Factors Associated with Atypical Moles in New Hampshire, USA

Only a few studies, conducted in Sweden, assessed factors associated with the presence of atypical moles in the general population. We conducted a population-based, case-control study in New Hampshire, USA, to identify factors associated with atypical moles. In our study, atypical moles affected 14% of the study population. The adjusted odds ratio (OR) was 0.34 (95% confidence interval (CI)=0.14-0.80) for those with the highest adulthood recreational sun exposure, relative to the lowest. The OR for any freckles, compared to none, was 2.24 (95% CI=1.18-4.25). We found a linear relationship between the number of benign moles and the presence of atypical moles (p for trend=0.0001). The OR was 7.34 (95% CI=3.03-17.80) for \u3e15 benign moles, relative to 0-4. Our data indicate that freckles and benign moles, which may reflect melanocytic inducibility, are strongly associated with atypical moles. The inverse association with sun exposure should be considered with caution

Smart density: a more accurate method of measuring rural residential density for health-related research

<p>Abstract</p> <p>Background</p> <p>Studies involving the built environment have typically relied on US Census data to measure residential density. However, census geographic units are often unsuited to health-related research, especially in rural areas where development is clustered and discontinuous.</p> <p>Objective</p> <p>We evaluated the accuracy of both standard census methods and alternative GIS-based methods to measure rural density.</p> <p>Methods</p> <p>We compared residential density (units/acre) in 335 Vermont school neighborhoods using conventional census geographic units (tract, block group and block) with two GIS buffer measures: a 1-kilometer (km) circle around the school and a 1-km circle intersected with a 100-meter (m) road-network buffer. The accuracy of each method was validated against the actual residential density for each neighborhood based on the Vermont e911 database, which provides an exact geo-location for all residential structures in the state.</p> <p>Results</p> <p>Standard census measures underestimate residential density in rural areas. In addition, the degree of error is inconsistent so even the relative rank of neighborhood densities varies across census measures. Census measures explain only 61% to 66% of the variation in actual residential density. In contrast, GIS buffer measures explain approximately 90% of the variation. Combining a 1-km circle with a road-network buffer provides the closest approximation of actual residential density.</p> <p>Conclusion</p> <p>Residential density based on census units can mask clusters of development in rural areas and distort associations between residential density and health-related behaviors and outcomes. GIS-defined buffers, including a 1-km circle and a road-network buffer, can be used in conjunction with census data to obtain a more accurate measure of residential density.</p

Menstrual and reproductive factors in relation to ovarian cancer risk

We assessed menstrual and reproductive factors in relation to ovarian cancer risk in a large, population-based, case–control study. 563 cases in Massachusetts and New Hampshire were ascertained from hospitals and statewide tumour registries; control women (n= 523) were selected through random digit dialing and matched to case women by age and telephone sampling unit. We used multivariate logistic regression to evaluate factors in relation to risk of ovarian cancer and the major tumour histologic subtypes. Ovarian cancer risk was reduced among parous women, relative to nulliparous women (OR = 0.4; 95% CI = 0.3−0.6). Among parous women, higher parity (P= 0.0006), increased age at first (P= 0.03) or last (P= 0.05) birth, and time since last birth (P= 0.04) were associated with reduced risk. Early pregnancy losses, abortions, and stillbirths were unrelated to risk, but preterm, term, and twin births were protective. Risk was lower among women who had breast-fed, relative to those who had not (OR = 0.7; 95% CI = 0.5–1.0), but the average duration of breast-feeding per child was unrelated to risk (P for trend = 0.21). Age at menarche and age at menopause were unrelated to risk overall, although increasing menarcheal age was protective among premenopausal women (P= 0.02). Menstrual cycle characteristics and symptoms were generally unrelated to risk, although cycle-related insomnia was associated with decreased risk (OR = 0.5; 95% CI = 0.3–0.8). We found no association between the type of sanitary product used during menstruation and ovarian cancer risk. In analyses by histologic subtype, reproductive and menstrual factors had most effect on risk of endometrioid/clear cell tumours, and least influential with regard to risk of mucinous tumours. Overall, our findings offer some support to current hypotheses of ovarian pathogenesis, and show aetiologic differences among the tumour subtypes. © 2001 Cancer Research Campaign http://www.bjcancer.co

No difference between red wine or white wine consumption and breast cancer risk.

Epidemiologic studies have reported an increased risk of breast cancer among women who drink alcohol, including wine (1, 2) Two meta-analyses estimated a ∼10% [95% confidence interval (CI), 5-15%] increased risk of breast cancer with each additional 10 grams (∼1 drink) of alcohol/day regardless of beverage type (3, 4). Few studies have evaluated breast cancer risk separately for red and white wine (5-8). There is some evidence of beneficial health effects of red wine from laboratory (9) and epidemiologic studies of heart disease (10) and prostate cancer (11, 12). We evaluated overall alcohol as well as red and white wine consumption to examine beverage-specific effects on breast cancer

Left-handedness and risk of breast cancer

Left-handedness may be an indicator of intrauterine exposure to oestrogens, which may increase the risk of breast cancer. Women (n=1786) from a 1981 health survey in Busselton were followed up using death and cancer registries. Left-handers had higher risk of breast cancer than right-handers and the effect was greater for post-menopausal breast cancer (hazard ratio=2.59, 95% confidence interval 1.11–6.03)

Prediagnostic use of hormone therapy and mortality after breast cancer.

BACKGROUND: A few studies have observed reduced breast cancer mortality in women who used hormone therapy before diagnosis. Due to the high prevalence of past and current hormone use, it is important to investigate whether these preparations are related to breast cancer mortality. METHODS: To evaluate the influence of prediagnostic use of hormone therapy on breast cancer mortality, a prospective cohort of 12,269 women ages 50 years or more diagnosed with incident invasive breast cancer and residents of Wisconsin, Massachusetts, or New Hampshire were enrolled in three phases beginning in 1988. They were followed for death until December 31, 2005, using the National Death Index. Cumulative mortality and multivariable adjusted hazard rate ratios for breast cancer and other mortality causes were calculated for women according to any hormone therapy use, and for exclusive use of estrogen or estrogen-progestin (EP). RESULTS: During an average 10.3 years of follow-up, 1,690 deaths from breast cancer were documented. Cumulative mortality from breast cancer was lower among hormone therapy users, specifically current users at the time of diagnosis, and EP users, compared with nonusers. Adjusted survival varied by type and duration of hormone therapy before diagnosis. A reduced risk of death from breast cancer was associated with EP preparations (hazard rate ratio, 0.73; 0.59-0.91) and with > or =5 years of EP use (0.60; 0.43-0.84). No association was observed for women who were former or current users of E-alone preparations. CONCLUSIONS: Although use of combined EP preparations increases breast cancer risk, in this study, use of these hormones before diagnosis was associated with reduced risk of death after a breast cancer diagnosis. The better survival among users, particularly of EP, persisted after adjustment of screening, stage, and measured confounders

Secondary Sex Ratio among Women Exposed to Diethylstilbestrol in Utero

BACKGROUND. Diethylstilbestrol (DES), a synthetic estrogen widely prescribed to pregnant women during the mid-1900s, is a potent endocrine disruptor. Previous studies have suggested an association between endocrine-disrupting compounds and secondary sex ratio. METHODS. Data were provided by women participating in the National Cancer Institute (NCI) DES Combined Cohort Study. We used generalized estimating equations to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the relation of in utero DES exposure to sex ratio (proportion of male births). Models were adjusted for maternal age, child's birth year, parity, and cohort, and accounted for clustering among women with multiple pregnancies. RESULTS. The OR for having a male birth comparing DES-exposed to unexposed women was 1.05 (95% CI, 0.95-1.17). For exposed women with complete data on cumulative DES dose and timing (33%), those first exposed to DES earlier in gestation and to higher doses had the highest odds of having a male birth. The ORs were 0.91 (95% C, 0.65-1.27) for first exposure at ≥ 13 weeks gestation to < 5 g DES; 0.95 (95% CI, 0.71-1.27) for first exposure at ≥ 13 weeks to ≥ 5 g; 1.16 (95% CI, 0.96-1.41) for first exposure at < 13 weeks to < 5 g; and 1.24 (95% CI, 1.04-1.48) for first exposure at < 13 weeks to ≥ 5 g compared with no exposure. Results did not vary appreciably by maternal age, parity, cohort, or infertility history. CONCLUSIONS. Overall, no association was observed between in utero DES exposure and secondary sex ratio, but a significant increase in the proportion of male births was found among women first exposed to DES earlier in gestation and to a higher cumulative dose.National Cancer Institute (N01-CP-21168, N01-CP-51017, N01-CP-01289

Urogenital Abnormalities in Men Exposed to Diethylstilbestrol in Utero: A Cohort Study

Background: Diethylstilbestrol (DES), a synthetic estrogen widely prescribed to pregnant women during the 1940s70s, has been shown to cause reproductive problems in the daughters. Studies of prenatally-exposed males have yielded conflicting results. Methods: In data from a collaborative follow-up of three U.S. cohorts of DES-exposed sons, we examined the relation of prenatal DES exposure to occurrence of male urogenital abnormalities. Exposure status was determined through review of prenatal records. Mailed questionnaires (1994, 1997, 2001) asked about specified abnormalities of the urogenital tract. Risk ratios (RR) were estimated by Cox regression with constant time at risk and control for year of birth. Results: Prenatal DES exposure was not associated with varicocele, structural abnormalities of the penis, urethral stenosis, benign prostatic hypertrophy, or inflammation/infection of the prostate, urethra, or epididymus. However, RRs were 1.9 (95% confidence interval 1.13.4) for cryptorchidism, 2.5 (1.54.3) for epididymal cyst, and 2.4 (1.54.4) for testicular inflammation/ infection. Stronger associations were observed for DES exposure that began before the 11th week of pregnancy: RRs were 2.9 (1.65.2) for cryptorchidism, 3.5 (2.06.0) for epididymal cyst, and 3.0 (1.75.4) for inflammation/infection of testes. Conclusion: These results indicate that prenatal exposure to DES increases risk of male urogenital abnormalities and that the association is strongest for exposure that occurs early in gestation. The findings support the hypothesis that endocrine disrupting chemicals may be a cause of the increased prevalence of cryptorchidism that has been seen in recent years