Bhattacharjee Pritha, Paul Somnath, Bhattacharjee Pritha
Department of Environmental Science, University of Calcutta, 35, Ballygunge Circular Road, Kolkata 700019, India.
Division of Molecular Genetics, CSIR-Indian Institute of Chemical Biology, Jadavpur, Kolkata 700032, India.
Environ Res. 2016 May;147:425-34. doi: 10.1016/j.envres.2016.02.038. Epub 2016 Mar 9.
Epidemiological studies suggest strong association of lung disorders with occupational exposure to asbestos, silicon and arsenic. The chronic occupational exposure primarily through inhalation results in adverse outcome on the respiratory tract which may also be fatal. Although several mechanisms have attributed towards these diseases; the molecular pathogenesis is still unknown.
In this review, we investigated the plausible molecular mechanism based on current research that may identify the genetic and epigenetic susceptibility of respiratory disorders upon such occupational exposures in humans.
We considered genetic variants and epigenetic alterations associated with pulmonary exposure hazards leading to asbestosis, silicosis and arsenicosis. Our review is stringently based on the literatures available through peer-reviewed articles mostly published in the last 10 years. Relevant search were conducted using keywords like "occupational lung disorders" along with "asbestos", "silicon" and "arsenic".
Till September 2015, pubmed search yielded approximately 780 articles relating to asbestos exposure; 240 articles for silicon exposure and 60 articles for arsenic exposure. Extensive screening for genetic and epigenetic factors identified certain genes and related pathways that are important to determine the susceptibility of an individual towards such occupational exposure.
The link between genotype and phenotype and its association with disease susceptibility is very complex in nature due to several factors like person's environment, lifestyle and nutritional status. The epigenome is dynamic as well as reversible and can be reshaped further by certain dietary components throughout its life. In the present review, we have addressed the role of molecular pathogenesis of occupational lung diseases based on the genetic variability and epigenetic alterations and also attempted to highlight the promising aspect of dietary interventions to counter toxic outcomes upon occupational exposure to asbestos, silicon or arsenic.
流行病学研究表明,肺部疾病与职业性接触石棉、硅和砷之间存在密切关联。主要通过吸入造成的慢性职业性接触会对呼吸道产生不良影响,甚至可能致命。尽管有多种机制与这些疾病有关,但分子发病机制仍不清楚。
在本综述中,我们基于当前研究调查了可能的分子机制,这些机制或许能确定人类在这种职业接触下呼吸道疾病的遗传和表观遗传易感性。
我们考虑了与导致石棉肺、矽肺和砷中毒的肺部接触危害相关的基因变异和表观遗传改变。我们的综述严格基于大多在过去10年发表的同行评审文章中的现有文献。使用“职业性肺部疾病”以及“石棉”“硅”和“砷”等关键词进行了相关搜索。
截至2015年9月,在PubMed上搜索到约780篇与石棉接触相关的文章;240篇与硅接触相关的文章和60篇与砷接触相关的文章。对遗传和表观遗传因素的广泛筛选确定了某些基因和相关途径,这些对于确定个体对这种职业接触的易感性很重要。
由于个人环境、生活方式和营养状况等多种因素,基因型与表型之间的联系及其与疾病易感性的关联本质上非常复杂。表观基因组是动态且可逆的,并且在其整个生命过程中可被某些饮食成分进一步重塑。在本综述中,我们基于遗传变异性和表观遗传改变探讨了职业性肺病分子发病机制的作用,并试图强调饮食干预在对抗职业性接触石棉、硅或砷后的毒性后果方面的前景。