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Cardiovascular-respiratory
2.0
2.0
1.0
1.0
0.0
0.0
−1.0
−1.0
20
10
5
<3.5 overall
≥ 60 20 10
5
<3.5 overall
≥60
Days
Days
FIGURE  23.33  Pooled estimates of log relative rates of mortality at different timescales for cardiovas-
cular-respiratory (left panel) and other causes of mortality (right panel) for four U.S. cities (Pittsburgh, PA;
Minneapolis, MN; Seattle, WA; Chicago, IL), 1987-1994. Shaded regions are ±2 standard errors of the esti-
mates. Percentage increases in mortality were greater at longer than shorter exposure intervals before death.
(From Dominici, F. et al., Am. J. Epidemiol ., 157, 1055, 2003.)
0.75
0.5
0.25
0
−0.25
−0.5
−0.75
−0.75
0
Effects at time scales shorter than 5 days
harvesting prone
0.25
0.5
0.75
−0.5
−0.25
FIGURE  23.34  Estimated relative rates of mortality due to PM at timescales shorter than 5 days
(harvesting-prone) versus relative rate estimates obtained at timescales longer than 5 days (harvesting-resistant)
from four U.S. cities (Pittsburgh, PA; Minneapolis, MN; Seattle, WA; Chicago, Il) and three mortality out-
comes (total, cardiovascular-respiratory, and other causes), 1987-1994. A large square is placed at the aver-
ages of the 12 estimates. (From Dominici, F. et al., Am. J. Epidemiol ., 157, 1055, 2003.)
The lining cells of blood vessels (endothelial cells) are known to play an important role in the
regulation of blood low and vascular tone. Studies in rats have observed alterations in the produc-
tion of endothelin 1, a potent constrictor of blood vessels that is produced by endothelial cells after
exposure to concentrated ambient PM (CAPS) and O 3 in combination [117] and vasoconstriction of
small pulmonary arteries with CAPS alone [262]. The relevance of these observations to humans
was demonstrated with controlled 2 h exposure of 25 healthy adults to a mixture of CAPS and O 3
compared to exposure to iltered air [263]. Brachial artery vasoconstriction was observed after the
CAPS1O 3 exposure but not with iltered air.
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