Despite research on rats that shows the placenta can block certain
combustion-related pollutants, researchers have found that a marker of
secondhand cigarette smoke accumulates at greater levels in the plasma
of fetuses than that in mothers. They also discovered that
cancer-causing benzo[a]pyrene (BP) has more harmful effects on fetal
than on maternal DNA.
This study bolstered previous findings in Poland, where women were
exposed to secondhand smoke and levels of BP that were 30 times higher.
Corresponding author Frederica P. Perera, director of the Columbia
Center of Children’s Environmental Health at Columbia University, says
the results are a concern, because exposure to BP has been linked to
DNA damage and increased risk of cancer.
“This study demonstrates that the fetus is more susceptible to DNA
damage from combustion-related pollutants than previously thought,”
says Perera. Researchers from the Columbia Center and the Center for
Disease Control and Prevention tracked 265 nonsmoking mothers and their
newborns in New York City. The mothers are exposed to significant air
pollution in their neighborhood, where the average ambient BP
concentration was less than 0.5 nanograms per cubic meter of air.
Perera says higher levels can be found in California and many European
cities. This study was published in the July issue of Environmental
Health Perspectives (Environ. Health Perspect. 2004, 12, 1133–1136).
The researchers found that 45% of newborns had detectable BP-DNA
adducts, as did 41% of mothers. The levels of adduct formation were
similar in mother and child: 0.24 adducts per 100 milllion nucleotides
in mothers and 0.22 adducts per 100 million nucleotides in newborns.
Cotinine, a metabolite of nicotine, was detected in the serum of 47% of
newborns and 44% of mothers. The levels were also quite similar, at 1.7
nanograms per milliliter (ng/mL) in newborns versus 1.28 ng/mL in
mothers. The higher levels of cotinine in newborns indicate that the
effects of environmental tobacco smoke are only slowly cleared from the
Previous research on the same cohort of New Yorkers found that elevated
levels of BP-DNA adducts in combination with secondhand smoke
correlated with poor birth outcomes, including smaller head
circumference and lower birth weight.
“We know that there is a lot of smoking in these neighborhoods, but you
would think that with nonsmoking mothers that these babies would be
protected,” says Ellen F. Crain, professor of pediatrics at the Albert
Einstein College of Medicine. “What I find interesting about this study
is that we’re finally starting to look for a mechanism for some of the
outcomes we find clinically.” —PAUL D. THACKER
I circulated the abstract of the paper described above on July 17 and
include it again below:
Perera, F., Tang, D., Tu, Y.-H., Cruz, L., Borjas, M., Bernert, T.,
R., 2004. Biomarkers in maternal and newborn blood indicate heightened
fetal susceptibility to procarcinogenic DNA damage. Environ Health
112:1133–1136 . doi:10.1289/ehp.6833 available via
[Online 22 March 2004]
Polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene (BaP) are
widespread air contaminants released by transportation vehicles, power
generation, and other combustion sources. Experimental evidence
indicates that the developing fetus is more susceptible than the adult
to carcinogenic effects of PAHs, although laboratory studies in rodents
suggest that the
dose to fetal tissues is an order of magnitude lower than that to
maternal tissues. To assess fetal versus adult susceptibility to PAHs
and environmental tobacco smoke (ETS), we compared carcinogen- DNA
adducts (a biomarker associated with increased cancer risk) and
cotinine (a biomarker of tobacco smoke exposure) in paired blood
samples collected from mothers and newborns in New York City. We
enrolled 265 nonsmoker African-American and Latina mother–newborn pairs
in New York City between 1997 and 2001 (estimated average ambient air
BaP concentrations < 0.5 ng/m3). Despite the estimated 10-fold lower
fetal dose, mean levels of BaP- DNA adducts as determined by
high-performance liquid chromatography–fluorescence were comparable in
paired New York City newborn and maternal samples (0.24 adducts per 108
nucleotides, 45% of newborns with detectable adducts vs. 0.22 per 108
nucleotides, 41% of mothers with detectable adducts). However, by the
Wilcoxon signed-rank test, the levels in newborns were higher (p 0.02).
Mean cotinine was higher in newborns than in mothers (1.7 ng/mL, 47%
detectable vs. 1.28 ng/mL, 44% detectable).
Consistent with our prior study in a Caucasian Polish population, these
results indicate increased susceptibility of the fetus to DNA damage
and reduced ability to clear TS constituents. The findings have
implications for risk assessment, given the need to protect children
as a sensitive subset of the population.