Chronic obstructive pulmonary diseases (COPD) may increase air pollution–related mortality. The relationship of immune mechanisms to mortality caused by fine particulates in healthy and COPD populations is incompletely understood. The objective of this study was to determine whether fine particulates from a single biomass fuel alter stress and inflammation biomarkers in people with COPD. Healthy and COPD subjects were exposed to smoke in a controlled indoor setting. Immune responses were quantified by measuring cell surface marker expression with flow-cytometric analysis and mRNA levels with quantitative reverse transcriptase–polymerase chain reactions in whole blood before and after exposure. Preexposure COPD subjects had more leukocytes, mainly CD14+ monocytes and neutrophils, but fewer CD3+ T cells. Fifty-seven of 186 genes were differentially expressed between healthy and COPD subjects' peripheral blood mononuclear cells (PBMCs). Of these, only nuclear factor (NF)-κ B1, TIMP-1, TIMP-2, and Duffy genes were up-regulated in COPD subjects. At 4 hours post smoke exposure, monocyte levels decreased only in healthy subjects. Fifteen genes, particular to inflammation, immune response, and cell-to-cell signaling, were differentially expressed in COPD subjects, versus 4 genes in healthy subjects. The authors observed significant differences in subjects' PBMCs, which may elucidate the adverse effects of air pollution particulates on people with COPD.
As indoor smoking bans have become widely adopted, some U.S. communities are considering restricting smoking outdoors, creating a need for measurements of air pollution near smokers outdoors. Personal exposure experiments were conducted with four to five participants at six sidewalk bus stops located 1.5–3.3 m from the curb of two heavily traveled California arterial highways with 3300–5100 vehicles per hour. At each bus stop, a smoker in the group smoked a cigarette. Gravimetrically calibrated continuous monitors were used to measure fine particle concentrations (aerodynamic diameter ≤2.5 µm; PM2.5) in the breathing zones (within 0.2 m from the nose and mouth) of each participant. At each bus stop, ultrafine particles (UFP), wind speed, temperature, relative humidity, and traffic counts were also measured. For 13 cigarette experiments, the mean PM2.5 personal exposure of the nonsmoker seated 0.5 m from the smoker during a 5-min cigarette ranged from 15 to 153 µg/m3. Of four persons seated on the bench, the smoker received the highest PM2.5 breathing-zone exposure of 192 µg/m3. There was a strong proximity effect: nonsmokers at distances 0.5, 1.0, and 1.5 m from the smoker received mean PM2.5 personal exposures of 59, 40, and 28 µg/m3, respectively, compared with a background level of 1.7 µg/m3. Like the PM2.5 concentrations, UFP concentrations measured 0.5 m from the smoker increased abruptly when a cigarette started and decreased when the cigarette ended, averaging 44,500 particles/cm3 compared with the background level of 7200 particles/cm3. During nonsmoking periods, the UFP background concentrations showed occasional peaks due to traffic, whereas PM2.5 background concentrations were extremely low. The results indicate that a single cigarette smoked outdoors at a bus stop can cause PM2.5 and UFP concentrations near the smoker that are 16–35 and 6.2 times, respectively, higher than the background concentrations due to cars and trucks on an adjacent arterial highway. Implications: Rules banning smoking indoors have been widely adopted in the United States and in many countries. Some communities are considering smoking bans that would apply to outdoor locations. Although many measurements are available of pollutant concentrations from secondhand smoke at indoor locations, few measurements are available of exposure to secondhand smoke outdoors. This study provides new data on exposure to fine and ultrafine particles from secondhand smoke near a smoker outdoors. The levels are compared with the exposure measured next to a highway. The findings are important for policies that might be developed for reducing exposure to secondhand smoke outdoors.
This study examined the differences in environmental tobacco smoke exposure between smokers and non-smokers.A probability sample of 1579 California adults completed a 1-day time diary of a full day's activities in which they reported whether any smoker was present during each activity.Some 61% of respondents reported at least some environmental tobacco smoke exposure in these diary accounts (for an average of up to 5 hours per day), and potential exposure rose monotonically with number of cigarettes actively smoked. Heaviest smokers reported about four times as much such exposure as nonsmokers.Because smokers lead life-styles that expose them to far higher levels of environmental tobacco smoke exposure, that factor needs to be controlled in studies estimating the effects of active smoking.
