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.
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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.
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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.
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