Biomonitorization of concentrations of 28 elements in serum and urine among workers exposed to indium compounds.

Many studies have documented the abnormal concentrations of metals/metalloids in serum or urine of occupational workers, but no works systematically analysed the concentrations of elements in serum or urine of indium-exposed workers. This study was aimed to assess 28 elements in serum and urine from 57 individuals with occupational exposure to indium and its compounds. Control subjects were 63 workers without metal exposure. We collected information on occupation and lifestyle habits by questionnaire. Biological samples were collected to quantify elements by inductive coupled plasma-mass spectrometer. Air in the breathing zones was drawn at flow rates of 1.5-3 L/min for a sampling period of 6 to 8 h, using a Model BFC-35 pump. The average ambient indium level was 0.078 mg/m3. Serum/urine Indium levels were significantly higher in indium-exposed workers than in controls (P < 0.01). Moreover, serum/urine indium concentrations in the group with 6-14 years and ≥15 years of employment were significantly higher than those with ≤5 employment years(P < 0.05). Ten of the other 27 elements/metals measured were higher in serum/urine in indium-exposed workers compared to the controls (aluminum, beryllium, cadmium, cesium, chromium, lithium, manganese, magnesium, molybdenum and vanadium). Zinc levels in serum/urine were significantly decreased in the indium-exposed workers. Additionally, other elements/metals were higher in one specimen (serum or urine) but lower in the other (Selenium was lower in serum but higher in urine in the indium-exposed workers compared with the controls; likewise Thallium and Rubidium were higher in serum but lower in urine). Linear regression analyses, revealed significant correlations between serum and urine for indium, aluminum, arsenic, barium, cadmium, cesium, cobalt, selenium, silver, and zinc (P < 0.05). These data suggest that occupational exposure to indium and its compounds may disturb the homeostasis of trace elements in systemic circulation, indium concentrations in serum or urine appear reflective of workers' exposure to ambient indium and their years of working, respectively. The serum/urine levels of essential metals are modified by exposure to indium in occupationally exposed workers. Further studies including larger sample size and more kinds of biological sample are needed to validate our findings.

Assessment of DNA/Chromosome Damage in the Peripheral Blood Lymphocytes of Workers Exposed to Indium Compounds.

This study was conducted to investigate possible genotoxic effects resulting from occupational exposure to indium compounds. We performed a cytogenetic analysis of peripheral blood lymphocytes gathered from 57 individuals exposed to indium at an indium ingot production plant in Guangxi, China, and compared the results with those obtained from 63 control subjects. The lymphocytes from both groups were examined in the chromosomal aberrations (CAs) assay, cytokinesis-block micronucleus (CBMN) assay, and single-cell gel electrophoresis (comet) assay. Samples of personal breathing zone air were collected throughout the work shift of each subject. Blood and urine samples were collected before and after each work shift on the same day as the air samples were collected. Our assay results showed that workers in the indium production plant were exposed to significantly higher levels of indium (median exposure, 8.00 µg/m3) than the control subjects. Also, higher concentrations of urinary indium (U-In) were found in the exposed workers than the control subjects. When compared with the control subjects, the exposed workers showed higher levels of DNA damage as detected by the comet assay (tail length and TDNA%), significantly higher frequencies of CAs/100 cells, and increased CBMN frequencies. Moreover, the mean CBMN frequency in the non-smokers exposed to indium was significantly higher than that in the non-smoker control subjects (3.14‰ vs 1.00‰, respectively; P < .01). U-In levels, comet assay, CBMN, and CA test proved to be the most sensitive biological markers for detecting occupational exposure to indium compounds and can also be used to assess the health risks of the exposed workers.

Occupational Exposure to Indium of Indium Smelter Workers.

Case reports of indium-related lung disease in workers have raised public concern to the human toxicity of indium (In) and its compounds. However, studies evaluating the exposure or health of workers in In smelting plants are rare. Therefore, in this study, we focused on four In smelting plants, with the main objective of characterizing In in smelter plants in China and discussing the potential exposure biomarkers of In exposure. We recruited 494 subjectsat four In smelting plants in China. Personal air samples, first morning urine and spot blood samples were collected. In concentrations in samples were analyzed using inductively coupled plasma mass spectrometry. In concentrations in air samples did not exceed the permissible concentration-time weighed average, but the smelter workers had a higher internal exposure to In. Positive correlations were observed between the air In and urine In concentrations, and between the air In and blood In concentrations. This study provides basic data for the following In exposure and health risk assessment.

Effects of a powered air-purifying respirator intervention on indium exposure reduction and indium related biomarkers among ITO sputter target manufacturing workers.

This study aimed to evaluate the efficacy of powered air-purifying respirators (PAPRs) worn by the workers, and to investigate the effect of this application on exposure and preclinical effects in terms of workplace measuring and biomarker monitoring in ITO sputter target manufacturing plants and workers, respectively. Fifty-four workers were recruited and investigated from 2010-2012, during which PAPRs were provided to on-site workers in September 2011. Each worker completed questionnaires and provided blood and urine samples for analysis of biomarkers of indium exposure and preclinical effects. Area and personal indium air samples were randomly collected from selected worksites and from participants. The penetration percentage of the respirator (concentration inside respirator divided by concentration outside respirator) was 6.6%. Some biomarkers, such as S-In, SOD, GPx, GST, MDA, and TMOM, reflected the decrease in exposure and showed lower levels, after implementation of PAPRs. This study is the first to investigate the efficacy of PAPRs for reducing indium exposure. The measurement results clearly showed that the implementation of PAPRs reduces levels of indium-related biomarkers. These findings have practical applications for minimizing occupational exposure to indium and for managing the health of workers exposed to indium.

Determination of trace indium in urine after preconcentration with a chelating-resin-packed minicolumn.

A simple and rapid chelating-resin-packed column has been developed for preconcentration of trace indium in biological samples. A large-sized urine sample was pumped through a minicolumn at a flow rate of 1.0 mL/min by using a peristaltic pump, and the eluents were analyzed using graphite furnace atomic absorption spectrometry (GFAAS). Four commercially available chelating resins including Chelex-100, Amberlite IRC-50, Duolite GT-73, and Celite 545-AW were studied for evaluating the indium sorption performance. Several parameters, such as pH, resin amount, eluent volume, eluent flow rate, and the volume of sample, were investigated and optimized. A 100-200 mL of the sample was loaded into a column containing 1.2 g of wet Chelex-100 and subjected to the ion-exchange procedure. The retained analytes were eluted with 5.0 mL of 0.1 M HNO(3) and quantified by GFAAS. The correlation coefficient in the range 10-250 ng/mL was of 0.9994. The limit of detection of the proposed method was 2.75 ng/mL. The method developed was successfully applied to analysis of spiked urine samples with good recoveries of 93-103% (n = 6) and reproducibility (relative standard deviation < 4.9%). The accuracy of procedure was confirmed by indium determination in spiked certified reference materials.

Occupational exposure to indium: what does biomonitoring tell us?

BACKGROUND: The industrial uses of indium, a rare metal with no known physiological role in humans, have increased dramatically over the past 15 years. The results of animal toxicity studies showing pulmonary and systemic effects as well as some reports in workers have created a growing concern about the possible occurrence of toxic effects in exposed workers. Validated biomarkers to assess exposure to indium are not available. OBJECTIVES: This work aimed at investigating the kinetics of indium in urine (In-U) and plasma (In-Pl) in workers manufacturing In ingots and mainly exposed to hardly water-soluble In compounds. All nine workers from the In department of a large metallurgical concern participated in the study as well as 5 retired workers and 20 controls. METHODS: Personal breathing zone air was collected throughout the work shift on Monday and Friday. Blood and urine samples were collected, before and after the shift, on the same day as the air sampling and on preshift the next Monday after a non-working week-end. Moreover, rats were given either InCl(3) by intraperitoneal injection or In(2)O(3) by pharyngeal aspiration, In was followed in plasma during 120 days and measured in tissues 120 days after exposure. RESULTS: Higher In-Pl and In-U concentrations were found in both current (range 0.32-12.61 µg/L plasma; 0.22-3.50 µg/g creat) and former (0.03-4.38 µg/L plasma; 0.02-0.69 µg/g creat) workers compared with controls (<0.03 µg/L plasma; <0.02 µg/g creat). Both biological parameters were highly correlated but no correlation was found between In-air (10-1030 µg/m(3)) and In-Pl or In-U. Normalizing In-U by the urinary creatinine concentration reduced the inter- (from 90% to 70%) and intra-individual variability (from 54% to 35%). In-Pl remained remarkably stable along the working week (inter- and intra-individual variability: 89% and 10%, respectively). Neither In-U nor In-Pl significantly increased during the day or the week. A week-end without occupational exposure was not sufficient to reach the background In-Pl and In-U levels measured in controls. The results of the experimental investigations confirmed the hypothesis that inhalation of hardly soluble In compounds may cause accumulation of In in the body leading to a prolonged "endogenous exposure" from both a lung depot of "insoluble" particles that are progressively absorbed and from a retention depot in other internal organs. CONCLUSION: This study shows that in workers exposed to hardly soluble In compounds, In-U and In-Pl are very sensitive to detect exposure and mainly reflect long-term exposure. In-Pl levels are particularly stable for a given individual. In-U might be more influenced than In-Pl by recent exposure. Both parameters remained high years after withdrawal from exposure, indicating a possible endogenous exposure and a prolonged risk of pulmonary and systemic diseases even after work exposure has ceased.

Pulmonary toxicity in mice by 2- and 13-week inhalation exposures to indium-tin oxide and indium oxide aerosols.

OBJECTIVES: Inhalation toxicities of indium-tin oxide (ITO) and indium oxide (IO) in mice were characterized in comparison with those previously reported in rats. METHODS: B6C3F(1) mice of both sexes were exposed by inhalation to ITO or IO aerosol for 6 h/day, 5 day/wk for 2 wk at 0, 0.1, 1, 10 or 100 mg/m(3) or 13 wk at 0, 0.1or 1 mg/m(3). RESULTS: ITO and IO particles were deposited in the lung, mediastinal lymph node (MLN) and nasal-associated lymphoid tissue. Alveolar proteinosis, infiltrations of alveolar macrophages and inflammatory cells and increased lung weight were induced by 2- and 13-week exposures to ITO and IO, while alveolar epithelial hyperplasia occurred only in the 2-week exposures. Thickened pleural wall, hyperplastic MLN, extramedullary hematopoiesis in the spleen and increased levels of erythrocyte parameters were induced by 13-week exposure to ITO. The ITO- and IO-induced pulmonary lesions were milder in mice than those previously reported in rats, and the fibrotic lesions were different between these two species. Indium levels in the lung and pooled blood were analyzed in the mice exposed to ITO and IO for 13 wk. In the 13-week inhalation exposure of mice to ITO, alveolar proteinosis and significantly increased lung weight were induced at the same exposure concentration as the current threshold limit value for indium and its compounds.

Lipid peroxidation in workers exposed to aluminium, gallium, indium, arsenic, and antimony in the optoelectronic industry.

OBJECTIVE: The objective of this study was to investigate whether exposure to aluminum, gallium, indium, arsenic, and antimony induces lipid peroxidation in humans. METHODS: Whole blood and urine levels of 103 exposed electronic industry workers and 67 referents were analyzed by use of inductively coupled plasma mass spectrometry. Malondialdehyde (MDA), the product of lipid peroxidation, was determined by high-performance liquid chromatography. RESULTS: The mean plasma MDA level in the 103 workers was significantly higher than that in 67 referents. The levels of MDA in the exposed workers were correlated significantly with the levels of urinary gallium and arsenic. CONCLUSIONS: Malondialdehyde as an index of lipid peroxidation can be induced by gallium and arsenic exposure. By reducing exposure to these metals, biologic effects such as lipid peroxidation may also be diminished.

Biological monitoring of exposures to aluminium, gallium, indium, arsenic, and antimony in optoelectronic industry workers.

The main objective of this study was to investigate aluminum, gallium, indium, arsenic, and antimony exposures on blood and urine levels in the optoelectronic workers. One hundred seventy subjects were enrolled in this cohort study. Whole blood and urine levels were determined by inductively coupled plasma-mass spectrometry. Blood indium and urine gallium and arsenic levels in the 103 workers were significantly higher than that in 67 controls during the follow-up period. In regression models, the significant risk factors of exposure were job title, preventive equipment, Quetelet's index, sex, and education level. The findings of this study suggest that gallium, indium, and arsenic exposure levels may affect their respective levels in blood and urine. The use of clean, preventive equipment is recommended when prioritizing the administration of safety and hygiene in optoelectronics industries.

Metabolism of subcutaneous administered indium arsenide in the hamster.

Indium arsenide (InAs) is partially dissociated in vivo to form inorganic arsenic and indium and excreted into the urine and feces. InAs dissolves slowly over time with deposits at the site of injection. Results of this study demonstrated that the principal metabolite of arsenic in the urine of hamsters was dimethylated arsenic (DMA). Inorganic arsenic and DMA accumulated in the fur, but the concentrations of indium were very low in this matrix. Urine and feces were the principal routes of elimination from the body. Analysis of tissues for arsenic demonstrated as concentrations in the parts per billion range. Results of these studies indicate that InAs is dissociated in vivo with release of both the indium and arsenic moieties to target tissues.

[Determination of urinary lead through optic emission spectrography using the double-arch method]. / Determinazione della piomburia per spettrografia di emissione ottica con la tecnica del doppio arco.

A new method for the determination of urinary lead by means of the emission spectroscopy is described. The sample is concentrated by lyophilization and the homogeneous dust obtained is analysed using the "double arc" method. The matrix effects and the source unstability are compensated by the use of the internal standard. The influence of the volatilization of the elements of the analytical pairs are studied and the pair thallium-lead is selected. The method is reproducible and the detection limit is 5 microgram/l of urinary lead.