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Studies have shown that fluoridated reagents for oil and water resistance are harmful to the human bodies and the environment. Consequently, the developments of nontoxic, environmentally friendly, fluorine‐free and degradable materials have received increasing attentions. Here, we introduce a novel method for fabricating a hydrophobic and oleophobic paper‐based packaging material through the application of chitosan/carnauba wax emulsions. These emulsions were prepared via high‐shear homogenization, blending melted carnauba wax with chitosan in acetic acid aqueous solutions. The stable chitosan/carnauba wax emulsion with particle size of 430 nm was prepared at the chitosan concentration of 1.5 wt%, the carnauba wax concentration of 8 wt% and temperature of 85 °C. After 10 g/m2 of chitosan/carnauba wax emulsion was applied to the paper surface, the oil and water resistance of the paper was significantly improved. The experimental results of kit rating value, oil contact angle, Cobb60 value and water contact angle were 9.5 ± 0.6, 86.6 ± 2.1°, 8.90 ± 1.62 g/m2 and 123.5 ± 2.6°, respectively. The application of chitosan/carnauba wax emulsion coating on papers provided a significantly lower water vapour transmission rate (WVTR, 78.45 ± 18.92 g/m2·24 h) and oxygen transmission rate (OTR, 94.26 ± 20.21 g/m2·24 h) as compared to the original paper, which met the needs of strawberry packaging. [ABSTRACT FROM AUTHOR]

In marine applications, the scaled wind turbine model (SWTM) based aerodynamic testing apparatus is regarded as one of the most effective approaches to predict the aerodynamic performance of offshore floating wind turbines (OFWTs). To fully disclose the aerodynamics of OFWTs, such kind of apparatus should meet two design requirements: (1) accurate representation of the aerodynamic characteristics of reference wind turbines and (2) reasonable reproduction of the environmental factors from real-world wind-wave-coupled field. Baring with these considerations, the authors propose a cost-effective SWTM-based aerodynamic testing apparatus, which consists of an innovative SWTM, a wind-wave simulator (WWS) and a data acquisition and analyses system. The proposed SWTM is featured by a double-deck tower, which satisfies the requirements of similarity in geometry, stiffness and mass, and a set of redesigned blades. The proposed WWS is capable of simulating both the time-varying inflow wind and the wave-induced platform motions through a wind field generator and a motion simulator. Based on the developed apparatus, a series of aerodynamic tests are conducted to validate the effectiveness of the apparatus design. In addition, the coupling effects of inflow wind and platform motions on the aerodynamics of OFWT are further revealed through experimental tests. [ABSTRACT FROM AUTHOR]

Ionic conductors have great application prospects in the field of flexible electronics, but the widely used hydrogels and ionic gels suffer from water loss of hydrogels and leakage of ionic liquids, so all-solid-state ionic conductors are more adaptable to complex and variable environments. Nevertheless, material design solutions for all-solid-state ionic conductors that can balance mechanical strength and tensile properties and cohesion and adhesion simultaneously are still rare. The lack of excellent self-adhesive and mechanical properties will limit the applicability and stability of all-solid-state ionic conductors for various applications (e.g., in the field of self-adhesive flexible sensing). Therefore, based on the double-network strategy, the stretchable and self-adhesive poly(AA-CDC) type supramolecular deep eutectic polymer was selected as the first network and the rigid and adhesive lignin as the second network to synthesise high-strength, high-stretch and high-adhesive all-solid-state double-network ionic conductors (ADNICs). Among them, ADNICs are rich in polymer networks with dynamic hydrogen bonding and have extremely strong mechanical properties (tensile strength, strain at break and toughness of ADNIC-0.5 can reach 13.59 MPa, 1013% and 115.04 MJ m−3, respectively), and can instantly form various interfacial interactions with various substrates (adhesion strength reaches 5500 N m−1) and firmly adhere to various substrates. At the same time, the decrease in its adhesion strength is less than 15% after 5 cycles of separation-re-adhesion. In addition, it has strong self-healing properties (electrical self-healing efficiency up to 90% in 0.4 s at room temperature), good electrical conductivity (9.63 × 10−3 S m−1), and adequate transparency (∼85% in the visible range). Due to their ease of preparation and exceptional comprehensive performance, ADNICs would facilitate the exploration of utilizing all-solid-state ionic conductors in flexible electronic devices. [ABSTRACT FROM AUTHOR]

This paper investigates the payment scheme and forecast information sharing issues in the express delivery logistics with the high-speed railway. The HSR carriers need to coordinate the transportation capacity between passenger and freight. It is widely recognized that the advance payment scheme (APS) using as deposit is a beneficial way for the HSR carriers to make decisions on the transportation capacity preserved for express delivery. However, the express service providers, who possess private forecast information of express delivery demand, may share inaccurate information with the HSR carriers to acquire sufficient preserved transportation capacity. This paper discusses what payment scheme is preferred by the HSR carrier, the express service provider through discussing the deposit decisions with or without forecast information sharing. We show that sharing demand forecast information can reduce the prereserved capacity and increase the profits of the HSR carrier. With the delayed payment scheme (DPS), the express service provider has no motivation to share the information; while with the APS, the HSR carrier can reasonably choose the deposit to encourage the express service provider to share the demand information. Our analysis also shows that the HSR carrier's profits with the APS is restricted by the investment returns and the express service provider's information sharing decisions. We also analyze the value range of the deposit, which is a proportion of the overall payment, that allows both the HSR carrier and the express service provider to prefer the APS, as well as to encourage the express service provider to share the demand information. [ABSTRACT FROM AUTHOR]

Diesel engine exhaust (DEE) is an established lung carcinogen, but the biological mechanisms of diesel‐induced lung carcinogenesis are not well understood. MicroRNAs (miRNAs) are small noncoding RNAs that play a potentially important role in regulating gene expression related to lung cancer. We conducted a cross‐sectional molecular epidemiology study to evaluate whether serum levels of miRNAs are altered in healthy workers occupationally exposed to DEE compared to unexposed controls. We conducted a two‐stage study, first measuring 405 miRNAs in a pilot study of six DEE‐exposed workers exposed and six controls. In the second stage, 44 selected miRNAs were measured using the Fireplex circulating miRNA assay that profiles miRNAs directly from biofluids of 45 workers exposed to a range of DEE (Elemental Carbon (EC), median, range: 47.7, 6.1–79.7 μg/m3) and 46 controls. The relationship between exposure to DEE and EC with miRNA levels was analyzed using linear regression adjusted for potential confounders. Serum levels of four miRNAs were significantly lower (miR‐191‐5p, miR‐93‐5p, miR‐423‐3p, miR‐122‐5p) and one miRNA was significantly higher (miR‐92a‐3p) in DEE exposed workers compared to controls. Of these miRNAs, miR‐191‐5p (ptrend =.001, FDR = 0.04) and miR‐93‐5p (ptrend =.009, FDR = 0.18) showed evidence of an inverse exposure–response with increasing EC levels. Our findings suggest that occupational exposure to DEE may affect circulating miRNAs implicated in biological processes related to carcinogenesis, including immune function. [ABSTRACT FROM AUTHOR]

Objectives Diesel exhaust is an established human carcinogen, however the mechanisms by which it leads to cancer development are not fully understood. Mitochondrial dysfunction is an established contributor to carcinogenesis. Recent studies have improved our understanding of the role played by epigenetic modifications in the mitochondrial genome on tumorigenesis. In this study, we aim to evaluate the association between diesel engine exhaust (DEE) exposure with mitochondrial DNA (mtDNA) methylation levels in workers exposed to DEE. Methods The study population consisted of 53 male workers employed at a diesel engine manufacturing facility in Northern China who were routinely exposed to diesel exhaust in their occupational setting, as well as 55 unexposed male control workers from other unrelated factories in the same geographic area. Exposure to DEE, elemental carbon, organic carbon, and particulate matter (PM2.5) were assessed. mtDNA methylation for CpG sites (CpGs) from seven mitochondrial genes (D-Loop , MT-RNR1 , MT-CO2 , MT-CO3 , MT-ATP6 , MT-ATP8 , MT-ND5) was measured in blood samples. Linear regression models were used to estimate the associations between DEE, elemental carbon, organic carbon and PM2.5 exposures with mtDNA methylation levels, adjusting for potential confounders. Results DEE exposure was associated with decreased MT-ATP6 (difference = −35.6%, P -value = 0.019) and MT-ATP8 methylation (difference = −30%, P -value = 0.029) compared to unexposed controls. Exposures to elemental carbon, organic carbon, and PM2.5 were also significantly and inversely associated with methylation in MT-ATP6 and MT-ATP8 genes (all P -values < 0.05). Conclusions Our findings suggest that DEE exposure perturbs mtDNA methylation, which may be of importance for tumorigenesis. [ABSTRACT FROM AUTHOR]

The behavior of changing lanes has a great impact on road traffic with heavy traffic. Traffic flow density is one of the important parameters that characterize the characteristics of traffic flow, and it will also be affected by the behavior of changing lanes, especially in the case of each lane. The penetration of autonomous vehicles can effectively reduce lane-changing behavior. Studying the relationship between traffic flow density and lane-changing behavior under different autonomous vehicle penetration rates is of great significance for describing the operation mechanism of mixed traffic flow and the control of mixed traffic. In this article, we use empirical, simulation, and data-driven methods to analyze the urban expressway of autonomous vehicles with penetration rates of 10%, 20%, 30%, 40%, 50%, 60%, 70%, and 80%, respectively. A simulation experiment was carried out on the road, and data related to density, the rate of changing into the lanes, and the rate of changing out lanes were collected. The analysis of the experimental results found the following: (1) The increase in penetration of autonomous vehicles leads to a certain degree of downward trend in density, the rate of changing into the lanes, and the rate of changing out lanes. (2) Different lanes have different effects on the penetration of autonomous vehicles. In a 4-lane road, the two lanes farther from the entrance and exit are closer in appearance, while the two lanes closer to the entrance and exit are similar. (3) The relationship between density and the rate of changing into the lanes and the rate of changing out lanes shows a linear relationship with the penetration of autonomous vehicles. Although the performance of each lane is slightly different, in general, it can be carried out by a multiple regression model. The given parameter value range is relatively close under different permeability. In summary, autonomous vehicles effectively reduce the traffic density and lane-changing behavior of each lane. There is a linear relationship between traffic flow density and lane-changing behavior with the penetration of autonomous vehicles. The density-lane-changing behavior model proposed in this paper can better describe the relationship between the density of the circular multilane urban expressway and the lane-changing behavior in the case of a large traffic flow in mixed traffic. [ABSTRACT FROM AUTHOR]

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]

Urinary mutagenicity reflects systemic exposure to complex mixtures of genotoxic/carcinogenic agents and is linked to tumor development. Coal combustion emissions (CCE) and diesel engine exhaust (DEE) are associated with cancers of the lung and other sites, but their influence on urinary mutagenicity is unclear. We investigated associations between exposure to CCE or DEE and urinary mutagenicity. In two separate cross‐sectional studies of nonsmokers, organic extracts of urine were evaluated for mutagenicity levels using strain YG1041 in the Salmonella (Ames) mutagenicity assay. First, we compared levels among 10 female bituminous (smoky) coal users from Laibin, Xuanwei, China, and 10 female anthracite (smokeless) coal users. We estimated exposure–response relationships using indoor air concentrations of two carcinogens in CCE relevant to lung cancer, 5‐methylchrysene (5MC), and benzo[a]pyrene (B[a]P). Second, we compared levels among 20 highly exposed male diesel factory workers and 15 unexposed male controls; we evaluated exposure‐response relationships using elemental carbon (EC) as a DEE‐surrogate. Age‐adjusted linear regression was used to estimate associations. Laibin smoky coal users had significantly higher average urinary mutagenicity levels compared to smokeless coal users (28.4 ± 14.0 SD vs. 0.9 ± 2.8 SD rev/ml‐eq, p = 2 × 10−5) and a significant exposure‐response relationship with 5MC (p = 7 × 10−4). DEE‐exposed workers had significantly higher urinary mutagenicity levels compared to unexposed controls (13.0 ± 10.1 SD vs. 5.6 ± 4.4 SD rev/ml‐eq, p =.02) and a significant exposure‐response relationship with EC (p‐trend = 2 × 10−3). Exposure to CCE and DEE is associated with urinary mutagenicity, suggesting systemic exposure to mutagens, potentially contributing to cancer risk and development at various sites. [ABSTRACT FROM AUTHOR]

Carbon black (CB) particulates as virtually pure elemental carbon can deposit deep in the lungs of humans. International Agency for Research on Cancer classified CB as a Group 2B carcinogen due to inconclusive human evidence. A molecular epidemiological study was conducted in an established cohort of CB packers (CBP) to assess associations between CB exposure and genomic instability in peripheral lymphocytes using cytokinesis-block micronucleus assay (CBMN). Carbon content in airway macrophages (CCAM) was quantified as a bio-effective dosimeter for chronic CB exposure. Dose–response observed in CBPs was compared to that seen in workers exposed to diesel exhaust. The association between CB exposure status and CBMN endpoints was identified in 85 CBPs and 106 non-CBPs from a 2012 visit and replicated in 127 CBPs and 105 non-CBPs from a 2018 visit. The proportion of cytoplasm area occupied by carbon particles in airway macrophages was over fivefold higher in current CBPs compared to non-CBPs and was associated with CBMN endpoints in a dose-dependent manner. CB aerosol and diesel exhaust shared the same potency of inducing genomic instability in workers. Circulatory pro-inflammatory factors especially TNF-α was found to mediate associations between CB exposure and CBMN endpoints. In vitro functional validation supported the role of TNF-α in inducing genomic instability. An estimated range of lower limits of benchmark dose of 4.19–7.28% of CCAM was recommended for risk assessment. Chronic CB exposure increased genomic instability in human circulation and this provided novel evidence supporting its reclassification as a human carcinogen. [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]

The International Agency for Research on Cancer has classified diesel engine exhaust (DEE) as a human lung carcinogen. Given that inflammation is suspected to be an important underlying mechanism of lung carcinogenesis, we evaluated the relationship between DEE exposure and the inflammatory response using data from a cross‐sectional molecular epidemiology study of 41 diesel engine testing workers and 46 unexposed controls. Repeated personal exposure measurements of PM2.5 and other DEE constituents were taken for the diesel engine testing workers before blood collection. Serum levels of six inflammatory biomarkers including interleukin (IL)‐1, IL‐6, IL‐8, tumor necrosis factor (TNF)‐α, macrophage inflammatory protein (MIP)‐1β, and monocyte chemotactic protein (MCP)‐1 were analyzed in all subjects. Compared to unexposed controls, concentrations of MIP‐1β were significantly reduced by ∼37% in DEE exposed workers (P < 0.001) and showed a strong decreasing trend with increasing PM2.5 concentrations in all subjects (Ptrend < 0.001) as well as in exposed subjects only (Ptrend = 0.001). Levels of IL‐8 and MIP‐1β were significantly lower in workers in the highest exposure tertile of PM2.5 (>397 µg/m3) compared to unexposed controls. Further, significant inverse exposure‐response relationships for IL‐8 and MCP‐1 were also found in relation to increasing PM2.5 levels among the DEE exposed workers. Given that IL‐8, MIP‐1β, and MCP‐1 are chemokines that play important roles in recruitment of immunocompetent cells for immune defense and tumor cell clearance, the observed lower levels of these markers with increasing PM2.5 exposure may provide insight into the mechanism by which DEE promotes lung cancer. Environ. Mol. Mutagen. 59:144–150, 2018. © 2017 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

The relationship between diesel engine exhaust (DEE), a known lung carcinogen, and immune/inflammatory markers that have been prospectively associated with lung cancer risk is not well understood. To provide insight into these associations, we conducted a cross-sectional molecular epidemiology study of 54 males highly occupationally exposed to DEE and 55 unexposed male controls from representative workplaces in China. We measured plasma levels of 64 immune/ inflammatory markers in all subjects using Luminex bead-based assays, and compared our findings to those from a nested case-control study of these markers and lung cancer risk, which had been conducted among never-smoking women in Shanghai using the same multiplex panels. Levels of nine markers that were associated with lung cancer risk in the Shanghai study were altered in DEE-exposed workers in the same direction as the lung cancer associations. Among these, associations with the levels of CRP (β= −0.53; P = 0.01) and CCL15/MIP-1D (β = 0.20; P = 0.02) were observed in workers exposed to DEE and with increasing elemental carbon exposure levels (Ptrends <0.05) in multivariable linear regression models. Levels of a third marker positively associated with an increased lung cancer risk, CCL2/MCP-1, were higher among DEE-exposed workers compared with controls in never and former smokers, but not in current smokers (Pinteraction = 0.01). The immunological differences in these markers in DEE-exposed workers are consistent with associations observed for lung cancer risk in a prospective study of Chinese women and may provide some insight into the mechanistic processes by which DEE causes lung cancer. [ABSTRACT FROM AUTHOR]

The International Agency for Research on Cancer has classified carbon black (CB) as a possible (Group 2B) human carcinogen. Given that most CB manufacturing processes result in the emission of various types of chemicals, it is uncertain if the adverse health effects that have been observed in CB-exposed workers are related to CB specifically or are due to other exposures. To address this issue, we conducted a cross-sectional molecular epidemiology study in China of 106 male factory workers who were occupationally exposed to pure CB and 112 unexposed male workers frequency-matched by age and smoking status from the same geographic region. Repeated personal exposure measurements were taken in workers before biological sample collection. Peripheral blood from all workers was used for the complete blood cell count and lymphocyte subsets analysis. Compared to unexposed workers, eosinophil counts in workers exposed to CB were increased by 30.8% ( P = 0.07) after adjusting for potential confounders. When stratified by smoking status, statistically significant differences in eosinophils between CB exposed and unexposed workers were only present among never smokers ( P = 0.040). Smoking is associated with alterations in various cell counts; however, no significant interaction between CB exposure and smoking status for any cell counts was observed. Given that inflammation, characterized in part by elevated eosinophils in peripheral blood, may be associated with increased cancer risk, our findings provide new biologic insights into the potential relationship between CB exposure and lung carcinogenesis. Environ. Mol. Mutagen. 57:589-604, 2016. © 2016 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Recently, diesel engine exhaust (DEE) was reclassified as a known carcinogen to humans. DNA methylation alterations in DNA damage response (DDR)-related genes have the potential to affect DEE exposure-related cancer risk. However, the evidence regarding the association between DEE exposure and methylation alterations in DDR-related genes is limited. In 117 DEE-exposed workers and 112 non-DEE-exposed workers, we measured urinary concentrations of six mono-hydroxylated polycyclic aromatic hydrocarbons (OH-PAHs). We also determined the methylation levels of three DDR-related genes (p16, RASSF1A, and MGMT) and LINE-1 by bisulfite-pyrosequencing assay. We found that DEE-exposed workers exhibited significantly lower mean promoter methylation levels of p16, RASSF1A, and MGMT than non-DEE-exposed workers (all p < 0.001). In all study subjects and non-smoking workers, increasing quartiles of urinary summed OH-PAHs was associated with hypomethylation of p16, RASSF1A, and MGMT (all p < 0.05). In non-smoking workers, methylation in p16, RASSF1A, and MGMT decreased by 0.36 % [95 % confidential interval (CI): −0.60, −0.11 %], 0.46 % (95 % CI: −0.79, −0.14 %), and 0.55 % (95 % CI: −0.95, −0.15 %), respectively, in association with highest versus lowest quartile of urinary summed OH-PAHs. In addition, p16, RASSF1A, MGMT, and LINE-1 methylation levels showed negative correlations with cytokinesis-block micronucleus cytome index which was previously measured in the same workers (all p < 0.05). In conclusion, our results clearly indicated that DEE exposure and increased genetic damage were associated with hypomethylation of p16, RASSF1A, and MGMT. Future studies with larger sample size are needed to confirm these associations. [ABSTRACT FROM AUTHOR]

Diesel engine exhaust (DEE), a ubiquitous environmental pollutant, has been associated with adverse health effects. Revelation of cellular and molecular changes is critical for understanding environmental exposure-related diseases. Although the molecular-level effects of DEE exposure have been investigated, whether it is associated with aberrant changes at cellular level is largely unknown at the population level. In the present study, we measured urinary concentrations of 6 mono-hydroxylated PAHs (OH-PAHs) and cytotoxicity-related endpoints including apoptosis and necrosis frequencies, and nuclear division cytotoxicity index (NDCI) in peripheral blood lymphocytes (PBLs) of 79 DEE-exposed workers and 59 non-DEE-exposed workers. We found that DEE-exposed workers had significantly higher necrosis frequency and lower NDCI than did non-DEE-exposed workers (bothp < 0.001). In all study subjects and nonsmoking workers, urinary summed OH-PAHs was associated with increased necrosis frequency and reduced NDCI. In nonsmoking workers, an interquartile range increase in urinary summed OH-PAHs was associated with 105.03% increase in necrosis frequency and 8.70% decrease in NDCI. Taking advantage of the previous measure of micronucleus frequency, we observed that micronucleus frequency was positively correlated with apoptosis and necrosis frequencies (r = 0.277,p = 0.047 andr = 0.452,p = 0.001, respectively) and negatively correlated with NDCI (r = −0.477,p < 0.001). In conclusion, our results suggested that DEE exposure was associated with increased necrosis frequency and further with reduced NDCI in PBLs, providing evidence of DEE exposure-induced cytotoxicity in humans. [ABSTRACT FROM PUBLISHER]

Diesel engine exhaust (DEE) is a predominant contributor to urban air pollution. The International Agency for Research on Cancer classified DEE as a group I carcinogen. Inflammatory response is considered to be associated with various health outcomes including carcinogenesis. However, human data linking inflammation with long-term DEE exposure are still lacking. In this study, a total of 137 diesel engine testing workers with an average exposure of 8.2 years and 108 unexposed controls were enrolled. Peripheral blood samples were collected from all subjects, and the association of DEE exposure with inflammatory biomarkers was analyzed. Overall, DEE exposed workers had a significant increase in the C-reactive protein (CRP) and a significant decrease in cytokines including interleukin (IL)-1β, IL-6, IL-8, and macrophage inflammatory protein (MIP)-1β compared to controls after adjusting for age, BMI, smoking status, and alcohol use, and findings were highly consistent when stratified by smoking status. In addition, exposure time dependent patterns for IL-6 and CRP were also found (Ptrend = 0.006 and 0.026, respectively); however, the levels of IL-1β and MIP-1β were significantly lower in subjects with a DEE working time of less than 10 years compared with the controls and then recovered to control levels in workers exposed for >10 years. There were no significant differences in blood cell counts and major lymphocyte subsets between exposed workers and the controls. Our results provide epidemiological evidence for the relationship between DEE exposure and immunotoxicity considering the important roles of cytokines in immunological processes. [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]

The International Agency for Research on Cancer has recently reclassified diesel engine exhaust (DEE) as a Group 1 carcinogen. Micronucleus (MN), nucleoplasmic bridge (NPB), and nuclear bud (NBUD) frequencies in peripheral blood lymphocytes (PBLs) are associated with cancer risk. However, the impact of DEE exposure on MN frequency has not been thoroughly elucidated due to mixed exposure and its impact on NPB and NBUD frequencies has never been explored in humans. We recruited 117 diesel engine testing workers with exclusive exposure to DEE and 112 non-DEE-exposed workers, and then we measured urinary levels of 4 mono-hydroxylated polycyclic aromatic hydrocarbons (OH-PAHs) using high-performance liquid chromatography-mass spectrometry as well as MN, NPB, and NBUD frequencies in PBLs using cytokinesis-block MN assay. The DEE-exposed workers exhibited significantly higher MN, NPB, and NBUD frequencies than the non-DEE-exposed workers (P < 0.05). Among all study subjects, increasing levels of all 4 urinary OH-PAHs, on both quartile and continuous scales, were associated with increased MN, NPB, and NBUD frequencies (all P < 0.05). When the associations were analyzed separately in DEE-exposed and non-DEE-exposed workers, we found that the association between increasing quartiles of urinary 9-hydroxyphenanthrene (9-OHPh) and MN frequencies persisted in DEE-exposed workers (P = 0.001). The percent of MN frequencies increased, on average, by 23.99% (95% confidential interval, 9.64–39.93) per 1-unit increase in ln-transformed 9-OHPh. Our results clearly show that exposure to DEE can induce increases in MN, NPB, and NBUD frequencies in PBLs and suggest that DEE exposure level is associated with MN frequencies. [ABSTRACT FROM AUTHOR]

Formaldehyde (FA) is a well-known irritant, and it is suggested to increase the risk of immune diseases and cancer. The present study aimed to evaluate the distribution of major lymphocyte subsets and cytokine expression profiles in the peripheral blood of FA-exposed workers. A total of 118 FA-exposed workers and 79 controls were enrolled in the study. High performance liquid chromatography, flow cytometry, and cytometric bead array were used to analyze FA in air sample and formic acid in urine, blood lymphocyte subpopulations, and serum cytokines, respectively. The FA-exposed workers were divided into low and high exposure groups according to their exposure levels. The results showed that both the low and high FA-exposed groups had a significant increase of formic acid in urine when compared to the controls. Both the low and high exposure groups had a significant increase in the percentage of B cells (CD19+) compared to the control group (p<0.01). A significant increase in the percentage of the natural killer (NK) cells (CD56+) was observed in the low exposure group compared to the control (p = 0.013). Moreover, the FA-exposed workers in both exposure groups showed a significant higher level of IL-10 but lower level of IL-8 than the control (p<0.01). Subjects in the high exposure group had a higher level of IL-4 but a lower level of IFN-γ than the control (p<0.05). Finally, there is a significant correlation between the levels of IL-10, IL-4, and IL-8 and formic acid (p<0.05). The findings from the present study may explain, at least in part, the association between FA exposure and immune diseases and cancer. [ABSTRACT FROM AUTHOR]

Global hypomethylation, gene-specific methylation, and genome instability are common events in tumorigenesis. To date, few studies have examined the aberrant DNA methylation patterns in coke oven workers, who are highly at risk of lung cancer by occupational exposure to polycyclic aromatic hydrocarbons (PAHs). We recruited 82 PAH-exposed workers and 62 unexposed controls, assessed exposure levels by urinary 1-hydroxypyrene, and measured genetic damages by comet assay, bleomycin sensitivity, and micronucleus assay. The PAHs in coke oven emissions (COE) were estimated based on toxic equivalency factors. We used bisulfite-PCR pyrosequencing to quantitate DNA methylation in long interspersed nuclear element-1 (LINE-1) and O-methylguanine-DNA methyltransferase (MGMT). Further, the methylation alteration was also investigated in COE-treated human bronchial epithelial (16HBE) cells. We found there are higher levels of PAHs in COE. Among PAH-exposed workers, LINE-1 and MGMT methylation levels (with CpG site specificity) were significantly lowered. LINE-1, MGMT, and its hot CpG site-specific methylation were negatively correlated with urinary 1-hydroxypyrene levels ( r = −0.329, p < 0.001; r = −0.164, p = 0.049 and r = −0.176, p = 0.034, respectively). In addition, LINE-1 methylation was inversely associated with comet tail moment and micronucleus frequency, and a significant increase of micronucleus in low MGMT methylation group. In vitro study revealed that treatment of COE in 16HBE cells resulted in higher production of BPDE-DNA adducts, LINE-1 hypomethylation, hypomethylation, and suppression of MGMT expression. These findings suggest hypomethylation of LINE-1 and MGMT promoter could be used as markers for PAHs exposure and merit further investigation. [ABSTRACT FROM AUTHOR]

Identification of aberrant microRNA (miRNA) expression during chemical carcinogen–induced cell transformation will lead to a better understanding of the substantial role of miRNAs in cancer development. To explore whether aberrant miRNAs expression can be used as biomarkers of chemical exposure in risk assessment of chemical carcinogenesis, we analyzed miRNA expression profiles of human bronchial epithelial cells expressing an oncogenic allele of H-Ras (HBER) at different stages of transformation induced by benzo(a)pyrene (BaP) by miRNA array. It revealed 12 miRNAs differentially expressed in HBER cells at both pretransformed and transformed stages. Differentially expressed miRNAs were confirmed in transformed cells and examined in 50 pairs of primary human non–small-cell lung cancer (NSCLC) tissues using real-time PCR. Among these miRNAs, downregulation of miR-638 was found in 68% (34/50) of NSCLC tissues. However, the expression of miR-638 in HBER cells increased upon treatment of BaP in a dose-dependent manner. The expression of miR-638 was also examined in peripheral lymphocytes from 86 polycyclic aromatic hydrocarbons (PAHs)-exposed (PE) workers. We found that the average expression level of miR-638 in peripheral lymphocytes from 86 PE workers increased by 72% compared with control group. The levels of miR-638 were correlated with the concentration of urinary 1-hydroxypyrene (1-OHP) and external levels of PAHs. Overexpression of miR-638 aggravated cell DNA damage induced by BaP, which might be mediated by suppression of breast cancer 1 (BRCA1), one of the target genes of miR-638. In summary, we suggest that miR-638 is involved in the BaP-induced carcinogenesis by targeting BRCA1. [ABSTRACT FROM PUBLISHER]

The purpose of this study was to address the association between the ataxia telangiectasia mutated (ATM) gene polymorphisms and susceptibility to DNA repair capacity (DRC) among polycyclic aromatic hydrocarbons (PAHs)–exposed workers. Polymorphisms of ATM were genotyped. DRC was determined by comet assay. Chromosomal damage was detected by cytokinesis-block micronucleus (CBMN) assay. Flow cytometry was used to detect the distributions of cell cycle. Expressions of ATM and rH2AX were determined by immunoblotting analysis. Luciferase assays were performed to determine the functional difference of ATM promoter region allele. Subjects carrying T allele of rs228589 had significantly lower DRC compared with those with AA genotype. Subjects carrying G allele of rs652311 had significantly lower DRC than those with zero copy number of haplotype CGGT. SH ataxia telangiectasia mutated (SHATM) cells had significantly lower DRC than SH green fluorescent protein (SHGFP) cells induced by bleomycin and higher CBMN frequencies treated by benzo(a)pyrene [B(a)P] than SHGFP cells. After B(a)P treatment, a decrease in the percentage of G1 phase cells was observed in SHATM cells compared with SHGFP cells, rH2AX expressions were increased in SHATM cells and SHGFP cells, but ATM expressions had no change in 16HBE-SHGFP cells and HEK-SHGFP cells. Luciferase expression was not different between rs228589T and rs228589A plasmid constructs. In conclusions, it is suggested that ATM polymorphisms are associated with DRC among PAHs-exposed workers and ATM plays key roles in repair of chromosomal damage and cell cycle control with the treatment of B(a)P. [ABSTRACT FROM AUTHOR]

The Froude-scaled offshore floating wind turbine model is inevitably affected by the Reynolds number effect, making the model unable to correctly reproduce the thrust performance of the reference wind turbine (RWT). To solve this problem, an Xfoil-AirfoilPrep-Matlab (XAM) system and a wide tip speed ratio search method (WTSM) are proposed to design a wide tip speed ratio (TSR) thrust-match model blade. The XAM system is utilized to select the best airfoil for WTSM by calculating the lift and drag coefficients of several airfoils. The WTSM is utilized to optimize the blade chord and twist. It formalizes the blade chord and twist by polynomials and then optimizes the polynomial coefficients. The thrust coefficients construct the optimization object at different TSRs. For validating the effect of the redesigned blade, the thrust performance is compared to that of the RWT blade. In addition, the thrust performance of redesigned blade at different pitch angles is also calculated and compared to those of the RWT blade. Results show that the thrust performance of redesigned blade matches well with that of the RWT blade at 0 pitch angle, and it can also match the variations of that of the RWT blade at the other pitch angles well. [ABSTRACT FROM AUTHOR]

In the natural marine environment, offshore floating wind turbines (OFWTs) inevitably experience yawed inflow conditions, which will make their aerodynamics more complicated than those experiencing uniform inflow conditions and difficult to understand. In the present study, the thrust characteristics of a wake-influenced OFWT under dynamic, static, and coupled yawed inflow conditions are investigated thoroughly. Analytical characterizations of yawed inflow and upstream wake are integrated into the blade element momentum (BEM) method to achieve the investigation. Based on this method, simulations by the FAST code have been conducted, and the results are analyzed. It is shown that the three inflow conditions have considerable influences on the thrust coefficient of the wind rotor or the normal force at the blade section, especially in the wake case where the downstream OFWT is located at a specific offset from the central line of a single upstream wake. In order to validate the analyses of simulation results, experimental tests by a set of dedicated apparatus are conducted. The comparison results are good, proving the reliability of simulation results. This work can provide some theoretical contributions to the aerodynamic design and control of OFWTs. [ABSTRACT FROM AUTHOR]

Duan, H.-W.; Ma, C.-S., and Ding, X.-D., 2019. Profit calculation and allocation for rail-sea intermodal transportation alliance in port. In: Gong, D.; Zhu, H., and Liu, R. (eds.), Selected Topics in Coastal Research: Engineering, Industry, Economy, and Sustainable Development. Journal of Coastal Research, Special Issue No. 94, pp. 385–391. Coconut Creek (Florida), ISSN 0749-0208. In order to promote the alliance of railway and marine transport enterprises in port and ensure the alliance stability, the alliance profit calculation model and allocation scheme is studied. Firstly, the essence of the alliance is analyzed. Secondly, the pricing game models of different alliance structures are established and solved to get the alliance profit. Thirdly, the alliance profit is allocated by Myerson value method. Then the allocation scheme is adjusted considering the difference of the resources invested by the alliance members. Finally, numerical example is contructed to verify the validity of the profit calculation model and allocation scheme. Following conclusions are drawn. The more enterprises to participate in the alliance, the more favorable to the customer and the port. Alliance profit is related to the number of enterprises participating in the alliance, but is not related to the nature of the participation. The smaller transportation cost, the greater the alliance profit. It is feasible to allocate the alliance profit in an effective and fair manner based on Myerson value method, but adjustments are necessary to express the influence exerted by resource inputs. [ABSTRACT FROM AUTHOR]

Trichloroethylene induced hypersensitivity syndrome is dose-independent and potentially life threatening disease, which has become one of the serious occupational health issues and requires intensive treatment. To discover the genetic risk factors and evaluate the performance of risk prediction model for the disease, we conducted genomewide association study and replication study with total of 174 cases and 1761 trichloroethylene-tolerant controls. Fifty seven SNPs that exceeded the threshold for genome-wide significance (P < 5 × 10−8) were screened to relate with the disease, among which two independent SNPs were identified, that is rs2857281 at MICA (odds ratio, 11.92; Pmeta = 1.33 × 10−37) and rs2523557 between HLA-B and MICA (odds ratio, 7.33; Pmeta = 8.79 × 10−35). The genetic risk score with these two SNPs explains at least 20.9% of the disease variance and up to 32.5-fold variation in inter-individual risk. Combining of two SNPs as predictors for the disease would have accuracy of 80.73%, the area under receiver operator characteristic curves (AUC) scores was 0.82 with sensitivity of 74% and specificity of 85%, which was considered to have excellent discrimination for the disease, and could be considered for translational application for screening employees before exposure. [ABSTRACT FROM AUTHOR]