Biological Monitoring of Glyphosate Exposure among Knapsack Sprayers in Khon Kaen, Thailand.

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.

Biomatrix of health risk assessment of benzene-exposed workers at Thai gasoline stations.

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.

Factors Affecting Adverse Health Effects of Gasoline Station Workers.

This cross-sectional study examined the risk factors affecting adverse health effects from benzene exposure among gasoline station workers in Khon Kean province, Thailand. An interview questionnaire of adverse symptoms relating to benzene toxicity was administered to 151 workers. Area samplings for benzene concentration and spot urine for tt-muconic acid (tt-MA), a biomarker of benzene exposure, were collected. The factors associated with adverse symptoms were analysed by using multiple logistic regression. It was found that these symptoms mostly affected fuelling workers (77.5%), and the detected air benzene reached an action level or higher than 50% of NIOSH REL (>50 ppb). The top five adverse symptoms, i.e., fatigue, headache, dizziness, nasal congestion, and runny nose, were reported among workers exposed to benzene. More specific symptoms of benzene toxicity were chest pain, bleeding/epistaxis, and anaemia. The detected tt-MA of workers was 506.7 ug/g Cr (IQR), which was a value above the BEI and higher than that of asymptomatic workers. Risk factors significantly associated with adverse symptoms, included having no safety training experience (ORadj = 5.22; 95% CI: 2.16-12.58) and eating during work hours (ORadj = 16.08; 95% CI: 1.96-131.74). This study urges the tightening of health and safety standards at gasoline stations to include training and eating restrictions while working in hazardous areas.

Human exposure to synthetic endocrine disrupting chemicals (S-EDCs) is generally negligible as compared to natural compounds with higher or comparable endocrine activity: how to evaluate the risk of the S-EDCs?

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.

Human exposure to synthetic endocrine disrupting chemicals (S-EDCs) is generally negligible as compared to natural compounds with higher or comparable endocrine activity. How to evaluate the risk of the S-EDCs?

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 than S-EDCs. 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.

Human exposure to synthetic endocrine disrupting chemicals (S-EDCs) is generally negligible as compared to natural compounds with higher or comparable endocrine activity. How to evaluate the risk of the S-EDCs?

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. 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.

Human exposure to synthetic endocrine disrupting chemicals (S-EDCs) is generally negligible as compared to natural compounds with higher or comparable endocrine activity. How to evaluate the risk of the S-EDCs?

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.

Human exposure to synthetic endocrine disrupting chemicals (S-EDCs) is generally negligible as compared to natural compounds with higher or comparable endocrine activity. How to evaluate the risk of the S-EDCs?

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.

Human exposure to synthetic endocrine disrupting chemicals (S-EDCs) is generally negligible as compared to natural compounds with higher or comparable endocrine activity. How to evaluate the risk of the S-EDCs?

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.

Factors Affecting Urinary tt-Muconic Acid Detection among Benzene Exposed Workers at Gasoline Stations.

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.

Risk Assessment on Benzene Exposure among Gasoline Station Workers.

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.

Obfuscating transparency?

Several recent and prominent articles in Science and Nature deliberately mischaracterized the nature of genuine scientific evidence. Those articles take issue with the United States Environmental Protection Agency's recent proposal to structure its policies and rules only from studies with transparently published raw data. The articles claim it is an effort to obfuscate with transparency, by eliminating a host of studies not offering raw data. A remarkable declaration by a Science editorial is that properly trained experts can verify the scientific evidence of studies without access to raw data, We assert the Agency's proposal must be sustained. Transparency in reporting is a fundamental ethical imperative of objective scientific research justifying massive official regulations and policies. Putative hazards bereft of independent scientific evidence will continue to stoke public anxieties, calling for precautionary regulations and policies. These should rely not on spurious science but on transparent tradeoffs between the smallest exposures compatible with utility and with social perceptions of affordable precaution.

Silver nanoparticles increase connexin43-mediated gap junctional intercellular communication in HaCaT cells through activation of reactive oxygen species and mitogen-activated protein kinase signal pathway.

Silver nanoparticles (AgNPs) are widely used in health and consumer products that routinely contact skin. However, the biological effects and possible mechanisms of AgNPs on skin remain unclear. Gap junctional intercellular communication (GJIC) plays a critical role in multicellular organisms to maintain tissue homeostasis. The aim of this study is to examine if non-coated AgNPs affect GJIC in human keratinocytes (HaCaT cells), and to identify the possible molecular mechanisms responsible for the effects. GJIC, connexin (Cx)43 protein and mRNA expression, and the effect of siRNA-mediated knockdown of Cx43 on GJIC were assessed. HaCaT cells exposed to non-coated AgNPs at different doses after a 24 hour exposure. To explore further the underlying mechanism, reactive oxygen species and mitogen-activated protein kinase pathway were evaluated after 2, 6, 12 and 24 hours. Our results revealed that non-coated AgNP exposure at subcytotoxic doses increase GJIC partially via Cx43 upregulation. Reactive oxygen species and extracellular signal-regulated kinase and activation of c-Jun N-terminal kinase were involved in the AgNP-induced upregulation of Cx43. This study provides new insight into the potential mechanism of AgNP biological activity.

Upholding science in health, safety and environmental risk assessments and regulations.

A public appeal has been advanced by a large group of scientists, concerned that science has been misused in attempting to quantify and regulate unmeasurable hazards and risks.1 The appeal recalls that science is unable to evaluate hazards that cannot be measured, and that science in such cases should not be invoked to justify risk assessments in health, safety and environmental regulations. The appeal also notes that most national and international statutes delineating the discretion of regulators are ambiguous about what rules of evidence ought to apply. Those statutes should be revised to ensure that the evidence for regulatory action is grounded on the standards of the scientific method, whenever feasible. When independent scientific evidence is not possible, policies and regulations should be informed by publicly debated trade-offs between socially desirable uses and social perceptions of affordable precaution. This article explores the premises, implications and actions supporting the appeal and its objectives.

Silver nanoparticles induced oxidative and endoplasmic reticulum stresses in mouse tissues: implications for the development of acute toxicity after intravenous administration.

Concerns have arisen about the health and environmental impacts of the increasing commercial use of silver nanoparticles (AgNPs). However, the toxic mechanisms and target tissues of AgNPs have not been fully defined. In this paper, we investigated the tissue toxicity of mice after intravenous administration of AgNPs at a single-dose of 0.2, 2 or 5 mg per kg (body weight), respectively. Biodistribution, endoplasmic reticulum stress, and oxidative stress were examined in mouse organs at eight hours after exposure. Stress markers, e.g. HSP70, BIP, p-IRE1, p-PERK, chop and xbp-1s proteins/genes, were significantly upregulated in a dose-dependent manner. In the liver, spleen, lung and kidney, high stress accompanied by apoptosis occurred. Low stress levels were observed in the heart and brain. Thus, it is proposed that the liver, spleen, lung and kidney are dominant target tissues of AgNP exposure. The lower stress and toxicity in the heart and brain were in agreement with lower AgNP accumulation. The present results demonstrated that AgNP exposure eventually resulted in permanent toxic damage by gradually imposing stress impacts on target organs. These findings highlight the potent applications of stress markers in future risk evaluation of silver nanoparticle toxicity.

Nanosilver pathophysiology in earthworms: Transcriptional profiling of secretory proteins and the implication for the protein corona.

Previously we have identified lysenin as a key protein constituent of the secretome from Eisenia fetida coelomocytes and revealed its critical importance in priming interactions between the cells and the protein corona around nanosilver. As alterations of the protein environment can directly affect the corona composition, the extent to which nanoparticles influence the cells' protein secretion profile is of remarkable interest that has rarely acquired attention. Here, we have probed transcriptional responses of E. fetida coelomocytes to the representative nanosilver NM-300K (15 nm) in a time-dependent manner (2, 4, 8 and 24 h at a low-cytotoxic concentration), and examined the implication of the temporal changes in transcriptional profiles of secretory proteins with a particular reference to that of lysenin. NM-300K was accumulated in/at the cells and lysenin was, after transient induction, gradually suppressed over time indicating a negative feedback cycle. This may limit further enrichment of lysenin in the corona and thereby decrease the lysenin-assisted uptake of the nanoparticles. Other differentially expressed genes were those involved in metal stress (likewise in AgNO3-stressed cells) and in Toll-like receptor (TLR) signaling. This offers an intriguing perspective of the nanosilver pathophysiology in earthworms, in which the conserved pattern recognition receptor TLRs may play an effector role.