Adverse Health Effects In Animals Research Articles

104 Exposure to Environmental Pollutant GenX Chemical Modulates Innate and Adaptive Immunity Genes in Cow Neutrophils

Abstract GenX is an environmental contaminant with wide industrial use and found in drinking water. These chemicals have high bioaccumulation and cause adverse health effects in animals and humans. Previous study has shown that pre GenX perfluoroalkyl/polyfluoroalkyl substances (PFAS) and GenX affect immune cells but there is limited study on their impact on innate immune cells (neutrophils) in livestock, such as cows. This study evaluated the effect of GenX exposure on innate and adaptive immune response gene transcription in bovine neutrophils ex vivo. Whole blood was collected using Acid citrate dextrose as a coagulant from cows (n = 5). Neutrophils were isolated using differential centrifugation and hypotonic lysis of red cells. Isolated neutrophils were treated with GenX (100 ng), or untreated (control group) for hour at 37oC, 5%CO2 and 85% relative humidity. After treatment, total RNA was extracted using Trizol reagent, reverse transcribed to cDNA, and quantitative PCR was performed using the innate and adaptive immunity RT2 profiler array (Qiagen) with 84 genes. The qPCR data were analyzed using Livak’s method to calculate fold change (FC) in gene expression between GenX-treated and control neutrophils, and FC >2, (p < 0.05) was considered significant. Normalization of data was performed with GAPDH and Beta Actin as an internal control. Out of the 84 genes tested, 78 were expressed, 25 were upregulated and4 were downregulated, in response to GenX exposure. Exposure to GenX upregulated the expression of TLR8 (FC = 24.75), NOD2 (FC = 7.65), STAT1 (FC = 49.35), HLA-A (FC = 14.07), and NKB1A (FC = 16.52). Treatment with GenX decreased the expression TICAM1 (FC = -2.30), CD86 (FC = -2.27) and RAG1 (FC = -2.50). These results indicate that GenX exposure can activate and modulate the expression of innate and adaptive immune response genes in cow neutrophils. STAT1 is involved in transcriptional regulation and activation of TLR7/8 shifts neutrophil function from phagocytosis to NETosis. Thus, the mechanism of action of GenX on identified gene targets and their function and possible animal health consequences warrants further study.

Study of Impact of Mycotoxins on the Human Health

Mycotoxins are secondary metabolites produced by fungi and are capable of causing various diseases in humans and animals. They are naturally occurring chemical substances and are chemically stable which is why they pose a great threat to public health. Accumulation of mycotoxins in the food chain can cause hazardous effects in human. The gut microbiota has a bidirectional relationship with mycotoxin, being the leading cause of the development of mycotoxicosis. These fungal toxins exhibit a number of adverse health effects in animals, even at very low concentrations, and have been associated to cases of acute and chronic poisoning of humans and farm animals since historical times. Preventive measure for controlling contamination should be adopted both before and after harvest. Mycotoxin occurrence cannot be completely avoided, but a number of measures aiming at minimizing mycotoxin levels and mycotoxin exposure can be implemented at multiple points in the food and feed chains.

The Epitranscriptomic Mechanism of Metal Toxicity and Carcinogenesis.

Metals are common toxic environmental pollutants. Acute or chronic exposure to metal pollutants causes severe adverse health effects in animals and humans, such as developmental retardation, abnormal metabolism, and disorders of cardiovascular, neurologic, respiratory, reproductive, and urologic systems. Moreover, several metals (arsenic, cadmium, chromium, and nickel) are classified as potent Group I carcinogens and cause various types of cancer in humans. Although the toxicity and carcinogenicity of metal pollutants are well recognized, the underlying mechanisms have not been clearly defined. The epitranscriptome includes all kinds of chemical modifications of all forms of RNA molecules inside a cell. Recent progresses in demonstrating the reversible pattern of RNA modifications and their roles in physiology and pathogenesis represent a breakthrough in the field of RNA biology and function study. The epitranscriptomic study is now an exciting emerging field in toxicology research. While few studies have been conducted so far to determine the epitranscriptomic effects of metal pollutants, they offer novel insights for understanding the mechanisms of metal toxicity and carcinogenesis. The goal of this review is to discuss recent studies on the epitranscriptomic effects of metals and propose some thoughts for future studies in the field.

Flame Retardancy of Biobased Composites-Research Development.

Due to the thermal and fire sensitivity of polymer bio-composite materials, especially in the case of plant-based fillers applied for them, next to intensive research on the better mechanical performance of composites, it is extremely important to improve their reaction to fire. This is necessary due to the current widespread practical use of bio-based composites. The first part of this work relates to an overview of the most commonly used techniques and different approaches towards the increasing the fire resistance of petrochemical-based polymeric materials. The next few sections present commonly used methods of reducing the flammability of polymers and characterize the most frequently used compounds. It is highlighted that despite adverse health effects in animals and humans, some of mentioned fire retardants (such as halogenated organic derivatives e.g., hexabromocyclododecane, polybrominated diphenyl ether) are unfortunately also still in use, even for bio-composite materials. The most recent studies related to the development of the flame retardation of polymeric materials are then summarized. Particular attention is paid to the issue of flame retardation of bio-based polymer composites and the specifics of reducing the flammability of these materials. Strategies for retarding composites are discussed on examples of particular bio-polymers (such as: polylactide, polyhydroxyalkanoates or polyamide-11), as well as polymers obtained on the basis of natural raw materials (e.g., bio-based polyurethanes or bio-based epoxies). The advantages and disadvantages of these strategies, as well as the flame retardants used in them, are highlighted.

Perturbations in glycerophospholipid levels of PC12 cells after exposure to PCB95 based on targeted lipidomics analysis

Polychlorinated biphenyls (PCBs) are a group of organic chlorine chemicals that can induce various adverse health effects in animals and humans. The toxicology of PCBs is a significant public health concern because of their long-term presence in the environment. Among the 209 PCB congeners, PCB95 has been reported to be neurotoxic, however, there has been limited researches on evaluating whether and how PCB95 affects cellular lipids, the most abundant components of the brain. In this study, PCB95 was found to inhibit cell proliferation at concentrations of 0.1 μM, 2 μM and 10 μM for 120 h. Additionally, there may be a shift in apoptosis to necrosis at 2 μM PCB95 exposure for 24 h. However, lipid peroxidation was found not dominant for PCB95 exposure, especially at the concentrations of 0.1 μM and 2 μM. Because of playing vital roles in cell metabolism, 20 glycerophospholipids in PC12 cells were investigated after exposure to PCB95 for 120 h. The distinctions in the orthogonal projection to latent structures-discriminant analysis (OPLS-DA) models indicated that different concentrations of PCB95 leaded to aberrant glycerophospholipid metabolism. Based on the principles of t-test P-value < 0.05, variable importance at projection (VIP) value >1 and fold change >1, PC (14:0/14:0) and PC (16:0/14:0) were screened as potential biomarkers from all the target glycerophospholipids. This study is the first time that identifies the effects of PCB95 on specific glycerophospholipids in PC12 cells, and the observed changes in glycerophospholipids provides the basis for further evaluation of PCB95-induced neurotoxicity mechanisms.

Are Persistent Organic Pollutants Linked to Lipid Abnormalities, Atherosclerosis and Cardiovascular Disease? A Review.

The term persistent organic pollutants (POPs) denotes chemicals with known or suspected adverse health effects in animals or humans and with chemical properties that make them accumulate in the environment, including animals or humans. Lipid-soluble POPs, like dioxins, polychlorinated biphenyls (PCBs) and organochlorine pesticides are transported by lipoproteins and accumulate in adipose tissue. High levels of these compounds in the circulation have been associated with elevated cholesterol and triglycerides in cross-sectional studies and with an increase in mainly low-density lipoprotein cholesterol in a longitudinal study. Also, non-lipid-soluble POPs, such as perfluoroalkyl substances (PFASs) compounds have been associated with increased total cholesterol levels. Carotid artery atherosclerosis has been related to elevated levels of mainly highly chlorinated PCBs and to highly fluorinated PFASs, but in this case only in women. Both cross-sectional and prospective studies have shown dioxins, PCBs, as well as PFASs to be linked to cardiovascular disease (CVD) and mortality. In conclusion, as highlighted in this review, several lines of evidence support the view that POPs of different chemical classes could be linked to lipid abnormalities, carotid atherosclerosis and overt CVD like myocardial infarction and stroke.

Evaluation of the cytotoxic properties, gene expression profiles and secondary signalling responses of cultured cells exposed to fumonisin B1, deoxynivalenol and zearalenone mycotoxins.

Mycotoxins are toxic secondary metabolites produced by a range of fungi and are common contaminants of agricultural crops. These toxins are chemically diverse and structurally stable, enabling them to enter the food chain which can lead to numerous adverse health effects in animals and humans. Although mycotoxin exposure is associated with the development of several cancers, it has proved challenging to show a direct connection between exposure and oncogenic change. This study investigates the in vitro cytotoxicity, molecular mechanisms and secondary signalling responses associated with the exposure to three major mycotoxins, fumonisin B1 (FB1), deoxynivalenol (Don) and zearalenone (Zea). The cytotoxicity of FB1, Don and Zea were investigated in cultured HepG2 and Caco-2 cells using cell viability assays as well as flow cytometry. FB1 proved to be less cytotoxic than its counterparts, while Don and Zea demonstrated high cytotoxicity through an apoptotic mechanism. Expression profiles of 84 genes involved in mediating communication between tumour cells and the cellular mediators of inflammation as well as the innate immune system were also studied. The expression profiles associated with the different mycotoxins were further explored for functional networks, biological functions, canonical pathways, toxicological association as well as to predict network associations between the differentially expressed genes. RT-qPCR revealed the significant differential expression of 46 genes, including the expression of several genes strongly associated with cancer and aberrant inflammatory signalling, after mycotoxin exposure. Aberrant inflammatory signalling seems to be a credible contributing factor that initiates the malignant change observed in cells exposed to mycotoxins.

Polychlorinated biphenyls: New evidence from the last decade.

Millions of pounds of polychlorinated biphenyl (PCB) compounds have been produced in multiple countries for industrial applications over the last several decades. PCB exposure induces various adverse health effects in animals and humans. Environmental and occupational exposures to PCBs have been associated with liver, kidney, endocrine, and neurodevelopmental adverse effects. We have collected and reviewed animal and human data cited in the US National Library of Medicine from 2000 to 2010. In brief, our review shows new evidence, that is, in animal studies, exposure to one of the PCBs, A1221, induces a significant alteration of serum luteinizing hormone. The effects were more profound in the F2 generation, particularly with respect to fluctuations in hormones and reproductive tract tissues across the estrous cycle. Morphological analyses of brain tissue from rats exposed to A1254 confirmed the results of an earlier work which showed that the relative size of the intra- and infrapyramidal (II-P) mossy fibers was smaller than that in the controls and also reduction in growth was selective for the II-P mossy fibers. PCB exposure increased anogenital distance and prostate size but decreased epididymal weight, epididymal sperm count, and motile epididymal sperm count. No effects were observed on testicular weight or size. The epidemiological data showed an association between diabetes mellitus prevalence and elevated concentrations of PCB 153. Additionally, prenatal PCB exposure studies were associated with a smaller thymic index at birth and could adversely affect immune responses to childhood vaccinations and resistance to respiratory infections. PCB exposure was also reported to adversely affect enamel development in children in a dose-dependent manner. Because PCBs and their metabolites are potential health hazards, understanding the risk factors associated with individual PCBs, PCB mixtures, and PCB metabolites is important. PCB exposures of vulnerable populations (pregnant women, fetuses, infants, and children) are of particular concern because of heightened sensitivity during this period of brain development.

Deoxynivalenol inhibits proliferation and induces apoptosis in human umbilical vein endothelial cells.

Deoxynivalenol (DON) is a stable mycotoxins found in cereals infected by certain fungal species and causes adverse health effects in animals and human such as vomiting, diarrhea and reproductive toxicity. In this study, we investigated the toxic and apoptotic effects of DON in human umbilical vein endothelial cells (HUVECs), a good model for studying inflammation. The results show that DON significantly inhibited the viability of HUVECs. DON could also inhibit the proliferation of HUVECs through G2/M phase arrest in cell cycle progression. Moreover, oxidative stress induced by DON was indicated by observations of increased levels of reactive oxygen species (ROS). In addition, DON also causes mitochondrial damage by decreasing the mitochondrial membrane potential and inducing apoptosis by up-regulation of apoptosis-related genes like caspase-3, caspase-9, and Bax genes, and down-regulation of Bcl-2 gene. These results together suggest that DON could induce cell cycle arrest, oxidative stress, and apoptosis in HUVECs.

Alkylphenol ethoxylates and brominated flame retardants in water, fish (carp) and sediment samples from the Vaal River, South Africa

Alkylphenol ethoxylates (APEs) and brominated flame retardants (BFRs) are known to be bio-accumulative, persistent, and endocrine disruptors and can cause adverse health effects in animals and humans. In this study, environmental samples were collected from sites along the Vaal River, South Africa in order to determine the concentrations of APEs and BFRs in water, sediment, and fish samples. The highest concentrations of these pollutants were observed from discharge of the Rietspruit WWTW. Measurable levels of both APEs and BFRs were observed with APEs exhibiting higher concentrations than BFRs in all the matrices. The concentrations observed for APEs and BFRs were as follows: 1.00-3.85 μg/L APEs, 0.09-0.26 μg/L PBDEs, ND- 0.14 PBBs and 0.51-1.77 μg/L HBCD for water samples; 47-63 ng/g lipid APEs, 3.24-12.4 ng/g lipid PBB, 4.63-33 ng/g lipid PBDEs and 10-13 ng/g lipid HBCD for fish; and 40-184 ng/g (wet weight (ww)) APEs, 2.93-5.9 ng/g (ww) PBB, 10-24 ng/g (ww) PBDEs, and 15-52 ng/g (ww) HBCD for sediment samples. The concentrations of APEs and BFRs in water samples were found to be in the range with the results reported in the literature while the concentration in fish and sediment were lower than the concentrations reported in other studies.

Influence of physicochemical and chemical parameters on polybrominated diphenyl ethers in selected landfill leachates, sediments and river sediments from Gauteng, South Africa.

Polybrominated diphenyl ethers (PBDEs) are known to be persistent, endocrine disruptors and bioaccumulative and can cause adverse health effects in animals and humans. In this study, river and landfill sediment samples were collected from selected rivers and municipal solid waste landfill (MSWL) sites across Gauteng Province in South Africa to determine the levels of common PBDEs (BDE-17, BDE-47, BDE-99, BDE-100, BDE-153, BDE-154, BDE-183 and BDE-209). The mean and median concentrations of Σ8 PBDEs from river sediment samples was 2.4 and 0.4 ng g(-1), respectively, and a range of 0.8-114 ng g(-1). The highest concentration of Σ8 PBDEs (43.6 ng g(-1)) was observed at Jukskei River with more than two orders of magnitude greater than the rest. The observed total PBDE concentrations in landfill sediment and leachate samples ranged from 0.8 to 8.4 ng g(-1) and 127-3,702 pg L(-1) for the two matrices. BDE-209 was predominantly detected in most of the sediment samples. Two of the MSWLs which are lined with geomembranes gave the highest concentrations of ∑7 PBDEs (2,678 and 3,702 pg L(-1)). Correlation values for ∑7 PBDEs versus Co (r = 0.65), Cu (r = 0.52), Mn (r = 0.10), Mg (r = 0.76), Ca (r = 0.66) and Ni (r = 0.77) with a statistical significance (p < 0.05) were observed except for Na, Cr, Pb, K, Fe and Zn (p > 0.05). The observed positive correlation may suggest a possible influence of trace metals on PBDE concentrations in leachates. Furthermore, a test of relationship between major anions and PBDEs yielded positive relationship with Cl(-) (r = 0.94, p = 0.16), F(-) (r = 0.97, p = 0.21), Br(-) (r = 0.6, p = 0.29) and NO3 (2-) (r = 0.96, p = 0.08) with an insignificant statistical difference. However, evaluation of the relationship between some water quality parameters (pH, dissolved oxygen and electrical conductivity) gave negative correlation with PBDE concentrations.

Influence of Mycotoxins and a Mycotoxin Adsorbing Agent on the Oral Bioavailability of Commonly Used Antibiotics in Pigs

It is recognized that mycotoxins can cause a variety of adverse health effects in animals, including altered gastrointestinal barrier function. It is the aim of the present study to determine whether mycotoxin-contaminated diets can alter the oral bioavailability of the antibiotics doxycycline and paromomycin in pigs, and whether a mycotoxin adsorbing agent included into diets interacts with those antibiotics. Experiments were conducted with pigs utilizing diets that contained blank feed, mycotoxin-contaminated feed (T-2 toxin or deoxynivalenol), mycotoxin-contaminated feed supplemented with a glucomannan mycotoxin binder, or blank feed supplemented with mycotoxin binder. Diets with T-2 toxin and binder or deoxynivalenol and binder induced increased plasma concentrations of doxycycline administered as single bolus in pigs compared to diets containing blank feed. These results suggest that complex interactions may occur between mycotoxins, mycotoxin binders, and antibiotics which could alter antibiotic bioavailability. This could have consequences for animal toxicity, withdrawal time for oral antibiotics, or public health.

Deoxynivalenol transport across the human placental barrier

Deoxynivalenol (DON) is the most commonly detected mycotoxin contaminant of cereal crops and cereal based food products in temperate regions of the world. DON causes adverse health effects in animals, passes through to the foetus and causes foetal abnormalities in animals. Biomonitoring for DON has revealed frequent human exposure. This study reports on DON transfer across the human placenta. Firstly, in vitro studies with the BeWo b30 clone were used as a rapid screening model showing transfer of DON through a stable confluent cell monolayer. Five term placentas were then used to study DON transfer with the ex vivo dual perfusion model. The concentration of DON on the foetal side after 4h was about 21% of that on the maternal side at t=0. These results support the data from the BeWo monolayer model in respect to the transport rate of DON, and are consistent with our hypothesis of foetal exposure to DON during pregnancy.

The Pharmacokinetics of BPA: Similarities in Human and Animal Metabolism Suggest Higher Exposure than Thought

Vol. 119, No. 4 NewsOpen AccessThe Pharmacokinetics of BPA: Similarities in Human and Animal Metabolism Suggest Higher Exposure than Thought Julia R. Barrett Julia R. Barrett Search for more papers by this author Published:1 April 2011https://doi.org/10.1289/ehp.119-a177aCited by:2AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit Bisphenol A (BPA) has been shown to cause adverse health effects in animals, but attempts to extrapolate human health effects from this evidence are impeded by unanswered questions about routes and levels of exposure, metabolism, and whether animal models are appropriate proxies for humans. New findings show the kinetics of BPA metabolism are very similar in humans, monkeys, and mice and also suggest greater human exposure than previously estimated [EHP119(4):422–430; Taylor et al.].BPA in food and beverage packaging likely underlies most human oral exposure, and dermal and inhalation exposure may occur from other sources. BPA has been assumed to undergo rapid metabolism (conjugation) and clearance from the body. However, recent human biomonitoring data showed serum concentrations of unconjugated BPA, the bioactive form, at levels much higher than predicted given earlier assumptions about the amount of BPA ingested by humans and its expected rate of clearance.The authors of the current study studied clearance of radiolabeled unconjugated BPA in rhesus macaques and CD-1 mice, then compared the results with those from a previous oral dosing study in women. In the first experiment, female monkeys received deuterated BPA (dBPA) at 400 μg per kg body weight once a day for a week. Blood samples were collected prior to dosing and several times on days 1 and 7. The second experiment involved an oral dose of 400 μg 3H-BPA per kg body weight to female CD-1 mice and measurements of the unconjugated compound in serum over the next 24 hours. A second group of mice received a single dose of varying amounts of 3H-BPA, with unconjugated serum levels measured 24 hours later, and a third group received a single dose of BPA at 100,000 μg/kg, with serum assessed for unconjugated BPA several times over the next 24 hours.Unconjugated dBPA concentrations in monkeys averaged 0.5 ng/mL over 24 hours and peaked at 3.94 ng/mL 1 hour after treatment. These values are comparable to medians of 0.3–4.0 ng/mL reported in human biomonitoring studies. The amount of BPA needed to achieve the serum concentrations in monkeys far exceeded the 2007 U.S. Food and Drug Administration human exposure estimate of 0.16 μg/kg/day as well as the U.S. Environmental Protection Agency’s daily intake dose of 50 μg/kg. Results from the mouse experiments showed a linear relationship between BPA dose and unconjugated BPA in serum, with the kinetics of metabolism remarkably similar to those observed in monkeys and humans.If the reported plasma BPA concentrations in humans are accurate, the results suggest human exposure is currently underestimated and that there may be significant sources of exposure though non-oral routes. Additionally, they support CD-1 mouse studies as being relevant for estimating serum levels of unconjugated BPA in humans.FiguresReferencesRelatedDetailsCited by Poet T and Hays S (2017) Extrapolation of plasma clearance to understand species differences in toxicokinetics of bisphenol A, Xenobiotica, 10.1080/00498254.2017.1379626, 48:9, (891-897), Online publication date: 2-Sep-2018. Chevrier J and Chalifour L (2018) Influence of Exposure to Bisphenols on Cardiac Structure/Function Comprehensive Toxicology, 10.1016/B978-0-12-801238-3.64270-8, (447-468), . Vol. 119, No. 4 April 2011Metrics About Article Metrics Publication History Originally published1 April 2011Published in print1 April 2011 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

PERSONAL CARE PRODUCTS: Triclosan Comes under Scrutiny

PERSONAL CARE PRODUCTS: Triclosan Comes under Scrutiny

Halogenated Flame Retardants: Do the Fire Safety Benefits Justify the Risks?

Since the 1970s, an increasing number of regulations have expanded the use of brominated and chlorinated flame retardants. Many of these chemicals are now recognized as global contaminants and are associated with adverse health effects in animals and humans, including endocrine and thyroid disruption, immunotoxicity, reproductive toxicity, cancer, and adverse effects on fetal and child development and neurologic function. Some flame retardants such as polybrominated diphenyl ethers (PBDEs) have been banned or voluntarily phased out by manufacturers because of their environmental persistence and toxicity, only to be replaced by other organohalogens of unknown toxicity. Despite restrictions on further production in some countries, consumer products previously treated with banned retardants are still in use and continue to release toxic chemicals into the environment, and the worldwide use of organohalogen retardants continues to increase. This paper examines major uses and known toxic effects of commonly-used organohalogen flame retardants, replacements for those that have been phased out, their combustion by-products, and their effectiveness at reducing fire hazard. Policy and other solutions to maintain fire safety while reducing toxicity are suggested. The major conclusions are: (1) Flammability regulations can cause greater adverse environmental and health impacts than fire safety benefits. (2) The current options for end-of-life disposal of products treated with organohalogens retardants are problematic. (3) Life-cycle analyses evaluating benefits and risks should consider the health and environmental effects of the chemicals, as well as their fire safety impacts. (4) Most fire deaths and most fire injuries result from inhaling carbon monoxide, irritant gases, and soot. The incorporation of organohalogens can increase the yield of these toxic by-products during combustion. (5) Fire-safe cigarettes, fire-safe candles, child-resistant lighters, sprinklers, and smoke detectors can prevent fires without the potential adverse effects of flame retardant chemicals. (6) Alternatives to organohalogen flame retardant chemicals include using less flammable materials, design changes, and safer chemicals. To date, before evaluating their health and environmental impacts, many flame retardant chemicals have been produced and used, resulting in high levels of human exposure. As a growing literature continues to find adverse impacts from such chemicals, a more systematic approach to their regulation is needed. Before implementing new flammability standards, decision-makers should evaluate the potential fire safety benefit versus the health and environmental impacts of the chemicals, materials, or technologies likely to be used to meet the standard. Reducing the use of toxic or untested flame retardant chemicals in consumer products can protect human and animal health and the global environment without compromising fire safety.

Risks and Benefits of Pool Chlorination, with Manolis Kogevinas

Chlorine is one of the most common disinfectants used to kill microbes in water and make it safe for humans to swim in and drink. But when chlorine and other disinfectants combine with organic matter in pools such as sweat, urine, and skin cells, the results are disinfection by-products (DBPs), which have been linked with adverse health effects in animals and humans. In this podcast, Manolis Kogevinas discusses recent research on the carcinogenic and genotoxic potential of DBPs, but he also explains why people don't necessarily need to stop swimming in pools. Kogevinas is a professor and co-director of the Centre for Research in Environmental Epidemiology in Barcelona, Spain.

Protective role of buffalo pineal proteins on arsenic-induced oxidative stress in blood and kidney of rats

Objective: Exposure to various toxic metals has become an increasingly recognized source of ill- ness in human and animals, worldwide. Arsenic (As) and its compounds cause adverse health effects in animals and humans. Recently, it has been suggested that the pineal gland may also have antioxidants role due to secretary product other than melatonin. With keeping this view, pre-sent investigation tested effect of buffalo (Bubalus bubalis) pineal proteins (PP) on arsenic-induced oxidative stress in RBCs (Red blood cells) and kidney of rats. Methods: Eighteen adult female Wistar rats were grouped into group-I (Control), group-II (Arsenic control), and group-III (Arsenic + Pineal proteins). Experimental rats were given 100 ppm arsenic (p.o.) for 4 weeks alone or along with pineal proteins at a dose of 100 µg/kg body weight (i.p.). Results: Interestingly, arsenic ex-posure led to the stimulation of kidney catalase (CAT) activity, but inhibition of RBCs CAT activ-ity and significantly (P<0.05) increased the RBCs and kidney lipid peroxidation level (LPO). How-ever, arsenic treatment caused depletion of glu- tathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GR) in kidney tissues. In RBCs, only GR and CAT activity were significantly (P<0.05) declined. These changes were significantly (P<0.05) reversed by PP treatment in arsenic exposed animals. Conclusion: Therefore, present study indicated the significant protecting effect of buf-falo (Bubalus bubalis) PP against arsenic in-duced-oxidative stress through antioxidant de-fense systems in rats.

Epidemiology, toxicokinetics, and health effects of methyltert-butyl ether (MTBE)

This paper reviews the published information assessing the kinetics and potential for adverse health effects related to exposure to the fuel oxygenate, methyl tert-butyl ether (MTBE). Data were obtained from previously published reports, using human data where possible. If human data were not available, animal studies were cited. The kinetic profile of MTBE in humans is similar for ingestion and inhalation. The concentrations of MTBE to which the general public is expected to be exposed are orders of magnitude below concentrations that have caused adverse health effects in animals. Controlled human studies have not replicated early epidemiology studies that suggested, but did not confirm, a possible association between MTBE exposure and nonspecific health complaints.

Mercury in the Environment: Effect on Health and Reproduction

Mercury is a heavy metal that is found naturally in the environment in various forms. Human activity can release mercury into the air, water, and soil. Mercury is also released into the environment after its conversion to methylmercury by bacteria. Mercury was once used in medicine, but the medicinal aspect changed because of its devastating poisoning effect on humans and animals. Today, mercury is one of the most potent neurotoxins known, having a number of adverse health effects in animals and humans. As the sources of mercury are many, the general population is exposed to mercury in day-to-day life, in occupational settings, and in cases of accidental exposure. In addition, ignorance about the use of mercury in cosmetics and religious materials has opened an additional source of exposure. Therefore, making people aware of mercury's effects on health, its sources of entry into the environment, and its chelating remedies becomes a necessity so that strategies can be adopted to minimize use and exposure.