Toxicological Sciences,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 4, 2024
Abstract
Microplastics
are
ubiquitous
in
the
atmosphere,
leading
to
human
exposure
through
inhalation.
Airborne
microplastics
undergo
degradation
due
sunlight
irradiation,
yet
respiratory
risks
associated
with
degraded
remain
poorly
understood.
In
this
study,
we
investigated
effects
of
polyethylene
terephthalate
(PET)
by
artificial
and
created
a
transport
model
PET
for
risk
assessment.
fibers
were
cut
subjected
irradiation.
Mice
exposed
aged
showed
increased
airway
resistance
induced
methacholine
(MCh)
inhalation,
along
lung
inflammation
neutrophil
infiltration.
Terephthalic
acid
(TPA)
was
continuously
released
from
sunlight.
Exposure
TPA
also
caused
enhanced
MCh
mice.
These
findings
indicate
that
can
cause
impairment
via
release.
A
simple
developed
quantitatively
relate
abundance
produced
study
(i.e.
4,000
×
96
W
m−2
h)
fractions
be
generated
atmosphere.
Our
results
suggested
10%
60%
as
over
sunny
regions
summer,
whereas
only
lower
than
1%
high-latitude
cities
Europe
winter.
This
demonstrates
importance
considering
further
development
assess
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(10), P. 1256 - 1256
Published: Oct. 17, 2024
Environmental
pollution
continues
to
increase
with
industrial
development
and
has
become
a
threat
human
health.
Atmospheric
particulate
matter
(PM)
was
designated
as
Group
1
carcinogen
by
the
International
Agency
for
Research
on
Cancer
in
2013
is
an
emerging
global
environmental
risk
factor
that
major
cause
of
death
related
cardiovascular
respiratory
diseases.
PM
complex
composed
highly
reactive
organic
matter,
chemicals,
metal
components,
which
mainly
excessive
production
oxygen
species
(ROS)
can
lead
DNA
cell
damage,
endoplasmic
reticulum
stress,
inflammatory
responses,
atherosclerosis,
airway
remodeling,
contributing
increased
susceptibility
exacerbation
various
diseases
infections.
effects
health
depending
particle
size,
physical
chemical
characteristics,
source,
exposure
period.
smaller
than
5
μm
penetrate
accumulate
alveoli
circulatory
system,
causing
harmful
skin,
brain.
In
this
review,
we
describe
relationship
mechanism
ROS-mediated
oxidative
responses
caused
organs,
well
comprehensively
discuss
harmfulness
PM.
Cells,
Journal Year:
2024,
Volume and Issue:
13(10), P. 803 - 803
Published: May 8, 2024
Recent
evidence
indicates
that
exposure
to
environmental
toxins,
both
short-term
and
long-term,
can
increase
the
risk
of
developing
neurological
disorders,
including
neurodegenerative
diseases
(i.e.,
Alzheimer's
disease
other
dementias)
acute
brain
injury
stroke).
For
stroke,
latest
systematic
analysis
revealed
ambient
particulate
matter
is
second
most
frequent
stroke
after
high
blood
pressure.
However,
preclinical
clinical
investigations
on
deleterious
consequences
pollutants
are
scarce.
This
review
examines
recent
how
absorbed
along
digestive
tract
or
inhaled
through
lungs,
affect
host
cellular
response.
We
particularly
address
toxins
immune
response
microbiome
at
gut
lung
barrier
sites.
Additionally,
this
highlights
findings
showing
potential
contribution
an
increased
stroke.
A
better
understanding
biological
mechanisms
underlying
has
mitigate
disorders.
Long-term
exposure
of
humans
to
air
pollution
is
associated
with
an
increasing
risk
cardiovascular
diseases
(CVDs).
Astaxanthin
(AST),
a
naturally
occurring
red
carotenoid
pigment,
was
proved
have
multiple
health
benefits.
However,
whether
or
not
AST
also
exerts
protective
effect
on
fine
particulate
matter
(PM2.5)-induced
cardiomyocyte
damage
and
its
underlying
mechanisms
remain
unclear.In
vitro
experiments,
the
H9C2
cells
were
subjected
pretreatment
varying
concentrations
AST,
then
injury
model
induced
by
PM2.5
established.
The
cell
viability
ferroptosis-related
proteins
expression
measured
in
different
groups.
In
vivo
rats
pretreated
for
21
days.
Subsequently,
rat
myocardial
established
intratracheal
instillation
every
other
day
1
week.
effects
tissue
caused
indicating
histological,
serum,
protein
analyses
examined.AST
significantly
ameliorated
PM2.5-induced
injury,
inflammatory
infiltration,
release
factors,
damage.
Mechanistically,
increased
SLC7A11,
GPX4
down-regulated
TfR1,
FTL
FTH1
vivo.Our
study
suggest
that
ferroptosis
plays
significant
role
pathogenesis
PM2.5.
may
serve
as
potential
therapeutic
agent
mitigating
through
inhibition
ferroptosis.
Ecotoxicology and Environmental Safety,
Journal Year:
2025,
Volume and Issue:
292, P. 117990 - 117990
Published: March 1, 2025
Human
are
widely
exposed
to
polycyclic
aromatic
hydrocarbon
(PAHs),
but
existing
evidence
about
exposure
urinary
PAHs
metabolites
for
pulmonary
health
in
children
and
adolescents
is
limited.
Our
aim
was
examine
the
effect
of
single
mixed
on
lung
function
among
adolescents.
We
included
1417
individuals
aged
6-19
years
from
3
survey
cycles
(2007-2008,
2009-2010,
2011-2012)
NHANES
program.
Multivariable
linear
regression
model
conducted
relationship
between
index
including
FEV1,
FVC
FEV1/FVC.
BKMR
WQS
were
used
evaluate
joint
effects
index.
Mediation
analyses
performed
investigate
mediating
role
inflammation
related
Hub
proteins
screened
by
network
toxicology
validated
using
molecular
docking.
results
indicated
that
3-FLU
negatively
linked
with
FEV1
FEV1/FVC;
1-OHP
FEV1;
1-PYR
FVC.
In
addition,
3-OHP
positively
corrected
three
parameters.
models,
co-exposure
all
Systemic
response
mediated
I-PYR
as
well
FVC,
8
%
6
proportion.
IL-6,
STAT3,
TNF,
TP53
common
targets
PAHs,
docking
analysis.
Taken
together,
our
findings
raise
concerns
potential
hazards
environmentally
relevant
respiratory
system
vulnerable
population
guide
future
research
into
toxic
mechanisms
metabolites-mediated
injury,
which
has
important
public
implications.
The Journal of Toxicological Sciences,
Journal Year:
2025,
Volume and Issue:
50(3), P. 147 - 159
Published: Jan. 1, 2025
Exposure
to
fine
particulate
matter
(PM2.5)
has
been
epidemiologically
reported
worsen
the
prognosis
of
ischemic
stroke;
however,
details
have
not
investigated.
One
major
toxic
mechanisms
PM2.5
inhalation
is
oxidative
stress,
which
mediated
by
reactive
oxygen
species
generated
components
such
as
metals
and
polycyclic
aromatic
hydrocarbons.
In
this
study,
we
examined
effects
long-term
exposure
urban
matter,
focusing
on
after
stroke
in
mice.
When
mice
were
intranasally
exposed
for
28
days
an
aerosol
collected
Beijing,
China
(CRM28),
microglial
activation
was
observed
cerebral
cortex,
indicating
that
CRM28
induced
neuroinflammation.
resulted
increased
serum
levels
brain
natriuretic
peptide
troponin
I,
suggesting
cardiac
injury
elicited
CRM28.
Lung
inflammation
also
following
exposure;
systemic
detected.
Mice
showed
exacerbation
mortality
induction
compared
with
vehicle
A
vitamin
E-rich
diet
suppressed
CRM28-induced
lipid
peroxidation
heart
lungs
but
brain.
attenuated
lung
exposure,
whereas
neuroinflammation
affected.
Mortality
improved
administration
a
diet.
Considering
did
occur,
stress
under
may
be
involved
stroke.
Antioxidation
air
pollution
fundamental
protection
against
Asian Biomedicine,
Journal Year:
2025,
Volume and Issue:
19(1), P. 21 - 35
Published: Feb. 1, 2025
Air
pollution
exposure
has
become
an
international
health
issue
that
poses
many
risks
to
life
and
health.
The
bidirectional
regulatory
network,
known
as
the
oral-gut-brain
axis
connects
oral
cavity,
intestine,
central
nervous
system,
well
its
influence
on
outcomes
from
air
is
receiving
increased
attention.
This
article
systematically
details
epidemiological
evidence
linking
pollutants
diseases
affecting
oral,
respiratory,
intestinal,
systems,
while
also
explaining
route
of
via
axis.
anomalies
resulting
their
underlying
molecular
processes
are
covered.
study
provides
a
fresh
viewpoint
how
affects
investigates
cutting-edge
preventative
therapeutic
techniques.
The Journal of Toxicological Sciences,
Journal Year:
2024,
Volume and Issue:
49(2), P. 61 - 68
Published: Jan. 1, 2024
Particulate
matter
(PM)
is
among
the
major
air
pollutants
suspended
in
atmosphere.
PM2.5
has
a
particle
size
of
2.5
µm;
it
known
to
cause
inflammation,
especially
respiratory
tract
and
skin.
Since
skin
acts
primary
barrier
against
harmful
environmental
substances
that
may
enter
body,
highly
exposed
present
environment.
However,
adverse
health
effects
exposure
on
human
have
not
been
accurately
examined
due
lack
system
exposes
epidermal
tissue
actual
concentration
PM2.5.
In
this
study,
we
developed
an
air–liquid
interface
for
exposing
cultured
3D
epidermis
cornea
collected
through
cyclonic
separation.
suspension
was
nebulized
acrylic
chamber,
resulting
mist
pumped
diffusion
dryer
into
glass
chamber.
A
counter
connected
chamber
continuously
measure
spatial
mass
PM.
Human
Exposure
PM
aerosol
increased
interleukin-8
release
media
around
50
µg/m3.
Mass
concentrations
above
100
µg/m3
caused
cell
death.
Furthermore,
corneal
model
showed
similar
responses
as
epidermis.
The
study
considered
useful
evaluating
induced
by
can
be
used
alternative
experiments
involving
or
animals.