The Chernobyl accident resulted in a number of cases of thyroid cancer in females under the age of 20 y. Many of these individuals were treated with surgical removal of the thyroid gland followed by 131I ablation of residual thyroid tissue. Epidemiologic evidence demonstrates that 131I treatment for thyroid cancer or hyperthyroidism in adult women confers negligible risk of breast cancer. However, comparable data for younger women do not exist. Studies of external radiation exposure indicate that, for radiation exposures of as low as 0.2-0.7 Gy, the risk of breast cancer is greater for infant and adolescent female breast tissues than for adult female breast tissues. METHODS: The effective half-time of 131I measured in athyrotic patients was used together with the OLINDA/EXM computer code to estimate doses to breast tissue in 10-y-old, 15-y-old, and young adult females from ablation treatment. RESULTS: The dose to pediatric and young adult female breast tissue associated with a 5.6-GBq (150 mCi) ablation treatment may range from 0.35 to 0.55 Gy, resulting in a lifetime risk of breast cancer ranging from 2-4 cases per 100 such individuals exposed and a lifetime risk of solid tumors ranging from 8 to 17 solid tumors per 100 such individuals exposed. Administration of multiple ablation treatments, as often occurs with metastases, could result in doses ranging from 0.7 to 1 Gy, with corresponding increases in the lifetime cancer risk. CONCLUSION: These estimates suggest the need for additional research and a possible need for surveillance of young Chernobyl thyroid cancer patients who received 131I ablation treatment.
It has been suggested that abortions leave the breast epithelium in a proliferative state with an increased susceptibility to carcinogenesis. Results from previous studies of induced or spontaneous abortions and risk of subsequent breast cancer are contradictory, probably due to methodological considerations. We investigated the relationship between abortions and subsequent breast cancer risk in a case-control study using prospectively recorded exposure information. The study population comprised women recorded in the population-based Swedish Medical Birth Register between 1973-91. Cases were defined by linkage of the birth register to the Swedish Cancer Register and controls were randomly selected from the birth register. From the subjects' antenatal care records we abstracted prospectively collected information on induced and spontaneous abortions, as well as a number of potential confounding factors. Relative risk of breast cancer was estimated by odds ratios (OR) with 95% confidence intervals (95% CI). A reduced risk of breast cancer was observed for women with a history of at least 1 compared to no abortions (adjusted OR = 0.84, 95% CI = 0.72-0.99). The adjusted OR decreases step-wise with number of abortions to 0.59 (95% CI = 0.34-1.03) for 3 or more compared to no abortions. The patterns are similar for induced and spontaneous abortions. In conclusion, neither a history of induced nor spontaneous abortions is associated with an increased risk of breast cancer. Our data suggest a protective effect of pregnancies regardless of outcome.
Comment In: Int J Cancer. 2004 May 10;109(6):945-6; author reply 947-815027130
Four authoritative reviews of active smoking and breast cancer have been published since 2000, but only one considered data after 2002 and conclusions varied. Three reviews of secondhand smoke (SHS) and breast cancer (2004-2006) each came to different conclusions. With 30 new studies since 2002, further review was deemed desirable. An Expert Panel was convened by four Canadian agencies, the Ontario Tobacco Research Unit, the Public Health Agency of Canada, Physicians for a Smoke-Free Canada and the Canadian Partnership Against Cancer to comprehensively examine the weight of evidence from epidemiological and toxicological studies and understanding of biological mechanisms regarding the relationship between tobacco smoke and breast cancer. This article summarises the panel's full report (http://www.otru.org/pdf/special/expert_panel_tobacco_breast_cancer.pdf). There are 20 known or suspected mammary carcinogens in tobacco smoke, and recognised biological mechanisms that explain how exposure to these carcinogens could lead to breast cancer. Results from the nine cohort studies reporting exposure metrics more detailed than ever/never and ex/current smoker show that early age of smoking commencement, higher pack-years and longer duration of smoking increase breast cancer risk 15% to 40%. Three meta-analyses report 35% to 50% increases in breast cancer risk for long-term smokers with N-acetyltransferase 2 gene (NAT2) slow acetylation genotypes. The active smoking evidence bolsters support for three meta-analyses that each reported about a 65% increase in premenopausal breast cancer risk among never smokers exposed to SHS. The Panel concluded that: 1) the association between active smoking and breast cancer is consistent with causality and 2) the association between SHS and breast cancer among younger, primarily premenopausal women who have never smoked is consistent with causality.
The relationship of breast cancer to early reproductive development and height suggests that fetal and childhood nutrition may be important in its aetiology. Caloric restriction sufficient to reduce adult height may reduce breast cancer risk. During World War II (WWII) there was a marked reduction in average caloric intake in Norway that resulted in greater nutritional diversity. We hypothesized that a positive association between height and risk of breast cancer would be stronger among women who were born during this period than among women born before or after the war. A total of 25 204 Norwegian women were followed up for approximately 11 years, and 215 incident cases of breast cancer were registered. We found the strongest positive association between height and breast cancer among women born during WWII: women in the tallest tertile (>167 cm) had a relative risk of 2.5 (95% confidence interval = 1.2-5.5) compared with the shortest (
A case-control study was conducted over a period of 11 months in an area containing one-third of the Swedish population. One thousand and one patients participated, constituting 94% of all women newly diagnosed as having breast cancer within the area. They were compared with 1,001 age-matched, non-hospitalized controls without breast cancer, selected by paired sampling from a population register. The risk of breast cancer was slightly, but significantly, related to parity, the standardized relative risk (SRR) being 1.35 for nulliparous women as compared to ever parous. In the different parity groups a risk significantly lower than that for nulliparous women was found only for women with more than 2 children (SRR = 0.59) but the trend with parity was highly significant (P less than 0.001). Age at first birth was not found to be an important risk factor for breast cancer. SRR was lower than for nulliparous women in all groups of women with their first birth before the age of 35 years, but the difference was significant (P less than 0.05) only for those with the first birth between 20 and 24 (SSR = 0.69) and 25 and 29 (SRR = 0.69) years of age. The trend with age at first birth (P less than 0.05) disappeared after stratification for parity, suggesting that it was a confounding factor.
A population-based cohort study of 36 856 women diagnosed with alcoholism in Sweden between 1965 and 1995 found that alcoholic women had only a small 15% increase in breast-cancer incidence compared to the general female population. It is therefore apparent, contrary to expectation, that alcoholism does not increase breast-cancer risk in proportion to presumed ethanol intake.
In order to demonstrate how possible causal relationships are critically evaluated in epidemiologic research, literature on the association between alcohol and breast cancer is reviewed and discussed. A cause can be defined as a factor which, in combination with other factors, known and unknown, is sufficient to produce an effect. Since the hypothesis-generating study was published in 1977, a total of 34 positive and 16 negative studies have been published. Methodological problems, such as chance, bias and confounding, cannot be considered as plausible explanations for the above majority of positive findings. The question of causality was then evaluated using the guidelines developed by Bradford Hill in 1965. Among these, the strength of the association, consistency, temporality, biological gradient and biological plausibility, are the most important. In spite of the relatively weak association and somewhat inconsistent results, it is concluded that alcohol consumption should be considered as a cause of breast cancer. It is estimated that in Norway, between 24 and 180 cases of breast cancer may be attributed to alcohol consumption. Future research should focus on the question of effect-modification and on the possible implications of different patterns of alcohol consumption.
A case-control study of 177 premenopausal and 216 postmenopausal breast cancer patients diagnosed in the southern Swedish Health Care Region between 1981 and 1984, and 195 premenopausal and 254 postmenopausal controls randomly chosen during 1984 from the same population by means of a computerized population register was used to estimate the relations among alcohol consumption, cigarette smoking, and the risk of cancer. Cigarette smoking did not seem to be related to the risk for breast cancer among pre- or postmenopausal women. Beer consumption did not show any consistent relation to the risk of breast cancer. An occasional (less frequent than once a week) or a weekly consumption of wine and spirits appeared to be protective compared with abstaining (RRadj = 0.4, 95% CI = 0.3-0.7 for weekly wine consumption, and RRadj = 0.6, 95% CI = 0.4-0.9 for occasional consumption of spirits) among postmenopausal but not among premenopausal women (RRadj = 0.8, 95% CI = 0.7-2.3 and RRadj = 1.0, 95% CI = 0.7-1.8 respectively). The risk estimates were adjusted for differences between cases and controls in age at menarche, age at first full-term pregnancy, age at diagnosis, smoking, and use of exogenous hormones, and for postmenopausal women, age at menopause. The study was based on observations of women with a relatively low exposure to cigarette smoking and alcohol. More frequent exposure or exposure to greater quantities of alcohol and smoking may exhibit different relationships with breast cancer risk.
The influence of alcohol consumption on breast cancer risk was evaluated in a population-based case-control study, including 1,486 cases diagnosed over a one-year (1983-84) period in Denmark. Cases were identified from the files of the nationwide clinical trial of the Danish Breast Cancer Cooperative Group and the Danish Cancer Registry. The control group was an age-stratified random sample of 1,336 women from the general population. Data on risk factors were collected by self-administered questionnaires. The association of alcohol consumption with breast cancer risk varied with age and dietary fat intake. Among women aged 50-59 years, with a fat intake in the lowest quartile, the risk of breast cancer increased with increasing consumption of alcohol. A consumption of 24 g or more per day was associated with an 18-fold increased risk compared with abstainers. For women in other age groups, alcohol consumption had no significant association with breast cancer risk.