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Equine asthma (EA) is an important cause of wastage in the USA horse industry. Exposure to organic particulates, from stable dust, airborne pollen, and fungal loads, is posited to be the main cause. Dust arising from the earth's crust has been largely ignored as a contributor to EA in the veterinary literature. The objectives of this study were to investigate the occurrence of birefringent particulates in the bronchoalveolar lavage fluid (BALF) of horses with a clinical complaint of EA residing in the arid West of the USA v. the East, in an effort to determine the contribution of geolocation to geogenic dust exposure. We analyzed BALF cytology and historical data sent to our referral clinical laboratory from 148 horses from the West Coast and 233 horses from the East Coast of the USA over a 6-year period, using light microscopy to determine cell proportions and other visible elements as well as a polarizing lens to detect birefringent material. Univariate analysis showed that horses from the West coast were significantly more likely to have birefringent particulates in the BALF than horses from the East coast (40.5% v. 8.6%, p < 0.001); while horses from the East had higher BALF neutrophil proportions. Horses from the West also had lower proportions of neutrophils in the BALF than those from the East (27.1 v. 10.9, p < .001). Using historical and BAL data in a forward stepwise binary logistic regression model with presence of birefringent particulates found within alveolar macrophages as the outcome, geographical location in the West retained significance as a predictor (OR 8.0, CI [4.3-14.8], p< .001). While the birefringent particulates cannot be identified on the basis of polarizing microscopy alone, this study provides evidence that horses from the West are exposed to inorganic particulates that may contribute to signs of equine asthma., Competing Interests: The authors declare that no competing interests exist., (Copyright: © 2024 Mazan, Deveney. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Background: Hemosiderophages in bronchoalveolar lavage fluid (BALF) are commonly ascribed to exercise-induced pulmonary hemorrhage (EIPH). Little information exists regarding the presence of these cells in horses that perform light or no work and that are referred for respiratory problems., Objectives: Evaluate the presence of hemosiderophages in BALF of horses suspected of respiratory disease without history of or risk factors for EIPH and determine predictors of hemosiderophages in BALF in this population., Methods: Observational retrospective cross-sectional study using STROBE (Strengthening the Reporting of Observational Studies in Epidemiology) guidelines. Bronchoalveolar lavage fluid cytology reports of 353 horses evaluated for respiratory disease between 2012 and 2022 at the Cummings School for Veterinary Medicine were reviewed retrospectively. Horses with a history or likelihood of having performed past strenuous exercise were removed, and the remaining 91 horses were divided into hemosiderin-positive (HSD-POS) and hemosiderin-negative groups based on Perls' Prussian blue staining. Potential predictors for the presence of hemosiderophages in BALF (history, clinical evaluation, baseline lung function, airway reactivity, BALF cytology, and hemosiderin score) were compared between the 2 groups, using univariate and multivariate analyses., Results: Horses with a diagnosis of severe equine asthma (sEA; odds ratio, 11.1; 95% confidence interval, 3.2-38.5; P < .001) were significantly more likely to be HSD-POS than horses with mild-to-moderate equine asthma., Conclusions and Clinical Importance: Hemosiderophages were found in the BALF cytology in a subset of horses that perform light or no work and presented for respiratory signs; these cells were found more frequently in horses with sEA. The link between hemosiderophages and sEA highlights previously unstudied pathology associated with this common disease., (© 2023 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine.)

The airways are the first part of the pathway in the oxygen transport chain that is critical to excellent athletic performance, and the lower airways are considered the final gatekeeper before oxygen enters the blood and carbon dioxide exits. Horses are blessed with large airways and lungs that allow them to be superb athletes, but the down side of this largesse on the part of evolution is that unless they are truly elite athletes they may withstand noninfectious disease of the lower respiratory tract for months to years before the owner or trainer notices. The two conditions of the lower respiratory tract that affect the athletic horse during exercise are exercise-induced pulmonary hemorrhage and inflammatory airway disease. The former may be considered, at least at the onset, as a problem of physiology rather than a disease, and the latter is a disease primarily of domestication: both are widespread among the athletic horse population and account for an impressive number of horses that fail to perform to their potential. Because of the high demands for oxygen in the athletic horse, even minor insults to the oxygen-carrying capacity of the body can affect performance, so it is of critical importance to keep the lungs as healthy as possible., (Copyright © 2018 Elsevier Inc. All rights reserved.)

While aging leads to a reduction in the capacity for regeneration after pneumonectomy (PNX) in most mammals, this biological phenomenon has not been characterized over the lifetime of mice. We measured the age-specific (3, 9, 24 month) effects of PNX on physiology, morphometry, cell proliferation and apoptosis, global gene expression, and lung fibroblast phenotype and clonogenicity in female C57BL6 mice. The data show that only 3 month old mice were fully capable of restoring lung volumes by day 7 and total alveolar surface area by 21 days. By 9 months, the rate of regeneration was slower (with incomplete regeneration by 21 days), and by 24 months there was no regrowth 21 days post-PNX. The early decline in regeneration rate was not associated with changes in alveolar epithelial cell type II (AECII) proliferation or apoptosis rate. However, significant apoptosis and lack of cell proliferation was evident after PNX in both total cells and AECII cells in 24 mo mice. Analysis of gene expression at several time points (1, 3 and 7 days) post-PNX in 9 versus 3 month mice was consistent with a myofibroblast signature (increased Tnc, Lox1, Col3A1, Eln and Tnfrsf12a) and more alpha smooth muscle actin (aSMA) positive myofibroblasts were present after PNX in 9 month than 3 month mice. Isolated lung fibroblasts showed a significant age-dependent loss of clonogenicity. Moreover, lung fibroblasts isolated from 9 and 17 month mice exhibited higher &agr;SMA, Col3A1, Fn1 and S100A expression, and lower expression of the survival gene Mdk consistent with terminal differentiation. These data show that concomitant loss of clonogenicity and progressive myofibroblastic differentiation contributes to the age-dependent decline in the rate of lung regeneration. [ABSTRACT FROM AUTHOR]