Environmental Chemicals (environmental + chemical)

Distribution by Scientific Domains

Selected Abstracts

Endocrine disruptor issues in Japan

Taisen Iguchi
ABSTRACT, Monitoring of environmental chemicals in Japan has revealed that several endocrine active chemicals are in river water, sediments, and wildlife as well as in the human umbilical cord. In 2001, risk assessments of tributyltin and nonylphenol have been conducted by the Ministry of the Environment, Japan. Risk assessments of di(2-ethylhexyl)phthalate and di-isononyl phthalate have also been performed by the Ministry of Health, Labour and Welfare using a toxicological point of view in 2001. In this review, an overview of recent progress in endocrine disruptor research in Japan will be provided. [source]

Competitive binding comparison of endocrine-disrupting compounds to recombinant androgen receptor from fathead minnow, rainbow trout, and human

Vickie S. Wilson
Abstract Typically, in vitro hazard assessments for the identification of endocrine-disrupting compounds (EDCs), including those outlined in the Endocrine Disruptor Screening and Testing Advisory Committee (EDSTAC) Tier 1 Screening protocols, utilize mammalian receptors. Evidence, however, exists that fish sex steroid hormone receptors differ from mammalian receptors both structurally and in their binding affinities for some steroids and environmental chemicals. Most of the binding studies to date have been conducted using cytosolic preparations from various tissues. In the present study, we compare competitive binding of a set of compounds to full-length recombinant rainbow trout androgen receptor , (rtAR), fathead minnow androgen receptor (fhAR), and human androgen receptor (hAR), each expressed in COS cells. Saturation binding and subsequent Scatchard analysis using [3H]R1881, a high-affinity synthetic androgen, revealed an equilibrium dissociation constant (Kd) of 0.11 nM for the rtAR, 1.8 nM for the fhAR, and 0.84 nM for the hAR. Compounds, including endogenous and synthetic steroids, known mammalian antiandrogens, and environmental compounds, were tested for competitive binding to each of the three receptors. Overall, agreement existed across receptors as to binding versus nonbinding for all compounds tested in this study. Minor differences, however, were found in the relative order of binding of the compounds to the individual receptors. Studies such as these will facilitate the identification of EDCs that may differentially affect specific species and aid in the development and support of future risk assessment protocols. [source]

Development of a daphnia magna DNA microarray for evaluating the toxicity of environmental chemicals

Hajime Watanabe
Abstract Toxic chemical contaminants have a variety of detrimental effects on various species, and the impact of pollutants on ecosystems has become an urgent issue. However, the majority of studies regarding the effects of chemical contaminants have focused on vertebrates. Among aquatic organisms, Daphnia magna has been used extensively to evaluate organism- and populationlevel responses of invertebrates to pollutants in acute toxicity or reproductive toxicity tests. Although these types of tests can provide information concerning hazardous concentrations of chemicals, they provide no information about their mode of action. Recent advances in molecular genetic techniques have provided tools to better understand the responses of aquatic organisms to pollutants. In the present study, we adapted some of the techniques of molecular genetics to develop new tools, which form the basis for an ecotoxicogenomic assessment of D. magna. Based on a Daphnia expressed sequence tag database, we developed an oligonucleotide-based DNA microarray with high reproducibility. The DNA microarray was used to evaluate gene expression profiles of neonatal daphnids exposed to several different chemicals: Copper sulfate, hydrogen peroxide, pentachlorophenol, or ,-naphthoflavone. Exposure to these chemicals resulted in characteristic patterns of gene expression that were chemical-specific, indicating that the Daphnia DNA microarray can be used for classification of toxic chemicals and for development of a mechanistic understanding of chemical toxicity on a common freshwater organism. [source]

Differential binding of endogenous steroids and chemicals to androgen receptors in rainbow trout and goldfish

Kelly Wells
Abstract Androgen receptors (ARs) from fish were characterized in order to evaluate differences in the binding affinities of steroids and environmental chemicals between mammals and fish, among species offish, and among target tissues within a species of fish. High-affinity, low-capacity ARs were identified in cytosolic fractions of rainbow trout brains (Oncorhynchus mykiss) and the brains, ovaries, and testes of goldfish (Carassius auratus) using [3H]testosterone. The binding specificities of endogenous steroids to the ARs did not differ between goldfish tissues but did differ between goldfish and rainbow trout. Interspecies differences in binding specificities were also seen using cyproterone acetate, which bound to the ARs in the goldfish tissues, but not in the rainbow trout brains. The mammalian antiandrogens flutamide, vinclozolin and its metabolites 2-(((3,5)-dichlorophenyl-carbamo-yl)oxy)-2-methyl-3-butenoic acid and 3,,5,-dichloro-2-hydroxy-2-methylbut-3-enanilide, along with procymidone did not bind to the ARs in any of the fish tissues tested. However, other mammalian antiandrogens including methoxychlor and its metabolite 2,2-bis(p -hydroxyphenyl)-1,1,1-trichloroethane, o,p,-DDT, o,p,-dichlorodiphenyldichloroethylene (DDE) and p,p,-DDE did bind to the fish ARs, but only in the goldfish testes, demonstrating tissue differences in AR binding specificities of environmental chemicals. These results may be due to the presence of multiple AR isoforms in the different fish species and tissues. This study supports the growing evidence of species differences in the potency and actions of endocrine-disrupting chemicals and suggests that multiple species need to be tested when screening the receptor binding ability of potential endocrine-disrupting chemicals. [source]

Data analysis of environmental air pollutant monitoring systems in Europe

Kristina Voigt
Abstract Public access to information about the environment is being strengthened across Europe. The concept of public's right to information gives the basis for the access to environmental information. In this paper the quality of air pollutant monitoring systems in the 15 European member states is analyzed. For pragmatic reasons only the capitals are looked upon. Comprehensive data on environmental monitoring programs concerning air pollutants like ozone (O3), nitrogen dioxide (NO2), nitrogen oxide (NO), carbon dioxide (CO2) and carbon monoxide (CO), and sometimes suspended dust, benzene and other environmental chemicals are available on the free Internet. As different monitoring information systems exist in the European member states a comparison of these systems with their pros and cons is of great interest to the public. Environmental air pollutant monitoring systems in the capitals of the 15 EEC member countries (objects) are evaluated by applying 5 evaluation criteria for the differentiation of these systems. The scores run from 0,=,insufficient, 1,=,medium, to 2,=,excellent. Different data-analysis methods will be applied. As order theory is still not sufficiently presented in the scientific literature, a short overview about the so-called Hasse diagram technique and POSAC method is outlined. In several steps the data-matrix is analyzed coming to the conclusion that all methods (additionally PCA is used) identify one criterion as specifically important. Not unexpected, each method has its own advantage. The aim of this data-analysis is the evaluation of the publicly available air quality monitoring systems in Europe with their pros and cons. This might help the interested public to find and understand the information given on the Internet. Furthermore our evaluation approach might give some recommendations for an improvement of the air quality monitoring systems. Copyright 2004 John Wiley & Sons, Ltd. [source]

Chemical and Physical Sensing by Organic Field-Effect Transistors and Related Devices

Takao Someya
Abstract Organic semiconductor films are susceptible to noncovalent interactions, trapping and doping, photoexcitation, and dimensional deformation. While these effects can be detrimental to the performance of conventional circuits, they can be harnessed, especially in field-effect architectures, to detect chemical and physical stimuli. This Review summarizes recent advances in the use of organic electronic materials for the detection of environmental chemicals, pressure, and light. The material features that are responsible for the transduction of the input signals to electronic information are discussed in detail. [source]

The ,oestrogen hypothesis', where do we stand now?,

Richard M. Sharpe
Summary The original ,oestrogen hypothesis' postulated that the apparent increase in human male reproductive developmental disorders (testis cancer, cryptorchidism, hypospadias, low sperm counts) might have occurred because of increased oestrogen exposure of the human foetus/neonate; five potential routes of exposure were considered. This review revisits this hypothesis in the light of the data to have emerged since 1993. It addresses whether there is a secular increasing trend in the listed disorders and highlights the limitations of available data and how these are being addressed. It considers whether new data has emerged to support the suggestion that increased oestrogen exposure could cause these abnormalities and reviews new data on potential routes via which such increased exposure could have occurred. Secular trends: The disorders listed above are now considered to represent a syndrome of disorders (testicular dysgenesis syndrome, TDS) with a common origin in foetal life. Testicular cancer has increased in incidence in Caucasian men worldwide and lifetime risk is 0.3,0.8%. Secular trends in cryptorchidism are unclear but it is by far the commonest (2,4% at birth) congenital abnormality in either sex. Secular trends for hypospadias are not robust, although most studies suggest a progressive increase; registry data probably under-estimates incidence, but based on this data hypospadias is the second most common (0.3,0.7% at birth) congenital malformation. Retrospective analyses of sperm count data show a global downward trend but this is inconclusive , prospective studies using standardized methodology show significant differences between countries and very low sperm counts in the youngest cohort of men. For all disorders, other then testis cancer, standardized prospective studies are the best way forward and are in progress across Europe. Oestrogen effects: Evidence that foetal exposure to oestrogens can induce the above disorders has strengthened. New pathways via which such changes could be induced have been identified, including suppression of testosterone production by the foetal testis, suppression of androgen receptor expression and suppression of insulin-like factor-3 (InsL3) production by foetal Leydig cells. Other evidence suggests that the balance between androgen and oestrogen action may be important in induction of reproductive tract abnormalities. Oestrogen exposure: Although many new environmental oestrogens have been identified, their uniformly weak oestrogenicity excludes the possibility that they could induce the above disorders. However, emerging data implicates various environmental chemicals in being able to alter endogenous levels of androgens (certain phthalates) and oestrogens (polychlorinated biphenyls, polyhalogenated hydrocarbons), and the former have been shown to induce a similar collection of disorders to TDS. Other mechanisms via which increased fetal exposure to pregnancy oestrogens might occur (increasing trend in obesity, dietary changes) are also discussed. [source]

The joint effects of larval density and 14C-cypermethrin on the life history and population growth rate of the midge Chironomus riparius

Helen L. Hooper
Summary 1Chemical effects on organisms are typically assessed using individual-level endpoints or sometimes population growth rate (PGR), but such measurements are generally made at low population densities. In contrast most natural populations are subject to density dependence and fluctuate around the environmental carrying capacity as a result of individual competition for resources. As ecotoxicology aims to make reliable population projections of chemical impacts in the field, an understanding of how high-density or resource-limited populations respond to environmental chemicals is essential. 2Our objective was to determine the joint effects of population density and chemical stress on the life history and PGR of an important ecotoxicological indicator species, Chironomus riparius, under controlled laboratory conditions. Populations were fed the same ration but initiated at different densities and exposed to a solvent control and three concentrations of 14C-cypermethrin in a sediment,water test system for 67 days at 20 1 C. 3Density had a negative effect on all the measured life-history traits, and PGR declined with increasing density in the controls. Exposure to 14C-cypermethrin had a direct negative effect on juvenile survival, presumably within the first 24 h because the chemical rapidly dissipated from the water column. Reductions in the initial larval densities resulted in an increase in the available resources for the survivors. Subsequently, exposed populations emerged sooner and started producing offspring earlier than the controls. 14C-cypermethrin had no effect on estimated fecundity and adult body weight but interacted with density to reduce the time to first emergence and first reproduction. As a result, PGR increased with cypermethrin concentration when populations were initiated at high densities. 4Synthesis and applications. The results showed that the effects of 14C-cypermethrin were buffered at high density, so that the joint effects of density and chemical stress on PGR were less than additive. Low levels of chemical stressors may increase carrying capacity by reducing juvenile competition for resources. More and perhaps fitter adults may be produced, similar to the effects of predators and culling; however, toxicant exposure may result in survivors that are less tolerant to changing conditions. If less than additive effects are typical in the field, standard regulatory tests carried out at low density may overestimate the effects of environmental chemicals. Further studies over a wide range of chemical stressors and organisms with contrasting life histories are needed to make general recommendations. [source]

Adrenal toxicology: a strategy for assessment of functional toxicity to the adrenal cortex and steroidogenesis

Philip W. Harvey
Abstract The adrenal is the most common toxicological target organ in the endocrine system in vivo and yet it is neglected in regulatory endocrine disruption screening and testing. There has been a recent marked increase in interest in adrenal toxicity, but there are no standardised approaches for assessment. Consequently, a strategy is proposed to evaluate adrenocortical toxicity. Human adrenal conditions are reviewed and adrenocortical suppression, known to have been iatrogenically induced leading to Addisonian crisis and death, is identified as the toxicological hazard of most concern. The consequences of inhibition of key steroidogenic enzymes and the possible toxicological modulation of other adrenal conditions are also highlighted. The proposed strategy involves an in vivo rodent adrenal competency test based on ACTH challenge to specifically examine adrenocortical suppression. The H295R human adrenocortical carcinoma cell line is also proposed to identify molecular targets, and is useful for measuring steroids, enzymes or gene expression. Hypothalamo-pituitary-adrenal endocrinology relevant to rodent and human toxicology is reviewed (with an emphasis on multi-endocrine axis effects on the adrenal and also how the adrenal affects a variety of other hormones) and the endocrinology of the H295R cell line is also described. Chemicals known to induce adrenocortical toxicity are reviewed and over 60 examples of compounds and their confirmed steroidogenic targets are presented, with much of this work published very recently using H295R cell systems. In proposing a strategy for adrenocortical toxicity assessment, the outlined techniques will provide hazard assessment data but it will be regulatory agencies that must consider the significance of such data in risk extrapolation models. The cases of etomindate and aminoglutethimide induced adrenal suppression are clearly documented examples of iatrogenic adrenal toxicity in humans. Environmentally, sentinel species, such as fish, have also shown evidence of adrenal endocrine disruption attributed to exposure to chemicals. The extent of human sub-clinical adrenal effects from environmental chemical exposures is unknown, and the extent to which environmental chemicals may act as a contributory factor to human adrenal conditions following chronic low-level exposures will remain unknown unless purposefully studied. Copyright 2007 John Wiley & Sons, Ltd. [source]

Ecotoxicity testing of chemicals with particular reference to pesticides

Colin H Walker
Abstract Ecotoxicity tests are performed on vertebrates and invertebrates for the environmental risk assessment of pesticides and other chemicals and for a variety of ecotoxicological studies in the laboratory and in the field. Existing practices and strategies in ecotoxicity testing are reviewed, including an account of current requirements of the European Commission for the testing of pesticides and the recent REACH (Registration, Evaluation, Authorisation and Restrictions of Chemicals) proposals for industrial chemicals. Criticisms of existing practices have been made on both scientific and ethical grounds, and these are considered before dealing with the question of possible alternative methods and strategies both for environmental risk assessment and for ecotoxicological studies more generally. New approaches from an ecological point of view are compared with recent developments in laboratory-based methods such as toxicity tests, biomarker assays and bioassays. With regard to the development of new strategies for risk assessment, it is suggested that full consideration should be given to the findings of earlier long-term studies of pollution, which identified mechanisms of action by which environmental chemicals can cause natural populations to decline. Neurotoxicity and endocrine disruption are two cases in point, and biomarker assays for them could have an important role in testing new chemicals suspected of having these properties. In a concluding discussion, possible ways of improving testing protocols are discussed, having regard for current issues in the field of environmental risk assessment as exemplified by the debate over the REACH proposals. The importance of flexibility and the roles of ecologists and ecotoxicologists are stressed in the context of environmental risk assessment. Copyright 2006 Society of Chemical Industry [source]

Method for the elucidation of the elemental composition of low molecular mass chemicals using exact masses of product ions and neutral losses: application to environmental chemicals measured by liquid chromatography with hybrid quadrupole/time-of-flight mass spectrometry

Shigeru Suzuki
A method for elucidating the elemental compositions of low molecular weight chemicals, based primarily on mass measurements made using liquid chromatography (LC) with time-of-flight mass spectrometry (TOFMS) and quadrupole/time-of-flight mass spectrometry (LC/QTOFMS), was developed and tested for 113 chemicals of environmental interest with molecular masses up to ,400,Da. As the algorithm incorporating the method is not affected by differences in the instrument used, or by the ionization method and other ionization conditions, the method is useful not only for LC/TOFMS, but also for all kinds of mass spectra measured with higher accuracy and precision (uncertainties of a few mDa) employing all ionization methods and on-line separation techniques. The method involves calculating candidate compositions for intact ionized molecules (ionized forms of the sample molecule that have lost or gained no more than a proton, i.e., [M+H]+ or [M,H],) as well as for fragment ions and corresponding neutral losses, and eliminating those atomic compositions for the molecules that are inconsistent with the corresponding candidate compositions of fragment ions and neutral losses. Candidate compositions were calculated for the measured masses of the intact ionized molecules and of the fragment ions and corresponding neutral losses, using mass uncertainties of 2 and 5,mDa, respectively. Compositions proposed for the ionized molecule that did not correspond to the sum of the compositions of a candidate fragment ion and its corresponding neutral loss were discarded. One, 2,5, 6,10, 11,20, and >20 candidate compositions were found for 65%, 39%, 1%, 1%, and 0%, respectively, for the 124 ionized molecules formed from the 113 chemicals tested (both positive and negative ions were obtained from 11 of the chemicals). However, no candidate composition was found for 2% of the test cases (i.e., 3 chemicals), for each of which the measured mass of one of the product ions was in error by 5,6.7,mDa. Copyright 2005 John Wiley & Sons, Ltd. [source]

Microarray analysis of murine limb bud ectoderm and mesoderm after exposure to cadmium or acetazolamide

Claire M. Schreiner
Abstract BACKGROUND: A variety of drugs, environmental chemicals, and physical agents induce a common limb malformation in the offspring of pregnant mice exposed on day 9 of gestation. This malformation, postaxial, right-sided forelimb ectrodactyly, is thought to arise via an alteration of hedgehog signaling. METHODS: We have studied two of these teratogens, acetazolamide and cadmium, using the technique of microarray analysis of limb bud ectoderm and mesoderm to search for changes in gene expression that could indicate a common pathway to postaxial limb reduction. RESULTS: Results indicated a generalized up-regulation of gene expression after exposure to acetazolamide but a generalized down-regulation due to cadmium exposure. An intriguing observation was a cadmium-induced reduction of Mt1 and Mt2 expression in the limb bud mesoderm indicating a lowering of embryonic zinc. CONCLUSIONS: We propose that these two teratogens and others (valproic acid and ethanol) lower sonic hedgehog signaling by perturbation of zinc function in the sonic hedgehog protein. Birth Defects Research (Part A), 2009. 2009 Wiley-Liss, Inc. [source]

Molecular epidemiology of hypospadias: Review of genetic and environmental risk factors

Jeanne M. Manson
Hypospadias is one of the most common congenital anomalies in the United States, occurring in approximately 1 in 125 live male births. It is characterized by altered development of the urethra, foreskin, and ventral surface of the penis. In this review, the embryology, epidemiology, risk factors, genetic predisposition, and likely candidate genes for hypospadias are described. Recent reports have identified increases in the birth prevalence of mild and severe forms of hypospadias in the United States from the 1960s to the present. Studies in consanguineous families and small case series have identified allelic variants in genes controlling androgen action and metabolism that cause hypospadias, but the relevance of these findings to the general population is unknown. Concern has also focused on whether exposure to endocrine disrupting chemicals (EDC) with antiandrogenic activity is the cause of this increase. Hypospadias is believed to have a multifactorial etiology in which allelic variants in genes controlling androgen action and metabolism predispose individuals to develop this condition. When genetic susceptibility is combined with exposure to antiandrogenic agents, a threshold is surpassed, resulting in the manifestation of this birth defect. A clear role for exposure to antiandrogenic environmental chemicals has yet to be established in the etiology of hypospadias, although results from laboratory animal models indicate that a number of environmental chemicals could be implicated. Molecular epidemiology studies that simultaneously examine the roles of allelic variants in genes controlling androgen action and metabolism, and environmental exposures are needed to elucidate the risk factors for these anomalies and the causes of the increased rate of hypospadias. Birth Defects Research (Part A), 2003. 2003 Wiley-Liss, Inc. [source]

Metabolic activation of polycyclic aromatic hydrocarbons to carcinogens by cytochromes P450 1A1 and1B1

CANCER SCIENCE, Issue 1 2004
Tsutomu Shimada
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitously distributed environmental chemicals. PAHs acquire carcinogenicity only after they have been activated by xenobiotic-metabolizing enzymes to highly reactive metabolites capable of attacking cellular DNA. Cytochrome P450 (CYP) enzymes are central to the metabolic activation of these PAHs to epoxide intermediates, which are converted with the aid of epoxide hydrolase to the ultimate carcinogens, diol-epoxides. Historically, CYP1A1 was believed to be the only enzyme that catalyzes activation of these procarcinogenic PAHs. However, recent studies have established that CYP1B1, a newly identified member of the CYP1 family, plays a very important role in the metabolic activation of PAHs. In CYP1B1 gene-knockout mice treated with 7,12-dimethyl-benz[a]anthracene and dibenzo[a, l]pyrene, decreased rates of tumor formation were observed, when compared to wild-type mice. Significantly, gene expression of CYP1A1 and 1B1 is induced by PAHs and polyhalogenated hydrocarbons such as 2,3,7,8-tetrachlorodibenzo- p -dioxin through the arylhydrocarbon receptor. Differences in the susceptibility of individuals to the adverse action of PAHs may, in part, be due to differences in the levels of expression of CYP1A1 and 1B1 and to genetic variations in the CYP1A1 and 1B1 genes. [source]