[The study on biological exposure index of occupational exposure to arsenic and its inorganic compounds].

Objective: To establish biological exposure index (BEI) of occupational exposure to arsenic and its inorganic compounds through occupational epidemiology and the regression analysis of internal and external exposure of workers. Methods: In November 2021, 125 workers with occupational exposure to arsenic and its inorganic compounds and 49 office administrators in a non-ferrous metal smelter in Yunnan Province were selected as the exposure group and control group, respectively. Air samples from the workplace of the study subjects on weekdays were collected and arsenic concentrations were determined. Urine samples were collected in end-of-work weekend and high performance liquid chromatography-inductively coupled plasma mass spectrometry (HPLC-ICP-MS) was used to detect the levels of trivalent inorganic arsenic (iAs(3+)) , pentavalent inorganic arsenic (iAs(5+)) , monomethyl arsenic (MMA) and dimethyl arsenic (DMA) in urine. The correlations between arsenic concentration in the workplace air and arsenic species in urine of workers were analyzed. Arsenic exposure concentration and the level of urinary arsenic (ΣiAs+MMA+DMA) of workers was analyzed by linear regression and the BEI of arsenic and its inorganic compounds in the workplace was proposed based on the results of micronucleus test. Results: The median of time-weighted average concentration (C(TWA)) of arsenic in the workplace air of the exposure group was 0.0116 mg/m(3), and the over-standard rate was 71.2% (89/125) . The concentrations of iAs(3+), iAs(5+), inorganic arsenic (iAs=ΣiAs(3+)+iAs(5+)) 、MMA、DMA and urinary arsenic in the exposure group were higher than those in the control group at the end of shift, and the differences were statistically significant (P<0.05) . The concentration of arsenic in the workplace air had the strongest correlation with the concentration of urinary arsenic at the end of the shift (r(s)=0.909, P<0.001) . The regression equation was lg (y) =7.662+2.968lg (x) (r=0.821, P<0.05) . According to the occupational exposure limit (OEL) of arsenic in China, the concentration of urinary arsenic in the end-of-work weekend was calculated to be 53.2 µg/L. Combined with the results of micronucleus test, the BEI of occupational exposure to arsenic and its inorganic compounds in the workplace was proposed to be 50 µg/L. Conclusion: The urinary arsenic in the end-of-work weekend can be used as a biomarker of occupational exposure to arsenic, and its BEI is recommended to be 50 µg/L.

[Correlation analysis of urinary arsenic species and health effect indicators of occupational arsenic exposure workers].

Objective: To explore the correlation between urinary arsenic and health effects through the determination and analysis of urinary arsenic levels in occupational arsenic exposed workers. Methods: In November 2021, 95 workers exposed to arsenic and its inorganic compounds and 31 administrative personnel from a non-ferrous metal smelter in Yunnan Province were selected as the contact group and control group, respectively. Urine forms of arsenic, blood tumor markers, liver function were detected, and micronucleus test was used to analyze the chromosome damage. The correlation between urine forms of arsenic and health effects were analyzed. Results: Compared with the control group, the concentrations of urinary trivalent inorganic arsenic (iAs(3+)) , pentavalent inorganic arsenic (iAs(5+)) , inorganic arsenic (iAs=ΣiAs(3+)+iAs(5+)) , monomethyl arsenic (MMA) , dimethyl arsenic (DMA) and urinary arsenic (ΣiAs+MMA+DMA) at the end of class in contact group were higher (P<0.05) . There was no statistically significant difference in blood tumor markers and liver function indicators between the two groups (P>0.05) . Compared with the control group, the peripheral blood micronucleus rate and cell micronucleus rate in the contact group were significantly increased (P<0.05) . The urinary arsenic, iAs(5+), inorganic arsenic and DMA were positively correlated with peripheral blood micronucleus rate in contact group (r(s)=0.48, 0.34, 0.37, 0.23, P<0.05) , and the urinary arsenic, iAs(5+), DMA were positively correlated with peripheral blood micronucleus rate (r(s)=0.48, 0.34, 0.26, P<0.05) . Conclusion: There is a significant correlation between different valence states of arsenic in the urine and abnormal health effects of occupational arsenic exposed workers. It is necessary to strengthen the detection of arsenic species in the urine of occupational arsenic exposed workers to better protect their health.

[The research progress of metabolism and occupational biological exposure index metabolism of inorganic arsenic and its compounds].

Arsenic is a common metal-like element. Drinking arsenic-containing water and occupational exposure to arsenic are the main ways exposure to arsenic for population. Long-term exposure to arsenic can cause various organs dysfunction and cancer. After entering the body, inorganic arsenic is mainly methylated into monomethyl arsenic and dimethyl arsenic in the liver. Only a small part of inorganic arsenic is metabolized in the kidneys and lungs, and finally the metabolites of arsenic are excreted in the urine. understanding the biological characteristics of arsenic absorption, metabolism, and distribution in the body and formulating biological indicators related to occupational exposure to arsenic and can provide a scientific basis for the prevention and treatment of arsenic-related diseases. This article will review the biological monitoring indicators of occupational exposure to arsenic and the metabolic process of arsenic in the body.

[Effect of autologous skin paste on repairing wound of donor site of medium-thickness skin graft].

Objective: To explore the effect of autologous skin paste on repairing wound of medium-thickness skin donor site. Methods: The prospective randomized controlled research method was applied. From October 2018 to December 2019, 18 patients with flame burn or hydrothermal scald, met the inclusion criteria were admitted to Jinhua Hospital Affiliated to Zhejiang University School of Medicine, including 15 males and 3 females, aged (45±6) years, and the wounds were repaired with medium-thickness skin grafts. The wound area after medium-thickness skin grafting was (121±33) cm2. The wound of donor site of medium-thickness skin graft in each patient was divided into 2 wounds in equal area and included into autologous skin paste group and conventional treatment group with random number table, with 18 wounds in each group.The wounds in autologous skin paste group were repaired with skin paste prepared with remaining skin fragments after autologous medium-thickness skin grafting, and the wounds in conventional treatment group were repaired with petroleum jelly gauze and sterile gauze. On 3, 7, 14, 21 d after operation, the wound healing in 2 groups was observed, and the wound healing rate was calculated. The wound healing time in 2 groups was recorded. Occurrences of subcutaneous effusion and infection on 3, 7, 14, 21 d after operation and wound rupture in 3 months after operation were observed. In 6 months after operation, the Vancouver scar scale (VSS) was used to evaluate the scar formation of wounds in 2 groups. Data were statistically analyzed with analysis of variance for repeated measurement, chi-square test, and group t test. Results: The wounds in 2 groups did not heal on 3 and 7 d after operation. The wound healing rate in autologous skin paste group was (29.8±2.5)% and (95.6±4.7)% on 14 and 21 d after operation, which were significantly higher than (25.8±2.9)% and (82.6±8.9)% in conventional treatment group (t=4.3, 5.6, P<0.01). The wound healing time in autologous skin paste group was (21.8±1.4) d, which was significantly shorter than (25.6±2.0) d in conventional treatment group (t=6.24, P<0.01). On 3, 7, 14, 21 d after operation, there were no complications such as subcutaneous effusion and infection in wounds of 2 groups. In 3 months after operation, ulceration occurred in wounds of 2 patients in autologous skin paste group, which was significantly less than 12 patients in conventional treatment group (χ2=11.688, P＜0.01). The wounds with ulceration healed after dressing change. In 6 months after operation, the VSS score of wounds in autologous skin paste group was (9.1±1.1) points, which was significantly lower than (11.3±1.2) points in conventional treatment group (t=-5.75, P＜0.01). Conclusion: The remaining fragments after autologous medium-thickness skin grafting are prepared into skin paste to repair wound of donor site of medium-thickness skin graft can shorten wound healing time, improve wound healing quality, reduce degree of scar hyperplasia, which has a good clinical effect.

[The role of renal tubular epithelial cells in cadmium-induced renal fibrosis].

Objective: To investigate the role of renal tubular epithelial cells in cadmium-induced renal fibrosis. Methods: Established a sub-chronic cadmium exposure mouse model and analyzed the progress of renal fibrosis induced by cadmium exposure through Masson staining and immunohistochemistry, and then a co-culture system of renal tubular epithelial cells and renal fibroblasts was established, the levels of proliferation and activation of renal fibroblasts were detected by Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting. Results: Sub-chronic cadmium exposure led to weight loss in mice (P<0.05) , and the levels of ß-microglobulin (ß-MG) and N-acetyl ß-D-glucosaminidase (NAG) in urine were increased in mice exposed to cadmium (P<0.05) ; pathological analysis revealed that sub-chronic cadmium exposure damaged renal tubular structure, causing infiltration of inflammatory cells and deposition of collagen fiber by Masson (P<0.05) , which in turn induced kidney fibrosis in mice; the results of in vitro co-culture experiments showed that cadmium-exposed renal tubular epithelial cells accelerated the synthesis of collagen in renal fibroblasts and promoted the proliferation and activation of renal fibroblasts (P<0.05) . Conclusion: In the progression of cadmium-induced renal fibrosis, a deleterious renal epithelial-fibroblast cross talk was formed, which may be one of the important mechanisms of cadmium-induced renal fibrosis.

Ligand preorganization in metal ion complexation: molecular mechanics/dynamics, kinetics, and laser-excited luminescence studies of trivalent lanthanide complex formation with macrocyclic ligands TETA and DOTA.

The molecular mechanics and dynamics calculations, kinetics, and laser-excited luminescence studies were carried out for trivalent lanthanide (Ln(3+)) complexes of macrocyclic polyaminopolycarboxylate ligands TETA and DOTA (where TETA is 1,4,8,11-tetraazacyclotetradecane-1,4,8,11-tetraacetic acid and DOTA is 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid) to further understand the observed thermodynamic, kinetic, and structural properties and to examine how ligand preorganization affects metal ion complexation. Excitation spectroscopy (emission monitored at 614.0 nm) of the (7)F(0) --> (5)D(0) transition of Eu(3+) was used to study the aqueous properties of the Eu(3+)-TETA system. A stopped-flow spectrophotometric method was used to study the formation kinetics of the aqueous Ce(3+)-TETA/DOTA systems in the pH range 6.1-6.7. Molecular mechanics calculation results are consistent with the proposed mechanism of Ln(DOTA)(-) formation, i.e., formation of a carboxylate O-bonded precursor, followed by metal ion moving into the preformed macrocyclic cavity. For Ln(TETA)(-) formation, at least two carboxylate O-bonded intermediates have been predicted and Ln(3+) ion assisted reorganization of the TETA ligand is present. The calculated bond distances and overall structures of Ln(DOTA)(-) and Ln(TETA)(-) were in agreement with the single-crystal and solution NMR structural data. The origin of the difference in thermodynamic stability of Ln(DOTA)(-) and Ln(TETA)(-) complexes and the corresponding formation intermediates is mainly due to the differences in water-occupancy energy (i.e., whether there is an apical coordinated water molecule), the ligand strain energy, and the cation-ligand interaction energy. Kinetic studies revealed that the formation rates of the Ce(TETA)(-) complex are smaller at lower pH and temperature but become greater at higher pH and temperature, as compared to those of the Ce(DOTA)(-) complex. This is attributed to the lanthanide ion and both mono- and di-hydroxide ion assisted TETA conformational reorganization and higher kinetic activation parameters. The presence of a di-hydroxide ion assisted intermediate rearrangement pathway could make the Ce(TETA)(-) complex formation rate faster at higher pH, and the higher activation barrier makes Ce(TETA)(-) complex formation rate slower at lower pH, as compared to those of the Ce(DOTA)(-) complex.

Dentinogenesis imperfecta 1 with or without progressive hearing loss is associated with distinct mutations in DSPP.

Dentinogenesis imperfecta 1 (DGI1, MIM 125490) is an autosomal dominant dental disease characterized by abnormal dentin production and mineralization. The DGI1 locus was recently refined to a 2-Mb interval on 4q21 (ref. 1). Here we study three Chinese families carrying DGI1. We find that the affected individuals of two families also presented with progressive sensorineural high-frequency hearing loss (gene DFNA39). We identified three disease-specific mutations within the dentin sialophosphoprotein gene (DSPP) in these three families. We detected a G-->A transition at the donor-splicing site of intron 3 in one family without DFNA39, a mutation predicted to result in the skipping of exon 3. In two other families affected with both DGI1 and DFNA39, however, we identified two independent nucleotide transversions in exons 2 and 3 of DSPP, respectively, that cause missense mutations of two adjacent amino-acid residues in the predicted transmembrane region of the protein. Moreover, transcripts of DSPP previously reported to be expressed specifically in teeth are also detected in the inner ear of mice. We have thus demonstrated for the first time that distinct mutations in DSPP are responsible for the clinical manifestations of DGI1 with or without DFNA39.