Metabolomic profiling identifies plasma sphingosine 1-phosphate levels associated with welding exposures.

BACKGROUND: Despite a number of known health hazards of welding fume exposure, it is unclear how exposure affects the human metabolome. OBJECTIVE: We assessed the metabolic profiles of welders before and after a 6-hour welding shift, controlling for circadian rhythm of metabolism on a non-welding day. METHODS: Welders were recruited from a training centre in Quincy, Massachusetts, in 2006 and 2010-2012 and donated blood samples on a welding shift day before and after work, as well as on a non-welding day spent in an adjacent classroom. In total, we collected 509 samples from 74 participants. Liquid chromatography-mass spectrometry quantified 665 metabolites from thawed plasmas. Metabolites with significant time (afternoon compared with morning) and day (welding/classroom) interactions were identified by two-way analysis of variance, and the overnight changes were evaluated. RESULTS: Sphingosine 1-phosphate (S1P) and sphingasine 1-phosphate (SA1P) exhibited significant interaction effects between day and time with false discovery rate-adjusted p values of 0.03 and <0.01, respectively. S1P, SA1P and sphingosine shared similar trends over time: high relative levels in the morning of a non-welding day declining by afternoon, but with lower starting levels on a welding day and no decline. There was no obvious pattern related to current smoking status. CONCLUSION: S1P and SA1P profiles were different between welding day and classroom day. The S1P pathway was disrupted on the day of welding exposure. The levels of S1P, SA1P and sphingosine were highly correlated over time. S1P is a signalling lipid with many vital roles; thus, the underlying mechanism and clinical implications of this alteration need further investigation.

Global DNA (LINE-1) methylation is associated with lead exposure and certain job tasks performed by electronic waste workers.

OBJECTIVE: This study assessed the associations between blood and urine levels of toxic metals; cadmium (Cd) and lead (Pb), and methylation levels of the LINE-1 gene among e-waste and control populations in Ghana. METHODS: The study enrolled 100 male e-waste workers and 51 all-male non-e-waste workers or controls. The concentrations of Cd and Pb were measured in blood and urine using inductively coupled plasma mass spectrometry, while LINE1 methylation levels were assessed by pyrosequencing of bisulfite-converted DNA extracted from whole blood. Single and multiple metals linear regression models were used to determine the associations between metals and LINE1 DNA methylation. RESULTS: Blood lead (BPb) and urine lead (UPb) showed higher median concentrations among the e-waste workers than the controls (76.82 µg/L vs 40.25 µg/L, p ≤ 0.001; and 6.89 µg/L vs 3.43 µg/L, p ≤ 0.001, respectively), whereas blood cadmium (BCd) concentration was lower in the e-waste workers compared to the controls (0.59 µg/L vs 0.81 µg/L, respectively, p = 0.003). There was no significant difference in LINE1 methylation between the e-waste and controls (85.16 ± 1.32% vs 85.17 ± 1.11%, p = 0.950). In our single metal linear regression models, BPb was significantly inversely associated with LINE1 methylation in the control group (ßBPb = - 0.027, 95% CI - 0.045, - 0.010, p = 0.003). In addition, a weak association between BPb and LINE1 was observed in the multiple metals analysis in the e-waste worker group (ßBPb = - 0.005, 95% CI - 0.011, 0.000, p = 0.058). CONCLUSION: Continuous Pb exposure may interfere with LINE1 methylation, leading to epigenetic alterations, thus serving as an early epigenetic marker for future adverse health outcomes.

Increased aluminum and lithium and decreased zinc levels in plasma is related to cognitive impairment in workers at an aluminum factory in China: A cross-sectional study.

BACKGROUND: Previous studies have shown that multiple imbalances of metal ions in the brain are closely associated with the neurodegenerative disorders. Our studies have shown that long-term working exposure to aluminum induces increased plasma aluminum levels and causes cognitive impairment in workers at aluminum factories. OBJECTIVE: To explore the levels of nine metals in plasma and the effect on cognitive function among in-service workers. METHODS: In this cross-sectional study, cognitive function was assessed using the Montreal Cognitive Assessment (MoCA), which included seven subitems: executive/visuospatial abilities; naming; attention and calculation; language; abstract; recall; and orientation. The plasma levels of nine kinds of metals were measured by inductively coupled plasma-mass spectrometry (ICP-MS). A multivariate generalized linear regression model and Bayesian kernel machine regression (BKMR) were selected to estimate the relationship between metal plasma level and MoCA scores with adjustment for confounders. RESULTS: One hundred and eighty-seven workers participated in this study. In the multivariable generalized linear model, among these nine metals studied, five were related to the MoCA score: aluminum, lithium, cobalt, zinc and chromium. In the BKMR model, a significantly negative correlation between the plasma aluminum, lithium and the total MoCA score was observed. Moreover, for subitems on the MoCA scale, the plasma levels of lithium, aluminum, and zinc had a significant correlation with the executive/visuospatial abilities, naming, and orientation abilities, respectively. The log-transformation concentrations of plasma aluminum and lithium were negatively correlated with the executive/visuospatial abilities and naming abilities, respectively. The log-transformation plasma zinc concentration was positively correlated with orientation abilities. CONCLUSION: Based on the results, we determined that increased aluminum and lithium and decreased zinc levels in plasma were associated with the incidence of mild cognitive impairment (MCI) in workers at a Chinese aluminum plant.

Assessment of lead exposure controls on bridge painting projects using worker blood lead levels.

A retrospective analysis of worker blood lead levels (BLL) was conducted using blood lead data collected by four bridge painting contractors before and after lead exposure. The objective of the study was to evaluate the effectiveness of exposure controls in preventing elevated blood lead levels (>25 µg/dl) during bridge painting projects. The contractors selected for the study submitted BLL data for 289 workers representing ten work tasks and 11 bridge painting projects. In total, 713 blood lead levels results were evaluated. The mean blood lead level for all work classifications combined was 10.9 µg/dl at baseline compared with 14.9 µg/dl after two months of exposure and 15.0 µg/dl after four months of exposure. Two months after initial exposure, 29% of the painters and 35% of the laborers had a 10 µg/dl incremental increase or greater in blood lead level. Likewise, 18% of the painters and 26% of the laborers had a blood lead level greater than 25 µg/dl during the same time. The blood lead levels that exceeded the 25 µg/dL threshold ranged from 30µg/dL-63 µg/dL for painters and 26 µg-56 µg/dL for laborers. All work tasks with high-intensity exposure (abrasive blaster/painter, abrasive blaster, painter & laborer) experienced an average blood lead level increase that ranged from 0.2 µg/dl to 8.9 µg/dl two months after initial exposure. Blood lead testing conducted after modified exposure controls (two months after the initial follow-up blood testing) were implemented showed a decrease in average blood lead levels (range -0.14 µg/dl to -2.7 µg/dl) for two high-intensity exposure work tasks. In comparison, the other two high-intensity work tasks had moderate increases (range 1 µg/dl to 2.4 µg/dl). The modified exposure controls included an increase in the air velocity inside of the work containment and an administrative control in the form of additional worker training on lead exposure prevention. The reduction in the 95th percentile (point estimate) BLL exposure profile for each exposure group at the 4-month follow-up blood testing period is associated with modified exposure controls. Ineffective exposure controls were identified through the analysis of worker BLLs. We found two exposure groups (laborer and painter) whose 95th percentile (point estimate) exposure profile was greater than the OSHA construction lead standard's targeted BLL goal (25 µg/dl) during the first two months of exposure. Our research findings provide support for monthly blood lead testing after baseline until blood lead levels are controlled to an acceptable concentration.

Influence of task-based airborne lead exposures on blood lead levels: a case study of informal automobile repair artisans in Nakuru town, Kenya.

Lead poisoning is an emerging worldwide public health concern, especially in the developing countries. Occupational tasks such as spray painting and welding in informal automobile repair enterprises present risks of exposures to lead generally through inhalation and ingestion. The artisans therefore risk high blood lead (BPb) levels, which is critical to chronic adverse health effects of lead. The study aimed at assessing the influence of occupational tasks on personal airborne lead exposures and to evaluate the association between these exposures with blood lead (BPb) levels among the artisans. A cross-sectional study was conducted in ten informal automobile repair workshops. Task-specific personal inhalable air samples and blood samples were collected concurrently for 20 participants performing five distinct occupational tasks. Lead levels were analysed using inductively coupled plasma atomic emission spectroscopy and data analysed by analysis of variance, simple and multiple linear regressions. The results indicated significant differences in airborne lead (PbA) exposure levels in different occupational tasks (p = 0.000). Lead-acid battery repairs recorded mean PbA exposure level of [76.11 ± (10.81 SE) µg/m3] exceeding the WHO 50 µg/m3 airborne lead permissible exposure limit. The average (PbA) exposure level was 22.55 ± (5.05 SE) µg/m3, while the mean (BPb) level was 25.08 ± (3.48 SE) µg/dl. A significant positive correlation between task-based airborne lead with blood lead levels was observed (r = 0.68, p = 0.001). In conclusion, the occupational tasks influenced personal airborne lead exposure levels, which in turn was an important predictor of blood lead levels. The study recommends lead exposure assessments, medical screening and intervention measures to minimize the risk and consequences of occupational exposures to lead among the study population.

[Serum polychlorinated biphenyls in workers of a second-smelting steel mill]. / Policlorobifenili sierici nei lavoratori di una acciaieria di seconda fusione.

SUMMARY: In the steel industry polychlorodibenzodioxins (PCDD), polychlorinated dibenzofurans (PCDF) and polychlorinated biphenyls (PCBs) may be present deriving from the fusion of ferrous and non-ferrous scrap, as well as for the thermal decomposition of the plastic materials (thermoplastic and thermosetting resins) contained therein and not removed before melting at high temperatures. The aim of the study was to assess in 52 workers of a secondmelting steel plant the PCBs exposure deriving from the manual handling of ferrous scrap waste eventually contaminated. The population was divided by production department (scrap, casting and office). Static air sampling of PCDD, PCDF, PCBs and biological monitoring of serum dioxin-like PCBs (DL-PCBs) were performed. The comparison of serum DL-PCB values between workers from the scrap department and those from the casting did not find any statistically significant differences (Mann- Whitney U test). The range of serum DL-PCBs was 7.74-78.55 ng/g lipids with an average of 24.21 ng/g lipids, much lower than the reference values measured in the Italian general population in 2011. Mean and median TEQ WHO 1998 of DL-PCBs were 0.22 pg/g lipids and 0.15 pg/g lipids respectively. The low concentrations of serum DL-PCBS in the studied population can be explained by the progressive reduction of environmental PCBs contamination.

Quantification of eight bisphenol analogues in blood and urine samples of workers in a hazardous waste incinerator.

Bisphenol A (BPA) has been widely used in the manufacture of polycarbonate plastic and epoxy resins. In recent years, producers have started replacing BPA by other chemical analogues, such as bisphenol -S (BPS) and -F (BPF), all of them under the label "BPA-free". However, despite bisphenol (BP) analogues have a very similar structure, their endocrine-disrupting properties could differ from those of BPA. Unfortunately, information regarding human exposure to BP analogues is very limited, not only as single substances, but also as chemical mixtures. The aim of this study was to determine the levels of 8 BP analogues (A, S, F, B, AF, Z, E, and AP) in biological samples from a controlled cohort of workers in a hazardous waste incinerator (HWI) located in Constantí (Catalonia, Spain). Firstly, a chemical method to analyze a mixture of those 8 analogues in total blood and urine was optimized, being samples quantified by means of gas chromatography coupled to mass spectrometry (GC-MS). Furthermore, a biomonitoring study was performed by collecting samples of total blood and urine of 29 people working in the HWI. Among the 8 BP analogues assessed, BPA presented the highest levels in both biological samples, with mean total (free + conjugated) BPA concentrations of 0.58 and 0.86 µg/L in blood and urine, respectively. Free vs. total BPA levels presented a mean percentage of 79% in blood and 19% in urine. Beyond BPA, traces of BPB were also found in a single sample of blood. Furthermore, none of the remaining BP analogues was detected in blood or urine. Despite BPA has been regulated, it is still very present in the environment, being human exposure to this chemical still an issue of concern for the public health.

Simultaneous analysis of bisphenol A fractions in maternal and fetal compartments in early second trimester of pregnancy.

Background Bisphenol A (BPA) is an estrogenic, endocrine-disrupting compound widely used in the industry. It is also a ubiquitous environmental pollutant. Its presence was confirmed in human fetuses, which results from maternal exposure during pregnancy. The mechanisms behind maternal-fetal transfer, and relationships between pregnant women and fetal exposures remain unclear. The aim of this study was to assess the impact of maternal exposure to BPA on the exposure of the fetus. Methods Maternal plasma and amniotic fluid samples were collected from 52 pregnant women undergoing amniocentesis for prenatal diagnosis of chromosomal abnormalities. BPA was measured by gas chromatography-mass spectrometry (GC-MS). The permeability factor - a ratio of fetal-to-maternal BPA concentration - was used as a measure delineating the transplacental transfer of BPA. Results The median concentration of maternal plasma BPA was 8 times higher than the total BPA concentration in the amniotic fluid (8.69 ng/mL, range: 4.3 ng/mL-55.3 ng/mL vs. median 1.03 ng/mL, range: 0.3 ng/mL-10.1 ng/mL). There was no direct relationship between the levels of BPA in maternal plasma and amniotic fluid levels. The permeability factor, in turn, negatively correlated with fetal development (birth weight) (R = -0.54, P < 0.001). Conclusion Our results suggest that the risk of fetal BPA exposure depends on placental BPA permeability rather than the levels of maternal BPA plasma concentration and support general recommendations to become aware and avoid BPA-containing products.

lncRNAVNN3 mediated benzene-induced hematotoxicity through promoting autophagy and apoptosis.

The potential toxicity of low-dose benzene exposure to human health has received attention, but the mechanisms of low-dose benzene-induced hematotoxicity remain largely unknown. The purpose of our study was to investigate the relationships between lncRNAVNN3 expression with benzene-induced autophagy and apoptosis in control and benzene-exposed workers. Seventy benzene-exposed workers and seventy non-benzene-exposed healthy workers were recruited. The expression of lncRNAVNN3, serum autophagy-associated and apoptosis-associated proteins were evaluated, and the relationship among them were also analysed. Furthermore, the mechanism of lncRNAVNN3 on autophagy and apoptosis induced by benzene metabolite (1, 4-benzoquinone, 1, 4-BQ) was investigated in vitro. The results showed that the expression of lncRNAVNN3 increased in benzene-exposed workers (p < 0.05). A positive correlation was found between lncRNAVNN3, serum autophagy-associated and apoptosis-associated proteins. In addition, we found that the knockdown of lncRNAVNN3 reduced phosphorylation of beclin1 and Bcl-2, which mediated 1, 4-benzoquinone-induced autophagy and apoptosis. Overall, lncRNAVNN3 mediated 1, 4-benzoquinone-induced autophagy and apoptosis though regulating phosphorylation of beclin1 and Bcl-2, suggesting that lncRNAVNN3 might be a novel early sensitive biomarker of benzene-induced hematotoxicity.

Investigation of occupational exposure to lead and its relation with blood lead levels in electrical solderers.

Occupational exposure to lead compounds can cause headache, nausea, encephalopathy, anemia, chronic muscle pain, and saturnism. Exposure to lead in women can affect fertility, and cause abortion or low IQ in the offspring. The aim of this study was to investigate occupational exposure to lead and its relation with blood lead levels in female electrical parts solderers. This cross-sectional (descriptive and analytical) study was carried out on 40 female solderers, working in two electrical parts manufacturing factories in Neyshabur city in 2017-2018. Occupational exposure to lead was determined by the OSHA 121 method, and the NIOSH 8003 method was used to determine the concentration of lead in blood. Lead in blood and air samples were determined by using a flame atomic absorption analyzer. Blood was measured using a Cell Dyn Hematology device. Data were analyzed using STATA 15. The mean age of the solderers was 35.42 ± 6.80 years, and their average work experience was 7.85 ± 5.60 years. Mean occupational exposure to lead was 0.09 ± 0.01 mg/m3, and the mean levels of lead in the blood of solderers were 10.59 ± 3.25 µg/dL. The mean of red blood cells (RBC) was 4.88 mil/uL, white blood cells (WBC) = 8.53 Tho/uL, hemoglobin = 14.02 g/dL, and hematocrit = 42.38%. There was a significant correlation between the concentrations of lead in air and the level of lead in workers' blood (p = 0.012, r = 0.31). The level of lead in the workers' respiratory region (ß = 0.36, p = 0.033), body mass index (ß = 0.25, p = 0.028), and the season of the year (ß = 0.21, p = 0.019) were the strongest factors affecting blood lead levels. There was a significant relation between lead in workers' air and their blood, although all blood indices were in normal range. Using lead-free alloys and local ventilation systems, and reducing exposure times are recommended to decrease exposure to lead among solderers.

Exposure, respiratory symptoms, lung function and inflammation response of road-paving asphalt workers.

BACKGROUND: Controversy exists as to the health effects of exposure to asphalt and crumb rubber modified (CRM) asphalt, which contains recycled rubber tyres. OBJECTIVE: To assess exposures and effects on airway symptoms, lung function and inflammation biomarkers in conventional and CRM asphalt road pavers. METHODS: 116 conventional asphalt workers, 51 CRM asphalt workers and 100 controls were investigated. A repeated-measures analysis included 31 workers paving with both types of asphalt. Exposure to dust, nitrosamines, benzothiazole and polycyclic aromatic hydrocarbon (PAH) was measured in worksites. Self-reported symptoms, spirometry test and blood sampling were conducted prework and postwork. Symptoms were further collected during off-season for asphalt paving. RESULTS: Dust, PAHs and nitrosamine exposure was highly varied, without difference between conventional and CRM asphalt workers. Benzothiazole was higher in CRM asphalt workers (p<0.001). Higher proportions of asphalt workers than controls reported eye symptoms with onset in the current job. Decreased lung function from preworking to postworking was found in CRM asphalt workers and controls. Preworking interleukin-8 was higher in CRM asphalt workers than in the controls, followed by a decrement after 4 days of working. No differences in any studied effects were found between conventional and CRM asphalt paving. CONCLUSION: CRM asphalt workers are exposed to higher benzothiazole. Further studies are needed to identify the source of nitrosamines in conventional asphalt. Mild decrease in lung function in CRM asphalt workers and work-related eye symptoms in both asphalt workers were observed. However, our study did not find strong evidence for severe respiratory symptoms and inflammation response among asphalt workers.

Mono-, di-, and trichlorinated biphenyls (PCB 1-PCB 39) in the indoor air of office rooms and their relevance on human blood burden.

Exposure to polychlorinated biphenyls (PCBs) from indoor air can lead to a significant increase in lower chlorinated congeners in human blood. Lower chlorinated congeners with short biological half-lives can exhibit an indirect genotoxic potential via their highly reactive metabolites. However, little is known about their occurrence in indoor air and, therefore, about the effects of possible exposure to these congeners. We analyzed all mono-, di-, and trichlorinated biphenyls in the indoor air of 35 contaminated offices, as well as in the blood of the 35 individuals worked in these offices for a minimum of 2 years. The median concentration of total PCB in the indoor air was 479 ng/m3 . The most prevalent PCBs in the indoor air samples were the trichlorinated congeners PCB 31, PCB 18, and PCB 28, with median levels of 39, 31, and 26 ng/m3 , respectively. PCB 8 was the most prevalent dichlorinated congener (median: 9.1 ng/m3 ). Monochlorinated biphenyls were not detected in relevant concentrations. In the blood samples, the most abundant congener was PCB 28; nearly 90% of all mono-, di-, and trichlorinated congeners were attributed to this congener (median: 12 ng/g blood lipid).

Validity of different biomonitoring parameters for the assessment of occupational exposure to N,N-dimethylformamide (DMF).

This study was performed to assess the relation between occupational exposure to N,N-dimethylformamide after an 8 h work shift in the acrylic fibre industry and its three biological markers N-methylformamide (NMFtotal), N-acetyl-S-(N-methylcarbamoyl)cysteine (AMCC), and N-methylcarbamoyl adduct at haemoglobin (MCVal). External DMF exposure of 220 workers was determined during the whole shift. A standardised questionnaire was used to obtain information about the worker's general health status, medical treatment, smoking habits, protective measures, and possible symptoms caused by DMF exposure. NMF and AMCC were analysed in post-shift urine samples and MCVal in blood. For longitudinal assessment the average AMCC concentration was determined over a period of 4 weeks (weekly sampling) in a sub-collective of 89 workers. The median of DMF concentration in air was 3.19 mg/m3 (range < 0.15-46.9 mg/m3). The biological markers showed a median of 4.80 mg/L (range 0.20-50.6 mg/L) for NMFtotal, 4.75 mg/g creatinine (range 0.06-49.6 mg/g creatinine) for AMCC, and 57.5 nmol/g globin (range 0.5-414 nmol/g) for MCVal. A significant linear relationship was observed between DMF in air and NMF as well as between DMF in air and AMCC in post-shift urine samples. The mean AMCC values measured weekly over a period of 4 weeks correlated significantly with MCVal adducts too. Excluding workers who had been using breathing masks on the day of the study led to even tighter correlations. The results of the present study demonstrate the applicability of the DMF biomonitoring parameters NMFtotal in post-shift urine for the present-day exposure assessment, AMCC in the post-shift urine after several shifts for assessment of the cumulative exposure of the previous working days, and MCVal for assessment of long-term exposure during previous weeks and months. The data of the present study enable now the estimation of valid equivalents of these biomonitoring parameters to the external DMF exposure. From the risk assessment point of view, the exposure limit values for AMCC and MCVal, which are directly linked to the presumed toxic intermediate MIC, exhibit a significant advance.

Occupational exposure to asphalt fume can cause oxidative DNA damage among road paving workers.

OBJECTIVES: We designed the present study to determine the effect of occupational exposure to asphalt fumes on oxidative status and DNA damage in road paving workers. METHODS: Sixty road paving workers exposed to asphalt fumes and forty non-exposed control subjects were recruited. Occupational exposure to PAHs was assessed by urinary 1-hydroxypyrene (1-OHP) excretion. Serum thiol disulfide homeostasis (TDH), total oxidant status (TOS) and total antioxidant status (TAS) and urinary 8-hydro-deoxyguanosine (8-OH-dG) level were evaluated by automated colourimetric method. RESULTS: The urinary concentrations of 1-OHP and 8-OH-dG were significantly higher in the exposed group than in the control group (P < 0.001). Disulfide/thiol ratio, TOS, and TAS were also significantly higher for the asphalt workers. A positive correlation existed between urinary 1-OHP and 8-OH-dG, TOS and TAS. CONCLUSION: Study results indicate that exposure to PAHs induces oxidative stress and causes genotoxic effects in asphalt workers.

[Study on the health effects of occupational exposure to low concentrations of benzene].

Objective: The main purpose of this study was to ascertain whether (or not) exposure to benzene, toluene, xylene and ethylbenzene (BTXE) , under normal working conditions, was associated with any health effects. Methods: From January to December 2014, the workplaces concentrations of BTXE were measured of 71 enterprises in Suzhou Industrial Park. Occupational health examination were investigated on 764 employees who exposed to BTXE, as well as 4409 employees of the corresponding enterprises who unexposed to BTXE, and analyzed the data of the two groups. Results: A total of 6 monitoring sites in 3 enterprises BTXE concentrations excess of the standards, the unexposed group was under the limit of detection. The means of red blood cell count, hemoglobin, hematocrit, intermediate cell count and percentage of intermediate cells were significantly higher in exposed group than in unexposed group (P<0.05) . Conversely, platelet count was significantly lower in exposed group than in unexposed group (P<0.05) . The proportion of red blood cell volume, lymphocyte count and percentage of intermediate cells were significantly lower in exposed group than in unexposed group (P<0.05) . Both means and proportion of glutamic pyruvic transaminase and urea nitrogen were significantly higher in exposed group than in unexposed group (P<0.05) . The positive rate of protein, urine, urine red blood cell were significantly higher in exposed group than in unexposed group (P<0.05) . The abnormal rate of electrocardiogram, liver and kidney B scan were significantly higher in exposed group than in unexposed group (P<0.05) . Multivariate logistic regression analysis revealed that percentage of intermediate cells increased, urea nitrogen increased, urine protein positived, urine red blood cells positived in exposed group the OR values were 1.689, 3.291, 3.163 and 1.743 (P<0.05) . Conclusion: Occupational exposure to low concentrations of BTXE had a certain impact on the blood system and liver and kidney function of the employees, occupational health surveillance for such people should be strengthened.

The risk of occupational exposure to mercury vapor in some public dental clinics of Baghdad city, Iraq.

BACKGROUND: Dental workers are exposed to elevated levels of elemental mercury vapor substantially above the occupational exposure standards when placing or removing mercury/silver tooth restorations and disposing of mercury waste. This results in a significant increase in occupational exposure and risk of mercury intoxication. METHODS: To evaluate the occupational exposure of dental workers to amalgam in four dental clinics in Baghdad city, the concentrations of mercury vapor were measured seasonally from February to November 2016. Samples of blood and urine were collected from 30 dental workers (exposed individuals) and five non-occupationally exposed individuals. Biochemical parameters such as cholesterol, liver enzymes (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase), renal enzymes (urea and creatinine), total protein and reduced glutathione (GSH) were observed. RESULTS: The results indicated that mercury vapor levels varied from 84.7 ± 18.67 to 609.3 ± 238.90 µg/m3 and most concentrations were above the occupational exposure standards. The results of the biochemical parameters showed a significant increase in levels of cholesterol, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and no significant increase in blood urea and creatinine in dental workers in comparison with unexposed persons (control). Although the results showed a significant reduction in the levels of glutathione and total protein, there was no significant decrease in the levels of alkaline phosphatase (ALP) in exposed dental workers when compared with non-occupationally exposed individuals. CONCLUSIONS: It is concluded that mercury vapor concentrations in the indoor air of some dental clinics in Baghdad city are high and exceed the OSHA STEL(Occupational Safety and Health Administration Short Term Exposure Limit). The present data showed that altered biochemical parameters can be used as efficient bioindicators for mercury toxicity.

Correlation between airborne manganese concentration at the workstations in the iron foundry and manganese concentration in workers' blood.

BACKGROUND: Manganese (Mn) used as raw material for melting process in the ferrous foundry is considered as hazardous neurotoxic substance because it accumulates in the central nervous system and may cause neurological disorders. The furnace-men and melting department workers are potentially exposed to manganese particles or fume in the workplace. The objective of the research has been to investigate the sources and levels of manganese exposure in the foundry by correlation of blood-manganese (B-Mn) and air-manganese (air-Mn) measurement. MATERIAL AND METHODS: Air-Mn and Mn of blood serum were measured involving workers who worked in a big-sized foundry during 1 year. The standard method of the Occupational Safety and Health Administration (OSHA) ID-121 was used for air and blood assessment and atomic absorption spectroscopy (AAS) was carried out for air and blood sample analysis. RESULTS: The air sampling results have revealed that there is a high exposure to manganese (4.5 mg/m3) in the workplace as compared to the National Institute for Occupational Safety and Health's (NIOSH) time weighted average (the reference time-weighted average (TWA) = 1 mg/m3). The average blood serum Mn concentration was 2.745 µg/l for subjects working for shorter than 3 months and 274.85 µg/l for subjects working 3-12 months. CONCLUSIONS: Against the research hypothesis there was no correlation between the air-Mn concentration and the B-Mn (serum) level of manganese in the serum of the exposed subjects. It may be due to short time of air sampling of manganese airborne particles, and a real-time monitoring of airborne manganese particles is suggested for any future study. Med Pr 2017;68(4):449-458.

Blood morphology and the levels of selected cytokines related to hematopoiesis in occupational short-term exposure to lead.

The aim of the study was to investigate the influence of a short-term exposure to lead on the blood morphology and the levels of selected cytokines related to hematopoiesis in occupationally exposed workers. The study population included 37 males occupationally exposed to lead for 36 to 44days. Their blood lead level raised from 10.7±7.67µg/dl at baseline to the level of 49.1±14.1µg/dl at the end of the study. The level of hemoglobin and values of MCH and MCHC were decreased due to a short-term exposure to lead by 2%, 2%, and 1%, respectively. The counts of WBC, LYM, and MXD increased significantly by 5%, 7%, and 35%. Similarly, the count of PLT increased by 7%, while PDW, MPV, and P-LCR decreased by 6%, 3%, and 9%, respectively. The levels of IL-7, G-CSF, HGF, PDGF AB/BB, SCF, and PECAM-1, decreased significantly by 30%, 33%, 8%, 30%, 25%, and 20%, respectively. A short-term occupational exposure to lead results in a decreased hemoglobin level and increased counts of WBC and PLT. Changes in counts and proportions of different types of leukocytes and decreased values of PLT indices, such as PDW, MPV, and P-LCR, due to the subacute lead-exposure may be associated with lead-induced decreased levels of cytokines related to hematopoiesis, including SCF, G-CSF, IL-7, and PDGF.

Occupational exposure levels of bioaerosol components are associated with serum levels of the acute phase protein Serum Amyloid A in greenhouse workers.

BACKGROUND: Occupational exposure to particles may be associated with increased inflammation of the airways. Animal experiments suggest that inhaled particles also induce a pulmonary acute phase response, leading to systemic circulation of acute phase proteins. Greenhouse workers are exposed to elevated levels of bioaerosols. The objective of this study is to assess whether greenhouse workers personal exposure to bioaerosol components was associated with serum levels of the acute phase proteins Serum Amyloid A (SAA) and C-reactive protein (CRP). METHODS: SAA and CRP levels were determined in serum sampled repeatedly from 33 greenhouse workers. Blood was drawn repeatedly on Mondays and Thursdays during work weeks. Acute phase protein levels were compared to levels in a comparison group of 42 people and related to individual exposure levels to endotoxin, dust, bacteria, fungi and ß-glucan. RESULTS: Serum levels of SAA and CRP were not significantly different in greenhouse workers and a reference group, or on the two work days. In a mixed model, SAA levels were positively associated with endotoxin exposure levels (p = 0.0007). Results for fungi were not clear. CRP levels were positively associated with endotoxin exposures (p = 0.022). Furthermore, when workers were categorized into three groups based on SAA and CRP serum levels endotoxin exposure was highest in the group with the highest SAA levels and in the group with middle and highest CRP levels. SAA and CRP levels were elevated in workers with asthma. CONCLUSION: Greenhouse workers did not have elevated serum levels of SAA and CRP compared to a reference group. However, occupational exposure to endotoxin was positively associated with serum levels of the acute phase proteins SAA and CRP. Preventive measures to reduce endotoxin exposure may be beneficial.

Using exposure windows to explore an elusive biomarker: blood manganese.

PURPOSE: We sought to understand the time course between exposure to manganese (Mn) and uptake into the blood, to allow a more meaningful interpretation of exposure biomarker data, and to determine the utility of blood as a biomarker of Mn exposure. METHODS: Welder trainees were monitored over the course of a five-quarter training program. Each quarter, trainees gave eight blood samples and had personal air monitoring four times. A mixed model was fit to obtain estimates of airborne exposure by welding type (fixed effect), adjusted for subject (random effect). Considering weekends and days absent as zero exposure, estimated exposures were summed over various exposure windows and related to measured blood manganese (MnB) using a mixed model. RESULTS: A relationship consistent with zero was found between MnB and modeled 1 or 7 days of exposure. After 30 days of preceding exposure, a 1 mg-days/m(3) increase in air Mn is associated with a 0.57 ng/mL increase in MnB (95% CI -0.04, 1.19). Considering a 90-day exposure window and a cumulative exposure window, a 1 mg-days/m(3) increase in air Mn is associated with a 0.26 (95% CI 0.005, 0.51) and 0.09 (95% CI 0.006, 0.17) ng/mL increase in MnB, respectively. CONCLUSIONS: From this analysis, MnB may begin to act as a biomarker of Mn exposure over longer time periods, or at higher levels of exposure. This novel study design allowed investigation of how MnB relates to different time windows of exposure, representing the most robust Mn exposure assessment in the biomarker literature.