Toxic Chemical Exposure Research Articles

Environmental Health: Advancing Emancipatory Policies for the Common Good.

Human health is substantially impacted by the state of the environment, and environmental degradation has a disproportionate impact on persons with less immediate access to financial and social power. This article calls for upstream nursing action to address the natural environment in order to turn about health injustices and improve health for all. Such action would move nursing towards a greater actualization of the nursing environmental domain. The health impacts of climate change, air and water quality, and toxic chemical exposure are substantiated and specific policy leadership recommendations are proposed. Recommended actions include work to build environmental health literacy and empowerment, advocacy for regulatory protection and enforcement, and environmental engagement within health care systems.

Obesogens and Nuclear Receptors

Obesity is so common within the world’s population and prevalence has increased markedly over. And we know that toxic chemical substance exposure increased that both of obesity prevalence and formation of health problems related with obesity. Nuclear receptors that are sensors of exposure to xenobiotics. In addition recent studies have proposed a first set of obesogens that target nuclear hormone receptor signaling pathways with relevance to adipocyte biology and the developmental origins of health and disease. In this paper assesses the information about a huge puclic helath problem that is obesity and its relationship also evaluated that nuclear receptor signaling pathways of obesogens.

The environmental injustice of beauty: framing chemical exposures from beauty products as a health disparities concern

The obstetrics-gynecology community has issued a call to action to prevent toxic environmental chemical exposures and their threats to healthy human reproduction. Recent committee opinions recognize that vulnerable and underserved women may be impacted disproportionately by environmental chemical exposures and recommend that reproductive health professionals champion policies that secure environmental justice. Beauty product use is an understudied source of environmental chemical exposures. Beauty products can include reproductive and developmental toxicants such as phthalates and heavy metals; however, disclosure requirements are limited and inconsistent. Compared with white women, women of color have higher levels of beauty product-related environmental chemicals in their bodies, independent of socioeconomic status. Even small exposures to toxic chemicals during critical periods of development (such as pregnancy) can trigger adverse health consequences (such as impacts on fertility and pregnancy, neurodevelopment, and cancer). In this commentary, we seek to highlight the connections between environmental justice and beauty product-related chemical exposures. We describe racial/ethnic differences in beauty product use (such as skin lighteners, hair straighteners, and feminine hygiene products) and the potential chemical exposures and health risks that are associated with these products. We also discuss how targeted advertising can take advantage of mainstream beauty norms to influence the use of these products. Reproductive health professionals can use this information to advance environmental justice by being prepared to counsel patients who have questions about toxic environmental exposures from beauty care products and other sources. Researchers and healthcare providers can also promote health-protective policies such as improved ingredient testing and disclosure for the beauty product industry. Future clinical and public health research should consider beauty product use as a factor that may shape health inequities in women's reproductive health across the life course.

Liver and Serum miRNAs in Toxic Liver Fibrosis

Toxic chemical exposure is a risk factor for toxic liver injury in the military, chemical plant workers, and the general public. Early indicators of disease would facilitate medical and strategic decisions involving treatment, protective equipment, and/or relocation. Here, we map liver miRNA to their predicted mRNA targets in a rodent model of hepatotoxicity. We report a panel of serum miRNA that may serve as early, blood‐based indicators of toxic liver injury or fibrosis.Rats were orally administered vehicle control or the hepatotoxicant 4, 4′‐methylenedianiline (MDA; 22, 60 or 162 mg/kg) for 1 or 5 consecutive days. Serum and liver tissue were collected at necropsy, 24 hours after the last exposure. Liver sections were stained with hematoxylin and eosin for histology. Liver tissue and serum miRNA expression was determined by next‐generation sequencing for selected doses of MDA. mRNA gene expression in the liver was measured by microarray. Known and novel miRNAs were mapped to the rat genome using miRDeep2 and differential expression was determined by DESeq (FDR<0.05). mRNA changing by at least 1.5 fold were used for the target analysis using Ingenuity Pathway Analysis (IPA) software. Pathway enrichment analysis was also conducted in IPA.MDA poisoning caused moderate liver fibrosis and bile duct hyperplasia after 5 consecutive doses, as shown by histological analysis. One day after the final dosing, we identified 0, 7, and 38 differentially expressed liver miRNA at 22, 60, and 162 mg/kg, respectively. After 5 doses, 0, 126, and 127 liver miRNA were differentially expressed at 22, 60, and 162 mg/kg, respectively. Sixteen miRNAs were modulated in the serum of the rats exposed to 162 mg/kg of MDA. We also identified novel, previously undescribed differentially expressed miRNAs which may play a role in liver injury progression. We predicted mRNA targets of each differentially expressed miRNA. Pathway enrichment analysis of the predicted targets identified pathways involved in the liver fibrosis adverse outcome pathway, including inflammation, collagen accumulation, and stellate cell activation. Many of the modulated mRNAs targeted by these miRNAs have been previously associated with liver fibrosis.In conclusion, we identified liver miRNAs that may target and regulate gene expression contributing to liver fibrosis. The miRNAs in the serum may serve as prognostic indicators of disease progression.Support or Funding InformationDisclaimer: Research was conducted in compliance with the Animal Welfare Act and all other Federal requirements. The views expressed are those of the authors and do not constitute endorsement by the U.S. Army.

Oxidative Enzyme Response of Watercress (Nasturtium officinale) to Sublethal Fuel Exposure

Biomarkers such as oxidase enzyme activity from flora exposed to chemicals in the water column and sediments have been widely used by ecotoxicologists to assess the quality of an environment. Biomarkers such as oxidase enzymes are especially useful indicators because they represent a direct biological response to environmental toxicity. A luminometer was used to quantify oxidase enzyme production in watercress (Nasturtium officinale) due to toxic chemical exposure of E85 (85% ethanol and 15% gasoline blend), gasoline, and 99% pure ethanol over a 72-h period in aquatic root exposure and volatile leaf exposure experiments. Aquatic exposure to E85 caused an increase in oxidative enzyme production while gasoline and ethanol caused no significant changes in oxidase concentrations. Aquatic root exposure results were compared to volatile leaf exposures where effects of E85, gasoline, and ethanol caused increases in oxidase production. Morphometric measurements were also conducted as plant stress comparisons to oxidative enzyme analyses. Measurements of root length showed increases in root growth at some concentrations of fuels with only the highest concentration of E85 resulting in a decrease in root growth when compared to the control.

Environmental and Economic Strategies for Primary Prevention of Cancer in Early Life.

This article summarizes the evidence for environmental toxic exposures contributing to cancers in early life, focusing on the most common cancer sites in this age group. It provides examples of widespread avoidable exposures to human carcinogens through air, water, and food and then describes recent examples of successful initiatives to reduce exposure to chemicals linked to these cancer sites, through government policy, industry initiatives, and consumer activism. State government initiatives to reduce toxic chemical exposures have made important gains; the Toxics Use Reduction Act of Massachusetts is now 25 years old and has been a major success story. There are a growing number of corporate initiatives to eliminate toxics, especially carcinogens, from the products they manufacture and sell. Another important opportunity for cancer prevention is provided by online databases that list chemicals, their toxicity, and lower-toxicity alternatives; these can be used by businesses, health care institutions, consumers, and workers to reduce exposures to chemicals of concern. The article concludes by inviting pediatricians and public health professionals to include elimination of carcinogen exposures in their work to promote primary prevention of cancer in early life.

Breath biomarkers in toxicology.

Exhaled breath has joined blood and urine as a valuable resource for sampling and analyzing biomarkers in human media for assessing exposure, uptake metabolism, and elimination of toxic chemicals. This article focuses current use of exhaled gas, aerosols, and vapor in human breath, the methods for collection, and ultimately the use of the resulting data. Some advantages of breath are the noninvasive and self-administered nature of collection, the essentially inexhaustible supply, and that breath sampling does not produce potentially infectious waste such as needles, wipes, bandages, and glassware. In contrast to blood and urine, breath samples can be collected on demand in rapid succession and so allow toxicokinetic observations of uptake and elimination in any time frame. Furthermore, new technologies now allow capturing condensed breath vapor directly, or just the aerosol fraction alone, to gain access to inorganic species, lung pH, proteins and protein fragments, cellular DNA, and whole microorganisms from the pulmonary microbiome. Future applications are discussed, especially the use of isotopically labeled probes, non-targeted (discovery) analysis, cellular level toxicity testing, and ultimately assessing "crowd breath" of groups of people and the relation to dose of airborne and other environmental chemicals at the population level.

Power Failure: The Battered Legacy of Leaded Batteries

Viewpoint pubs.acs.org/est Power Failure: The Battered Legacy of Leaded Batteries Oladele A. Ogunseitan* Program in Public Health and School of Social Ecology, University of California, Irvine, California 92697, United States flow of toxic products intact. The U.S. has not ratified the Basel Convention. Rather, lead-acid batteries are regulated under the Resource Conservation and Recovery Act (RCRA) of 1976, as part of negotiations to harmonize U.S. policies with initiatives of the Organization for Economic Cooperation and Develop- ment. 4 Individual states in the U.S. stipulate either mandatory or voluntary cash deposits, typically $5−10, for used batteries returned by consumers at the point of purchase of a new lead- acid battery. The U.S. Environmental Protection Agency (EPA) considers the high “recycling” rate of lead-acid battery as evidence of successful public-private partnerships in pollution prevention policy. 4 The apparent success of the retailer take-back program masked growing concerns about pollution and health impacts created by battery recycling in developing countries, until similar problems emerged within continental U.S., exemplified by a recent case in California. In February, 2016, California Governor Jerry Brown proposed spending $176.6 million to accelerate the testing and cleanup of thousands of lead- contaminated homes surrounding the troubled Exide battery recycling facility in the Vernon district of Los Angeles, which is predominantly populated by families in the lower socio- he history of automobiles is inextricable from the story of economic category. 5 The funds will support testing 10 000 one of the most pervasive toxic chemical exposures in homes within 1.7 miles of the closed facility and the removal of modern human history. Globally, billions of people were lead-contaminated soil from about 2500 homes where levels poisoned by lead (Pb) between 1921, when General Motors pose the greatest risk of poisoning. 5 Corporation introduced tetraethyl lead as an antiknock agent in Unfortunately, the Exide-linked pollution in Los Angeles is gasoline-powered cars, until 2015, when leaded gasoline was only a “tip of the iceberg” in terms of global impacts of lead scheduled to be phased out in Algeria, the last country still poisoning from batteries. The international market for using leaded gasoline. reclaiming lead is growing rapidly, 2 and battery-recycling The elimination of lead from gasoline is one of the greatest operations can be found in almost every city in the developing milestones in public health. Regulatory policies were world. Battery smelting operations are often located in densely instrumental in achieving the phase-out of leaded gasoline, populated areas with inadequate pollution controls. Regulatory and these were informed by incontrovertible scientific evidence policies that supported high rates of battery recycling also that there are no safe levels of exposure to lead and that dampened interest in developing safer lead-free alternatives. children are particularly susceptible to its adverse health The emergence of hybrid and full electric automobiles has effects. 1 Unfortunately, lead remains a tenacious toxicant spurred the development of advanced lithium-ion batteries, but because of ubiquitous lead-acid batteries that power more these may have their own safety concerns. than a billion cars on the road today. T EMPOWERING INNOVATION California’s landmark Safer Consumer Products Law of 2013 requires manufacturers to seek safer alternatives to harmful chemical ingredients in widely used products. At the federal level, the U.S. EPA uses alternatives analysis (AA) as part of chemical action plans in its chemical management program. Similarly, the European Union’s Registration, Evaluation, Authorisation and Restriction of Chemicals (REACH) program imposes alternatives analysis obligations upon certain partic- A FAILED POLICY ON RECYCLING In 2015, ∼90% of 1.62 million tons of lead consumed in the United States was for production of >94.1 million lead-acid batteries. 2 These batteries have an international life cycle: during the first 8 months of 2015, 19.3 million spent lead-acid batteries, containing an estimated 167 000 tons of lead, 2 were exported to low- and middle income countries where they fed hazardous industries for materials recovery. Spent lead-acid batteries are recognized as hazardous waste under Annex VIII of the United Nation’s Basel Convention on the Control of Transboundary Hazardous Wastes and Their Disposal. 3 However, several loopholes keep the international © 2016 American Chemical Society Received: June 24, 2016 Published: July 28, 2016 DOI: 10.1021/acs.est.6b03174 Environ. Sci. Technol. 2016, 50, 8401−8402

Predicting Behaviors to Reduce Toxic Chemical Exposures Among New and Expectant Mothers: The Role of Distal Variables Within the Integrative Model of Behavioral Prediction.

There is a growing body of evidence linking childhood exposure to environmental toxins and a range of adverse health outcomes, including preterm birth, cognitive deficits, and cancer. Little is known, however, about what drives mothers to engage in health behaviors to reduce such risks. Guided by the integrative model of behavioral prediction, this study surveyed women who were pregnant and/or had children younger than 7 years (N = 819) to identify the factors that determine engagement in behaviors to reduce childhood exposure to toxic chemicals in the environment. Structural equation modeling pertaining to three different environmental toxins-bisphenol A, arsenic, and pesticides-demonstrated that perceived normative pressure was the primary determinant of behavior across all three models. Additionally, we identified two key distal variables-perceived risk and information seeking-that not only increased the model's predictive power but also consistently and positively predicted perceived social norms regarding exposure reduction behaviors. Findings also suggest important differences across these behaviors. Implications for health communication researchers and practitioners developing interventions, communication campaigns, and persuasive messages to promote prenatal and pediatric environmental health are discussed.

Changes in Chemical Composition, Total Phenolics and Antioxidant Activity of Alpinia (<i>Alpinia zerumbet</i>) Leaves Exposed to UV

Alpinia zerumbet (Pers.) B.L. Burtt. & R.M. Sm is an important perennial ginger plant in the tropics with various uses as foods, dietary supplement, cosmetics, essential oil production and traditional medicines. In this study, essential oils, phenolic acids, fatty acids, kavains, total phenols and antioxidant activity in A. zerumbet plants exposed to UV-C were investigated. Number and weights of essential oils increased rapidly from 1 to 3 days of exposure. Major extend of essential oils was recorded in methyl cinnamate and followed by benzyl acetone. The correspondence to the accumulation of palmitic acid was 15 folds, in contrast to the strong reduction of stearic quantity was 10 folds at 3 days of treatment. Changes in chemical components and antioxidant capacity in A. zerumbet are differed reversely between the exposure of UV-C and heavy toxic chemicals. The exposure of UV-C is beneficial for the increasing of essential oil production in A. zerumbet.

Changes in Chemical Composition, Total Phenolics and Antioxidant Activity of Alpinia (<i>Alpinia zerumbet</i>) Leaves Exposed to UV

Alpinia zerumbet (Pers.) B.L. Burtt. & R.M. Sm is an important perennial ginger plant in the tropics with various uses as foods, dietary supplement, cosmetics, essential oil production and traditional medicines. In this study, essential oils, phenolic acids, fatty acids, kavains, total phenols and antioxidant activity in A. zerumbet plants exposed to UV-C were investigated. Number and weights of essential oils increased rapidly from 1 to 3 days of exposure. Major extend of essential oils was recorded in methyl cinnamate and followed by benzyl acetone. The correspondence to the accumulation of palmitic acid was 15 folds, in contrast to the strong reduction of stearic quantity was 10 folds at 3 days of treatment. Changes in chemical components and antioxidant capacity in A. zerumbet are differed reversely between the exposure of UV-C and heavy toxic chemicals. The exposure of UV-C is beneficial for the increasing of essential oil production in A. zerumbet.

Systems toxicology of chemically induced liver and kidney injuries: histopathology-associated gene co-expression modules.

Organ injuries caused by environmental chemical exposures or use of pharmaceutical drugs pose a serious health risk that may be difficult to assess because of a lack of non‐invasive diagnostic tests. Mapping chemical injuries to organ‐specific histopathology outcomes via biomarkers will provide a foundation for designing precise and robust diagnostic tests. We identified co‐expressed genes (modules) specific to injury endpoints using the Open Toxicogenomics Project‐Genomics Assisted Toxicity Evaluation System (TG‐GATEs) – a toxicogenomics database containing organ‐specific gene expression data matched to dose‐ and time‐dependent chemical exposures and adverse histopathology assessments in Sprague–Dawley rats. We proposed a protocol for selecting gene modules associated with chemical‐induced injuries that classify 11 liver and eight kidney histopathology endpoints based on dose‐dependent activation of the identified modules. We showed that the activation of the modules for a particular chemical exposure condition, i.e., chemical‐time‐dose combination, correlated with the severity of histopathological damage in a dose‐dependent manner. Furthermore, the modules could distinguish different types of injuries caused by chemical exposures as well as determine whether the injury module activation was specific to the tissue of origin (liver and kidney). The generated modules provide a link between toxic chemical exposures, different molecular initiating events among underlying molecular pathways and resultant organ damage. Published 2016. This article is a U.S. Government work and is in the public domain in the USA. Journal of Applied Toxicology published by John Wiley & Sons, Ltd.

In silico docking of methyl isocyanate (MIC) and its hydrolytic product (1, 3-dimethylurea) shows significant interaction with DNA Methyltransferase 1 suggests cancer risk in Bhopal-Gas- Tragedy survivors.

DNA methyltransferase 1 (DNMT1) is a relatively large protein family responsible for maintenance of normal methylation, cell growth and survival in mammals. Toxic industrial chemical exposure associated methylation misregulation has been shown to have epigenetic influence. Such misregulation could effectively contribute to cancer development and progression. Methyl isocyanate (MIC) is a noxious industrial chemical used extensively in the production of carbamate pesticides. We here applied an in silico molecular docking approach to study the interaction of MIC with diverse domains of DNMT1, to predict cancer risk in the Bhopal population exposed to MIC during 1984. For the first time, we investigated the interaction of MIC and its hydrolytic product (1,3-dimethylurea) with DNMT1 interacting (such as DMAP1, RFTS, and CXXC) and catalytic (SAM, SAH, and Sinefungin) domains using computer simulations. The results of the present study showed a potential interaction of MIC and 1,3-dimethylurea with these domains. Obviously, strong binding of MIC with DNMT1 interrupting normal methylation will lead to epigenetic alterations in the exposed humans. We suggest therefore that the MIC- exposed individuals surviving after 1984 disaster have excess risk of cancer, which can be attributed to alterations in their epigenome. Our findings will help in better understanding the underlying epigenetic mechanisms in humans exposed to MIC.

Induction of thioredoxin reductase 1 by crotonaldehyde as an adaptive mechanism in human endothelial cells

Cigarette smoking is one of the main sources of toxic chemical exposure to humans and is the greatest cause of progression of vascular disease. Crotonaldehyde is one of the major constituents of cigarette smoke and a product of endogenous lipid peroxidation. Thioredoxin reductase (TrxR) is a key element of the intact thioredoxin (Trx) system, which is predominant in modulating the intracellular redox homeostasis. In this study, we showed the effects of crotonaldehyde on the induction of TrxR1 expression in human endothelial cells. Crotonaldehyde exposure caused notably increased phosphorylation of p38 mitogen-activated protein kinase (MAPK). Introduction of siRNA against nuclear factor erythroid 2-related factor 2 (Nrf2) downregulated TrxR1 expression. Furthermore, treatment with auranofin, a TrxR inhibitor, significantly increased the death rate of crotonaldehyde-exposed cells. In summary, these results suggest a role for TrxR1 upregulation through p38 MAPK-Nrf2 activation in the adaptive response of human endothelial cells to crotonaldehyde.

Sub-chronic exposure to EOMABRS leachate induces germinal epithelial cell lesions, sperm abnormalities and oxidative damage in rats

Abstract Objectives To explore the possible link between reproductive abnormalities among men and exposure of toxic chemicals in the environment. Methods The study investigated the sperm functions and the antioxidant defence system of rats exposed to leachate obtained from Elewi Odo municipal battery recycling site (EOMABRSL) via oral route. Results EOMABRSL had significant effects on both absolute and relative testicular weight. Formation of sperm abnormalities was observed following EOMABRSL exposure. Antioxidant enzymes including superoxide dismutase and catalase were significantly altered in the testes resulting into increased lipid peroxidation. Reduced glutathione (GSH) levels were found to be significantly ( P Conclusion The study concluded that possible mechanisms by which EOMABRSL at the investigated doses elicits spermatotoxicity could be linked to the testicular oxidative stress and damage to germinal epithelial cells by mixed-metal exposure. However, this may suggest possible reproductive health hazards in subjects with environmental or industrial exposure.

Endogenous nitric oxide in Pseudomonas fluorescens ZY2 as mediator against the combined exposure to zinc and cefradine.

A better understanding on the mechanism involved in bacterial resistance to combined exposure to antibiotics and heavy metals is helpful in implementing practices to mitigate their ecological risk and spread of resistance genes in microbial population. Pseudomonas fluorescens ZY2, a strain isolated from swine wastewater, was chosen to study its growth (bacterial density OD600), the formation of reactive oxygen species (ROS), nitric oxide (NO) and NO synthases (NOS) under Zn, cefradine or Zn+cefradine treatments. Using Zn and cefradine as representative heavy metal and antibiotic in this investigation, respectively, the resistance of P. fluorescens ZY2 to toxic chemical exposure was investigated. Bacterial densities of treatment groups significantly increased over the time of incubation, but less than the control. ROS, NO and NOS initially increased, but then decreased after the initial 8h of culturing, and were positively related to Zn concentrations. Moreover, the formation of ROS, NOS, and NO was activated by cefradine at Zn of up to 160mg/L, but inhibited at Zn of 200mg/L whether cefradine was added or not. Zn concentration affected ROS and NO concentrations between treatments and also was closely related to the variation of the relative bacterial density. For P. fluorescens ZY2, the mediation of endogenous NO to overcome ROS in response to the combined exposure of Zn and cefradine was suggested as a co-resistance mechanism, which would be beneficial to evaluate the ecological risk of heavy metals and antibiotics.

Water quality monitoring using abnormal tail-beat frequency of crucian carp

Fish are rapidly becoming favored as convenient sentinels for behavioral assays of toxic chemical exposure. Tail-beat frequency (TBF) of fish is highly correlated with swimming speed, which has been used to detect toxicants. Here we examined the effect on TBF of exposure to two chemicals, and evaluated the ability of this novel behavioral parameter to accurately monitor water quality. To further refine our approach, the Wall-hitting rate (WHR) was used to characterize behavioral avoidance after exposure. Overall, exposure to test chemicals at different levels induced significant increase in both behavioral parameters of the red crucian carp during 1-h exposure periods. Furthermore, the TBF achieved better performance as an indicator when it was calculated in cases where the fish hit the tank wall. Collectively, this study demonstrates the capacity of the TBF of fish to assess water quality in a reliable manner.

Health Consequences Of Benzene Exposure Among Children Following a Flaring Incident At Petroleum Refinery In Texas City

Objective Human exposure to benzene is associated with multiple adverse health effects leading to hematological malignancies. The objective of this retrospective study was to evaluate the health consequences of benzene and other toxic chemical exposure in children following a flaring incident at the British petroleum refinery in the Texas City, Texas. Methods The study included children aged < 17 years who had been exposed and unexposed to benzene due to a flaring incident at the British petroleum refinery facility. Using medical charts, clinical data including white blood cell (WBC) counts, platelets counts, hemoglobin, hematocrit, blood urea nitrogen (BUN,) creatinine, alkaline phosphatase (ALP), aspartate amino transferase (AST), alanine amino transferase (ALT), and somatic symptom complaints by the children exposed to benzene were reviewed and analyzed. Results A total of 312 subjects (benzene exposed, n=157 and unexposed, n=155) were included. Hematologic analysis showed that WBC counts were significantly decreased in benzene exposed children compared with the unexposed children (6.8 ± 2.1 versus 7.3 ± 1.7, P=0.022). Conversely, platelet (X 103 per µL) counts were increased significantly in the benzene exposed group compared with the unexposed group (278.4 ± 59.9 versus 261.6 ± 51.7, P=0.005). Similarly, benzene exposed children had significantly higher levels of ALP (183.7± 95.6 versus 165 ± 70.3 IU/L, P=0.04), AST (23.6 ± 15.3versus 20.5 ± 5.5 IU/L, P = 0.015), and ALT (19.2 ± 7.8 versus 16.9 ± 6.9 IU/L, P=0.005) compared with the unexposed children. Conclusion Together, the results of the study reveal that children exposed to benzene experienced significantly altered blood profiles, liver enzymes and somatic symptoms indicating that children exposed to benzene are at a higher risk of developing hepatic or blood related disorders. Disclosures: No relevant conflicts of interest to declare.

Protecting children from toxic chemicals: Putting it on Australia’s public health agenda

The high volume and widespread use of industrial chemicals, the backlog of internationally untested chemicals, the uptake of synthetic chemicals found in babies in utero, cord blood, and in breast milk, and the lack of a unified and comprehensive regulatory framework all necessitate developing policies that protect the most vulnerable in our society - our children. Australia's failure to do so raises profound intergenerational ethical issues. This article tells a story of international policy, and where Australia is falling down. It demonstrates that we can learn from countries already taking critical steps to reduce the toxic chemical exposure, and that the development of a comprehensive, child-centered chemical regulation framework is central to turning around Australia's failure.

Review: Sacrifice Zones

Author(s): Little, Peter C. | Abstract: Book Review: Sacrifice Zones: The front lines of tocix chemical toxic chemical exposure in the United States