Two new species of the genus Microplitis Förster, 1862 (Hymenoptera, Braconidae, Microgastrinae) from China.

Two new species of Microplitis Förster, 1862, M.bomiensis Zhang, sp. nov., and M.paizhensis Zhang, sp. nov. from Tibet, China are described and illustrated. A key to the species of the genus Microplitis Förster from China is added.

Co-exposure to metals and polycyclic aromatic hydrocarbons, microRNA expression, and early health damage in coke oven workers.

BACKGROUND: All humans are now co-exposed to multiple toxic chemicals, among which metals and polycyclic aromatic hydrocarbons (PAHs) are of special concern as they are often present at high levels in various human environments. They can also induce similar early health damage, such as genetic damage, oxidative stress, and heart rate variability (HRV). Exposure to metals, PAHs, and their combined pollutants can alter microRNA (miRNA) expression patterns. OBJECTIVES: To explore the associations of metal-PAH co-exposure with miRNA expression, and of the associated miRNAs with early health damage. METHODS: We enrolled 360 healthy male coke oven workers and quantified their exposure levels of metals and PAHs by urinary metals, urinary monohydroxy-PAHs (OH-PAHs), and plasma benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts, respectively. We selected and measured ten miRNAs: let-7b-5p, miR-126-3p, miR-142-5p, miR-150-5p, miR-16-5p, miR-24-3p, miR-27a-3p, miR-28-5p, miR-320b, and miR-451a. For miRNAs influenced by the effect modification of metals or PAHs and/or metal-PAH interactions, we further evaluated their associations with biomarkers for genetic damage, oxidative stress, and HRV. RESULTS: After adjusting for PAHs and other metals, miRNA expression was found to be negatively associated with aluminum, antimony, lead, and titanium, and positively associated with molybdenum and tin (p < 0.05). Antimony showed modifying effects on the PAH-miRNA associations, while OH-PAHs and BPDE-Alb adducts modified the associations of metals with miRNAs (p for modifying effect < 0.05). Furthermore, miRNA expression was influenced by the antagonistic interactions between antimony and OH-PAHs, and by the synergistical interactions between metals and BPDE-Alb adducts (pinteraction < 0.05). Let-7b-5p, miR-126-3p, miR-16-5p, and miR-320b were additionally found to be associated with increased genetic damage in the present study [false discovery rate (FDR)-adjusted p < 0.05]. CONCLUSIONS: Associations of metal-PAH co-exposure with miRNA expression, and of associated miRNAs with early health damage, suggested potential mechanistic connections between the complex metal-PAH interactions and their deleterious effects that are worthy of further investigation.

Revision of Microplitis species from China with description of a new species.

Microplitis bicoloratus Chen 2004 is a synonym of Microplitis prodeniae Rao & Kurian 1950, and is also the junior homonym of Microplitis bicoloratus Xu & He 2003. A new species, Microplitis fujianica sp. nov. is described and illustrated. The new species is compared with its related species from the Oriental region.

Polycyclic aromatic hydrocarbons exposure and lung function decline among coke-oven workers: A four-year follow-up study.

OBJECTIVES: This study aimed to investigate quantitative relationships of urinary PAH metabolites with lung function declines among coke-oven workers. METHODS: We performed a prospective investigation involving 1243 workers with follow-up periods from 2010 to 2014. Their lung function measurements, including forced vital capacity (FVC), forced expiratory volume in one second (FEV1), the percentage of predicted FVC (FVC%) and FEV1 (FEV1%), FEV1/FVC ratio, and forced expiratory flow between 25% and 75% of vital capacity (FEF25-75), were detected in both baseline (2010) and follow-up study (2014). We also detected the urinary concentrations of 12 PAH metabolites in the baseline study. The relationships between the baseline urinary PAH metabolites and 4-year lung function declines were analyzed by multivariate linear regressions, with adjustment for potential confounders. RESULTS: We found that the baseline concentrations of urinary 1-hydroxynaphthalene (1-OHNa), 2-OHNa, 2-hydroxyfluorene (2-OHFlu), 9-OHFlu, 1-hydroxyphenanthrene (1-OHPh), 2-OHPh, and ΣOH-PAHs were significantly associated with accelerated decline in FEV1/FVC [all ß>0 and false discovery rate (FDR) P<0.05]. Additionally, the baseline levels of urinary 1-OHNa, 1-OHPh, 2-OHPh, 9-OHPh, 1-hydroxypyrene (1-OHP), and ΣOH-PAHs were associated with significantly deeper decline in FEF25-75 (all ß>0 and FDR P<0.10). When using backward selection to adjustment for 10 urinary PAH metabolites, the most significant determiner for FEV1/FVC decline was 1-OHNa among nonsmokers and 9-OHFlu among smokers, and the significant determiner for FEF25-75 decline was 9-OHPh among nonsmokers and 1-OHP among smokers. CONCLUSIONS: This longitudinal study revealed that higher baseline exposure levels of PAHs could lead to greater decline in lung function over a 4-year follow-up.

Polycyclic aromatic hydrocarbon exposure, miR-146a rs2910164 polymorphism, and heart rate variability in coke oven workers.

BACKGROUND: Exposure to ubiquitous polycyclic aromatic hydrocarbons (PAHs) has been associated with decreased heart rate variability (HRV). Evidence accumulates that microRNAs (miRNAs) might be the intermediate factors between environmental exposures and their adverse health effects. Single nucleotide polymorphisms (SNPs) in miRNA genes may affect phenotypes and disease morbidity. OBJECTIVE: We sought to investigate the influences of four well-studied SNPs in miRNA genes (rs2910164, rs11614913, rs2292832, and rs3746444) on HRV, and their modifying effects on the associations between PAH exposure and HRV. METHODS: We measured the concentrations of ten urinary monohydroxy PAHs (OH-PAHs), seven HRV parameters, and genotypes of these four SNPs in 1222 coke oven workers. RESULTS: There were significant differences among different rs2910164 genotype carriers in terms of all seven HRV indices: workers with rs2910164 CC genotype had significant lower HRV than those with GG or GC genotype (P<0.05). The number of rs2910164 C allele was negatively associated with HRV indices in the high PAH exposure group (ß<0, P<0.05), and the association between rs2910164 and high-frequency (HF) power was significantly stronger in high exposure group (Pinteraction=0.042). Interestingly, the negative associations between the sum of 10 OH-PAHs and HRV (ß<0, P<0.05) were significantly or marginally significantly stronger in workers with rs2910164 CC genotype (Pinteraction≤0.050). CONCLUSIONS: Coke oven workers with miR-146a rs2910164 CC genotype may be more susceptible to decreased HRV. The modifying effect of rs2910164 on the PAHs-HRV associations suggested miR-146a may mediate the effects of PAH exposure on HRV.

Exposure to Polycyclic Aromatic Hydrocarbons, Plasma Cytokines, and Heart Rate Variability.

Epidemiological studies have suggested associations between polycyclic aromatic hydrocarbons (PAHs) and heart rate variability (HRV). However, the roles of plasma cytokines in these associations are limited. In discovery stage of this study, we used Human Cytokine Antibody Arrays to examine differences in the concentrations of 280 plasma cytokines between 8 coke-oven workers and 16 community residents. We identified 19 cytokines with significant different expression (fold change ≥2 or ≤-2, and q-value <5%) between exposed workers and controls. 4 cytokines were selected to validate in 489 coke-oven workers by enzyme-linked immunosorbent assays in validation stage. We found OH-PAHs were inversely associated with brain-derived neurotrophic factor (BDNF) (p < 0.05), and interquartile range (IQR) increases in OH-PAHs were associated with >16% BDNF decreases. Additionally, OH-PAHs were positively associated with activated leukocyte cell adhesion molecule (ALCAM) and C-reactive protein (CRP) (p < 0.05), and IQR increases in OH-PAHs were associated with >20% increases in CRP. We also found significant associations between these cytokines and HRV (p < 0.05), and IQR increases in BDNF and CRP were associated with >8% decreases in HRV. Our results indicated PAH exposure was associated with plasma cytokines, and higher cytokines were associated with decreased HRV, but additional human and potential mechanistic studies are needed.

Essential Metals Zinc, Selenium, and Strontium Protect against Chromosome Damage Caused by Polycyclic Aromatic Hydrocarbons Exposure.

Essential metals play important roles in maintaining cellular homeostasis, but the effects of their interaction with the environmental pollutants are still not very well-known in human subjects. The aim of this study was to evaluate the roles of essential metals and their interactions with polycyclic aromatic hydrocarbons (PAHs) on chromosome damage, an early carcinogenic event. A total of 1245 male workers were included in this study and the levels of 11 urinary essential metals, 12 urinary PAH metabolites, plasma concentrations of benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts, and lymphocyte micronucleus (MN) frequencies were monitored. We found that zinc (Zn), selenium (Se), and strontium (Sr) have significant inverse dose-response relationships with MN frequencies (all P < 0.05). Furthermore, the protective roles of Zn, Se, and Sr were mainly shown among subjects with high levels of BPDE-Alb adducts. Significant effect modification of BPDE-Alb adducts on the associations of Zn, Se, and Sr with MN frequencies was observed (all Pinteraction < 0.05). Our study showed evidence that Zn, Se, and Sr play protective roles in reducing chromosome damage, and these effects can be modified by PAH exposure levels. These findings add potential evidence for the preventive effects of Zn, Se, and Sr against carcinogenesis in human subjects.

The effects of heavy metals and their interactions with polycyclic aromatic hydrocarbons on the oxidative stress among coke-oven workers.

Heavy metals and polycyclic aromatic hydrocarbons (PAHs) are predominate toxic constituents of particulate air pollution that may be related to the increased risk of cardiopulmonary events. We aim to investigate the effects of the toxic heavy metals (arsenic, As; cadmium, Cd; chromium, Cr; nickel, Ni; and lead, Pb), and their interactions with PAHs on oxidative stress among coke-oven workers. A total of 1333 male workers were recruited in this study. We determined their urinary levels of As, Cd, Cr, Ni, Pb, twelve PAH metabolites, 8-hydroxydeoxyguanosine (8-OHdG), and 8-iso-prostaglandin-F2α (8-iso-PGF2α). Multivariate linear regression models were used to analyze the effects of these metals and their interactions with PAHs on 8-OHdG and 8-iso-PGF2α levels. It was found that only urinary As and Ni showed marginal or significant positive linear dose-dependent effects on 8-OHdG in this study population, especially among smokers (ß=0.103, P=0.073 and ß=0.110, P=0.002, respectively). After stratifying all participants by the quartiles of ΣOH-PAH, all five metals showed linear association with 8-OHdG in the highest quartile subgroup (Q4) of ΣOH-PAHs. However, these five urinary metals showed significantly consistent linear associations with 8-iso-PGF2α in all subjects and each stratum. Urinary ΣOH-PAHs can significant modify the effects of heavy metals on oxidative stress, while co-exposure to both high levels of ΣOH-PAHs and heavy metals render the workers with highest 8-OHdG and 8-iso-PGF2α (all P(interaction)≤0.005). This study showed evidence on the interaction effects of heavy metals and PAHs on increasing the oxidative stress, and these results warrant further investigation in more longitudinal studies.

Association of body mass index with chromosome damage levels and lung cancer risk among males.

Epidemiological studies have shown an etiological link between body mass index (BMI) and cancer risk, but evidence supporting these observations is limited. This study aimed to investigate potential associations of BMI with chromosome damage levels and lung cancer risk. First, we recruited 1333 male workers from a coke-oven plant to examine their chromosome damage levels; and then, a cohort study of 12,052 males was used to investigate the association of BMI with lung cancer incidence. We further carried out a meta-analysis for BMI and male lung cancer risk based on cohort studies. We found that men workers with excess body weight (BMI ≥ 25 kg/m(2)) had lower levels of MN frequencies than men with normal-weight (BMI: 18.5-24.9). Our cohort study indicated that, the relative risk (RR) for men with BMI ≥ 25 to develop lung cancer was 35% lower than RR for normal-weight men. Further meta-analysis showed that, compared to normal-weight men, men with BMI ≥ 25 had decreased risk of lung cancer among both the East-Asians and others populations. These results indicate that men with excess body weight had significant decreased chromosome damage levels and lower risk of lung cancer than those with normal-weight. However, further biological researches were needed to validate these associations.

Associations between 25 lung cancer risk-related SNPs and polycyclic aromatic hydrocarbon-induced genetic damage in coke oven workers.

BACKGROUND: Genome-wide association studies (GWAS) have identified multiple single-nucleotide polymorphisms (SNP) associated with lung cancer. However, whether these SNPs are associated with genetic damage, a crucial event in cancer initiation and evolution, is still unknown. We aimed to establish associations between these SNPs and genetic damage caused by the ubiquitous carcinogens, polycyclic aromatic hydrocarbons (PAH). METHODS: We cross-sectionally investigated the associations between SNPs from published GWAS for lung cancer in Asians and PAH-induced genetic damage in 1,557 coke oven workers in China. Urinary PAH metabolites, plasma benzo[a]pyrene-r-7,t-8,c-10-tetrahydrotetrol-albumin (BPDE-Alb) adducts, urinary 8-hydroxydeoxyguanosine (8-OHdG), and micronuclei (MN) frequency were determined by gas chromatography-mass spectrometry, sandwich ELISA, high-performance liquid chromatography, and cytokinesis-block micronucleus assay, respectively. RESULTS: 13q12.12-rs753955C was suggestively associated with elevated 8-OHdG levels (P = 0.003). Higher 8-OHdG levels were observed in individuals with rare allele homozygotes (CC) than in TT homozygotes (ß, 0.297; 95% confidence interval, 0.124-0.471; P = 0.001). 9p21-rs1333040C, 10p14-rs1663689G, and 15q25.1-rs3813572G were significantly associated with lower MN frequency (P values were 0.002, 0.001, and 0.005, respectively). 10p14-rs1663689G polymorphism downregulated the relationship of the total concentration of PAH metabolites to 8-OHdG levels (Pinteraction = 0.002). TERT-rs2736100G and VTI1A-rs7086803A aggravated the relationship of BPDE-Alb adducts to MN frequency, whereas BPTF-rs7216064G attenuated that correlation (all Pinteraction < 0.001). CONCLUSIONS: Lung cancer risk-associated SNPs and their correlations with PAH exposure were associated with 8-OHdG levels and MN frequency. IMPACT: Lung cancer risk-associated SNPs might influence one's susceptibility to genetic damage caused by PAHs. Cancer Epidemiol Biomarkers Prev; 23(6); 986-96. ©2014 AACR.

Plasma microRNA expression and micronuclei frequency in workers exposed to polycyclic aromatic hydrocarbons.

BACKGROUND: Ubiquitous polycyclic aromatic hydrocarbons (PAHs) have been shown to alter gene expression patterns and elevate micronuclei (MN) frequency, but the underlying mechanisms are largely unknown. MicroRNAs (miRNAs) are key gene regulators that may be influenced by PAH exposures and mediate their effects on MN frequency. OBJECTIVES: We sought to identify PAH-associated miRNAs and evaluate their associations with MN frequency. METHODS: We performed a two-stage study in healthy male coke oven workers to identify miRNAs associated with PAH exposures quantified using urinary monohydroxy-PAHs and plasma benzo[a]pyrene-r-7,t-8,c-10-tetrahydrotetrol-albumin (BPDE-Alb) adducts. In the discovery stage, we used Solexa sequencing to test differences in miRNA expression profiles between pooled plasma samples from 20 exposed workers and 20 controls. We then validated associations with eight selected miRNAs in 365 workers. We further evaluated associations between the PAH-associated miRNAs and MN frequency. RESULTS: In the discovery stage, miRNA expression profiles differed between the exposed and control groups, with 68 miRNAs significantly down-regulated [fold change (FC) ≤ -5] and 3 miRNAs mildly up-regulated (+2 ≤ FC < +5) in the exposed group. In the validation analysis, urinary 4-hydroxyphenanthrene and/or plasma BPDE-Alb adducts were associated with lower miR-24-3p, miR-27a-3p, miR-142-5p, and miR-28-5p expression (p < 0.030). Urinary 1-hydroxynaphthalene, 2-hydroxynaphthalene, 2-hydroxyphenanthrene, and the sum of monohydroxy-PAHs were associated with higher miR-150-5p expression (p < 0.030). These miRNAs were associated with higher MN frequency (p < 0.005), with stronger associations in drinkers (pinteraction < 0.015). CONCLUSIONS: Associations of PAH exposures with miRNA expression, and of miRNA expression with MN frequency, suggest potential mechanisms of adverse effects of PAHs that are worthy of further investigation.

Women are more susceptible than men to oxidative stress and chromosome damage caused by polycyclic aromatic hydrocarbons exposure.

Exposure to environmental polycyclic aromatic hydrocarbons (PAHs) has been associated with increased risk of cancer, but evidence for gender differences in this association is limited. The aim of this study was to examine the gender differences in PAHs caused early genotoxic effects such as oxidative stress and chromosome damage, which are potential carcinogenic etiology of PAHs. A total of 478 nonsmoking workers (272 men and 206 women) from a coke oven plant were recruited. We determined 16 environmental PAHs in their workplaces, and measured concentrations of 12 urinary PAH metabolites (OH-PAHs), plasma benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts, urinary 8-hydroxydeoxyguanosine (8-OHdG) and 8-iso-prostaglandin-F2α (8-iso-PGF2α), and micronucleus frequencies in lymphocytes in all subjects. It showed that, women working at the office, adjacent to the coke oven, and on the bottom or side of the coke oven displayed significantly higher levels of urinary 8-OHdG and 8-iso-PGF2α, and lymphocytic micronucleus frequencies compared with men working at above areas, respectively (all P < 0.05). These gender differences remain significant after adjusted for potential confounders and urinary ΣOH-PAHs or plasma BPDE-Alb adducts. A significant interaction existed between gender and BPDE-Alb adducts on increasing micronucleus frequencies (Pinteraction < 0.001). We further stratified all workers by the tertiles of urinary ΣOH-PAHs or plasma BPDE-Alb adducts, and the above gender differences were more evident in the median- and high-exposure groups (all P < 0.05). In conclusion, women were more susceptible than men to oxidative stress and chromosome damage induced by PAHs, which may add potential evidence underlying gender differences in PAH exposure-related lung cacinogenesis.

Polycyclic aromatic hydrocarbons-associated microRNAs and their interactions with the environment: influences on oxidative DNA damage and lipid peroxidation in coke oven workers.

We previously identified five polycyclic aromatic hydrocarbons (PAHs)-associated microRNAs (miRNAs) and found they were associated with chromosome damage. As oxidative damage is the common contributory cause of various PAHs-related diseases, we further investigated the influences of these miRNAs and their interactions with environmental factors on oxidative DNA damage and lipid peroxidation. We measured PAHs internal exposure biomarkers [urinary monohydroxy-PAHs (OH-PAHs) and plasma benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts], the expression levels of PAHs-associated plasma miRNAs (miR-24-3p, miR-27a-3p, miR-142-5p, miR-28-5p, and miR-150-5p), and urinary biomarkers of oxidative DNA damage [8-hydroxydeoxyguanosine (8-OH-dG)] and lipid peroxidation [8-iso-prostaglandin-F2α (8-iso-PGF2α)] in 365 healthy male coke oven workers. These miRNAs were associated with a dose-response increase in 8-OH-dG (ß > 0), and with a dose-response decrease in 8-iso-PGF2α (ß < 0), especially in workers with lower PAHs exposure levels, in nonsmokers, and in nondrinkers. These miRNAs interacted antagonistically with ΣOH-PAHs and BPDE-Alb adducts (ßinteraction < 0) and synergistically with drinking status (ßinteraction > 0) to influence 8-OH-dG, while they interacted synergistically with BPDE-Alb adducts (ßinteraction > 0) and antagonistically with smoking status (ßinteraction < 0) to influence 8-iso-PGF2α. Our results suggested that miRNAs and their interactions with environmental factors might be novel mechanisms mediating the effects of PAHs exposure on oxidative DNA damage and lipid peroxidation.

Dose-response relationships of polycyclic aromatic hydrocarbons exposure and oxidative damage to DNA and lipid in coke oven workers.

Polycyclic aromatic hydrocarbons (PAHs) are known to induce reactive oxygen species and oxidative stress, but the dose-response relationships between exposure to PAHs and oxidative stress levels have not been established. In this study, we recruited 1333 male coke oven workers, monitored the levels of environmental PAHs, and measured internal PAH exposure biomarkers including 12 urinary PAH metabolites and plasma benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts, as well as the two oxidative biomarkers urinary 8-hydroxydeoxyguanosine (8-OHdG) and 8-iso-prostaglandin-F2α (8-iso-PGF2α). We found that the total concentration of urinary PAH metabolites and plasma BPDE-Alb adducts were both significantly associated with increased 8-OHdG and 8-iso-PGF2α in both smokers and nonsmokers (all p < 0.05). This exposure-response effect was also observed for most PAH metabolites (all p(trend) < 0.01), except for 4-hydroxyphenanthrene and 8-OHdG (p(trend) = 0.108). Furthermore, it was shown that only urinary 1-hydroxypyrene has a significant positive association with both 8-OHdG and 8-iso-PGF2α after a Bonferroni correction (p < 0.005). Our results indicated that urinary ΣOH-PAHs and plasma BPDE-Alb adducts can result in significant dose-related increases in oxidative damage to DNA and lipids. Furthermore, when a multianalyte method is unavailable, our findings demonstrate that urinary 1-hydroxypyrene is a useful biomarker for evaluating total PAHs exposure and assessing oxidative damage in coke oven workers.

The dose-response decrease in heart rate variability: any association with the metabolites of polycyclic aromatic hydrocarbons in coke oven workers?

BACKGROUND: Air pollution has been associated with an increased risk of cardiopulmonary mortality and decreased heart rate variability (HRV). However, it is unclear whether coke oven emissions (COEs) and polycyclic aromatic hydrocarbons (PAHs) are associated with HRV. OBJECTIVES: Our goal in the present study was to investigate the association of exposure to COEs and the urinary metabolite profiles of PAHs with HRV of coke oven workers. METHODS: We measured benzene soluble matter, carbon monoxide, sulfur dioxide, particulate matters, and PAHs at different workplaces of a coke oven plant. We determined 10 urinary PAH metabolites and HRV indices of 1333 workers using gas chromatography-mass spectrometry and a 3-channel digital Holter monitor, respectively. RESULTS: Our results showed that there was a significant COEs-related dose-dependent decrease in HRV, and an inverse relationship between the quartiles of urinary 2-hydroxynaphthalene and five HRV indices (p(trend)<0.01 for all). After adjustment for potential confounders, elevation per interquartile range (IQR) (1.81 µg/mmol creatinine) of urinary 2-hydroxynaphthalene was associated with a 5.46% (95% CI, 2.50-8.32) decrease in standard deviation of NN intervals (SDNN). As workers worked more years, SDNN gradually declined in the same quartiles of 2-hydroxynaphthalene levels (p(trend) = 1.40×10(-4)), especially in workers with the highest levels of 2-hydroxynaphthalene. CONCLUSIONS: Occupational exposure to COEs is associated with a dose-response decrease in HRV. In particular, increased exposure to 2-hydroxynaphthalene is associated with significantly decreased HRV. Increase of working years and exposure levels has resulted in a gradual decline of HRV.

[Characteristics of particulate matter pollution in coke oven plant].

OBJECTIVE: To explore the characteristics of particulate matter pollution in coke oven plant, so as to provide scientific data for establishing occupational exposure limits for coke oven emissions. METHODS: Concentrations of CO, SO2, BSM, BTEX (concentrations of benzene, toluene and xylene were determined in this study), PM10, PM2.5, 16 selected PAHs in PM10 and PM2.5 were determined in the work environment of a coke oven plant in Wuhan. The work environment was divided into the adjunct area, the bottom of, the side of and the top of coke oven. RESULTS: The concentrations of CO, SO2, BSM, BETX, PM10, PM2.5, PAHs in PM10 and PM2.5 were significantly related to working environmental categories, respectively, and were increasing as the adjunct area < bottom < side < top (P (trend) < 0.05). PM10 was statistically significantly correlated with CO, SO2, benzene, BTEX and BSM (0.705, 0.823, 0.664, 0.624 and 0.734, respectively). PM2.5 was statistically significantly correlated with CO, SO2, benzene, BTEX and BSM (0.635, 0.916, 0. 680, 0.553 and 0.726, respectively). BSM was statistically significantly correlated with benzene (0.689). The ratios of PM2.5 to PM10 between different work environments were not significantly different in one-way ANOVA (P > 0.05). The distribution of aromatic rings and the concentrations of total benzo[a] pyrene equivalents in PM10 and PM2.5 were not statistically different between work environments. CONCLUSION: The concentrations of particulate matter was related with other contents of coke oven emissions in coke work environment, and the contents and types of PAHs in PM10 and PM2.5 were similar.

[Effects of smoking on the concentrations of urinary 10 metabolites of polycyclic aromatic hydrocarbons in coke oven workers].

OBJECTIVE: To explore the effects of smoking on urinary 10 metabolites of polycyclic aromatic hydrocarbons (PAHs) in the coke oven workers. METHODS: Occupational health examination was performed on 1401 coke oven workers in one coking plant, their urine were collected respectively. The concentrations of the ten monohydroxy polycyclic aromatic hydrocarbons in urine were detected by gas chromatography/mass spectrometry. The 1401 workers were divided into four groups, namely control, adjunct workplaces, bottom and side, top group according to their workplaces and the different concentrations of PAHs in the environment. The concentrations of the ten monohydroxy polycyclic aromatic hydrocarbons between smokers and nonsmokers in each workplace group were compared using analysis of covariance, respectively. RESULTS: The levels of concentrations of the sixteen polycyclic aromatic hydrocarbons we detected at control were significantly higher than those at other areas (P < 0.05). Comparing the ten monohydroxy polycyclic aromatic hydrocarbons levels between smokers and nonsmokers, the levels of 1-hydroxynaphthalene and 2-hydroxynaphthalene among smokers were higher than nonsmokers with statistically significance in control, adjunct workplaces, bottom and side and top groups (P < 0.05). However, the levels of 1-hydroxypyrene had no statistically significant differences between the four areas. CONCLUSION: Urinary 1-hydroxynaphthalene and 2-hydroxynaphthalene may be used as biomarkers for the impact of smoking on monohydroxy polycyclic aromatic hydrocarbons in the coke oven workers.