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 fetuses’  blood.

 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.,
 Whyatt,
 R., 2004.  Biomarkers in maternal and newborn blood indicate heightened
 fetal susceptibility to procarcinogenic DNA damage. Environ Health
 Perspect
 112:1133–1136 . doi:10.1289/ehp.6833 available via http://dx.doi.org/
 [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.