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Purpose: Moderate alcohol consumption (15 g/day) has been consistently associated with increased breast cancer risk; however, the association between alcohol and mammographic density, a strong marker of breast cancer risk, has been less consistent. Less is known about the effect of patterns of alcohol intake across the lifecourse.Methods: Using the Early Determinants of Mammographic Density study, an adult follow-up of women born in two US birth cohorts (n = 697; Collaborative Perinatal Project in Boston and Providence sites and the Childhood Health and Development Studies in California), we examined the association between alcohol intake in early adulthood (ages 20-29 years) and at time of interview and mammographic density (percent density and total dense area). We report the difference between nondrinkers and three levels of alcohol intake. We considered confounding by age at mammogram, body mass index, geographic site, race/ethnicity, and reproductive characteristics.Results: Seventy-nine percent of women reported ever consuming alcohol. Compared to nondrinkers in early adulthood, we observed an inverse association between >7 servings/week and percent density in fully adjusted models (β = -5.1, 95% CI -8.7, -1.5; p for trend = <0.01). Associations with dense area were inverse for the highest category of drinking in early adulthood but not statistically significant (p for trend = 0.15). Compared to noncurrent drinkers, the association for current intake of >7 servings/week and percent density was also inverse (β = -3.1, 95% CI -7.0, 0.8; p for trend = 0.01). In contrast, moderate alcohol intake (>0-≤7 servings/week) in either time period was positively associated with dense area; but associations were not statistically significant in fully adjusted models.Conclusions: Our study does not lend support to the hypothesis that the positive association between alcohol intake and breast cancer risk is through increasing mammographic density. [ABSTRACT FROM AUTHOR]

Background: Elevated levels of the pesticide DDT (dichlorodiphenyltrichloroethane) have been positively associated with blood pressure and hypertension in studies among adults. Accumulating epidemiologic and toxicologic evidence suggests that hypertension during adulthood may also be affected by earlier life and possibly the prenatal environment. Objectives: We assessed whether prenatal exposure to the pesticide DDT increases risk of adult hypertension. Methods: We examined concentrations of DDT (p,p´- and o,p´-) and its metabolite p,p´-DDE (dichlorodiphenyldichloroethylene) in prenatal serum samples from a subset of women (n = 527) who had participated in the prospective Child Health and Development Studies birth cohort in the San Francisco Bay area while they were pregnant between 1959 and 1967. We surveyed daughters 39-47 years of age by telephone interview from 2005 to 2008 to obtain information on self-reported physician-diagnosed hypertension and use of hypertensive medication. We used multi­variable regression analysis of time to hypertension based on the Cox proportional hazards model to estimate relative rates for the association between prenatal DDT exposures and hypertension treated with medication in adulthood, with adjustment for potential confounding by maternal, early-life, and adult exposures. Results: Prenatal p,p´-DDT exposure was associated with hypertension [adjusted hazard ratio (aHR) = 3.6; 95% CI: 1.8, 7.2 and aHR = 2.5; 95% CI: 1.2, 5.3 for middle and high tertiles of p,p´-DDT relative to the lowest tertile, respectively]. These associations between p,p´-DDT and hypertension were robust to adjustment for independent hypertension risk factors as well as sensi­tivity analyses. Conclusions: These findings suggest that the association between DDT exposure and hyperten­sion may have its origins early in development. [ABSTRACT FROM AUTHOR]

Intrauterine and early-life exposures, including intrauterine smoke exposures and infant growth are associated with mammographic breast density (MBD), a strong breast cancer risk factor. We investigated whether placental morphometry, which is affected by intrauterine smoke exposure and also influences infant growth, predicts %MBD at ages 37-47. In 247 daughters in the Child Health and Development Studies, we found that larger placental surface area and placental thickness were associated with lower %MBD (-0.32 per cm 2 , 95% CI -0.6, -0.05; -37.8 per 0.5 cm, 95% CI= -73.3, -2.3 respectively) independent of mothers' smoking, age, weight, parity and daughters' birthweight and age at mammogram. We also observed a positive interaction between placental surface area and thickness (p < 0.05) such that the highest breast dense area was observed for offspring with the thickest and largest placentas. Factors that impact placental morphometry, in addition to in utero smoke exposure, may influence adult breast architecture and breast cancer risk., Competing Interests: Declaration of Competing Interest The authors report no declarations of interest., (Copyright © 2019. Published by Elsevier Inc.)

Prior studies in the Child Health and Development Studies (CHDS) found in utero exposure to the pesticide, dichlorodiphenyltrichloroethane (DDT), increased breast cancer risk by age 52. Mammographic density is considered a primary risk factor for breast cancer. We conducted a study of 309 daughters from the CHDS to examine in utero DDT exposure and mammographic density in midlife. Among daughters with high (>75th percentile) exposure to p,p'-Dichlorodiphenyldichloroethylene (DDE), p,p'-DDT was significantly correlated with increased dense area and percent density regardless of her body mass in midlife. In the subset of women with lower (<75th percentile) p,p-DDE, p,p'-DDT was associated with increased non-dense breast area. This was explained by adjustment for midlife BMI suggesting that p,p'-DDT may be obesogenic. In aggregate our findings indicate that early life p,p'-DDT exposure impacts breast density in a complex way that depends on the hosts biological ability to sequester and process DDT and levels of exposure., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2019 Elsevier Inc. All rights reserved.)