Transcript Assessing effects of prenatal pah exposure on birth outcomes and

Assessing effects of prenatal
PAH exposure on birth outcomes
and neurocognitive development
among a cohort of Polish
mothers and newborns.
Ulka Bawle*, Wieslaw Jedrychowski**, Robin Whyatt*,
David Camann***, John Spengler***, Tom Dumyahn***,
Frederica Perera*
*/ Center for Children’s Environmental Health,
Columbia University, New York, USA
**/Chair of Epidemiology and Preventive Medicine,
Coll.Med.. Jagiellonian University, Krakow, Poland
What is the role of
early life exposures
to PAH?
Vulnerability of the Fetus and Child
Exposure
Effect
Lead (Needleman et al.,1979)
D
Radiation (Shimizu et al., 1991)
C
Pesticides (NAS, 1993)
D,C
PCBs (Jacobsen and Jacobsen, 1996)
D
Polycyclic aromatic hydrocarbons (PAH)
D,G
(Perera, Whyatt et al., 1998)
D
Developmental
D -- Developmental
damage
- Cancer G - Genetic
G - Genetic
C -CCancer
damage
HEALTH HAZARDS DUE TO PAH COMPONENTS
Macromolecules
PAHs
Biotransformation
Mixed-function
oxidases
P-450 enzymes
Aryl hydrocarbon
hydrolase (AHH)
Epoxides
DNA
Impairment of fetal
and early childhood
growth and development
A. SPECIFIC AIMS OF THE STUDY
1.To test the hypothesis that prenatal exposure to airborne
polycyclic aromatic hydrocarbons (PAH) adversely affects fetal
growth, after controlling for non-PAH components of particulate
matter < 2.5 m (PM2.5), environmental tobacco smoke ( ETS),
nutritional status and other potential confounders.
2. To test the hypothesis that prenatal exposure to airborne PAH
adversely affects early childhood growth and development, after
controlling for non-PAH components of PM2.5, ETS and other
potential confounders
3. To explore whether non-PAH components of PM2.5, and ETS have
independent effects on birth outcomes and childhood growth and
development, after controlling for PAH, and to explore possible
interactions between PAH, PM2.5 and ETS.
4. To estimate the relative contribution of ambient PAH pollution vs.
ETS and other indoor PAH sources to a) personal PAH exposure and
PAH-DNA adducts; and b) impairment of fetal growth and early child
development
Research Design of study “Vulnerability of the Fetus/Infant
to PAH, PM2.5 and ETS”
Recruitment
in Pregnancy
1. Questionnaires:
a. Prenatal I, II Trimester (mother)
b. Dietary (FFQ)
c. Dietary (24-Hour Recall)
d. 48-Hour Exposure Assessment
e. Prenatal III Trimester
f. Health /Asthma (in child)
I tri. II tri. III tri. Delin=96 n=400
very
3m
6m
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9m
12 m
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2. Air monitoring exposure:
personal
indoor/ outdoor
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3. Infant cord blood
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4. Maternal blood
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5. Birth outcomes:
Mother’s Med. Chart Review
Newborn’s Med. Chart Review
6. Neurodevelopmental test
of infant:
Fagan test
Bayley Scale
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Characteristics of recruited pregnant women:
age of women
N = 30
N = 105
36,7%
32,4%
48,6%
19,0% 43,3%
<=25
Age group:
>25 and <=30
20,0%
>30
Characteristics of recruited pregnant women:
by educational level and marital status
N = 30
26,7%
Education level:
Primary
10,0%
Occupational
Technical
N = 105
22,9%
9,5%
9,5%
6,7%
13,3%
2,9%
14,3%
College
High school
University
Marital status:
Married
41,0%
43,3%
76,7%
88,6%
Single
11,4%
23,3%
Characteristics of recruited pregnant women:
number of pregnancies
N = 30
N = 105
49,5%
56,7%
1,0%
2,9%
3,3%
6,7%
6,7%
40,0%
33,3%
Number of pregnancies:
1
2
3
4
5
PAH concentrations in low and high polluted areas
of Krakow (N=30). Air monitoring over 48 hours.
Low polluted area
High polluted area
Benzo(a)pyrene
Benz(a)anthracene
Benzo(b)fluoranthene
Benzo(k)fluoranthene
Benzo(g,h,i)perylene
Chrysene
Dibenz(a,h)anthracene
Indeno(1,2,3-cd)pyrene
0
5
10
15
20
25
ng/m3
30
PM2.5 concentration in Krakow
N = 30
Mean
56,729
Median
56,758
Standard deviation
26,181
(Q3-Q1)/2
14,652
PAH concentrations in Krakow and New York City
ng/m3
Contribution of various chemical substances (in %)
in the total PAH concentration in Krakow and New York City
Krakow
New York City