Computational models are useful for understanding respiratory physiology. Crucial to such models are the boundary conditions specifying the flow conditions at truncated airway branches (terminal flow rates). However, most studies make assumptions about these values, which are difficult to obtain in vivo. We developed a computational fluid dynamics (CFD) model of airflows for steady expiration to investigate how terminal flows affect airflow patterns in respiratory airways. First, we measured in vitro airflow patterns in a physical airway model, using particle image velocimetry (PIV). The measured and computed airflow patterns agreed well, validating our CFD model. Next, we used the lobar flow fractions from a healthy or chronic obstructive pulmonary disease (COPD) subject as constraints to derive different terminal flow rates (i.e., three healthy and one COPD) and computed the corresponding airflow patterns in the same geometry. To assess airflow sensitivity to the boundary conditions, we used the correlation coefficient of the shape similarity (R) and the root-mean-square of the velocity magnitude difference (Drms) between two velocity contours. Airflow patterns in the central airways were similar across healthy conditions (minimum R, 0.80) despite variations in terminal flow rates but markedly different for COPD (minimum R, 0.26; maximum Drms, ten times that of healthy cases). In contrast, those in the upper airway were similar for all cases. Our findings quantify how variability in terminal and lobar flows contributes to airflow patterns in respiratory airways. They highlight the importance of using lobar flow fractions to examine physiologically relevant airflow characteristics.

BACKGROUND: There is significant concern about the respiratory health of deployed military service members given the reported airborne hazards in southwest Asia, which range from geologic dusts, burn pit emissions, chemical exposures, and increased rates of smoking. There has been no previous comparison of pre- and post-deployment lung function in these individuals. METHODS: Military personnel who deployed to southwest Asia in support of ongoing military operations were recruited from the Soldier Readiness Processing Center at Fort Hood, Texas, from 2011 to 2014. The participants were asked to complete a brief survey on their respiratory health and perform both spirometry and impulse oscillometry studies at baseline with repeated survey and testing after deployment. RESULTS: Of the 1,693 deployed personnel who completed baseline examinations, 843 (50%) completed post-deployment testing. Post-deployment values demonstrated no statistical or clinical change in spirometry, with an increase in mean ± SD FEV ₁ (% predicted) from 95.2 ± 12.6 to 96.1 ± 12.4 ( P = .14), increase in mean ± SD FVC (% predicted) from 95.9 ± 11.8 to 96.4 ± 11.9 ( P = .32), and increase in mean ± SD FEV ₁ /FVC from 81.5 ± 5.9 to 81.8 ± 6.1 ( P = .29). Impulse oscillometry values showed statistical improvement with reduction in resistance (at 5 Hz and 20 Hz) and reactance (at 5 Hz). The presence of pre-deployment obstruction, self-reported asthma, smoking history, or increased body mass index also did not change spirometry values after deployment. DISCUSSION: To our knowledge, this was the first prospective evaluation of deploying military by using spirometry as an indicator for the possible development of pulmonary disease related to environmental exposures. Pre-deployment testing with spirometry and impulse oscillometry was unable to detect any significant change. In those with abnormal spirometry pre-deployment or asthma history, there was also not identifiable change that indicated worsening lung function. CONCLUSIONS: Utilization of spirometry for the deploying military population had little benefit and did not identify individuals with lung disease after deployment. Routine use was not warranted before or after deployment in the absence of pulmonary symptoms.

Military personnel are a unique group of individuals referred to the pulmonary physician for evaluation. Despite accession standards that limit entrance into the military for individuals with various pre-existing lung diseases, the most common disorders found in the general population such as asthma and chronic obstructive pulmonary disease remain frequently diagnosed. Military personnel generally tend to be a more physically fit population who are required to exercise on a regular basis and as such may have earlier presentations of disease than their civilian counterparts. Exertional dyspnea is a common complaint; establishing a diagnosis may be challenging given the subtle nature of symptoms and lack of specificity with pulmonary function testing. The conflicts over the past 10 years in Iraq and Afghanistan have also given rise to new challenges for deployed military. Various respiratory hazards in the deployed environment include suspended geologic dusts, burn pits, vehicle exhaust emissions, industrial air pollution, and isolated exposure incidents and may give rise to both acute respiratory symptoms and chronic lung disease. In the evaluation of deployed military personnel, establishing the presence of actual pulmonary disease and the relationship of existing disease to deployment is an ongoing issue to both military and civilian physicians. This paper reviews the current evidence for chronic lung disease in the deployed military population and addresses any differences in diagnosis and management.

We have identified candidate protein and microRNA (miRNA) biomarkers for dyspnea by studying serum, lavage fluid, and urine from military personnel who reported serious respiratory symptoms after they were deployed to Iraq or Afghanistan. Forty-seven soldiers with the complaint of dyspnea who enrolled in the STudy of Active Duty Military Personnel for Environmental Dust Exposure (STAMPEDE) underwent comprehensive pulmonary evaluations at the San Antonio Military Medical Center. The evaluation included fiber-optic bronchoscopy with bronchoalveolar lavage. The clinical findings from the STAMPEDE subjects pointed to seven general underlying diagnoses or findings including airway hyperreactivity, asthma, low diffusivity of carbon monoxide, and abnormal cell counts. The largest category was undiagnosed. As an exploratory study, not a classification study, we profiled proteins or miRNAs in lavage fluid, serum, or urine in this group to look for any underlying molecular patterns that might lead to biomarkers. Proteins in lavage fluid and urine were identified by accurate mass tag (database-driven) proteomics methods while miRNAs were profiled by a hybridization assay applied to serum, urine, and lavage fluid. Over seventy differentially expressed proteins were reliably identified both from lavage and from urine in forty-eight dyspnea subjects compared to fifteen controls with no known lung disorder. Six of these proteins were detected both in urine and lavage. One group of subjects was distinguished from controls by expressing a characteristic group of proteins. A related group of dyspnea subjects expressed a unique group of miRNAs that included one miRNA that was differentially overexpressed in all three fluids studied. The levels of several miRNAs also showed modest but direct associations with several standard clinical measures of lung health such as forced vital capacity or gas exchange efficiency. Candidate proteins and miRNAs associated with the general diagnosis of dyspnea have been identified in subjects with differing medical diagnoses. Since these markers can be measured in readily obtained clinical samples, further studies are possible that test the value of these findings in more formal classification or case–control studies in much larger cohorts of subjects with specific lung diseases such as asthma, emphysema, or some other well-defined lung disease.