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.     

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.     

Biomonitoring for chromium and arsenic in timber treatment plant workers exposed to CCA wood Preservatives

This study reports a survey of occupational exposure to copper chrome arsenic (CCA) based wood preservatives during vacuum pressure timber impregnation. The survey involved biological monitoring based on analysis of chromium and arsenic in urine samples collected from UK workers. The aim of the study was to determine the extent of occupational exposure to arsenic and chromium in the UK timber treatment industry. The objectives were to collect and analyse urine samples from as many workers as possible, where CCA wood preservatives might be used, at 6 monthly intervals for 2 years. In addition, to investigate day-to-day variations in urinary excretion of chrome and arsenic by collecting and analysing three samples a week for 3 weeks in subsets of workers and controls (people not occupationally exposed). All urine samples were analysed for chromium and inorganic arsenic. To investigate any residual interference every sample was accompanied by a short questionnaire about recent consumption of seafood and smoking. The analytical methods for arsenic used a hydride generation technique to reduce interference from dietary sources of arsenic and also a technique that would measure total arsenic concentration in urine. The main findings show that workers exposed to CCA wood preservatives have concentrations of inorganic arsenic and chromium in urine that are significantly higher than those from non-occupationally exposed people but below biological monitoring guidance values that would indicate inhalation exposure at UK occupational exposure limits for chromium and arsenic. The effects of consumption of seafood on urinary arsenic were not significant using the hydride generation method for inorganic arsenic but were significant if 'total' arsenic was measured. The 'total' arsenic method could not distinguish CCA workers from controls and is clearly unsuitable for assessment of occupational exposure to arsenic. There was a significant increase in the urinary concentration of chromium in workers over the four sample collection rounds indicating increasing exposure to chromium during the 2 years of the study. This unexpected finding may be worth further investigation. Overall, the study demonstrated the utility of biological monitoring for assessment of occupational exposure to chromium and arsenic.     

Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites.

The relation between exposure to As2O3 fumes and dust, and the urinary excretion of inorganic arsenic metabolites (monomethylarsonic acid, dimethylarsinic acid, unchanged inorganic arsenic) has been studied in 18 workers from a sulphuric acid producing plant. The concentration of arsenic in the breathing zone of each worker was measured during five consecutive days and urine samples were obtained after one shift and before the next. The collection efficiency of the air sampling system exceeded 95%. The time weighted average exposure (TWA) concentrations of As2O3 ranged from 6 to 502 micrograms As/m3 and were log normally distributed. Although exposure probably occurred by ingestion as well as inhalation, statistically significant correlations (log scales) were found between airborne TWA of As2O3 and the inorganic arsenic metabolites in urine collected immediately after the shift, or just before the next shift. For a TWA of 50 micrograms As/m3, the mean concentration of the sum of the three inorganic arsenic metabolites in a postshift urine sample amounted to about 55 micrograms arsenic/g creatinine (95% confidence interval (95% CI) 47-62). Higher estimates of urinary arsenic reported by other authors are probably due either to the influence of dietary organoarsenicals when total arsenic is measured in urine or to a low retention efficiency of the air sampling system for As2O3 in the vapour phase.     

Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites.

The relation between exposure to As2O3 fumes and dust, and the urinary excretion of inorganic arsenic metabolites (monomethylarsonic acid, dimethylarsinic acid, unchanged inorganic arsenic) has been studied in 18 workers from a sulphuric acid producing plant. The concentration of arsenic in the breathing zone of each worker was measured during five consecutive days and urine samples were obtained after one shift and before the next. The collection efficiency of the air sampling system exceeded 95%. The time weighted average exposure (TWA) concentrations of As2O3 ranged from 6 to 502 micrograms As/m3 and were log normally distributed. Although exposure probably occurred by ingestion as well as inhalation, statistically significant correlations (log scales) were found between airborne TWA of As2O3 and the inorganic arsenic metabolites in urine collected immediately after the shift, or just before the next shift. For a TWA of 50 micrograms As/m3, the mean concentration of the sum of the three inorganic arsenic metabolites in a postshift urine sample amounted to about 55 micrograms arsenic/g creatinine (95% confidence interval (95% CI) 47-62). Higher estimates of urinary arsenic reported by other authors are probably due either to the influence of dietary organoarsenicals when total arsenic is measured in urine or to a low retention efficiency of the air sampling system for As2O3 in the vapour phase.     

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.     

Pathways of human exposure to arsenic in a community surrounding a copper smelter

Several studies have found elevated levels of urinary arsenic among residents living near a copper smelter in Tacoma, Washington. To assess pathways of exposure to arsenic from the smelter, biological and environmental samples were collected longitudinally from 121 households up to 8 miles from the smelter. The concentration of inorganic and methylated arsenic compounds in spot urine samples was used as the primary measure of exposure to environmental arsenic. Urinary concentration of arsenic dropped off to a constant background level within one-half mile of the smelter in contrast to environmental concentrations, which decreased more steadily with increasing distance. Among all age-sex-specific groups in all areas, only children ages 0-6 living within one-half mile of the smelter had elevated levels of arsenic in urine. A separate analysis of data for these children suggests that hand-to-mouth activity was the primary source of exposure. Inhalation of ambient air and resuspension of contaminated soil were not important sources of exposure for children or adults.     

Airborne arsenic and urinary excretion of metabolites of inorganic arsenic among smelter workers

Summary The relationship between airborne concentrations of arsenic and the urinary excretion of inorganic arsenic metabolites (inorganic arsenic + methylarsonic acid + dimethylarsinic acid) have been studied among smelter workers exposed to arsenic trioxide. The urinary concentrations of arsenic metabolites were found to increase steadily during the first day of the working week (after 2–3 d off from work), whereafter they reached a steady state. The concentration in the late evening after a day of exposure was very similar to that in the early morning after. Both were well correlated to the total daily excretion. In the second part of the study, comprising 18 subjects, the first-void morning urine of each participant was collected for 2 to 3 d during the steady-state phase. Total concentration of arsenic in the breathing zones was measured by personal air samplers. Airborne arsenic (8-h values) varied between 1 and 194 g As/m³, and urinary arsenic between 16 and 328 g As/g creatinine. With the urinary arsenic concentrations (mean values of 2–3 d for each subject) plotted against the corresponding airborne arsenic concentrations, the best fit was obtained by a power curve with the equation y = 17 x x^0.56. However, four of the participants were found to excrete far more (105–260%) arsenic in the urine than possibly could have been inhaled, most likely due to oral intake of arsenic via contaminated hands, cigarettes or snuff. If these four were excluded, the best fit was obtained by a straight regression line with the slope 2.0 and the intercept 29 g As/g creatinine (coefficient of correlation 0.92; P < 0.001).     

Airborne arsenic and urinary excretion of arsenic metabolites during boiler cleaning operations in a Slovak coal-fired power plant.

Little information is available on the relationship between occupational exposure to inorganic arsenic in coal fly ash and urinary excretion of arsenic metabolites. This study ws undertaken in a coal-fired power plant in Slovakia during a routine maintenance outage. Arsenic was measured in the breathing zone of workers during 5 consecutive workdays, and urine samples were obtained for analysis of arsenic metabolites--inorganic arsenic (Asi), monomethylarsonic acid (MMA), and dimethylarsinic acid (DMA)--prior to the start of each shift. Results from a small number of cascade impactor air samples indicated that approximately 90% of total particle mass and arsenic was present in particle size fractions >/= 3.5 micron. The 8-hr time-weighted average (TWA) mean arsenic air concentration was 48.3 microg/m3 (range 0.17-375.2) and the mean sum of urinary arsenic (SigmaAs) metabolites was 16.9 microg As/g creatinine (range 2.6-50.8). For an 8-hr TWA of 10 microg/m3 arsenic from coal fly ash, the predicted mean concentration of the SigmaAs urinary metabolites was 13.2 microg As/G creatinine [95% confidence interval (CI), 10.1-16.3). Comparisons with previously published studies of exposure to arsenic trioxide vapors and dusts in copper smelters suggest that bioavailability of arsenic from airborne coal fly ash (as indicated by urinary excretion) is about one-third that seen in smelters and similar settings. Arsenic compound characteristics, matrix composition, and particle size distribution probably play major roles in determining actual uptake of airborne arsenic.     

Vasospastic tendency and Raynaud's phenomenon in smelter workers exposed to arsenic

The long-term drinking of water with a high content of inorganic arsenic can lead to Raynaud's phenomenon, acrocyanosis, and gangrene of the lower legs ("black foot disease"). We have measured the systolic blood pressure in the finger after local cooling in 47 workers from a copper smelter who were habitually exposed to moderate amounts of arsenic dust. The controls were 48 workers not exposed to arsenic. The concentration of inorganic arsenic including its metabolites in urine was determined. We found a difference between As-exposed workers and the controls in the finger systolic pressure at skin temperatures of 10 degrees C and/or 15 degrees C expressed as a percentage of the pressure at 30 degrees C (FSP%), P less than 0.01; and the prevalence of Raynaud's phenomenon, P less than 0.05. A low FSP% was taken to indicate vasospastic tendency. There was a covariation between the duration of exposure to arsenic and the decrease in finger systolic pressure between the measurements at 30 and 10 degrees C (P less than 0.05). The uptake of arsenic at the time of the study probably did not exceed 300 micrograms/day. This was confirmed by estimation of the urinary excretion. The average total arsenic uptake was estimated to be about 4 g over 23 years, which is less than the total uptake of 20 g of arsenic by subjects who developed black foot disease. Increased vasospastic reactivity in the fingers and Raynaud's phenomenon in smelter workers seems to be due to functional alterations in the vessels caused by inhalation of arsenic.     

Human arsenic exposure in relation to a copper smelter

Children living near a copper smelter in Tacoma, Washington, were shown to have increased levels of arsenic in hair and urine. The urinary arsenic level decreased with distance of residence from the smelter stack. House vacuum-cleaner dust showed a similar distance relationship. Urine arsenic levels in children varied synchronously over a 5-wk period, indicating that inhalation was the most likely exposure route. In children urinary arsenic level showed an inverse relationship to age with younger children showing consistently higher urine arsenic levels.A death-record analysis indicated an increased respiratory cancer incidence in men working at this smelter. Since published urinary arsenic levels for men working at this smelter were similar to those seen in people residing near the smelter, it was felt that the community surrounding the smelter might be exposed to an increased respiratory cancer risk. Accordingly, action was taken to reduce arsenic emissions from the smelter.     

Biomarkers of exposure: a case study with inorganic arsenic

The environmental contaminant inorganic arsenic (iAs) is a human toxicant and carcinogen. Most mammals metabolize iAs by reducing it to trivalency, followed by oxidative methylation to pentavalency. iAs and its methylated metabolites are primarily excreted in urine within 4-5 days by most species and have a relatively low rate of bioaccumulation. Intra- and interindividual differences in the methylation of iAs may affect the adverse health effects of arsenic. Both inorganic and organic trivalent arsenicals are more potent toxicants than pentavalent forms. Several mechanisms of action have been proposed for arsenic-induced toxicity, but a scientific consensus has not been achieved. Biomarkers of exposure may be used to quantify exposure to iAs. The most common biomarker of exposure for iAs is the measurement of total urinary arsenic. However, consumption of seafood containing high concentrations of organic arsenic can confound estimation of iAs exposure. Because these organic species are thought to be relatively nontoxic, their presence in urine may not represent increased risk. Speciation of urinary arsenic into inorganic and organic forms, and even oxidation state, gives a more definitive indication of the exposure to iAs. Questions still remain, however, as to how reliably the measurement of urinary arsenic, either total or speciated, may predict arsenic concentrations at target tissues as well as how this measurement could be used to assess chronic exposures to iAs.     

Exposure to inorganic arsenic in drinking water and total urinary arsenic concentration in a Chilean population

The relationship of inorganic arsenic exposure through drinking water and total urinary arsenic excretion in a nonoccupationally exposed population was evaluated in a cross-sectional study in three mayor cities of Chile (Antofagasta, Santiago, and Temuco). A total of 756 individuals in three population strata (elderly, students, and workers) provided first morning void urine specimens the day after exposure and food surveys were administered. Arsenic intake from drinking water was estimated from analysis of tap water samples, plus 24-h dietary recall and food frequency questionnaires. Multilevel analysis was used to evaluate the effects of the age group and city factors adjusted by predictor variables. Arsenic levels in drinking water and urine were significantly higher in Antofagasta compared with the other cities. City-and individual-level factors, 12% and 88%, respectively, accounted for the variability in urinary arsenic concentration. The main predictors of urinary arsenic concentration were total arsenic consumption through water and age. These findings indicate that arsenic concentration in drinking water continues to be the principal contributing factor to exposure to inorganic arsenic in the Chilean population.     

House dust and inorganic urinary arsenic in two Arizona mining towns

Residents of copper mining and smelting towns may have increased risk of arsenic exposure from elevated arsenic contained in environmental media. To determine the relation of arsenic in house dust to inorganic urinary arsenic concentrations, a door-to-door survey was conducted in Hayden and Winkelman, Arizona. A total of 122 households (404 individuals) participated; 85 provided dust samples. Urine was collected at first morning void and analyzed for total and speciated arsenic. Speciation of arsenic was performed in samples with total arsenic above 10 micro g/l (N=106). The generalized estimating equation was used to determine the relation between urinary and house dust arsenic concentrations, allowing adjustment for the correlation of measurements obtained from the same home. Seafood consumption during the past 3 days and smoking contributed significantly to inorganic urinary arsenic, after adjusting for age and gender. Arsenic in house dust was not significantly associated with inorganic urinary arsenic measurements in this population.     

Effects of low-level lead and arsenic exposure on copper smelter workers

An analysis of reported symptoms and their relationship with indicators of lead absorption--blood lead (Pb-B) and zinc protoporphyrin (ZPP)--and of arsenic absorption--urinary arsenic (As-U)--was undertaken among 680 active copper smelter workers. Lead and arsenic absorption in the copper smelter employees were characterized by the median values of 30.4 micrograms/dl for Pb-B, 41.5 micrograms/dl for ZPP, and 26 micrograms/L for As-U. Blood lead was 40 micrograms/dl or higher in 16.7% of cases, ZPP was 50 micrograms/dl or higher in 31.2%, and urinary arsenic was 50 micrograms/L or higher in 16.4% of currently active copper smelter workers. The number of reported symptoms (from a total of 14 symptoms) increased with ZPP levels; the relationship with Pb-B was less marked. Arsenic contributed relatively little. Mean Pb-B, ZPP, and As-U levels for subjects reporting each of the 14 symptoms were compared with those of subjects who did not report the symptoms. Mean Pb-B was found to differ significantly for one symptom, fatigue. Significant differences in mean ZPP levels were found for fatigue, sleep disturbances, weakness, paresthesia, and joint pain. Prevalence rates for these symptoms rose more markedly with increasing ZPP than with Pb-B levels. The results indicate a relationship between certain CNS and musculo-skeletal symptoms and increased lead absorption in this population. Adherence to exposure standards that preclude undue lead absorption and appropriate biological monitoring including ZPP levels, are necessary to prevent adverse, especially long-term, health effects.     

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   

Saccadic eye movements among copper smelter workers

Saccade accuracy was studied in 87 copper smelter workers. Findings were compared with those obtained in 52 lead-exposed automobile production workers and 52 controls examined as part of a separate study. Both groups of workers showed a decrease in saccade accuracy compared to controls. Saccade accuracy was reduced in copper smelter workers over 50 years of age compared to automobile production workers in this age group. Decreased saccade accuracy was not correlated with blood lead (Pb-B), zinc protoporphyrin (ZPP), or urinary arsenic (As-U) levels among copper smelter workers, but was significantly correlated with both Pb-B and ZPP in the group of automobile production workers. Saccade accuracy decreased significantly with age and duration of exposure only in the group of copper smelter workers. Complex exposures to lead and other toxic agents present in the smelter may account for the reduction in saccade accuracy among copper smelter workers.     

Comparison of several methods for the determination of arsenic compounds in water and in urine

Summary Several arsenic species (inorganic tri- or pentavalent arsenic, mono-and dimethylated arsonic acids) can be determined in water samples by electrothermal atomic absorption spectrometry after appropriate acidification procedures (concentrated HCl or a mixture HCl/HClO₄/HBr) and extraction by toluene in the presence or absence of KI; the determination of aromatic derivatives and of arsenic thiol complexes needs a wet or dry ashing step. The procedures for water analysis are not directly applicable to urine samples; in the best conditions, total inorganic plus 85% on the average of the methylated arsenicals present in urine are measured after acidification with concentrated HCl and extraction by toluene in the presence of KI. Total arsenic content (including arsenic from marine origin) is measured only after a drastic mineralization step like MgO treatment at 600°C. The results obtained by the electrothermal atomic absorption technique and those obtained by neutron activation analysis are in excellent agreement.When the presence of arsenic of marine origin is suspected in urine, the analysis of inorganic arsenic and its metabolites is preferably performed by an arsine generation technique. The sum of inorganic arsenic and of its mono and dimethylated derivatives determined by such a technique is identical with the results obtained by electrothermal atomic absorption spectrometry after complete mineralization of the samples as long as no arsenic from marine origin is present.After oral ingestion of As₂O₃ by man, the urinary excretion of inorganic arsenic and its metabolites is important and rapid (approximately 60% are eliminated by the oral route with a half life of 30 h).While the excretion occurs in the form of inorganic species during the first hours following the ingestion, a methylating process is rapidly triggered and leads to a preponderant excretion of dimethylarsinic acid 1 day after ingestion. In the case of ingestion of seafood containing arsenic, the urinary excretion occurs at a higher rate (half life 18 h) apparently without transformation.The absence of interference of arsenic from marine origin and the capacity of measuring separately inorganic arsenic and its main urinary metabolites makes the arsine generation technique the best suited for the monitoring of workers exposed to inorganic arsenic. However, since the technique may sometimes be too elaborate and time-consuming for routine work, the biological monitoring of workers can be performed by determining total arsenic concentration in urine after mineralization with MgO. Samples with high arsenic content are then re-analyzed to distinguish between occupational exposure and ingestion of the organic arsenic present in marine organisms. This is carried out either by the arsine generation method or, if this technique is not available, by a direct extraction procedure in the presence of KI of a sample acidified with HCI. With the latter procedure, 85% of the methylated arsenic is measured on average without interference of arsenic from marine origin.     

Metabolic profile in workers occupationally exposed to arsenic: role of GST polymorphisms

Arsenic is a well-known human carcinogen with a ubiquitous distribution in the natural environment. Chronic exposure to inorganic arsenic involves a biotransformation process that leds to the main excretion of organic methylated metabolites, such as monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA), as well as the parental inorganic species. Interindividual variation in arsenic metabolism has been extensively reported, and polymorphisms in genes involved in such process could be related to changes in the arsenic excretion profile and the response to chronic exposures. Our analysis of the metabolic profiles in three groups of workers exposed to different arsenic exposure levels showed high amounts of inorganic arsenic and MMA in the most-exposed workers versus the least-exposed workers, in whom high amounts of DMA were observed. With respect to the role of different genetic polymorphisms in the glutathione S-transferase (GST) genes in the modulation of the urinary profiles, for the overall population only a tendency was just observed between GSTM1 null and MMA excretion as well as between GSTP1 val/val and DMA excretion.     

砷冶炼厂工人皮肤损害与尿中砷甲基化产物的关系

目的探讨职业砷接触致皮肤病发生与尿中砷甲基化产物的关系。方法选择偏远山区冶炼厂为研究现场,暴露组为91名工人,对照组58人。监测作业场所工作岗位中砷化合物浓度,进行健康监护体检和尿砷形态分析,计算3种砷化合物百分率及一、二级甲基化指数。结果冶炼厂所有检测岗位砷化合物浓度均超过国家职业卫生标准,91名工人中36人存在明显慢性砷中毒样皮肤损害,尿中3种砷化合物(无机砷、甲基砷酸、二甲基砷酸)浓度(Log10)分别为(2.18±0.40)、(2.26±0.35)和(2.77±0.31)μg/g肌酐,明显示高于接砷但无皮肤损害的工人及对照组工人,差异均有统计学意义,冶炼厂存在皮肤损害的工人尿中甲基砷酸浓度占总砷百分率和二级甲基化指数均明显高于其他工人。结论尿中甲基化产物在冶炼厂工人皮肤损害中具有重要作用,二级甲基化指数与砷致皮肤损害有关。