Exposures of Elderly Volunteers with and without Chronic Obstructive Pulmonary Disease (COPD) to Concentrated Ambient Fine Particulate Pollution

The elderly and individuals who have chronic obstructive pulmonary disease (COPD) may be sensitive to particulate matter (PM) air pollution. We evaluated short-term health responses of 13 elderly volunteers with COPD and 6 age-matched healthy adults to controlled exposures of ambient PM pollution in suburban Los Angeles. Using a Harvard particle concentrator and a whole-body chamber, we exposed each person on separate occasions to approximately 200 μg/m³ concentrated ambient particles (CAP) less than 2.5 μm in diameter and to filtered air (FA). Each exposure lasted 2 h with intermittent mild exercise. We found no significant effects of CAP on symptoms, spirometry, or induced sputum. A significant negative effect of CAP on arterial oxygenation (measured by pulse oximetry) immediately postexposure was more pronounced in healthy subjects. Peripheral blood basophils increased after CAP in healthy but not in COPD subjects. In both groups, red cell counts increased slightly 1 day after exposure to FA but not to CAP. Preexposure ectopic heartbeats were infrequent in healthy subjects, but increased modestly during/after CAP exposure relative to FA. Ectopic beats were more frequent in COPD subjects, but decreased modestly during/after CAP relative to FA. Heart-rate variability over multihour intervals was lower after CAP than after FA in healthy elderly subjects but not in COPD subjects. Thus, in this initial small-scale study of older volunteers experimentally exposed to ambient PM, some acute cardiopulmonary responses were consistent with effects reported from epidemiologic studies. Unexpectedly, individuals with COPD appeared less susceptible than healthy elderly individuals. Further investigation of older adults is warranted to understand the pathophysiology and public health significance of these findings.     

Respiratory responses to exposures with fine particulates and nitrogen dioxide in the elderly with and without COPD

Elderly people, with and without chronic obstructive pulmonary disease (COPD), may be susceptible to particulate matter (PM) air pollution. However, the respiratory impacts of inhaled PM combined with copollutant(s) in controlled exposure studies are unclear and warrant investigation since exposures to PMgas mixtures constitute realistic scenarios. Thus, we exposed 6 healthy subjects and 18 volunteers with COPD (mean age 71 yr) on separate days to (a) filtered air (FA); (b) 0.4 ppm NO2; (c) concentrated ambient particles (CAP), predominantly in the fine (PM2.5) size range, at concentrations near 200 microg/m3; and (d) CAP and NO2 together. Each 2-h exposure included exercise for 15 min every half hour. Most respiratory responses, including symptoms, spirometry, and total and differential counts of induced sputum cells, showed no statistically significant responses attributable to separate or combined effects of CAP and NO2. However, maximal mid-expiratory flow and arterial O2 saturation (measured by pulse oximetry) showed small but statistically significant decrements associated with CAP, greater in healthy than COPD subjects. CAP exposure was also associated with decreased percentages of columnar epithelial cells in sputum. The results suggest that the respiratory effect of the PMNO2 mixture may be primarily PM driven since coexposure to NO2 did not significantly enhance the responses. In conclusion, older adults exposed to urban fine particles may experience acute small-airways dysfunction with impaired gas exchange. Healthy subjects appear more susceptible, suggesting that the respiratory effect may be related to efficient penetration and deposition of inhaled toxic particles in distal small airways. More clinical investigation of the elderly population is warranted.     

Respiratory Responses to Exposures With Fine Particulates and Nitrogen Dioxide in the Elderly With and Without COPD

Elderly people, with and without chronic obstructive pulmonary disease (COPD), may be susceptible to particulate matter (PM) air pollution. However, the respiratory impacts of inhaled PM combined with copollutant(s) in controlled exposure studies are unclear and warrant investigation since exposures to PM–gas mixtures constitute realistic scenarios. Thus, we exposed 6 healthy subjects and 18 volunteers with COPD (mean age 71 yr) on separate days to (a) filtered air (FA); (b) 0.4 ppm NO₂; (c) concentrated ambient particles (CAP), predominantly in the fine (PM_2.5) size range, at concentrations near 200 μg/m₃; and (d) CAP and NO₂ together. Each 2-h exposure included exercise for 15 min every half hour. Most respiratory responses, including symptoms, spirometry, and total and differential counts of induced sputum cells, showed no statistically significant responses attributable to separate or combined effects of CAP and NO₂. However, maximal mid-expiratory flow and arterial O₂ saturation (measured by pulse oximetry) showed small but statistically significant decrements associated with CAP, greater in healthy than COPD subjects. CAP exposure was also associated with decreased percentages of columnar epithelial cells in sputum. The results suggest that the respiratory effect of the PM–NO₂ mixture may be primarily PM driven since coexposure to NO₂ did not significantly enhance the responses. In conclusion, older adults exposed to urban fine particles may experience acute small-airways dysfunction with impaired gas exchange. Healthy subjects appear more susceptible, suggesting that the respiratory effect may be related to efficient penetration and deposition of inhaled toxic particles in distal small airways. More clinical investigation of the elderly population is warranted.     

Controlled exposures of healthy and asthmatic volunteers to concentrated ambient fine particles in Los Angeles

Information about health effects from controlled exposure to particulate matter (PM) air pollution is relatively limited but potentially critical in urban locations such as Los Angeles, where abundant mobile sources generate combustion-related particles. Nonsmoking healthy (n = 12) and asthmatic (n = 12) volunteers, age 18-45 yr, were exposed to concentrated ambient particulates (CAP) in the fine (PM(2.5)) size range at an average concentration of 174 micro g/m(3) (range 99-224), and to filtered air (FA). Exposures used a two-stage Harvard virtual-impactor concentrator and whole-body chamber and lasted 2 h with alternating rest-exercise periods. Neither group showed significant (p <.05) changes in spirometry or routine hematologic measurements attributable to CAP exposure, relative to FA. Both groups showed CAP-related decreases of columnar cells in postexposure induced sputum, slight changes in certain mediators of blood coagulability and systemic inflammation, and modest increases in parasympathetic stimulation of heart rate variability. Systolic blood pressure decreased in asthmatics and increased in healthy subjects during CAP exposure relative to FA. Cardiovascular (but not respiratory) symptoms increased slightly with CAP in both groups. In summary, the urban fine PM exposures elicited different biologic endpoints with statistically significant differences between CAP and FA. The observed changes in blood inflammation and heart-rate variability were consistent with systemic (rather than respiratory) effects reported from other laboratory and epidemiologic studies. Further studies involving other biologic endpoints, PM size modes, and risk factors will be needed to clarify these results.     

Controlled Exposures of Healthy and Asthmatic Volunteers to Concentrated Ambient Fine Particles in Los Angeles

Information about health effects from controlled exposure to particulate matter (PM) air pollution is relatively limited but potentially critical in urban locations such as Los Angeles, where abundant mobile sources generate combustion-related particles. Nonsmoking healthy (n = 12) and asthmatic (n = 12) volunteers, age 18-45 yr, were exposed to concentrated ambient particulates (CAP) in the fine (PM 2.5) size range at an average concentration of 174 µg/m 3 (range 99-224), and to filtered air (FA). Exposures used a two-stage Harvard virtual-impactor concentrator and whole-body chamber and lasted 2 h with alternating rest-exercise periods. Neither group showed significant (p < .05) changes in spirometry or routine hematologic measurements attributable to CAP exposure, relative to FA. Both groups showed CAP-related decreases of columnar cells in postexposure induced sputum, slight changes in certain mediators of blood coagulability and systemic inflammation, and modest increases in parasympathetic stimulation of heart rate variability. Systolic blood pressure decreased in asthmatics and increased in healthy subjects during CAP exposure relative to FA. Cardiovascular (but not respiratory) symptoms increased slightly with CAP in both groups. In summary, the urban fine PM exposures elicited different biologic endpoints with statistically significant differences between CAP and FA. The observed changes in blood inflammation and heart-rate variability were consistent with systemic (rather than respiratory) effects reported from other laboratory and epidemiologic studies. Further studies involving other biologic endpoints, PM size modes, and risk factors will be needed to clarify these results.     

Relative contributions of PM2.5 chemical constituents to acute arterial vasoconstriction in humans

Studies have shown associations between acute ambient particulate matter (PM) levels and increases in morbidity and mortality from cardiovascular diseases. We have previously reported in 24 healthy adults that exposure to concentrated ambient particles plus ozone (CAP + O(3)) caused a mean decrease of 0.09 mm in brachial artery diameter (BAD), which was significantly larger than a mean increase of 0.01 mm among the same individuals exposed to filtered air (FA). Our current objective is to examine the relationship between total and constituent PM(2.5) mass concentrations and the acute vascular response. We have analyzed both ambient and exposure filters from the brachial artery study for major chemical constituents, allowing us to compare the strength of the associations between each constituent and an individual's arterial response. We determined gravimetric PM(2.5) mass concentration and inorganic ion content from exposure filters. Twenty-three-hour ambient PM(2.5) filters collected from the same site and on the same day were used to estimate exposure concentrations of trace elements and organic and elemental carbon. We performed linear regression analyses on the levels of measured or estimated PM constituents using each subject's FA exposure as a control. We found, from our regression analyses, a significant negative association between both the organic and elemental carbon concentrations and the difference in the postexposure change in the BAD (Delta BAD) between and CAP + O(3) and FA exposure days. An understanding of the PM constituents most responsible for adverse health outcomes is critical for efforts to develop pollution abatement strategies that maximize benefits to public health.     

Ambient Air Pollution Particles and the Acute Exacerbation of Chronic Obstructive Pulmonary Disease

Investigation has repeatedly demonstrated an association between exposure to ambient air pollution particles and numerous indices of human morbidity and mortality. Individuals with chronic obstructive pulmonary disease (COPD) are among those with an increased sensitivity to air pollution particles. Current and ex-smokers account for 80 to 85% of all those with COPD. The human breathing in an urban site with a significant level of particulate matter (PM) may be exposed to 720 μ g daily. A single cigarette introduces 15,000 to 40,000 μ g particle into the respiratory tract of the smoker. It is subsequently confounding why such a relatively small mass of airborne PM should have any biological effect in the patient with COPD, as these individuals are repeatedly exposed to particles (with a similar size and composition) at perhaps a thousandfold the mass of ambient PM. Regarding this increased sensitivity of COPD patients to air pollution particles, there are several possible explanations for this seeming contradiction, including correlations of PM levels with other components of air pollution, an accumulation of multiple independent risk factors in a patient, changes in individual activity patterns, disparities in dosimetry between healthy subjects and COPD patients, and some unique characteristic of an ambient air pollution PM. Regardless of the underlying mechanism for the increased sensitivity of COPD patients, exposures of these individuals to elevated levels of PM should be discouraged. To provide a greater awareness of PM levels, the U.S. Environmental Protection Agency now includes levels of air pollution particles in an air quality index.     

Ambient air pollution particles and the acute exacerbation of chronic obstructive pulmonary disease

Investigation has repeatedly demonstrated an association between exposure to ambient air pollution particles and numerous indices of human morbidity and mortality. Individuals with chronic obstructive pulmonary disease (COPD) are among those with an increased sensitivity to air pollution particles. Current and ex-smokers account for 80 to 85% of all those with COPD. The human breathing in an urban site with a significant level of particulate matter (PM) may be exposed to 720 microg daily. A single cigarette introduces 15,000 to 40,000 microg particle into the respiratory tract of the smoker. It is subsequently confounding why such a relatively small mass of airborne PM should have any biological effect in the patient with COPD, as these individuals are repeatedly exposed to particles (with a similar size and composition) at perhaps a thousandfold the mass of ambient PM. Regarding this increased sensitivity of COPD patients to air pollution particles, there are several possible explanations for this seeming contradiction, including correlations of PM levels with other components of air pollution, an accumulation of multiple independent risk factors in a patient, changes in individual activity patterns, disparities in dosimetry between healthy subjects and COPD patients, and some unique characteristic of an ambient air pollution PM. Regardless of the underlying mechanism for the increased sensitivity of COPD patients, exposures of these individuals to elevated levels of PM should be discouraged. To provide a greater awareness of PM levels, the U.S. Environmental Protection Agency now includes levels of air pollution particles in an air quality index.     

Relative Contributions of PM2.5 Chemical Constituents to Acute Arterial Vasoconstriction in Humans

Studies have shown associations between acute ambient particulate matter (PM) levels and increases in morbidity and mortality from cardiovascular diseases. We have previously reported in 24 healthy adults that exposure to concentrated ambient particles plus ozone (CAP + O₃) caused a mean decrease of 0.09 mm in brachial artery diameter (BAD), which was significantly larger than a mean increase of 0.01 mm among the same individuals exposed to filtered air (FA). Our current objective is to examine the relationship between total and constituent PM_2.5 mass concentrations and the acute vascular response. We have analyzed both ambient and exposure filters from the brachial artery study for major chemical constituents, allowing us to compare the strength of the associations between each constituent and an individual's arterial response. We determined gravimetric PM_2.5 mass concentration and inorganic ion content from exposure filters. Twenty-three-hour ambient PM_2.5 filters collected from the same site and on the same day were used to estimate exposure concentrations of trace elements and organic and elemental carbon. We performed linear regression analyses on the levels of measured or estimated PM constituents using each subject's FA exposure as a control. We found, from our regression analyses, a significant negative association between both the organic and elemental carbon concentrations and the difference in the postexposure change in the BAD (Δ BAD) between and CAP + O₃ and FA exposure days. An understanding of the PM constituents most responsible for adverse health outcomes is critical for efforts to develop pollution abatement strategies that maximize benefits to public health.     

Altered heart-rate variability in asthmatic and healthy volunteers exposed to concentrated ambient coarse particles

Twelve mildly asthmatic and four healthy adults were exposed to filtered air (FA) and concentrated ambient coarse particles (CCP) supplied to a whole-body exposure chamber via a coarse particle concentrator with 15 parallel virtual impactors. Exposures were conducted in a Los Angeles suburb with high levels of motor-vehicle pollution and lasted 2 h with intermittent exercise. Mean CCP concentration was 157 microg/m(3) (range: 56-218 microg/m(3)) measured by continuous monitoring with a tapered-element oscillating microbalance (TEOM). On average, 80% of mass was coarse (2.5-10 microm aerodynamic diameter) and the rest <2.5 microm. Relative to FA, CCP exposure did not significantly alter respiratory symptoms, spirometry, arterial oxygen saturation, or airway inflammation according to exhaled nitric oxide and total and differential cell counts of induced sputum. After CCP exposure, Holter electrocardiograms showed small (p <.05) increases in heart rate and decreases in heart-rate variability, which were larger in healthy than in asthmatic subjects. Cardiac ectopy did not increase. In conclusion, acute exposure to elevated concentrations of ambient coarse particles elicited no obvious pulmonary effects but appeared to alter the autonomic nervous system of the heart in adult volunteers.     

Altered Heart-Rate Variability in Asthmatic and Healthy Volunteers Exposed to Concentrated Ambient Coarse Particles

Twelve mildly asthmatic and four healthy adults were exposed to filtered air (FA) and concentrated ambient coarse particles (CCP) supplied to a whole-body exposure chamber via a coarse particle concentrator with 15 parallel virtual impactors. Exposures were conducted in a Los Angeles suburb with high levels of motor-vehicle pollution and lasted 2 h with intermittent exercise. Mean CCP concentration was 157 μ g/m ³ (range: 56–218 μ g/m³) measured by continuous monitoring with a tapered-element oscillating microbalance (TEOM). On average, 80% of mass was coarse (2.5–10 μ m aerodynamic diameter) and the rest < 2.5 μ m. Relative to FA, CCP exposure did not significantly alter respiratory symptoms, spirometry, arterial oxygen saturation, or airway inflammation according to exhaled nitric oxide and total and differential cell counts of induced sputum. After CCP exposure, Holter electrocardiograms showed small (p <. 05) increases in heart rate and decreases in heart-rate variability, which were larger in healthy than in asthmatic subjects. Cardiac ectopy did not increase. In conclusion, acute exposure to elevated concentrations of ambient coarse particles elicited no obvious pulmonary effects but appeared to alter the autonomic nervous system of the heart in adult volunteers.     

Effects of inhaled ambient particulate matter on pulmonary antimicrobial immune defense

Respiratory-tract infection, specifically pneumonia, contributes substantially to the increased morbidity and mortality among elderly individuals exposed to airborne particulate matter of <10 microm diameter (PM(10)). These epidemiological findings suggest that PM(10) may act as an immunosuppressive factor that can undermine normal pulmonary antimicrobial defense mechanisms. To investigate whether, and how, compromised pulmonary immunocompetence might contribute to increased mortality, two sets of laboratory studies were performed. The first examined the effects of a single inhalation exposure to concentrated ambient PM(2.5) (CAPS) from New York City air on pulmonary/systemic immunity and on the susceptibility of exposed aged rats to subsequent infection with Streptococcus pneumoniae. The second set of studies determined whether CAPS exposure, at a concentration approximating or somewhat greater than the promulgated 24-h NAAQS of 65 microg/m(3), could exacerbate an ongoing infection. Taken together, results demonstrated that a single exposure of healthy animals to CAPS had little effect on pulmonary immune function or bacterial clearance during subsequent challenge with S. pneumoniae. Alternatively, CAPS exposure of previously infected rats significantly increased bacterial burdens and decreased percentages of lavageable neutrophils and proinflammatory cytokine levels compared to those in infected filtered-air-exposed controls. These studies demonstrate that a single exposure to ambient PM(2.5) compromises a host's ability to handle ongoing pneumococcal infections and support the epidemiological findings of increased pneumonia-related deaths in ambient PM-exposed elderly individuals.     

Effects of Inhaled Ambient Particulate Matter on Pulmonary Antimicrobial Immune Defense

Respiratory-tract infection, specifically pneumonia, contributes substantially to the increased morbidity and mortality among elderly individuals exposed to airborne particulate matter of <10 µm diameter (PM 10) . These epidemiological findings suggest that PM 10 may act as an immunosuppressive factor that can undermine normal pulmonary antimicrobial defense mechanisms. To investigate whether, and how, compromised pulmonary immunocompetence might contribute to increased mortality, two sets of laboratory studies were performed. The first examined the effects of a single inhalation exposure to concentrated ambient PM 2.5 (CAPS) from New York City air on pulmonary/systemic immunity and on the susceptibility of exposed aged rats to subsequent infection with Streptococcus pneumoniae. The second set of studies determined whether CAPS exposure, at a concentration approximating or somewhat greater than the promulgated 24-h NAAQS of 65 µg/m 3, could exacerbate an ongoing infection. Taken together, results demonstrated that a single exposure of healthy animals to CAPS had little effect on pulmonary immune function or bacterial clearance during subsequent challenge with S. pneumoniae. Alterna­tively, CAPS exposure of previously infected rats significantly increased bacterial burdens and decreased percentages of lavageable neutrophils and proinflammatory cytokine levels compared to those in infected filtered-air-exposed controls. These studies demonstrate that a single exposure to ambient PM 2.5 compromises a host's ability to handle ongoing pneumococcal infections and support the epidemiological findings of increased pneumonia-related deaths in ambient PM-exposed elderly individuals.     

The effect of coarse ambient particulate matter on first, second, and overall hospital admissions for respiratory disease among the elderly

The objective of this article is to examine differences in the effect of ambient particulate matter on first, second, and overall hospital admissions for respiratory disease among the elderly. We studied 8989 adults 65 yr of age or older living in the greater Vancouver area who were admitted to hospital for any acute respiratory disease (ICD-9 codes 460-519) between June 1, 1995, and March 31, 1999. Time-series analysis was used to evaluate the association between respiratory admissions and daily measures of particulate matter (PM10, PM2.5, and PM10 - 2.5) in urban air, after adjustment for gaseous copollutants (CO, O3, NO2, and SO2) and meteorological variables. Repeated admissions for respiratory disease were common among the elderly. Approximately 30% of the subjects were readmitted to hospital after the first admission; 9% had more than 2 admissions for respiratory disease during the 4-yr study period. PM10 - 2.5 was significantly associated with the second and overall admissions for respiratory disease, but not with the first admission. The adjusted relative risks for an increment of 4.2 microg/m(3) in -day average PM10 - 2.5 concentrations were 1.03 (95% confidence interval: 0.98-1.09) for the first admission, 1.22 (1.10-1.36) for the second admission, and 1.06 (1.02, 1.11) for overall admissions. There was no significant association between PM2.5 and hospital admissions for respiratory disease among the elderly. Our data suggest that (1) people with a history of respiratory admissions are at a higher risk of respiratory disease in relation to particulate air pollution in urban areas, (2) analyses based on overall rather than repeated hospital admissions lead to lower estimates of the risk of respiratory disease associated with particulate air pollution, and (3) PM10 - 2.5 has a larger effect on respiratory admissions than PM2.5.     

Influence of season and location on pulmonary response to California's San Joaquin Valley airborne particulate matter

Season and location have documented impacts on particulate matter (PM)-induced morbidity and mortality. Seasonal and regional influences on the physical and chemical properties of PM?.? (also known as fine/ultrafine PM) contribute to differences in exposure burden and adverse respiratory health outcomes experienced in California's San Joaquin Valley (SJV), which ranks among the worst in the nation for PM pollution. Current regulations are driven by the association between mass concentrations and adverse health outcomes. However, this association is difficult to reproduce in toxicological studies and suggests a role for other parameters, such as chemical composition, involved in PM-induced adverse pulmonary health effects. Pulmonary toxicity of summer/winter and rural/urban SJV PM was evaluated given the unique geography, metereology and sources of the region. Healthy juvenile male mice inhaled summer/winter and urban/rural concentrated ambient PM (CAP) or ambient PM for 6 h/d for 10 d, and pulmonary inflammatory responses were measured 48 h postexposure. Exposure concentrations ranged from 10 to 20 μg/m3 for ambient air control mice and from 86 to 284 μg/m3. Mice exposed to rural but not urban CAP, displayed significant neutrophil influx that was more than 50-fold greater than control levels, which ranged from 21 to 60 neutrophils/ml for all experiments. Pulmonary neutrophilic inflammation was measured despite lower CAP concentrations in the rural compared to the urban location and in the absence of cytotoxicity, oxidative stress, or elevations in cytokine and chemokines expression. Further, the inflammatory responses induced by rural winter CAP were associated with the highest levels of organic carbon (OC) and nitrates (NO??). Evidence indicates that regional/seasonal influences on PM chemical composition rather than PM mass may be associated with increased PM-induced adverse health effects.     

Total lung deposition of ultrafine particles in elderly subjects during controlled breathing

Ultrafine particulate matter (PM) in the air may be harmful to health, particularly in elderly subjects. From the dosimetry point of view, it is not known if the elderly subjects are more susceptible to exposure to ultrafine PM. We measured the total deposition fraction (TDF) of ultrafine PM (NMD = 0.04-0.1 microm in number median diameter) in the lungs of healthy, elderly subjects (age = 69 +/- 5 yr) and compared the results with those obtained from young adults (age = 31 +/- 4 yr) in an earlier study. Subjects inhaled the aerosols with six different breathing patterns: three different tidal volumes (V(t) = 500, 750, and 1000 ml) and two flow rates (Q) for each V(t). TDF was measured breath by breath in situ by measuring aerosol concentrations on inhalation and exhalation using an ultrafine condensation particle counter. Mean TDF (+/-SD) of the elderly subjects was 0.43 +/- 0.03, 0.36 +/- 0.04, 0.31 +/- 0.03, and 0.27 +/- 0.02 for NMD = 0.04, 0.06, 0.08, and 0.1 microm, respectively, for V(t) = 500 ml and Q = 250 ml/s. These and all other results were very similar to those of young adults. The results suggest that healthy, elderly subjects are not subjected to a greater respiratory dose of ultrafine PM than young adults under the same exposure conditions.     

Total Lung Deposition of Ultrafine Particles in Elderly Subjects During Controlled Breathing

Abstract

Ultrafine particulate matter (PM) in the air may be harmful to health, particularly in elderly subjects. From the dosimetry point of view, it is not known if the elderly subjects are more susceptible to exposure to ultrafine PM. We measured the total deposition fraction (TDF) of ultrafine PM (NMD = 0.04–0.1 μm in number median diameter) in the lungs of healthy, elderly subjects (age = 69 ± 5yr) and compared the results with those obtained from young adults (age = 31 ± 4 yr) in an earlier study. Subjects inhaled the aerosols with six different breathing patterns: three different tidal volumes (V_t = 500, 750, and 1000 ml) and two flow rates (Q) for each V_t. TDF was measured breath by breath in situ by measuring aerosol concentrations on inhalation and exhalation using an ultrafine condensation particle counter. Mean TDF (±SD) of the elderly subjects was 0.43 ± 0.03, 0.36 ± 0.04, 0.31 ± 0.03, and 0.27 ± 0.02for NMD = 0.04, 0.06, 0.08, and 0.1 μm, respectively, for V_t = 500ml and Q = 250ml/s. These and all other results were very similar to those of young adults. The results suggest that healthy, elderly subjects are not subjected to a greater respiratory dose of ultrafine PM than young adults under the same exposure conditions.     

Influence of relatively low level of particulate ar pollution on hospitalization for COPD in elderly people

To assess the association between relatively low levels of size-fractioned particulate matter (PM) and hospitalization for chronic obstructive pulmonary disease (COPD), we conducted a time-series analysis among elderly people 65 yr of age or more living in Vancouver between June 1995 and March 1999. Measures of thoracic PM (PM(10)), fine PM (PM(2.5)), coarse PM (PM(10-2.5)), and coefficient of haze (COH) were examined over periods varying from 1 to 7 days prior to hospital admissions. Generalized additive models (GAMs; general linear models, GLMs) were used, and temporal trends and seasonal and subseasonal cycles in COPD hospitalizations were removed by using GLM with parametric natural cubic splines. The relative risks were calculated based on an incremental exposure corresponding to the interquartile range of these measures, and were adjusted for daily weather conditions and gaseous pollutants. PM measures had a positive effect on COPD hospitalization, especially 0 to 2 days prior to the admissions, before copollutants were accounted for. For 3-day average levels of exposure the relative risk estimates were 1.13 (95% confidence interval: 1.05-1.21) for PM(10), 1.08 (1.02-1.15) for PM(2.5), 1.09 (1.03-1.16) for PM(10-2.5), and 1.05 (1.01-1.09) for COH. The associations were no longer significant when NO(2) was included in the models. We concluded that the particle-related measures were significantly associated with COPD hospitalization in the Vancouver area, where the level of air pollution is relatively low, but the effects were not independent of other air pollutants.     

Airway and systemic inflammatory responses to ultrafine carbon black particles and ozone in older healthy subjects

Increased adverse health effects in older subjects due to exposure to ambient air pollutants may be related to the inflammatory response induced by these contaminants. The aim of this study was to assess airway and systemic inflammatory responses in older healthy subjects to a controlled experimental exposure with spark-generated elemental carbon black ultrafine particles (cbUFPs) and ozone (O₃). Twenty healthy subjects, age 52–75 years, were exposed on three occasions separated by at least 8 weeks. The exposures to filtered air (FA), to cbUFP (50 μg/m³), or to cbUFP in combination with 250 ppb ozone (cbUFP + O₃) for 3 h with intermittent exercise were performed double blind, and in random order. Sputum and blood samples were collected 3.5 h after each exposure. Exposure to cbUFP + O₃ significantly increased plasma club cell protein 16 (CC16), the number of sputum cells, the number and percent of sputum neutrophils, and sputum interleukin 6 and matrix metalloproteinase 9. Exposure to cbUFP alone exerted no marked effect, except for an elevation in sputum neutrophils in a subgroup of 13 subjects that displayed less than 65% sputum neutrophils after FA exposure. None of the inflammatory markers was correlated with age, and serum cardiovascular risk markers were not markedly affected by cbUFP or cbUFP + O₃. Exposure to cbUFP+O₃ induced a significant airway and systemic inflammatory response in older healthy volunteer subjects. The effects induced by cbUFP alone suggest that the inflammation was predominantly mediated by O₃, although one cannot rule out that the interaction of cbUFP and O₃ played a role.