The Role of Occupational and Environmental Exposures in the Pathogenesis of Idiopathic Pulmonary Fibrosis: A Narrative Literature Review

Trethewey, Samuel P; Walters, Gareth

doi:10.3390/medicina54060108

Cited by 27 publications

(19 citation statements)

References 70 publications

(85 reference statements)

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“…Aside from bleomycin, fluorescein isothiocyanate (FITC) has also been widely used to induce experimental lung fibrosis which results in alveolar injury and acute fibrotic reaction that persist up to 24 weeks. Occupational exposure to environmental risk factors has been extensively associated with pulmonary fibrosis (183). Reports suggested that inhalation of silica and asbestos particles in rats results in fibrotic nodule formation which closely mimics prominent features of silicosis and asbestosis in humans with long-term occupational exposure (184,185).…”

Section: In Vivo and In Vitro Models Of Pulmonary Fibrosismentioning

confidence: 99%

Human-Based Advanced in vitro Approaches to Investigate Lung Fibrosis and Pulmonary Effects of COVID-19

et al. 2021

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The coronavirus disease 2019 (COVID-19) pandemic has caused considerable socio-economic burden, which fueled the development of treatment strategies and vaccines at an unprecedented speed. However, our knowledge on disease recovery is sparse and concerns about long-term pulmonary impairments are increasing. Causing a broad spectrum of symptoms, COVID-19 can manifest as acute respiratory distress syndrome (ARDS) in the most severely affected patients. Notably, pulmonary infection with Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2), the causing agent of COVID-19, induces diffuse alveolar damage (DAD) followed by fibrotic remodeling and persistent reduced oxygenation in some patients. It is currently not known whether tissue scaring fully resolves or progresses to interstitial pulmonary fibrosis. The most aggressive form of pulmonary fibrosis is idiopathic pulmonary fibrosis (IPF). IPF is a fatal disease that progressively destroys alveolar architecture by uncontrolled fibroblast proliferation and the deposition of collagen and extracellular matrix (ECM) proteins. It is assumed that micro-injuries to the alveolar epithelium may be induced by inhalation of micro-particles, pathophysiological mechanical stress or viral infections, which can result in abnormal wound healing response. However, the exact underlying causes and molecular mechanisms of lung fibrosis are poorly understood due to the limited availability of clinically relevant models. Recently, the emergence of SARS-CoV-2 with the urgent need to investigate its pathogenesis and address drug options, has led to the broad application of in vivo and in vitro models to study lung diseases. In particular, advanced in vitro models including precision-cut lung slices (PCLS), lung organoids, 3D in vitro tissues and lung-on-chip (LOC) models have been successfully employed for drug screens. In order to gain a deeper understanding of SARS-CoV-2 infection and ultimately alveolar tissue regeneration, it will be crucial to optimize the available models for SARS-CoV-2 infection in multicellular systems that recapitulate tissue regeneration and fibrotic remodeling. Current evidence for SARS-CoV-2 mediated pulmonary fibrosis and a selection of classical and novel lung models will be discussed in this review.

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Section: In Vivo and In Vitro Models Of Pulmonary Fibrosismentioning

confidence: 99%

Human-Based Advanced in vitro Approaches to Investigate Lung Fibrosis and Pulmonary Effects of COVID-19

et al. 2021

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“…By comparison, chemical exposure does not promote such a cell specific response, often leading to varying degrees of stress, ranging from susceptibility to disease later in life to irreversible senescence and pathogenesis of disease (101,102). Particulate matter exposure has been widely studied for its importance in lung health (Figure 4).…”

Section: Cell Type-specific Responsesmentioning

confidence: 99%

Senescence in Pulmonary Fibrosis: Between Aging and Exposure

Venosa

2020

Front. Med.

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“…Apart from the genetic predispositions, numerous non-genetic risk factors for IPF have been identified. Older age, male sex, and cigarette smoking represent the most widely recognized [ 61 ], although microaspirations and gastroesophageal reflux disease, certain viruses, and occupational exposures (metal and wood dust) have also been suggested to increase the risk of IPF [ 61 , 62 , 63 , 64 , 65 ]. Despite notable research interest in air pollution relationship with respiratory diseases, very little is known on the short and long-term effects of air pollution in IPF.…”

Section: Impact Of Air-pollution On Disease Initiation and Health mentioning

confidence: 99%

Air Pollution—An Overlooked Risk Factor for Idiopathic Pulmonary Fibrosis

Majewski

Piotrowski

2020

JCM

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Air pollution is a major environmental risk to health and a global public health concern. In 2016, according to the World Health Organization (WHO), ambient air pollution in cities and rural areas was estimated to cause 4.2 million premature deaths. It is estimated that around 91% of the world’s population lives in places where air pollution exceeds the limits recommended by the WHO. Sources of air pollution are multiple and context-specific. Air pollution exposures are established risk factors for development and adverse health outcomes in many respiratory diseases, including asthma, chronic obstructive pulmonary disease (COPD), or lung cancer. However, possible associations between air pollution and idiopathic pulmonary fibrosis (IPF) have not been adequately studied and air pollution seems to be an underrecognized risk factor for IPF. This narrative review describes potential mechanisms triggered by ambient air pollution and their possible roles in the initiation of the pathogenic process and adverse health effects in IPF. Additionally, we summarize the most current research evidence from the clinical studies supporting links between air pollution and IPF.

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The Role of Occupational and Environmental Exposures in the Pathogenesis of Idiopathic Pulmonary Fibrosis: A Narrative Literature Review

Cited by 27 publications

References 70 publications

Human-Based Advanced in vitro Approaches to Investigate Lung Fibrosis and Pulmonary Effects of COVID-19

Human-Based Advanced in vitro Approaches to Investigate Lung Fibrosis and Pulmonary Effects of COVID-19

Senescence in Pulmonary Fibrosis: Between Aging and Exposure

Air Pollution—An Overlooked Risk Factor for Idiopathic Pulmonary Fibrosis

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