Environmental Engineering Reference
In-Depth Information
synergy between Ni and V. Cardiovascular effects became apparent on the third day
of exposure and persisted for more than 72 h. Exactly 50% of the rats exposed to the
highest concentration of Ni + V (1.3 mg/m
3
) died. The exposure levels to Ni and V
used in this study were approximately one million times the mean ambient levels of
1.3 ng/m
3
and 1.1 ng/m
3
, respectively, in the 2008 STN data as shown in Table
1
.
In the companion study by this research group (Campen et al.
2002
), healthy
(normotensive) and pulmonary hypertensive induced with monocrotaline (MCT)
Sprague Dawley rats were fi tted with telemetry devices and instilled with either
0.3 ml saline, or various masses (Table
9
) of sulfates of Fe (III), Ni (II), V (II), or
combinations of the three metal sulfates in the same volume of saline. Telemetry
data were collected for 48 h before instillation and for 96 h following instillation,
after which the animals were sacrifi ced, and BALF and tissue samples collected. In
both healthy and MCT-treated rats, instillation of V produced an acute decrease in
both heart rate and core temperature and an increase in arrhythmias, which persisted
for 3 days post instillation. Somewhat surprisingly, these effects were of lesser
magnitude in MCT-treated rats. Ni did not cause an immediate effect but rather
produced delayed and prolonged bradycardia, hypothermia and arrhythmogenesis,
with similar responses in both healthy and MCT-treated rats; 50% of the MCT-
treated rats instilled with Ni subsequently died. The combination of Ni + V produced
a greater acute hypothermic and arrhythmic response than V alone. The hypother-
mic and rhythm effects of Ni + V were somewhat attenuated by the addition of Fe.
Treatment with MCT (in the absence of metals) produced signifi cant increases in
indicators of cardiac damage and proteins that were associated with cell injury
[LDH; microalbumin (MIA); N-acetyl glucosaminidase (NAG); glutathione (GSH)]
in BALF as compared to saline controls. In MCT-treated rats, the following metals
caused signifi cant increases in BALF proteins compared to controls: Ni (LDH);
Fe + Ni (LDH); Ni + V (LDH, GSH); Fe + Ni + V (LDH). In healthy rats, the effects
of Fe alone were no different than controls. V produced signifi cant increases in
LDH and MIA. Ni produced signifi cant increases in total protein, LDH, MIA, NAG
and GSH. In these two studies (Campen et al.
2001
and
2002
), instillation of 263
g
of Ni produced signifi cantly greater effects on cardiac function, regulation of core
body temperature and BALF indicators of pulmonary injury than did 245
ʼ
g of V.
In two companion papers, Gilmour et al. (
2006
) investigated the following
parameters: systemic effects of intratracheal zinc sulfate exposure on metal homeo-
stasis of essential metals (Zn, Cu and Se), changes in cardiac gene expression and
changes in sequestering proteins, Zn transporter-2 (ZT-2) and metallothionein-1
(MT-1), in the heart, lung and liver in rats exposed to 2
ʼ
mol/kg of zinc sulfate or
saline. This Zn concentration is approximately 100,000 times environmentally-
relevant concentrations (Table
9
), but may be relevant to occupational exposures at
levels that could induce Zn fume fever, an acute occupational heavy metal intoxica-
tion that is classically associated with welders. Rats were euthanized at various time
points and responses were measured in plasma, heart, lung and liver tissue. Plasma
Zn levels increased 20% at 1 h post exposure and levels in the liver increased 35%
in 24-48 h post exposure. Signifi cant increases in liver levels of Cu and Se were also
observed at 24-48 h post exposure, which suggested that disruption of systemic
ʼ
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