7. Inhala&on Exposure and Mental
Health
Power MC, Kioumourtzoglou MA, Hart JE, Okereke OI, Laden F, Weisskopf MG et al. The rela&on
between past exposure to fine par&culate air pollu&on and prevalent anxiety: observa&onal
cohort study BMJ 2015; 350 :h1111
compared with 12.7 (4.2 μg/m3) for the one month aver-
aging period.
Residential proximity to roadways
Nurses who lived 50 to 200 m from the nearest major
road were more likely to have increased Crown-Crisp
index phobic anxiety scale scores than those living
>200 m away (adjusted odds ratio 1.06, 95% confi-
dence interval 1.01 to 1.12; P=0.03). However, there was
no evidence of a dose-response pattern, as those living
within 50 m of the nearest major road did not have
increased odds (adjusted odds ratio 1.01, 0.95 to 1.08;
P=0.74). Findings of all sensitivity analyses were simi-
lar or more uniformly null (see supplementary table e2
and figure e1).
Particulate matter
We observed associations between higher PM2.5 and
high anxiety across several averaging periods. Given
evidence for slightly non-linear dose-response patterns
in some averaging periods (see supplementary figure
e2), we report associations with both fifths of exposure
(fig 2) and per 10 μg/m3 increase in exposure (table 2).
Notably, while associations were similar across 1, 3, 6,
and 12 month averaging periods, associations for the
1988–2003 averaging period were weaker than for the
shorter averaging periods. All sensitivity analyses were
reasonably consistent with our primary models (see
supplementary tables e4 to e10). Mutually adjusted
models suggest that these associations were primarily
driven by an association between anxiety and shorter
averaging periods (fig 3). There was little evidence to
support an association between high anxiety and expo-
sure to PM2.5–10 in either our primary (see supplemen-
tary table e3 and figure e3) or our sensitivity analyses
(see supplementary tables e4 to e10). We did not
observe significant effect modification of the associa-
tion with one month PM2.5 by any of the proposed vari-
6 months 11.59 (2.77) 1.14 (1.05 to 1.23) 0.002
12 months 11.38 (2.60) 1.15 (1.06 to 1.25) 0.001
1988–2003 13.75 (2.82) 1.09 (1.01 to 1.18) 0.03
PM2.5=particulate matter <2.5 μm in diameter.
*Adjusted for month of questionnaire return, nurse’s education, husband’s education, age, age squared,
whether the nurse has a partner, employment status, physical activity, percent of residential census tract that
is white, percent of residential census tract adults who lack a high school education, median home value of
residential census tract, geographic region, residence within a metropolitan statistical area, and social
support.
Fifths of PM2.5 exposure
Lowest
fifth (ref)
Second
fifth
Third
fifth
Fourth
fifth
Highest
fifth
0.9
1.0
3 months
Oddsratio(95%CI)
0.9
1.1
1.2
1.3
1.0
6 months
Oddsratio(95%CI)
0.9
1.1
1.2
1.3
1.0
12 months
Oddsratio(95%CI)
0.9
1.1
1.2
1.3
1.0
1988-2003
Oddsratio(95%CI)
0.9
1.1
1.2
1.3
1.0
RESEARCH
e month aver-
nearest major
Crown-Crisp
n those living
6, 95% confi-
osure to PM2.5
nts of Nurses’
P value
0.0001
0.0004
0.002
0.001
0.03
e squared,
census tract that
home value of
and social
1 month
Oddsratio(95%CI)
0.9
1.1
1.2
1.3
1.0
3 months
Oddsratio(95%CI)
0.9
1.1
1.2
1.3
1.0
6 months
5%CI)
1.3
one month aver-
he nearest major
sed Crown-Crisp
han those living
1.06, 95% confi-
wever, there was
n, as those living
ad did not have
1.01, 0.95 to 1.08;
alyses were simi-
mentary table e2
higher PM2.5 and
g periods. Given
esponse patterns
lementary figure
fifths of exposure
xposure (table 2).
lar across 1, 3, 6,
ociations for the
aker than for the
ity analyses were
ary models (see
utually adjusted
ns were primarily
xiety and shorter
ittle evidence to
nxiety and expo-
(see supplemen-
nsitivity analyses
10). We did not
n of the associa-
he proposed vari-
Fifths of PM2.5 exposure
Lowest
fifth (ref)
Second
fifth
Third
fifth
Fourth
fifth
Highest
fifth
Oddsratio(9
0.9
1.1
1.2
1.0
6 months
Oddsratio(95%CI)
0.9
1.1
1.2
1.3
1.0
12 months
Oddsratio(95%CI)
0.9
1.1
1.2
1.3
1.0
1988-2003
Oddsratio(95%CI)
0.9
1.1
1.2
1.3
1.0
10. Inhala&on Exposure in Maternity and
Mental Health
between the sexes in childhood outcomes fol-
lowing maternal stress during pregnancy (Cao
et al. 2012; Fang et al. 2011).
Our data from isolated CD11b+ and
CD11b– cells demonstrate that microglia—
not neurons or astrocytes—are the primary
source of the measured cytokines in the
brain, suggesting that they are a target of
“programming” by the prenatal stressors.
Microglia begin to colonize the rodent brain
animals we used for protein analysis
went behavioral testing, whereas the
used for CD11b isolation and gene
sion analysis were behaviorally naïv
possible that behavioral testing may
a sufficient stressor to elicit relativel
term increases in cytokine levels (i.e.,
ing until tissue collection) in the b
the DEP/NR animals, which would
observed at baseline. Alternatively, th
2.5
2.0
1.5
1.0
0.5
0
1.8
1.6
1.4
1.2
1.0
0.8
0.6
0.4
0.2
0
#
#
#
**
#
**
Control
r = –0.33
p < 0.05
r = 0.27
p = 0.09
Males Females
Memory
Males Females
Males Female
NR Control NR Control NR Control
IL-1β(pg/mL)
IL-10(pg/mL)
Percentfreezing
infearcontext
Percentfreezing
infearcontext
IL-1β (pg/mL) IL-1β (pg/mL)
Timeinclosed
arms(sec)
0 0 00.5 0.5 01.0 1.02.0 2.03.0 3.0 4.03.51.5 1.52.5 2.5
50
40
30
20
10
0
100
80
60
40
20
0
350
300
250
200
150
100
50
0
VEH
DEP
on analysis were behaviorally naïve. It is
ossible that behavioral testing may serve as
sufficient stressor to elicit relatively long-
erm increases in cytokine levels (i.e., endur-
ng until tissue collection) in the brains of
he DEP/NR animals, which would not be
bserved at baseline. Alternatively, there may
patterns (e.g., lipopolysaccharide), as well
as endogenous danger-associated molecu-
lar patterns released in response to cellular
distress (e.g., DEP-induced hyaluronan or
high-mobility group box 1) (Bianchi 2007).
Notably, glucocorticoids may up-regulate
TLRs on microglia, augmenting subsequent
1.8
1.6
1.4
1.2
1.0
0.8
0.6
0.4
0.2
0
35
30
25
20
15
10
5
0
†
†
#
**
#
**
r = 0.27
p = 0.09
r = 0.37
p < 0.05
r = –0.46
p < 0.01
Anxiety
Females Males Females
Males Females Males Females
Control NR Control NR Control NR Control NRIL-1β/IL-10ratio
IL-1β (pg/mL) IL-1β (pg/mL) IL-1β (pg/mL)
Timeinclosed
arms(sec)
Timeinclosed
arms(sec)
0 00.5 0.50 1.0 1.02.0 2.0 2.03.0 3.0 3.0 4.04.03.51.5 1.5 1.52.5 2.5 2.5 3.5
350
300
250
200
150
100
50
0
350
300
250
200
150
100
50
0
Bolton JL, Huff NC, Smith SH, Mason SN, Foster WM, Auten RL, Bilbo SD. 2013. Maternal stress and
effects of prenatal air pollu&on on offspring mental health outcomes in mice. Environ Health
Perspect 121:1075–1082
11. Mechanisms for Air Pollutant Exposure
and Mental Health ology 3
Reactive astrocytosis
Nasal pathway
Direct transport
Respiratory intake
Olfactory bulb
Systemic inflammation
Circulating cytokines
Respiratory inflammation
Systemic circulation
Neuroinflammation
Oxidative stress
Protein aggregation
Neuronal death
Trigeminal
pathway
Neuronal transport (?)
Microglial
activation
ROS
BBB
Vagal
pathway
Air pollutants
TNFα, IL-1β, IL-6
Figure 1: The impact of air pollution on the brain through multiple pathways.
f the route of entry, NPs that reach the damage, endothelial cell activation, and brain lesions in the
Genc et al, 2011
Vitamin D prevents autoimmunity through different mechanisms: there is a significant association between vitamin D de
Fig. 1. Air pollution exposure and mechanisms in multiple sclerosis pathogenesis: Inflammation and oxidative stress lead to blood brain barrier breakdown, im
cascades by nuclear factors and activated microglia, mitochondrial dysfunction and neurodegeneration, and vitamin D deficiency could culminate in brain a
(COX-2, cyclooxygenase2; ET-1, endothelin1; HO-1, heme oxygenase1; ICAM-1, intercellular adhesion molecule1; IL, interleukin; iNOS, inducible nitric oxide sy
1, monocyte chemoattractant protein1; MIF, macrophage inhibitory factor; MIP1a, macrophage inflammatory protein1-a; MMP, matrix metalloproteinase; N
factor kappa B; SOD, superoxide dismutase; TNF-a, tumor necrosis factor alpha; UVB, ultraviolet B, VCAM-1, vascular adhesion molecule1).
S. Esmaeil Mousavi et al. / Medical Hypotheses 100 (2017) 23–30
Mousavi et al, 2017
12. Figure 1. High-resolution mapping of time-integrated concentrations. Annual median daytime concentrations for 30 m-length road segments based on
1 year of repeated driving for a 16 km2
domain in West Oakland [WO] and Downtown (a), and for a 0.6 km2
industrial-residential area in WO (b).
Median ± SE concentrations are tabulated by road type in c. Annual median daytime ambient concentrations Camb at a regulatory fixed-site monitor in
WO are plotted as shaded stars. Localized hotspots in b correspond to major intersections, industries, and businesses with truck traffic, and are
Environmental Science & Technology Article
Apte et al., 2017
Issues from IAQ Perspec&ve
13. Issues from IAQ Perspec&ve
18 Ch. Mom et al. / The Science of the Total Environment 208 (1997) 15-21
A B C D E F
Home
G
Fig. 1. I/O ratios for PM,, in different homes (mean ratio,
minimum ratio and maximum ratio).
of indoor particulates. The relationship between
outdoor and indoor particulates was investigated
using linear regression analysis. Fig. 2 shows a
scatter diagram for the indoor and outdoor mea-
‘preference
n activity
I
PM-10 PM-Z.5
Fig. 3. Effect of activity on I/O ratios for PM,, and PM,,,
(homes A and Cl.
siderably below 1 and in home C, greater than 1.
Fig. 3 shows the influence of activity on I/O
ratios. In homes A and C, where PM,, and PM,,
were measured, a distinction was made between
grades of activity: The ‘reference cases’, refers to
a situation with no activity (an absence of inhabi-
Monn et al., 1998
Differences in Built Environment
Both TSP and 48-h geometric mean fine-mode
number concentration measurements showed a strong
correlation between rooms. Figure 1a shows the
correlation between the TSP measurements in the
kitchen and the living room (R2
=0.95, smoking house-
hold included; R2
=0.63, y=0.77x+15.45, smoking
household excluded). Figure 1b shows the even stronger
correlation between 48-h geometric mean fine-mode
number concentrations in the kitchen and living room
(R2
=0.99, smoking household included; R2
=0.82,
y=1.14xÀ32.12, smoking household excluded).
Besides the good correlation shown between mea-
surements in different rooms there was also a small but
significantly larger 48-h geometric mean fine-mode
particle number concentration in the living room
compared to that found in the kitchen both with and
without the smoking household included (p=0.05 and
0.04, respectively), and a significantly higher TSP value
in the living room compared to that found in the
kitchen, both with and without the smoking household
included (p=0.02 and 0.01 respectively).
Continuous Measurement
The graphs of particle number concentration (1-min
moving average median particle number per litre)
against time for the 48-h period in both the kitchen
and living room reveal that many of the short-term
peak concentrations in either of the rooms were
frequently mirrored in the other room. This is illustrated
in Figures 2±4.
The peak number concentrations in the living room
were often mirrored in terms of time and duration to
those found in the kitchen, e.g., those generated by
cooking activities in the kitchen. These results are
consistent despite many potential uncertainties such as
the effect of different air exchange rates, any pre-
existing differences in number concentrations and any
unidentified activities in the living room that are likely
to occur near meal times. It is also interesting to note
that whilst the background night time number concen-
tration was usually different on the two consecutive
nights monitored it was very similar between rooms for
each night with the average arithmetic mean difference
Figure 2. Fine-mode particle number concentration against time for house number 5 (smoking household).
Particulate matter variation within the home Wigzell et al.
Journal of Exposure Analysis and Environmental Epidemiology (2000) 10(3) 311
Concentra&on Spikes
Kendall et al., 2000