Abstract
BackgroundCoal workers' pneumoconiosis (CWP) is characterized by chronic pulmonary inflammation and fibrotic nodular lesions that usually lead to progressive fibrosis. Inflammation is the first step in the development of CWP. E-selectin, an adhesion molecule, is involved in the development of various inflammatory diseases.MethodsWe investigated the association between the functional polymorphisms in SELE and the risk of CWP in Han Chinese population. Three polymorphisms (T1880C/rs5355, T1559C/rs5368, A16089G/rs4786) in SELE were genotyped and analyzed in a case-control study with 697 CWP cases and 694 controls. The genotyping was based on the TaqMan method with the ABI 7900HT Real Time PCR system.ResultsThe SELE rs5368 CT genotype was associated with a significantly increased risk of CWP (OR = 1.28, 95% CI = 1.02–1.60, P = 0.03) relative to the CC genotype. The statistical analysis of classification and regression tree (CART) and multifactor dimensionality reduction (MDR) were used to predict the interactions among risk factors of CWP. The MDR analysis found that the best interaction model was the two-factor model that contains pack-years smoked and SELE rs5368 genotypes. For non-smokers, the CART analysis showed an increased risk of CWP for carriers of the SELE rs_5368 variant genotype compared with the common genotype (OR = 1.51; 95% CI = 1.11–2.05, P = 0.0069).ConclusionThe results suggest that the T1559C/rs5368 polymorphism and smoking are involved in the susceptibility to CWP. Further studies are warranted to validate these findings.
Highlights
Coal workers’ pneumoconiosis (CWP) is a chronic occupational lung disease caused by the long-term inhalation and deposition of coal mine dust
The minor allele frequency (MAF) of these three polymorphisms were consistent with those reported in the HapMap database
In the stratification analysis (Table 4), significant associations were observed between the SELE rs-5368 CT/TT genotypes and patients with stage II CWP (OR = 1.55, 95% confidence intervals (95%CIs) = 1.12–2.15)
Summary
Coal workers’ pneumoconiosis (CWP) is a chronic occupational lung disease caused by the long-term inhalation and deposition of coal mine dust. The dust triggers a persistent inflammatory response and generation of pro-inflammatory and pro-fibrotic mediators, eventually resulting in irreversible lung damage [1,2]. Underground mining is associated with exposures to silica, metals, and coal dust generated during tunnel drilling, mining, roof bolting, and transportation. Most cases of CWP are caused by silica exposure. Inhalation of respirable silica particles leads to lung injury and alveolar macrophage activation, which initiate inflammation. Coal workers’ pneumoconiosis (CWP) is characterized by chronic pulmonary inflammation and fibrotic nodular lesions that usually lead to progressive fibrosis. E-selectin, an adhesion molecule, is involved in the development of various inflammatory diseases
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