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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.
Citation:
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).
Impact/Purpose:
The purpose of this study was to determine if current or ex-smokers are more susceptible to PM than non-smokers.
Description:
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.
