Environmental Engineering Reference
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Lewis et al. (
2003
) further examined the role of ROS induced by transition met-
als on lipid peroxidation as a mechanism of lung injury by exposing rats to ROFA
that had been separated into soluble and insoluble fractions that were taken from the
a Boston power plant (Table
8
). Sprague Dawley rats were instilled with 1 mg/100 g
body wt with total ROFA suspension, ROFA-soluble fraction, ROFA-insoluble frac-
tion, total ROFA suspension plus the chelating agent deferoxamine and antioxidant
enzyme catalase, or saline controls. At 4, 24 and 72 h post-instillation, animals were
sacrifi ced and BALF analyzed for total and differential cell counts. Non-lavaged
lungs were evaluated for evidence of lipid peroxidation as an indicator of infl amma-
tory injury. The presence of ROS was determined by ESR in a cell-free system, and
cellular oxidant potential was measured by chemiluminescence. ROFA-total and
ROFA-soluble preparations had signifi cantly more oxidant potential by ESR than
the ROFA-insoluble fraction (no p value given). The oxidant potential was reduced
by the addition of deferoxamine. There were no differences in alveolar macrophages
amongst any of the treatment groups at any time points. All forms of ROFA increased
neutrophils, but had somewhat different time courses. ROFA-total and ROFA-
insoluble signifi cantly increased lipid peroxidation at 24 and 72 h, compared to
saline controls. ROFA-soluble had no effect on lipid peroxidation at any time inter-
val. This fi nding contradicts other studies that report signifi cant effects from solu-
ble, but not insoluble fractions.
The effects of ROFA metals on susceptibility to bacterial lung infection in
Sprague Dawley rats was investigated by Roberts et al. (
2004
) by using the same
ROFA source as used in the previous study (Lewis et al.
2003
). The rats were
instilled with 1 mg/100 g body wt with one of the three ROFA solutions or saline
and then inoculated with
Listeria monocytogenes
3 days later. At days 6, 8 and 10,
rats were sacrifi ced and the lungs removed for histology and determination of clear-
ance of
L. monocytogenes
. The ROFA-insoluble treatments had no signifi cant effect
on rat survival of
L. monocytogenes
infection. On the other hand, mortality after
inoculation was 40% in ROFA-total and 80% in ROFA-soluble treatment groups,
with the majority of animals dying 7-8 days post-ROFA instillation. Bacterial lung
burdens were also correspondingly much higher in those animals administered the
ROFA-total or ROFA-soluble treatments, compared to the saline or ROFA-insoluble
ones. Rats exposed to ROFA-soluble treatments in the presence of a chelating agent
were able to clear the majority of bacteria from their lungs by day 10 and were simi-
lar to controls. The fact that adding a chelating agent appeared to nullify the
increased susceptibility to infection caused by the ROFA-soluble fraction supports
the hypothesis that soluble metals are involved.
In an extension of the previous study (Roberts et al.
2004
), Antonini et al. (
2004
)
tested ROFA collected from the precipitator and air-heater of the same Boston
power plant on the response of Sprague-Dawley rats to infection with
L. monocyto-
genes
. The metal content of the precipitator ROFA was considerably higher, and
was more water-soluble than that from the air-heater (Table
8
). The dosing protocol
with the different ROFA preparations and with silica (positive control) or saline
(negative control), infection with
L. monocytogenes
, and determination of pulmo-
nary bacterial clearance was the same as described for the Roberts et al. (
2004
)
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