CORVALLIS, Ore. The cancer-causing potential of fetal exposure to carcinogens can vary substantially, a recent study suggests, causing different types of problems much later in life depending on the stage of pregnancy when the fetus is exposed.
The research sheds further light on the way in which toxic damage early in life can later manifest itself as cancer, due to "epigenetic" changes in cells. It was done by scientists in the Linus Pauling Institute at Oregon State University, and other institutions, in laboratory studies with mice.
In this study, published in the journal Cancer Letters, mice received four separate doses of a carcinogen commonly found in air pollutants or other combustion products. As a result, they had triple the level of ovarian cancer at the rodent equivalent of middle age. About 80 percent of them also got lung cancer, and many of the male mice had abnormally small testes a phenomenon not seen before.
In previous research, by contrast, the same amount of this carcinogen given in a single dose had caused a much higher rate of T-cell lymphoma, a type of blood cancer, which this study found to almost disappear when the carcinogen exposure was spread out over time. Liver cancer also was largely absent.
"There's still a lot of uncertainty about how the fetus responds to carcinogens and at what points in time it is most vulnerable," said David Williams, a professor of environmental and molecular toxicology at OSU.
"We know it's far more sensitive than adults for several reasons, including faster cell division and the lack of protective detoxifying enzymes," he said. "But it's interesting that the timing of fetal exposure makes such a difference in which organs are targeted. These results were somewhat surprising."
The mice in these experiments were exposed to one type of polycyclic aromatic hydrocarbon, a group of compounds commonly produced by everything from coal combustion to a
|Contact: David Williams|
Oregon State University