University of Groningen, University Medical Center Groningen, Department of Epidemiology, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands.
University of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD (GRIAC), Groningen, The Netherlands.
Sci Rep. 2020 Jul 31;10(1):12963. doi: 10.1038/s41598-020-69372-6.
In this cross-sectional study, we investigated the association between occupational exposures and sickness absence (SA), the mediating role of respiratory symptoms, and whether genetic susceptibility to SA upon occupational exposures exists. Logistic regression was used to examine associations and structural equation modelling was used for mediation analyses. Genetic susceptibility was investigated by including interactions between occupational exposures and 11 candidate single nucleotide polymorphisms (SNPs). Biological dust, mineral dust, and pesticides exposure were associated with a lower prevalence of any SA (OR (95% CI) = 0.72 (0.58-0.89), 0.88 (0.78-0.99), and 0.70 (0.55-0.89), respectively) while gases/fumes exposure was associated with a higher prevalence of long-term SA (1.46 (1.11-1.91)). Subjects exposed to solvents and metals had a higher prevalence of any (1.14 (1.03-1.26) and 1.68 (1.26-2.24)) and long-term SA (1.26 (1.08-1.46) and 1.75 (1.15-2.67)). Chronic cough and chronic phlegm mediated the association between high gases/fumes exposure and long-term SA. Two of 11 SNPs investigated had a positive interaction with exposure on SA and one SNP negatively interacted with exposure on SA. Exposure to metals and gases/fumes showed a clear dose-response relationship with a higher prevalence of long-term SA; contrary, exposure to pesticides and biological/mineral dust showed a protective effect on any SA. Respiratory symptoms mediated the association between occupational exposures and SA. Moreover, gene-by-exposure interactions exist.
在这项横断面研究中，我们调查了职业暴露与病假（SA）之间的关联，以及呼吸道症状的中介作用，以及职业暴露是否存在对 SA 的遗传易感性。使用逻辑回归检查关联，使用结构方程模型进行中介分析。通过包括职业暴露与 11 个候选单核苷酸多态性（SNP）之间的相互作用，研究遗传易感性。生物粉尘、矿物粉尘和农药暴露与任何 SA 的患病率较低相关（OR（95%CI）=0.72（0.58-0.89）、0.88（0.78-0.99）和 0.70（0.55-0.89）），而气体/烟雾暴露与长期 SA 的患病率较高相关（1.46（1.11-1.91））。暴露于溶剂和金属的受试者任何（1.14（1.03-1.26）和 1.68（1.26-2.24））和长期 SA（1.26（1.08-1.46）和 1.75（1.15-2.67））的患病率较高。慢性咳嗽和慢性咳痰介导了高气体/烟雾暴露与长期 SA 之间的关联。在所研究的 11 个 SNP 中，有两个与 SA 的暴露具有阳性相互作用，一个 SNP 与 SA 的暴露具有负相互作用。金属和气体/烟雾暴露与长期 SA 的患病率较高呈明显的剂量反应关系；相反，农药和生物/矿物粉尘暴露对任何 SA 都有保护作用。呼吸道症状介导了职业暴露与 SA 之间的关联。此外，还存在基因-暴露相互作用。
