Environmental Engineering Reference
In-Depth Information
Epidemiological studies have clearly established that PM 2.5 air pollution is associated with
cardiopulmonary effects. However, because of the very low ambient air concentration levels
measured in these studies, particularly of the trace metal components, the biological plausibility of
these epidemiologically demonstrated associations needs to be substantiated. While we would prefer
to substantiate them in human controlled exposure studies with an experimental design, such studies
are not feasible and animal experimental studies can serve the purpose effectively. To date, while
there are many toxicological studies that investigated the response of animals to ambient PM by
inhalation or IT instillation, only a few had investigated the contributions from speciic air pollution
components, either as an individual compound or as part of a mixture, in producing adverse health
effects. It is, therefore, critical to systematically investigate the potential cardiopulmonary effects
of components of ambient PM in different regions of the United States, since PM of different
composition and from different sources may vary markedly in their potency for producing adverse
health effects. In this section, we irst discuss short-term inhalation exposure studies (up to 1 week in
duration). This discussion is followed by a review of longer-term CAPs exposure studies in animals.
14.3.2  s Hort -t erM  caP s  i nHalation  s tudies
In order to determine if CAPs inhalation can induce cardiopulmonary effects, Clarke et al. (2000)
investigated pulmonary inlammatory and hematological responses of canines after exposure to
Boston PM 2.5 CAPs. For pulmonary inlammatory studies, normal dogs were exposed in pairs to
either CAPs or iltered air (paired studies) for 6 h/day on 3 consecutive days. For hematological
studies, dogs were exposed for 6 h/day for 3 consecutive days with one receiving CAPs while the
other was simultaneously exposed to iltered air; crossover of exposure took place the following week
(crossover studies). No statistical differences in biologic responses were found when all CAPs and
all sham exposures were compared. However, the variability in biologic response was considerably
higher with CAPs exposure. Subsequent exploratory graphical analyses and mixed linear regression
analyses suggested associations between CAPs constituents and biologic responses. Factor analysis
was applied to the compositional data from paired and crossover experiments to determine elements
consistently associated with each other in CAPs samples. In paired experiments, four factors
were identiied; in crossover studies, a total of six factors (V/Ni, S, Al/Si, Br, Na/Cl, and Cr) were
observed. Increased BAL PMN percentage, total peripheral WBC counts, circulating PMNs, and
circulating lymphocytes (LYM) were associated with increases in the Al/Si factor. Increased PMNs
and increased BAL macrophages were associated with the V/Ni factor. Increased BAL PMNs were
associated with the Br/Pb factor only when the compositional data from the third day of CAPs
exposure were used. Decreases in RBC counts and hemoglobin levels were correlated with the
S factor. BAL or hematologic parameters were not associated with increases in total CAPs mass
concentration. In terms of signiicant individual components, SO 4 = was associated with increased
WBC; BC, Al, Mn, Si, Zn, Ti, V, Ni, and Fe were associated with increased PMNs; Na was associated
with increased LYM; and Al, Mn, and Si were associated with decreased LYM. These data suggest
that speciic components of CAPs may be responsible for biologic responses, but the lack of overall
statistically signiicant alterations in pulmonary and systemic responses diminished the impact of
this study.
Saldiva et al. (2002) studied the effects of CAPs inhalation on lung inlammation. They
exposed normal and bronchitic rats to Boston PM 2.5 CAPs or iltered air for 5 h/day for 3 days.
The CAPs produced signiicant pulmonary inlammation. Some inorganic CAPs components
(Si, V, Pb, SO 4 = , and Br) were signiicantly associated with increases in PMN in BALF and lung
tissue.
Rhoden et al. (2004) reported that N -Acetylcysteine (NAC) could prevent lung inlammation due
to Boston PM 2.5 CAPs inhalation. They also reported the results of regression analyses showing
strong associations between increases in thiobarbituric reactive substances (TBARS) accumulation
and the CAPs content of Al, Si, and Fe, and between BALF PMN count and Cr, Zn, and Na.
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