Current Environmental Health Reports

Genomic imprinting refers to the epigenetic mechanism that results in the mono-allelic expression of a subset of genes in a parent-of-origin manner. These haploid genes are highly active in the placenta and are functionally implicated in the appropriate development of the fetus. Furthermore, the epigenetic marks regulating imprinted expression patterns are established early in development. These characteristics make genomic imprinting a potentially useful biomarker for environmental insults, especially during the in utero or early development stages, and for health outcomes later in life. Herein, we critically review the current literature regarding environmental influences on imprinted genes and summarize findings that suggest that imprinted loci are sensitive to known teratogenic agents, such as alcohol and tobacco, as well as less established factors with the potential to manipulate the in utero environment, including assisted reproductive technology. Finally, we discuss the potential of genomic imprinting to serve as an environmental sensor during early development.

A scoping review was conducted to identify interventions that successfully alter biomarker concentrations of phenols, glycol ethers, and phthalates resulting from dietary intake and personal care product (PCPs) use. Twenty-six interventions in populations ranging from children to older adults were identified; 11 actively removed or replaced products, 9 provided products containing the chemicals being studied, and 6 were education-only based interventions. Twelve interventions manipulated only dietary intake with a focus on bisphenol A (BPA) and phthalates, 8 studies intervened only on PCPs use and focused on a wider range of chemicals including BPA, phthalates, triclosan, parabens, and ultraviolet absorbers, while 6 studies intervened on both diet and PCPs and focused on phthalates, parabens, and BPA and its alternatives. No studies assessed glycol ethers. All but five studies reported results in the expected direction, with interventions removing potential sources of exposures lowering EDC concentrations and interventions providing exposures increasing EDC concentrations. Short interventions lasting a few days were successful. Barriers to intervention success included participant compliance and unintentional contamination of products. The identified interventions were generally successful but illustrated the influence of participant motivation, compliance, ease of intervention adherence, and the difficulty of fully removing exposures due their ubiquity and the difficulties of identifying “safer” replacement products. Policy which reduces or removes EDC in manufacturing and processing across multiple sectors, rather than individual behavior change, may have the greatest impact on population exposure.

Arsenic toxicity is a worldwide health concern as several millions of people are exposed to this toxicant via drinking water, and exposure affects almost every organ system in the body including the brain. Recent studies have shown that even low concentrations of arsenic impair neurological function, particularly in children. This review will focus on the current epidemiological evidence of arsenic neurotoxicity in children and adults, with emphasis on cognitive dysfunction, including learning and memory deficits and mood disorders. We provide a cohesive synthesis of the animal studies that have focused on neural mechanisms of dysfunction after arsenic exposure including altered epigenetics; hippocampal function; glucocorticoid and hypothalamus-pituitary-adrenal axis (HPA) pathway signaling; glutamatergic, cholinergic and monoaminergic signaling; adult neurogenesis; and increased Alzheimer’s-associated pathologies. Finally, we briefly discuss new studies focusing on therapeutic strategies to combat arsenic toxicity including the use of selenium and zinc.

The first author’s name should should be “Fariba Zare Sakhvidi”.

Inference in epidemiologic studies is plagued by exposure misclassification. Several methods exist to correct for misclassification error. One approach is to use point estimates for the sensitivity (Sn) and specificity (Sp) of the tool used for exposure assessment. Unfortunately, we typically do not know the Sn and Sp with certainty. Bayesian methods for exposure misclassification correction allow us to model this uncertainty via distributions for Sn and Sp. These methods have been applied in epidemiologic literature, but are not considered a mainstream approach, especially in occupational epidemiology. Here, we illustrate an occupational epidemiology application of a Bayesian approach to correct for the differential misclassification error generated by estimating occupational exposures from job codes using a job exposure matrix (JEM). We argue that analyses accounting for exposure misclassification should become more commonplace in the literature.

Bài báo này trình bày một đánh giá phân tích về các nghiên cứu gần đây liên quan đến sự bất bình đẳng xã hội do ô nhiễm không khí xung quanh gây ra hoặc làm trầm trọng thêm trong Liên minh châu Âu. Trong khi các nghiên cứu thực nghiệm đã phát triển đáng kể cả trong lĩnh vực học thuật và thể chế, chúng chủ yếu tập trung vào chỉ một khía cạnh: sự tiếp xúc và nhạy cảm của các cá nhân và nhóm đối với ô nhiễm không khí theo các tiêu chí khác nhau, ghi nhận sự bất bình đẳng đáng kể và chồng chéo. Trong khi chính sách của EU nên giải quyết tốt hơn sự bất bình đẳng về ảnh hưởng đã được chứng minh này, cũng cần có nghiên cứu về các lĩnh vực mới của chất lượng không khí (cụ thể là tác động đến sức khỏe tinh thần và chất lượng không khí trong nhà) cũng như các loại bất bình đẳng không khí khác (chẳng hạn như bất bình đẳng về trách nhiệm và tác động của chính sách giảm thiểu ô nhiễm không khí).