{'fraction_non_alphanumeric': 0.02528658125421443, 'fraction_numerical': 0.0077545515846257585, 'mean_word_length': 5.549668874172186, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Pulmonary Function Evaluation in Elite Swimmers: A Case Series of Environmental Considerations

Introduction Reactive airway disease, airway hyperresponsiveness (AHR), and/or asthma are terms that encompass a variety of complex clinical syndromes with many phenotypes. Asthma has been described broadly as transient narrowing of the airway that is reversible following inhalation of a A2 agonist. When the narrowing of the airway occurs only with exercise, this phenomenon has been termed exercise-induced bronchoconstriction (EIB) (1). When evaluating elite athletes, it has been noted that respiratory symptoms alone cannot be relied upon to make a diagnosis of asthma and/or AHR and that the diagnosis should be confirmed with documentation of increased airflow in response to A2 agonists or decreased airflow in response to bronchial provocation testing, such as a methacholine challenge testing or eucapnic voluntary hyperventilation (2). In the setting of such testing, spirometry should demonstrate a 12% increase in forced expiratory volume in 1 s (FEV1) above baseline measurements after administration of a A2 agonist or a 10% decline in response to eucapnic voluntary hyperventilation (2,3). Although the specific etiology of EIB/AHR among competitive swimming athletes is not always clear, the diagnosis of this pathology is quite common in this population (4). Interestingly, despite having similar environmental exposures, it has been demonstrated that participation in competitive swimming activities is associated with the highest prevalence of asthma/ AHR, even when compared with five other aquatic disciplines (5). In the setting of competitive swimming, air quality can be influenced by chlorine derivatives, ozone, and combustionderived pollutants, such as oxides of nitrogen, as well as particulate matter (2). To complicate the accuracy of diagnosis further, it also has been shown that self-reporting of symptoms among elite athletes is not particularly reliable in identifying EIB or AHR (6). In addition, the reference range criteria for postexercise FEV1 decrement in the elite athlete population is discordant with the current recommended guidelines used to assess the general population (3,7). Another challenge in diagnosing EIB/AHR among swimming athletes is that the requisite bronchial provocation tests may not be performed in the appropriate setting (8,9). As a result of these various factors, a large number of misdiagnoses and inappropriate treatments may occur in this population when EIB/AHR screening is either not performed or is performed without adequate exercise and environmental stress exposure (8). To overcome these diagnostic challenges, swimming athletes must have both access to resources that accurately capture the relevant data as well as the cooperation of a team’s infrastructure and athletes. As an example of spirometry assessments in a clinically relevant environment, we present the following case series.