Pulmonary responses in current smokers and ex-smokers following a two hour exposure at rest to clean air and fine ambient air particles

Abstract

BackgroundIncreased susceptibility of smokers to ambient PM may potentially promote development of COPD and accelerate already present disease.ObjectivesTo characterize the acute and subacute lung function response and inflammatory effects of controlled chamber exposure to concentrated ambient fine particles (CAFP) with MMAD ≤ 2.5 microns in ex-smokers and lifetime smokers.MethodsEleven 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 μg/m3) or CAFP (mean 108.7 ± 24.8 μg/m3 ) lasted 2 h with subjects at rest.ResultsAt 3 h post-exposure subjects’ DTPA clearance half-time significantly increased by 6.3 min per 100 μg/m3 of CAFP relative to “clean air”. At 22 h post-exposure they showed significant reduction of 4.3% per 100 μg/m3 in FEV1 and a significant DLCO decrease by 11.1% per 100 μg/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.ConclusionsThe 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.

Satellite-Surface Perspectives of Air Quality and Aerosol-Cloud Effects on the Environment: An Overview of 7-SEAS/BASELInE

“…The findings suggested that the quality of people's lives in this region could be compromised by the presence of biomass-burning particles that may be deposited in the lungs. In susceptible groups, these particles are more likely to remain in the alveolar regions for longer times due to air trapping, leading to elevated particle toxicity (Hazucha et al, 2013;Patterson et al, 2014).…”

Air pollution exposure and lung function in highly exposed subjects in Beijing, China: a repeated-measure study

“…Short-term exposure to PM has been repeatedly associated with decreased forced expiratory volume in 1 second (FEV1) in human studies in Boston [ 5 ], Salt Lake City [ 6 ], Italy [ 7 ], and The Netherlands [ 8 ]. In a human controlled-exposure experiment including current smokers and ex-smokers, a 2-hour exposure to concentrated ambient fine particles was sufficient to determine a significant decrease in FEV1 compared to clean air experiments [ 9 ]. Elemental components of PM have been suggested to play critical roles in determining PM toxicity [ 10 - 12 ].…”

Associations of autophagy with lung diffusion capacity and oxygen saturation in severe COPD: effects of particulate air pollution

“…This finding is consistent with previous reports that D L CO reduction occurred with acute exposure to particulates in healthy smokers. 18 Generally, deposition of PM 2.5 in the lungs is higher in COPD patients and smokers compared to healthy nonsmokers, which could increase particle deposition and was proportional to the severity of obstruction. 18 The lung diffusion capacity, D L CO, provides a quantitative and qualitative assessment of pulmonary gas exchange across the alveolar–capillary membrane.…”

“… 18 Generally, deposition of PM 2.5 in the lungs is higher in COPD patients and smokers compared to healthy nonsmokers, which could increase particle deposition and was proportional to the severity of obstruction. 18 The lung diffusion capacity, D L CO, provides a quantitative and qualitative assessment of pulmonary gas exchange across the alveolar–capillary membrane. In COPD patients, the D L CO can reflect alveolar–capillary membrane damage subsequent to emphysema and increased pressure in the pulmonary circulation or secondary to heart failure.…”