BackgroundAir 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.ObjectivesOur 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.MethodsWe 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.ResultsOur 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.ConclusionsOccupational 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.

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Due to widely commercial applications of silver nanoparticles (Ag NPs), toxicity assessment of this NP is of great importance. This study aimed to investigate the oxidative stress and heat shock response of Ag NPs at different doses to A549 and HepG2 cells. After treatment with different concentrations of Ag NPs for 24 h, oxidative damage indicated by malondialdehyde (MDA), 8-epi-PGF2α, and 8-hydroxy-2′-deoxyguanosine (8-oxo-dG) concentrations and protein levels of heat shock protein A1A (HSPA1A) and heme oxygenase 1 (HO-1) were determined. Ag NPs induced dose-dependent increases in MDA, 8-epi-PGF2α, and 8-oxo-dG concentrations in both A549 and HepG2 cells. Stress-inducible HSPA1A and HO-1 were also significantly upregulated in a dose-dependent manner. A higher level of HSPA1A and HO-1 activation by Ag NPs occurred in HepG2 cells than that in A549 cells. Compared with that of HSPA1A, Ag NPs induced a stronger increase in protein level of HO-1 in both cell lines. Significant positive correlations between protein levels of HSPA1A and HO-1 and oxidative damage were also observed. In conclusion, Ag NPs could induce oxidative stress in human cell lines. In addition to the products of oxidative stress such as MDA and 8-oxo-dG, HSPs can be used as potential biomarkers in nanotoxicity assessment, especially HO-1.

Mu opioid receptor (OPRM1), a member of the G-protein coupled receptor superfamily, mediates the analgesic and euphoric effects of opioid drugs. The sequences of OPRM1 cDNA and reported splice variants were used to search the public and Celera genomic databases. The matched sequences were analyzed to assemble an OPRM1 genomic contig. Human OPRM1 gene was estimated to span at least 90 kb in the chromosome 6q24-25 region. Four coding exons are separated by 3 introns. While intron 2 has only 773 bp, these databases for the first time provide the precise length of and other information about long introns 1 and 3, containing 50 and 27 kb, respectively. When a consensus exon/intron splice junction at the end of the coding exon 3 was not utilized, it may have resulted in continuous translation of the exon to yield the splice variant OPRM1A. The study did not identify human orthologs of other OPRM1 variants that had been reported for mouse OPRM1, although several proposed exons were found to be included in mouse genomic clones. Single nucleotide polymorphisms in the OPRM1 gene were also analyzed and summarized, which could provide potential polymorphic markers for molecular genetic studies.

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