A food chemical known to cause cancer in rats has been discovered in human breast milk, according to a group of Canadian researchers. This is the first time that the chemical, mostly associated with grilled meats, has been found in human breast milk, the scientists add.
Although no one is certain whether the chemical, called PhIP, actually causes cancer in humans, the researchers suggest that it may increase the risk of breast cancer in women as well as pose a cancer risk to nursing infants. Although they stress that breast-feeding remains preferable to formula feeding, and there are ways to minimise PhIP exposure.
"Since exposure to [PhIP] is chiefly from dietary meats, reduction in the intake of cooked meats and avoidance of "very well-done" meats might minimise exposure to these compounds,"," said P. David Josephy, a professor in the department of chemistry and biochemistry at the University of Guelph in Guelph, Ontario. "Very well-done" is interpreted as charbroiled or grilled meats, considered the major dietary source of the chemical, he added.
Many toxic chemicals have been found in human breast milk, including PCBs, dioxin, nitrosamines, ethanol and nicotine. Few are strongly associated with breast cancer. PhIP is one of the few suspected mammary carcinogens found in breast milk that is almost exclusively associated with grilled meat, commented Josephy. It is also the first member of its chemical class, a group of highly mutagenic compounds known as heterocyclic amines (HCAs), to be found in human breast milk.
Milk samples were obtained from 11 healthy lactating volunteers, all residing in or near Guelph, Canada. Using chemical tests, the researchers detected trace levels of PhIP in nine of the samples at levels as high as 59 parts per trillion. All but one of the women tested had eaten grilled meat at least once during their last three meals, according to the researcher.
In the woman who did not eat meat, no PhIP was detected. Unexpectedly, no PhIP was found in the milk sample from one of the meat-eaters, says Josephy. Individual differences or differences in the type of meat and preparation of the meat may help explain this result, but these factors have not been fully analysed, he says. Future studies are planned to evaluate these factors.
PhIP is formed by pyrolysis, a chemical reaction that is caused by the heating of muscle (meat), particularly the reaction between meat proteins and a nitrogenous compound called creatinine. The higher the temperature at which meat is heated, the more PhIP that is formed. The process also forms other heterocyclic amines, but PhIP is considered the most abundant in cooked meat.
The chemical is formed mostly through grilling, broiling and frying of meats, as these processes expose the muscle to extremely high temperatures for prolonged periods. Grilled meat is the largest source of the chemical, said Josephy.
There are many ways to reduce HCA levels in meat. Most involve cooking meat at lower temperatures. Baking, roasting and microwaving of meat - processes that produce less heat - may significantly reduce levels of PhIP, according to recent studies. Cooking methods that involve liquids, including boiling, steaming, and poaching, generally do not produce significant amounts of the chemical. When grilling, turning the meat frequently or marinating the meat before cooking is thought to significantly reduce PhIP as well as other HCAs, according to Josephy.
Little or no PhIP is produced by the cooking of vegetables and fruit, regardless of the process, studies show.
A number of epidemiological studies have shown an increased risk of breast cancer among women who eat a lot of meat. Many factors are thought to contribute to this risk, including fat intake, caloric intake and hormone exposure, as well as exposure to HCAs such as PhIP, said Josephy.
Some studies have suggested that increased exposure to PhIP may be linked to an increased risk of colon and prostate cancer in men.
Josephy and his associates are planning larger studies to compare PhIP levels in vegetarians versus meat-eaters to further clarify how diet affects these levels.
Full findings appear in the November 19 print edition of Chemical Research in Toxicology, a peer-reviewed journal of the American Chemical Society.