Tampa (US), Guyana (SA), and Bolivia (SA), are geographically, socially, economically, and politically unique which make them ideal sites to study issues of mercury and sustainability. Mercury’s innate ability to bioaccumulate and biomagnify in aquatic and terrestrial ecosystems poses a severe threat to both human and environmental health. The most vulnerable populations affected by mercury consumption include coastal communities, children, women of child-bearing age, the indigenous poor and persons with high environmental/occupational exposure factors. Communities in the regions of Florida, Bolivia, and Guyana whose diets are high in fish and are environmentally/occupationally exposed to mercury may be at a higher risk of mercury intoxication, especially in the absence of education on the topic. Mercury loadings in rivers, streams, and mine tailing waters and sediments ranged from 0.9-114 ng/L and 29- 2891 ng/g, respectively; whilst fish mercury loadings were 0.02-1.034 mg/kg wet wt. Although mining sites had the highest mercury sediment and water loadings there were no significant differences when compared to pristine sites in Guyana. Fish loadings above recommended EPA/WHO regulatory limits were observed at all sites and none had signage, informational warnings or educational material available. A pilot study that included four elementary schools in Tampa showed that Water Awareness Research Education (WARE), a community based participatory environmental educational program, is a sustainable solution to addressing issues of mercury exposure.

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior / The environmental contamination by methyl mercury (MeHg) is a great health public problem in some world regions like Amazonia. The MeHg toxic effects seem to be influenced by environmental and genetic factors. However, there are few studies evaluating the genetic influence on MeHg toxicity in humans. Therefore, the aim of this present study was to evaluate the genetic influence of Ala16Val superoxide dismutase manganese dependent gene polymorphism (Ala16Val-MnSOD) on cytotoxic effects of in vitro human leucocytes exposed to MeHg. Subjects were selected from 100 individuals genotyped to Ala16Val-MnSOD polymorphism (26,4±7,3 years) with different genotpypes (AA=08, VV=06 and AV=12) to perform the in vitro tests. The reactive oxygen species (ROS) production was measured using 2� 7�-dichlorofluorescein diacetate (DCFDA) fluorimetric assay and the cell viability was measured using the MTT assay were performed in leucocyte samples with the same subjects exposed and not exposed to MeHg (2,5μM for 6h). The results showed that AA and VVleucocytes exposed to MeHg did not increase the ROS levels when compared to the cells that were not exposed. However, the AV-leucocyte MeHg exposure increased the ROS levels. The cellular viability comparison among different genotypes exposed to MeHg showed lower AAleucocyte viability when compared to VV-leucocytes, whereas heterozygous cells (AV) presented intermediary values. This occurred probabibly due to the fact of AA-leucocytes present a higher basal H2O2 production than other genotypes. The whole of these results suggests toxicogenetic effects of Ala16Val-SOD polymorphism in human cells exposed to MeHg. / A contaminação ambiental por metilmercúrio (MeHg) é uma grande problema para a saúde pública em algumas regiões do mundo, como a Amazônia. Entretanto, os seus efeitos tóxicos parecem ser influenciados tanto por fatores ambientais como genéticos. Porém ainda há poucos estudos avaliando a influencia genética em humanos expostos ao MeHg. Assim, o presente estudo buscou avaliar a influência de um polimorfismo genético presente na enzima superóxido dismutase dependente de manganês (Ala16Val-MnSOD) sobre os efeitos citotóxicos relacionados a exposição ex vivo ao MeHg em leucócitos humanos. A partir da genotipagem de 100 indivíduos (26,4±7,3 anos) foram selecionados sujeitos com diferentes genótipos (AA=08, VV=06 e AV=12) para a realização dos testes. Foi avaliada a citotoxicidade (via ensaio MTT) e a produção de radicais livres RL (via ensaio da fluorescência do DCFDA) em amostras de leucócitos, dos mesmos sujeitos, expostas e não expostas ao MeHg (2,5μM por 6h). Os resultados mostraram que leucocitos AA e VV expostos ao MeHg não aumentaram os níveis de produção de ROS quando comparados ao grupo controle. Enquanto os leucocitos AV quando expostos ao MeHg aumentaram a produção de EROs. Contudo, leucocitos-AA expostos ao MeHg apresentaram menor viabilidade quando comparados aos leucócitos dos genótipos VV e AV sob as mesmas condições. Isto ocorre provavelmente pelo ao fato do genótipo AA apresentar maior produção basal de H2O2 do que os demais genótipos. Estes resultados sugerem efeito toxicogenético na resposta de células humanas expostas ao MeHg.

The effects of Hg2+, methyl mercury, and flufenamic acid, all of which inhibit mitochondria, were examined at frog motor nerve terminals. Unbiased estimates of m (no. of transmitter quanta released), n (no. of functional release sites), p (probability of release), and vars p (spatial variance in p) were obtained using K+-induced asynchronous neurosecretion (m, n and p not having the same definitions as with nerve-evoked release). Transient but significant increases in m, n, p and vars p were found with all three agents. These findings indicate that mitochondrial inhibition and release of sequestered Ca2+ can be detected as a real-time increase in vars p. The results also suggest that changes in vars p might be used to differentiate between cellular (membrane) and subcellular (organellar) actions of drugs at the nerve terminal.

Widespread consumption of canned tuna fish since the 1950s may explain some of the increase in breast cancer prevalence in the United States and Europe. Although canned tuna is the primary source of human exposure to methylmercury, its role as an estrogen activating metalloestrogen has been overlooked in the etiology and incidence of breast cancer. Carcinogenic theory asserts that increased exposure to estrogen elevates the risk of breast cancer. The purpose of this population-based, case control study was to examine the association between canned tuna consumption, total blood mercury, and breast cancer in the NHANES 2003-2006 surveys. A multivariable logistic regression model representing 138,747,398 U.S. adult females, controlling for covariates, was applied to investigate whether canned tuna consumption or blood mercury level had a relationship to breast cancer. According to study results, women who reported eating canned tuna at one level of increased frequency out of 11 had a 6.8% increased odds of being diagnosed with breast cancer (p =0. 000 OR 1.068 and 95% CI 1.067-1.069). Women with only a 0.01 Ug/L increase in total blood mercury level were found to have a 0.2% increased odds of being diagnosed with breast cancer (p =. 000 OR 1.002 and 95% CI 1.002-1.003). Additional research individuating the canned tuna fish variable in nutrition, fish, mercury, and breast cancer studies is recommended. This research contributes to positive social change by providing evidence to improve understanding and specification of canned tuna fish in future research and better identification of methylmercury levels in canned tuna fish for public knowledge.

The contamination of seafood with methylmercury (MeHg) is a global health issue, as MeHg is a well known neurotoxin. Since dietary nutrients may interact with MeHg toxicity, and oxidative stress is one of the primary mechanisms underlying MeHg neurotoxicity, we characterized dietary antioxidant-MeHg interactions. Firstly, we used an ethnobotanical study to confirm the antioxidant activity of Northern Labrador Tea, Rhododendron tomentosum ssp. subarcticum (Tea), for the Canadian Inuit, a population with elevated MeHg exposure. Secondly, we determined the ability of Tea to ameliorate MeHg-induced toxicity in a rat perinatal exposure study. MeHg exposure (2 mg/KgBW/d) was associated with perturbed development and behaviour, elevated brain N-methyl-D-aspartate receptors, and serum lipid peroxidation. Surprisingly, Tea co-exposure (100 mg/KgBW/d) modulated MeHg’s effects on brain NMDA-R levels and lipid peroxidation, but also increased mercury serum concentrations. Thirdly, using a toxicogenomics approach we determined that MeHg exposure caused the down-regulation of Nr4a2 and its protein product Nurr1. These novel MeHg targets are implicated in developmental learning functions and were corrected with MeHg + Tea co-exposure. Lastly, we conducted a risk assessment survey and cross-sectional dietary epidemiology study in Costa Rica to further investigate dietary nutrient-MeHg interactions. Costa Rica is a Central American country with multiple sources of Hg and a high per capital fish consumption. Here, 5 of the 14 populations we studied exceeded the recommended MeHg provisional tolerable daily intake (pTDI) of 0.2 µg/KgBW/d. In Heredia the pTDI was exceeded by 34% of woman participants, primarily associated with canned tuna consumption. Interestingly, we detected that Hg body burden was significantly reduced by the consumption of antioxidant-rich dietary items. Considering our collective results, we hypothesized that MeHg toxicokinetics may be altered by dietary nutrients at the site of intestinal absorption from the disruption of gut flora, or at the site of cellular demethylation in tissues from the improvement of cellular redox state. The interaction of dietary nutrients on MeHg outcomes has a large impact on risk assessment and may provide a public health approach for managing the risk associated with MeHg exposure without reducing local fish consumption.

The contamination of seafood with methylmercury (MeHg) is a global health issue, as MeHg is a well known neurotoxin. Since dietary nutrients may interact with MeHg toxicity, and oxidative stress is one of the primary mechanisms underlying MeHg neurotoxicity, we characterized dietary antioxidant-MeHg interactions. Firstly, we used an ethnobotanical study to confirm the antioxidant activity of Northern Labrador Tea, Rhododendron tomentosum ssp. subarcticum (Tea), for the Canadian Inuit, a population with elevated MeHg exposure. Secondly, we determined the ability of Tea to ameliorate MeHg-induced toxicity in a rat perinatal exposure study. MeHg exposure (2 mg/KgBW/d) was associated with perturbed development and behaviour, elevated brain N-methyl-D-aspartate receptors, and serum lipid peroxidation. Surprisingly, Tea co-exposure (100 mg/KgBW/d) modulated MeHg’s effects on brain NMDA-R levels and lipid peroxidation, but also increased mercury serum concentrations. Thirdly, using a toxicogenomics approach we determined that MeHg exposure caused the down-regulation of Nr4a2 and its protein product Nurr1. These novel MeHg targets are implicated in developmental learning functions and were corrected with MeHg + Tea co-exposure. Lastly, we conducted a risk assessment survey and cross-sectional dietary epidemiology study in Costa Rica to further investigate dietary nutrient-MeHg interactions. Costa Rica is a Central American country with multiple sources of Hg and a high per capital fish consumption. Here, 5 of the 14 populations we studied exceeded the recommended MeHg provisional tolerable daily intake (pTDI) of 0.2 µg/KgBW/d. In Heredia the pTDI was exceeded by 34% of woman participants, primarily associated with canned tuna consumption. Interestingly, we detected that Hg body burden was significantly reduced by the consumption of antioxidant-rich dietary items. Considering our collective results, we hypothesized that MeHg toxicokinetics may be altered by dietary nutrients at the site of intestinal absorption from the disruption of gut flora, or at the site of cellular demethylation in tissues from the improvement of cellular redox state. The interaction of dietary nutrients on MeHg outcomes has a large impact on risk assessment and may provide a public health approach for managing the risk associated with MeHg exposure without reducing local fish consumption.

The contamination of seafood with methylmercury (MeHg) is a global health issue, as MeHg is a well known neurotoxin. Since dietary nutrients may interact with MeHg toxicity, and oxidative stress is one of the primary mechanisms underlying MeHg neurotoxicity, we characterized dietary antioxidant-MeHg interactions. Firstly, we used an ethnobotanical study to confirm the antioxidant activity of Northern Labrador Tea, Rhododendron tomentosum ssp. subarcticum (Tea), for the Canadian Inuit, a population with elevated MeHg exposure. Secondly, we determined the ability of Tea to ameliorate MeHg-induced toxicity in a rat perinatal exposure study. MeHg exposure (2 mg/KgBW/d) was associated with perturbed development and behaviour, elevated brain N-methyl-D-aspartate receptors, and serum lipid peroxidation. Surprisingly, Tea co-exposure (100 mg/KgBW/d) modulated MeHg’s effects on brain NMDA-R levels and lipid peroxidation, but also increased mercury serum concentrations. Thirdly, using a toxicogenomics approach we determined that MeHg exposure caused the down-regulation of Nr4a2 and its protein product Nurr1. These novel MeHg targets are implicated in developmental learning functions and were corrected with MeHg + Tea co-exposure. Lastly, we conducted a risk assessment survey and cross-sectional dietary epidemiology study in Costa Rica to further investigate dietary nutrient-MeHg interactions. Costa Rica is a Central American country with multiple sources of Hg and a high per capital fish consumption. Here, 5 of the 14 populations we studied exceeded the recommended MeHg provisional tolerable daily intake (pTDI) of 0.2 µg/KgBW/d. In Heredia the pTDI was exceeded by 34% of woman participants, primarily associated with canned tuna consumption. Interestingly, we detected that Hg body burden was significantly reduced by the consumption of antioxidant-rich dietary items. Considering our collective results, we hypothesized that MeHg toxicokinetics may be altered by dietary nutrients at the site of intestinal absorption from the disruption of gut flora, or at the site of cellular demethylation in tissues from the improvement of cellular redox state. The interaction of dietary nutrients on MeHg outcomes has a large impact on risk assessment and may provide a public health approach for managing the risk associated with MeHg exposure without reducing local fish consumption.

The contamination of seafood with methylmercury (MeHg) is a global health issue, as MeHg is a well known neurotoxin. Since dietary nutrients may interact with MeHg toxicity, and oxidative stress is one of the primary mechanisms underlying MeHg neurotoxicity, we characterized dietary antioxidant-MeHg interactions. Firstly, we used an ethnobotanical study to confirm the antioxidant activity of Northern Labrador Tea, Rhododendron tomentosum ssp. subarcticum (Tea), for the Canadian Inuit, a population with elevated MeHg exposure. Secondly, we determined the ability of Tea to ameliorate MeHg-induced toxicity in a rat perinatal exposure study. MeHg exposure (2 mg/KgBW/d) was associated with perturbed development and behaviour, elevated brain N-methyl-D-aspartate receptors, and serum lipid peroxidation. Surprisingly, Tea co-exposure (100 mg/KgBW/d) modulated MeHg’s effects on brain NMDA-R levels and lipid peroxidation, but also increased mercury serum concentrations. Thirdly, using a toxicogenomics approach we determined that MeHg exposure caused the down-regulation of Nr4a2 and its protein product Nurr1. These novel MeHg targets are implicated in developmental learning functions and were corrected with MeHg + Tea co-exposure. Lastly, we conducted a risk assessment survey and cross-sectional dietary epidemiology study in Costa Rica to further investigate dietary nutrient-MeHg interactions. Costa Rica is a Central American country with multiple sources of Hg and a high per capital fish consumption. Here, 5 of the 14 populations we studied exceeded the recommended MeHg provisional tolerable daily intake (pTDI) of 0.2 µg/KgBW/d. In Heredia the pTDI was exceeded by 34% of woman participants, primarily associated with canned tuna consumption. Interestingly, we detected that Hg body burden was significantly reduced by the consumption of antioxidant-rich dietary items. Considering our collective results, we hypothesized that MeHg toxicokinetics may be altered by dietary nutrients at the site of intestinal absorption from the disruption of gut flora, or at the site of cellular demethylation in tissues from the improvement of cellular redox state. The interaction of dietary nutrients on MeHg outcomes has a large impact on risk assessment and may provide a public health approach for managing the risk associated with MeHg exposure without reducing local fish consumption.

No description available.

Abstract Mercury is a global pollutant that accumulates easily in forest soils, even in remote areas. Mercury accumulated in soils can be subsequently released into surface waters causing an increased eco-toxicological and human health risk. The most toxic form of mercury to humans and wildlife is methyl mercury (MeHg), which can be formed in the environment via methylation processes. In freshwaters, MeHg is readily accumulated in fish, which are the main source of human exposure to MeHg. The determination of both total mercury and MeHg concentrations in environmental samples, such as natural waters and soils, is important in environmental risk assessment. This study involved the development of analytical methods for the determination of ultra-trace total mercury and MeHg concentrations in humic-rich natural water and peat soil samples. Each developed method was carefully optimized and validated by using real natural water and peat soil samples, certified reference materials and/or reference methods. The cold vapor inductively coupled plasma mass spectrometry (CV-ICP-MS) method developed during this study was found to be a reliable method for the determination of total ultra-trace mercury concentrations in natural freshwaters. Purge and trap gas chromatography, coupled to an ICP-MS, was used in mercury speciation analysis. Together with species-specific isotope dilution this technique proved to be a reliable method in MeHg determinations. Prior to instrumental determination, MeHg was successfully isolated from humic-rich water and peat soil samples using N2-assisted distillation. The analytical methods developed in this study were successfully applied to an investigation of the effects of forest harvesting practices on the mobilization of mercury in boreal forest catchments. / Tiivistelmä Elohopeaa pääsee ilmakehään sekä luonnollisista lähteistä (mm. tulivuorenpurkaukset ja kiviaineksen rapautuminen), että ihmisen toiminnan kautta. Elohopean viipymäaika ilmakehässä on hyvin pitkä, minkä vuoksi se voi kulkeutua kauas päästölähteestä ennen päätymistään maaperään ja vesistöihin. Ympäristössä olevasta epäorgaanisesta elohopeasta voi muodostua erittäin myrkyllistä metyylielohopeaa, joka rikastuu helposti ravintoketjussa. Metyylielohopean muodostuminen on merkittävä osa elohopean biogeokemiallista kiertoa, minkä vuoksi metyylielohopean määrittäminen näytteen kokonaiselohopeapitoisuuden ohella antaa tärkeää tietoa elohopean käyttäytymisestä ympäristössä. Tutkimuksessa kehitettiin analyysimenetelmät, joilla määritettiin ultrapieniä kokonaiselohopea- ja metyylielohopeapitoisuuksia humuspitoisista luonnonvesistä ja turvemaanäytteistä. Tutkimuksessa käytetyt näytteet oli kerätty turvemaametsien valuma-alueilta Sotkamosta. Luonnonvesinäytteiden kokonaiselohopeapitoisuuksien määrityksessä käytettiin kylmähöyrymenetelmää (CV) yhdistettynä induktiiviplasma-massaspektrometriaan (ICP-MS). Vesi- ja turvenäytteiden metyylielohopeapitoisuuksien määrityksessä elohopeaspesiekset erotettiin kaasukromatografisesti (GC) ja määritettiin isotooppilaimennus-ICP-MS:lla. Ennen GC-ICP-MS -määritystä näytteet esikäsiteltiin typpiavusteisella tislausmenetelmällä ja esikonsentroitiin ’purge and trap’ -tekniikalla. CV-ICP-MS ja ’purge and trap’ GC-ICP-MS -menetelmät optimoitiin huolellisesti sekä laiteparametrien, että reagenssimäärien suhteen. Menetelmillä saatavien tulosten oikeellisuus varmistettiin vertailumateriaalien ja/tai vertailumenetelmien avulla. Kehitettyjä analyysimenetelmiä hyödynnettiin tutkimuksessa, jossa seurattiin metsähakkuiden mahdollisia vaikutuksia elohopean huuhtoutumiseen ja metyloitumiseen ojitetuilla turvemailla.