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In the last few years, microplastics research has exploded, with the field exploring new procedures and techniques that focus on a variety of scientific and policy issues. As there are not standardized definitions for many terms in the field, including the term microplastic itself, researchers utilize the same labels to describe different aspects of microplastic pollution. Here we provide a visual tool, called a Hub for Interactive Literature (HIL), to assist researchers in identifying and targeting specific literature. Currently, there are four Hubs for Interactive Learning (HILs) corresponding to previously published reviews, including a scoping review of microplastics literature as well as three reviews examining the human exposure and health effects of microplastics, the unique liver carcinogenicity of polyvinyl chloride (PVC) microplastics, and micro and nanoplastics found in the air. The HILs incorporate all of the literature used to produce the corresponding reviews. A couple of advantages that HILs provide in their capacity as a supportive instrument are the filtering options and easily accessed original references. This tool can be leveraged by researchers to rapidly review microplastics research and isolate specific subtopics of interest to develop new conclusions and quickly identify data gaps. We give an in-depth look at the HIL corresponding to a scoping review of microplastics literature to exhibit the novel functionality and advantages of this exciting tool. We demonstrate a novel world map of the literature to show that microplastics are a global scientific and public health issue. The map offers the additional functionality of filtering the references by country. We also provide a brief description of the current HILs to show the flexibility and personalization available when using this method. [ABSTRACT FROM AUTHOR]

Prolonged exposure to the flame retardants found in many household products and building materials is associated with adverse developmental, reproductive, and carcinogenic consequences. While these compounds have been studied in numerous epidemiological and animal models, less is known about the effects of flame retardant exposure on cell function. This study evaluated the toxicity of the commonly used fire retardant tris(1,3-dichloro-2-propyl)phosphate (TDCPP) in cell line derived from the kidney, a major tissue target of organohalogen toxicity. TDCPP inhibited cell growth at lower concentrations (IC50 27 μM), while cell viability and toxicity were affected at higher concentrations (IC50 171 μM and 168 μM, respectively). TDCPP inhibited protein synthesis and caused cell cycle arrest, but only at higher concentrations. Additionally, the antioxidant N-acetylcysteine (NAC) reduced cell toxicity in cells treated with TDCPP, suggesting that exposure to TDCPP increased oxidative stress in the cells. In summary, these data show that low concentrations of TDCPP result in cytostasis in a kidney cell line, whereas higher concentrations induce cell toxicity. Furthermore, TDCPP toxicity can be attenuated by NAC, suggesting that antioxidants may be effective countermeasures to some organohalogen exposures.

Serum concentrations of 35 ortho-substituted polychlorinated biphenyl congeners (PCBs) were measured in 765 adults from Anniston, Alabama, where PCBs were manufactured between 1929 and 1971. As part of the Anniston Community Health Survey (ACHS), demographic data, questionnaire information, and blood samples were collected from participants in 2005-2007. Forty-six percent of study participants were African-American, 70% were female, and the median age was 56 years. The median concentration of the sum of 35 PCB congeners (ΣPCBs) was 528 ng/g lipid, with a 90th percentile of 2,600 ng/g lipid, minimum of 17.0 ng/g lipid, and maximum of 27,337 ng/g lipid. The least square geometric mean ΣPCBs was more than 2.5 times higher for African-American participants than for White participants (866 ng/g lipid vs. 331 ng/g lipid); this difference did not change materially after adjustment for age, sex, body mass index (BMI) and current smoking. In spite of large differences in absolute PCB levels, relative contributions of individual congeners to ΣPCBs were quite similar between race groups. Nevertheless, while percent contributions to ΣPCBs for most of the most abundant penta- to heptachlorobiphenyls were higher among African-Americans, the percentages were higher in Whites for the lower-chlorinated PCBs 28 and 74 and for octa- to decachlorinated PCBs. No major differences were observed in geometric mean ΣPCBs between women and men when adjusted for age, race, BMI and current smoking (516 ng/g lipid vs. 526 ng/g lipid). Principal component analysis revealed groups of co-varying congeners that appear to be determined by chlorine substitution patterns. These congener groupings were similar between ACHS participants and the National Health and Nutrition Examination Survey (NHANES) 2003-04 sample of the general United States population, despite ACHS participants having serum concentrations of ΣPCBs two to three times higher than those in comparable age and race groups from NHANES.

The influence of exposure duration on chemical toxicity has important implications for risk assessment. Although a default 10-fold extrapolation factor is commonly applied when the toxicological dataset includes a subchronic (90-day) study but lacks studies of chronic duration, little consensus has been reached on an appropriate extrapolation factor to apply when the dataset includes a 28-day study but lacks studies of longer durations. The goal of the present assessment was to identify a 28-day to 90-day extrapolation factor by analyzing distributions of ratios of No-Observed-Adverse-Effect Levels (NOAELs) and Benchmark Doses (BMDs) derived from 28-day and 90-day studies. The results of this analysis suggest that a default 10-fold extrapolation factor in chemical risk assessment applications is sufficient to account for the uncertainty associated with evaluating human health risk based on results from a 28-day study in the absence of results from a 90-day study. This analysis adds significantly to the growing body of literature interpreting the influence of exposure duration on chemical toxicity that will likewise facilitate discussions on the future state of testing requirements in the international regulatory community. [ABSTRACT FROM AUTHOR]

Risk evaluations play an important role in environmental management, remediation and restoration. Yet when different agencies and groups evaluate risk, the objectives and methods may differ, leading to different conclusions, which can confuse managers, policy-makers and the public. In this paper, we examine two evaluations of the potential risk from mercury contamination deriving from the Y-12 facility at the Department of Energy’s Oak Ridge Reservation (Tennessee, USA). The US Agency for Toxic Substances and Disease Registry (ATSDR) examined the past and present risks from mercury to humans, using data provided in government reports and publications. The Consortium for Risk Evaluation with Stakeholder Participation (CRESP) used a risk-informed prioritization model, developed for managers to evaluate different remediation projects. The CRESP prioritization model considered both human and ecological receptors, as well as future potential risks. Risk was an important component of both evaluations, and both evaluations found that there was a completed pathway of mercury from the source on the Oak Ridge Reservation to offsite human receptors, although the evaluations differed in their final conclusions. CRESP evaluated the risk as ‘high’, while the ATSDR noted that the risk was ‘moderate’ for people consuming fish from East Fork Poplar Creek. In both cases, the pathway to off-site human exposure was through fish consumption. The two evaluations are compared with respect to purpose, specific goals, target audience, receptors, assumptions, time frames, evaluation criteria and conclusions. When these aspects are considered, the risk evaluations are congruent, although the risk communication messages differ. We conclude that there are many different possible risk evaluations, and the aforementioned variables must be carefully considered when making management decisions, determining remediation goals, and communicating with regulators, managers, public policy-makers and the public. [ABSTRACT FROM PUBLISHER]

Background: Cancer clusters garner considerable public and legislative attention, and there is often an expectation that cluster investigations in a community will reveal a causal link to an environmental exposure. At a 1989 national conference on disease clusters, it was reported that cluster studies conducted in the 1970s and 1980s rarely, if ever, produced important findings. We seek to answer the question: Have cancer cluster investigations conducted by US health agencies in the past 20 years improved our understanding of cancer etiology, or informed cancer prevention and control? Methods: We reviewed publicly available cancer cluster investigation reports since 1990, obtained from literature searches and by canvassing all 50 states and the District of Columbia. Investigations were categorized with respect to cancer type(s), hypothesized exposure, whether perceived clusters were confirmed (e.g. by elevated incidence), and conclusions about a link between cancer(s) of concern and hypothesized environmental exposure(s). Results: We reviewed 428 investigations evaluating 567 cancers of concern. An increase in incidence was confirmed for 72 (13%) cancer categories (including the category 'all sites'). Three of those were linked (with variable degree of certainty) to hypothesized exposures, but only one investigation revealed a clear cause. Conclusions: It is fair to state that extensive efforts to find causes of community cancer clusters have not been successful. There are fundamental shortcomings to our current methods of investigating community cancer clusters. We recommend a multidisciplinary national dialogue on creative, innovative approaches to understanding when and why cancer and other chronic diseases cluster in space and time. [ABSTRACT FROM AUTHOR]

Since 1995, the Agency for Toxic Substances and Disease Registry (ATSDR) has evaluated environmental contaminants and human health risks at nearly 3000 sites. Hazardous substances at these sites include newly emerging problems as well as historically identified threats. ATSDR classifies sites according to the degree of hazard they represent to the public. Less than 1% of the sites investigated are considered urgent public health hazards where chemical or physical hazards are at levels that could cause an immediate threat to life or health. Approximately 20% of sites have a potential for long-term human exposures above acceptable risk levels. At almost 40% of sites, hazardous substances do not represent a public health hazard. Completed exposure pathways for contaminants in air, water, and soil have been reported at approximately 30% of evaluated sites. The most common contaminants of concern at these sites include heavy metals, volatile organic compounds, and polychlorinated biphenyls. This article reviews ATSDR's ongoing work by examining the historic hazard of lead, the contemporary hazard of asbestos, and the emerging issue of perchlorate contamination. [ABSTRACT FROM AUTHOR]

Di(2-ethylhexyl)phthalate (also known as DEHP, bis(2-ethylhexyl)phthalate, or BEHP; CAS Registry Number 117-81-7) is a widely-used plasticizer. It is found in numerous plastic articles, such as paints, inks, floor tiles, upholstery, shower curtains, footwear, plastic bags, food-packaging materials, toys, and medical tubing. Not surprisingly, DEHP appears at many waste sites. As part of its mandate, the Agency for Toxic Substances and Disease Registry (ATSDR) prepares toxicological profiles on hazardous chemicals that are of greatest public health concern at Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) National Priority List (NPL) sites. These profiles comprehensively summarize toxicological and environmental information. This article constitutes the release of the bulk of ATSDR's profile for DEHP (ATSDR, 1993) into the mainstream scientific literature. An extensive listing of human and animal health effects, organized by route, duration, and endpoint, is presented. Toxicological information on toxicokinetics, biomarkers, interactions, sensitive subpopulations, reducing toxicity after exposure, and relevance to public health is also included. Environmental information encompasses physical properties, production and use, environmental fate, levels seen in the environment, analytical methods, and a listing of regulations. ATSDR, at the behest of Congress and therefore the citizenry, prepares these profiles to inform the public about site contaminants. [ABSTRACT FROM AUTHOR]

Objectives: The Agency for Toxic Substances and Disease Registry (ATSDR) and the Environmental Protection Agency (EPA) derive minimal risk levels (MRLs) and reference concentrations and doses (RfCs and RfDs), respectively, for environmental contaminants to help identify potential health risks to exposed populations. MRLs, RfDs, and RfCs involve similar derivation methods, but the values sometimes differ for the same chemical. The objectives of this manuscript are to quantitatively assess similarities and differences between MRLs, RfCs, and RfDs, qualitatively describe how a number of factors can influence the development of the health guidance values (HGVs) and identify ongoing collaborations and opportunities for increased coordination of efforts., Materials and Methods: We collected MRLs and RfCs/RfDs, assessment date, and description of the derivation process from ATSDR's toxicological profiles and EPA's Integrated Risk Information System (IRIS) and Office of Pesticide Program (OPP) and identified reasons for differences between MRLs and RfCs/RfDs., Results: The most frequent types of differences in values that we found in our analysis included use of different methodologies, use of different studies, and/or completion of a more recent chemical evaluation. These can stem from differences in scientific judgement., Conclusion: To avoid confusion when disparate HGVs occur between government agencies, a keen understanding of these differences can be helpful for appropriate risk characterization and communication when applying HGVs.

Serum concentrations of 35 ortho-substituted polychlorinated biphenyl congeners (PCBs) were measured in 765 adults from Anniston, Alabama, where PCBs were manufactured between 1929 and 1971. As part of the Anniston Community Health Survey (ACHS), demographic data, questionnaire information, and blood samples were collected from participants in 2005-2007. Forty-six percent of study participants were African-American, 70% were female, and the median age was 56 years. The median concentration of the sum of 35 PCB congeners (ΣPCBs) was 528 ng/g lipid, with a 90th percentile of 2,600 ng/g lipid, minimum of 17.0 ng/g lipid, and maximum of 27,337 ng/g lipid. The least square geometric mean ΣPCBs was more than 2.5 times higher for African-American participants than for White participants (866 ng/g lipid vs. 331 ng/g lipid); this difference did not change materially after adjustment for age, sex, body mass index (BMI) and current smoking. In spite of large differences in absolute PCB levels, relative contributions of individual congeners to ΣPCBs were quite similar between race groups. Nevertheless, while percent contributions to ΣPCBs for most of the most abundant penta- to heptachlorobiphenyls were higher among African-Americans, the percentages were higher in Whites for the lower-chlorinated PCBs 28 and 74 and for octa- to decachlorinated PCBs. No major differences were observed in geometric mean ΣPCBs between women and men when adjusted for age, race, BMI and current smoking (516 ng/g lipid vs. 526 ng/g lipid). Principal component analysis revealed groups of co-varying congeners that appear to be determined by chlorine substitution patterns. These congener groupings were similar between ACHS participants and the National Health and Nutrition Examination Survey (NHANES) 2003-04 sample of the general United States population, despite ACHS participants having serum concentrations of ΣPCBs two to three times higher than those in comparable age and race groups from NHANES., (Published by Elsevier B.V.)

Metals are a threat to human health by increasing disease risk. Experimental data have linked altered miRNA expression with exposure to some metals. MiRNAs comprise a large family of non-coding single-stranded molecules that primarily function to negatively regulate gene expression post-transcriptionally. Although several human populations are exposed to low concentrations of As, Cd and Pb as a mixture, most toxicology research focuses on the individual effects that these metals exert. Thus, this study aims to evaluate global miRNA and mRNA expression changes induced by a metal mixture containing NaAsO2, CdCl2, Pb(C2H3O2)2·3H2O and to predict possible metal-associated disease development under these conditions. Our results show that this metal mixture results in a miRNA expression profile that may be responsible for the mRNA expression changes observed under experimental conditions in which coding proteins are involved in cellular processes, including cell death, growth and proliferation related to the metal-associated inflammatory response and cancer., (© 2013 Elsevier B.V. All rights reserved.)

Background: There is limited research examining the relationship between lead (Pb) exposure and medically diagnosed attention deficit hyperactivity disorder (ADHD) in children. The role of mercury (Hg) and cadmium (Cd) exposures in ADHD development is even less clear., Objectives: To examine the relationship between Pb, Hg, and Cd and ADHD in children living inside and outside a Lead Investigation Area (LIA) of a former lead refinery in Omaha, NE., Methods: We carried out a case-control study with 71 currently medically diagnosed ADHD cases and 58 controls from a psychiatric clinic and a pediatric clinic inside and outside of the LIA. The participants were matched on age group (5-8, 9-12 years), sex, race (African American or Caucasians and others), and location (inside or outside LIA). We measured whole blood Pb, total Hg, and Cd using inductively coupled plasma mass spectrometry., Results: Inside the LIA, the 27 cases had blood Pb geometric mean (GM) 1.89 µg/dL and the 41 controls had 1.51 µg/dL. Outside the LIA, the 44 cases had blood Pb GM 1.02 µg/dL while the 17 controls had 0.97 µg/dL. After adjustment for matching variables and maternal smoking, socioeconomic status, and environmental tobacco exposure, each natural log unit blood Pb had an odds ratio of 2.52 with 95% confidence interval of 1.07-5.92. Stratification by the LIA indicated similar point estimate but wider CIs. No associations were observed for Hg or Cd., Conclusions: Postnatal Pb exposure may be associated with higher risk of clinical ADHD, but not the postnatal exposure to Hg or Cd., (© 2013 Published by Elsevier Inc.)

The contribution of genomics and associated technologies to human health risk assessment for environmental chemicals has focused largely on elucidating mechanisms of toxicity, as discussed in other articles in this issue. However, there is interest in moving beyond hazard characterization to making more direct impacts on quantitative risk assessment (QRA)--i.e., the determination of toxicity values for setting exposure standards and cleanup values. We propose that the evolution of QRA of environmental chemicals in the post-genomic era will involve three, somewhat overlapping phases in which different types of approaches begin to mature. The initial focus (in Phase I) has been and continues to be on "augmentation" of weight of evidence--using genomic and related technologies qualitatively to increase the confidence in and scientific basis of the results of QRA. Efforts aimed towards "integration" of these data with traditional animal-based approaches, in particular quantitative predictors, or surrogates, for the in vivo toxicity data to which they have been anchored are just beginning to be explored now (in Phase II). In parallel, there is a recognized need for "expansion" of the use of established biomarkers of susceptibility or risk of human diseases and disorders for QRA, particularly for addressing the issues of cumulative assessment and population risk. Ultimately (in Phase III), substantial further advances could be realized by the development of novel molecular and pathway-based biomarkers and statistical and in silico models that build on anticipated progress in understanding the pathways of human diseases and disorders. Such efforts would facilitate a gradual "reorientation" of QRA towards approaches that more directly link environmental exposures to human outcomes., (Published by Elsevier Inc.)

In 2011 the Taiwan Food and Drug Administration reported that plasticizers di(2-ethylhexyl) phthalate (DEHP) and di-iso-nonyl phthalate (DiNP), endocrine disruptors, were illegally added to clouding agents used in foods and beverages. 965 products were found contaminated, of which 206 were exported to 22 countries. This study's purpose was to obtain English names for 28 contaminated products for which DEHP levels were reported, calculate estimated average daily intake (mg/kg/day) for a 50 kg woman consuming one portion, and compare to U.S. and E.U. guidelines for daily intake. We found that drinking just one bottle (500 ml) of sports drinks would result in an average DEHP intake of 0.14 mg/kg bw/day (range 0.091-0.341), which exceeds by several fold government guidelines (0.02-0.06 mg/kg bw/day). One (2 g) serving from 4/14 samples of contaminated dietary supplements exceeds the guideline of 0.02 mg/kg bw/day. In conclusion, consuming even one portion of tainted drinks and some powders would lead to daily intake of DEHP that greatly exceeds established safety guidelines, raising concerns about potential adverse effects, particularly reproductive tract development in the male fetus. Global distribution of DEHP-contaminated and other adulterated products should prompt governments to become proactive in food safety regulations and chemical testing., (Copyright © 2013 Elsevier Ltd. All rights reserved.)