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Mercury and Methylmercury Toxicology and Risk Assessment

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A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Toxicology".

Deadline for manuscript submissions: closed (31 August 2018) | Viewed by 55153

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Prof. Laurie Hing Man Chan

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Department of Biology, University of Ottawa, Ottawa, Ontario, K1N 6N5, Canada
Interests: Toxicology and Environmental Health

Special Issue Information

Dear Colleagues,

Mercury (Hg) is a global pollutant that affects human and ecosystem health. Wildlife and humans are exposed to Hg primarily through diet in the form of methylmercury (MeHg), since MeHg bioaccumulates and biomagnifies in the food web. Among Hg species, MeHg toxicity is much more damaging to the nervous system in early developmental stages as it leads to alterations in its structure and function. Even at low doses, prenatal exposure to MeHg can disrupt fetal brain development. Since the initial identification of MeHg poisoning in Minamata, Japan, in 1956, the clinical neurology and neurotoxic effects of MeHg have been widely studied. However, the mechanisms responsible for MeHg-induced changes in neuronal function, particularly the delayed effects observed when exposure occurred during fetal development, are not fully understood. Increasing epidemiological evidence is showing that MeHg exposure is also a risk factor for cardiovascular diseases but the toxicological evidence is scarce. Recent advances in toxicology using “omics” approach provide new tools to study the complex effects of MeHg on system biology. Effects of MeHg on stem/progenitor cells show great promise in understanding MeHg toxicology. Increasing understanding of the roles of genetic determinants and the gut-microbiota in determining the toxicokinetics of MeHg also allows for more accurate risk assessment focusing on the sensitive populations. The understanding of interactive effects between Hg and nutrients, such as n-3 fatty acids and selenium, are improving the relevance of risk assessment. This Special Issue calls for papers that report new findings on MeHg toxicology and new information for the improvement of risk assessment of MeHg.

Prof. Laurie Hing Man Chan
Guest Editor

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Keywords

mercury
methylmercury
toxicology
risk assessment
exposure
toxicokinetics
mechanisms

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Published Papers (10 papers)

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Editorial

Jump to: Research, Review

3 pages, 157 KiB

Open AccessEditorial

Advances in Methylmercury Toxicology and Risk Assessment

by Hing Man Chan

Toxics 2019, 7(2), 20; https://doi.org/10.3390/toxics7020020 - 1 Apr 2019

Cited by 7 | Viewed by 3743

Abstract

Mercury (Hg) is a global pollutant that affects the health of both humans and ecosystems [...] Full article

(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)

Research

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10 pages, 2081 KiB

Open AccessArticle

Sub-Micromolar Methylmercury Exposure Promotes Premature Differentiation of Murine Embryonic Neural Precursor at the Expense of Their Proliferation

by Xiaoyang Yuan, Jing Wang and Hing Man Chan

Toxics 2018, 6(4), 61; https://doi.org/10.3390/toxics6040061 - 10 Oct 2018

Cited by 6 | Viewed by 3576 | Correction

Abstract

Methylmercury (MeHg) is a ubiquitous environmental pollutant that is known to be neurotoxic, particularly during fetal development. However, the mechanisms responsible for MeHg-induced changes in adult neuronal function, when their exposure occurred primarily during fetal development, are not yet understood. We hypothesized that fetal MeHg exposure could affect neural precursor development leading to long-term neurotoxic effects. Primary cortical precursor cultures obtained from embryonic day 12 were exposed to 0 µM, 0.25 µM, 0.5 µM, 2.5 µM, and 5 µM MeHg for 48 or 72 h. All of the concentrations tested in the study did not affect cell viability. Intriguingly, we observed that cortical precursor exposed to 0.25 µM MeHg showed increased neuronal differentiation, while its proliferation was inhibited. Reduced neuronal differentiation, however, was observed in the higher dose groups. Our results suggest that micromolar MeHg exposure may deplete the pool of neural precursors by increasing premature neuronal differentiation, which can lead to long-term neurological effects in adulthood as opposed to the higher MeHg doses that cause more immediate toxicity during infant development. Full article

(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)

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16 pages, 602 KiB

Open AccessFeature PaperArticle

Methylmercury Exposure and Developmental Outcomes in Tohoku Study of Child Development at 18 Months of Age

by Nozomi Tatsuta, Kunihiko Nakai, Mineshi Sakamoto, Katsuyuki Murata and Hiroshi Satoh

Toxics 2018, 6(3), 49; https://doi.org/10.3390/toxics6030049 - 21 Aug 2018

Cited by 18 | Viewed by 4814

Abstract

Seafood is an important component in a healthy diet and may contain methylmercury or other contaminants. It is important to recognize the risks and benefits of consuming seafood. A longitudinal prospective birth cohort study has been conducted to clarify the effects of neurotoxicants on child development—the Tohoku Study of Child Development (TSCD) in Japan. TSCD comprises two cohorts; a polychlorinated biphenyls (PCB) cohort (urban area) and a methylmercury cohort (coastal area). Our previous results from the coastal area showed prenatal methylmercury exposure affected psychomotor development in 18-month-olds, and boys appear to be more vulnerable to the exposure than girls. In this report, we have added the urban area cohort and we reanalyzed the impact of prenatal exposure to methylmercury, which gave the same results as before. These findings suggest prenatal exposure to low levels methylmercury may have adverse effects on child development, especially in boys. Full article

(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)

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9 pages, 2406 KiB

Open AccessFeature PaperArticle

Effect of Metallothionein-III on Mercury-Induced Chemokine Gene Expression

by Jin-Yong Lee, Maki Tokumoto, Gi-Wook Hwang, Min-Seok Kim, Tsutomu Takahashi, Akira Naganuma, Minoru Yoshida and Masahiko Satoh

Toxics 2018, 6(3), 48; https://doi.org/10.3390/toxics6030048 - 12 Aug 2018

Cited by 3 | Viewed by 3692

Abstract

Mercury compounds are known to cause central nervous system disorders; however the detailed molecular mechanisms of their actions remain unclear. Methylmercury increases the expression of several chemokine genes, specifically in the brain, while metallothionein-III (MT-III) has a protective role against various brain diseases. In this study, we investigated the involvement of MT-III in chemokine gene expression changes in response to methylmercury and mercury vapor in the cerebrum and cerebellum of wild-type mice and MT-III null mice. No difference in mercury concentration was observed between the wild-type mice and MT-III null mice in any brain tissue examined. The expression of Ccl3 in the cerebrum and of Cxcl10 in the cerebellum was increased by methylmercury in the MT-III null but not the wild-type mice. The expression of Ccl7 in the cerebellum was increased by mercury vapor in the MT-III null mice but not the wild-type mice. However, the expression of Ccl12 and Cxcl12 was increased in the cerebrum by methylmercury only in the wild-type mice and the expression of Ccl3 in the cerebellum was increased by mercury vapor only in the wild-type mice. These results indicate that MT-III does not affect mercury accumulation in the brain, but that it affects the expression of some chemokine genes in response to mercury compounds. Full article

(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)

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9 pages, 970 KiB

Open AccessFeature PaperArticle

Health Impacts and Biomarkers of Prenatal Exposure to Methylmercury: Lessons from Minamata, Japan

by Mineshi Sakamoto, Nozomi Tatsuta, Kimiko Izumo, Phuong Thanh Phan, Loi Duc Vu, Megumi Yamamoto, Masaaki Nakamura, Kunihiko Nakai and Katsuyuki Murata

Toxics 2018, 6(3), 45; https://doi.org/10.3390/toxics6030045 - 3 Aug 2018

Cited by 60 | Viewed by 8207

Abstract

The main chemical forms of mercury are elemental mercury, inorganic divalent mercury, and methylmercury, which are metabolized in different ways and have differing toxic effects in humans. Among the various chemical forms of mercury, methylmercury is known to be particularly neurotoxic, and was identified as the cause of Minamata disease. It bioaccumulates in fish and shellfish via aquatic food webs, and fish and sea mammals at high trophic levels exhibit high mercury concentrations. Most human methylmercury exposure occurs through seafood consumption. Methylmercury easily penetrates the blood-brain barrier and so can affect the nervous system. Fetuses are known to be at particularly high risk of methylmercury exposure. In this review, we summarize the health effects and exposure assessment of methylmercury as follows: (1) methylmercury toxicity, (2) history and background of Minamata disease, (3) methylmercury pollution in the Minamata area according to analyses of preserved umbilical cords, (4) changes in the sex ratio in Minamata area, (5) neuropathology in fetuses, (6) kinetics of methylmercury in fetuses, (7) exposure assessment in fetuses. Full article

(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)

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36 pages, 7987 KiB

Open AccessFeature PaperArticle

Survey of the Extent of the Persisting Effects of Methylmercury Pollution on the Inhabitants around the Shiranui Sea, Japan

by Shigeru Takaoka, Tadashi Fujino, Yoshinobu Kawakami, Shin-ichi Shigeoka and Takashi Yorifuji

Toxics 2018, 6(3), 39; https://doi.org/10.3390/toxics6030039 - 20 Jul 2018

Cited by 16 | Viewed by 7567 | Correction

Abstract

In 1956 methylmercury poisoning, known as Minamata disease, was discovered among the inhabitants around the Shiranui Sea, Kyushu, Japan. Although about five hundred thousand people living in the area had supposedly been exposed to methylmercury, administrative agencies and research institutes had not performed any subsequent large scale, continuous health examination, so the actual extent of the negative health effects was not clearly documented. In 2009, we performed health surveys in order to examine residents in the polluted area and to research the extent of the polluted area and period of pollution. We analyzed data collected on 973 people (age = 62.3 ± 11.7) who had lived in the polluted area and had eaten the fish there and a control group, consisting of 142 persons (age = 62.0 ± 10.5), most of whom had not lived in the polluted area. Symptoms and neurological signs were statistically more prevalent in the four groups than in the control group and were more prevalent and severe in those who had eaten most fish. The patterns of positive findings of symptoms and neurological findings in the four groups were similar. Our data indicates that Minamata disease had spread outside of the central area and could still be observed recently, almost 50 years after the Chisso Company’s factory had halted the dumping of mercury polluted waste water back in 1968. Full article

(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)

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9 pages, 1900 KiB

Open AccessFeature PaperArticle

Chemokine CCL4 Induced in Mouse Brain Has a Protective Role against Methylmercury Toxicity

by Tsutomu Takahashi, Min-Seok Kim, Miyuki Iwai-Shimada, Masatake Fujimura, Takashi Toyama, Akira Naganuma and Gi-Wook Hwang

Toxics 2018, 6(3), 36; https://doi.org/10.3390/toxics6030036 - 7 Jul 2018

Cited by 11 | Viewed by 5047

Abstract

Methylmercury (MeHg) is selectively toxic to the central nervous system, but mechanisms related to its toxicity are poorly understood. In the present study, we identified the chemokine, C-C motif Chemokine Ligand 4 (CCL4), to be selectively upregulated in the brain of MeHg-administered mice. We then investigated the relationship between CCL4 expression and MeHg toxicity using in vivo and in vitro approaches. We confirmed that in C17.2 cells (a mouse neural stem cell line) and the mouse brain, induction of CCL4 expression occurs prior to cytotoxicity caused by MeHg. We also show that the addition of recombinant CCL4 to the culture medium of mouse primary neurons attenuated MeHg toxicity, while knockdown of CCL4 in C17.2 cells resulted in higher MeHg sensitivity compared with control cells. These results suggest that CCL4 is a protective factor against MeHg toxicity and that induction of CCL4 expression is not a result of cytotoxicity by MeHg but is a protective response against MeHg exposure. Full article

(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)

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9 pages, 237 KiB

Open AccessArticle

Expression of Genes Involved in Stress, Toxicity, Inflammation, and Autoimmunity in Relation to Cadmium, Mercury, and Lead in Human Blood: A Pilot Study

by Rebecca N. Monastero, Caterina Vacchi-Suzzi, Carmen Marsit, Bruce Demple and Jaymie R. Meliker

Toxics 2018, 6(3), 35; https://doi.org/10.3390/toxics6030035 - 6 Jul 2018

Cited by 16 | Viewed by 4733

Abstract

There is growing evidence of immunotoxicity related to exposure to toxic trace metals, and an examination of gene expression patterns in peripheral blood samples may provide insights into the potential development of these outcomes. This pilot study aimed to correlate the blood levels of three heavy metals (mercury, cadmium, and lead) with differences in gene expression in 24 participants from the Long Island Study of Seafood Consumption. We measured the peripheral blood mRNA expression of 98 genes that are implicated in stress, toxicity, inflammation, and autoimmunity. We fit multiple linear regression models with multiple testing correction to correlate exposure biomarkers with mRNA abundance. The mean blood Hg in this cohort was 16.1 µg/L, which was nearly three times the Environmental Protection Agency (EPA) reference dose (5.8 µg/L). The levels of the other metals were consistent with those in the general population: the mean Pb was 26.8 µg/L, and the mean Cd was 0.43 µg/L. The expression of three genes was associated with mercury, four were associated with cadmium, and five were associated with lead, although none were significant after multiple testing correction. Little evidence was found to associate metal exposure with mRNA abundance for the tested genes that were associated with stress, toxicity, inflammation, or autoimmunity. Future work should provide a more complete picture of physiological reactions to heavy metal exposure. Full article

(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)

Review

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15 pages, 348 KiB

Open AccessReview

Oxidative Stress in Methylmercury-Induced Cell Toxicity

by Alessandra Antunes dos Santos, Beatriz Ferrer, Filipe Marques Gonçalves, Aristides M. Tsatsakis, Elisavet A. Renieri, Anatoly V. Skalny, Marcelo Farina, João B. T. Rocha and Michael Aschner

Toxics 2018, 6(3), 47; https://doi.org/10.3390/toxics6030047 - 9 Aug 2018

Cited by 80 | Viewed by 8136

Abstract

Methylmercury (MeHg) is a hazardous environmental pollutant, which elicits significant toxicity in humans. The accumulation of MeHg through the daily consumption of large predatory fish poses potential health risks, and the central nervous system (CNS) is the primary target of toxicity. Despite well-described neurobehavioral effects (i.e., motor impairment), the mechanisms of MeHg-induced toxicity are not completely understood. However, several lines of evidence point out the oxidative stress as an important molecular mechanism in MeHg-induced intoxication. Indeed, MeHg is a soft electrophile that preferentially interacts with nucleophilic groups (mainly thiols and selenols) from proteins and low-molecular-weight molecules. Such interaction contributes to the occurrence of oxidative stress, which can produce damage by several interacting mechanisms, impairing the function of various molecules (i.e., proteins, lipids, and nucleic acids), potentially resulting in modulation of different cellular signal transduction pathways. This review summarizes the general aspects regarding the interaction between MeHg with regulators of the antioxidant response system that are rich in thiol and selenol groups such as glutathione (GSH), and the selenoenzymes thioredoxin reductase (TrxR) and glutathione peroxidase (Gpx). A particular attention is directed towards the role of the PI3K/Akt signaling pathway and the nuclear transcription factor NF-E2-related factor 2 (Nrf2) in MeHg-induced redox imbalance. Full article

(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)

14 pages, 1102 KiB

Open AccessFeature PaperReview

Assessment of Cardiac Autonomic Function in Relation to Methylmercury Neurotoxicity

by Kanae Karita, Toyoto Iwata, Eri Maeda, Mineshi Sakamoto and Katsuyuki Murata

Toxics 2018, 6(3), 38; https://doi.org/10.3390/toxics6030038 - 20 Jul 2018

Cited by 11 | Viewed by 4655

Abstract

After the European Food Safety Authority reviewed reports of methylmercury and heart rate variability (HRV) in 2012, the panel concluded that, although some studies of cardiac autonomy suggested an autonomic effect of methylmercury, the results were inconsistent among studies and the implications for health were unclear. In this study, we reconsider this association by adding a perspective on the physiological context. Cardiovascular rhythmicity is usually studied within different frequency domains of HRV. Three spectral components are usually detected; in humans these are centered at <0.04 Hz, 0.15 Hz (LF), and 0.3 Hz (HF). LF and HF (sympathetic and parasympathetic activities, respectively) are evaluated in terms of frequency and power. By searching PubMed, we identified 13 studies examining the effect of methylmercury exposure on HRV in human populations in the Faroe Islands, the Seychelles and other countries. Considering both reduced HRV and sympathodominant state (i.e., lower HF, higher LF, or higher LF/HF ratio) as autonomic abnormality, eight of them showed the significant association with methylmercury exposure. Five studies failed to demonstrate any significant association. In conclusion, these data suggest that increased methylmercury exposure was consistently associated with autonomic abnormality, though the influence of methylmercury on HRV (e.g., LF) might differ for prenatal and postnatal exposures. The results with HRV should be included in the risk characterization of methylmercury. The HRV parameters calculated by frequency domain analysis appear to be more sensitive to methylmercury exposure than those by time domain analysis. Full article

(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)

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