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In order to make photocuring ink or coating cured by UV-LED illuminant, we synthesized (4-((hexahydropyrrolo[1,2-a]pyrimidin-1 (2H)-yl)methyl)phenyl)(phenyl)methanone(PL -DBN) and (4-((octahydropyrimido[1,2-a]azepin-1(2H)-yl)methyl)phenyl)(phenyl)met hanone(PL -DBU) as photoinitiators. Different mass fraction of the photoinitiators was mixed with bisphenol A epoxy acrylate, cured by different wavelengths and power of UV-LED illuminant,and investigated the curing effects of photoinitiators on bisphenol A epoxy acrylate. The results show that the conversion of C=C double bonds of bisphenol A epoxy acrylate will increase as the mass fraction of the photoinitiators or the power of UV-LED illuminant increase. In the same conditions, the curing effect of using 365nm UV-LED illuminant on bisphenol A epoxy acrylate is better than using 395nm UV-LED illuminant. PL-DBU has a better curing effect on the bisphenol A epoxy acrylate rather than PL-DBN. When using the 8W/cm2 of 365nm UV-LED illuminant to cure a mixture of 3% PL-DBU and 97% bisphenol A epoxy acrylate, it will be dry completely in 2 seconds, moreover, the conversion reach 79%.

BACKGROUND: Trichloroethylene (TCE) is used extensively as an industrial solvent and has been recognized as one of the major environmental pollutants. To date, > 200 cases of TCE-induced hypersensitivity dermatitis among exposed workers have been reported worldwide, and TCE exposure has become one of the critical occupational health issues in Asia. OBJECTIVES: The study aimed to identify genetic susceptible biomarkers associated with the TCE-induced hypersensitivity dermatitis in genes located in the human leukocyte antigen (HLA) region. METHODS: From 1998 to 2006, 121 cases with TCE-induced hypersensitivity dermatitis and 142 tolerant controls were recruited into the population-based case-control study. We determined HLA alleles B, DRB1, DQA1, and DQB1, by sequence-based typing. p-Values were corrected for comparisons of multiple HLA alleles. In addition, we compared and analyzed the structure character of amino acid residues of HLA molecules found in participants. RESULTS: We obtained complete genotyping data of 113 cases and 142 controls. The allele HLA-B*1301 was present in 83 (73.5%) of 113 patients compared with 13 (9.2%) of 142 tolerant workers (odds ratio = 27.5; 95% confidence interval, 13.5-55.7; corrected p = 1.48 X [10.sup.-21]). In addition, the HLA-B*44 alleles were present in 6.2% (7/113) of patients, but were absent in TCE-tolerant workers. Residue 95 shared by HLA-B*1301 and HLA-B*44 molecules formed a different pocket F than other residues. CONCLUSIONS: The allele HLA-B*1301 is strongly associated with TCE-induced hypersensitivity dermatitis among exposed workers and might be used as a biomarker to predict high risk individuals to TCE. KEY WORDS: biomarkers, genetic polymorphism, human leukocyte antigen, hypersensitivity dermatitis, trichloroethylene. Environ Health Perspect 115:1553-1556 (2007). doi:10.1289/ehp.10325 available via http://dx.doi.org/ [Online 24 August 2007], Trichloroethylene (TCE) is known as a major pollutant that affects both the occupational and general environment. It has been used as an industrial degreasing agent, solvent, and extraction agent for [...]

Diesel engine exhaust (DEE) is classified as a Group 1 human carcinogen. Using a targeted proteomics approach, we aimed to identify proteins associated with DEE and characterize these markers to understand the mechanisms of DEE‐induced carcinogenicity. In this cross‐sectional molecular epidemiology study, we measured elemental carbon (EC) using a personal air monitor and quantified 1317 targeted proteins in the serum using the SOMAScan assay (SOMALogic) among 19 diesel exposed factory workers and 19 unexposed controls. We used linear regressions to identify proteins associated with DEE and examined their exposure‐response relationship across levels of EC using linear trend tests. We further examined pathway enrichment of DEE‐related proteins using MetaCore. Occupational exposure to DEE was associated with altered levels of 22 serum proteins (permutation p <.01). Of these, 13 proteins (CXCL11, HAPLN1, FLT4, CD40LG, PES1, IGHE.IGK..IGL, TNFSF9, PGD, NAGK, CCL25, CCL4L1, PDXK, and PLA2G1B) showed an exposure‐response relationship with EC (p trend <.01), with serum levels of all but PLA2G1B declining with increasing air levels of EC. For instance, C‐X‐C Motif Chemokine Ligand 11 (CXCL11) showed the most significant association with DEE (β = −0.25; permutation p =.00004), where mean serum levels were 4121.1, 2356.7, and 2298.8 relative fluorescent units among the unexposed, lower exposed (median, range : 56.9, 40.2–62.1 μg/m3 EC), and higher exposed (median, range of EC: 72.9, 66.9–107.7 μg/m3 EC) groups, respectively (p trend =.0005). Pathway analysis suggested that these proteins are enriched in pathways related to inflammation and immune regulation. Our study suggests that DEE exposure is associated with altered serum proteins, which play a role in inflammation and immune regulation. [ABSTRACT FROM AUTHOR]

Diesel exhaust (DE) as the major source of vehicle-emitted particle matter in ambient air impairs lung function. The objectives were to assess the contribution of local (eg, the fraction of exhaled nitric oxide [FeNO] and serum Club cell secretory protein [CC16]) and systemic (eg, serum C-reaction protein [CRP] and interleukin-6 [IL-6]) inflammation to DE-induced lung function impairment using a unique cohort of diesel engine testers (DETs, n=137) and non-DETs (n=127), made up of current and noncurrent smokers. Urinary metabolites, FeNO, serum markers, and spirometry were assessed. A 19% reduction in CC16 and a 94% increase in CRP were identified in DETs compared with non-DETs (all p values <10-4), which were further corroborated by showing a dose-response relationship with internal dose for DE exposure (all p values <.04) and a time-course relationship with DE exposure history (all p values <.005). Mediation analysis showed that 43% of the difference in FEV1 between DETs and non-DETs can be explained by circulating CC16 and CRP (permuted p<.001). An inverse dose-dependent relationship between FeNO and internal dose for cigarette smoke was identified (p=.0003). A range of 95% lower bounds of benchmark dose of 1.0261-1.4513 μg phenanthrols/g creatinine in urine as an internal dose was recommended for regulatory risk assessment. Local and systemic inflammation may be key processes that contribute to the subsequent development of obstructive lung disease in DE-exposed populations. [ABSTRACT FROM AUTHOR]

Antimony (Sb) poses a significant threat to human health due to sharp increases in its exploitation and application globally, but few studies have explored the pathophysiological mechanisms of acute hepatotoxicity induced by Sb exposure. We established an in vivo model to comprehensively explore the endogenous mechanisms underlying liver injury induced by short-term Sb exposure. Adult female and male Sprague-Dawley rats were orally administrated various concentrations of potassium antimony tartrate for 28 days. After exposure, the serum Sb concentration, liver-to-body weight ratio, and serum glucose levels significantly increased in a dose-dependent manner. Body weight gain and serum concentrations of biomarkers of hepatic injury (e.g., total cholesterol, total protein, alkaline phosphatase, and the aspartate aminotransferase/alanine aminotransferase ratio) decreased with increasing Sb exposure. Through integrative non-targeted metabolome and lipidome analyses, alanine, aspartate, and glutamate metabolism; phosphatidylcholines; sphingomyelins; and phosphatidylinositols were the most significantly affected pathways in female and male rats exposed to Sb. Additionally, correlation analysis showed that the concentrations of certain metabolites and lipids (e.g., deoxycholic acid, N-methylproline, palmitoylcarnitine, glycerophospholipids, sphingomyelins, and glycerol) were significantly associated with hepatic injury biomarkers, indicating that metabolic remodeling may be involved in apical hepatotoxicity. Our study demonstrated that short-term exposure to Sb induces hepatotoxicity, possibly through a glycolipid metabolism disorder, providing an important reference for the health risks of Sb pollution. Adult female and male Sprague-Dawley rats were orally administrated various concentrations of potassium antimony tartrate for 28 days. After antimony (Sb) exposure, the alanine, aspartate, and glutamate metabolism; glycine, serine, and threonine metabolism; phosphatidylcholines; phosphatidylethanolakines; phosphatidylinositols and sphingomyelins pathways were significantly affected in both female and male rats. And the liver-to-body ratio, and serum glucose concentration significantly increased in a dose-dependent manner. Body weight gain and serum concentrantions of biomarkers of hepatic injury (e.g. alkaline phosphatase, and the aspartate aminotransferase/alanine aminotransferase ratio) decreased with increasing Sb exposure. Short-term exposure to Sb induced hepatotoxicity, possibly through disturbances in glucolipid metabolism. [Display omitted] • Short-term exposure to Sb induced hepatotoxicity and serum glucose increased in female and male rats. • The most significantly affected pathways induced by Sb were alanine, aspartate, and glutamate metabolism and PCs in rats. • Sb exposure caused hepatotoxicity possibly through changes of metabolites and lipids. [ABSTRACT FROM AUTHOR]

Objectives: Diesel engine exhaust (DEE) is a ubiquitous environmental pollutant and is carcinogenic to humans. To seek early and sensitive biomarkers for prediction of adverse health effects, we analysed the components of DEE particles, and examined the genetic and oxidative damages in DEE-exposed workers.Methods: 101 male diesel engine testing workers who were constantly exposed to DEE and 106 matched controls were enrolled in the present study. The components of DEE were analysed, including fine particulate matter (PM2.5), element carbon (EC), nitrogen dioxide (NO2), sulfur dioxide (SO2) and polycyclic aromatic hydrocarbons (PAHs). Postshift urine samples were collected and analysed for 1-hydroxypyrene (1-OHP), an internal exposure marker for DEE. Levels of DNA strand breaks and oxidised purines, defined as formamidopyrimidine-DNA glycosylase (FPG) sites in leucocytes, were measured by medium throughput Comet assay. Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) was also used to determine the level of oxidative stress.Results: We found higher levels of PM2.5, EC, NO2, SO2 and PAHs in the diesel engine testing workshop and significantly higher urinary 1-OHP concentrations in exposed subjects (p<0.001). Compared with controls, the levels of parameters in normal Comet and FPG-Comet assay were all significantly higher in DEE-exposed workers (p<0.001), and in a dose-dependent and time-dependent manner. There were no significant differences between DEE-exposed workers and controls in regard to leucocyte FPG sensitive sites and urinary 8-OHdG levels.Conclusions: These findings suggest that DEE exposure mainly induces DNA damage, which might be used as an early biomarker for risk assessment of DEE exposure. [ABSTRACT FROM AUTHOR]