Biomarkers of mercury exposure at a mercury recycling facility in Ukraine

This study evaluates biomarkers of occupational mercury exposure among workers at a mercury recycling operation in Gorlovka, Ukraine. The 29 study participants were divided into three occupational categories for analysis: (1) those who worked in the mercury recycling operation (Group A, n = 8), (2) those who worked at the facility but not in the yard where the recycling was done (Group B, n = 14), and (3) those who did not work at the facility (Group C, n = 7). Urine, blood, hair, and nail samples were collected from the participants, and a questionnaire was administered to obtain data on age, gender, occupational history, smoking, alcohol consumption, fish consumption, tattoos, dental amalgams, home heating system, education, source of drinking water, and family employment in the former mercury mine/smelter located on the site of the recycling facility. Each factor was tested in a univariate regression with total mercury in urine, blood, hair, and nails. Median biomarker concentrations were 4.04 microg/g-Cr (urine), 2.58 microg/L (blood), 3.95 microg/g (hair), and 1.16 microg/g (nails). Occupational category was significantly correlated (p < 0.001) with both blood and urinary mercury concentrations but not with hair or nail mercury. Four individuals had urinary mercury concentrations in a range previously found to be associated with subtle neurological and subjective symptoms (e.g., fatigue, loss of appetite, irritability), and one worker had a urinary mercury concentration in a range associated with a high probability of neurological effects and proteinuria. Comparison of results by occupational category found that workers directly involved with the recycling operation had the highest blood and urinary mercury levels. Those who worked at the facility but were not directly involved with the recycling operation had higher levels than those who did not work at the facility.     

Organochlorines in breast milk from two cities in Ukraine.

Reports of environmental problems in the former Soviet Union, including excess use of pesticides, have led to concerns about high levels of contamination in humans, but little information is available to assess whether these concerns are warranted. Samples of breast milk from 197 women from two cities in Ukraine were analyzed for p,p'-DDT, p,p'-DDE, endrin, dieldrin, heptachlor epoxide, trans-nonachlor, oxychlordane, hexachlorobenzene, ss-hexachlorocyclohexane (HCH), and 18 polychlorinated biphenyl congeners, and results were compared to previous reports from Europe. The median ss-HCH concentration was 731 ng/g milk fat, which is higher than other reports from Europe but lower than reports from other parts of the world. The median DDE concentration was 2,457 ng/g milk fat, which is higher than most but not all other reports from Europe. Concentrations of other chemicals were comparable to or lower than other reports from Europe. Concentrations from the city of Kyiv were generally lower than those from Dniprodzerzhinsk, but the magnitudes of these differences were modest.     

Biomarkers of low-level mercury exposure through fish consumption in pregnant and lactating Slovenian women

In order to assess the mercury exposure of pregnant and lactating women in Slovenia, levels of total mercury (THg) and methylmercury (MeHg) were determined in hair, cord blood and breast milk. In addition, the frequency of fish consumption was estimated, because fish is generally the main pathway for human exposure to MeHg. Hair samples were collected from 574 women participating in this study, while cord blood and breast milk samples were collected from 446 and 284 women, respectively. As expected, the levels of THg in hair (median (Med)=297 ng/g, 10th percentile (P10)=73 ng/g, 90th percentile (P90)=781 ng/g), cord blood (Med=1.5 ng/g, P10=0.5 ng/g, P90=4.2 ng/g) and breast milk (Med=0.2 ng/g, P10=0.06 ng/g, P90=0.6 ng/g) were low, due to low consumption of fish (X=25 g/day). A significant linear correlation was found between levels of ln THg in hair and ln THg in cord blood (r=0.87, 95% confidence interval (CI): 0.84–0.89), between levels of ln THg in hair and ln MeHg in cord blood (r=0.94, 95% CI: 0.90–0.96) and between ln THg levels in cord blood and ln THg levels in breast milk (r=0.36, 95% CI: 0.25–0.47). Spearman's rank correlations between the frequency of fish consumption and THg in hair (r_s=0.35, 95% CI: 0.28–0.42), and between the frequency of fish consumption and THg in cord blood (r_s=0.43, 95% CI: 0.36–0.51) or MeHg in cord blood (r_s=0.31, 95% CI: 0.06–0.52) were weak. This could be due to the approximate information on fish consumption obtained from the questionnaires, the high variability of MeHg concentrations in fish and a relatively high proportion of inorganic mercury in the biomarkers which originates from sources other than fish. In conclusion, THg levels in cord blood, THg levels in hair and MeHg levels in cord blood are suitable biomarkers of low-level Hg exposure through fish consumption. Compared to cord blood, hair samples are easy to collect, store and analyse.     

Biomarkers of lead exposure

Biomarkers of exposure, effect, and susceptibility are reviewed in relation to lead exposure. Of the biomarkers of lead exposure, blood lead (Pb-B), mainly red cell lead, is a representative of soft tissue lead, and most widely used as measures of body burden and absorbed (internal) doses of lead. Urine lead (Pb-U) as well as plasma lead (Pb-P) increases exponentially with increasing Pb-B under a steady-state situation and is a reflection of recent exposure. The amount of lead in plasma and urine (MPb-P and MPb-U) after administration of a chelating agent (e.g. CaEDTA) can be useful for biomarkers of internal exposure of lead, reflecting the mobilizable pool of lead which consists of mainly blood and soft tissue lead with only a small fraction derived from bones. The critical effects in bone marrow arise mainly from the interaction of lead with some enzymatic process responsible for heme synthesis. The effects can be used for the biomarkers of effects. They are the inhibition of delta-aminolevulinic acid dehydratase (ALAD) and the variation in some metabolite concentrations (e.g. delta-aminolevulinic acid in urine (ALA-U), blood (ALA-B) or plasma (ALA-P), coproporphyrin in urine (CP), zinc protoporphyrin (ZP) in blood). The activities of pyrimidine nucleotidase (P5'N) and nicotinamide adenine dinucleotide synthetase (NADS) in blood are also decreased in lead exposure, and nucleotide contents in blood is altered in lead exposure. These effects of lead on human can be also useful biomarkers of effect. The differences in levels of heme precursors between two types of ALAD genotypes might be attributable to those in the affinity of different ALAD isozymes to lead. ALAD1 homozygotes have higher levels of ZP and ALA in comparison with ALAD2 carriers at the high lead exposure, suggesting that ALAD1 homozygotes might be more susceptible for disturbance in heme biosynthesis by lead than ALAD2 carriers.     

Biomarkers of Mn exposure in humans

BACKGROUND: Studies have reported associations between manganese (Mn) exposures and Mn levels in blood and urine, though the suitability of these biological measures as biomarkers of exposure is not well known. METHODS: We evaluated whether whole blood, plasma, and urine Mn levels reflect exposures in occupationally exposed humans. RESULTS: In active ferroalloy workers, blood Mn was associated with total air Mn levels in subjects currently exposed to low (median = 0.42 microg/m(3), P = 0.009) and moderate (median = 4.2 microg/m(3), P = 0.007) air Mn levels, but not in workers exposed to the highest Mn levels (median = 292 microg/m(3), P = 0.31). In bridge welders blood Mn (P < 0.01), but not plasma or urine Mn was significantly associated with their cumulative respiratory exposure index. In welders, approximately 6% (range approximately 3-9%) of whole blood Mn was contained in the plasma fraction, though there was no association between whole blood and plasma Mn levels (Pearson's R = 0.258, P = 0.12). In contrast, in fresh whole blood samples spiked with Mn ex vivo approximately 80% or more of added Mn partitioned in the plasma, while only approximately 20% or less partitioned in the cellular fraction. CONCLUSIONS: These data suggest a complex and limited relationship between exposure and blood Mn levels that may depend upon exposure attributes and the latency of blood sampling relative to exposure; plasma and urine Mn appear to be of little utility as exposure biomarkers. This underscores the need to fully characterize and validate these or other biomarkers for use in constructing appropriate exposure metrics and determining exposure-effect relationships.     

Comparison of microenvironmental CO concentrations in two cities for human exposure modeling.

The microenvironmental components of the CO concentration in two cities are compared by subtracting the ambient background concentration from personal exposures measured in Denver, Colorado, and Washington, DC. Two surrogate measures for the ambient background concentration are tested. Both improve the similarity of the means in the two cities, but the Denver standard deviations are higher than those in Washington, DC. Microenvironments containing the internal combustion engine have both higher means and standard deviations in Denver compared with Washington, DC. The Washington, DC, mean concentration for automobiles, for example, was 59% of the Denver mean (2.0 ppm versus 4.9 ppm). Washington, DC, had approximately 57% of the Denver emissions, and the difference in mean CO concentrations is roughly consistent with the lower emissions in Washington, DC, due to lower elevation. A surprising finding is that mean CO exposure levels caused by cooking with gas stoves in Washington, DC, were only 58% of the levels in Denver (1.9 ppm and 3.3 ppm, respectively). This result suggests that elevation may exert an influence on gas stove emissions that is similar to its influence on internal combustion engines. Using an averaging time model, analysis of the autocorrelation of sleeping and office microenvironments suggests that considerable serial dependency exists. The microenvironmental data and findings in this paper have important implications for constructing human exposure-activity pattern models. For future human exposure field studies, the findings emphasize the importance of measuring background values in a location that is extremely close to each microenvironment studied.     

Biomarkers of toluene diisocyanate exposure

Biomarkers are very useful tools when the metabolic fate of the compound or the etiology of a resultant disease is completely understood. They may contribute to confusion if it is not possible to distinguish between markers of exposure and markers of disease. Such is the case for biomarkers used in the assessment of diisocyanate exposure. Biomarkers for diisocyanate exposure result from both direct and indirect effects. Molecules such as hemoglobin, albumin, tubulin, glutathione, and laminin have been implicated as having been directly modified as a result of exposure to toluene diisocyanate (TDI). In addition, indirect biomarkers have included profiles of molecules such as antibodies, cytokines, cell accumulation or proliferation, and markers of oxidative stress. While a brief presentation of each of these markers is provided here, the focus is primarily on immunological markers as an example of the difficulties with using biomarkers in assessing diisocyanate exposure in general, and TDI specifically. Compiled data will be used to demonstrate where gaps exist in our understanding of how the results of measured biomarkers are used with regard to isocyanate exposure, and whether it may be possible to develop these tools to define thresholds between exposure and disease. Issues addressed include whether the marker represents a measure of exposure or disease, whether the methods are sufficiently uniform between labs to be able to compare between studies, and whether the ambiguities are the result of the complexity of the isocyanate reactivity in the biological system, or our inability to accurately measure the end point of the reactions.     

Sisters with mercury exposure

The same iron pot in which their father had boiled lead with mercury (from a glass thermometer) for the purpose of alchemy, was also used for cooking in the kitchen. Although his wife had died of mercury poisoning, and his 14-year-old and 11-year-old daughters were found to excrete 322 and 455 micrograms/l mercury in the urine, respectively, (1-10 micrograms/l in controls), he stubbornly refused to give permission for them to be examined further. Nine months later, the daughters were permitted to be sent to our clinical ward. While the blood level of mercury had already come down to near normal, its excessive deposition in hair, kidneys and other parts of the body as well as its excessive urinary excretion, were still persistent (beyond tenfold the normal). According to our measurement values, mercury ranged from 14 to 49 micrograms/g in every 1-cm-piece of 10 cm hair of the elder sister, and ranged from 21 to 85 micrograms/g in 14 cm hair from the younger sister. About a 75% decrease in mercury deposition was estimated during these 9 months, based on the speculation of 1.5 cm/month hair-lengthening.     

Occupational noise exposure and hearing loss of workers in two plants in eastern Saudi Arabia.

OBJECTIVE: To determine the prevalence of hearing loss associated with occupational noise exposure and other risk factors. DESIGN: A cross-sectional study involving 269 exposed and 99 non-exposed subjects (non-industrial noise exposed subjects) randomly selected. Current noise exposure was estimated using both sound level meter and noise-dosimeter. Past noise exposure was estimated by interview questionnaire. Otoscopic examination and conventional frequency (0.25-8 kHz) audiometry were used to assess the hearing loss in each subject. RESULTS: 75% (202 subjects) from the exposed group were exposed to a daily Leq above the permissible level of 85 dB(A) and most (61%) of these did not and had never used any form of hearing protection. Hearing loss was found to be bilateral and symmetrical in both groups. Bivariate analysis showed a significant hearing loss in the exposed vs non-exposed subjects with a characteristic dip at 4 kHz. Thirty eight percent of exposed subjects had hearing impairment, which was an 8-fold higher rate than that found for non-exposed subjects. Multivariate analysis indicated exposure to noise was the primary, and age the secondary predictor of hearing loss. Odds of hearing impairment were lower for a small sub-group of exposed workers using hearing protection (N=19) in which logistic regression analysis showed the probability of workers adopting hearing protective devices increased with noise exposure, education, and awareness of noise control. Hearing loss was also greater amongst those who used headphones to listen to recorded cassettes. CONCLUSION: Gross occupational exposure to noise has been demonstrated to cause hearing loss and the authors believe that occupational hearing loss in Saudi Arabia is a widespread problem. Strategies of noise assessment and control are introduced which may help improve the work environment.     

Biomarkers of environmental and workplace boron exposure

The purpose of this work was to identify an accurate, noninvasive biomarker of boron exposure that could be used in worker populations. Occupational exposure to boron is of concern due to high numbers of workers exposed, animal toxicity data suggesting reproductive effects, and lack of human studies. Total daily boron exposure was determined from duplicate samples of 24-hr food and fluid intake, plus workplace personal air monitoring in boron workers and comparison groups in northern China during 2003 and 2004. Boron was also measured in blood, semen, creatinine-corrected postshift urine, and 24-hr urine. Total daily boron exposure (mg/day) averaged 41.2 for men working in the boron industry and 2.3 for the comparison group. Boron concentration in postshift urine was correlated with 24-hr urine boron concentration (Pearson correlation coefficient = 0.85, p < 0.0001). Boron concentration in postshift urine was correlated with total daily boron exposure measured through food, fluid, and personal air monitoring (Pearson correlation coefficient = 0.83, p < 0.0001). Boron concentration in postshift urine was also correlated with internal dose measures of boron in blood and semen (Pearson correlation coefficient = 0.85, 0.80 respectively, p < 0.0001). This work suggests that creatinine-corrected, postshift urine boron concentration can be used as a biomarker of human boron exposure in worker populations.     

Mobilized mercury in subjects with varying exposure to elemental mercury vapour

Summary In a mercury mobilization test, 0.3 g of the complexing agent sodium 2,3-dimercaptopropane-1-sulfonate (DMPS) was given orally to 10 workers with moderate occupational exposure to elemental mercury vapour, controls, and to 5 referents without amalgam fillings. In the workers, DMPS caused an increase in 24-h urinary mercury excretion by a factor of 10; in the dentists, 5.9; in the controls, 5.3; and in the amalgam-free referents, 3.8. Of the mercury excreted during 24 h, 59% appeared during the first 6 h. Close, albeit non-linear, associations were found between mobilized mercury and the premobilization mercury levels in plasma and urine, but not with the duration of occupational exposure or the rough estimate of the integrated function of blood levels vs. time. The present data indicate that mercury mobilized after a single DMPS dose in close connection with exposure is mainly an index of recent exposure and is not significantly affected by slow body pools or long-term exposure.     

Microenvironmental exposure to mercury vapor

Work area and breathing zone samples were collected in a factory utilizing metallic mercury and analyzed for mercury vapor content. Breathing zone samples averaged several fold higher in concentration than concurrent area samples, reflecting a "microenvironmental" exposure to mercury vapor, presumably from contaminated clothing and hands. Blood and corrected total urine mercury values correlated well with the average microenvironmental exposure level for each worker. Measurements of unbound mercury in urine samples were sensitive at picking up minimal exposures. Excessive amounts of unbound mercury were not found in the urine, even with wide day-to-day swings in microenvironmental mercury vapor levels, suggesting that the human body can adapt to a chronic, moderate exposure to mercury vapor.     

Biomarkers of kidney integrity in children and adolescents with dental amalgam mercury exposure: findings from the Casa Pia children's amalgam trial

Mercury is toxic to the kidney, and dental amalgam is a source of mercury exposure. Few studies have evaluated the effects of dental amalgam on kidney function in a longitudinal context in children. Here, we evaluated urinary concentrations of glutathione S-transferases (GSTs) α and π as biomarkers of renal proximal and distal tubular integrity, respectively, and albumin as a biomarker of glomerular integrity in children and adolescents 8-18 years of age over a 7-year course of dental amalgam treatment. Five hundred seven children, 8-12 years of age at baseline, participated in a clinical trial to evaluate the neurobehavioral and renal effects of dental amalgam in children. Subjects were randomized to either dental amalgam or resin composite treatments. Urinary GSTs α and π, albumin, and creatinine concentrations were measured at baseline and annually in all subjects. Results were evaluated using linear regression analysis. GST-α concentrations were similar between treatment groups and in each sex and race (white vs. non-white) group in each follow-up year. GST-π levels tended upward over the course of follow-up by four- to six-fold. This increase was seen in all groups irrespective of the treatment, race, or gender. Females had GST-π levels approximately twice those of males at all ages. Albumin concentrations were constant throughout the follow-up period and did not differ by treatment, although females had 39% higher albumin levels than males. Additionally, we found no significant effects of amalgam treatment on the proportion of children with microalbuminuria (>30 mg/g creatinine). These findings are relevant within the context of children's health risk assessment as relates to the safety of mercury exposure from dental amalgam on kidney function. These data also provide normative values for sensitive indices of renal functional integrity that may serve in the evaluation of children and adolescents with renal disorders.     

Relation of mercury exposure to elemental mercury levels in the urine and blood

The levels of elemental and inorganic mercury were measured in urine and blood samples from workers in thermometer manufacturing factories. The inorganic mercury levels in the urine did not correlate with the levels of mercury exposure for each worker. However, a significant correlation was noted between elemental mercury levels in the urine and the levels of individual exposure. A significant correlation was also found between elemental mercury levels in the urine and mercury levels in the blood. These findings suggest that the determination of elemental mercury in urine may serve as a useful indicator for assessing levels of recent exposure to mercury vapor, as well as the level of inorganic mercury in the blood.