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Molecular and cellular mechanisms linking air pollution and bone damage.
Environmental Research ( IF 7.7 ) Pub Date : 2020-04-06 , DOI: 10.1016/j.envres.2020.109465
Diddier Prada 1 , Gerard López 2 , Helena Solleiro-Villavicencio 3 , Claudia Garcia-Cuellar 4 , Andrea A Baccarelli 5
Affiliation  

Air pollution is the second most important risk factor associated with noncommunicable diseases after smoking. The effects of pollution on health are commonly attributable to particulate matter (PM), a complex mixture of particles suspended in the air. PM can penetrate the lower respiratory tract and has harmful direct and indirect effects on different organs and tissues. Direct effects are caused by the ability of PM components to cross the respiratory membrane and enter the bloodstream; indirect effects are systemic consequences of the local airway response. Recent work suggests that PM is an independent risk factor for low bone mineral density and osteoporosis-related fractures. Osteoporosis is a common age-related disease closely linked to bone fractures, with severe clinical consequences affecting quality of life, morbidity, and mortality. In this review, we discuss potential mechanisms behind the association between outdoor air pollution, especially PM, and bone damage. The discussion features four main mechanisms: 1) several different atmospheric pollutants can induce low-grade systemic inflammation, which affects bone metabolism through a specific effect of cytokines such as TNFα, IL-1β, IL-6, and IL-17 on osteoblast and osteoclast differentiation and function; 2) some pollutants, particularly certain gas and metal compounds, can cause oxidative damage in the airway and bone cells; 3) different groups of pollutants can act as endocrine disruptors when binding to the receptors in bone cells, changing their functioning; and 4) air pollution can directly and indirectly cause vitamin D deficiency. Characterizing these mechanisms will better define the physiopathology of bone damage, and recognizing air pollution as a modifiable risk factor for osteoporosis will inform environmental policies. Such knowledge will also guide the prevention of fractures due to fragility and help reduce health-related costs.

中文翻译:

分子和细胞机制将空气污染与骨骼损害联系起来。

空气污染是仅次于吸烟的与非传染性疾病有关的第二重要风险因素。污染对健康的影响通常归因于颗粒物(PM),这是悬浮在空气中的颗粒的复杂混合物。PM可以穿透下呼吸道,对不同器官和组织具有有害的直接和间接影响。直接影响是由PM成分穿过呼吸膜进入血液的能力引起的。间接影响是局部气道反应的全身性后果。最近的工作表明,PM是导致骨密度低和与骨质疏松症相关的骨折的独立危险因素。骨质疏松症是一种常见的与年龄相关的疾病,与骨折密切相关,严重的临床后果影响生活质量,发病率和死亡率。在这篇综述中,我们讨论了室外空气污染(尤其是PM)与骨骼损伤之间关联的潜在机制。讨论的主要机制有四个:1)几种不同的大气污染物可以诱发低度全身性炎症,这通过诸如TNFα,IL-1β,IL-6和IL-17等细胞因子对成骨细胞和细胞的特定作用来影响骨骼代谢。破骨细胞的分化和功能;2)一些污染物,尤其是某些气体和金属化合物,可能会在气道和骨细胞中引起氧化损伤;3)当与骨细胞中的受体结合时,不同种类的污染物可以充当内分泌干扰物,从而改变其功能;4)空气污染会直接和间接导致维生素D缺乏。表征这些机制将更好地定义骨骼损伤的生理病理学,并且认识到空气污染是可改变的骨质疏松危险因素,将为环境政策提供参考。这些知识还将指导预防由于脆性引起的骨折,并有助于降低与健康相关的成本。
更新日期:2020-04-06
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