Work and Female Breast Cancer: The State of the Evidence, 2002-2017.

The authors undertook a scoping review to assess the literature from 2002 to 2017 on the relationship between occupation and female breast cancer. Case-control, cohort, and meta-analytic studies suggest that women working as flight attendants, in medical professions, some production positions, sales and retail, and scientific technical staff are likely to have elevated risk of breast cancer. In addition, occupational exposures to night-shift work, ionizing radiation, some chemicals, job stress, and sedentary work may increase risk of breast cancer. Occupational physical activity appears to decrease risk. Workplace exposures to passive smoke and occupational exposure to nonionizing radiation do not appear to affect breast cancer risk. Some studies of occupational categories and workplace exposures indicate that risk may be modified by duration of exposure, timing of exposure, dose, hormone-receptor subtypes, and menopausal status at diagnosis. The compelling data from this review reveal a substantial need for further research on occupation and breast cancer.

Work and Breast Cancer: Recommendations to Address Research Needs.

A review of case-control, cohort, and meta-analytic studies on breast cancer, occupation, and work-related exposures from 2002 to 2017 revealed significant methodological limitations in the current literature. As part of our review, we tabulated the demographic and life history data, breast cancer risk factors, occupational history, and exposure estimates collected and analyzed in each study. Opportunities exist for future research to explore occupation and breast cancer more rigorously and with greater nuance by gathering specific data on age at diagnosis, menopausal status, tumor characteristics, demographics, breast cancer risk factors, and occupational histories, work roles and settings, and exposures. Inclusion of workers in the planning and implementation of research on their occupational risks and exposures is one effective way to refine research questions and ensure research is relevant to workers' needs and concerns.

State of the evidence 2017: an update on the connection between breast cancer and the environment.

BACKGROUND: In 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. Singly 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. CONCLUSION: Increasing 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.

Temporal variability of urinary di(2-ethylhexyl) phthalate metabolites during a dietary intervention study.

Exposure to di(2-ethylhexyl) phthalate (DEHP) may be related to adverse health effects including developmental and reproductive disorders, prompting interest in strategies for reducing human exposure. We previously reported a reduction of DEHP metabolite levels in composite urine samples by more than 50% (geometric means) during a 3-day dietary intervention avoiding plastics in food packaging, preparation, and storage. In the present study, we analyzed individual spot urine samples before compositing in order to evaluate temporal variability. There were no meaningful changes in any of the previous findings when using individual rather than composited samples. Individual urine samples, like the composites, showed significant decreases of ≥50% in all three measured DEHP metabolites during the intervention. Compositing urine samples provided sufficient information to observe the effect of the intervention, whereas reducing analytical expenses compared with analyzing multiple samples individually. Low intraclass correlations (ICCs) for samples collected from the same person before the intervention indicate the importance of collecting multiple samples per exposure condition. Substantially larger ICCs during and after the intervention suggest that much of the variability observed in DEHP metabolite levels originates from dietary exposure.

Mancozeb-induced behavioral deficits precede structural neural degeneration.

Manganese-containing fungicides like Mancozeb have been associated with neurodegenerative conditions like Parkinson's disease. We examined the behavioral damage and differential neuronal vulnerability resulting from Mancozeb exposure using Caenorhabditis elegans, an important mid-trophic level soil organism that is also a powerful model for studying mechanisms of environmental pollutant-induced neurodegenerative disease. The dopamine-mediated swim to crawl locomotory transition behavior is exquisitely vulnerable to Mancozeb, with functional impairment preceding markers of neuronal structural damage. The damage is partially rescued in mutants lacking the divalent metal transporter, SMF-1, demonstrating that some, but not all, of the damage is mediated by manganese. Increasing concentrations of Mancozeb recruit additional behavioral dysfunction, notably serotonin-mediated egg-laying behavior, but without evident serotonergic neuronal structural damage. Thus, measurements of behavioral dysfunction are a sensitive early marker of fungicide toxicity that could be exploited to examine further mechanisms of neuron damage and possible therapeutic interventions. These results also provide important insight into the consequences of fungicide use on the ecological behavior of nematodes.

Food packaging and bisphenol A and bis(2-ethyhexyl) phthalate exposure: findings from a dietary intervention.

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.

Exploration of gerontogenes in the nervous system: a multi-level neurogenomics laboratory module for an intermediate neuroscience and behavior course.

In this paper, we describe and assess a laboratory module that we introduced into an intermediate-level undergraduate course in Neuroscience and Behavior (NEUR201) in order to expose students to the new and rapidly developing neurogenomic and bioinformatics approaches to neuroscience research. The laboratory accompanies a topics-based, highly process-oriented course that explores research methodologies and integrative approaches to particular topics in the field. The laboratory comprises multi-week modules that expand upon the topics being covered in class. In the class for which this module was developed, a key topic under discussion is the role played by the nervous system in aging and/or lifespan. This laboratory module focuses on the model organism, Caenorhabditis elegans (C. elegans), which has been studied extensively. There is a large and ongoing literature elucidating a number of genes involved in determining or modulating lifespan in C. elegans. Students choose a candidate gerontogene expressed in neurons in C. elegans from a provided list for which we have mutant strains. Students use available databases to become experts on their candidate gene and design, carry out and analyze a behavioral experiment. In addition, students use available bioinformatics and genomic tools to conduct a protein sequence phylogenetic analysis of their candidate protein across at least 10 different taxa of animals. The laboratory module thus focuses on the integration of behavioral, genetic and bioinformatics approaches, as well as on the evolutionary considerations of the role played by gerontogenes in different organisms.