Høyer, AP, P Grandjean, T Jørgensen, JW Brock and HB Hartvig. 1998. Organochlorine exposure and risk of breast cancer. Lancet 352:1816-1820.

Most studies of the relationship between breast cancer and organochlorines have focused on the classic suspects, DDT or its metabolites and PCBs. This research by an international group of scientists (including the US Centers for Disease Control) expands this body of research by assessing links between dieldrin exposures and breast cancer risk. They find that women with the highest serum concentration of dieldrin had more than a two-fold increased risk of developing breast cancer compared to those with the lowest concentration.

Data from subjects enrolled in the "Copenhagen City Heart Study," a study population selected randomly from around Copenhagen, Denmark, were analyzed. Women were enrolled in 1976, at which time serum samples were obtained. The health of the participants was then tracked for the next 17 years. During that time, 268 of the 7712 participants developed invasive breast cancer. For this analysis, each woman with breast cancer was matched with two breast cancer free women also in the study, and a comparison was made of the chemical constituents of the serum stored in 1976.

This study has several strengths: prospective design, long-term follow-up, and random selection of participants independent of the occurrence of breast cancer.

Dieldrin was associated with a significant increase in the risk of breast cancer. The result for dieldrin showed a dose-related increase in risk with an adjusted odds ratio of 2.05. The risk of breast cancer was twice as high in women with the highest serum concentrations of dieldrin compared to women with the lowest concentrations. At right, the reference group (R) is compared with quartiles of dieldrin exposure (adapted from Høyer et al. 1998). Vertical bars indicate 95% confidence interval. The dose response relationship is statistically significant (p=0.01).

This result is especially important because dieldrin is unequivocally an estrogen mimic, shown to interact with the estrogen receptor in analyses using Soto and Sonneschein's E-screen test.

The study also examined DDT (and its metabolites) and PCB. No risk increase was detected for these compounds.

Lifetime exposure to estrogen has been identified as a significant risk factor for breast cancer in people. While DDT is slightly estrogenic, its principle metabolite, DDE, anti-androgenic in human tissue. With respect to DDT, the authors of this article state: "Information on o,p'-DDT was insufficient because only 20% of the serum samples contained this compound in detectable amounts."

The negative results were more definitive on p,p'-DDE, the most common metabolite of DDT. Much confusion has been generated in the popular media about the failure of DDE to yield positive links. As an anti-androgen, DDE would not be predicted to increase the risk of breast cancer on the basis of its hormonal activity. Hence it is particularly inappropriate for industry spokes-scientists like Steven Safe to claim that the failure of research to reveal links between DDT and breast cancer proves that estrogenic organochlorines do not cause breast cancer. He knows better.