Several information sources provided data on traffic volumes on roads in question for the years from 1960 to 2002 and tail-pipe emissions, including measurements from tunnels and tests on individual vehicles. A geographic model was used to reconstruct historic traffic PAHs, using measurements of benzo[a]pyrene, a known potent mutagen and carcinogen, as a surrogate for total PAH exposure. Cruise emissions, cold engine emissions and intersection emissions were used to estimate total traffic PAH emissions.
In addition, meteorological information was used in a geographic dispersion model to determine PAH exposure at each participant's residence.
While the researchers found increased risk for exposure at menarche and first birth for premenopausal and postmenopausal participants, respectively, who were lifetime nonsmokers, there was no association of traffic emissions with breast cancer for the other time periods.
Nie said these findings related to PAHs need to be interpreted with caution, because they could be explained by other compounds in vehicle exhaust or by other exposures related to the traffic emissions.
"While these results are subject to the limitations of epidemiologic observational studies, they are provocative in providing evidence both of the importance of early exposures and of the potential importance of an environmental agent in risk of breast cancer," said Nie. "Further examination of PAH exposure in early life is clearly warranted."
The UB researchers currently are examining whether genetic polymorphisms involving PAH metabolism may modify the risk, if lifeline cumulative exposure may be associated with the risk and if this study may be replicated in another geographic settings.
Source:University of Buffalo