure and identifying at-risk populations of arsenic exposure.Methods:Pertinent studies were identified by searching PubMed, Embase, Web of Science, China Biology Medicine Disc (CBM), China National Knowledge Infrastructure (CNKI), Wanfang Data and VIP Database through March 2020. The studies that reported arsenic exposure and lung function dysfunction published at home and abroad were collected comprehensively. According to the inclusion and exclusion criteria, two reviewers independently screened and extracted the literatures. All of the Meta-analysis were performed by using Review Manager 5.3 software, the mean difference value ( MD) was used as the effect index, the fixed effect model or the random effect model were performed for comprehensive quantitative analysis according to the heterogeneity results, and subgroup analysis was conducted to explore the source of heterogeneity. Stata SE 15 software for funnel mapping and Egger's regression test were used to evaluate publication bias. Results:Totally 10 documents were included, all in English. The Meta-analysis showed that arsenic exposure could significantly reduce forced expiratory volume in one second (FEV1) and forced vital capacity (FVC), and the MD (95% CI) was - 23.82 ( - 39.93 -- 7.72) ml and - 47.47 (- 73.97 -- 20.98) ml, respectively. The differences were statistically significant ( Ζ = 2.90, 3.51, P < 0.01). FEV1/FVC was reported in three documents, and MD (95% CI) was - 4.72 (- 13.10 - 3.67). There was no evidence of an association between arsenic exposure and FEV1/FVC ( Ζ = 1.10, P > 0.05). The results of subgroup analysis showed that there were significant differences in FEV1 and FVC among subgroups by region (χ 2 = 6.80, 30.06, P < 0.01). Conclusion:Arsenic exposure is negatively correlated with vital capacity measurement indexes FEV1 and FVC, but not with FEV1/FVC, indicating that arsenic exposure may mainly lead to restrictive pulmonary ventilation dysfunction.

Objective:To investigate the antagonistic and therapeutic effects of Ginkgo biloba on arsenic-induced lung injury in rats and its mechanism.Methods:A total of 42 healthy clean grade Wistar rats, half male and half female, weighing 120 - 130 g, were randomly divided into 7 groups with 6 rats in each group. Two intervention models of Ginkgo biloba antagonism and treatment were established, respectively. The specific treatments were as follows: (1) Experimental study on the antagonism of Ginkgo biloba (4 groups): the control A group was given deionized water; the Ginkgo biloba control (GBE) group was given Ginkgo biloba solution (50 mg·kg -1·bw); the arsenic-treated (As) group was given sodium arsenite solution (10 mg·kg -1·bw); the Ginkgo biloba antagonistic (As + GBE) group was treated with sodium arsenite solution (10 mg·kg -1·bw) and Ginkgo biloba solution (50 mg·kg -1·bw), and the above administration was by gavage for 6 days/week, for 4 months. (2) Experimental study on the treatment of Ginkgo biloba (3 groups): the control B group was given deionized water for 5.5 months; in the arsenism natural recovery (recovery) group, sodium arsenite solution (10 mg·kg -1·bw) was administered by gavage for 4.0 months and deionized water for 1.5 months; the Ginkgo biloba treatment (treatment) group was given sodium arsenite solution (10 mg·kg -1·bw) by gavage for 4.0 months and Ginkgo biloba solution (50 mg·kg -1·bw) for 1.5 months, and the above administration was for 6 days/week. Masson staining was used to evaluate collagen fiber deposition in lung tissue. Western blotting was used to detect the expression level of related proteins in lung tissue homogenates, including inflammatory cytokines matrix metalloproteinase-9 (MMP-9), interleukin (IL)-1β, IL-18; high mobility group box 1 (HMGB1) and receptor for advanced glycation end-products (RAGE) of the HMGB1/RAGE pathway; phosphatidylinositol-4, 5-bisphosphate 3-kinase (PI3K), protein kinase B (AKT), phosphorylated AKT (p-AKT) of the PI3K/AKT pathway; transforming growth factor (TGF)-β1, SMAD2, p-SMAD2, SMAD3, p-SMAD3 and SMAD4 of the TGF-β1/SMAD pathway. Results:(1) Antagonistic effect of Ginkgo biloba: compared with the control A group, there was no significant change in protein expression and collagen fiber deposition in the lung tissue of GBE group ( P > 0.05); the levels of MMP-9, IL-1β and IL-18 protein expression and collagen fiber deposition in the lung tissue of As group were significantly increased ( P < 0.05); and the levels of HMGB1, RAGE, PI3K, p-AKT, TGF-β1, p-SMAD2, p-SMAD3 and SMAD4 protein expression were significantly increased ( P < 0.05). Compared with As group, the levels of MMP-9, IL-1β and IL-18 protein expression and collagen fiber deposition were significantly decreased in As + GBE group ( P < 0.05); and levels of HMGB1, RAGE, PI3K, p-AKT, TGF-β1, p-SMAD2, and p-SMAD3 protein expression were significantly decreased ( P < 0.05). (2) Therapeutic effect of Ginkgo biloba: compared with control B group, the levels of MMP-9, IL-1β, IL-18 protein expression and collagen fiber deposition were significantly increased in recovery group ( P < 0.05); and the levels of HMGB1, RAGE, PI3K, p-AKT, TGF-β1, p-SMAD2, p-SMAD3 and SMAD4 protein expression were significantly increased ( P < 0.05). Compared with recovery group, the levels of MMP-9, IL-1β, IL-18, HMGB1, RAGE, PI3K and p-AKT protein expression were significantly decreased in treatment group ( P < 0.05); and there was no significant change in collagen fiber deposition and TGF-β1, p-SMAD2, p-SMAD3 and SMAD4 protein expression levels in lung tissue ( P > 0.05). In both experiments, there was no significant difference in the protein expression levels of AKT, SMAD2 and SMAD3 between the groups ( P > 0.05). Conclusion:Ginkgo biloba intervention has ameliorated inflammatory injury and collagen fiber deposition in lung tissue of arsenic-treated rats possibly by inhibiting the expression levels of HMGB1/RAGE pathway-related proteins.