Assessment of occupational exposure to inorganic arsenic based on urinary concentrations and speciation of arsenic.

An analytical speciation method, capable of separating inorganic arsenic (As (V), As (III] and its methylated metabolites (MMAA, DMAA) from common, inert, dietary organoarsenicals, was applied to the determination of arsenic in urine from a variety of workers occupationally exposed to inorganic arsenic compounds. Mean urinary arsenic (As (V) + As (III) + MMAA + DMAA) concentrations ranged from 4.4 micrograms/g creatinine for controls to less than 10 micrograms/g for those in the electronics industry, 47.9 micrograms/g for timber treatment workers applying arsenical wood preservatives, 79.4 micrograms/g for a group of glassworkers using arsenic trioxide, and 245 micrograms/g for chemical workers engaged in manufacturing and handling inorganic arsenicals. The maximum recorded concentration was 956 micrograms/g. For the most exposed groups, the ranges in the average urinary arsenic speciation pattern were 1-6% As (V), 11-14% As (III), 14-18% MMAA, and 63-70% DMAA. The highly raised urinary arsenic concentrations for the chemical workers, in particular, and some glassworkers are shown to correspond to possible atmospheric concentrations in the workplace and intakes in excess of, or close to, recommended and statutory limits and those associated with inorganic arsenic related diseases.     

Biological monitoring of occupational exposure to inorganic arsenic

OBJECTIVES: This study was undertaken to assess reliable biological indicators for monitoring the occupational exposure to inorganic arsenic (iAs), taking into account the possible confounding role of arsenicals present in food and of the element present in drinking water. METHODS: 51 Glass workers exposed to As trioxide were monitored by measuring dust in the breathing zone, with personal air samplers. Urine samples at the end of work shift were analysed for biological monitoring. A control group of 39 subjects not exposed to As, and eight volunteers who drank water containing about 45 micrograms/l iAs for a week were also considered. Plasma mass spectrometry (ICP-MS) was used for the analysis of total As in air and urine samples, whereas the urinary As species (trivalent, As3; pentavalent, As5; monomethyl arsonic acid, MMA; dimethyl arsinic acid, DMA; arsenobetaine, AsB) were measured by liquid chromatography coupled with plasma mass spectrometry (HPLC-MS) RESULTS: Environmental concentrations of As in air varied widely (mean 84 micrograms/m3, SD 61, median 40) and also the sum of urinary iAs MMA and DMA, varied among the groups of exposed subjects (mean 106 micrograms/l, SD 84, median 65). AsB was the most excreted species (34% of total As) followed by DMA (28%), MMA (26%), and As3 + As5 (12%). In the volunteers who drank As in the water the excretion of MMA and DMA increased (from a median of 0.5 to 5 micrograms/day for MMA and from 4 to 13 micrograms/day for DMA). The best correlations between As in air and its urinary species were found for total iAs and As3 + As5. CONCLUSIONS: To avoid the effect of As from sources other than occupation on urinary species of the element, in particular on DMA, it is proposed that urinary As3 + As5 may an indicator for monitoring the exposure to iAs. For concentrations of 10 micrograms/m3 the current environmental limit for iAs, the limit for urinary As3 + As5 was calculated to be around 5 micrograms/l, even if the wide variation of values needs critical evaluation and application of data. The choice of this indicator might be relevant also from a toxicological point of view. Trivalent arsenic is in fact the most active species and its measure in urine could be the best indicator of some critical effects of the element, such as cancer.

 

     

职业性砷暴露对尿砷及外周血miRNA的影响

目的 探讨职业性砷暴露工人尿中不同化学形态砷含量及甲基化能力与外周血miRNA的关系。方法 采用自身对照，选取某矿山55名工人，问卷收集基本信息；采集研究对象正在接触时与脱离接触3个月后的尿液和外周血，高效液相色谱-电感耦合等离子质谱联用(HPLC-ICP-MS)法检测尿中三价及五价无机砷(inorganic arsenic, iAs³⁺、iAs⁵⁺)、一甲基砷酸(monomethylarsonic acid, MMA)、二甲基砷酸(dimethylarsinic acid, DMA)的含量；以尿中四种形态砷含量总和为总砷(total arsenic, tAs),并以一甲基化率(primary methylated index, PMI)、二甲基化率(secondary methylated index, SMI)为指标，计算甲基化能力；同时，采用实时荧光定量PCR检测外周血miR-155、miR-191、miR-200b相对表达量。结果 正在接触时工人尿中iAs³⁺、MMA、DMA、iAs⁵⁺、t...     

Risk factors for increased urinary inorganic arsenic concentrations from low arsenic concentrations in drinking water

A large number of drinking water supplies worldwide have greater than 50 microg l(- 1) inorganic arsenic in drinking water, and there is increasing pressure to reduce concentrations. Few studies have specifically considered low concentrations of arsenic in water supplies and the significance of other factors which may contribute to increased exposure. This study aimed to investigate risk factors for increased urinary inorganic arsenic concentrations, in a population exposed to 10 - 100 microg l(- 1) of arsenic in drinking water, as well as a control population with lower arsenic concentrations in their drinking water. Inorganic arsenic in urine was used as the measure of exposure. The median drinking water arsenic concentration in the exposed population was 43.8 microg l(- 1) (16.0 - 73 microg l(- 1)) and less than the analytical limit of detection of 1 microg l(- 1) (相似文献   

HPLC-ICP-MS speciation analysis of arsenic in urine of Japanese subjects without occupational exposure

The toxicity and carcinogenicity of arsenic depend on its species. Individuals living in Japan consume much seafood that contains high levels of organoarsenics. Speciation analysis of urinary arsenic is required to clarify the health risks of arsenic intake. There has been no report of urinary arsenic analysis in Japan using high performance liquid chromatography with inductively coupled plasma mass spectrometry (HPLC-ICP-MS). We performed speciation analysis of urinary arsenic for 210 Japanese male subjects without occupational exposure using HPLC-ICP-MS. The median values of urinary arsenics were as follows: sodium arsenite (AsIII), 3.5; sodium arsenate (AsV), 0.1; monomethylarsonic acid (MMA), 3.1; dimethylarsinic acid (DMA), 42.6; arsenobetaine (AsBe), 61.3; arsenocholine, trimethylarsine oxide, and unidentified arsenics (others), 5.2; and total arsenic (total As), 141.3 microgAs/l. The median creatinine-adjusted values were as follows: AsIII, 3.0; AsV, 0.1; MMA, 2.6; DMA, 35.9; AsBe, 52.1; others 3.5; and total As, 114.9 microgAs/g creatinine. Our findings indicate that DMA and AsBe levels in Japan are much higher than those found in Italian and American studies. It appears that the high levels of DMA and AsBe observed in Japan may be due in part to seafood intake. ACGIH and DFG set the BEI and BAT values for occupational arsenic exposure as 35 microgAs/l and 50 microgAs/l, respectively, using the sum of inorganic arsenic (iAs), MMA, and DMA. In the general Japanese population, the sums of these were above 50 microgAs/l in 115 (55%) samples. We therefore recommend excluding DMA concentration in monitoring of iAs exposure.     

Monitoring of arsenic exposure with speciated urinary inorganic arsenic metabolites for ion implanter maintenance engineers

For wafer fabrication in the semiconductor industry, maintenance engineers are potentially exposed to hazards during their work of disassembling machine components for cleanup. One special concern is the presence of arsenic or arsenic compounds in the working environment. This study analyzed speciated urinary inorganic arsenic metabolites of the maintenance engineers using high-performance liquid chromatography-hydride generation atomic absorption spectrometry to study the potential arsenic exposure during their maintenance work. In total, from six wafer fabrication facilities, 30 maintenance engineers were recruited as the exposed group and another 12 office-based engineers served as the control group. First morning-voided urine samples of each study subject were collected for 7 consecutive days. The levels of total urinary inorganic arsenic metabolites for the exposed group were 1.7+/-1.4, 1.4+/-1.1, 6.2+/-6.7, 20.2+/-14.1, and 29.5+/-17.2 micro g/L for As3+, As5+, monomethylarsonic acid, dimethylarsinic acid, and total inorganic arsenic, respectively. Both the concentration of monomethylarsonic acid and its percentage in total urinary inorganic arsenic metabolites showed significantly ascending trends for the control group, for the engineers without preventative maintenance work prior to their urine sampling, and for the engineers with such work prior to their urine sampling (P<0.05 and P<0.0005, respectively). The data also suggested that, at low-level occupational arsenic exposure, the concentration of total urinary inorganic arsenic metabolites might be misleading due to the confounding effect resulting from intake of seafood, such as arsenosuger. Nevertheless, monitoring of urinary arsenic species by using the percentage change of monomethylarsonic acid in total urinary inorganic arsenic metabolites as an indicator for the verification of arsenic exposure is helpful and appropriate in such cases.     

Binational arsenic exposure survey: methodology and estimated arsenic intake from drinking water and urinary arsenic concentrations

The Binational Arsenic Exposure Survey (BAsES) was designed to evaluate probable arsenic exposures in selected areas of southern Arizona and northern Mexico, two regions with known elevated levels of arsenic in groundwater reserves. This paper describes the methodology of BAsES and the relationship between estimated arsenic intake from beverages and arsenic output in urine. Households from eight communities were selected for their varying groundwater arsenic concentrations in Arizona, USA and Sonora, Mexico. Adults responded to questionnaires and provided dietary information. A first morning urine void and water from all household drinking sources were collected. Associations between urinary arsenic concentration (total, organic, inorganic) and estimated level of arsenic consumed from water and other beverages were evaluated through crude associations and by random effects models. Median estimated total arsenic intake from beverages among participants from Arizona communities ranged from 1.7 to 14.1 μg/day compared to 0.6 to 3.4 μg/day among those from Mexico communities. In contrast, median urinary inorganic arsenic concentrations were greatest among participants from Hermosillo, Mexico (6.2 μg/L) whereas a high of 2.0 μg/L was found among participants from Ajo, Arizona. Estimated arsenic intake from drinking water was associated with urinary total arsenic concentration (p < 0.001), urinary inorganic arsenic concentration (p < 0.001), and urinary sum of species (p < 0.001). Urinary arsenic concentrations increased between 7% and 12% for each one percent increase in arsenic consumed from drinking water. Variability in arsenic intake from beverages and urinary arsenic output yielded counter intuitive results. Estimated intake of arsenic from all beverages was greatest among Arizonans yet participants in Mexico had higher urinary total and inorganic arsenic concentrations. Other contributors to urinary arsenic concentrations should be evaluated.     

砷的职业接触生物监测指标

砷是一种自然界中多以化合物形式存在的常见类金属元素,在生产中应用广泛。随着职业接触人群越来越多,砷中毒越来越受到人们的重视。环境中的砷主要通过消化道、呼吸道和皮肤黏膜等进入人体,长期暴露于无机砷环境中可引起人体多种脏器损伤及其功能障碍,严重时可引发癌前病变。本文将对职业接触人群有关砷的生物监测指标予以综述。     

砒霜厂工人外周血淋巴细胞Dicer基因相对表达与尿砷代谢产物的关系研究

目的 通过比较职业性砷暴露人群与对照人群外周血淋巴细胞Dicer基因表达的差异,探讨职业性砷暴露人群外周血淋巴细胞中Dicer基因的表达与尿砷代谢产物之间的关系.方法 于2011年选取43名砒霜厂职业性砷暴露工人为暴露组,23名无砷暴露史人群为对照组,采用TRIzol法提取淋巴细胞中的总RNA,利用实时荧光定量PCR方法检测Dicer基因的表达,采用氢化物发生原子吸收分光光度法检测尿中各类砷化合物的含量.结果 砒霜厂工人无机砷、甲基胂酸、二甲基胂酸、总砷含量均高于对照组,二级甲基化指数低于对照组,外周血淋巴细胞中Dicer基因mRNA的表达(6.90±0.24)高于对照组(5.08±0.24),差异均有统计学意义(P＜0.01).尿中无机砷、甲基胂酸、二甲基胂酸、总砷与外周血淋巴细胞中Dicer基因mRNA表达呈正相关(P＜0.01);二级甲基化指数与Dicer基因mRNA表达呈负相关(r=-0.384,P＜0.05).结论 职业性砷暴露工人外周血淋巴细胞Dicer基因表达升高,可能与砷代谢甲基化过程有关.     

Assessment of occupational exposure to aromatic polycyclic hydrocarbons determining urinary levels of 1-pyrenol

In conformity with Italian law 626/94, occupational exposure to Polycyclic Aromatic Hydrocarbons (PAH) in several types of work environments was assessed by analysing urinary levels of 1-pyrenol. A total of 231 non-smokers exposed to PAH (82 workers, employed in two different thermoelectric power plants using combustible oil (30 subjects from plant A and 52 from plant B), 18 subjects working for a company recovering exhausted oils, 12 working on rubber production, 10 on road surface asphalting operations, 22 working in the anodizing section of an aluminium plant, 27 chimney-sweeps, and 60 coke-oven workers (30 topside workers, and 30 doing other jobs)) were enrolled. There were also 53 non-smoker control subjects, not occupationally exposed to PAH. Current smokers were excluded, since smoking is an important confounding factor when occupational exposure to low PAH concentrations are monitored. Confounding factors, i.e., diet and passive smoking, were checked by means of a questionnaire which, in addition to personal data and habits, also requested specific details about the type of diet followed and possible exposure to passive smoking during the 24-hour period preceding urine collection. In controls, exposure to PAH in the diet significantly increased 1-pyrenol levels in urine: in subjects introducing > or = 1 microgram of pyrene with the diet, the mean urinary level of 1-pyrenol was significantly higher than that introduced with < 1 microgram (high versus low dietary intake, mean +/- SD, 0.08 +/- 0.13 and 0.04 +/- 0.06 1-pyrenol mumoles/mole of creatinine, respectively; Mann-Whitney U-test Z = 2.67, p < 0.01). Conversely, passive smoking did not influence 1-pyrenol levels. In the overall population (controls and exposed), multiple linear regression analysis showed that levels of urinary 1-pyrenol were significantly influenced by occupational exposure to PAH in asphalt workers, anodizing plant workers, chimney-sweeps, and coke-oven workers, both those working at the top side of the oven and those doing other jobs (t = 2.19, p = 0.02; t = 2.56, p = 0.01; t = 5.25, p = 0.001; t = 3.34, p = 0.001; t = 7.82, p = 0.001, respectively; F = 9.7, p < 0.01), but not in power plant workers in contact with combustible oils, workers recovering exhausted oils, or rubber production workers. Diet and passive smoking did not influence urinary 1-pyrenol levels in the entire sample population. This biomarker also allowed an assessment of exposure levels among certainly exposed subjects. The percentage of subjects with urinary 1-pyrenol values higher than the 99th percentile of the reference population (0.67 mumoles 1-pyrenol/mole of creatinine) was significantly higher than that of controls in asphalt workers (20%), anodizing plant workers (14%), chimney-sweeps (13%) and coke-oven workers (33%) (chi-square test: asphalt workers = 6.1, p = 0.01; anodizing plant workers = 4.3, p = 0.04; chimney-sweeps = 7.1, p = 0.008; coke-oven workers with other duties = 4.4, p = 0.04; top side workers = 16.5, p < 0.001). In chimney sweeps and top side workers, respectively 2 and 4 subjects (7% and 13%) exceeded the precautionary level of 1.4 mumoles 1-pyrenol/mole of creatinine; of these, 1 chimney sweep and 3 top side workers (4% and 10%) exceeded the recommended biological threshold of 2.3 mumoles 1-pyrenol/mole of creatinine.     

Association between arsenic exposure from a coal-burning power plant and urinary arsenic concentrations in Prievidza District,Slovakia

To assess the arsenic exposure of a population living in the vicinity of a coal-burning power plant with high arsenic emission in the Prievidza District, Slovakia, 548 spot urine samples were speciated for inorganic As (Asinorg), monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), and their sum (Assum). The urine samples were collected from the population of a case-control study on nonmelanoma skin cancer (NMSC). A total of 411 samples with complete As speciations and sufficient urine quality and without fish consumption were used for statistical analysis. Although current environmental As exposure and urinary As concentrations were low (median As in soil within 5 km distance to the power plant, 41 micro g/g; median urinary Assum, 5.8 microg/L), there was a significant but weak association between As in soil and urinary Assum(r = 0.21, p < 0.01). We performed a multivariate regression analysis to calculate adjusted regression coefficients for environmental As exposure and other determinants of urinary As. Persons living in the vicinity of the plant had 27% higher Assum values (p < 0.01), based on elevated concentrations of the methylated species. A 32% increase of MMA occurred among subjects who consumed homegrown food (p < 0.001). NMSC cases had significantly higher levels of Assum, DMA, and Asinorg. The methylation index Asinorg/(MMA + DMA) was about 20% lower among cases (p < 0.05) and in men (p < 0.05) compared with controls and females, respectively.     

Renal and immunological effects of occupational exposure to inorganic mercury.

Seven parameters of renal dysfunction (urinary excretion of albumin, orosomucoid, beta 2-microglobulin, N-acetyl-beta-glucosaminidase (NAG), and copper; serum creatinine concentration, and relative clearance of beta 2-microglobulin) were examined in a group of chloralkali workers exposed to mercury vapour (n = 89) and in an unexposed control group (n = 75). Serum concentrations of immunoglobulins (IgA, IgG, IgM) and auto-antibodies towards glomeruli and other tissues were also determined. The parameters examined were compared between the two groups and related to different exposure parameters. In the chloralkali group median blood mercury concentration (B-Hg) was 55 nmol/l, serum mercury (S-Hg) 45 nmol/l, and urine mercury concentration (U-Hg) 14.3 nmol/mmol creatinine (25.4 micrograms/g creatinine). Corresponding concentrations for the control group were 15 nmol/l, 4 nmol/l, and 1.1 nmol/mmol creatinine (1.9 micrograms/g creatinine) respectively. None of the parameters of renal dysfunction differed significantly between the two groups, but there was a tendency to increased excretion of NAG in the exposed group compared with the controls. Also, a statistically significant relation existed between U-Hg and U-NAG (p less than 0.001). Serum immunoglobulin concentrations did not differ between the groups, and serum titres of autoantibodies (including antiglomerular basement membrane and antilaminin antibodies) were low in both groups. Thus the results gave no evidence of glomerular damage or of a tubular reabsorption defect at the current relatively low exposures. The findings still indicate slight, dose related tubular cell damage in the mercury exposed group. There were no signs of a mercury induced effect on the immune system.     

Renal and immunological effects of occupational exposure to inorganic mercury.

Seven parameters of renal dysfunction (urinary excretion of albumin, orosomucoid, beta 2-microglobulin, N-acetyl-beta-glucosaminidase (NAG), and copper; serum creatinine concentration, and relative clearance of beta 2-microglobulin) were examined in a group of chloralkali workers exposed to mercury vapour (n = 89) and in an unexposed control group (n = 75). Serum concentrations of immunoglobulins (IgA, IgG, IgM) and auto-antibodies towards glomeruli and other tissues were also determined. The parameters examined were compared between the two groups and related to different exposure parameters. In the chloralkali group median blood mercury concentration (B-Hg) was 55 nmol/l, serum mercury (S-Hg) 45 nmol/l, and urine mercury concentration (U-Hg) 14.3 nmol/mmol creatinine (25.4 micrograms/g creatinine). Corresponding concentrations for the control group were 15 nmol/l, 4 nmol/l, and 1.1 nmol/mmol creatinine (1.9 micrograms/g creatinine) respectively. None of the parameters of renal dysfunction differed significantly between the two groups, but there was a tendency to increased excretion of NAG in the exposed group compared with the controls. Also, a statistically significant relation existed between U-Hg and U-NAG (p less than 0.001). Serum immunoglobulin concentrations did not differ between the groups, and serum titres of autoantibodies (including antiglomerular basement membrane and antilaminin antibodies) were low in both groups. Thus the results gave no evidence of glomerular damage or of a tubular reabsorption defect at the current relatively low exposures. The findings still indicate slight, dose related tubular cell damage in the mercury exposed group. There were no signs of a mercury induced effect on the immune system.