Interventional Chest/Diagnostic Procedures

Pulmonary Physiology, Function, and Rehabilitation

Wildfires, particulate matter, and lung function

In the last 3 decades, human-caused climate change contributed to wildfires in an additional 4.2 million hectares of land across the western US alone. Human impact on climate is responsible for nearly doubling the expected wildfire area (Abatzoglou, et al. PNAS. 2016;113:11770). Year 2017 saw the most destructive wildfires in California recorded to date, and over $2 billion dollars was spent by the US Forest Service, the most-expensive on record. Besides the devastating effects on the forestry and nearby communities, wildfires also generate a large amount of particulate matter (PM). In western US, wildfires contributed to 71.3% of total PM2.5 on days exceeding regulatory PM2.5 standards during 2004-2009 (Liu et al. Clim Change. 2016;138:655). Acute PM exposure is associated with respiratory health effects, such as exacerbation of asthma and COPD, increased ED visits and hospitalization for pneumonia, and increased mortality. Chronic PM2.5 exposure may also affect lung function. Cross-shift and cross-season FEV1 declined by 0.150 L and 0.104 L, respectively in forest firefighters (Betchley, et al. Am. J Ind Med. 1997;31:503). The Children’s Health Study conducted in California found that subjects who were exposed to the highest level of exposure to PM2.5 were five times more likely to have an FEV1 less than 80% of expected FEV1 when they reached 18 years of age than subjects exposed to the lowest level of PM2.5 (Gauderman et al. N Engl J Med. 2004;351:1057). Clinicians should educate patients and the public how to protect our environment and, when wildfires occur, how to protect themselves from exposure to PM.

Thomas W. DeCato, MD
Fellow-in-Training Committee Member

Yuh-Chin T. Huang, MD, FCCP
Steering Committee Member
 

Pulmonary Vascular Disease

Small increases in pulmonary pressures—big impact

Pulmonary hypertension (PH) is a progressive, life-limiting pulmonary vascular disease that is diagnosed hemodynamically by right-sided heart catheterization (RHC) and defined by a mean pulmonary artery pressure (mPAP) >25 mm Hg (Hoeper MM, et al. JACC. 2013;62(25 Suppl):D42).

The impact of PH on survival both in its “pure” form, pulmonary arterial hypertension, and in the setting of underlying cardiopulmonary disease, is well established. However, the clinical relevance of mildly elevated mPAP, defined as mPAP between 18 and 24 mm Hg, has been unclear until recently. Two large cohort studies have suggested that mild increases in mPAP are clinically relevant. A large retrospective analysis of hemodynamic data from 21,727 US veterans found mildly increased mPAP (19-24 mm Hg) was associated with increased hospitalization and decreased survival (Maron, et al. Circulation. 2016;133:1240).

While this population was skewed toward elderly men, a study from Vanderbilt University that included equal numbers of men and women showed similar results. Patients with mPAP 19-24 mm Hg experienced incrementally increased mortality (HR:1.31, P=.001). Importantly, in the subset of patients who underwent a repeat RHC in follow-up, 61% developed progressive increases of pulmonary pressures (>25 mm Hg) on follow-up RHC suggesting that the disease process may progress in a substantial proportion of patients (Assad, et al. JAMA Cardiol. 2017;2[1]):1361). Combined with prior data from smaller cohorts, these studies highlight the impact of mildly increased pulmonary pressures on outcomes. Given the dearth of available data regarding interventions for these patients, there is an urgent need to study to role of specific therapy for mildly elevated pulmonary pressures.

Vijay Balasubramanian, MD, FCCP
Steering Committee Member

Jean Elwing, MD, FCCP
Steering Committee Vice-Chair