ACS Nano,
Год журнала:
2022,
Номер
17(1), С. 12 - 19
Опубликована: Дек. 30, 2022
As
one
of
the
major
pollutants
in
air,
ambient
fine
particles
are
gaining
considerable
attention
terms
public
health
concerns.
Significant
progress
has
been
achieved
recent
years
understanding
biological
effects
and
mechanisms
particles.
The
airborne
can
enter
human
body
through
various
pathways
translocate
to
a
range
different
organs
further
stay
these
for
extended
periods.
Current
studies
making
substantial
achievements,
while
many
challenges
remain.
On
hand,
whole
picture
concurrent
exposure
translocation
should
be
explored,
requiring
technological
advances
systematic
biobanking
samples
analysis.
other
correlation
between
environmental
concentration
internal
fate
(i.e.,
dose,
distribution
patterns,
kinetics)
invasive
needs
investigated.
Moreover,
biotransformation
vivo
considered,
more
information
is
needed
differentiate
exogenous
from
macromolecules
biogenically
formed
We
recapitulate
current
knowledge
gaps
extra-pulmonary
related
also
propose
future
research
directions
support
both
fundamental
policy
making.
Proceedings of the National Academy of Sciences,
Год журнала:
2022,
Номер
119(26)
Опубликована: Июнь 22, 2022
There
are
still
significant
knowledge
gaps
in
understanding
the
intrusion
and
retention
of
exogeneous
particles
into
central
nervous
system
(CNS).
Here,
we
uncovered
various
fine
human
cerebrospinal
fluids
(CSFs)
identified
ambient
environmental
or
occupational
exposure
sources
these
particles,
including
commonly
found
(e.g.,
Fe-
Ca-containing
ones)
other
compositions
that
have
not
been
reported
previously
(such
as
malayaite
anatase
TiO
2
),
by
mapping
their
chemical
structural
fingerprints.
Furthermore,
using
mouse
vitro
models,
unveiled
a
possible
translocation
pathway
inhaled
from
lung
to
brain
through
blood
circulation
(via
dedicated
biodistribution
mechanistic
studies).
Importantly,
with
aid
isotope
labeling,
obtained
kinetics
mice,
indicating
much
slower
clearance
rate
localized
exogenous
than
main
metabolic
organs.
Collectively,
our
results
provide
piece
evidence
on
CNS
support
association
between
inhalation
transport
tissues.
This
work
thus
provides
additional
insights
for
continued
investigation
adverse
effects
air
pollution
brain.
Environmental Science & Technology,
Год журнала:
2022,
Номер
56(11), С. 6847 - 6856
Опубликована: Фев. 23, 2022
Exposure
to
particulate
matter
(PM)
pollution
damages
the
human
brain.
Fossil
fuel
burning
for
transportation
energy
accounts
a
significant
fraction
of
urban
air
and
climate
pollution.
While
current
United
States
(US)
standards
limit
PM
ambient
concentrations
emissions,
they
do
not
regulate
explicitly
ultrafine
particles
(UFP
≤
100
nm
in
diameter).
There
is
growing
body
evidence
suggesting
UFP
may
play
bigger
role
inflicting
adverse
health
impacts
than
has
been
recognized,
this
perspective,
we
highlight
effects
on
brain,
particularly
young
individuals.
penetrate
through
nasal/olfactory,
respiratory,
gastrointestinal,
placenta,
brain–blood
barriers,
translocating
bloodstream
reaching
glymphatic
central
nervous
systems.
We
discuss
one
case
study.
The
21.8
million
residents
Metropolitan
Mexico
City
(MMC)
are
regularly
exposed
fine
(PM2.5)
above
US
12
μg/m3
annual
average
standards.
Alzheimer's
disease
(AD),
Parkinson's
(PD),
TAR
DNA-binding
protein
(TDP-43)
pathologies
nanoparticles
(NP
50
diameter)
critical
brain
organelles
have
documented
MMC
children
adult
autopsies.
cognitive
olfaction
deficits,
altered
gait
equilibrium,
brainstem
auditory
evoked
potentials,
sleep
disorders.
Higher
risk
AD
vascular
dementia
associated
with
residency
close
high
traffic
roadways
documented.
ready
or
prepared
adopt
quality
emission
will
continue
focus
regulations
only
total
mass
PM2.5
PM10.
Thus,
approach
raises
question:
dropping
ball?
As
research
continues
answer
remaining
questions
about
sources,
exposures,
impacts,
controls,
precautionary
principle
should
call
us
accelerate
expand
policy
interventions
abate
eliminate
emissions
mitigate
exposures.
For
highly
polluted
cities,
developing
world
where
there
likely
older
dirtier
vehicles,
equipment,
fuels
use
less
regulatory
oversight,
embark
strong
campaign
raise
public
awareness
associations
between
pollution,
heavy
traffic,
UFP,
NP,
neuropsychiatric
outcomes,
including
dementia.
Neurodegenerative
diseases
evolving
from
childhood
polluted,
anthropogenic,
industrial
environments
ought
be
preventable.
Environmental Science & Technology,
Год журнала:
2022,
Номер
56(11), С. 6857 - 6869
Опубликована: Фев. 24, 2022
Exposure
to
airborne
fine
particles
(PM2.5,
particulate
matter
with
aerodynamic
diameter
<2.5
μm)
severely
threatens
global
human
health.
Understanding
the
distribution
and
processes
of
inhaled
PM2.5
in
body
is
crucial
clarify
causal
links
between
pollution
diseases.
In
contrast
extensive
research
on
emission
formation
ambient
environment,
reports
about
occurrence
fate
humans
are
still
limited,
although
many
studies
have
focused
exposure
adverse
effects
animal
models.
It
has
been
shown
that
PM2.5,
especially
ultrafine
(UFPs),
potential
go
across
different
biological
barriers
translocate
into
organs
(i.e.,
blood
circulation,
brain,
heart,
pleural
cavity,
placenta).
this
Perspective,
we
summarize
factors
affecting
internal
relevant
analytical
methodology
review
current
knowledge
pathways
humans.
We
also
discuss
challenges
call
for
more
identification
characterization
key
toxic
species
quantification
doses
general
population,
further
clarification
translocation,
metabolism,
clearance
body.
way,
it
possible
develop
toxicity-based
air
quality
standards
instead
currently
used
mass-based
standards.
International Journal of Environmental Research and Public Health,
Год журнала:
2021,
Номер
18(21), С. 11568 - 11568
Опубликована: Ноя. 3, 2021
We
appraise
newly
accumulated
evidence
of
the
impact
particle
pollution
on
brain,
portals
entry,
neural
damage
mechanisms,
and
ultimately
neurological
psychiatric
outcomes
statistically
associated
with
exposures.
PM
comes
from
natural
anthropogenic
sources
such
as
fossil
fuel
combustion,
engineered
nanoparticles
(NP
≤
100
nm),
wildfires,
wood
burning.
are
all
constantly
exposed
during
normal
daily
activities
to
some
level
various
sizes-PM2.5
(≤2.5
µm),
ultrafine
(UFP
or
NPs.
Inhalation,
ingestion,
dermal
absorption
key
entry.
Selected
literature
provides
context
for
US
Environmental
Protection
Agency
(US
EPA)
ambient
air
quality
standards,
conclusions
an
Independent
Particulate
Matter
Review
Panel,
importance
internal
combustion
emissions,
suggesting
UFPs/NPs
cross
biological
barriers
reach
brain.
NPs
produce
oxidative
stress
neuroinflammation,
neurovascular
unit,
mitochondrial,
endoplasmic
reticulum
DNA
damage,
protein
aggregation
misfolding,
other
effects.
Exposure
PM2.5
concentrations
at
below
current
standards
can
increase
risk
TIAs,
ischemic
hemorrhagic
stroke,
cognitive
deficits,
dementia,
Alzheimer's
Parkinson's
diseases.
Residing
in
a
highly
polluted
megacity
is
Alzheimer
neuropathology
hallmarks
99.5%
residents
between
11
months
≤40
y.
PD
aggravation
linked
exposure
diesel
exhaust
increases
ALS
risk.
Overall,
supports
that
contributes
targeted
highlights
complexity
pathophysiologic
mechanisms
marked
differences
profiles
inducing
damage.
Factors
emission
source
intensity,
genetics,
nutrition,
comorbidities,
others
also
play
role.
threat
Thus,
future
research
should
address
specifically
potential
role
