Organophosphorous pesticides (OPs), with high efficiency, broad-spectrum and low residue, are widely used in China. Omethoate is a broad category of organophosphorous pesticides and is more domestically utilized which has chronic toxic effect on human health caused by long-term, low-dose exposure to Ops, recently its potential genotoxicity has attracted wide attention which can cause chromosomal DNA damage. Thus, the aim of this study is screen susceptible biomarkers and explore the mechanism of canceration induced by omethoate. 180 long-term organophosphorus pesticide–exposed workers and 115 healthy controls were recruited. Quantitative polymerase chain reaction method was applied to determine the relative telomere length in peripheral lymphocyte DNA as well as p53 and p21 gene expression levels. Genetic polymorphisms were determined by the polymerase chain reaction–restriction fragment length polymorphism method. Multiple linear regression was conducted to explore the effects of exposure, expression levels, and polymorphisms in genes on the telomere length. The results showed the relative telomere lengths in the exposure group were significantly longer than that in the control group. The messenger RNA expression levels of p53 and p21 in exposure group were significantly lower than that in the control group; telomere lengths of the CA genotype individuals of p21 rs1801270 polymorphism locus were significantly longer than that of the CC genotype in the control group that were estimated using the Bonferroni method; and bivariate correlation analysis showed that the messenger RNA expression level of gene p53 was negatively correlated with telomere length, and the messenger RNA expression level of gene p21 was positively correlated with telomere length. Multivariate analysis found that p53 messenger RNA and p21 messenger RNA had an impact on telomere length. These results demonstrated that the messenger RNA expression levels of p53 and p21 may have a relationship with the changes in telomere length induced by omethoate and provided strong evidence for the mechanism of canceration induced by poison.

The evidence on the effects of polycyclic aromatic hydrocarbons (PAHs) on sleep disorders is limited. This study aimed to explore the association between PAH exposure and sleep-related disorders, and the potential mediating roles of inflammation in these relationships were further been examined. This study utilized data from adult participants (≥ 20 years of age) in the US National Health and Nutrition Examination Survey 2005–2008. Weighted logistic regression models were used to estimate the associations between each urinary PAH biomarker and sleep-related disorders. Structural Equation Modelling (SEM) was applied to evaluate the association between PAH exposure and sleep-related disorders and to assess the mediating effect of inflammatory markers that include C-reactive protein (CRP) and white blood cell counts (WBC). One or more urinary PAH metabolites were associated with an increased risk of long sleep-onset latency, obstructive sleep apnea (OSA), sleep problems, and daytime sleepiness. The latent PAH exposure variable in SEM was positively associated to long sleep-onset latency (β = 0.054, p = 0.035), OSA (β = 0.071, p = 0.002), sleep problems (β = 0.089, p < 0.001) and daytime sleepiness (β = 0.066, p = 0.003). Mediation analysis suggested that WBC mediated the link between PAH exposure and sleep problems (Indirect effect = 0.009, 95%CI: 0.002 ~ 0.017, Proportion: 10.8%), as well as daytime sleepiness (Indirect effect = 0.011, 95%CI: 0.005 ~ 0.019, Proportion: 15.7%). PAH exposure was associated with an increased risk of long sleep-onset latency, obstructive sleep apnea, sleep problems, and daytime sleepiness. Inflammation may be one potential mechanism by which PAH exposure contributes sleep problems and daytime sleepiness.