Background: Bisphenol A (BPA) and bis(2-ethylhexyl) phthalate (DEHP) are high-production-volume chemicals used in plastics and resins for food packaging. They have been associated with endocrine disruption in animals and in some human studies. Human exposure sources have been estimated, but the relative contribution of dietary exposure to total intake has not been studied empirically.Objectives: To evaluate the contribution of food packaging to exposure, we measured urinary BPA and phthalate metabolites before, during, and after a “fresh foods” dietary intervention.Methods: We selected 20 participants in five families based on self-reported use of canned and packaged foods. Participants ate their usual diet, followed by 3 days of “fresh foods” that were not canned or packaged in plastic, and then returned to their usual diet. We collected evening urine samples over 8 days in January 2010 and composited them into preintervention, during intervention, and postintervention samples. We used mixed-effects models for repeated measures and Wilcoxon signed-rank tests to assess change in urinary levels across time.Results: Urine levels of BPA and DEHP metabolites decreased significantly during the fresh foods intervention [e.g., BPA geometric mean (GM), 3.7 ng/mL preintervention vs. 1.2 ng/mL during intervention; mono-(2-ethyl-5-hydroxy hexyl) phthalate GM, 57 ng/mL vs. 25 ng/mL]. The intervention reduced GM concentrations of BPA by 66% and DEHP metabolites by 53–56%. Maxima were reduced by 76% for BPA and 93–96% for DEHP metabolites.Conclusions: BPA and DEHP exposures were substantially reduced when participants’ diets were restricted to food with limited packaging.

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BackgroundIn this review, we examine the continually expanding and increasingly compelling data linking radiation and various chemicals in our environment to the current high incidence of breast cancer.AbstractSingly and in combination, these toxicants may have contributed significantly to the increasing rates of breast cancer observed over the past several decades. Exposures early in development from gestation through adolescence and early adulthood are particularly of concern as they re-shape the program of genetic, epigenetic and physiological processes in the developing mammary system, leading to an increased risk for developing breast cancer. In the 8 years since we last published a comprehensive review of the relevant literature, hundreds of new papers have appeared supporting this link, and in this update, the evidence on this topic is more extensive and of better quality than that previously available.ConclusionIncreasing evidence from epidemiological studies, as well as a better understanding of mechanisms linking toxicants with development of breast cancer, all reinforce the conclusion that exposures to these substances – many of which are found in common, everyday products and byproducts – may lead to increased risk of developing breast cancer. Moving forward, attention to methodological limitations, especially in relevant epidemiological and animal models, will need to be addressed to allow clearer and more direct connections to be evaluated.

ICI 182,780 is one of a new class of steroidal antiestrogens that differs from nonsteroidal antiestrogens, such as tamoxifen, in a number of respects. 1) It is bound by estrogen receptors with a high affinity, similar to that for estradiol. 2) It is a "pure" antiestrogen in that it does not mimic any of the effects of estradiol. 3) This class of antiestrogens does not seem to be bound by antiestrogen binding sites. 4) ICI 182,780 may not be active in the brain after peripheral administration. Indeed, ICI 182,780 blocked in vivo cell nuclear binding of [3H]estradiol in uterus, pituitary, and adipose tissue but not in hypothalamus-preoptic area. In vitro, ICI 182,780 competed for binding by neural estrogen receptors with an affinity comparable with that for estradiol. When given to ovariectomized rats, ICI 182,780 did not mimic any of the actions of estradiol. Instead, ICI 182,780 treatment completely blocked the uterotrophic effects of estradiol and attenuated the actions of estradiol on linear growth, carcass fat content, fat pad weight, and sexual receptivity. Treatment with ICI 182,780 also attenuated the estrogenic effects of tamoxifen on food intake, body weight and composition, linear growth, and uterine weight. These findings support the concept that, in addition to its actions in the brain, estradiol can act peripherally to modulate regulatory behaviors, energy balance, and estrous behavior. They are also consistent with the hypothesis that nonsteroidal antiestrogens, such as tamoxifen, affect energy balance via estrogen receptors, rather than antiestrogen binding sites.

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