-
Nature Materials Jun 2022In principle, porous physisorbents are attractive candidates for the removal of volatile organic compounds such as benzene by virtue of their low energy for the capture...
In principle, porous physisorbents are attractive candidates for the removal of volatile organic compounds such as benzene by virtue of their low energy for the capture and release of this pollutant. Unfortunately, many physisorbents exhibit weak sorbate-sorbent interactions, resulting in poor selectivity and low uptake when volatile organic compounds are present at trace concentrations. Herein, we report that a family of double-walled metal-dipyrazolate frameworks, BUT-53 to BUT-58, exhibit benzene uptakes at 298 K of 2.47-3.28 mmol g at <10 Pa. Breakthrough experiments revealed that BUT-55, a supramolecular isomer of the metal-organic framework Co(BDP) (HBDP = 1,4-di(1H-pyrazol-4-yl)benzene), captures trace levels of benzene, producing an air stream with benzene content below acceptable limits. Furthermore, BUT-55 can be regenerated with mild heating. Insight into the performance of BUT-55 comes from the crystal structure of the benzene-loaded phase (CH@BUT-55) and density functional theory calculations, which reveal that C-H···X interactions drive the tight binding of benzene. Our results demonstrate that BUT-55 is a recyclable physisorbent that exhibits high affinity and adsorption capacity towards benzene, making it a candidate for environmental remediation of benzene-contaminated gas mixtures.
Topics: Adsorption; Benzene; Gases; Metal-Organic Frameworks; Volatile Organic Compounds
PubMed: 35484330
DOI: 10.1038/s41563-022-01237-x -
International Journal of Environmental... Apr 2021The main anthropic sources of exposure to airborne benzene include vehicular traffic, cigarette smoke, and industrial emissions.
BACKGROUND
The main anthropic sources of exposure to airborne benzene include vehicular traffic, cigarette smoke, and industrial emissions.
METHODS
To detect early genotoxic effects of environmental exposure to benzene, we monitored environmental, personal, and indoor airborne benzene in children living in an urban area and an area near a petrochemical plant. We also used urinary benzene and S-phenylmercapturic acid (S-PMA) as biomarkers of benzene exposure and urinary 8-hydroxydeoxyguanosine (8-OHdG) as a biomarker of early genotoxic effects.
RESULTS
Although always below the European Union limit of 5 μg/m, airborne benzene levels were more elevated in the indoor, outdoor, and personal samples from the industrial surroundings compared to the urban area ( = 0.026, = 0.005, and = 0.001, respectively). Children living in the surroundings of the petrochemical plant had urinary benzene values significantly higher than those from the urban area in both the morning and evening samples ( = 0.01 and = 0.02, respectively). Results of multiple regression modelling showed that age was a significant predictor of 8-OHdG excretion, independent of the sampling hour. Moreover, at the low exposure level experienced by the children participating in this study, neither personal or indoor airborne benzene level, nor personal monitoring data, affected 8-OHdG excretion.
CONCLUSIONS
Our results suggest the importance of biological monitoring of low-level environmental exposure and its relation to risk of genotoxic effects among children.
Topics: Benzene; Biomarkers; Child; DNA Damage; Environmental Exposure; Environmental Monitoring; Humans; Italy; Occupational Exposure; Oxidative Stress; Schools
PubMed: 33925535
DOI: 10.3390/ijerph18094644 -
Environmental Health Perspectives Feb 1991
Topics: Benzene; Humans; Leukemia; Occupational Diseases; Risk Factors
PubMed: 2040245
DOI: 10.1289/ehp.9191165 -
Carcinogenesis Feb 2012Benzene causes acute myeloid leukemia and probably other hematological malignancies. As benzene also causes hematotoxicity even in workers exposed to levels below the US... (Review)
Review
Benzene causes acute myeloid leukemia and probably other hematological malignancies. As benzene also causes hematotoxicity even in workers exposed to levels below the US permissible occupational exposure limit of 1 part per million, further assessment of the health risks associated with its exposure, particularly at low levels, is needed. Here, we describe the probable mechanism by which benzene induces leukemia involving the targeting of critical genes and pathways through the induction of genetic, chromosomal or epigenetic abnormalities and genomic instability, in a hematopoietic stem cell (HSC); stromal cell dysregulation; apoptosis of HSCs and stromal cells and altered proliferation and differentiation of HSCs. These effects modulated by benzene-induced oxidative stress, aryl hydrocarbon receptor dysregulation and reduced immunosurveillance, lead to the generation of leukemic stem cells and subsequent clonal evolution to leukemia. A mode of action (MOA) approach to the risk assessment of benzene was recently proposed. This approach is limited, however, by the challenges of defining a simple stochastic MOA of benzene-induced leukemogenesis and of identifying relevant and quantifiable parameters associated with potential key events. An alternative risk assessment approach is the application of toxicogenomics and systems biology in human populations, animals and in vitro models of the HSC stem cell niche, exposed to a range of levels of benzene. These approaches will inform our understanding of the mechanisms of benzene toxicity and identify additional biomarkers of exposure, early effect and susceptibility useful for risk assessment.
Topics: Animals; Benzene; Hematopoietic Stem Cells; Humans; Leukemia; Risk Assessment; Systems Biology; Toxicogenetics
PubMed: 22166497
DOI: 10.1093/carcin/bgr297 -
Ecotoxicology and Environmental Safety Jan 2021Low benzene exposure leads to hematotoxicity, but we still lack sensitive early monitoring and early warning markers. Benzene is associated with inflammation, which is...
BACKGROUND
Low benzene exposure leads to hematotoxicity, but we still lack sensitive early monitoring and early warning markers. Benzene is associated with inflammation, which is mainly mediated by cytokines network. However, until now few studies have conducted high-throughput detection of multi-cytokines to get a global view of cytokine changes and screen for markers of benzene-induced toxicity. We hypothesized that cytokine profiles mediate benzene-induced hematotoxicity.
METHODS
228 subjects consisting of 114 low benzene exposed workers and 114 healthy controls were recruited at Research Center of Occupational Medicine, Peking University Third Hospital, Beijing. The serum concentrations of 27 cytokines were detected by cytokinomics array, urinary benzene series metabolites were measured by UPLC-MS/MS, and peripheral blood cell counts were observed by basic blood test.
RESULTS
Among 27 cytokines, IL-9 and MIP1-α were significantly lower, but IL-4, IL-10, IL-15, MCP-1, TNF-α and VEGF were significantly higher in benzene exposure group than controls. Urinary benzene metabolite S-phenylmercapturic acid (S-PMA) was significantly higher in benzene exposure group and had a negative linear relationship with WBC count. S-PMA was only significantly associated with IL-9, meanwhile IL-9, IL-15 and VEGF had a positive linear relationship with WBC count. The bootstrapping mediation models showed that the effect of S-PMA on WBC count was partially explained by IL-9 for 10.11%.
CONCLUSION
This study suggests that exposure to benzene was associated with alternation of blood cell count and cytokine profiles in workers exposed to low levels of benzene, especially decreases of WBC count and IL-9. We also found IL-9 partially mediated the effect of low benzene exposure on WBC count, which may be a potential and promising early monitoring and early warning marker of benzene hematotoxicity.
Topics: Acetylcysteine; Adult; Air Pollutants, Occupational; Asian People; Benzene; Biomarkers; Blood Cell Count; Chromatography, Liquid; Cross-Sectional Studies; Cytokines; Female; Humans; Leukocyte Count; Male; Middle Aged; Occupational Exposure; Tandem Mass Spectrometry
PubMed: 33254416
DOI: 10.1016/j.ecoenv.2020.111562 -
Angewandte Chemie (International Ed. in... May 2021The electrophotocatalytic heterofunctionalization of arenes is described. Using 2,3-dichloro-5,6-dicyanoquinone (DDQ) under a mild electrochemical potential with...
The electrophotocatalytic heterofunctionalization of arenes is described. Using 2,3-dichloro-5,6-dicyanoquinone (DDQ) under a mild electrochemical potential with visible-light irradiation, arenes undergo oxidant-free hydroxylation, alkoxylation, and amination with high chemoselectivity. In addition to batch reactions, an electrophotocatalytic recirculating flow process is demonstrated, enabling the conversion of benzene to phenol on a gram scale.
Topics: Benzene; Benzoquinones; Catalysis; Electrochemical Techniques; Light; Molecular Structure; Phenols
PubMed: 33661562
DOI: 10.1002/anie.202100222 -
Annals of Work Exposures and Health Oct 2019Occupational exposures in population-based case-control studies are increasingly being assessed using decision rules that link participants' responses to occupational... (Review)
Review
OBJECTIVES
Occupational exposures in population-based case-control studies are increasingly being assessed using decision rules that link participants' responses to occupational questionnaires to exposure estimates. We used a hierarchical process that incorporated decision rules and job-by-job expert review to assign occupational benzene exposure estimates in a US population-based case-control study of non-Hodgkin lymphoma.
METHODS
We conducted a literature review to identify scenarios in which occupational benzene exposure has occurred, which we grouped into 12 categories of benzene exposure sources. For each source category, we then developed decision rules for assessing probability (ordinal scale based on the likelihood of exposure > 0.02 ppm), frequency (proportion of work time exposed), and intensity of exposure (in ppm). The rules used the participants' occupational history responses and, for a subset of jobs, responses to job- and industry-specific modules. For probability and frequency, we used a hierarchical assignment procedure that prioritized subject-specific module information when available. Next, we derived job-group medians from the module responses to assign estimates to jobs with only occupational history responses. Last, we used job-by-job expert review to assign estimates when job-group medians were not available or when the decision rules identified possible heterogeneous or rare exposure scenarios. For intensity, we developed separate estimates for each benzene source category that were based on published measurement data whenever possible. Frequency and intensity annual source-specific estimates were assigned only for those jobs assigned ≥75% probability of exposure. Annual source-specific concentrations (intensity × frequency) were summed to obtain a total annual benzene concentration for each job.
RESULTS
Of the 8827 jobs reported by participants, 8% required expert review for one or more source categories. Overall, 287 (3.3%) jobs were assigned ≥75% probability of exposure from any benzene source category. The source categories most commonly assigned ≥75% probability of exposure were gasoline and degreasing. The median total annual benzene concentration among jobs assigned ≥75% probability was 0.11 ppm (interquartile range: 0.06-0.55). The highest source-specific median annual concentrations were observed for ink and printing (2.3 and 1.2 ppm, respectively).
CONCLUSIONS
The applied framework captures some subject-specific variability in work tasks, provides transparency to the exposure decision process, and facilitates future sensitivity analyses. The developed decision rules can be used as a starting point by other researchers to assess occupational benzene exposure in future population-based studies.
Topics: Benzene; Case-Control Studies; Decision Support Techniques; Humans; Lymphoma, Non-Hodgkin; Occupational Exposure; Occupations; Retrospective Studies; Risk Assessment; Surveys and Questionnaires
PubMed: 31504127
DOI: 10.1093/annweh/wxz063 -
Analytical and Bioanalytical Chemistry May 2007Surface-enhanced Raman spectroscopy (SERS) has developed into one of the most important tools in analytical and surface sciences since its discovery in the mid-1970s.... (Review)
Review
Surface-enhanced Raman spectroscopy (SERS) has developed into one of the most important tools in analytical and surface sciences since its discovery in the mid-1970s. Recent work on the SERS of transition metals concluded that transition metals, other than Cu, Ag, and Au, can also generate surface enhancement as high as 4 orders of magnitude. The present article gives an overview of recent progresses in the field of Raman spectroscopy on transition metals, including experimental, theory, and applications. Experimental considerations of how to optimize the experimental conditions and calculate the surface enhancement factor are discussed first, followed by a very brief introduction of preparation of SERS-active transition metal substrates, including massive transition metal surfaces, aluminum-supported transition metal electrodes, and pure transition metal nanoparticle assembled electrodes. The advantages of using SERS in investigating surface bonding and reaction are illustrated for the adsorption and reaction of benzene on Pt and Rh electrodes. The electromagnetic enhancement, mainly lightning-rod effect, plays an essential role in the SERS of transition metals, and that the charge-transfer effect is also operative in some specific metal-molecule systems. An outlook for the field of Raman spectroscopy of transition metals is given in the last section, including the preparation of well-ordered or well-defined nanostructures, and core-shell nanoparticles for investigating species with extremely weak SERS signals, as well as some new emerging techniques, including tip-enhanced Raman spectroscopy and an in situ measuring technique.
Topics: Adsorption; Benzene; Electrochemistry; Electrodes; Metal Nanoparticles; Surface Plasmon Resonance; Surface Properties; Transition Elements
PubMed: 17318524
DOI: 10.1007/s00216-007-1141-2 -
Environmental Health Perspectives Dec 1996The pathways of metabolism of benzene appear to be qualitatively similar in all species studied thus far. However, there are quantitative differences in the fraction of... (Comparative Study)
Comparative Study Review
The pathways of metabolism of benzene appear to be qualitatively similar in all species studied thus far. However, there are quantitative differences in the fraction of benzene metabolized by the different pathways. These species differences become important for risk assessments based on animal data. Mice have a greater overall capacity to metabolize benzene than rats or primates, based on mass balance studies conducted in vivo using radiolabled benzene. Mice and monkeys metabolize more of the benzene to hydroquinone metabolites than do rats or chimpanzees, especially at low doses. Nonhuman primates metabolize less of the benzene to muconic acid than do rodents or humans. In all species studied, a greater proportion of benzene is converted to hydroquinone and ring-breakage metabolites at low doses than at high doses. This finding should be considered in attempting to extrapolate the toxicity of benzene observed at high doses to predicted toxicity at low doses. Because ring-breakage metabolites and hydroquinone have both been implicated in the toxicity of benzene, the higher formation of those metabolites in the mouse may partially explain why mice are more sensitive to benzene than are rats. Metabolism of benzene in humans, the species of interest, does not exactly mimic that of any animal species studied. More information on the urinary and blood metabolites of occupationally exposed people is required to determine the fractional conversion of benzene to putative toxic metabolites and the degree of variability present in human subjects.
Topics: Animals; Benzene; Bone Marrow; Humans; Mice; Primates; Rats; Species Specificity; Tissue Distribution
PubMed: 9118889
DOI: 10.1289/ehp.961041173 -
Chemico-biological Interactions Mar 2010Toxicogenomic studies, including genome-wide analyses of susceptibility genes (genomics), gene expression (transcriptomics), protein expression (proteomics), and... (Review)
Review
Toxicogenomic studies, including genome-wide analyses of susceptibility genes (genomics), gene expression (transcriptomics), protein expression (proteomics), and epigenetic modifications (epigenomics), of human populations exposed to benzene are crucial to understanding gene-environment interactions, providing the ability to develop biomarkers of exposure, early effect and susceptibility. Comprehensive analysis of these toxicogenomic and epigenomic profiles by bioinformatics in the context of phenotypic endpoints, comprises systems biology, which has the potential to comprehensively define the mechanisms by which benzene causes leukemia. We have applied this approach to a molecular epidemiology study of workers exposed to benzene. Hematotoxicity, a significant decrease in almost all blood cell counts, was identified as a phenotypic effect of benzene that occurred even below 1 ppm benzene exposure. We found a significant decrease in the formation of progenitor colonies arising from bone marrow stem cells with increasing benzene exposure, showing that progenitor cells are more sensitive to the effects of benzene than mature blood cells, likely leading to the observed hematotoxicity. Analysis of transcriptomics by microarray in the peripheral blood mononuclear cells of exposed workers, identified genes and pathways (apoptosis, immune response, and inflammatory response) altered at high (>10 ppm) and low (<1 ppm) benzene levels. Serum proteomics by SELDI-TOF-MS revealed proteins consistently down-regulated in exposed workers. Preliminary epigenomics data showed effects of benzene on the DNA methylation of specific genes. Genomic screens for candidate genes involved in susceptibility to benzene toxicity are being undertaken in yeast, with subsequent confirmation by RNAi in human cells, to expand upon the findings from candidate gene analyses. Data on these and future biomarkers will be used to populate a large toxicogenomics database, to which we will apply bioinformatic approaches to understand the interactions among benzene toxicity, susceptibility genes, mRNA, and DNA methylation through a systems biology approach.
Topics: Benzene; Computational Biology; Epigenesis, Genetic; Hematopoietic System; Humans; Systems Biology; Toxicogenetics
PubMed: 20026094
DOI: 10.1016/j.cbi.2009.12.011