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Nanomaterials, especially silver nanoparticles (Ag NPs), are used in a rapidly increasing number of commercial products. Accordingly, the hazards associated with human exposure to nanomaterials should be investigated to facilitate the risk assessment process. A potential route of exposure to NPs is through the respiratory system. In the present study, we investigated the effects of well-characterized PVP-coated Ag NPs and silver ions (Ag+) in the human, alveolar cell line, A549. Dose-dependent cellular toxicity caused by Ag NPs and Ag+ was demonstrated by the MTT and annexin V/propidium iodide assays, and evidence of Ag NP uptake could be measured indirectly by atomic absorption spectroscopy and flow cytometry. The cytotoxicity of both silver compounds was greatly decreased by pretreatment with the antioxidant, N -acetyl-cysteine, and a strong correlation between the levels of reactive oxygen species (ROS) and mitochondrial damage ( r s  = −0.8810; p  = 0.0039) or early apoptosis ( r s  = 0.8857; p  = 0.0188) was observed. DNA damage induced by ROS was detected as an increase in bulky DNA adducts by 32 P postlabeling after Ag NP exposure. The level of bulky DNA adducts was strongly correlated with the cellular ROS levels ( r s  = 0.8810, p  = 0.0039) and could be inhibited by antioxidant pretreatment, suggesting Ag NPs as a mediator of ROS-induced genotoxicity.

Benzene is a human carcinogen presented in gasoline (1% by volume). It is also found in vehicle exhaust. The aim of this study was to assess the health risk of inhalation exposure to benzene among gasoline station workers. The ambient benzene concentration was measured by personal sampling from 150 gasoline station workers (137 fueling workers and 13 cashiers). Additional data of working characteristics were collected by interviews and on-site observations. All workers were non-smokers and passive smoking was limited. Risk assessment of inhalation exposure was determined using the United State Environmental Protection Agency (USEPA), and showed a high risk of adverse health effect (Hazard Quotients (HQ) >1) in 51.33% of workers. The cancer risk was increased from 1.35 × 10−8 to 1.52 × 10−4, and 70.67% of the workers had a lifetime cancer risk (>Inhalation Unit Risk (IUR): 2.2 × 10−6). A significantly higher risk was found in fueling workers compared to cashiers, and in workers at gasoline stations in inner-city zones (suburban and urban), compared to rural zones. All risk estimations were based upon a single measurement in an eight hour working period, which was assumed to be the average shift length for all working days in a year (250 days). The increased health risk suggests that there should be health surveillance for workers in order to protect them from exposure to benzene. In addition to benzene, the volatile organic compounds (VOCs) present in gasoline may influence health outcomes.

Objective This study assessed the health risk of benzene exposure among Thai gasoline station workers through biomarker detection and experience of adverse symptoms. Methods Trans, trans‐muconic acid (tt‐MA) metabolites of benzene were analyzed from spot urine sampled among gasoline station workers after shift work using HPLC‐UV. Air benzene monitoring was done with an active sampler connected to a charcoal sorbent tube, and analyzed by GC‐FID. The health risk was calculated by using the biomatrix of the likelihood of benzene exposure and the severity of adverse symptoms. Results The tt‐MA concentration, among 235 workers, ranged from less than 10–2159 µg/g Cr, which corresponded to the air benzene concentration range of <0.1 to 65.8 ppb. In total, 32.3% of workers had a higher than acceptable risk level and there was a significant association between gasoline station work zones and the likelihood of benzene exposure as well as the health risk of workers. The health risk levels estimated from the biomarker monitoring were consistent with the risk matrix of air benzene monitoring. Conclusion This tt‐MA biomarker monitoring and biomatrix of health risk assessment is suggested as useful for health surveillance of gasoline station workers exposed to benzene.

Trans, trans-muconic acid (tt-MA) is a metabolite that is widely used as a biomarker to identify low exposure to benzene, a human carcinogen. This study aimed to investigate occupational factors related to the urinary tt-MA detection of benzene exposed workers in gasoline stations. Spot urine samples were collected and analyzed for tt-MA using a high performance liquid chromatography. Additional data were collected via subject interviews using a structured questionnaire. The personal benzene concentration was measured and analyzed by gas chromatography with a flame ionization detector. Results showed that, among the 170 workers, tt-MA was detected in 24.7% of workers and the concentration ranged from 23.0 to 1127.8 µg/g creatinine. Over 25% of those detections possessing tt-MA exceeding the recommended 500 µg/g creatinine was safe. A multiple logistic regression analysis identified that factors significantly associated with the detectable tt-MA were having no other part-time jobs (ORadj = 4.2), personal benzene concentrations of 0.05 ppm or higher (ORadj = 10.3), close to fuel nozzle during refuelling (ORadj = 93.7), and no job training (ORadj = 2.74). Safety training is recommended for those tt-MA detected workers or under a reference benzene concentration of 0.05 ppm or higher. The proposed reference of occupational action level to benzene exposure is 0.05 ppm and compliance could be assessed tt-MA for biomonitoring of those benzene exposed workers.

Benzene is harmful to human health and early detection of haematological alterations is important in preventing adverse health effects. This study aimed to investigate the biomarkers of benzene exposure and its effects due to haematological alterations. Gasoline station workers with potential risks according to the biomatrix concerning benzene exposure underwent blood and urine evaluation for the biological monitoring of urinary trans, trans-muconic acid (tt-MA), and haematological and biochemical parameter evaluation. The results were analysed for correlations between biological and haematological effects. The tt-MA biomarker was detected in some workers and approximately 50% of workers had a blood profile that showed abnormal parameters with respect to the haemoglobin (Hb), haematocrit (Hct) and white blood cell parameters, which were outside the normal range. A significant correlation was observed between the tt-MA biomarker’s level and the levels of the haematological and biochemical parameters, which were Hb, Hct, eosinophil, neutrophil, SGOT and blood creatinine. The level of urinary tt-MA as a marker of benzene exposure correlated with haematological and biochemical changes in the blood, suggesting that the gasoline station workers were affected by benzene exposure. Moreover, the current study suggests that early detection of haematological abnormalities may be possible by analysing biomarkers of their effects through regular health surveillance of workers.

Sprayers’ exposure to glyphosate was analyzed through detection of its biomarker in spot urine biological monitoring, and the health risk was assessed using the biomatrix model. Urine samples were collected from 15 sprayers after spraying, and the glyphosate concentration was determined by using the DLLME-HPLC method with a UV detector. The calibration curve for glyphosate was linear in the range of 0.4–100 µg/L, while the limits of detection and quantification were 0.1 µg/L and 0.4 µg/L, respectively. The human health risk was estimated using the hazard quotient (HQ) and the biomatrix of risk assessment. The internal dose ranged from 0.0001 to 0.0021 mg/kg b.w./day. The non-cancer HQ showed no potential health risk concerns (HQ < 1). The biomatrix of health risk assessment, based on urinary glyphosate concentration, exhibited a strong correlation with the health risk matrix model. This correlation was determined by considering the likelihood of exposure, calculated from the quantity of glyphosate used and the usage of personal protective equipment (r = 0.854, p < 0.001). Although low risk was observed in sprayers, proper PPE use and the application of more knowledge are required. The simplified health risk assessment can be used for easy self-assessment of risk in preventive action regarding health risk awareness among sprayers.

Theoretically, both synthetic endocrine disrupting chemicals (S-EDCs) and natural (exogenous and endogenous) endocrine disrupting chemicals (N-EDCs) can interact with endocrine receptors and disturb hormonal balance. However, compared to endogenous hormones, S-EDCs are only weak partial agonists with receptor affinities several orders of magnitude lower. Thus, to elicit observable effects, S-EDCs require considerably higher concentrations to attain sufficient receptor occupancy or to displace natural hormones and other endogenous ligands. Significant exposures to exogenous N-EDCs may result from ingestion of foods such as soy-based diets, green tea and sweet mustard. While their potencies are lower as compared to natural endogenous hormones, they usually are considerably more potent than S-EDCs. Effects of exogenous N-EDCs on the endocrine system were observed at high dietary intakes. A causal relation between their mechanism of action and these effects is established and biologically plausible. In contrast, the assumption that the much lower human exposures to S-EDCs may induce observable endocrine effects is not plausible. Hence, it is not surprising that epidemiological studies searching for an association between S-EDC exposure and health effects have failed. Regarding testing for potential endocrine effects, a scientifically justified screen should use in vitro tests to compare potencies of S-EDCs with those of reference N-EDCs. When the potency of the S-EDC is similar or smaller than that of the N-EDC, further testing in laboratory animals and regulatory consequences are not warranted.

Manganese superoxide dismutase (MnSOD) inhibits oxidative damage and cancer therapy effectiveness. A polymorphism in its encoding gene (SOD2: Val16Ala rs4880) may confer poorer breast cancer survival, but data are inconsistent. We examined the association of SOD2 genotype and breast cancer recurrence (BCR) among patients treated with cyclophosphamide-based chemotherapy (Cyclo). We compared our findings with published studies using meta-analyses. We conducted a population-based case-control study of BCR among women in Jutland, Denmark. Subjects were diagnosed with non-metastatic breast cancer from 1990-2001, received adjuvant Cyclo, and were registered in the Danish Breast Cancer Cooperative Group. We identified 118 patients with BCR and 213 matched breast cancer controls. We genotyped SOD2 and used conditional logistic regression to compute the odds ratio (OR) and associated 95% confidence intervals (95% CI) of BCR. We used random-effects meta-analytic models to evaluate the association of SOD2 polymorphisms and BCR. The frequency of the SOD2-Ala allele was 70% in cases versus 71% in controls; 40% versus 44% were heterozygotes, and 30% versus 25% were homozygotes, respectively. Heterozygote and homozygote carriers of the Ala allele had no increased rate of BCR (OR = 1.1, 95%CI = 0.65, 2.0, and OR = 0.87, 95%CI = 0.47, 1.6, respectively). Five studies informed the meta-analytic models; summary estimates associating BCR for homozygote, or any inheritance of the variant Ala allele were 1.18 (95%CI = 0.74, 1.88), and 1.18, (95%CI = 0.91, 1.54), respectively. Our findings do not suggest that MnSOD enzymatic activity, as measured by SOD2 genotype, affects rates of BCR among patients treated with Cyclo.

The aim of this study was to compare results obtained by eight different short-term assays of estrogenlike actions of chemicals conducted in 10 different laboratories in five countries. Twenty chemicals were selected to represent direct-acting estrogens, compounds with estrogenic metabolites, estrogenic antagonists, and a known cytotoxic agent. Also included in the test panel were 17β-estradiol as a positive control and ethanol as solvent control. The test compounds were coded before distribution. Test methods included direct binding to the estrogen receptor (ER), proliferation of MCF-7 cells, transient reporter gene expression in MCF-7 cells, reporter gene expression in yeast strains stably transfected with the human ER and an estrogen-responsive reporter gene, and vitellogenin production in juvenile rainbow trout. 17β-Estradiol, 17α-ethynyl estradiol, and diethylstilbestrol induced a strong estrogenic response in all test systems. Colchicine caused cytotoxicity only. Bisphenol A induced an estrogenic response in all assays. The results obtained for the remaining test compounds-tamoxifen, ICI 182.780, testosterone, bisphenol A dimethacrylate, 4-n-octylphenol, 4-n-nonylphenol, nonylphenol dodecylethoxylate, butylbenzylphthalate, dibutylphthalate, methoxychlor, o,p′-DDT, p,p′-DDE, endosulfan, chlomequat chloride, and ethanol-varied among the assays. The results demonstrate that careful standardization is necessary to obtain a reasonable degree of reproducibility. Also, similar methods vary in their sensitivity to estrogenic compounds. Thus, short-term tests are useful for screening purposes, but the methods must be further validated by additional interlaboratory and interassay comparisons to document the reliability of the methods.

This study of risk assessment of gasoline station workers was performed by using the following three models: the occupational safety and health (OSH) risk assessment aligned with ISO 45001, the biomatrix of health risk, and the benzene risk matrix assessment for gasoline station workers. Levels of inhaled air benzene and urine tt-muconic acid (tt-MA) were measured using samples collected from 151 gasoline station workers. Opportunity levels of benzene exposure were obtained by multiplying the frequency of benzene exposure by the levels of tt-MA, the inhaled benzene concentration levels, or the likelihood levels from contributing risk factors at gasoline stations. The final risk scores were calculated by multiplying the opportunity levels by the severity based on the adverse symptoms of benzene toxicity experienced by workers. A checklist regarding risk factors contributing to benzene exposure was used to collect data on occupational safety performance. The potential health risk was at an unacceptable level for 66.23%, 75.50%, and 60.26% of workers according to the OSH risk, the biomatrix of health risk, and the benzene risk matrix model, respectively. There was a significant linear relationship between the risk levels indicated by the three matrix models (r > 0.6, p < 0.001). These findings demonstrate that alternative risk assessments can be provided and simply used for preventive action against health hazards from benzene exposure in risk management programs.