medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: July 21, 2024
Abstract
Cognitive
impairment
among
older
adults
is
a
growing
public
health
challenge
and
environmental
chemicals
may
be
modifiable
risk
factors.
A
wide
array
of
has
not
yet
been
tested
for
association
with
cognition
in
an
environment-wide
framework.
In
the
US
National
Health
Nutrition
Examination
Survey
(NHANES)
1999-2000
2011-2014
cross-sectional
cycles,
was
assessed
using
Digit
Symbol
Substitution
Test
(DSST,
scores
0-117)
participants
aged
60
years
older.
Concentrations
measured
blood
or
urine
were
log
2
transformed
standardized.
Chemicals
at
least
50%
measures
above
lower
limit
detection
included
(n
=147,
n
classes
=14).
We
associations
between
chemical
concentrations
parallel
survey-weighted
multivariable
linear
regression
models
adjusted
age,
sex,
race/ethnicity,
education,
smoking
status,
fish
consumption,
cycle
year,
urinary
creatinine,
cotinine.
Participants
one
measurement
(n=4,982)
mean
age
69.8
years,
55.0%
female,
78.2%
non-Hispanic
White,
77.0%
high
school
educated.
The
DSST
score
50.4
(standard
deviation
(SD)=17.4).
analyses,
5
147
exposures
associated
p-value<0.01.
Notably,
SD
increase
-scaled
cotinine
concentration
2.71
points
(95%
CI
-3.69,
-1.73).
tungsten
1.34
-2.11,
-0.56).
Exposure
to
chemicals,
particularly
heavy
metals
tobacco
smoke,
factors
adults.
The Egyptian Journal of Internal Medicine,
Journal Year:
2025,
Volume and Issue:
37(1)
Published: Jan. 24, 2025
Abstract
This
narrative
review
explores
the
relationship
between
air
pollution
and
neurodegenerative
diseases
(NDs).
Historically,
has
been
linked
primarily
to
respiratory
cardiovascular
issues,
but
recent
evidence
suggests
that
it
may
also
impact
neurological
health.
With
global
increase
in
diseases,
understanding
environmental
risk
factors
become
crucial.
The
synthesizes
findings
from
studies,
highlighting
potential
role
of
pollutants—particularly
fine
particulate
matter
(PM2.5),
ozone,
nitrogen
dioxide
(NO2),
heavy
metals—in
onset
progression
NDs.
Key
mechanisms
under
investigation
include
brain
inflammation
microglial
activation,
which
are
believed
contribute
processes.
Animal
human
studies
have
shown
correlations
exposure
increased
cognitive
decline
disorders.
Research
indicates
exacerbate
neuroinflammation
cause
white
abnormalities,
disrupt
neural
communication
function.
Additionally,
emerging
like
residential
greenness
climate
action
could
mitigate
some
these
adverse
effects.
Despite
advancements,
significant
knowledge
gaps
remain,
particularly
regarding
long-term
chronic
specific
molecular
pathways
involved.
shows
need
for
further
research
clarify
develop
targeted
interventions.
Addressing
pollution’s
on
requires
comprehensive
public
health
strategies,
including
stricter
regulations
awareness,
alongside
continued
into
preventive
therapeutic
measures.
Scientific Reports,
Journal Year:
2023,
Volume and Issue:
13(1)
Published: June 2, 2023
Abstract
Atmospheric
particulate
matter
(PM)
causes
3.7
million
annual
deaths
worldwide
and
potentially
damages
every
organ
in
the
body.
The
cancer-causing
potential
of
fine
particulates
(PM
2.5
)
highlights
inextricable
link
between
air
quality
human
health.
With
over
half
world’s
population
living
cities,
PM
emissions
are
a
major
concern,
however,
our
understanding
exposure
to
urban
is
restricted
relatively
recent
(post-1990)
monitoring
programmes.
To
investigate
how
composition
toxicity
has
varied
within
an
region,
timescales
encompassing
changing
patterns
industrialisation
urbanisation,
we
reconstructed
pollution
records
spanning
200
years
from
sediments
ponds
Merseyside
(NW
England),
heartland
urbanisation
since
Industrial
Revolution.
These
archives
environmental
change
across
region
demonstrate
key
shift
coarse
carbonaceous
‘soot’
that
peaked
during
mid-twentieth
century,
finer
combustion-derived
post-1980,
mirroring
changes
infrastructure.
evolution
enhanced
signal
important
implications
for
lifetime
exposures
populations
generational
timescales.
Environmental Science & Technology,
Journal Year:
2024,
Volume and Issue:
58(10), P. 4571 - 4580
Published: March 2, 2024
Exposure
to
atmospheric
particulate
matter
(PM)
has
been
found
accelerate
the
onset
of
neurological
disorders
via
induction
detrimental
neuroinflammatory
responses.
To
reveal
how
astrocytes
respond
urban
PM
stimulation,
a
commercially
available
standard
reference
material
(SRM1648a)
was
tested
in
this
study
on
activation
rat
cortical
astrocytes.
The
results
showed
that
SRM1648a
stimulation
induced
both
A1
and
A2
phenotypes
astrocytes,
as
characterized
by
exposure
concentration-dependent
increases
Fkbp5,
Sphk1,
S100a10,
Il6
mRNA
levels.
Studying
functional
alterations
indicated
neurotrophic
factors
Gdnf
Ngf
were
transcriptionally
upregulated
due
astrocytic
A2-type
activation.
also
promoted
autonomous
motility
elevated
expressions
chemokines.
aryl
hydrocarbon
receptor
(AhR)
agonistic
components,
such
polycyclic
aromatic
hydrocarbons
(PAHs),
recognized
greatly
contribute
SRM1648a-induced
effects
which
confirmed
attenuation
PM-disturbed
AhR
blockage.
This
study,
for
first
time,
uncovered
direct
regulation
function
traced
containing
bioactive
components
(e.g.,
PAHs)
with
activity.
findings
provided
new
knowledge
understanding
ambiguous
disturbance
from
ambient
fine
pollution.
Frontiers in Neurology,
Journal Year:
2023,
Volume and Issue:
14
Published: June 23, 2023
Multiple
sclerosis
and
the
major
sporadic
neurogenerative
disorders,
amyotrophic
lateral
sclerosis,
Parkinson
disease,
Alzheimer
disease
are
considered
to
have
both
genetic
environmental
components.
Advances
been
made
in
finding
predispositions
these
but
it
has
difficult
pin
down
agents
that
trigger
them.
Environmental
toxic
metals
implicated
neurological
since
human
exposure
is
common
from
anthropogenic
natural
sources,
damaging
properties
suspected
underlie
many
of
disorders.
Questions
remain,
however,
as
how
enter
nervous
system,
if
one
or
combinations
sufficient
precipitate
metal
results
different
patterns
neuronal
white
matter
loss.
The
hypothesis
presented
here
damage
selective
locus
ceruleus
neurons
causes
dysfunction
blood-brain
barrier.
This
allows
circulating
toxicants
astrocytes,
where
they
transferred
to,
damage,
oligodendrocytes,
neurons.
type
disorder
arises
depends
on
(i)
which
damaged,
(ii)
variants
give
rise
susceptibility
uptake,
cytotoxicity,
clearance,
(iii)
age,
frequency,
duration
toxicant
exposure,
(iv)
uptake
various
mixtures
metals.
Evidence
supporting
this
presented,
concentrating
studies
examined
distribution
system.
Clinicopathological
features
shared
between
disorders
listed
can
be
linked
Details
provided
applies
multiple
neurodegenerative
Further
avenues
explore
for
suggested.
In
conclusion,
may
play
a
part
several
While
further
evidence
support
needed,
protect
system
would
prudent
take
steps
reduce
pollution
industrial,
mining,
manufacturing
burning
fossil
fuels.
Turkish Archives of Pediatrics,
Journal Year:
2025,
Volume and Issue:
60(1), P. 13 - 21
Published: Jan. 3, 2025
Social
determinants
of
health
(SDHs)
are
significant
and
potentially
modifiable
drivers
neurologic
diseases,
including
childhood
epilepsy.
greatly
influence
the
epidemiology,
management,
outcomes
associated
with
these
conditions.
affect
every
aspect
a
family's
journey
epilepsy-from
initial
diagnosis
to
accessing
effective
treatments
ongoing
care.
Despite
notable
advancements
in
understanding
genetic
molecular
underpinnings
pediatric
epilepsies,
there
remains
relative
lack
knowledge
about
nature
impact
SDHs
on
disorders.
Epilepsy
is
symptom
much
more
profound
underlying
health.
Addressing
broader
context
epilepsy
can
transform
outcomes.
This
narrative
review
appraises
some
available
evidence
explores
possible
solutions.
