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Pulmonary responses in current smokers and ex-smokers following a two hour exposure at rest to clean air and fine ambient air particles.
Hazucha, M., P. Bromberg, J. Lay, W. Bennett, K. Zeman, N. Alexis, H. Kehrl, A. Rappold, W. Cascio, AND R. Devlin. Pulmonary responses in current smokers and ex-smokers following a two hour exposure at rest to clean air and fine ambient air particles. Particle and Fibre Toxicology. BioMed Central Ltd, London, Uk, 10(1):58, (2013).
The purpose of this study was to determine if current or ex-smokers are more susceptible to PM than non-smokers.
BACKGROUND: Increased susceptibility of smokers to ambient PM may potentially promote development of COPD and accelerate already present disease. OBJECTIVES: To characterize the acute and subacute lung function response and inflammatory effects of controlled chamber exposure to concentrated ambient fine particles (CAFP) with MMAD s 2.5 microns in ex-smokers and lifetime smokers. METHODS: Eleven subjects, aged 35-74 years, came to the laboratory 5 times; a training day and two exposure days separated by at least 3 weeks, each with a post-exposure visit 22 h later. Double-blind and counterbalanced exposures to "clean air" (mean 1.5 ± 0.6 ug/m3) or CAFP (mean 108.7 ± 24.8 ug/m3 ) lasted 2 h with subjects at rest. RESULTS: At 3 h post-exposure subjects' DTPA clearance half-time significantly increased by 6.3 min per 100 ug/m3 of CAFP relative to "clean air". At 22 h post-exposure they showed significant reduction of 4.3% per 100 ug/m3 in FEV1 and a significant DLCO decrease by 11.1% per 100 g/m3 of CAFP relative to "clean air". At both 3 h and 22 h the HDL cholesterol level significantly decreased by 4.5% and 4.1%, respectively. Other blood chemistries and markers of lung injury, inflammation and procoagulant activity were within the normal range of values at any condition. CONCLUSIONS: The results suggest that an acute 2 h resting exposure of smokers and ex-smokers to fine ambient particulate matter may transiently affect pulmonary function (spirometry and DLCO.) and increase DTPA clearance half-time. Except for a post exposure decrease in HDL no other markers of pulmonary inflammation, prothrombotic activity and lung injury were significantly affected under the conditions of exposure.