Cadmium, a highly persistent heavy metal, has been categorized as a probable human carcinogen by the U.S. Environmental Protection Agency. Primary exposure sources include food and tobacco smoke. We carried out a population-based case–control study of 246 women, aged 20–69 years, with breast cancer and 254 age-matched control subjects. We measured cadmium levels in urine samples by inductively coupled plasma mass spectrometry and conducted interviews by telephone to obtain information on known breast cancer risk factors. Odds ratios (ORs) and 95% confidence intervals (CIs) for breast cancer by creatinine-adjusted cadmium levels were calculated by multivariable analysis. Statistical tests were two-sided. Women in the highest quartile of creatinine-adjusted cadmium level (≥0.58 μg/g) had twice the breast cancer risk of those in the lowest quartile (<0.26 μg/g; OR = 2.29, 95% CI = 1.3 to 4.2) after adjustment for established risk factors, and there was a statistically significant increase in risk with increasing cadmium level ( Ptrend = .01). Based on this study, the absolute risk difference is 45 (95% CI = 0 to 77) per 100 000 given an overall breast cancer rate of 124 per 100 000. Whether increased cadmium is a causal factor for breast cancer or reflects the effects of treatment or disease remains to be determined.
Background: Women are at higher risk of breast cancer if they have higher socioeconomic status (SES) or live in higher SES or urban communities. We examined whether women living in such communities remained at greater risk of breast cancer after controlling for individual education and other known individual-level risk factors. Methods: Data were from a population-based, breast cancer case-control study conducted in Wisconsin from 1988 to 1995 (n = 14,667). Data on community SES and urbanicity come from the 1990 census, measured at the census tract and zip code levels. We evaluated relationships between individual- and community-level variables and breast cancer risk using multilevel logistic regression models with random community intercepts. Results: After controlling for individual education and other individual-level risk factors (age, mammography use, family history of breast cancer, parity, age at first birth, alcohol intake, body mass index, hormone replacement use, oral contraceptive use, and menopausal status), women living in the highest SES communities had greater odds of having breast cancer than women living in the lowest SES communities (1.20; 95% confidence interval = 1.05–1.37). Similarly, the odds were greater for women in urban versus rural communities (1.17; 1.06–1.28). Conclusions: Community SES and urbanicity are apparently not simply proxies for individual SES. Future research should examine why living in such communities itself is associated with greater risk of breast cancer.
Evidence-based public health requires the existence of reliable information systems for priority setting and evaluation of interventions. Existing data systems in the United States are either too crude (e.g., vital statistics), rely on administrative data (e.g., Medicare) or, because of their national scope (e.g., NHANES), lack the discriminatory power to assess specific needs and to evaluate community health activities at the state and local level. This manuscript describes the rationale and methods of the Survey of the Health of Wisconsin (SHOW), a novel infrastructure for population health research.
Background Geographic information systems (GIS) and spatial statistics are useful for exploring the relation between geographic location and health. The ultimate usefulness of GIS depends on both completeness and accuracy of geocoding (the process of assigning study participants’ residences latitude/longitude coordinates that closely approximate their true locations, also known as address matching). The goal of this project was to develop an iterative geocoding process that would achieve a high match rate in a large population-based health study. Methods Data were from a study conducted in Wisconsin using mailing addresses of participants who were interviewed by telephone from 1988 to 1995. We standardized the addresses according to US Postal Service guidelines, used desktop GIS geocoding software and two versions of the Topologically Integrated Geographic Encoding and Referencing street maps, accessed Internet mapping engines for problematic addresses, and recontacted a small number of study participants’ households. We also tabulated the project’s cost, time commitment, software requirements, and brief notes for each step and their alternatives. Results Of the 14,804 participants, 97% were ultimately assigned latitude/longitude coordinates corresponding to their respective residences. The remaining 3% were geocoded to their zip code centroid. Conclusion The multiple methods described in this work provide practical information for investigators who are considering the use of GIS in their population health research.
Cadmium is a human lung carcinogen and possesses estrogen-like activity. This combination of carcinogenic and estrogenic activity makes cadmium a contaminant of high concern for hormone-related cancers. Diet and smoking are the main sources of cadmium exposure. The aim of this study was to investigate the association between dietary cadmium intake and risk of breast, endometrial and ovarian cancer in Danish postmenopausal woman. We estimated dietary cadmium intake in the Diet, Cancer and Health cohort at enrolment 1993-97. The estimates were based on food frequency questionnaires and cadmium contents in all foods. Among 23,815 postmenopausal women we identified 1390 breast, 192 endometrial, and 146 ovarian cancer cases from enrolment through December 31, 2010 using the Danish Cancer Registry. Cox regression was used to analyse the association between dietary cadmium intake and cancer risk. Mean dietary cadmium intake was 14 µg/day. Cadmium was not associated with breast cancer, incidence rate ratio (IRR) = 0.99, 95% confidence interval (CI): 0.87–1.13 per 10 µg higher dietary cadmium intake/day; endometrial cancer, IRR = 1.08, 95% CI: 0.76–1.53; or ovarian cancer, IRR = 1.15, 95% CI: 0.78–1.70. We found a positive association between cadmium and endometrial cancer for the women with BMI<25 (IRR = 1.50, 95% CI: 0.94–2.39), whereas an inverse association was seen for the women with BMI≥25 (IRR = 0.69, 95% CI: 0.42–1.12); p value for interaction = 0.02. Our study does not indicate that our estimated dietary cadmium intake is associated with hormone-related cancers in women.
One important function of sleep may be its contribution to the maintenance of the immune system and regulation of the circadian rhythms by melatonin. Researchers have speculated that disruption of immune functions involving cortisol levels and natural killer cell activity may increase breast cancer risk whereas increased melatonin exposure may protect against breast cancer. We conducted a multistate population-based case-control study of 4,033 women with invasive breast cancer and 5,314 community women without breast cancer in which we inquired about women's sleep habits in the recent past and during adult lifetime. Relative to women who slept 7.0-7.9 h/night, the multivariate odds ratio for developing breast cancer among women who slept an average of 9 h or more per night approximately 2 years prior to interview was 1.13 (95% CI 0.93-1.37). The multivariate-adjusted odds ratio for the continuous term was 1.06 (95% CI 1.01-1.11), suggesting a 6% increase in risk for every additional hour of sleep. Similar patterns were observed for average lifetime adult sleep duration. We found little evidence that sleeping few hours per night was associated with breast cancer risk. The results of this study suggest that increasing sleep duration is modestly associated with an increased breast cancer risk. In contrast, short duration of sleep (<7 h/night) is not substantially associated with increased risk. Further research in this area is warranted.