International Journal of Environmental Research and Public Health,
Journal Year:
2020,
Volume and Issue:
17(13), P. 4874 - 4874
Published: July 6, 2020
Epidemiological
studies
have
corroborated
that
respiratory
diseases,
including
lung
cancer,
are
related
to
fine
particulate
matter
(<2.5
μm)
(PM2.5)
exposure.
The
toxic
responses
of
PM2.5
greatly
influenced
by
the
source
PM2.5.
However,
effects
from
Beijing
on
bronchial
genotoxicity
scarce.
In
present
study,
was
sampled
and
applied
in
vitro
investigate
its
mechanisms
behind
it.
Human
epithelial
cells
16HBE
were
used
as
a
model
for
Low
(67.5
μg/mL),
medium
(116.9
high
(202.5
μg/mL)
doses
cell
After
exposure,
viability,
oxidative
stress
markers,
DNA
(deoxyribonucleic
acid)
strand
breaks,
8-OH-dG
levels,
micronuclei
formation,
repair
gene
expression
measured.
results
showed
significantly
induced
cytotoxicity
16HBE.
Moreover,
levels
reactive
oxygen
species
(ROS),
malondialdehyde
(MDA),
cellular
heme
oxygenase
(HO-1)
increased,
level
glutathione
(GSH)
decreased,
which
represented
occurrence
severe
micronucleus
rate
elevated,
damage
occurred
indicators
comet
assay,
γ-H2AX
8-OH-dG,
markedly
enhanced
PM2.5,
accompanied
influence
8-oxoguanine
glycosylase
(OGG1),
X-ray
cross-complementing
1
(XRCC1),
poly
(ADP-ribose)
polymerase-1
(PARP1)
expression.
These
support
significant
role
cells,
may
occur
through
combined
effect
genes.
Environmental Science & Technology,
Journal Year:
2019,
Volume and Issue:
53(17), P. 10479 - 10486
Published: Aug. 9, 2019
Nowadays,
knowledge
regarding
component-specific
inflammatory
effect
of
fine
particulate
matter
(PM2.5)
is
limited.
In
this
study,
an
omics
approach
based
on
time-of-flight
mass
spectrometry
was
established
to
identify
the
key
hydrophobic
components
PM2.5
associated
with
pro-inflammatory
cytokines
released
by
macrophages
after
in
vitro
exposure.
Of
764
compounds,
62
were
robustly
screened
firmly
identified
37
specific
chemicals.
addition
polycyclic
aromatic
hydrocarbons
(PAHs)
and
their
methylated
congeners,
novel
oxygen-
nitrogen-containing
PAHs
and,
especially,
oxygenated
(Oxy-PAHs)
identified.
Interleukin
(IL)-6
Oxy-PAHs
1,8-naphthalic
anhydride,
xanthone,
benzo[h]quinolone,
whereas
IL-1β
tumor
necrosis
factor
(TNF)-α
most
species.
Most
species
related
IL-1β,
which
significantly
higher
heating
season,
a
monotonic
dose–response
pattern
mainly
for
U-shaped
primary
On
basis
components,
four
sources
pollution
(coal
combustion,
traffic
emissions,
biomass
burning,
secondary
formation,
traced
such
as
anhydride
quinones)
resolved
positive
matrix
factorization
model.
TNF-α
sources,
IL-6
both
suggesting
different
effects
between
when
assessing
toxicity-driven
disparities
known
unknown
components.
Environmental Science & Technology,
Journal Year:
2020,
Volume and Issue:
54(17), P. 10570 - 10576
Published: Aug. 10, 2020
A
novel
pollutant,
tris(2,4-di-tert-butylphenyl)phosphate
(I168O),
was
identified
in
urban
fine
particulate
matter
(PM2.5)
samples
a
nontargeted
screening
based
on
mass
spectrometry
for
the
first
time.
I168O
detected
all
collected
from
two
typical
cities
far
away
each
other
China.
The
concentrations
of
reached
up
to
851
(median:
153)
ng/m3,
indicating
that
it
widespread
and
abundant
pollutant
air.
antioxidant
Irgafos
168
[I168,
tris(2,4-di-tert-butylphenyl)phosphite]
popularly
added
plastics
most
suspected
source
I168O.
Simulation
studies
indicated
heating,
UV
radiation,
water
contact
might
significantly
(p
<
0.05)
transform
I168
In
particular,
be
magnificently
evaporated
into
air
at
high
temperatures.
outdoor
inhalation
exposure
may
exert
substantial
health
risks.
International Journal of Environmental Research and Public Health,
Journal Year:
2020,
Volume and Issue:
17(13), P. 4874 - 4874
Published: July 6, 2020
Epidemiological
studies
have
corroborated
that
respiratory
diseases,
including
lung
cancer,
are
related
to
fine
particulate
matter
(<2.5
μm)
(PM2.5)
exposure.
The
toxic
responses
of
PM2.5
greatly
influenced
by
the
source
PM2.5.
However,
effects
from
Beijing
on
bronchial
genotoxicity
scarce.
In
present
study,
was
sampled
and
applied
in
vitro
investigate
its
mechanisms
behind
it.
Human
epithelial
cells
16HBE
were
used
as
a
model
for
Low
(67.5
μg/mL),
medium
(116.9
high
(202.5
μg/mL)
doses
cell
After
exposure,
viability,
oxidative
stress
markers,
DNA
(deoxyribonucleic
acid)
strand
breaks,
8-OH-dG
levels,
micronuclei
formation,
repair
gene
expression
measured.
results
showed
significantly
induced
cytotoxicity
16HBE.
Moreover,
levels
reactive
oxygen
species
(ROS),
malondialdehyde
(MDA),
cellular
heme
oxygenase
(HO-1)
increased,
level
glutathione
(GSH)
decreased,
which
represented
occurrence
severe
micronucleus
rate
elevated,
damage
occurred
indicators
comet
assay,
γ-H2AX
8-OH-dG,
markedly
enhanced
PM2.5,
accompanied
influence
8-oxoguanine
glycosylase
(OGG1),
X-ray
cross-complementing
1
(XRCC1),
poly
(ADP-ribose)
polymerase-1
(PARP1)
expression.
These
support
significant
role
cells,
may
occur
through
combined
effect
genes.
