Environmental Engineering Reference
In-Depth Information
exposure. This study provides evidence that at concentrations 8,000 times that of
ambient levels, zinc salts can produce infl ammatory lung injury.
Following up on the fi ndings of Adamson et al. (
2000
), Prieditis and Adamson
(
2002
) instilled mice with solutions of Zn, Cu, V, Ni, Fe, and Pb at concentrations
(4.8 mg/g in 0.1 mL saline) equal to the concentration of Zn (4.8 mg Zn/g dust) in
the EHC-93 dust and observed effects on markers of pulmonary infl ammation in
BALF and lung morphology. The doses (Table
9
) used in this study were approxi-
mately 100,000-1,000,000 times higher than people are exposed to in ambient air.
Markers of infl ammation and injury in BALF and lung morphology were then
examined to determine any associations with exposure. Only Zn and Cu were asso-
ciated with signifi cant lung injury as measured by the increased numbers of alveolar
macrophages, leukocytes and BALF protein in the exposed mice versus controls.
Morphological changes in the lungs of Cu- and Zn-exposed mice were similar to the
mice exposed to EHC-93 dust. The Zn levels found in the EHC-93 samples were
approximately four times higher than those found in STN samples (Table
1
), and the
exposure was more than 100,000 fold ambient levels.
Wallenborn et al. (
2008
) administered aerosolized zinc sulfate (10-100
g/m
3
) to
healthy rats via nasal inhalation for 5 h per day, 3 days per week for 16 weeks. The
animals were euthanized 48 h after the last exposure. No morphological changes
consistent with cardiac or pulmonary pathology were observed. Signifi cantly
increased levels of ferritin and decreased levels of glutathione peroxidase and suc-
cinate dehydrogenase were observed in cardiac cells, suggesting a mitochondrial-
specifi c effect of inhaled Zn sulfate. Cardiac gene expression was signifi cantly
altered at the highest dose of Zn sulfate (100
ʼ
g/m
3
), as evidenced by a microarray
analysis. As shown in Table
8
, the highest exposure level (100
ʼ
g/m
3
of Zn) was
equal to the NOAEL for BALF parameters and indicators of cardiac changes, and
the LOAEL for effects on cardiac enzymes.
According to the authors, this study demonstrates that inhalation exposures to
environmentally plausible concentrations of Zn are associated with cardiovascular
effects in healthy rats. However, the exposure concentrations of Zn used in this
study were hundreds to thousands of times higher than what has been reported in
ambient air (STN Zn = 0.014
ʼ
g/m
3
); hence, these
concentrations would not be considered as environmentally relevant levels. In two
related studies that were an extension of the work conducted by Costa and Dreher
(
1997
), Campen et al. (
2001
and 2002) examined the effects of Fe, Ni and V on
cardiovascular parameters and body core temperature in Sprague Dawley rats. In
the fi rst study (Campen et al.
2001
), rats were surgically fi tted with radiotelemetry
transmitters that were used to measure core temperature and ECG. Groups of 4 rats
were exposed by inhalation to concentrations (Table
9
) of V sulfate, Ni sulfate, Ni
and V sulfates concurrently, ranging from 0.3 to 2.4 mg/m
3
, or fi ltered air 6 h/day
for 4 days. Animals were observed for either 24 or 96 h following the fi nal exposure
and then were sacrifi ced. Blood and BALF were collected. Ni caused delayed bra-
dycardia, hypothermia and arrhythmia at concentrations greater than 1.2 mg/m
3
. Ni
and V together produced cardiovascular effects at lower concentrations than pro-
duced by the highest concentration of Ni alone (2.1 mg/m
3
), suggesting possible
ʼ
g/m
3
; IMPROVE Zn = 0.043
ʼ
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