Dermal exposure to jet fuel (JP-8) in US Air Force personnel

Limited research has been conducted on dermal exposure and risk assessment, owing to the lack of reliable measurement techniques and data for quantitative risk assessment. We investigated the magnitude of dermal exposure to jet propulsion fuel 8 (JP-8), using naphthalene as a surrogate, on the US Air Force fuel-cell maintenance workers. Dermal exposure of 124 workers routinely working with JP-8 was measured using a non-invasive tape-strip technique coupled with gas chromatography-mass spectrometry analysis. The contribution of job-related factors to dermal exposure was determined using multiple linear regression analyses. Average whole body dermal exposure to naphthalene (as a marker for JP-8) was 7.61 +/- 2.27 ln(ng m(-2)). Significant difference (P < 0.0001) between the high-exposure group [8.34 +/- 2.23 ln(ng m(-2))] and medium- and low-exposure groups [6.18 +/- 1.35 ln(ng m(-2)) and 5.84 +/- 1.34 ln(ng m(-2)), respectively] was observed reflecting the actual exposure scenarios. Skin irritation, use of booties, working inside the fuel tank and the duration of JP-8 exposure were significant factors explaining the whole body dermal exposure. This study clearly demonstrates the efficiency and suitability of the tape-strip technique for the assessment of dermal exposure to JP-8 and that naphthalene can serve as a useful marker of exposure and uptake of JP-8 and its components. It also showed that the skin provides a significant route for JP-8 exposure and that actions to reduce exposure are required. Studies to investigate the relative contribution of dermal uptake of JP-8 on total body dose and the toxicokinetics of dermal exposure to JP-8 are underway.     

Urinary biomarkers of exposure to jet fuel (JP-8)

Benzene, naphthalene, and 1- and 2-naphthol were measured in urine samples obtained from 322 U.S. Air Force personnel categorized a priori as likely to have low, moderate, or high exposure to jet fuel [jet propulsion fuel-8 (JP-8)]. In postexposure samples, levels of these analytes in the high-exposure group were 3- to 29-fold greater than in the low-exposure group and 2- to 12-fold greater than in the moderate-exposure group. Heavy exposure to JP-8 contributed roughly the same amount of benzene and more than three times the amount of naphthalene compared with cigarette smoking. Strong correlations were observed among postexposure levels of naphthalene-based biomarkers in urine and naphthalene in air and breath. We conclude that urinary naphthalene and the naphthols can serve as biomarkers of exposure to jet fuel. Of these, the naphthols are probably more useful because of their greater abundance and slower elimination kinetics.     

Urinary biomarkers of atrazine exposure among farm pesticide applicators

PURPOSE: This study assessed the feasibility of three laboratory methods for the detection of atrazine, a triazine herbicide, and its related metabolites in urine collected from field applicators.METHODS: Urine samples were collected from 256 randomly sampled field applicators 8 hours post application. Of these, 99 reported atrazine use during the application prior to sample collection and these samples were subsequently analyzed for urinary biomarkers.RESULTS: 37.4% (n = 37) samples showed detectable levels (minimum = 1.0 ng/mL) of deethylatrazine using gas chromatographic mass spectrometry (GCMS) analysis (X = 14.2 ng/mL; s.d. = 13.5). Fifty samples were tested using atrazine mercapturate in urine ELISA methods and 80% (n = 40) of these samples showed detectable levels of atrazine (X = 6.4 ng/mL; s.d. = 7.5). Of 10 samples tested by triazines in water ELISA methods, a common assay used for the detection of atrazine in groundwater, 100% showed detectable levels of atrazine (X = 22.4 ng/mL; s.d. = 13.9). Of the 21 samples collected from non-applicators and tested by GCMS, none evidenced detectable atrazine levels. Using GCMS as the gold standard, analyses showed that the mercapturate in urine ELISA was 48% sensitive and 91% specific whereas the triazines in water ELISA was 69% sensitive and 100% specific.CONCLUSIONS: It is possible to detect one-time atrazine exposures through analysis of urinary biomarkers among pesticide applicators. The feasibility of triazines in water ELISA methods for use in field studies for analyzing the presence of atrazine and related metabolites in urine was supported, but these methods need further testing on larger applicator samples before they can be used for standard screening.     

Urinary sevoflurane and hexafluoro-isopropanol as biomarkers of low-level occupational exposure to sevoflurane

Objectives: Sevoflurane is an inhalation halogenated anaesthetic widely used in day and paediatric surgery. We were interested in evaluating biological markers of exposure to sevoflurane, which should improve the health surveillance of occupationally exposed personnel. Methods: A group of 36 subjects (13 male, 23 female) occupationally exposed to volatile anaesthetics in paediatric operating rooms was studied in a 2-week survey. Post-shift urine samples and specimens from passive samplers (for personal monitoring) were collected after 1.75–6 h morning exposure and analysed by headspace gas chromatography–mass spectrometry (GC–MS). Multiple determinations were assumed as independent values (in total, n=78: 24 from men, 54 from women; 25 from smokers, 53 from non-smokers). Results: Median sevoflurane external values were 0.13 parts per million (ppm) (range 0.03–18.82) (n=78), urinary sevoflurane 0.6 g/l_urine (ND–18.5)(n=76) and total urinary hexafluoro-isopropanol (HFIP) 0.49 mg/l_urine (ND–6833.4) (n=75). A lower limit of detection (LOD) was achieved for urinary sevoflurane (0.03 g/l_urine), allowing quantitation of all but one of the samples; >25% of urine samples were unquantifiable by HFIP and were assigned a value equal to half the LOD of 0.10 mg/l_urine. Urinary sevoflurane correlated well with breathing-zone data (r²=0.697 at log–log linear regression), whereas total urinary HFIP (r²=0.562 at log–log linear regression) seemed to be better described by a three-parameter logistic function and appeared to be influenced by smoking habits. Biological indices corresponding to National Institute for Occupational Safety and Health (NIOSH) exposure limits, calculated as means of linear regression slope and y intercept, were 3.9 g/l_urine and 1.4 g/l_urine for sevoflurane (corresponding to 2 ppm and 0.5 ppm, respectively), and 2.66 mg/l_urine and 0.82 mg/l_urine for HFIP. Conclusions: On the basis of our data, urinary unmodified, sevoflurane seems to be a more sensitive and reliable biomarker of short-term exposure to sevoflurane with respect to total urinary metabolite HFIP, which appears to be influenced by physiological and/or genetic individual traits, and seems to provide an estimate of integrated exposure.     

Urinary biomarkers of occupational N,N-dimethylformamide (DMF) exposure attributed to the dermal exposure

OBJECTIVE: To evaluate whether the dermal exposure to N,N-dimethylformamide (DMF) exerts significant effects and to determine the unit increment of dermal exposure on the total body burden of two biomarkers in urine: metabolism-required N-methylformamide (U-NMF) and non-metabolized DMF (U-DMF) in actual occupational environments. METHODS: Exposure via respiratory and dermal routes was assessed on an individual basis for 75 workers from four DMF-related factories directly exposed to DMF. Respiratory exposure was determined by breathing-zone sampling for a full-work shift, and dermal exposure was assessed on the palms and forearms of both hands by an adhesive tape-patch method. U-NMF and U-DMF collected immediately postshift were measured. RESULTS: The average concentrations of airborne DMF, DMF on hands and on forearms, U-NMF, and U-DMF (GM) were 1.51 ppm, 0.04 microg/cm(2), 0.03 microg/cm(2), 0.47 mg/l, and 0.38 mg/l, respectively. In multiple linear regression tests, only airborne DMF and DMF on hands remained significantly (P<0.001) associated with U-NMF and U-DMF. Based on model estimates, the unit increment of hands' exposure (microg/cm(2)) could contribute to 0.53 and 0.46 mg/l of the increment of U-NMF and U-DMF, respectively, given a daily occupational airborne exposure to DMF at about 1.5 ppm. CONCLUSIONS: Dermal exposure provides a substantial contribution to the total body burden of DMF. A control remedy such as the enforcement of wearing impermeable gloves by workers occupationally exposed to DMF should be implemented with the highest priority.     

Exposures to jet fuel and benzene during aircraft fuel tank repair in the U.S. Air Force

Jet fuel and benzene vapor exposures were measured during aircraft fuel tank entry and repair at twelve U.S. Air Force bases. Breathing zone samples were collected on the fuel workers who performed the repair. In addition, instantaneous samples were taken at various points during the procedures with SUMMA canisters and subsequent analysis by mass spectrometry. The highest eight-hour time-weighted average (TWA) fuel exposure found was 1304 mg/m3; the highest 15-minute short-term exposure was 10,295 mg/m3. The results indicate workers who repair fuel tanks containing explosion suppression foam have a significantly higher exposure to jet fuel as compared to workers who repair tanks without foam (p < 0.001). It is assumed these elevations result from the tendency for fuel, absorbed by the foam, to volatilize during the foam removal process. Fuel tanks that allow flow-through ventilation during repair resulted in lower exposures compared to those tanks that have only one access port and, as a result, cannot be ventilated efficiently. The instantaneous sampling results confirm that benzene exposures occur during fuel tank repair; levels up to 49.1 mg/m3 were found inside the tanks during the repairs. As with jet fuel, these elevated benzene concentrations were more likely to occur in foamed tanks. The high temperatures associated with fuel tank repair, along with the requirement to wear vapor-permeable cotton coveralls for fire reasons, could result in an increase in the benzene body burden of tank entrants.     

Urinary fibres in occupational exposure to asbestos

Urine samples from 10 workers from an asbestos cement factory and from a control group of 10 workers from a foundry, were obtained; drastic precautions were taken to avoid contamination. Each urinary mineral fibre was sized and identified by transmission electron microscopy. Results show that contamination problems encountered by other authors have been overcome and that the workers exposed to chrysotile appear to excrete more chrysotile fibres, but that this difference is not statistically significant. Possibly only a few of the exposed workers are significantly exposed to asbestos, the overall exposure level being very low. The degradability of chrysotile fibres in biological fluids or the retention of fibres in some organ could explain the lack of apparent correlation between exposure and urinary concentration. Unexpectedly high concentrations of crocidolite fibres of unknown origin were detected in both groups of workers.     

职业性铅接触的生物标志物研究进展

随着现代工业生产的迅速发展,铅中毒多以低浓度铅接触导致的亚临床无症状中毒为主,给职业性铅中毒的早期发现、早期诊断、早期治疗带来了一定的困难。铅接触的生物标志物的日渐发展对现代职业卫生生物监测、铅损害效应的早期预警和早期干预具有重要作用。作者就职业性铅接触常用的生物标志物的研究进展做一归纳。     

职业暴露异氰酸酯生物标志物的研究进展

异氰酸酯是导致职业性哮喘的主要致病因素之一,选择合适的异氰酸酯生物标志物,对开展异氰酸酯暴露的生物监测,实现异氰酸酯易感者的早期预警、早期干预等具有重要的意义。作者就职业暴露异氰酸酯生物标志物的研究进展做一综述,以期为更好地保护异氰酸酯暴露者提供依据。     

医护人员血源性职业暴露的风险管理

血源性职业暴露是医护人员最常见的职业伤害。通过建立血源性职业暴露事件监控系统，加强对医护人员血源性职业暴露的培训，改进操作技术，严格的医疗垃圾分类管理，提供充足的个人防护设备等事前预防措施，以及建立血源性暴露事件报告流程，制定暴露后预防性治疗的事后干预等风险管理措施，在3年多的实施过程中，追踪所有暴露事件中的个案，无一人感染乙型肝炎、丙型肝炎和艾滋病。     

医务人员职业暴露调查分析

目的调查医务人员职业暴露发生人群、场所、时机及源患者携带血源性病原体分布,为进一步预防职业暴露提供依据和有效防护措施,从而减少职业暴露的发生。方法采用回顾性调查方法,对医院2007年1月-2012年6月71名医务人员职业暴露报告资料进行分析。结果 71名医务人员职业暴露中,护士、助理护士、实习护士,分别占46.48%、4.22%、19.72%,工龄≤10年者占74.64%;暴露类型中,锐器伤占95.77%;暴露发生场所前3位为病区、手术室、急诊科,分别占47.89%、35.21%、9.85%;暴露发生时机前3位为术中、拔针时、处理医疗废物过程,分别占35.21%、18.31%、16.90%;源患者携带血源性病原体38例,占53.52%。结论暴露人员操作不熟练、防护意识不到位、接触侵入性操作、锐器伤发生概率大、对操作环境是否安全未进行充分评估是职业暴露的主要原因,加强职业安全教育、规范操作行为、充分评估操作环境的安全性等措施,能有效预防职业暴露。     

Comparative evaluation of biomarkers of occupational exposure to toluene

Objectives This study was initiated to make comparative evaluation of five proposed urinary markers of occupational exposure to toluene, i.e., benzyl alcohol, benzylmercapturic acid, o-cresol, hippuric acid and un-metabolized toluene. Methods In practice, six plants in Japan were surveyed, and 122 Japanese workers (mostly printers; all men) together with 12 occupationally nonexposed control subjects (to be called controls; all men) agreed to participate in the study. Surveys were conducted in the second half of working weeks. Time-weighted average exposure (about 8 h) to toluene and other solvents were monitored by diffusive sampling. End-of-shift urine samples were collected and analyzed for the five markers by the methods previously described; simultaneous determination of o-cresol was possible by the method originally developed for benzyl alcohol analysis. Results The toluene concentration in the six plants was such that the grand geometric mean (GM) for the 122 cases was 10.4 ppm with the maximum of 121 ppm. Other solvents coexposed included ethyl acetate (26 ppm as GM), methyl ethyl ketone (26 ppm), butyl acetate (1 ppm) and xylenes (1 ppm). By simple regression analysis, hippuric acid correlated most closely with toluene in air (r = 0.85 for non-corrected observed values) followed by un-metabolized toluene (r = 0.83) and o-cresol (r = 0.81). In a plant where toluene in air was low (i.e., 2 ppm as GM), however, un-metabolized toluene and benzylmercapturic acid in urine showed better correlation with air-borne toluene (r = 0.79 and 0.61, respectively) than hippuric acid (r = 0.12) or o-cresol (r = 0.17). Benzyl alcohol tended to increase only when toluene exposure was intense. Correction for creatinine concentration or specific gravity of urine did not improve the correlation in any case. Multiple regression analysis showed that solvents other than toluene did not affect the levels of o-cresol, hippuric acid or un-metabolized toluene. Levels of benzylmercapturic acid and un-metabolized toluene were below the limits of detection [limit of detections (LODs); 0.2 and 2 μg/l, respectively] in the urine from the control subjects. Conclusions In over-all evaluation, hippuric acid, followed by un-metabolized toluene and o-cresol, is the marker of choice for occupational toluene exposure. When toluene exposure level is low (e.g., 2 ppm), un-metabolized toluene and benzylmercapturic acid in urine may be better indicators. Detection of un-metabolized toluene or benzylmercapturic acid in urine at the levels in excess of the LODs may be taken as a positive evidence of toluene exposure, because their levels in urine from the controls are below the LODs. The value of benzyl alcohol as an exposure marker should be limited.     

Evaluation of biomarkers for occupational exposure to benzene.

OBJECTIVE--To evaluate the relations between environmental benzene concentrations and various biomarkers of exposure to benzene. METHODS--Analyses were carried out on environmental air, unmetabolised benzene in urine, trans, trans-muconic acid (ttMA), and three major phenolic metabolites of benzene; catechol, hydroquinone, and phenol, in two field studies on 64 workers exposed to benzene concentrations from 0.12 to 68 ppm, the time weighted average (TWA). Forty nonexposed subjects were also investigated. RESULTS--Among the five urinary biomarkers studied, ttMA correlated best with environmental benzene concentration (correlation coefficient, r = 0.87). When urinary phenolic metabolites were compared with environmental benzene, hydroquinone correlated best with benzene in air. No correlation was found between unmetabolised benzene in urine and environmental benzene concentrations. The correlation coefficients for environmental benzene and end of shift catechol, hydroquinone, and phenol were 0.30, 0.70, and 0.66, respectively. Detailed analysis, however, suggests that urinary phenol was not a specific biomarker for exposure below 5 ppm. In contrast, ttMA and hydroquinone seemed to be specific and sensitive even at concentrations of below 1 ppm. Although unmetabolised benzene in urine showed good correlation with atmospheric benzene (r = 0.50, P < 0.05), data were insufficient to suggest that it is a useful biomarker for exposure to low concentrations of benzene. The results from the present study also showed that both ttMA and hydroquinone were able to differentiate the background level found in subjects not occupationally exposed and those exposed to less than 1 ppm of benzene. This suggests that these two biomarkers are useful indices for monitoring low concentrations of benzene. Furthermore, these two metabolites are known to be involved in bone marrow leukaemogenesis, their applications in biological monitoring could thus be important in risk assessment. CONCLUSION--The good correlations between ttMA, hydroquinone, and atmospheric benzene, even at concentrations of less than 1 ppm, suggest that they are sensitive and specific biomarkers for benzene exposure.     

Urinary elimination of acetone in experimental and occupational exposure

Fifteen volunteers were exposed to an acetone vapor concentration of 964-8, 610 mumol/m3 (56-500 mg/m3) for 2-4 h in an exposure chamber. Ten subjects were at rest during the exposure, and five were exposed at alternate rest and light physical exercise. Subsequently 104 workers occupationally exposed to acetone were studied. The relative uptake averaged about 53%, and the ratio of the alveolar concentration to the environmental concentration averaged about 0.28. Both for the experimentally exposed subjects and the occupationally exposed workers the urinary acetone concentration showed a linear relationship to the corresponding environmental time-weighted average concentration. A linear equation also existed between urinary concentrations and the amounts of acetone absorbed. The findings enable a consideration of the urinary concentration of the unaltered acetone as an appropriate exposure indicator and the proposal of a "biological equivalent threshold" to be used in the field of biological monitoring.     

职业苯暴露生物标志物的研究现状

苯作为有机化学生产过程中广泛使用的原料,在生产环境中多以蒸气形式由呼吸系统进入人体,主要分布在含类脂质较多的组织和器官,如骨髓、脑髓、脂肪组织和肝脏[1],体内苯主要在肝脏代谢,在肝微粒体上的细胞色素P450(CYP)介导下苯被氧化成环氧化苯.通过对DNA的直接损伤作用,而引起造血系统的损害[2].苯已被国际癌症研究机构定为Ⅰ类化学致癌物[3].发达国家现将苯接触阈值限值-时间加权平均浓度(TLV-TWA)降至32 mg/m3以下,美国则降至0.32 mg/m3,我国现行GBZ2-2002<工作场所有害因素职业接触限值>中规定生产环境空气中苯的时间加权平均容许浓度为6 mg/m3,而短时间接触容许浓度(PC-STEL)为10 mg/m3[4].1989年至2000年国内期刊报道有28例苯白血病[5].Stockstad等[6]报道在鞋厂工作的工人接触1 mg/m3的苯浓度仍可引起人体白细胞和淋巴细胞减少.Lan Q等[7]认为40 mg/m3以下苯作业工人易罹患骨髓瘤.苯还可诱导血清活性氧水平,引起细胞成分包括DNA氧化损伤[8].     

Identifying occupational and nonoccupational exposure to mercury in dental personnel

The objective of this study was to investigate the occupational and nonoccupational exposure to mercury (Hg) vapor in dental personnel by examining the relationships between blood mercury, urine mercury, and their ratio with air mercury. The method was performed on 50 occupational exposed and 50 unexposed controls (25 men and 25 women). The mercury concentrations in air and human biological samples were determined based on the National Institute for Occupational Safety and Health (NIOSH) method and standard method (SM) by a new mode of liquid-phase microextraction, respectively. The mean mercury concentrations in urine (μg Hg⁰/g creatinine) and blood were significantly higher than control group, respectively (19.41 ± 5.18 vs 2.15 ± 0.07 μg/g and 16.40 ± 4.97 vs 2.50 ± 0.02 μg/L) (p <.001). The relationships between mercury concentration in blood/urine ratio (r = .380) with dental office air are new indicators for assessing occupational exposure in dental personnel.