S. Petrovic et al., Cardiorespiratory effects of concentrated ambient PM2.5: A pilot study using controlled human exposures, INHAL TOXIC, 12, 2000, pp. 173-188
Epidemiological studies suggest that there may De adverse human health effe
cts associated with exposure to ambient fine particles (PM2.5). in a prelim
inary study, we examined the health Effects of PM2.5 concentrated from ambi
ent air (CAP) in downtown Toronto using the Harvard ambient particle concen
trator Four young healthy volunteers were each exposed to filtered air IFA)
and low mid, and high CAP levels ranging from 23 to 124 mu g/m(3) for 2 h.
Response measures included pulmonary function, symptom reports, inflammato
ry cells, blood coagulation factors, and cardiac effects. Exposures were fo
llowed by 30 min of exercise at a target heart rate of 130 bpm, during whic
h subjects were evaluated for cardiac response. Review of 12-lead electroca
rdiograph (ECG) data Dy a cardiologist revealed no clinically significant c
ardiac effects during Exposure, the following exercise period, or 24 h afte
r exposure. Following the high CAP exposure, plasma fibrinogen measured pos
texercise showed a trend to increase above the preexposure value (mean incr
ease of 10%) when compared with the FA response (mean increase of 2%). The
only statistically significant effect on pulmonary function (p < .01) was a
small mean decrease of 6.4% in thoracic gas volume after high CAP exposure
compared with a mean increase of 5.6% after TA. This was not accompanied D
y an increase in respiratory symptoms. There was no respiratory cellular in
flammatory response as evaluated by induced sputum; however, there was a tr
end toward an increase in the percentage of nasal neutrophils after CAP exp
osures. The results from this pilot study indicate that exposure of young h
ealthy volunteers to these levels of concentrated ambient PM2.5 in Toronto
may not cause significant acute health effects. Additional research with mo
re subjects and susceptible individuals will De required to further examine
the cardiorespiratory effects of PM2.5.