Chest
Volume 147, Issue 4, April 2015, Pages 1161-1167
Journal home page for Chest

Recent Advances in Chest Medicine
Air Pollution Exposure: A Novel Environmental Risk Factor for Interstitial Lung Disease?

https://doi.org/10.1378/chest.14-1299Get rights and content

Abstract

Air pollution exposure is a well-established risk factor for several adverse respiratory outcomes, including airways diseases and lung cancer. Few studies have investigated the relationship between air pollution and interstitial lung disease (ILD) despite many forms of ILD arising from environmental exposures. There are potential mechanisms by which air pollution could cause, exacerbate, or accelerate the progression of certain forms of ILD via pulmonary and systemic inflammation as well as oxidative stress. This article will review the current epidemiologic and translational data supporting the plausibility of this relationship and propose a new conceptual framework for characterizing novel environmental risk factors for these forms of lung disease.

Section snippets

Air Pollution Overview

Ambient air pollution includes chemical, biologic, and particulate materials released into the atmosphere. Of the six criteria air pollutants regulated by the US Environmental Protection Agency (particulate matter [PM], ozone [O3], nitrogen dioxide [NO2], sulfur dioxide, carbon monoxide, and lead), PM, ground-level O3, and NO2have been most strongly associated with adverse respiratory outcomes.

PM is a uniquely complex mixture that may include solid particles, liquids, and vapors. Sources of PM

Respiratory Health Effects of Air Pollution (Epidemiology)

Air pollution exposure has been linked extensively to respiratory-related morbidity, particularly with respect to airways disease. Increased exposure levels have been associated with poorly controlled asthma,9, 10 asthma hospitalizations,11 impaired lung function growth,12 COPD incidence,13 and COPD exacerbations.14 Proximity to a major road, as a proxy of traffic-related air pollution, was associated with elevated pulmonary and systemic markers of inflammation and an increased risk of

Potential Mechanisms

There are plausible mechanisms by which air pollution may cause or exacerbate ILD (Table 1). Early animal studies demonstrated that chronic and subchronic exposure to high O3levels in monkeys and rats was associated with irreversible increases in collagen deposition.30, 31 Rats exposed to moderately high O3concentrations showed epithelial lesions with increased DNA synthesis in bronchiolar and type 2 epithelial cells shortly after exposure.32 The same study showed that coexposure to mixtures of

Integrating Environmental Exposures Into Disease Models: The Exposome

We believe a comprehensive assessment of environmental risk factors (termed the “exposome”) must be undertaken to fully delineate the contribution of ambient air pollution (and other exposures) to the complex pathobiology of pulmonary fibrosis. This global approach has been pioneered in cancer research and could be applied to the study of ILD.

The concept of the exposome was initially proposed as a framework to complement the genome, accounting for an individual's nongenetic/environmental risk

Conclusions

Ambient air pollution is a well-established risk factor for the development and worsening of many forms of pulmonary disease, and based on our evidence, we propose it may have an important role in the ILDs, particularly IPF. While definitive evidence is lacking, translational and epidemiologic data support the plausibility of a contributory relationship. The exposome may be a useful research concept, promoting characterization of the cumulative environmental exposures and their contribution to

Acknowledgments

Financial/nonfinancial disclosures:The authors have reported toCHESTthe following conflicts of interest: Dr Johannson reports travel support from InterMune Inc. Dr Collard reports personal fees from Bayer AG, Biogen Idec Inc, FibroGen Inc, Gilead Sciences Inc, InterMune Inc, Mesoblast Ltd, Moerae Matrix Inc, Pfizer Inc, Promedior Inc, Takeda Pharmaceutical Co Ltd, and grants from Boehringer-Ingelheim GmbH, Genentech Inc, National Heart, Lung and Blood Institute, and the University of

References (61)

  • C Solomon et al.

    Effect of serial-day exposure to nitrogen dioxide on airway and blood leukocytes and lymphocyte subsets

    Eur Respir J

    (2000)
  • MW Frampton et al.

    Nitrogen dioxide exposure: effects on airway and blood cells

    Am J Physiol Lung Cell Mol Physiol

    (2002)
  • NE Alexis et al.

    Low-level ozone exposure induces airways inflammation and modifies cell surface phenotypes in healthy humans

    Inhal Toxicol

    (2010)
  • C Scannell et al.

    Greater ozone-induced inflammatory responses in subjects with asthma

    Am J Respir Crit Care Med

    (1996)
  • H Song et al.

    Ozone induces inflammation in bronchial epithelial cells

    J Asthma

    (2011)
  • ST Larsen et al.

    Ozone increases airway hyperreactivity and mucus hyperproduction in mice previously exposed to allergen

    J Toxicol Environ Health A

    (2010)
  • YY Meng et al.

    Outdoor air pollution and uncontrolled asthma in the San Joaquin Valley, California

    J Epidemiol Community Health

    (2010)
  • JK Mann et al.

    Short-term effects of air pollution on wheeze in asthmatic children in Fresno, California

    Environ Health Perspect

    (2010)
  • ZJ Andersen et al.

    Long-term exposure to air pollution and asthma hospitalisations in older adults: a cohort study

    Thorax

    (2012)
  • WJ Gauderman et al.

    Association between air pollution and lung function growth in southern California children: results from a second cohort

    Am J Respir Crit Care Med

    (2002)
  • T Schikowski et al.

    Long-term air pollution exposure and living close to busy roads are associated with COPD in women

    Respir Res

    (2005)
  • F Dominici et al.

    Fine particulate air pollution and hospital admission for cardiovascular and respiratory diseases

    JAMA

    (2006)
  • TS Nawrot et al.

    The impact of traffic air pollution on bronchiolitis obliterans syndrome and mortality after lung transplantation

    Thorax

    (2011)
  • CH Goss et al.

    Effect of ambient air pollution on pulmonary exacerbations and lung function in cystic fibrosis

    Am J Respir Crit Care Med

    (2004)
  • M Jerrett et al.

    Long-term ozone exposure and mortality

    N Engl J Med

    (2009)
  • M Jerrett et al.

    Spatial analysis of air pollution and mortality in California

    Am J Respir Crit Care Med

    (2013)
  • C Schindler et al.

    SAPALDIA Team. Improvements in PM10 exposure and reduced rates of respiratory symptoms in a cohort of Swiss adults (SAPALDIA)

    Am J Respir Crit Care Med

    (2009)
  • CA Pope et al.

    Fine-particulate air pollution and life expectancy in the United States

    N Engl J Med

    (2009)
  • G Raghu et al.

    ATS/ERS/JRS/ALAT Committee on Idiopathic Pulmonary Fibrosis. An official ATS/ERS/JRS/ALAT statement: idiopathic pulmonary fibrosis: evidence-based guidelines for diagnosis and management

    Am J Respir Crit Care Med

    (2011)
  • K Iwai et al.

    Idiopathic pulmonary fibrosis. Epidemiologic approaches to occupational exposure

    Am J Respir Crit Care Med

    (1994)
  • Cited by (86)

    • Inflammation resolution in environmental pulmonary health and morbidity

      2022, Toxicology and Applied Pharmacology
      Citation Excerpt :

      PM2.5 facilitates M2 polarization through HDAC2 inhibition, upregulating TGFβ, MMP9 and MMP12 (Jiang et al., 2020). Recent studies suggest PM also exacerbates interstitial lung diseases such as IPF (Johannson et al., 2015; Harari et al., 2020; Winterbottom et al., 2018). PM2.5 increased acute inflammation and fibrosis after intratracheal administration in mice (Gangwar et al., 2020; Qin et al., 2018) and chronic exposure led to scar formation through progressive loss of alveolar structure (Günther et al., 2012; Selman et al., 2001).

    • Effects of air pollution on health: A mapping review of systematic reviews and meta-analyses

      2021, Environmental Research
      Citation Excerpt :

      The exponential growth in publication rates was also verified in similar studies (Dhital and Rupakheti, 2019) as in the present study, since from 2014 an overall progressive increase in publication of SRs and MAs was verified. Considering the most commonly investigated health outcome – respiratory disease, according to the US Environmental Protection Agency, PM, ground-level O3, and NO2 have been most strongly associated with adverse respiratory outcomes (Johannson et al., 2015). In a bibliometric analysis of publications on outdoor air pollution and respiratory health, Sweileh et al. (2018) observed that this research topic has accelerated lately and is receiving a lot of interest from researchers.

    View all citing articles on Scopus

    Funding/Support: Dr Johannson was supported by the GlaxoSmithKline/University of Calgary Advanced Fellowship in Respirology. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.

    View full text