Occupational exposure to (benzene, toluene and xylene, BTX is common in the Chinese workplace. Chronic occupational exposure to benzene is associated with an increased risk of hematological malignancies such as acute myeloid leukemia (AML), but the underlying mechanisms are still unclear. This study investigates changes in poly(ADP-ribosyl)ation and DNA methylation in subjects occupationally exposed to a BTX. Blood DNA samples and exposure data were obtained from subjects with different levels of exposure, including 132 decorators, 129 painters, and 130 unexposed referents in a container-manufacturing factory in Shenzhen, China. Occupational exposure assessment included personal monitoring of airborne benzene, toluene and xylene. Hematological parameters were measured and the cytokinesis-block micronucleus (CBMN) assay was used to detect DNA damage in peripheral lymphocytes. Quantitative real-time PCR was used to detect the mRNA expression of poly(ADP-ribose) polymerase 1 (PARP1) and poly(ADP-ribose) glycohydrolase (PARG), DNA methyltransferases (DNMTs) including DNMT1, DNMT3a and DNMT3b, methyl-CpG-binding domain protein 2(MBD2). PARP1 assay was used to measure PARP activity. Airborne levels of benzene, toluene and xylene in the two exposed groups were significantly higher than those of controls (P<0.001). The two exposed groups (decorators, painters) showed decreased PARP1, DNMTs and MBD2 expression relative to controls (P<0.05), and PARP activity was also decreased (P<0.05). Decreased PARP1, DNMT1, DNMT3a, DNMT3b and MBD2 mRNA expression was correlated with increased airborne BTX (Pearson's r: −0.587, −0.314, −0.636, −0.567 and −0.592 respectively, P<0.001). No significant differences in hematological parameters and CBMN were found among the three groups. Together, these results suggest that decreased DNMTs, MBD2 and PARP1 might be involved in the global hypomethylation associated with BTX exposure, and the imbalance of PARP/PARG might participate in the down-regulation of DNMTs. This is the first human study to link altered poly(ADP-ribosyl)ation patterns, which reproduce the aberrant epigenetic patterns found in benzene-treated cells, to chronic occupational exposure to BTX.

Ozone pollution is a prominent public health issue, but there are few studies on the effect of ozone on the ultrastructure of respiratory system; we conducted this research. Exposed to 1.1 ppm O₃ 4 h per day, the mice lungs and bronchi were taken on the 15th or 30th day. The sections stained with HE and immunohistochemical streptavidin–peroxidase methods for NQO1, Nrf2, and Keap1 were observed and measured under the optical microscope. TEM was used for ultrastructure observation. The animals’ serums were detected for CRP and IL-6 levels. The HE-stained sections showed no obvious micromorphological changes in the O₃ exposure, but the NQO1 average optical density was higher than the control on the 15th day (p < 0.05). The ultrastructural changes were found in the O₃ exposure group, such as bulges and vacuoles in type I alveolar cells, the increased evacuation of substance from lamellar bodies in the type II alveolar cells, the increased space around the goblet nucleus, binuclear goblet, and columnar cells. CRP and IL-6 levels increased compared with the control (p < 0.05). Although inhaling 1.1 ppm O₃ had no significant effect on the micromorphology of the mice lungs and bronchi, it did affect the ultrastructure with oxidative stress and inflammatory responses.