BMC Cancer (2001) 1:8 http://www.biomedcentral.com/1471-2407/1/8 Table 4: Risk of breast cancer in relation to serum concentrations of organochlorines in quartiles by estrogen receptor status. Organochlorines in quartiles (ng/mL) Estrogen receptor positive Cases/controls Adjusted RR (95% CI)a p trendb Estrogen receptor negative Cases/controls Adjusted OR (95% CI) p trend a Odds ratio, 95% confidence interval, adjusted for age, weight, parity, and hormone replacement therapy; b two sided p-value for linear trend in OR's; c reference category. Cases with missing information on confounders were excluded. HCB I II III IV Dieldrin I II III IV ΣPCB I II III IV p,p'-DDE I II III IV <206.50 206.50-269.75 269.75-335.75 >335.75 <12.01 12.01-28.30 28.30-57.11 >57.11 <811.11 811.11-1076.04 1076.04-1405.73 >1405.73 <741.04 741.04-1129.75 1129.75-1688.85 >1688.85 36/56 20/55 22/56 36/55 27/57 28/56 33/57 28/56 36/57 24/56 20/57 36/56 33/57 29/56 25/57 29/56 1.0 ref.c 1.1 (0.6-1.8) 1.0 (0.6-1.7) 1.2 (0.7-2.1) 1.0 1.3 (0.7-2,2) 1.5 (0.8-2.7) 1.4 (0.8-2.5) 1.0 1.1 (0.6-1.7) 0.7 (0.4-1.2) 1.3 (0.8-2.2) 1.0 0.7 (0.4-1.2) 0.8 (0.5-1.3) 0.9 (0.6-1.5) Including other organochlorines than the particular one in question in the multivariate analysis did not have any modifying effect on the observed estimates on breast cancer risk and survival. The cases on whom a tumor tissue specimen could not be obtained were older at the time of entrance into the CCHS (>60 years of age, 42.3% vs. 19.1%), older at the time of diagnosis (>71 years of age at diagnosis, 32.1% vs. 19.1%), and more often nulliparous (nulliparity, 33.3% vs. 24.1%) compared to those with an available speci- men. Discussion It has been postulated that ERP and ERN breast cancers represent different entities of the disease [7]. If this hy- pothesis is correct the risk factor profiles may differ be- tween the two types of breast cancer, especially for hormone related factors as parity, hormone replacement therapy and body weight. The present study's results on these breast cancer risk factors according to ER are in ac- cordance with previous epidemiological studies, which do not provide consistent evidence to conclude that de- velopment of ERP breast cancer is associated with expo- sure to estrogen related factors [30–36]. >0.20 >0.20 >0.20 >0.20 19/23 8/23 11/23 6/23 6/23 5/23 13/23 20/23 14/23 11/23 11/23 8/23 14/23 11/23 10/23 9/23 1.0 0.5 (0.2-1.4) 0.8 (0.3-2.2) 0.4 (0.1-1.4) 1.0 1.2 (0.3-5.4) 4.9 (0.9-28.3) 7.6 (1.3-46.1) 1.0 1.0 (0.4-2.7) 1.3 (0.4-3.9) 0.8 (0.3-2.6) 1.0 0.9 (0.3-2.5) 0.7 (0.2-2.0) 0.6 (0.2-1.7) >0.20 0.01 >0.20 >0.20 Only few prior studies have evaluated the role of poten- tial estrogenic organochlorines relationship to breast cancer risk while accounting for estrogen receptor status of the primary tumors. An excess risk of developing ERP breast cancers associated with exposure to certain PCB congeners, and DDE have been demonstrated [16,19]. The present study could not confirm this. In fact, the pre- viously reported excess risk observed with exposure to dieldrin derived from women who developed an ERN tu- mor [13]. However, it is still uncertain what happens in the preclinical phases of breast cancer development [37]. Low levels of available estrogen may stimulate estrogen receptor expression [38]. It is also possible that down- regulation of the estrogen receptor gene to immunohis- to-chemically undetectable levels may occur in some tu- mors due to high circulating levels of estrogens [38]. A breast cancer initiated as an ERP cancer could therefor change receptor status during the process of carcinogen- esis prior to diagnosis. Thus ER status may merely repre- sent different stages in disease progress.