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Interstitial lung disease
Original research
Relative environmental and social disadvantage in patients with idiopathic pulmonary fibrosis
  1. Na'ama Avitzur1,
  2. Elizabeth M Noth2,
  3. Mubasiru Lamidi3,
  4. Steven D Nathan4,
  5. Harold R Collard5,
  6. Alison M DeDent5,
  7. Neeta Thakur5,
  8. Kerri A Johannson1,6
  1. 1Department of Medicine, University of Calgary, Calgary, Alberta, Canada
  2. 2Division of Environmental Health Sciences, School of Public Health, University of California Berkeley, Berkeley, California, USA
  3. 3Department of Biostatistics, University of Calgary, Calgary, Alberta, Canada
  4. 4Inova Heart and Vascular Institute, Inova Fairfax Hospital, Falls Church, Virginia, USA
  5. 5Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California San Francisco, San Francisco, California, USA
  6. 6Department of Community Health Sciences, University of Calgary, Calgary, Alberta, Canada
  1. Correspondence to Dr Kerri A Johannson, Department of Medicine, University of Calgary, Calgary, AB T2N 1N4, Canada; kerri.johannson{at}ahs.ca

Abstract

Background Air pollution exposure is associated with disease severity, progression and mortality in patients with idiopathic pulmonary fibrosis (IPF). Combined impacts of environmental and socioeconomic factors on outcomes in patients with IPF are unknown. The objectives of this study were to characterise the relationships between relative environmental and social disadvantage with clinical outcomes in patients with IPF.

Methods Patients with IPF were identified from a longitudinal database at University of California, San Francisco. Residential addresses were geocoded and linked to the CalEnviroScreen 3.0 (CES), a tool that quantifies environmental burden in California communities, combining population, environmental and pollution vulnerability into individual and composite scores (higher scores indicating greater disadvantage). Unadjusted and adjusted linear and logistic regression and Fine and Gray proportional hazards models were used.

Results 603 patients were included. Higher CES was associated with lower baseline forced vital capacity (β=−0.073, 95% CI −0.13 to −0.02; p=0.006) and diffusion capacity of the lung for carbon monoxide (β=−0.11, 95% CI −0.16 to −0.06; p<0.001). Patients in the highest population vulnerability quartile were less likely to be on antifibrotic therapy (OR=0.33; 95% CI 0.18 to 0.60; p=0.001) at time of enrolment, compared with those in the lowest quartile. An association between CES and mortality was suggested, but sensitivity analyses demonstrated inconsistent results. Relative disadvantage of the study cohort appeared lower compared with the general population.

Conclusions Higher environmental exposures and vulnerability were associated with lower baseline lung function and lower antifibrotic use, suggesting that relative socioenvironmental disadvantage has meaningful impacts on patients with IPF.

  • interstitial fibrosis
  • clinical epidemiology
  • idiopathic pulmonary fibrosis

Data availability statement

Data are available on reasonable request.

http://dx.doi.org/10.1136/thoraxjnl-2021-217652

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    Data availability statement

    Data are available on reasonable request.

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    Footnotes

    • Contributors NA, EMN, SDN and KAJ conceived of the study. All authors provided critical intellectual input on study design, data analysis and interpretation, and manuscript preparation. KAJ is the acting guarantor and accepts full responsibility for the work.

    • Funding This study was funded by the CHEST Foundation Research Grant for Pulmonary Fibrosis.

    • Map disclaimer The depiction of boundaries on the map(s) in this article does not imply the expression of any opinion whatsoever on the part of BMJ (or any member of its group) concerning the legal status of any country, territory, jurisdiction or area or of its authorities. The map(s) are provided without any warranty of any kind, either express or implied.

    • Competing interests SDN is a consultant and is on the speakers bureau for Roche-Genentech and Boehringer-Ingelheim. He is also a consultant for Bellerophon, United Therapeutics and Galapagos. KAJ reports grants, personal fees and other from Boehringer-Ingelheim, personal fees and other from Hoffman La Roche, personal fees and other from Theravance, personal fees and other from Blade Therapeutics, grants from Chest Foundation, grants from University of Calgary School of Medicine, grants from Pulmonary Fibrosis Society of Calgary, grants and personal fees from Three Lakes Foundation, personal fees from Pliant Therapeutic, outside the submitted work.

    • Provenance and peer review Not commissioned; externally peer reviewed.