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Original research
Ambient air pollution exposure and risk and progression of interstitial lung abnormalities: the Framingham Heart Study
  1. Mary B Rice1,
  2. Wenyuan Li2,
  3. Joel Schwartz3,
  4. Qian Di3,
  5. Itai Kloog4,
  6. Petros Koutrakis3,
  7. Diane R Gold3,
  8. Robert W Hallowell1,
  9. Chunyi Zhang1,
  10. George O'Connor5,6,
  11. George R Washko7,
  12. Gary M Hunninghake7,
  13. Murray A Mittleman2
  1. 1 Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
  2. 2 Epidemiology, Harvard University T H Chan School of Public Health, Boston, Massachusetts, USA
  3. 3 Environmental Health, Harvard University T H Chan School of Public Health, Boston, Massachusetts, USA
  4. 4 Geography and Environmental Development, Ben-Gurion University of the Negev, Beer-Sheva, Israel
  5. 5 Medicine, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts, USA
  6. 6 Framingham Heart Study, Framingham, Massachusetts, USA
  7. 7 Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
  1. Correspondence to Dr Mary B Rice, Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA; mrice1{at}


Background Ambient air pollution accelerates lung function decline among adults, however, there are limited data about its role in the development and progression of early stages of interstitial lung disease.

Aims To evaluate associations of long-term exposure to traffic and ambient pollutants with odds of interstitial lung abnormalities (ILA) and progression of ILA on repeated imaging.

Methods We ascertained ILA on chest CT obtained from 2618 Framingham participants from 2008 to 2011. Among 1846 participants who also completed a cardiac CT from 2002 to 2005, we determined interval ILA progression. We assigned distance from home address to major roadway, and the 5-year average of fine particulate matter (PM2.5), elemental carbon (EC, a traffic-related PM2.5 constituent) and ozone using spatio-temporal prediction models. Logistic regression models were adjusted for age, sex, body mass index, smoking status, packyears of smoking, household tobacco exposure, neighbourhood household value, primary occupation, cohort and date.

Results Among 2618 participants with a chest CT, 176 (6.7%) had ILA, 1361 (52.0%) had no ILA, and the remainder were indeterminate. Among 1846 with a preceding cardiac CT, 118 (6.4%) had ILA with interval progression. In adjusted logistic regression models, an IQR difference in 5-year EC exposure of 0.14 µg/m3 was associated with a 1.27 (95% CI 1.04 to 1.55) times greater odds of ILA, and a 1.33 (95% CI 1.00 to 1.76) times greater odds of ILA progression. PM2.5 and O3 were not associated with ILA or ILA progression.

Conclusions Exposure to EC may increase risk of progressive ILA, however, associations with other measures of ambient pollution were inconclusive.

  • interstitial fibrosis
  • imaging/CT MRI etc
  • clinical epidemiology

Statistics from


  • Contributors MBR, MAM and GMH designed the study with contributions from and the approval of all the other co-authors. GO and GRW obtained the Framingham chest imaging data and GMH designed and managed the process for ascertaining ILA status on each image. MBR performed all statistical analyses with assistance from CZ and WL, who reviewed and verified the code. RWH and GMH contributed as experts on interstitial lung disease. IK developed and validated the PM2.5 model and QD developed and validated the models for EC and ozone, under the supervision of JS. PK, DRG, MAM and JS provided input in the study design and interpretation of the data as part of Harvard’s Clean Air Research Center. All authors provided critical input and read and approved the final version of the manuscript.

  • Funding This work was supported by the National Institute for Environmental Health Sciences (K23 ES026204 and P30 00002). This work was also supported by the National Heart, Lung and Blood Institute (the Framingham Heart Study Contract Nos. N01-HC-25195), the US Environmental Protection Agency (RD-835872) and the US Department of Health and Human Services (HHSN268201500001I). This publication’s contents are solely the responsibility of the grantee and do not necessarily represent the official views of the US EPA; the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the US Department of Health and Human Services. Further, US EPA does not endorse the purchase of any commercial products or services.

  • Competing interests There are no competing interests for any author.

  • Patient consent for publication Not Required.

  • Process to replicate results Research applications can be submitted to the Framingham Heart Study Research Review Committees online at

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

  • Data availability statement Data are available upon reasonable request.

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