Environmental Health Perspectives • VOLUME 111 | NUMBER 2 | February 2003 201

Effects of Transplacental Exposure to Environmental Pollutants on Birth

Outcomes in a Multiethnic Population 

Frederica P. Perera,1 Virginia Rauh,1 Wei-Yann Tsai,1 Patrick Kinney,1 David Camann,2 Dana Barr,3 Tom Bernert,3

Robin Garfinkel,1 Yi-Hsuan Tu,1 Diurka Diaz,1 Jessica Dietrich,1 and Robin M. Whyatt1

1Columbia Center for Children’s Environmental Health, Mailman School of Public Health, Columbia University, New York, USA;

2Department of Analytical and Environmental Chemistry, Southwest Research Institute, San Antonio, Texas, USA; 3Centers for Disease

Control and Prevention, National Center for Environmental Health, Division of Laboratory Sciences, Atlanta, Georgia, USA

The impact of environmental toxicants on

children’s health is increasingly being recognized as significant (Faustman 2000; GBPSR

2000; Landrigan et al. 1999; Perera et al.

1999; U.S. EPA 1996). Human and experimental studies indicate that the fetus and

infant are more sensitive than adults to many

environmental toxicants, including environmental tobacco smoke (ETS), polycyclic aromatic hydrocarbons (PAHs), and pesticides

(Calabrese 1986; Mott et al. 1994; National

Academy of Sciences 1993; WHO 1986;

Whyatt and Perera 1995). Urban, minority

populations represent high-risk groups for

adverse birth outcomes (New York City

Department of Health 1998; Perera et al.

2002). These same populations are likely to

be more heavily exposed to ambient air pollution, ETS, and pesticides (Chen and Petitti

1995; Heritage 1992; Metzer et al. 1995;

Olden and Poje 1995; Pirkle et al. 1996;

Wagenknecht et al. 1993; Wernette and

Nieves 1992). However, only limited information is available on the extent and impact

of prenatal exposure to these environmental

contaminants on fetal growth and development. Etiologic studies have largely been ecologic, lacking individual-level data on

exposure.

In the present study we evaluated the

effects of prenatal exposure to common

urban pollutants: airborne PAHs monitored

during pregnancy by personal air sampling

of the mother; along with ETS, estimated by

plasma concentrations of cotinine; and the

organophosphate (OP) pesticide (CPF), estimated by plasma CPF concentrations. In

addition to being genotoxic and carcinogenic, PAHs such as benzo[a]pyrene (BaP)

are endocrine disruptors (Bostrom et al.

2002; Bui et al. 1986; Davis et al. 1993).

Prior laboratory and two human studies in

Central Europe indicate that transplacental

exposure to PAHs at relatively high concentrations (annual average airborne concentrations of 7–17 ng/m3 BaP in the human

studies) is associated with adverse birth outcomes (Barbieri et al. 1986; Bui et al. 1986;

Legraverend et al. 1984; Perera et al. 1998;

Dejmek et al. 2000). ETS is a complex mixture of over 4,000 chemicals, including

PAHs and carbon monoxide (Leikauf et al.

1995). Prenatal exposure to tobacco smoke

has been associated with deficits in birth

weight, birth length, and cognitive functioning at age 3 (Janerich et al. 1990; Martinez

et al. 1994; Schuster-Kolbe and Ludwig

1994; Sexton et al. 1990). OP pesticides can

act as developmental toxicants. For example,

CPF exerts neurodevelopmental and/or

behavioral effects in experimental studies

when administered during gestation or postnatally (reviewed in (Eskenazi et al. 1999;

GBPSR 2000; Landrigan et al. 1999;

Whyatt et al. 2002). Effects on human fetal

development have not yet been evaluated. As

previously reported, we have obtained multiple measures of pesticides on our parent

cohort of pregnant women and newborns

(Whyatt et al. 2002). In the present analysis,

CPF was selected as a covariate because it

was the most commonly detected pesticide

in plasma samples and because CPF levels in

cord plasma were highly correlated with

those of other frequently detected pesticides

in plasma, including the organophosphate

diazinon and carbamate bendiocarb (r = 0.8

and r = 0.5, respectively; p < 0.001,

Spearman’s rank). CPF and diazinon have

been used widely on fruits and vegetables

and in treatment of homes, although all residential uses are being phased out (Adgate et

al. 2001; U.S. EPA 2002).

Here we tested the hypothesis that prenatal

exposure to environmental pollutants is negatively associated with birth weight, length, and

head circumference, after controlling for the

effects of known physical, biologic, and toxic

determinants of fetal growth. As reported previously, the study cohort has substantial exposure to multiple contaminants during

pregnancy (Perera et al. 2002; Whyatt et al.

2001, 2002). Specifically, analysis of PAHs in

Address correspondence to F.P. Perera, Columbia

Center for Children’s Environmental Health,

Mailman School of Public Health, Columbia

University, 60 Haven Avenue, #B-109, New York,

NY 10032 USA. Telephone: (212) 304-7280. Fax:

(212) 544-1943. E-mail: Fpp1@columbia.edu 

We gratefully acknowledge the contributions of D.

Holmes, M. Borjas, A. Reyes, J. Ramirez, Y. Cosme,

S. Illman, and E. Evans from Columbia University

and L. Needham and R. Jackson from the Centers for

Disease Control and Prevention; the obstetrics/gynecology staffs at Harlem Hospital, Allen Pavillion, and

New York-Presbyterian Hospital. 

Grant support was provided by NIEHS/EPA P50

ES09600, NIEHS RO1 ES10165 and RO1

ES08977, EPA (NCER STAR Program), the W.

Alton Jones Foundation, Gladys and Roland

Harriman Foundation, Bauman Foundations, and

the New York Community Trust.

Received 30 April 2002; accepted 10 September 2002.

Inner-city, minority populations are high-risk groups for adverse birth outcomes and also are more

likely to be exposed to environmental contaminants, including environmental tobacco smoke

(ETS), polycyclic aromatic hydrocarbons (PAHs), and pesticides. In a sample of 263 nonsmoking

African-American and Dominican women, we evaluated the effects on birth outcomes of prenatal

exposure to airborne PAHs monitored during pregnancy by personal air sampling, along with

ETS estimated by plasma cotinine, and an organophosphate pesticide (OP) estimated by plasma

chlorpyrifos (CPF). Plasma CPF was used as a covariate because it was the most often detected in

plasma and was highly correlated with other pesticides frequently detected in plasma. Among

African Americans, high prenatal exposure to PAHs was associated with lower birth weight (p =

0.003) and smaller head circumference (p = 0.01) after adjusting for potential confounders. CPF

was associated with decreased birth weight and birth length overall (p = 0.01 and p = 0.003,

respectively) and with lower birth weight among African Americans (p = 0.04) and reduced birth

length in Dominicans (p < 0.001), and was therefore included as a covariate in the model with

PAH. After controlling for CPF, relationships between PAHs and birth outcomes were essentially

unchanged. In this analysis, PAHs and CPF appear to be significant independent determinants of

birth outcomes. Further analyses of pesticides will be carried out. Possible explanations of the failure to find a significant effect of PAHs in the Hispanic subsample are discussed. This study provides evidence that environmental pollutants at levels currently encountered in New York City

adversely affect fetal development. Key words: birth outcomes, development, environmental, ETS,

PAH, pesticides, pollutants, prenatal. Environ Health Perspect 111:201–205 (2003). [Online

31 October 2002] 

doi:10.1289/ehp.5742 available via http://dx.doi.org/

Children’s Health | Articles
air samples from the first 250 subjects showed

that all samples had detectable levels of one or

more carcinogenic PAHs, ranging over 4

orders of magnitude (Perera et al. 2002).

Almost half of the mothers and infants initially

enrolled had cotinine levels indicative of ETS

exposure (≥ 0.05–25 ng/mL). Maternal and

newborn plasma cotinine levels were significantly higher for mothers who reported smoking by others in the household than for

mothers who reported no smoking in the

home (p < 0.001). In addition, 85% of the

subjects reported that some form of pest control was used during pregnancy, and 35%

reported that their homes were sprayed by an

exterminator during pregnancy (Whyatt et al.

2002). One-third of pest control users also

reported use of can sprays or pest bombs during pregnancy (Whyatt et al. 2002). Pesticide

concentrations measured in a subset of the prenatal air monitoring filters showed that 100%

of the women had detectable exposure to multiple pesticides, including CPF at levels ranging from 0.7 to 193 ng/m3 (Whyatt et al.

2002). CPF was significantly higher in African

Americans than Dominicans in the full cohort

after controlling for neighborhood of residence

(Whyatt et al. 2002). 

Methods

Study subjects. Study subjects are Dominican

and African-American women residing in

Washington Heights, Central Harlem, and

the South Bronx, New York, who delivered at

New York Presbyterian Medical Center

(NYPMC), Harlem Hospital (HH), or their

satellite clinics (Perera et al. 2002; Whyatt et

al. 2002) (see Table 1 for demographic and

exposure characteristics of the population).

Ethnicity was self-identified. Nonsmoking

women, ages 18–35, who registered at the

obstetrics and gynecology clinics at NYPMC

and HH by the 20th week of pregnancy, were

free of diabetes, hypertension, or known HIV,

and resided in the area for at least one year

were eligible. Subjects included in the present

analysis are those with valid prenatal personal

monitoring data on PAHs, cord or maternal

blood samples, complete questionnaire data,

and birth outcome data. Subjects with missing

information on any of these data points were

excluded from the analysis. Seven subjects

with plasma cotinine concentrations > 25

were excluded to rule out active smoking.

Analyses were also run restricting to cotinine

≤ 15, which has also been used as a cutoff for

ETS. There were no significant differences in

sociodemographic characteristics or levels of

exposure between subjects with missing data

and those included in the present sample. 

Personal interview. A 45-minute questionnaire was administered by a trained bilingual interviewer during the last trimester of

pregnancy. The questionnaire included

demographic information, lifetime residential

history (country of birth, location, and duration of residence), travel outside the current

area of residence during the past year, history

of active and passive smoking [household

members who smoke and estimated cigarettes

smoked per day by smoker(s)], alcohol use

during each trimester of pregnancy, and consumption of PAH-containing meat (frequency of consumption of fried, broiled, and

barbecued meat). Socioeconomic information

related to income and education was also collected. The questionnaire was based on that

used in a prior study of women and newborns

and adapted for the New York City population (Perera et al. 1998). 

Prenatal personal PAHs assessment.

During the third trimester of pregnancy,

women were asked to wear a small backpack

containing a personal monitor during the daytime hours for 2 consecutive days and to place

the monitor near the bed at night. The personal air sampling pumps operated continuously over this period, collecting vapors and

particles of ≤ 2.5 μg in diameter on a precleaned quartz microfiber filter and a precleaned polyurethane foam (PUF) cartridge

backup. The samples were analyzed at

Southwest Research Institute (SwRI) for eight

carcinogenic PAHs: benz[a]anthracene, chrysene, benzo[b]fluroanthene, benzo[k]fluroanthene, B[a]P, indeno[1,2,3-cd]pyrene,

disbenz[a,h]anthracene and benzo[g,h,i]perylene as described (Camann et al. 1995; Geno

et al. 1993; Majumdar et al. 1993). To determine whether subjects complied with requests

to carry backpacks equipped with environmental monitoring devices, motion detectors

were installed in the backpacks of randomly

selected women. For the average woman,

nearly 95% of the total number of motion

detections occurred during waking hours,

consistent with the verbal reports of our subjects that they were complying with our

request to wear the backpacks during daytime

hours over the environmental monitoring

period. 

For quality control, each personal monitoring result was coded as to accuracy in flow

rate, time, and completeness of documentation. A code of 0–1 indicated high quality, 2

indicated intermediate quality, and 3 indicated unacceptable quality. We restricted

analysis to 263 subjects with code 0,1 samples

and other relevant data (excluding 19 subjects

with code 2 and 3 samples). 

Biologic sample collection and analysis.

Maternal blood (30–35 mL) was collected

within 1 day postpartum, and umbilical cord

blood (30–60 mL) was collected at delivery.

Samples were transported to the laboratory

immediately. The buffy coat, packed red blood

cells, and plasma samples were separated and

stored at –70°C. A portion of each sample was

shipped to the Centers for Disease Control

and Prevention (CDC) for analysis of cotinine

and pesticides. Plasma cotinine was analyzed

by the CDC using high-performance liquid

chromatography atmospheric-pressure ionization tandem mass spectrometry as described

(Bernert et al. 1997, 2000). Plasma levels of

CPF were analyzed using isotope dilution gas

chromatography–high resolution mass spectrometry as described (Barr et al. 2002).

Measures of fetal growth. Information was

abstracted by the research workers from mothers’ and infants’ medical records following

delivery including date of delivery, gestational

age at birth, infant sex, birth weight, length,

head circumference, infant malformations,

Apgar scores, maternal height, prepregnancy

weight, total weight gain, complications of

pregnancy and delivery, and medications used

during pregnancy.

Statistical analysis. To exclude active

smokers, we restricted analyses to women and

newborns with cotinine levels ≤ 25 ng/mL.

Analyses were also done further restricting to

≤ 15 ng/mL (excluding 3 subjects). Because

the eight PAH air concentration measures

were significantly intercorrelated (r values

ranging from 0.45–0.94; all p-values < 0.001

by Spearman’s rank), a composite PAH variable was computed. This summed measure

was dichotomized at the median (2.66

ng/m3) to obtain a measure of high or low

exposure. The dichotomous variable was used

in the regression analysis because it is less vulnerable to error and uncertainty in the monitoring data. The results were similar when the

continuous PAH variable was used. The

maternal and cord plasma concentrations of

both cotinine and CPF were significantly correlated (r = 0.88, p < 0.001 for cotinine; r =

0.6, p < 0.001 for CPF by Spearman’s rank).

Therefore, in cases where the umbilical cord

levels were not available, the mothers’ values

were used. For CPF, we used the formula

derived from the regression model: Ln newborn CPF = 0.46 + 0.61 × Ln maternal CPF.

Cotinine and CPF and birth outcomes were

log (Ln) transformed to provide a better fit to

the data and/or to approximate the normal

distribution and stabilize the variance. The

relationships between the exposure variables

and the birth outcomes were analyzed by

multiple regression, adjusting for known or

potential confounders, and including all tests

of interactions between ethnicity and exposures. In addition to PAHs dichotomized as

high/low and CPF as a continuous variable,

the final regression model included covariates

representing known or suspected risk factors

that were associated with birth outcomes (p ≤

0.1). To measure the contribution of antenatal toxicant exposures to birth outcomes, we

conducted multiple regression analyses. As

shown in Table 2, regression analysis

Children’s Health | Perera et al.

202 VOLUME 111 | NUMBER 2 | February 2003 • Environmental Health Perspectives
proceeded in several steps. Model 1 evaluated

the effects of PAHs, adjusting for potential

confounders including body mass index

(BMI), parity, gestational age, and infant sex.

Cotinine, income, and alcohol consumption

were not significant predictors of outcomes

(p > 0.1) and were not included. Maternal age

and parity were significantly intercorrelated

(r = 0.26, p < 0.001) and inclusion of age

instead of parity gave similar results. Because

CPF was associated with decrements in birth

weight and birth length after adjusting for the

covariates in model 1, model 2 included CPF

as a covariate (Table 2). In a separate model,

because nonsmoking-related airborne PAHs

were of primary interest, we adjusted for

dietary PAHs as well as cotinine in addition to

the covariates in model 1. The test for interaction between PAHs and ethnicity on birth outcomes was significant (see “Results”);

therefore, stratified analyses were carried out

by race/ethnic group. The percent reduction in

each birth outcome associated with high prenatal PAHs was calculated using the formula

[1–exp (β)] × 100%.

Results 

Demographic and exposure characteristics for

the subjects included in the present analysis

are provided in Table 1 together with summary data on measured levels of PAHs, cotinine, and CPF. The subset did not differ from

the overall cohort in terms of demographic

variables. As noted above and in Table 1, the

present subset included only nonsmoking

women (cotinine ≤ 25 ng/mL). The results

were unchanged when we repeated the analyses restricting to women with cotinine ≤ 15

ng/mL. Among subjects in the present analysis, 100% had detectable inhalation levels of

one or more PAHs. Total PAH exposures

averaged 3.7 ng/m3 and varied substantially

among the women, with a range of 0.36

ng/m3 to 36.47 ng/m3. Forty-two percent of

mothers and 45% of newborns had cotinine

levels > 0.05 and ≤ 25 ng/mL, indicative of

ETS exposure. CPF was detected in 98% of

the maternal and 94% of the cord samples,

with means of 7.6 pg/g in cord blood and 7.1

in maternal blood. PAHs were correlated with

cotinine (r = 0.26, p < 0.001). Self-reported

ETS and plasma cotinine differed by ethnicity, with African Americans being significantly

more likely to report ETS exposure (p ≤ 0.01)

and to have higher cotinine levels (p ≤ 0.01).

The mean birth weight was 3382.6 g

(SD = 499.2). Mean head circumference was

34.1 cm (SD = 1.6). Mean birth weight,

birth length, and head circumference were

lower and there was greater variability in

these outcomes among African Americans

than in Dominican infants. The differences

between individual outcomes were not significant by t-test; however, by multivariate

Hotelling’s t-test, at least one of these

outcomes (weight, length, head circumference) was significantly lower in African

Americans (p < 0.001). Four percent of

infants were preterm (< 37 weeks gestation).

African-American infants had a significantly

lower mean gestational age than Dominican

infants (39 vs. 39.6 weeks, p ≤ 0.01), despite

the restriction of the sample to women who

completed the air monitoring in the third

trimester of pregnancy.

The test of interaction between PAHs

and ethnicity was significant for birth weight

(p = 0.002) and for head circumference (p =

0.012), such that PAHs had a significant

adverse effect on birth weight and head circumference among African-American but not

Dominican infants. Possible differential

effects of toxicant exposure on different

ethnic groups prompted us to conduct ethnic-specific regressions.

As shown in Table 2, among African

Americans prenatal exposure to PAHs was

associated with lower birth weight (β =

–0.09, p = 0.003) and smaller head circumference (β = –0.02, p = 0.01) after adjusting

for potential confounders (model 1). CPF

was significantly associated with decreased

birth weight overall (β = –0.04, p = 0.01) and

among African Americans (β = –0.05, p =

0.04), but not among Dominicans (β =

–0.03, p = 0.11). CPF was also associated

with reduced birth length overall (β = –0.01,

p = 0.003) and in Dominicans (β = –0.02, p

< 0.001), but was not significantly associated

with head circumference. After adjusting for

Children’s Health | Prenatal exposure to pollutants and birth outcomes 

Environmental Health Perspectives • VOLUME 111 | NUMBER 2 | February 2003 203

Table 1. Demographic and exposure characteristics of the population.a

All African American Dominican

(n = 263) (n = 116) (n = 146)

Maternal age (year)b 24.6 (5.2) (n = 262) 24.1 (5) (n = 115) 25 (5.3) (n = 146)

Maternal education (%)

< High school 32.8 31 34.3

High school 45.3 46.6 44.3

> High school 21.9 22.4 24.4

Maternal ETS 

(% reporting smoker in the home) 42.8 51.8* 35.9

Maternal alcohol consumption 

(% drank alcohol during pregnancy) 24 12.4* 33.3

Maternal height (cm)b 162.6 (8.3) (n = 263) 164.5 (8.4) (n = 116)* 161 (8) (n = 146)

Maternal prepregnancy weight (kg)b 67 (16.5) (n = 263) 71.6 (19.7) (n = 116)* 63.3 (12.4) (n = 146)

Gestational age (weeks)b 39.3 (1.5) (n = 263) 39 (1.7) (n = 116)* 39.6 (1.2) (n = 129)

Newborn birth weight (g) 3382.6 (499.2) (n = 262) 3299 (548.7) (n = 115)c 3348.5 (449.4) (n = 146)

Newborn birth length (cm)b 50.9 (2.7) (n = 259) 50.8 (3.4) (n = 115)c 51.1 (2.2) (n = 143)

Newborn head circumference (cm)b 34.1 (1.6) (n = 248) 33.8 (1.9) (n = 111)c 34.3 (1.2) (n = 136)

Sex of newborn (% females) 51.5 48.3 54.1

Plasma cotinine (ng/mL)b,d 0.5 (2.4) (n = 254) 0.6 (2) (n = 110)* 0.5 (2.7) (n = 143)

Inhalation PAH (ng/m3)

b 3.7 (3.6) (n = 263) 3.5 (2.8) (n = 116) 3.9 (4.1) (n = 146)

Plasma chlorpyrifos (CPF) (pg/g)b 7.5 (7.5) (n = 113) 8 (6.3) (n = 57) 7.1 (8.5) (n = 56)

aSubjects with prenatal monitoring data on PAH, either cord or maternal blood sample, complete questionnaire data, and

birth outcome data. There were no significant differences between the overall parent population and the present subset

in terms of demographic, questionnaire-derived, and birth outcome variables shown in Table 1. bMean (SD). Arithmetic

means are presented for ease of comparison with other studies; however, the reported analyses are based on log-transformed data. cBy Multivariate Hotelling’s t-test, at least one of these outcomes (weight, length, head circumference) was

significantly lower in African Americans (p < 0.001). dSubjects with cotinine > 25 ng/mL were excluded from analysis.

Cotinine represents the level in cord blood or, if unavailable, the level in maternal blood, using the formula provided in the

text. *p ≤ 0.01 for African American vs. Dominican (Student’s t-test for maternal height, prepregnancy weight, and gestational age; χ2 for ETS exposure and alcohol; Mann-Whitney for cotinine).

Table 2. Associations between prenatal PAH exposure and birth outcomes,a by ethnic group, with and

without CPF.

Birth weight Birth length Head circumference

Model 1 Model 2b Model 1 Model 2 Model 1 Model 2

All

β –0.02 –0.05 –0.003 –0.02 –0.006 –0.01

PAH p 0.27 0.08 0.57 0.08 0.24 0.12

No. 261 112 258 112 247 108

African American

β –0.09 –0.10 –0.01 –0.02 –0.02 –0.02

PAH p 0.003 0.02 0.30 0.24 0.01 0.06

No. 115 56 115 57 111 54

Dominican

β 0.03 –0.009 0.003 –0.02 0.005 0.003

PAH p 0.16 0.81 0.65 0.11 0.33 0.80

No. 146 56 143 55 136 54

Model 1: covariates included BMI, parity, cotinine, sex of baby, and gestational age. 

aBirth outcomes were log (LN) transformed. bModel 2 covariates included all variables in model 1 plus CPF. 
CPF, relationships between PAHs and birth

outcomes were essentially unchanged among

African Americans (model 2): (β = –0.1, p =

0.02 for birth weight; and β = –0.02, p =

0.06 for head circumference). Table 3 summarizes the effects of all covariates in model

2. PAHs and CPF appear to be significant

independent determinants of birth outcomes

in that no significant interactions were

observed between them; however, this analysis is limited by the number of subjects in the

combined analyses. When we adjusted further in the analysis of personal air PAHs for

other PAH sources (dietary PAHs and ETS as

measured by cotinine), the associations

between PAHs and birth outcomes remained

significant (β = –0.08, p = 0.02 for birth

weight; and β = –0.02, p = 0.04 for head

circumference among African Americans).

Discussion

The association of PAHs with decreased birth

weight and smaller head circumference among

African Americans, before and after adjusting

for CPF and other potential confounders, is of

concern because several studies have reported

that reduction in head circumference at birth

or during the first year of life correlates with

lower IQ as well as poorer cognitive functioning and school performance in childhood

(Dam et al. 1998; Hack et al. 1991; Song et al.

1997). The present finding is consistent with

our prior observation that the levels of

PAH–DNA adducts in cord blood of

Caucasian newborns in Poland were significantly associated with lower birth weight,

reduced length, and head circumference

(Perera et al. 1998). Fetal toxicity may be

caused by antiestrogenic effects (Bui et al.

1986), binding to the human Ah receptor to

induce P450 enzymes (Manchester et al.

1987), to DNA damage resulting in activation

of apoptotic pathways (Meyn 1995; Nicol et

al. 1995; Wood and Youle 1995), or to binding to receptors for placental growth factors

resulting in decreased exchange of oxygen and

nutrients (Dejmek et al. 2000).

In this study, among African Americans

high PAHs were associated with a 9% reduction in birth weight and with a head circumference decrement of 2%. After adjusting for

CPF, the corresponding reductions were 10%

in birth weight and 2% in head circumference. No other studies have carried out personal monitoring of PAHs in pregnant

women. However, we note that the mean

PAH concentration observed in this study

(3.7 ng/mL) is 46% lower than that measured in personal air samples from nonsmoking women who worked outdoors in a

moderately polluted area of the Czech

Republic (6.9 ± 4.4 ng/m3, range 2.7–18.8

ng/m3). However, the New York City range

is wider and the upper bound is higher.

PAHs are only one class of chemicals among

many found in particulate matter from combustion sources. Nevertheless, our results are

consistent with ecologic studies showing associations between ambient levels of air pollutants (including total suspended particulate

matter) and low birth weight (Bobak 2000;

Chen and Omaye 2001; Ha et al. 2001). A

study in Northern Bohemia found that estimated exposure to carcinogenic PAHs in

early gestation (based on ambient air monitoring data) was associated with reduced fetal

growth (Dejmek et al. 2000). 

The finding that effects of PAHs were

significant only among African Americans

may be attributed to unmeasured differences

in exposure and/or susceptibility, to our

limited sample size, or to the fact that birth

outcomes (weight, head circumference, and

gestational age) were generally less favorable

and more variable in African Americans than

in Dominicans. It is possible that with our

limited sample size we were able to observe

effects of prenatal exposure to pollutants only

in African-American women because of the

greater incidence of adverse outcomes and the

greater variability in birth outcomes within

this group compared with Dominicans.

Although African-American mothers had significantly higher self-reported exposure to

ETS and plasma cotinine levels, the personal

air concentrations of PAHs and CPF did not

differ significantly between ethnic groups

(Table 1). 

The data show an association between

CPF and reduced birth weight and birth

length. CPF is only one of a number of pesticides measured in the parent cohort study.

Comprehensive analyses of the main effects of

all measured pesticides on birth outcomes will

be carried out. There are no prior comparable

studies in humans, and the mechanism for

possible effects on fetal growth is not known.

However, exposure to CPF has been shown

to induce brain cell loss and neurochemical

and behavioral effects in the developing rat

when given prenatally (Campbell et al. 1997;

Chanda and Pope 1996). CPF has recently

been regulated and residential uses are being

phased out, but it has been the most heavily

applied pesticide throughout New York State

and in Manhattan in recent years (Landrigan

et al. 1999; Thier et al. 1998; Whyatt et al.

2002). 

In this study, cotinine was not a significant predictor of birth outcomes (p > 0.1).

The absence of a significant effect of ETS

(cotinine) may be due to the fact that the

cohort is nonsmoking and cotinine levels are

generally low. 

This study has the advantage of being

based on individual prenatal exposure data

from personal monitoring and biomarkers, as

well as extensive medical records and questionnaire data. However, it is limited by the

modest sample of subjects for whom data

from all relevant domains are currently available. Relationships observed in low-income,

minority women might be different in

women of other races or ethnic, cultural, or

socioeconomic backgrounds. In our study

cohort, adverse environmental conditions and

adverse outcomes are common. However, we

reported previously that DNA damage from

PAHs was associated with worse birth outcomes among Caucasians in Central Europe

who were exposed to air pollution from coal

burning (Perera et al. 1998). Finally, due to

budgetary constraints, we were able to obtain

only a single prenatal air sample over a 48-hr

period. Whether this single measurement is

representative of average exposure either during

Children’s Health | Perera et al.

204 VOLUME 111 | NUMBER 2 | February 2003 • Environmental Health Perspectives

Table 3. Associations between all covariates in Model 2a and birth outcomesb, by ethnic group.

All African American Dominican

BW BL HC BW BL HC BW BL HC

PAH

β –0.05 –0.02 –0.01 –0.10 –0.02 –0.02 –0.009 –0.02 0.003

p-Value 0.08 0.08 0.12 0.02 0.24 0.06 0.81 0.11 0.80

CPF

β –0.04 –0.02 –0.005 –0.05 –0.01 –0.003 –0.02 –0.02 –0.005

p-Value 0.01 0.04 0.28 0.04 0.15 0.70 0.26 0.002 0.31

Parity

β –0.02 0.01 0.002 0.02 0.03 0.006 –0.06 0.001 –0.005

p-Value 0.66 0.25 0.89 0.74 0.21 0.75 0.23 0.93 0.70

BMI

β 0.003 0.0003 0.0007 0.006 0.0007 0.001 0.003 0.0003 –0.0005

p-Value 0.14 0.69 0.26 0.06 0.56 0.17 0.47 0.76 0.65

Sex

β 0.04 0.02 0.02 0.06 0.03 0.02 0.04 0.02 0.02

p-Value 0.14 0.02 0.02 0.18 0.13 0.10 0.27 0.04 0.07

Gestational age

β 1.94 0.63 0.64 0.64 0.68 0.70 1.02 0.06 0.19

p-Value < 0.001 < 0.001 < 0.001 0.003 < 0.001 < 0.001 0.20 0.78 0.36

No. 112 112 108 56 57 54 56 55 54

Abbreviations: BL, birth length; BW, birth weight; HC, head circumference.

aModel 2 covariates included all variables in model 1 plus CPF. bBirth outcomes were log (LN) transformed.
the third trimester or the entire pregnancy is

unknown. Similarly, the biomarkers were

measured at a single time point. In cases of

chronic exposure, a single measure can be a

representative internal dosimeter; however,

this may not be true if exposures are sporadic

and biomarkers have short half-lives. Studies

are underway to determine the representativeness of a single 48-hr personal monitoring

sample and a single biomarker measurement

for various pollutants of interest. 

Conclusion

This study provides evidence that environmental pollutants at levels currently encountered in New York City adversely affect fetal

development.

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Children’s Health | Prenatal exposure to pollutants and birth outcomes 

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