1. INTRODUCTION
METHODS
AIM AND HYPOTHESIS
Figure 1. Estimated Association of TNF-α, IL-1β & Leptin
with Previous Cumulative 12-Month Exposure to PM2.5 &
NO2 Among Latino Participants in LA, CAa
• Increased obesity has been linked with the emergence of insulin
resistance and type 2 diabetes among youth.
• Meanwhile, growing evidence suggests that both ambient (AAP) and
traffic-related (TRAP) air pollution are strongly associated with
systemic inflammation and metabolic dysregulation, which can further
lead to risk factors for diabetes in children and adults.
• While the mechanisms underlying the associations between air
pollution exposure and adverse health outcomes remained uncertain,
studies indicate that increased exposures to AAP and/or TRAP may
induce systemic inflammation, leading to insulin resistance, impaired
glucose metabolism, and endothelial dysfunction.
• Aim: To investigate the cross-sectional associations between prior
year exposure to AAP and TRAP with systemic markers of
inflammation in overweight and obese Latino youth in LA, CA.
 Hypothesis: The previous cumulative 12-month exposure to
particulate matter (PM2.5), nitrogen dioxide (NO2), ozone (O3), and
nitric oxides (NOx) increased risk for obesity and type 2 diabetes
as defined by higher concentrations of systemic inflammatory
markers and altered levels of leptin and adiponectin.
Design and Recruitment: 200 obese and overweight Latino children (8-
15 years old) in urban Los Angeles were enrolled in this study, which is a
cross-sectional analysis of baseline data of SOLAR project.
Measures:
• AAP and TRAP exposures were estimated from residential addresses
for the year prior to each participant’s clinical visit.
• AAP exposure was estimated by interpolating concentrations from a
dense network of community monitors.
•TRAP was based on NOx concentrations estimated using CALINE4
models, and was also estimated using distance from freeways/highways
(FCC1) and minor collector roads (FCC3).
Statistical Analysis: Linear regression models were fitted to examine
associations between AAP (PM2.5, NO2, O3) and TRAP (Freeway NOx,
Non-freeway NOx, and Total NOx) exposure with measures of
inflammatory and metabolic markers, including TNF-α, IL-6, IL-1β,
adiponectin, and leptin. Analysis adjusted for age, sex, body fat percent,
season of testing, and social position.
Table 1. Characteristics of Latino Participants
RESULTS
Mean (SD)
Physical Characteristics
Age (years) 11.4 (1.6)
Sex (F/M, %) 90/110, 45
Adiposity
BMI (kg/m2
) 28.5 (5.5)
Total Fat Mass (kg)a
25.2 (9.8)
Total Percent Fat (%)a
38.7 (6.0)
Total Lean Mass (kg)a
31.7 (9.9)
Metabolic Outcomes
HOMA-IRb
Fasting Glucose (mg/dL)b
93.3 (6.2)
Fasting Insulin (μU/mL)b
19.6 (10.3)
SIb
(x10-4 min-1)/µU/mL) 2.0 (1.3)
AIRg
b
(µU/mL x 10min) 1,678.2 (1,160.7)
Disposition Indexb
(DI) 2,531.9 (1,177.2)
Table 2. Average Levels of Annual Air Pollution
Exposure and inflammatory biomarkers
Table 1 and 2. Unadjusted Mean (SD) for the 200 Latino participants included in this study. N= a
205, b
195, c
143.
Mean (SD)
12-Month Cumulative AAP
PM2.5 (μg/m3
) 19.8 (4.8)
NO2 (ppb) 30.3 (6.2)
O3 (ppb) 20.2 (3.2)
Annual TRAP
Freeway NOx 31.9 (29.3)
Non-Freeway NOx 8.8 (6.1)
Total NOx 40.7 (29.9)
Inflammatory and Metabolic Markers
TNF-α (pg/ml) 7.9 (4.1)
IL-6 (pg/ml) 9.3 (11.9)
IL-1β (pg/ml) 4.5 (5.0)
Adiponectin (pg/ml)c
10.1 (3.2)
Leptin (pg/ml) 25548.5 (15218.6)
a
Estimated percent change in metabolic indicates as a function of each 1-standard deviation increase in 12-month cumulative ambient
air pollution (AAP) were observed. Analysis adjusts for age, sex, pubertal stage, total percent fat mass, seasonality, and social position.
CONCLUSIONS
Effects of Ambient and Traffic-related Air Pollution Exposure on
Systemic Inflammation among Latino Youth in Los Angeles
Liu C1
, Alderete TL1
, Toledo-Corral CM1,2
, Habre R2
, Belcher B1
, Berhane K2
, Lurmann FW4
, Weigensberg MJ5
, Goran MI3,6
, Gilliland FD2
Support and Disclaimer:
This work is supported by the National Institute of Environmental Health Sciences Center (5P30ES07048).
Elevated AAP (PM2.5 and NO2) and TRAP (Non-freeway Nox) exposures were associated with higher levels of systemic inflammation and
alterations in metabolism. These findings suggest that increased exposure to AAP and TRAP may contribute to obesity and/or type 2 diabetes
and through inflammatory and metabolic pathways among overweight Latino adolescents.
1
Division of Environmental Health, 3
Diabetes and Obesity Research Institute, Department of Preventive Medicine, University of Southern California, Los Angeles, California
2
Department of Public Health, California State University, Los Angeles, California 4
Sonoma Technology, Inc.
5
Department of Pediatrics, 6
Department of Physiology and Biophysics, University of Southern California, Los Angeles, California
• Overall, AAP exposures had adverse effects on systemic inflammation.
• Higher PM2.5 exposure (5 μg/m3
) was associated with 10.4% higher IL-1β (p=0.02), 8.2% higher TNF-α (p=0.04), and 13.8% higher leptin
(p=0.005).
• Additionally, higher NO2 exposure (6 ppb) was associated with a 7.2% higher TNF-α (p=0.04) and 10.0% higher leptin (p=0.003).
• Living 500 to 1000 meters from highways/freeways was associated with lower leptin and higher adiponectin levels compared to shorter
distance.
• For TRAP exposures, 1 unit increase in non-freeway Nox was associated with 2.1% higher AIRg (p=0.01) and 1.2% DI (p=0.03).