ObjectivesPolycyclic aromatic hydrocarbons (PAHs) have been proven to be a risk factor for cardiovascular disease in coke oven workers, and increased plasma viscosity is a signal for higher risk of catching up cardiovascular disease. We want to explore whether the plasma viscosity is affected by the concentration of PAHs.DesignOur study is a cross-sectional dose–response study.SettingParticipants in this study came from a coke plant in Taiyuan, Shanxi.ParticipantsWe used data of 693 coke oven workers in Taiyuan.Primary and secondary outcome measuresWe assumed that plasma viscosity would increase as the concentration of PAHs metabolites in urine increases. We found that 2-hydroxyfluorene (OHFLU2) and plasma viscosity have a stable linear relationship in different statistical methods.ResultsWe found that plasma viscosity increased by 1.14 (mPa.s,30/s) for each ng/mL of 2-OHFLU urinary (correlation coefficient range: 0.54–1.74, p<0.05).ConclusionsThe results of this study could provide evidence for coke oven workers to prevent cardiovascular disease by checking whether plasma viscosity is elevated.
ObjectivesTo explore sex differences and dose–response relationships between nine urinary polycyclic aromatic hydrocarbon (PAH) metabolites and neutrophil–lymphocyte ratio (NLR), platelet–lymphocyte ratio (PLR) and complete blood counts among coke oven workers.Design and settingA cross-sectional study with stratified sex was conducted in Shanxi, China.ParticipantsA total of 458 male workers and 226 female workers were selected.Primary and secondary outcome measuresGeneral linear models, p values for trend tests and natural cubic spline models were used to explore the dose–response relationships between nine urinary PAH metabolites and NLR, PLR and complete blood counts.ResultCompared with male workers, female workers had lower exposure level of PAH (0.95 ng/mL vs 1.38 ng/mL). Only among female workers did we observe that a 1-unit increase in lg(1-OHPyr) was related to a 0.149 (95% CI: 0.055 to 0.242; p for trend=0.041) and 0.103 (95% CI: 0.025 to 0.181; p for trend=0.007) increase in lg(NLR) and lg(PLR), and a 0.116 (95% CI: −0.179 to –0.054; p for trend=0.007) decrease in lg(lymphocyte counts (LYMs)). A 1-unit increase in lg(2-OHNap) was related to a 0.045 (95% CI: 0.003 to 0.086; p for trend=0.037) increase in lg(PLR) and a 0.029 (95% CI: −0.056 to –0.002; p for trend=0.030) and 0.016 (95% CI: −0.029 to –0.003; p for trend=0.010) decrease in lg(white blood cell counts (WBCs)) and lg(haemoglobin (HGB)).ConclusionFemale workers’ NLR, PLR, WBCs, HGB and LYMs may be more susceptible than those of male workers when affected by PAH.
The mechanisms that long noncoding RNA (lncRNA) H19 binding to S-adenosylhomocysteine hydrolase (SAHH) interacted with DNA methyltransferase 1 (DNMT1) and then regulated DNA damage caused by PAHs remain unclear. A total of 146 occupational workers in a Chinese coke-oven plant in 2014 were included in the final analyses. We used high performance liquid chromatography mass spectrometry (HPLC-MS) equipped to detect urine biomarkers of PAHs exposure, including 2-hydroxynaphthalene (2-NAP), 2-hydroxyfluorene (2-FLU), 9-hydroxyphenanthrene (9-PHE), 1-hydroxypyrene (1-OHP). The levels of SAM and SAH in plasma were detected by HPLC-ultraviolet. By constructing various BEAS-2B cell models exposed to 16 µM Benzo[a]pyrene (BaP) for 24 h, toxicological parameters reflecting distinct mechanisms were evaluated. We documented that urinary 1-hydroxypyrene (1-OHP) levels were positively associated with blood H19 RNA expression (OR: 1.51, 95% CI: 1.03 - 2.19), but opposite to plasma SAHH activity (OR: 0.63, 95% CI: 0.41 - 0.98) in coke oven workers. Moreover, by constructing various BEAS-2B cell models exposed to Benzo[a]pyrene (BaP), we investigated that H19 binding to SAHH exaggerated DNMT1 expressions and activity. Suppression of H19 enhanced the interaction of SAHH and DNMT1 in BaP-treated cells, decreased OGG1 methylation, reduced oxidative DNA damage and lessened S phase arrest. However, SAHH or DNMT1 single knockdown and SAHH/DNMT1 double knockdown showed the opposite trend. A H19/SAHH/DNMT1 axis was involved in OGG1 methylation, oxidative DNA damage and cell cycle arrest by carcinogen BaP.
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