Environmental Engineering Reference
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Gurgueira et al. (2002) demonstrated that oxidative stress can be induced by exposure to high
levels of metals in Boston CAPs, and could be responsible for changes in cardiac parameters. In vivo
CAPs exposures also triggered adaptive responses.
Hamada et al. (2002) exposed female BALB/c mice for 30 min to an aerosol nebulized from a
solution of PM components dissolved from ROFA that had been collected at a Boston power plant,
Penh, an index of airway hyperresponsiveness (AHR), was increased in a time- and dose-related
manner, peaking at 48 h postexposure. PMNs in BAL peaked at 12 h postexposure. A simulated
ROFA extract, containing the same concentrations of Ni, V, Zn, Co, Mn, and Cu as the ROFA,
produced the same AHR response, but the summed responses to each metal separately did not.
Gurgueira et al. (2002) exposed adult SD rats exposed to Boston PM 2.5 CAPs at 300 μg/m 3 for
5 h and showed signiicant oxidative stress in the lung and heart, but not in the liver. The increase in
the lung concentrations of ROS upon exposure to CAPs was rapid, indicating an almost immediate
effect of PM, or PM components, on the intracellular sources of free radicals. Furthermore, the
transient nature of these increases points to a reversible interaction of PM components with cellular
targets. Both observations are compatible with Fenton-type reactions catalyzed by transition metals,
redox-cycling processes, or biochemical changes triggered by non-covalent binding to membrane
receptors. Using single-component regression analysis, increases in chemiluminescence (an index
of oxidant load) showed strong associations with the CAPs content of Fe, Mn, Cu, and Zn in the
lung and with Fe, Al, Si, and Ti in the heart. The oxidant stress imposed by 5 h exposure to CAPs
was associated with slight, but signiicant, increases in the lung and heart water content, and with
increased serum levels of lactate dehydrogenase (LDH), indicating mild damage to both tissues.
In addition, CAPs inhalation also led to tissue-speciic increases in the activities of the antioxidant
enzymes.
Morishita et al. (2004) exposed normal and allergic Brown Norway rats to PM 2.5 CAPs for 10 h
at concentrations ranging from 300 to 650 μg/m 3 in a mobile laboratory in Detroit. The allergic
rats had, compared to the normal rats, increased pulmonary retention of La, V, Mn, and S, as
well as increased lung inlammation. Using source-apportionment analyses, Morishita et al. (2006)
concluded that the pattern of the airway responses was likely associated with local reineries and
incinerators, and independent of SO 4 = and PM 2.5 mass.
Lippmann et al. (2006) exposed ApoE −/− mice to PM 2.5 CAPs in Sterling Forest (Tuxedo, NY)
on weekdays for 6 h/day, for 6 months at an average mass concentration of 85 μg/m 3 , and cardiac
function was monitored continuously over the 6 months and CAPs composition was determined for
each exposure day. Most of the results of this study are described in the following section on long-
term animal inhalation exposures. In effect, this was a time-series study as well as a chronic effects
study. Exposures to Ni, Cr, and Fe were much higher on 14 days than on the other 89 exposure days,
corresponding to days with unusually high HR and unusually low HRV. In addition, V was lower
than normal on the days with high Ni, since the source of high Ni was a distant Ni smelter rather
than residual oil combustion, the usual source of elevated Ni concentrations. The authors attributed
the acute effects on cardiac function to peaks in Ni.
Kodavanti et al. (2000a,b) performed a series of 2 and 3 day 6 h exposures to FA, PM 2.5 CAPs,
and aerosolized ROFA of SD rats in Research Triangle Park, NC (RTP) using rats with and without
SO 2 -induced bronchitis. The CAPs concentrations ranged from 475 to 907 μg/m 3 , and the ROFA
concentration was 1 mg/m 3 . The CAPs exposures produced some CAPs-concentration-related
pulmonary injury in the bronchitic rats, but not in the healthy rats, and the FA and ROFA did not
produce measurable effects in either group of rats. The concentrations of leachable SO 4 = and metals
in the CAPs were not associated with the effects.
An in vivo inhalation study by Kodavanti et al. (2005), utilizing two different rat strains,
made a number of important indings They exposed two different strains of rats (spontaneously
hypertensive [SHR] and Wistar-Kyoto [WKY]) to CAPs from ambient air in RTP, concentrated by a
factor of 40-60 times. The CAPs were drawn from an area in reasonably close proximity to a major
freeway near the intersection with another major road, suggesting that the effects seen might have
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