Toxics,
Journal Year:
2024,
Volume and Issue:
12(12), P. 878 - 878
Published: Dec. 1, 2024
As
one
of
the
most
common
air
pollutants,
fine
particulate
matter
(PM2.5)
increases
risk
diseases
in
various
systems,
including
urinary
system.
In
present
study,
we
exposed
male
and
female
C57BL/6J
mice
to
PM2.5
for
8
weeks.
Examination
renal
function
indices,
creatinine
(CRE),
blood
urea
nitrogen
(BUN),
uric
acid
(UA),
microalbumin,
indicated
that
kidneys
mice,
not
underwent
early
injury,
exhibiting
glomerular
hyperfiltration.
Meanwhile,
pathological
staining
showed
exhibited
enlarged
glomerulus
filled
entire
Bowman’s
capsule
mice.
Afterward,
explored
potential
causes
mechanisms
Variations
mRNA
levels
key
genes
involved
renin–angiotensin
system
(RAS)
kallikrein–kinin
(KKS)
demonstrated
led
elevated
capillary
hydrostatic
pressure
by
disturbing
balance
between
RAS
KKS,
which
turn
increased
filtration
rate
(GFR).
addition,
found
glucose
females,
enhanced
tubular
reabsorption
glucose,
attenuated
macular
dense
sensory
signaling,
induced
hypoxia,
affected
adenosine
triphosphate
(ATP)
synthesis,
thus
attenuating
tubuloglomerular
feedback
(TGF)-induced
afferent
arteriolar
constriction
leading
conclusion,
this
study
hyperfiltration
affecting
RAS/KKS
imbalances,
as
well
regulation
TGF;
innovatively
unveiled
association
subchronic
exposure
kidney
injury
its
gender
dependence;
enriched
toxicological
evidence
confirmed
importance
reducing
ambient
concentrations.
Wildfires
significantly
contribute
to
ambient
air
pollution,
yet
our
understanding
of
how
wildfire
smoke
influences
specific
chemicals
and
their
resulting
concentration
in
remains
incomplete.
We
combine
15
years
daily
species-specific
PM2.5
concentrations
from
700
pollution
monitors
with
satellite-derived
PM2.5,
use
a
panel
regression
estimate
smoke's
contribution
the
27
different
chemical
species
PM2.5.
Wildfire
drives
detectable
increases
25
out
largest
observed
for
organic
carbon,
elemental
potassium.
find
that
originating
wildfires
burned
structures
had
higher
copper,
lead,
zinc,
nickel
relative
fires
did
not
burn
structures.
is
responsible
an
increasing
share
multiple
species,
some
which
are
particularly
harmful
health.
Using
risk
assessment
approach,
we
wildfire-induced
enhancement
carcinogenic
could
cause
population
cancer
risk,
but
these
very
small
other
environmental
risks.
demonstrate
combining
ground-monitored
data
can
be
used
measure
influence
on
exposures
at
large
scales.
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.
Air
pollution
is
a
leading
contributor
to
the
global
disease
burden.
However,
complex
nature
of
chemicals
which
humans
are
exposed
through
inhalation
has
obscured
identification
key
compounds
responsible
for
diseases.
Here,
we
develop
network
topology-based
framework
identify
toxic
in
airborne
chemical
exposome.
Using
cardiovascular
diseases
(CVDs)
as
model
disease,
found
that
modules
various
closely
linked
CVDs.
The
proximity
compound
target
can
indicate
extent
toxicity
induced
by
compounds.
By
integrating
mass
spectrometry-based
external
exposure
concentrations
and
machine
learning-predicted
internal
concentrations,
established
comprehensive
linkage
connecting
disease-related
risk
These
findings
were
subsequently
validated
using
data
on
regional
scale.
This
work
provides
an
effective
strategy
identifying
within
environmental
exposomes
establishes
new
paradigm
understanding
pathogenicity
air
pollution.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(7), P. 3402 - 3402
Published: April 5, 2025
Air
pollution
is
a
major
global
health
threat,
responsible
for
over
8
million
deaths
in
2021,
including
700,000
fatalities
among
children
under
the
age
of
five.
It
currently
second
leading
risk
factor
mortality
worldwide.
Key
pollutants,
such
as
particulate
matter
(PM2.5,
PM10),
ozone,
sulfur
dioxide,
nitrogen
oxides,
and
carbon
monoxide,
have
significant
adverse
effects
on
human
health,
contributing
to
respiratory
cardiovascular
diseases,
well
neurodevelopmental
neurodegenerative
disorders.
Among
these,
poses
most
threat
due
its
highly
complex
mixture
organic
inorganic
compounds
with
diverse
sizes,
compositions,
origins.
Additionally,
it
can
penetrate
deeply
into
tissues
cross
blood-brain
barrier,
causing
neurotoxicity
which
contributes
development
diseases.
Although
link
between
air
neurological
disorders
documented,
precise
mechanisms
their
sequence
remain
unclear.
Beyond
oxidative
stress,
inflammation,
excitotoxicity,
studies
suggest
that
induces
epigenetic
changes.
These
alterations
may
affect
expression
genes
involved
stress
responses,
neuroprotection,
synaptic
plasticity.
Understanding
relationship
changes
induced
by
specific
pollutants
could
aid
early
detection
monitoring
central
nervous
system
The
effects
of
particulate
matter
(PMs)
from
different
cities
on
the
nervous
system
remain
unclear.
In
this
study,
aqueous
solutions
0.45
μm
membrane-filtered
PM
31
major
Chinese
were
intravenously
administered
to
rats.
Neurotoxicity
and
mechanisms
investigated
by
quantifying
rat
behavior,
analyzing
in
vivo
biomarkers,
examining
physicochemical
properties.
PMs
had
variable
impacts
responses,
as
manifested
movement
speed
right
ear,
particularly
at
1
h
4–6
days
postexposure.
Physiological
linked
regulation
glucocorticoids
via
hypothalamic-pituitary-adrenal
axis
miR-107/miR-124
expression
blood.
Additionally,
toxicity
was
strongly
influenced
particle
morphology,
size,
zeta
potential,
which
varied
greatly
across
cities.
Using
random
forest
multiple
linear
regression,
we
revealed
that
sizes
(458.67
531.17
nm)
potentials
(−3.78,
−17.01,
−20.31
mV)
most
important
responsiveness,
line
with
blood
biomarkers
levels
rats
such
Glucocorticoid,
IL-1β,
IFN-α.
These
findings
indicate
contribute
varying
neurotoxicity,
thus
presenting
a
possible
differential
burden
Alzheimer's
disease
aging
population
many
regions.
Molecular Brain,
Journal Year:
2025,
Volume and Issue:
18(1)
Published: Feb. 4, 2025
Abstract
Recent
studies
have
shown
that
abnormal
activity
of
acid
sphingomyelinase
(Asm)
has
been
associated
with
a
range
psychiatric
disorders
including
schizophrenia
and
depression.
However,
the
role
Asm
in
regulation
anxiety
remains
unclear.
In
present
study,
we
employed
Asm-knockout
(Asm
KO)
mice
to
investigate
association
between
using
behavioral
tests,
RNA
sequencing,
q-PCR,
immunohistochemical
staining,
other
methods.
The
results
showed
KO
exhibit
enhanced
anxiety-like
behaviors,
such
as
restricted
activity,
reduced
cumulative
times
central
area,
diminished
exploratory
interest,
delayed
latency
feed,
through
tests
open
field,
novelty-suppressed
feeding
test,
elevated
plus
maze
ect.
Transcriptional
profiling
combined
bioinformatics
analysis
revealed
upregulation
Toll-like
receptor
signaling
pathway
related
gene
Tlr1/2,
Ccl3,
Ccl4,
Ccl5
Cd86
mice,
which
was
further
confirmed
by
detection
activated
microglia
astrocytes
iba-1
GFAP
staining.
Collectively,
our
findings
uncover
for
regulating
behavior
suggest
it
may
be
essential
maintenance
emotional
stability,
indicating
its
potential
promising
target
treating
disorders.
Exposure
to
atmospheric
aerosols
threatens
human
health
and
is
yet
be
effectively
addressed
globally.
Aerosol
toxicity
strongly
depends
upon
components
whose
chemical
profiles
concentrations
can
constantly
evolve
throughout
transformation,
inhalation,
distribution,
metabolism,
excretion.
Despite
the
abundant
studies
on
aerosol
their
toxic
effects,
dynamics
in
component
related
biological
effects
from
air
body
remain
unclear.
Here,
we
propose
a
conceptual
toxicokinetic
framework
mathematically
deduce
bioavailable
concentration
changing
bulk
of
constituents
atmosphere.
The
single
or
multiple
are
further
predicted
via
toxicodynamic
modeling
according
concentrations.
Atmospheric
composition
turn
regulated
by
risk-based
guidelines,
aiming
alleviate
vivo
effects.
This
perspective
demonstrates
how
serial
toxicokinetic-toxicodynamic
equations
bridge
knowledge
gap
between
ambient
associated
bodies.
prediction
an
inhalation
also
allows
connecting
with
exposomes
aggregate
exposure
pathways.
We
call
for
development
model
validity
integrate
quantitative
adverse
outcome
pathways
apply
exposure-disease
modeling,
providing
novel
insights
into
quality
policymaking
public
management.
Electrophilic
compounds
belong
to
a
group
of
critical
components
fine
particulate
matter
(PM2.5)
with
significant
health
risk,
but
little
is
known
regarding
their
occurrence
and
sources
in
the
atmosphere.
In
this
study,
we
developed
nontargeted
approach
analyze
electrophilic
urban
Beijing
identified
147
ones
diurnal
variation,
among
which
oxygenated
aromatic
(OACs)
are
predominant
species.
The
discrepancy
hierarchical
clustering
analysis
atmospheric
transformation
markers,
e.g.,
9-nitroanthracene
(9NANT)
citraconic
anhydride
(CA),
PAHs,
fluoranthene
(FLT),
suggested
potential
secondary
formation
pathway
isomeric
ratio
acephenanthrylene
(ACP)
FLT,
product-to-precursor
11H-benzo[a]fluorene-11-one
(BaFO)
further
demonstrated
prevailing
existence
oxidation.
relationship
between
night-to-day
variation
molecular
characteristics,
particularly
negative
correlation
oxygen-related
features
such
as
carbon
oxidation
state,
confirmed
that
multigenerational
processes
during
daytime
predominantly
drive
diurnal/nocturnal
differences.
This
study
achieved
systematic
identification
atmosphere,
revealing
pivotal
role
on
fate
organic
chemicals
resulted
variation.
Russian Journal of Occupational Health and Industrial Ecology,
Journal Year:
2025,
Volume and Issue:
65(4), P. 265 - 270
Published: May 8, 2025
Introduction.
Currently,
the
problem
of
wildfires
is
acquiring
a
global
scale,
and
in
conditions
climate
change,
their
further
increase
predicted.
The
constant
scale
long-term
annual
smoke
pollution
vast
territories
dictate
need
to
study
mechanisms
combustion
products
toxicity,
including
assessment
neurotoxic
effect.
aims
assess
effect
acute
peat
intoxication
on
indices
functional
state
central
nervous
system
white
rats.
Materials
methods.
studies
were
performed
20
outbred
male
rats
exposed
for
4
hours.
A
day
after
end
exposure,
animals
examined
using
open
field
Morris
water
maze
tests.
EEG
also
assessed.
Results.
Exposure
hours
was
accompanied
by
pronounced
inhibition
motor
exploratory
activity
rats,
as
evidenced
decrease
distance
traveled
area
studied
arena
compared
control
group.
results
electroencephalography
revealed
statistically
significant
average
amplitude
left
right
hemispheres
23%
20%,
signal
power
θ-frequency
range
10–11%,
α-rhythm
β1-rhythm
—
22-27%.
Conclusion.
Our
indicate
that
single
4-hour
inhalation
exposure
from
thermal
destruction
containing
main
components:
CO
24
mg/m3
PM2.5
0.32
causes
changes
both
rats'
behavior
parameters.
In
formation
neurotoxicity
when
inhaling
peat,
leading
role
belongs
solid
particles
with
diameter
less
than
2.5
μm
(PM2.5).
Even
though
content
air
inoculation
chambers
close
maximum
permissible
level
working
area,
combination
other
gases
fraction,
occurrence
potentiation
toxic
likely.
Limitations.
limited
examining
behavioral
electroencephalographic
parameters
albino
Ethics.
carried
out
compliance
principles
set
European
Convention
Protection
Vertebrate
Animals
used
Experimental
Scientific
Purposes
ETS
N123,
GOST
33215-2014
approved
Ethics
Committee
East
Siberian
Institute
Medical
Ecological
Research
(Protocol
No.
7
dated
December
15,
2023).