INTRODUCTION: Inhalational injury is a known cause of primary bronchiolitis and a number of substances including chlorine, sulfur dioxide, and phosgene have been identified as inciting agents. A small cohort of US Army soldiers were diagnosed with biopsy proven bronchiolitis after service in Iraq. All had presented with duty-limiting dyspnea and many were exposed to the sulfur dioxide fires at the Mishraq Sulfur Mine near Mosul in June 2003.(1) A portion of this same group of soldiers reported no inhalational exposures despite similar symptoms. Thus, there appears to be other unknown inhalants producing similar pathophysiological manifestations as the sulfur. We report a case of an Army soldier who has developed limiting bronchiolitis after serving in Iraq during 2005 and 2009 despite the absence of exposure to sulfur dioxide fires.
CASE PRESENTATION: A 56-year-old non smoking male presented to his primary care physician with a complaint of dyspnea on exertion of one year's duration. He carries a history of obstructive sleep apnea with nightly non-invasive ventilation (NIV), post-traumatic stress disorder, peripheral neuropathy and post-vaccine encephalitis. He served as a surgeon for 1 month in Balad (2005) as well as 3 months in Tikrit (2009). For his dyspnea, he underwent an initial cardiac evaluation which was normal. His subsequent pulmonary evaluation was notable for an adequate 6 minute walk test, and mild gas exchange abnormality on his pulmonary function tests. A computed tomography (CT) scan demonstrated subpleural, posteriorly located right lower lobe airspace disease. Subsequent VATS lung biopsy revealed mild, chronic inflammation of the small airways with bronchiolectasia and mild peribronchial fibrosis. Physical examination was notable only for a body mass index of 40, with no physical manifestations of hypoxemia. Repeat pulmonary function testing demonstrated a mild restrictive ventilatory defect with a mild gas exchange abnormality. Cardiopulmonary exercise testing revealed normal functional capabilities with a mildly reduced VO2max. The patient was instructed to lose weight and required no systemic therapy.
DISCUSSIONS: Morbid obesity has been previously reported to be associated with reductions in expiratory reserve volumes as well as DLCO. It can also account for our patient’s suboptimal cardiopulmonary exercise test. However, the documented bronchiolitis and CT findings would be consistent with airway injury not explained by his obesity. Inhalation of a variety of toxic substances has the potential to cause bronchiolitis and an injury pattern similar to the one exhibited here. Furthermore, a similar pattern of findings were exhibited by the soldiers deployed from Fort Campbell to Iraq, specifically those without sulfur dioxide exposure. It is not clear what particular agent may be responsible for these findings, but given the variety of exposures associated with the intense combat environment within Iraq, including its desert location, burn pits, burning human waste, weapon operation and diesel exhaust, any number of possibilities could be implicated.(2) Given the large number of troops deployed during the Iraq War, the potential exists for a growing patient population with a similar presentation and duty-limiting complications.
CONCLUSION: Bronchiolitis should be on the differential diagnosis for soldiers serving in Iraq presenting with similar symptoms and imaging. Further research and insight will standardize an approach to diagnosis, treatment and potentially preventative measures.
DISCLOSURE: William Bender, No Financial Disclosure Information; No Product/Research Disclosure Information