Adams Traci N, Redlich Carrie A, Glazer Craig S, Gulati Mridu
Division of Pulmonary and Critical Care Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
Yale Occupational Medicine and Environmental Medicine, Yale School of Medicine, New Haven, Connecticut, United States of America.
PLoS One. 2025 May 8;20(5):e0323093. doi: 10.1371/journal.pone.0323093. eCollection 2025.
Home mold exposure is a commonly overlooked cause of hypersensitivity pneumonitis. This is in part due to the limited literature supporting the association as well as the lack of exposure characterization available in reported cases. Notably, climate change, extreme weather patterns and frequent flooding continue to create conditions that promote home mold growth. As remediation has the potential to improve outcomes, clinicians need to remain vigilant in searching for and identifying potential mold exposure in suspected HP patients. The purpose of this study is to describe a large retrospective cohort of patients with home mold associated HP.
HP patients were identified retrospectively from our single center interstitial lung disease (ILD) database between 2011-2019. Patients with a moderate, high, or definite confidence diagnosis of HP were included. The presence of residential mold exposure was confirmed by medical chart review by a pulmonologist trained in exposure assessment.
Home mold exposure was identified as the culprit antigen in 54 of 231 hypersensitivity pneumonitis patients. An invasive procedure (bronchoalveolar lavage, transbronchial biopsy, and/or surgical lung biopsy) was performed to confirm the diagnosis of HP in 85.7% of the cohort. Home mold was principally caused by chronic and/or recurring water intrusion. The most common locations of mold within the home included the bathroom, bedroom, and air conditioning unit. Transplant free survival was 97.7 months, which did not differ from the 50 HP patients in our cohort with HP associated with a mold exposure outside the home or patients in our cohort with HP associated with avian antigen exposure. Of the 41 patients who removed the exposure, 5 (12.2%) had a > 10% improvement in FVC, including 4 with fibrotic HP.
Our study is the largest to report an association between HP and home mold exposure and is the first report from the region of north Texas. As climate change continues to disrupt weather patterns causing storms and flooding in certain areas, clinicians should remain alert to the presence of mold and its potential contribution to development of HP.
家庭霉菌暴露是超敏性肺炎一个常被忽视的病因。部分原因在于支持这种关联的文献有限,以及报告病例中缺乏暴露特征描述。值得注意的是,气候变化、极端天气模式和频繁洪水持续创造促进家庭霉菌生长的条件。由于进行整治有可能改善预后,临床医生在疑似超敏性肺炎患者中寻找和识别潜在霉菌暴露时需保持警惕。本研究的目的是描述一大组与家庭霉菌相关的超敏性肺炎患者的回顾性队列。
通过回顾性研究,从我们单中心2011年至2019年的间质性肺病(ILD)数据库中识别出超敏性肺炎患者。纳入中度、高度或确诊为超敏性肺炎的患者。由接受过暴露评估培训的肺科医生通过病历审查确认是否存在家庭霉菌暴露。
在231例超敏性肺炎患者中,有54例被确定家庭霉菌暴露为致病抗原。85.7%的队列患者接受了侵入性检查(支气管肺泡灌洗、经支气管活检和/或外科肺活检)以确诊超敏性肺炎。家庭霉菌主要由慢性和/或反复的水侵入引起。家庭中霉菌最常见的位置包括浴室、卧室和空调设备。无移植生存时间为97.7个月,这与我们队列中50例与家庭外霉菌暴露相关的超敏性肺炎患者或与禽类抗原暴露相关的超敏性肺炎患者没有差异。在41例消除暴露的患者中,5例(12.2%)的用力肺活量(FVC)改善超过10%;其中4例为纤维化超敏性肺炎。
我们的研究是报告超敏性肺炎与家庭霉菌暴露之间关联的最大规模研究,也是北德克萨斯地区的首份报告。随着气候变化继续扰乱天气模式,在某些地区引发风暴和洪水,临床医生应警惕霉菌的存在及其对超敏性肺炎发病的潜在影响。