Small Airway Dysfunction and Abnormal Exercise Responses. A Study in Coal Miners.

RATIONALE: Coal mine dust exposure can cause symptoms and loss of lung function from multiple mechanisms, but the roles of each disease process are not fully understood. OBJECTIVES: We investigated the implications of small airway dysfunction for exercise physiology among a group of workers exposed to coal mine dust. METHODS: Twenty coal miners performed spirometry, first breathing air and then helium-oxygen, single-breath diffusing capacity, and computerized chest tomography, and then completed cardiopulmonary exercise testing. MEASUREMENTS AND MAIN RESULTS: Six participants meeting criteria for small airway dysfunction were compared with 14 coal miners who did not. At submaximal workload, miners with small airway dysfunction used a higher proportion of their maximum voluntary ventilation and had higher ventilatory equivalents for both O2 and CO2. Regression modeling indicated that inefficient ventilation was significantly related to small airway dysfunction but not to FEV1 or diffusing capacity. At the end of exercise, miners with small airway dysfunction had 27% lower O2 consumption. CONCLUSIONS: Small airway abnormalities may be associated with important inefficiency of exercise ventilation. In dust-exposed individuals with only mild abnormalities on resting lung function tests or chest radiographs, cardiopulmonary exercise testing may be important in defining causes of exercise intolerance.

Clinical manifestations of sleep apnea.

Obstructive sleep apnea (OSA) may manifest in a number of ways from subtle intrusion into daily life to profound sleepiness, snoring, witnessed apneas and other classic symptoms. Although there is increasing evidence suggesting OSA can adversely affect health in a variety of ways, this disorder remains underdiagnosed. The most well-escribed health consequences of OSA relate to the cardiovascular system. Hypertension and arrhythmias have a strong association with OSA, and evidence suggests that treatment of OSA in patients with refractory hypertension and in patients planning cardioversion for atrial fibrillation may be of particularly importance. Significant associations between heart failure and OSA as well as complex sleep apnea have also been well-described. Cerebrovascular insult, impaired neurocognition, and poorly controlled mood disorder are also associated with in OSA. Therapy for OSA may ameliorate atherosclerotic progression and improve outcomes post-cerebrovascular accident (CVA). OSA should be considered in patients complaining of poor concentration at work, actual or near-miss motor vehicle accidents, and patients with severe sleepiness as a component of their co-morbid mood disorders. The metabolic impact of OSA has also been studied, particularly in relation to glucose homeostasis. Also of interest is the potential impact OSA has on lipid metabolism. The adverse effect untreated OSA has on glucose tolerance and lipid levels has led to the suggestion that OSA is yet another constituent of the metabolic syndrome. Some of these metabolic derangements may be related to the adverse effects untreated OSA has on hepatic health. The cardiovascular, neurocognitive, and metabolic manifestations of OSA can have a significant impact on patient health and quality of life. In many instances, evidence exists that therapy not only improves outcomes in general, but also modifies the severity of co-morbid disease. To mitigate the long-term sequela of this disease, providers should be aware of the subtle manifestations of OSA and order appropriate testing as necessary.

Small airways involvement in coal mine dust lung disease.

Inhalation of coal mine dust results in a spectrum of symptoms, dysfunction, and pathological changes in the respiratory tract that collectively have been labeled coal mine dust lung disease. Recent reports from periodic health surveillance among underground and surface coal miners in the United States have demonstrated an increasing prevalence and severity of dust diseases, and have also documented that some miners experience rapid disease progression. The coal macule is an inflammatory lesion associated with deposited dust, and occurs in the region of the most distal conducting airways and proximal respiratory bronchioles. Inflammatory changes in the small airways have long been recognized as the signature lung pathology among coal miners. Human and laboratory studies have suggested oxidant injury, and increased recruitment and activity of macrophages play important roles in dust-induced lung injury. However, the functional importance of the small airway changes was debated for many years. We reviewed published literature that documents a pervasive occurrence of both physiologic and structural abnormalities in small airways among coal miners and other workers exposed to airborne particulates. There is increasing evidence supporting an important association of abnormalities in the small peripheral airways with the development of respiratory symptoms, deficits in spirometry values, and accelerated declines in ventilatory lung function. Pathologic changes associated with mineral dust deposition in the small airways may be of particular importance in contemporary miners with rapidly progressive respiratory impairment.

Rapid decline in lung function in coal miners: evidence of disease in small airways.

BACKGROUND: Coal mine dust exposure can cause both pneumoconiosis and chronic airflow limitation. The contributions of various pathophysiologic mechanisms to dust-related lung function decrements remain unclear. METHODS: Clinical and physiological findings were assessed for 15 underground coal miners who had demonstrated accelerated FEV1 losses (decliners) over 6-18 years. Decliners' findings were evaluated in comparison to a group of 11 miners who had shown relatively stable lung function (referents) during the same period. RESULTS: At follow-up examination, the decliners showed significantly greater mean airway resistance (10.47 vs. 6.78 cmH2 O/L/s; P = 0.05) and more air trapping (RV/TLC = 37.5 vs. 29.1%; P < 0.01) compared to the referents. Decliners also demonstrated more evidence of small airways dysfunction and tended to have more bronchospasm than the referent group. Total lung capacity, lung compliance, diffusing capacity, and chest radiography did not differ significantly between the two groups. After cessation of mine dust exposures, the decliners' mean rate of FEV1 loss normalized. CONCLUSION: In a series of working coal miners, accelerated lung function declines were associated with air trapping and evidence of small airways dysfunction. A preventive benefit from controlling dust exposures was suggested.