Unexplained dyspnea linked to mitochondrial myopathy following military deployment to Southwest Asia and Afghanistan.

We identified a case of probable mitochondrial myopathy (MM) in a soldier with dyspnea and reduced exercise tolerance through cardiopulmonary exercise testing (CPET) following Southwest Asia (SWA) deployment. Muscle biopsy showed myopathic features. We compared demographic, occupational exposure, and clinical characteristics in symptomatic military deployers with and without probable MM diagnosed by CPET criteria. We evaluated 235 symptomatic military personnel who deployed to SWA and/or Afghanistan between 2010 and 2021. Of these, 168 underwent cycle ergometer maximal CPET with an indwelling arterial line. We defined probable MM based on five CPET criteria: arterial peak exercise lactate >12 mEq/L, anaerobic threshold (AT) ≤50%, maximum oxygen consumption (VO2max ) <95% predicted, oxygen (O2) pulse percent predicted (pp) at least 10% lower than heart rate pp, and elevated ventilatory equivalent for O2 at end exercise (VE/VO2 ≥ 40). We characterized demographics, smoking status/pack-years, spirometry, and deployment exposures, and used descriptive statistics to compare findings in those with and without probable MM. We found 9/168 (5.4%) deployers with probable MM. Compared to symptomatic deployers without probable MM, they were younger (p = 0.0025) and had lower mean BMI (p = 0.02). They had a higher mean forced expiratory volume (FEV1)pp (p = 0.02) and mean arterial oxygen partial pressure (PaO2) at maximum exercise (p = 0.0003). We found no significant differences in smoking status, deployment frequency/duration, or inhalational exposures. Our findings suggest that mitochondrial myopathy may be a cause of dyspnea and reduced exercise tolerance in a subset of previously deployed military personnel. CPET with arterial line may assist with MM diagnosis and management.

Respiratory Diseases in Post-9/11 Military Personnel Following Southwest Asia Deployment.

OBJECTIVE: Persistent respiratory symptoms following post-9/11 military deployment to Iraq and Afghanistan are well-recognized, but the spectrum of respiratory diseases remains poorly characterized. This study describes deployment-related respiratory diseases and the diagnostic utility of resting and exercise pulmonary function testing. METHODS: Between 2009 and 2017, 127 consecutive military workers ("deployers") with new-onset respiratory symptoms underwent clinical evaluation. Deployment-related respiratory diseases were classified as proximal and/or distal. Using descriptive statistics and logistic regression, we analyzed lung function parameters associated with deployment-related distal lung disease (DDLD). RESULTS: Common deployment-related respiratory diseases included asthma (31.5%), intermittent laryngeal obstruction (14.2%), rhinosinusitis (15%), and DDLD (68.5%). Decreased diffusion capacity (odds ratio [OR] = 4.6, 95% confidence interval [CI]: 1.4 to 15.1, P = 0.01) was significantly associated with DDLD. CONCLUSIONS: A comprehensive diagnostic approach may identify a spectrum of proximal and distal respiratory diseases that can occur in symptomatic post-9/11 deployers, requiring a personalized approach to care.

Beryllium increases the CD14(dim)CD16+ subset in the lung of chronic beryllium disease.

CD14dimCD16+ and CD14brightCD16+ cells, which compose a minor population of monocytes in human peripheral blood mononuclear cells (PBMC), have been implicated in several inflammatory diseases. The aim of this study was to investigate whether this phenotype was present as a subset of lung infiltrative alveolar macrophages (AMs) in the granulomatous lung disease, chronic beryllium disease (CBD). The monocytes subsets was determined from PBMC cells and bronchoalveolar lavage (BAL) cells from CBD, beryllium sensitized Non-smoker (BeS-NS) and healthy subjects (HS) using flow cytometry. The impact of smoking on the AMs cell phenotype was determined by using BAL cells from BeS smokers (BeS-S). In comparison with the other monocyte subpopulations, CD14dimCD16+ cells were at decreased frequency in PBMCs of both BeS-NS and CBD and showed higher HLA-DR expression, compared to HS. The AMs from CBD and BeS-NS demonstrated a CD14dimCD16+phenotype, while CD14brightCD16+ cells were found at increased frequency in AMs of BeS, compared to HS. Fresh AMs from BeS-NS and CBD demonstrated significantly greater CD16, CD40, CD86 and HLA-DR than HS and BeS-S. The expression of CD16 on AMs from both CBD and BeS-NS was downregulated significantly after 10µM BeSO4 stimulation. The phagocytic activity of AMs decreased after 10µM BeSO4 treatment in both BeS-NS and CBD, although was altered or reduced in HS and BeS-S. These results suggest that Be increases the CD14dimCD16+ subsets in the lung of CBD subjects. We speculate that Be-stimulates the compartmentalization of a more mature CD16+ macrophage phenotype and that in turn these macrophages are a source of Th1 cytokines and chemokines that perpetuate the Be immune response in CBD. The protective effect of cigarette smoking in BeS-S may be due to the low expression of co-stimulatory markers on AMs from smokers as well as the decreased phagocytic function.