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We measured particulate matter (PM 2.5 and PM 10 ) exposures, home temperature, arterial blood oxygen saturation, blood pressure, and lung function in 30 volunteer Los Angeles area residents during four-day intervals. Continuous Holter electrocardiograms were recorded in a subgroup on the first two days. Subjects recorded symptoms and time-activity patterns in diaries during monitoring, and during a reference period one week earlier/later. All subjects had severe chronic obstructive pulmonary disease. PM 10 (24-hr mean) at monitoring stations near subjects' homes averaged 33 µg/m 3 , and ranged from 9 to 84 µg/m 3 . In longitudinal analyses, day-to-day changes in PM 2.5 and PM 10 outside subjects' homes significantly tracked concurrent station PM 10 (r 2 = 0.22 and 0.44, respectively). Indoor and personal concentrations were less related to station readings (r 2 ≤ 0.1), but tracked each other (r 2 ≥ 0.4). In-home temperatures tracked outdoor temperatures more for lows (r 2 = 0.27) than for highs (r 2 = 0.10). These longitudinal relationships of subject-oriented and station PM measurements were generally similar to cross-sectional relationships observed previously in similar subjects. Among health measurements, only blood pressure showed reasonably consistent unfavorable longitudinal associations with particulates, more with station or outdoor PM than with indoor or personal PM.
Adult volunteers (17 healthy, 14 asthmatic) were exposed in a controlled environmental chamber to concentrated ultrafine particles (UFP) collected in a Los Angeles suburb with substantial motor vehicle pollution. Exposures lasted 2 h with intermittent exercise. Inhaled particle counts (mean 145,000/cm 3 , range 39,000-312,000) were typically 7-8 times higher than ambient levels. Mass concentrations (mean 100 µg/m 3 , range 13-277) were not highly correlated with counts. Volunteers were evaluated for lung function, symptoms, exhaled nitric oxide (eNO), Holter electrocardiography, and inflammatory markers in peripheral blood and induced sputum. Relative to control (filtered air) studies, UFP exposures were associated with a 0.5% mean fall in arterial O 2 saturation estimated by pulse oximetry ( p < .01), a 2% mean fall in forced expired volume in 1 sec (FEV 1 ) the morning after exposure ( p < .05), and a transient slight decrease in lowfrequency (sympathetic) power in Holter recordings during quiet rest ( p < .05). Healthy and asthmatic subjects were not significantly different across most endpoints. Thus, this initial experimental study of human volunteers exposed to concentrated Los Angeles area ambient UFP showed some acute deleterious cardiopulmonary responses, which, although generally small and equivocal as in previous studies of larger sized concentrated ambient particles, might help to explain reported adverse health effects associated with urban 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 microg/m(3) concentrated ambient particles (CAP) less than 2.5 mum 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 multi-hour 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.
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