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The clinical management of idiopathic pulmonary fibrosis (IPF) is challenging. For patients with a progressive disease with no known cure, realistic goals include slowing the rate of disease progression, optimising comorbidities and functional status, managing symptoms, and preventing what is preventable. The latter is short however, mainly including smoking cessation and infection prevention measures. Despite adherence to recommended management, most patients deteriorate over time, with some experiencing acute exacerbation (AE), and the majority dying due to their IPF.1 Identifying modifiable risk factors that limit disease progression or death could change clinical practice, offering preventative tools with which to achieve the goal of improving patient quality and quantity of life.
Air pollution exposure is ubiquitous and a well-established risk factor for a wide range of adverse health outcomes including cardiovascular disease and all-cause mortality.2–4 Arguably the most common target is the respiratory system, given its exposure to the inhaled environment. Indeed, air pollution exposures are associated with increased risk of developing and exacerbating airway diseases, bronchiolitis obliterans post lung transplant, as well as being diagnosed with and dying from lung cancer.5–11 IPF was a relative latecomer to the world of air pollution epidemiology, although a number of plausible mechanisms exist to suggest a relationship.12 While it is unlikely that air pollution is the sole driver of disease, it may represent one form of environmental insult that precipitates or accelerates fibrosis in an already vulnerable lung.
In Thorax, Sesé and colleagues contribute novel data to a growing body of literature …
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