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The experience of poverty embodies complex, multidimensional stressors that may adversely affect physiological and psychological domains of functioning. Compounded by racial/ethnic discrimination, the financial aspect of family poverty typically coincides with additional social and physical environmental risks such as pollution exposure, housing burden, elevated neighborhood unemployment, and lower neighborhood education levels. In this study, we investigated the associations of multidimensional social disadvantage throughout adolescence with autonomic nervous system (ANS) functioning at 17 years. Two hundred and twenty nine low-income Mexican-American adolescents (48.6% female) and their parents were assessed annually between the ages of 10 and 16. Participants' census tracts were matched with corresponding annual administrative data of neighborhood housing burden, education, unemployment, drinking water quality, and fine particulate matter. We combined measures of adolescents' electrodermal response and respiratory sinuses arrhythmia at rest and during a social exclusion challenge (Cyberball) to use as ANS indices of sympathetic and parasympathetic activity, respectively. Controlling for family income-to-needs, youth exposed to greater cumulative water and air pollution from ages 10-16 displayed altered patterns of autonomic functioning at rest and during the social challenge. Conversely, youth living in areas with higher housing burden displayed healthy patterns of autonomic functioning. Altogether, results suggest that toxin exposure in youths' physical environments disrupts the ANS, representing a plausible mechanism by which pollutants and social disadvantage influence later physical and mental health.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancer types with a limited overall survival rate due to the asymptomatic progression of symptoms in metastatic stages of the malignancy and the lack of an early reliable diagnostic biomarker. MicroRNAs (miRs/miRNAs) are small (~18–24 nucleotides), endogenous, non-coding RNAs, which are closely linked to the development of numerous malignancies comprising PDAC. Recent studies have described the role of environmental pollutants such as nickel (Ni) in PDAC, but the mechanisms of Ni-mediated toxicity in cancer are still not completely understood. Specifically, Ni has been found to alter the expression and function of miRs in several malignancies, leading to changes in target gene expression. In this study, we found that levels of Ni were significantly higher in cancerous tissue, thus implicating Ni in pancreatic carcinogenesis. Hence, in vitro studies followed by using both normal and pancreatic tumor cell lines and increasing Ni concentration increased lethality. Comparing LC50 values, Ni-acetate groups demonstrated lower values needed than in NiCl2 groups, suggesting greater Ni-acetate. Panc-10.05 cell line appeared the most sensitive to Ni compounds. Exposure to Ni-acetate resulted in an increased phospho-AKT, and decreased FOXO1 expression in Panc-10.05 cells, while NiCl2 also increased PTEN expression in Panc-10.05 cells. Specifically, following NiCl2 exposure to PDAC cells, the expression levels of miR-221 and miR-155 were significantly upregulated, while the expression levels of miR-126 were significantly decreased. Hence, our study has suggested pilot insights to indicate that the environmental pollutant Ni plays an important role in the progression of PDAC by promoting an association between miRs and Ni exposure during PDAC pathogenesis.

Deoxynivalenol (DON) is a prevalent Fusarium mycotoxin, occurs predominantly in the global environment, especially in cereals, animal feed and food commodities. The widespread contamination causes a serious risk to human and animal health. DON usually impairs weight gain, which is presumably from its capacity to reduce feed intake by interfering with intestinal motility. To clarify the role of smooth muscle cells (SMCs) contractility intestinal motility and growth inhibition caused by DON, twelve weaned piglets were firstly divided into two groups to feed control or Fusarium mycotoxin-contaminated (MC) diet. Results showed that the final body weight, average daily gain and average daily feed intake were significantly reduced in piglets fed the MC diet. Exposure to the MC diet also significantly decreased the thickness of smooth muscle layer and SMCs contractile markers expression (myosin heavy chain 11, smooth muscle actin gamma 2, transgelin, calponin 1) in jejunum and ileum of piglets. Furthermore, oral DON supplementation (3 mg/kg body weight) to mice in six consecutive days could significantly inhibit the upper intestinal transit, impede normal defecation and downregulate SMCs contractile markers expression in small intestine. Finally, we generated a porcine enteric smooth muscle cell line (PISMC), and found that DON could depress its contractility by decreasing PISMC proliferation, migration and contractile markers expression. In conclusion, these findings in vivo and in vitro suggest that DON, as a common environmental toxin, can not only reduce proliferative and motile phenotype, but also decrease contractile apparatus components (contractile markers expression) in SMCs, which in turn influences SMCs contractility and then interferes with intestinal motility and growth performance. Jiangsu Modern Agricultural (Live Pig) Industry Technology System, China [JATS [2020] 412]; Science and Technology Innovation Team Project of Anhui Academy of Agricultural Sciences, China [2021YL027]; China Scholarship Council, ChinaChina Scholarship Council Published version This study was supported by a grant from the Jiangsu Modern Agricultural (Live Pig) Industry Technology System, China (JATS [2020] 412), and Science and Technology Innovation Team Project of Anhui Academy of Agricultural Sciences, China (2021YL027). The authors also would like to thank the China Scholarship Council, China that offered Xu Ji a scholarship for his studying at Virginia Tech as a visiting scholar.

The developing nervous system is remarkably sensitive to environmental signals, including disruptive toxins, such as polybrominated diphenyl ethers (PBDEs). PBDEs are an environmentally pervasive class of brominated flame retardants whose neurodevelopmental toxicity mechanisms remain largely unclear. Using dissociated cortical neurons from embryonic Rattus norvegicus, we found here that chronic exposure to 6-OH–BDE-47, one of the most prevalent hydroxylated PBDE metabolites, suppresses both spontaneous and evoked neuronal electrical activity. On the basis of our previous work on mitogen-activated protein kinase (MAPK)/extracellular signal-related kinase (ERK) (MEK) biology and our observation that 6-OH–BDE-47 is structurally similar to kinase inhibitors, we hypothesized that certain hydroxylated PBDEs mediate neurotoxicity, at least in part, by impairing the MEK–ERK axis of MAPK signal transduction. We tested this hypothesis on three experimental platforms: 1) in silico, where modeling ligand–protein docking suggested that 6-OH–BDE-47 is a promiscuous ATP-competitive kinase inhibitor; 2) in vitro in dissociated neurons, where 6-OH–BDE-47 and another specific hydroxylated BDE metabolite similarly impaired phosphorylation of MEK/ERK1/2 and activity-induced transcription of a neuronal immediate early gene; and 3) in vivo in Drosophila melanogaster, where developmental exposures to 6-OH–BDE-47 and a MAPK inhibitor resulted in offspring displaying similarly increased frequency of mushroom-body β–lobe midline crossing, a metric of axonal guidance. Taken together, our results support that certain ortho-hydroxylated PBDE metabolites are promiscuous kinase inhibitors and can cause disruptions of critical neurodevelopmental processes, including neuronal electrical activity, pre-synaptic functions, MEK–ERK signaling, and axonal guidance.

Background Parkinson’s disease (PD) is characterized by dopaminergic neuronal loss in the substantia nigra pars compacta and intracellular inclusions called Lewy bodies (LB). During the course of disease, misfolded α-synuclein, the major constituent of LB, spreads to different regions of the brain in a prion-like fashion, giving rise to successive non-motor and motor symptoms. Etiology is likely multifactorial, and involves interplay among aging, genetic susceptibility and environmental factors. Main body The prevalence of PD rises exponentially with age, and aging is associated with impairment of cellular pathways which increases susceptibility of dopaminergic neurons to cell death. However, the majority of those over the age of 80 do not have PD, thus other factors in addition to aging are needed to cause disease. Discovery of neurotoxins which can result in parkinsonism led to efforts in identifying environmental factors which may influence PD risk. Nevertheless, the causality of most environmental factors is not conclusively established, and alternative explanations such as reverse causality and recall bias cannot be excluded. The lack of geographic clusters and conjugal cases also go against environmental toxins as a major cause of PD. Rare mutations as well as common variants in genes such as SNCA, LRRK2 and GBA are associated with risk of PD, but Mendelian causes collectively only account for 5% of PD and common polymorphisms are associated with small increase in PD risk. Heritability of PD has been estimated to be around 30%. Thus, aging, genetics and environmental factors each alone is rarely sufficient to cause PD for most patients. Conclusion PD is a multifactorial disorder involving interplay of aging, genetics and environmental factors. This has implications on the development of appropriate animal models of PD which take all these factors into account. Common converging pathways likely include mitochondrial dysfunction, impaired autophagy, oxidative stress and neuroinflammation, which are associated with the accumulation and spread of misfolded α-synuclein and neurodegeneration. Understanding the mechanisms involved in the initiation and progression of PD may lead to potential therapeutic targets to prevent PD or modify its course.

Graphical abstract, Highlights • DON promotes PEDV entry and replication, and aggravates gut barrier injury. • CRISPR‐Cas9‐mediated LC3B knockout indicated a role of autophagy in the promotion. • p38 activation was required for the DON-enhanced autophagy in PEDV-infected cells. • Environmental toxins (eg, mycotoxins) might affect the prevalence of coronavirus., Mycotoxins are toxic metabolites produced by fungal species that commonly present in the global environment, especially in cereals and animal forages. The changing global environment may further increase the exposure to these toxins, posing a serious threat to humans and animals. Recently, coronavirus has become one of the most important pathogens threatening human and animal health. It is not clear whether environmental toxins, such as mycotoxins, will affect coronavirus infection. Given that pigs are among the animals most affected by coronavirus and highly homologous to humans, weaned piglets and IPEC-J2 cells were respectively chosen as in vivo and in vitro model to explore the impacts of deoxynivalenol (DON), the most abundant trichothecene mycotoxin in feed, on porcine epidemic diarrhea virus (PEDV) infection and the mechanisms involved. In vivo, twenty-seven piglets infected naturally with PEDV were randomly divided into three groups, receiving the basal diet containing 0, 750 and 1500 μg/kg DON, respectively. Significant increases in the diarrhea rates, gut barrier injury and PEDV proliferation of piglets’ small intestine were observed in experimental groups compared with the control. Additionally, the autophagosome-like vesicles and the autophagy-related proteins expression were also increased in experimental groups. In vitro, we observed that 0.1, 0.5 and 1.0 μM DON significantly promoted the entry and replication of PEDV in IPEC-J2 cells, along with the induction of a complete autophagy. CRISPR‐Cas9‐mediated knockout of LC3B indicated a vital role of autophagy in the promotion. Pretreatment with p38 signaling inhibitor could significantly block the induction of autophagy, indicating that DON could promote the PEDV infection by triggering p38-mediated autophagy. Our findings suggest that mycotoxin could influence the prevalence of coronavirus and provide new ideas for the prevention and control of coronavirus.

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by selective and progressive loss of dopaminergic neurons. Genetic and environmental risk factors are associated with this disease. The genetic factors are composed of approximately 20 genes, such as SNCA, parkin, PTEN-induced kinase1 (pink1), leucine-rich repeat kinase 2 (LRRK2), ATP13A2, MAPT, VPS35, and DJ-1, whereas the environmental factors consist of oxidative stress-induced toxins such as 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP), rotenone, and paraquat. The analyses of their functions and mechanisms have provided important insights into the disease process, which has demonstrated that these factors cause oxidative damage and mitochondrial dysfunction. The most invaluable studies have been performed using disease model organisms, such as mice, fruit flies, and worms. Among them, Drosophila melanogaster has emerged as an excellent model organism to study both environmental and genetic factors and provide insights to the pathways relevant for PD pathogenesis, facilitating development of therapeutic strategies. In this review, we have focused on the fly model organism to summarize recent progress, including pathogenesis, neuroprotective compounds, and newer approaches. [BMB Reports 2019; 52(4): 250-258].

Introduction: Environmental toxins, such as lead and other heavy metals, pesticides, and other compounds, represent a significant health concern within the USA and around the world. Even in the 21st century, a plethora of cities and towns in the U.S. have suffered from exposures to lead in drinking water or other heavy metals in food or the earth, while there is a high possibility of further places to suffer such exposures in the near future. Methods: We employed bioengineered 3D human liver and cardiac organoids to screen a panel of environmental toxins (lead, mercury, thallium, and glyphosate), and charted the response of the organoids to these compounds. Liver and cardiac organoids were exposed to lead (10 μM - 10 mM), mercury (200 nM - 200 μM), thallium (10 nM - 10 μM), or glyphosate (25 μM - 25 mM) for a duration of 48 hours. The impacts of toxin exposure were then assessed by LIVE/DEAD viability and cytotoxicity staining, measuring ATP activity and determining IC50 values, and determining changes in cardiac organoid beating activity. Results: As expected, all of the toxins induced toxicity in the organoids. Both ATP and LIVE/DEAD assays showed toxicity in both liver and cardiac organoids. In particular, thallium was the most toxic, with IC50 values of 13.5 μM and 1.35 μM in liver and cardiac organoids, respectively. Conversely, glyphosate was the least toxic of the four compounds, with IC50 values of 10.53 mM and 10.85 mM in liver and cardiac organoids, respectively. Additionally, toxins had a negative influence on cardiac organoid beating activity as well. Thallium resulting in the most significant decreases in beating rate, followed by mercury, then glyphosate, and finally, lead. These results suggest that the 3D organoids have significant utility to be deployed in additional toxicity screening applications, and future development of treatments to mitigate exposures. Conclusion: 3D organoids have significant utility to be deployed in additional toxicity screening applications, such as future development of treatments to mitigate exposures, drug screening, and environmental toxin detection.

Despite the benefits to the global food supply and agricultural economies, pesticides are believed to pose a threat to the health of both humans and wildlife. Chlorpyrifos (CP), a commonly used organophosphate insecticide, has poor target specificity and causes acute neurotoxicity in a wide range of species via the suppression of acetylcholinesterase. This effect is exacerbated 10- to 100-fold by chlorpyrifos oxon (CPO), a principal metabolite of CP. Since many animal-associated symbiont microorganisms are known to hydrolyze CP into CPO, we used a Drosophila melanogaster insect model to investigate the hypothesis that indigenous and probiotic bacteria could affect CP metabolism and toxicity. Antibiotic-treated and germfree D. melanogaster insects lived significantly longer than their conventionally reared counterparts when exposed to 10 μM CP. Drosophila melanogaster gut-derived Lactobacillus plantarum , but not Acetobacter indonesiensis , was shown to metabolize CP. Liquid chromatography tandem-mass spectrometry confirmed that the L. plantarum isolate preferentially metabolized CP into CPO when grown in CP-spiked culture medium. Further experiments showed that monoassociating germfree D. melanogaster with the L. plantarum isolate could reestablish a conventional-like sensitivity to CP. Interestingly, supplementation with the human probiotic Lactobacillus rhamnosus GG (a strain that binds but does not metabolize CP) significantly increased the survival of the CP-exposed germfree D. melanogaster . This suggests strain-specific differences in CP metabolism may exist among lactobacilli and emphasizes the need for further investigation. In summary, these results suggest that (i) CPO formation by the gut microbiota can have biologically relevant consequences for the host, and (ii) probiotic lactobacilli may be beneficial in reducing in vivo CP toxicity. IMPORTANCE An understudied area of research is how the microbiota (microorganisms living in/on an animal) affects the metabolism and toxic outcomes of environmental pollutants such as pesticides. This study focused specifically on how the microbial biotransformation of chlorpyrifos (CP; a common organophosphate insecticide) affected host exposure and toxicity parameters in a Drosophila melanogaster insect model. Our results demonstrate that the biotransformation of CP by the gut microbiota had biologically relevant and toxic consequences on host health and that certain probiotic lactobacilli may be beneficial in reducing CP toxicity. Since inadvertent pesticide exposure is suspected to negatively impact the health of off-target species, these findings may provide useful information for wildlife conservation and environmental sustainability planning. Furthermore, the results highlight the need to consider microbiota composition differences between beneficial and pest insects in future insecticide designs. More broadly, this study supports the use of beneficial microorganisms to modulate the microbiota-mediated biotransformation of xenobiotics.

It has been over 50 years since the first demonstration that levodopa was capable of reversing the motor dysfunction associated with Parkinson’s disease. In the intervening decades, although levodopa has remained the most effective treatment for the motor symptoms of Parkinson’s disease, it is limited by serious side effects and the fact that it provides symptomatic relief only. One of the main reasons suggested for the paucity of drug discovery for Parkinson’s disease is the lack of a relevant animal model for the disease. Parkinson’s disease is thought to be the net result of a combination of multiple risk factors encountered over a lifetime, such as genetic predisposition, exposure to pesticides and bacterial or viral infections. Therefore the overarching aim of this project was to develop a novel model of Parkinson’s disease incorporating both inflammatory and environmental exposures. This would serve to shed further light on the role of relevant inflammatory-environment interactions in Parkinson’s disease, and would also provide a novel inflammatory-environment model. In order to facilitate development of a novel inflammatory-environment model, we characterised the temporal changes that occur in the inflammatory system in neurotoxic, environmental, inflammatory and genetic models of Parkinson’s disease, with a particular focus on the pathogen-recognition Toll-like receptors (TLRs). We then went on to assess the impact of dual exposure of rats to a bacterial-like (i.e. lipopolysaccharide (LPS)) or viral-like (i.e. Poly I:C) inflammagen, followed by the environmental pesticide, rotenone. Finally, we investigated the impact of dual exposure of rats to rotenone, followed by Poly I:C or LPS. All Parkinsonian-associated toxins resulted in an increase in TLR3 and TLR4, and other inflammatory toxins, with varying temporal patterns. With the dual exposure inflammatory-environment studies we found that exposing rats to either Poly I:C or LPS followed by rotenone did not exacerbate the Parkinsonism caused by either toxin alone. In contrast, dual exposure to rotenone followed by LPS significantly exacerbated the motor dysfunction and neuroinflammation compared to that caused by either inflammagen or environmental factors alone. Overall, this research has shown that different Parkinson’s-associated challenges can induce different temporal neuroinflammatory responses, indicating the importance of the choice of toxin in preclinical Parkinson’s disease studies, and of time-point for secondary challenge administration in dual exposure studies. We have also shown that dual exposure of rats to the environmental pesticide, rotenone, and the bacterial endotoxin, LPS, induced a relevant model of Parkinson’s disease that may provide a suitable tool for testing novel neuroprotective therapies for this condition.

Chemokines play an important role in normal bone physiology and the pathophysiology of many bone diseases. The recent increased focus on the individual roles of this class of proteins in the context of bone has shown that members of the two major chemokine subfamilies—CC and CXC—support or promote the formation of new bone and the remodeling of existing bone in response to a myriad of stimuli. These chemotactic molecules are crucial in orchestrating appropriate cellular homing, osteoblastogenesis, and osteoclastogenesis during normal bone repair. Bone healing is a complex cascade of carefully regulated processes, including inflammation, progenitor cell recruitment, differentiation, and remodeling. The extensive role of chemokines in these processes and the known links between environmental contaminants and chemokine expression/activity leaves ample opportunity for disruption of bone healing by environmental factors. However, despite increased clinical awareness, the potential impact of many of these environmental factors on bone-related chemokines is still ill defined. A great deal of focus has been placed on environmental exposure to various endocrine disruptors (bisphenol A, phthalate esters, etc.), volatile organic compounds, dioxins, and heavy metals, though mainly in other tissues. Awareness of the impact of other less well-studied bone toxicants, such as fluoride, mold and fungal toxins, asbestos, and chlorine, is also reviewed. In many cases, the literature on these toxins in osteogenic models is lacking. However, research focused on their effects in other tissues and cell lines provides clues for where future resources could be best utilized. This review aims to serve as a current and exhaustive resource detailing the known links between several classes of high-interest environmental pollutants and their interaction with the chemokines relevant to bone healing.

Summary The First Emperor of China (Qin Shi Huang: 259–210 BCE) would have been interested in interstitial nephritis. He might conceivably be fascinated to know that consumption of mercury elixir, instead of giving him immortality, might have shortened his life by giving him interstitial nephritis. In the Balkan region of Eastern Europe, clustering of a peculiar interstitial nephritis is prevalent. One environmental risk contributing to Balkan endemic nephritis is aristolochic acid contamination of cooking flour, drinking water, and herbal medicine. In addition, the popular use of nonprescription Chinese weight reduction herbs and public unawareness of the consequential aristolochic acid nephropathy has become a worldwide problem. Finally, the mighty Romans of antiquity lost their empire, arguably due to lead in their wine containers, lead water pipes, and lead cooking utensils. In modern times, lead paint has become universally banned, which has resulted in a reduction of lead-induced interstitial nephritis. In recent decades, bisphenol A (BPA) has been identified as a new environmental risk. BPA is in the plastic coating of food and beverage containers to prevent corrosion. BPA is so ubiquitous that urinary BPA and proteinuria are present in a high percentage of the population. BPA-induced kidney injury and other health concerns have led certain countries to ban BPA. Now, BPA-free containers are being introduced with great fanfare by manufacturers, but safety issues on all plastic products remain. It begs the question whether “plastics” of today take the place of “lead” in ancient Rome. This is a challenging question without an answer at this point.

Congenital heart defects (CHDs) are a common birth defect of largely unknown etiology, with high fetal and neonatal mortality. A review of CHDs and environmental contaminant exposure found that meta-analyses showed only modest associations for smoking, vehicle exhaust components, disinfectant by-products and proximity to incinerators, with stronger results from the newer, larger and better quality studies masked by the typical absence of effect in older studies. Recent studies of exposure to agricultural pesticides, solvents, metals and landfill sites also showed associations. Certain contaminants have been associated with certain CHDs, with septal defects being the most common. Frequent methodological problems include failure to account for potential confounders or maternal/paternal preconception exposure, differences in diagnosing, defining and classifying CHDs, grouping of defects to increase power, grouping of contaminants with dissimilar mechanisms, exclusion of pregnancies that result in death or later life diagnosis, and the assumption that maternal residence at birth is the same as at conception. Furthermore, most studies use measurement estimates of one exposure, ignoring the many additional contaminant exposures in daily life. All these problems can distort and underestimate the true associations. Impaired methylation is a common mechanism, suggesting that supplementary folate may be protective for any birth defect.

The hypothalamic-pituitary-adrenal (HPA) axis activation and glucocorticoid responses are critical for survival from a number of bacterial, viral and toxic insults, demonstrated by the fact that removal of the HPA axis or GR blockade enhances mortality rates. Replacement with synthetic glucocorticoids reverses these effects by providing protection against lethal effects. Glucocorticoid resistance/insensitivity is a common problem in the treatment of many diseases. Much research has focused on the molecular mechanism behind this resistance, but an area that has been neglected is the role of infectious agents and toxins. We have recently shown that the anthrax lethal toxin is able to repress glucocorticoid receptor function. Data suggesting that the glucocorticoid receptor may be a target for a variety of toxins is reviewed here. These studies have important implications for glucocorticoid therapy.

Background Healthy post-pregnancy outcomes are contingent upon an informed regimen of prenatal care encouraging healthy maternal consumption habits. In this article, we describe aspects of maternal intake of food, drink, and medication in a population of predominantly Hispanic women in Southern California. Potential implications for unhealthy prenatal dietary choices are discussed. Methods The Food, Beverage, and Medication Intake Questionnaire (FBMIQ) measures common practices of maternal consumption during pregnancy. The FBMIQ was administered to English and Spanish speaking pregnant and recently pregnant (36 weeks pregnant - 8 weeks post-partum) women over the age of 18 who were receiving care from a private medical group in Downey CA. Results A total of 200 women completed the FBMIQ. Consumption habits of healthy foods and beverages, unhealthy foods, unhealthy beverages, and medication are characterized in this article. Data indicate widespread consumption of fresh fruit, meats, milk and juice and indicate most women used prenatal vitamin supplements. Studies in developmental neuroscience have shown that certain substances may cause teratogenic effects on the fetus when ingested by the mother during pregnancy. Those potentially harmful substances included in our study were Bisphenol-A (BPA), methylmercury, caffeine, alcohol and certain medications. Our results show that a proportion of the women surveyed in our study consumed BPA, methylmercury, caffeine, alcohol, and certain medications at varied levels during pregnancy. This represents an interesting finding and suggests a disconnect between scientific data and general recommendations provided to pregnant mothers by obstetricians. Conclusions The results of our study demonstrate that a proportion of pregnant women consume substances that are potentially teratogenic and may impact the health and well being of the offspring. It is important to appraise healthy and unhealthy consumption habits in order to encourage healthy practices and alleviate future effects of preventable, toxin-induced developmental issues. Prenatal advising should discourage the consumption of dangerous foods, beverages, and medications that women commonly report eating during pregnancy.

NIVA har undersøkt miljøtilstanden rundt AF Miljøbase Vats ved Raunes i Vindafjord kommune, Rogaland i 2012. Undersøkelsene omfattet bl.a. bløtbunnsfauna og analyser av miljøgifter i sedimenter, blåskjell, krabbe og fisk fra Vatsfjorden og Yrkefjorden. Miljøgifter ble også analysert i etasjemose og jord fra terrenget rundt anlegget og i vannprøver fra naturlige ferskvannstrømmer, grunnvann og utslippsvann fra bedriftens eget renseanlegg. Naturlig forekommende radioaktive stoffer ble analysert i en del av prøvematerialet. Undersøkelsene viser en generell menneskeskapt påvirkning av fjordområdet, en påvirkning som kan ha flere kilder. Miljøtilstanden varierer fra «Meget god» til «Dårlig» i de forskjellige mediene undersøkt. En del av resultatene tilsier at videre overvåking er viktig. Etasjemose viste forhøyede konsentrasjoner av metaller i avstander inntil ca 500 m fra bedriften. Fordelingsmønsteret av metallene lignet på fordelingsmønsteret tidligere funnet i oppsop fra bedriftsområdet. Påvirkningen rundt anlegget er større enn den var i 2008, men mindre enn i 2009 og 2010. Kvikksølv i noen av sedimentprøvene utenfor AF Miljøbase Vats, var noe høyere enn i 2009, men ingen av prøvene overskred øvre grense for tilstandsklasse I («Meget god») for dette metallet. Bekkene og elven igjennom anlegget inneholdt en del metaller, som kan skyldes påvirkning fra anlegget så vel som fra ustabile masser deponert utenfor anlegget. Analysene for renset utslippsvann viser ikke overskridelser av stoffer i forhold til utslippstillatelsen fra Klif, men det er spor av stoffer som man finner på Klif’s liste over prioriterte stoffer. Fortynning ved utløpet av utslippsledningen gjør at konsentrasjonen bare meter fra utløpet vil være under de som kan gi miljøeffekt. Stoffene bør analyseres videre i overvåkningsprogrammet. AF Decom Offshore

After the discovery of gammaglutamyltranspeptidase in 1950 by Hanes, the significance of its increased levels in clinical practice has mainly been focused on ethanol toxicity, and also some neoplasms and biliary tract obstruction. More recently, attention has swift to the metabolic functions of this enzyme, as a neutralizer of oxygen free radicals and as a glutathione donor to the cell. High serum levels of gamma-glutamyltranspeptidase is known to occur when oxidative stress is increased, or associated with several vascular risk factors and the insulin resistance syndrome, as an early marker of diabetes. There are also a number of drugs that induce the expression of the tissue enzyme (microsomes) with the result of high serum levels without structural damage to the liver. Because it is a ubiquitous enzyme, a very high number of causes can be involved, that may be difficult to recognize. Finally, because glutathione is necessary to conjugate a number of chemical compounds, from an epidemiological and toxicological perspective, the enzyme might be useful as a biomarker of several ambient toxins. In this review we want to emphasize the increasing clinical and diagnostic significance of this enzyme discovered half a century ago.

As an outcome of the EU FISH II project, information was produced about PCDD/F and PCB as well as PBDE levels in Baltic fish, domestic freshwater fish and farmed fish. Variations in the levels were studied by age and size of the fish as well as by species and areas. Analyses of the presence of perfluorinated compounds (PFC) and organotin compounds (OT) in muscles and liver were also carried out within the scope of the project. New data on the content of hazardous substances in fish were obtained for use in risk management. The 2009 results were compared with the results of the previous project conducted in 2002-2003. Analyses of PCDD/F and PCB levels in fish highlight the same species that have also previously been found to be susceptible to accumulation of these environmental toxins. Baltic herring, salmon and sea trout as well as river lamprey and now in this study also European flounder in Kotka area show levels of PCDD/F and PCB compounds exceeding the maximum stipulated limits. In Baltic fish, the median levels of dioxin equivalents in sprat, vendace, perch, pike, pike-perch, burbot and cod are not even half of the permitted maximum level, which is 4 pg/g of fresh weight. The comparison of the levels measured in 2002-2003 with the 2009 levels of PCDD/F and PCB as well as PBDE compounds shows that the mean levels have decreased in salmon and herring. The OT levels measured in the muscles of open sea fish were about one third lower than in the fish samples caught in 2005–2007. Dioxins and dioxin-like PCB compounds are still the worst contaminants in the Baltic Sea. The levels of PBDE, PFOS and OT were low, with a few exceptions. The Bothnian Sea and the fishing areas of Pori, Turku and Kotka took the lead in the contamination ranking, but the worst area was Vanhankaupunginlahti Bay of Helsinki, where both OT and PFOS levels give cause to recommend consumption restrictions, at least as far as large perch are concerned., FI; fi; efsafocalpoint@evira.fi

NIVA har utført en miljøundersøkelse ved og rundt AF Miljøbase Vats i Vindafjord kommune, Rogaland, på oppdrag fra AF Decom Offshore. Undersøkelsene hadde som mål å overvåke miljøsituasjonen rundt anlegget. Forurensingstilstanden er moderat til meget god for de aller fleste media og parametere som er undersøkt. Noen av resultatene indikerer at videre overvåkning er nødvendig. Dette gjelder spesielt undersøkelser av luftforurensing. Analyser av etasjemose indikerer at metallholdig støv ble spredt rundt anlegget i 2009. Det er klare indikasjoner på at AF Miljøbase Vats er forurensingskilden for disse funnene. Jordprøver langs utsiden av anlegget har også økt forurensing sammenlignet med året før, og en brønnprøve fra kaiområdet viste økt kvikksølvinnhold. Avrenning av ferskvann inneholdt noe forhøyete konsentrasjoner av tungmetaller. Disse, sammen med nitrogen, stammer trolig fra de endelige masseforflytningene i deponiområdene ovenfor anlegget og fra at disse enda ikke er tildekket og gjengrodd. Vi forventer at disse verdiene reduseres videre i 2011. Analyser av renset utslippsvann viser ingen overskridelser av stoffer det er gitt utslippstillatelse for. Vi finner imidlertid spor etter flere av Klifs prioriterte stoffer, da spesielt TBT, furaner, oktylfenol og etoksilater av nonyl- og oktylfenol over grenseverdiene som er gitt for sjøvann. Stoffene vil raskt fortynnes utenfor utløpet av utslippsledningen til under gjeldende grenseverdier for god økologisk tilstand. Vi anbefaler imidlertid at overvåkningen av de observerte stoffene videreføres. AF Decom Offshore

Introduction Adverse progression of autoimmune diseases is linked to the dysregulation of cytokines. In this regard we investigated the role of 4-nonylphenol (4-NP), as a potential contributing factor in the development of immune diseases and compared it to estrogens actions since 4-NP may work via estrogen processes. Material and methods The study made cytokine level expression changes in U937 cells by microarray technology coupled to RT PCR as a validating technique. Results It was determined that 4-NP significantly up-regulated proinflammatory cytokine expression (toll-like-receptor [TLR]-6, TLR-10, interleukin [IL]-1, IL-5, IL-6, IL-17C, IL-23A, IL-8RB, IL-receptor-associated-kinase [IRAK-2], tumor-necrosis-factor-receptor [TNFR]-5, and TNFR-10). Estrogen caused insignificant increases but the changes parralelled that of 4-NP. Simultaneously, 4-NP down-regulated the expression of anti-inflammatory cytokines (IL-4 and IL-10), while estrogen up-regulated them. Conclusions 4-Nonylphenol may initiate its toxic effects and pose a risk to autoimmunity-prone individuals by eliciting effects up to 4 times more potent than estrogen. Overall, exposure to 4-NP may contribute to autoimmune susceptibility and/or exacerbate existing autoimmune conditions by dys-regulating normal expression of cytokines.

WOS: 000261215500002 PubMed: 19032683 Air pollution is contemporarily considered to be a significant cause in impairing semen parameters. The aim of this study was to investigate possible effects of traffic pollutants, mainly the diesel exposure, on semen analysis. A total of 38 men working as toll collectors at motorways formed the study group. Simultaneously, 35 men working as office personnel constituted the control group. Factors including varicocele, chronic diseases that can affect sperm production were the exclusion criteria. No difference regarding smoking was present between the groups. Usual semen analysis according to WHO guidelines was performed. The results of semen analysis revealed decreased motility and low sperm counts in eight and seven men from the study group respectively. Besides, a man from the same group had combined abnormality of decreased motility and low sperm count. However, two men from the control group had slight motility defect and one had low sperm count. The differences regarding the abnormal sperm count and motility were significant between the groups (P = 0.002 and P = 0.003, respectively). Similarly, the ratio of sperm cells with normal morphology was significantly lower in the study group than that in the control group (P = 0.001). This observation proposes that air pollution particularly diesel exposure may have detrimental effects on sperm parameters.

Årsliste 2004 Etter en akutt forurensningsepisode i Etnevassdraget våren 2000 overvåkes innhold av miljøgifter (metaller og PAH-metabolitter) i fisk. Overvåking av miljøgifter i fisk, samt målinger i sedimenter fra innsjøer nedenfor ut-slippsstedet i 2000 og 2001 har dokumentert spredning av miljøgifter i vassdraget og forhøyete nivåer av miljøgifter i fisk. Forurensningsnivået har vært vurdert som moderat til markert. Her rapporteres resultater fra prøvetaking i 2002. Innholdet av metaller i filet av aure var lavt i hele vassdraget, og på nivå med en referansestasjon upåvirket av utslippet. Noe høyere verdier for bly og sink i fiskefilet målt i 2000-2001 var redusert i 2002. Det ble påvist to PAH-metabolitter i fiskens galle. I aure var nivået av PAH-metabolitter lavere eller likt med bakgrunnsnivået på alle stasjoner, og det synes som eksponering for PAH gjennom næringskjeden er tilbake til normalnivå. Imidlertid viste målinger på ungfisk av laks i Sørelva vesentlig høyere nivå. Dette kan indikere at PAH fortsatt er tilgjengelig i næringskjeden. Det anbefales ikke tiltak for å fjerne forurensede sedimenter, siden forurensningsnivået er moderat, og tiltak vil innebære risiko for ny spredning. Haugaland Kraft

Årsliste 2004 Etter en akutt forurensningsepisode i Etnevassdraget våren 2000 overvåkes innhold av miljøgifter (metaller og PAH-metabolitter) i fisk. Det er også tatt prøver av innsjøsediment for å kartlegge spredning av partikkelbundne miljøgifter i vassdraget. Her rapporteres resultater fra prøvetaking i 2001. Analyser av sediment fra Litledalsvatn (nedstrøms Hardelandsvatn hvor utslippet skjedde) viste tydelig økning i mengder av bly, sink og PAH-forbindelser. Forurensningsnivået for metallene vurderes som moderat, og for PAH-forbindelser som markert. Innholdet av metaller i filet av aure var lavt i hele vassdraget, men viste likevel forhøyet nivå av bly i fisk fra Hardelandsvatn og noe forhøyet nivå av sink i fisk fra Litledalsvatn og Sørelva. Sammenlignet med 2000 hadde nivået av bly sunket, mens nivået av sink hadde steget noe (på de to nederste stasjonene). Nivået av PAH-metabolitter var klart forhøyet i Hardelandsvatn, noe forhøyet i Sørelva, men likt med referansenivået i Litledalsvatn. I forhold til målinger fra 2000 var mengden PAH-metabolitter økt i Hardelandsvatn og Sørelva, og redusert i Litledalsvatn. Sjøaure fanget i Litledalsvatn hadde et noe høyere nivå av PAH-metabolitter enn stasjonær aure, men nivået var betydelig lavere enn i 2000. Haugaland Kraft

ObjectiveaaEnvironmental pollutants, especially environmental toxins (ET), may have the potential to disrupt neurodevelopmental pathways during early brain development. This study was designed to test our hypothesis that mothers with autism spectrum disorder (ASD) children would have less knowledge about ET and more chance to be exposed to ET than mothers with healthy children (MHC). MethodsaaOne hundred and six biologic mothers with ASD children (MASD) and three hundred twenty four biologic mothers with healthy children MHC were assessed using two questionnaires asking about ET. ResultsaaThe total score in response to questions related to knowledge about ET in MHC was higher than that in MASD. The possibility of exposure to ET was higher in MASD than MHC. MASD showed higher sub-scale scores in terms of exposures to canned food, plastics, waste incinerators, old electronics, microwavable food, and textiles. ConclusionaaThe current results show that reduced knowledge about ET and greater exposure to ET may be associated with autism spectrum disorder. Psychiatry Investig 2010;7:122-127 Key Wordsaa Environmental toxins, Autism spectrum disorders, Child behaviors.

Introduction: Environmental factors can play a role in the pathogenesis of Alzheimer’s disease. We present a case of the simultaneous onset of Alzheimer’s disease in two middle aged adults. Case presentation: A married couple ages 54 year and 51-year-old female cohabiting together were diagnosed with Alzheimer’s disease within the same year. The patient’s both developed cognitive decline shortly after a major renovation of their property and followed a similar disease course. The diagnosis was supported by clinical presentation and tissue pathology on autopsy. Conclusion: Environmental factors may play a role in the pathogenesis of Alzheimer’s disease. Further understanding of the disease cascade is required.