Background The prevalence of pleural abnormalities in the general population is an epidemiologically important index of asbestos exposure, which has not been investigated since a radiography-based study in 1980.
Methods We examined 2633 chest CT scans (mean 59.2 years, 50% female) from the Framingham Heart Study (FHS) for the presence and image characteristics of pleural plaques and diffuse pleural thickening. Demographics and pulmonary function were stratified by the presence of pleural abnormalities in association with interstitial lung abnormalities.
Results Pleural abnormalities were present in 1.5% (95% CI 1.1% to 2.1%). Pleural lesions were most commonly bilateral (90.0%), multiple (77.5%), calcified (97.5%) and commonly involved posterior (lower: 92.5%, middle: 87.5%), anterior (upper: 77.5%, middle: 77.5%) and diaphragmatic areas (72.5%). Participants with pleural abnormalities were significantly older (75.7 years, p <0.0001), male (92.5%, p <0.0001), former or current smokers (80.0%, p <0.001) with higher pack-years (33.3, p <0.0001). No significant reduction was noted in pulmonary function measures (p=0.07–0.94) when adjusted for the associated covariates, likely due to small number of cases with pleural abnormalities. Information about prior history of asbestos exposure and occupation was not available.
Conclusions Pleural plaques and diffuse pleural thickening are present on CT in 1.5% of the FHS cohort. The current prevalence of the pleural abnormalities is smaller than that reported in the previous population-based study using chest radiography, likely representing lower asbestos exposure in recent decades. The posterior portion of the pleura is most frequently involved but the anterior portion is also commonly involved.
- pleural plaque
- diffuse pleural thickening
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Contributors Each author has participated sufficiently in this submission to take public responsibility for its content. Publication has been approved by all authors and tacitly or explicitly by the responsible authorities where the work was carried out.
Funding MN is supported by NIH Grant Number: K23 CA157631. GRW is supported by NIH Grant Number: R01 HL122464, R01 HL116473 and R01 HL107246. GMH and this work were supported by NIH Grant Numbers: P01 HL114501, and R01 HL111024. This work was partially supported by the NHLBI’s Framingham Heart Study contract: N01 HC25195.
Competing interests MN reports consultancies or research grants with Bristol-Myers Aquibb Company, Canon Inc, and Merck & Co Inc. GW reports consultancies with GlaxoSmithKline and Genentech. HH reports research grants from Toshiba Corporation, AZE Ltd, Canon Inc and Konica Minolta Group.
Ethics approval Brigham and Women's Hospital, and Boston University.
Provenance and peer review Not commissioned; externally peer reviewed.