Smoke gets in your cervix and fetus.

When a cigarette smoker inhales, thousands of tobacco-derived compounds, many accused of being carcinogenic or otherwise toxic, gain easy access to the human body. Like detectives who document the actions of a suspect before and after a crime, investigators are tracing the steps of these suspicious compounds as they sneak about the body.

Three research groups now present evidence that some of those tobacco compounds enter a woman's cervix, where they may cause cancer, or pass into a fetus, where they may cause respiratory problems or genetic damage that will predispose the child to cancer.

Researchers have shown that the human papilloma virus plays an important role in triggering cervical cancer, but they believe that the virus alone is insufficient. "There must be another factor initially damaging the cervical DNA," says Bogdan Prokopczyk of the American Health Foundation in Valhalla, N.Y.

Epidemiological studies strongly suggest that smoking is one such factor, adds Prokopczyk. Consequently, he and his colleagues recently examined samples of cervical mucus taken from both smokers and nonsmokers. They found that compared to nonsmokers' cervical mucus, that of smokers contains much higher concentrations of nitrosamines, carcinogenic derivatives of nicotine that come from tobacco.

The new results mesh with earlier research by other groups showing that smokers have more DNA damage in cervical cells than nonsmokers do, says Prokopczyk. Previous studies had also established that the cervical cells of smokers contain tobacco-derived nicotine, the precursor of the nitrosamines.

A fetus may also pay a price for the smoking of its mom or the people around her. Babies born to smokers often have low weight at birth and respiratory problems, notes Steven R. Myers of the University of Louisville (Ky.) School of Medicine. Whether the children suffer higher cancer rates remains unclear, however. For many years, says Myers, the placenta was considered an effective barrier to tobacco-derived carcinogens.

To test that assumption, Myers and his colleagues recently obtained a detailed smoking history from 410 pregnant women. When the women gave birth, the investigators took maternal blood samples and samples of fetal blood from the umbilical cord. They then examined the blood for smoking-related adducts, the joining of a carcinogen to DNA or other molecules like hemoglobin.

Myers' group tested for three specific types of hemoglobin adducts that tobacco-derived carcinogens would form and found that the number in the fetus increased with the number of cigarettes its mother smoked. "She's passing a significant concentration [of carcinogens] into the baby," says Myers.

The investigators found that the babies of nonsmoking mothers who spent many hours a day around smokers also have greater than normal numbers of hemoglobin adducts. "The question remains what this all means to the baby," acknowledges Myers. He believes that the fetal hemoglobin adducts serve as markers of the number of DNA adducts that smoking creates in the fetus.

In general, fetal DNA may be more vulnerable than maternal DNA to adduct formation, notes Robin M. Whyatt of Columbia University School of Public Health. In a study examining the effects of air pollution and smoking on 170 newborns from Poland, Whyatt and her colleagues analyzed the DNA in white blood cells taken from blood in the umbilical cord.

The Polish infants, in general, had significantly more DNA adducts than their mothers, Whyatt says. To explain this puzzling result, she suggests that fetal cells, which divide more rapidly than adult cells, expose their DNA more often to adduct formation. In addition, suggests Whyatt, fetuses may not repair their DNA as efficiently as adults do.