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BACKGROUND:
Although mercury is an established neurotoxin, only few longitudinal studies have investigated the association between prenatal and early childhood mercury exposure and autistic behaviors.

METHODS:
We conducted a longitudinal cohort study using an ongoing prospective birth cohort initiated in 2006, wherein blood mercury levels were measured at early and late pregnancy; in cord blood; and at 2 and 3years of age. We analyzed 458 mother-child pairs. Autistic behaviors were assessed using the Social Responsiveness Scale (SRS) at 5years of age. Both continuous SRS T-scores and T-scores dichotomized by a score of ≥60 or <60 were used as outcomes.

RESULTS:
The geometric mean of mercury concentrations in cord blood was 5.52μg/L. In adjusted models, a doubling of blood mercury levels at late pregnancy (β=1.84, 95% confidence interval [CI]: 0.39, 3.29), in cord blood (β=2.24, 95% CI: 0.22, 4.27), and at 2years (β=2.12, 95% CI: 0.54, 3.70) and 3years (β=2.80, 95% CI: 0.89, 4.72) of age was positively associated with the SRS T-scores. When the SRS T-scores were dichotomized, we observed positive associations with mercury levels at late pregnancy (relative risk [RR]=1.31, 95% CI: 1.08, 1.60) and in cord blood (RR=1.28, 95% CI: 1.01, 1.63).

CONCLUSION:
We found that blood mercury levels at late pregnancy and early childhood were associated with more autistic behaviors in children at 5years of age. Further study on the long-term effects of mercury exposure is recommended.

In this study, the associations between mercury (Hg) exposure and cholesterol profiles were analyzed, and increased Hg levels and cholesterol profiles according to the amount of fish consumption were evaluated. Data on levels of blood Hg, the frequency of fish consumption, total blood cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) in 3951 adults were obtained from the Korea National Health and Nutrition Examination Survey 2010-2011 database. To compare the distribution for each log-transformed indicator, Student’s t-test and analysis of variance were carried out, and the groups were classified according to the frequency of fish consumption through linear regression analysis; the association between Hg level and cholesterol profiles in each group was analyzed. The blood Hg levels (arithmetic mean, median, and geometric mean) for all target participants were 4.59, 3.66, and 3.74 µg/L, respectively. The high cholesterol group, low HDL-C group, and high TG group showed a statistically and significantly higher blood Hg level than the low-risk group. In both sexes, as the frequency of fish consumption increased, blood Hg level also increased, but TC, HDL-C, LDL-C, and TG did not show a similar trend. Increased blood Hg level showed a significant association with increased TC and LDL-C. This statistical significance was maintained in the group with less frequent fish consumption (<4 times per month), but the group with frequent fish consumption (>8 times per month) did not show a similar trend. The results of this study suggest that fish consumption increases the level of Hg exposure, and that as the level of Hg exposure increases, the levels of cholesterol profiles increase. However, this study also suggests that the levels of cholesterol profiles in those with frequent fish consumption can be diminished.

BACKGROUND:
Conflicting evidence concerning possible harm from mercury (Hg) in regard to offspring cognition if the woman eats fish has prompted this study to examine evidence from a British pre-birth cohort to investigate the relationship between the two.

METHODS:
Pregnant women (median prenatal blood mercury 1.86μg/L) resident in the study area with delivery between April 1991 and December 1992 were followed up and verbal, performance and total intelligence quotient (IQ) of 2062 offspring were measured at age 8. Analysis treated IQ as (a) continuous and (b) the lowest 25% of the distribution. Multiple and logistic regression analyses took account of social and demographic variables. Stratification considered children of fish eaters separately.

RESULTS:
Before adjustment, mean full-scale IQ increased with increasing Hg (change with 1SD of Hg=+2.02; 95%CI+1.40,+2.64 IQ points; P <0.0001); after adjustment effect size was reduced although still positive (+0.61;95%CI -0.06,+1.29 IQ points; P=0.073). The adjusted positive relationship was stronger when fish-eating mothers were considered separately (+0.84:95%CI +0.13,+1.56 IQ points; P=0.021) in comparison with the outcomes for non-fish eaters, where the adjusted relationship was negative (-2.22;95%CI -5.00,+0.56 IQ points; P=0.117). The binary outcome showed a similar pattern with the adjusted OR for non-fish-eaters 1.79 (95%CI 1.10,2.93; P=0.019) per SD of Hg, significantly different from that for fish consumers (0.94;95%CI:0.82,1.08)(Pinteraction<0.05). There were no differences between the sexes in the associations, nor did the level of the mother’s blood selenium change the effect sizes.

CONCLUSION:
The relationship between intrauterine exposure to mercury and offspring IQ appears to be benign provided the mother consumes fish.

India is an industrial giant with one of the fastest growing major economies in the world. Primary energy consumption in India is third after China and the USA. Greater energy production brings the burden of increasing emissions of mercury (Hg). India ranks second for Hg emissions. Rising atmospheric Hg release, high Hg evasion processes, and increasing monomethylmercury (highly neurotoxin) accumulations in marine food products increase the potential for human and ecosystem Hg exposure. Hg has been identified to increase the risk of getting Alzheimer’s disease (AD). There are increasing reports of AD and dementia in different age groups in India. The relationship between increasing Hg exposure and increasing neurodegenerative disorder in India is not known. This commentary points to the need for better understanding of the relationship between Hg release and AD in India, and other countries, and how to protect human health and the environment from the adverse effects of Hg.

Prenatal exposure to mercury, a known neurotoxic metal, is associated with lower cognitive performance during childhood. Disruption of fetal epigenetic programming could explain mercury’s neurodevelopmental effects. We screened for epigenome-wide methylation differences associated with maternal prenatal blood mercury levels in 321 cord blood DNA samples and examined the persistence of these alterations during early (n = 75; 2.9-4.9 years) and mid-childhood (n = 291; 6.7-10.5 years). Among males, prenatal mercury levels were associated with lower regional cord blood DNA methylation at the Paraoxonase 1 gene (PON1) that persisted in early childhood and was attenuated in mid-childhood blood. Cord blood methylation at the PON1 locus predicted lower cognitive test scores measured during early childhood. Methylation at the PON1 locus was associated with PON1 expression in an independent set of cord blood samples. The observed persistent epigenetic disruption of the PON1 gene may modulate mercury toxicity in humans and might serve as a biomarker of exposure and disease susceptibility.

Environmental contamination has exposed humans to various metal agents, including mercury. It has been determined that mercury is not only harmful to the health of vulnerable populations such as pregnant women and children, but is also toxic to ordinary adults in various ways. For many years, mercury was used in a wide variety of human activities. Nowadays, the exposure to this metal from both natural and artificial sources is significantly increasing. Recent studies suggest that chronic exposure, even to low concentration levels of mercury, can cause cardiovascular, reproductive, and developmental toxicity, neurotoxicity, nephrotoxicity, immunotoxicity, and carcinogenicity. Possible biological effects of mercury, including the relationship between mercury toxicity and diseases of the cardiovascular system, such as hypertension, coronary heart disease, and myocardial infarction, are being studied. As heart rhythm and function are under autonomic nervous system control, it has been hypothesized that the neurotoxic effects of mercury might also impact cardiac autonomic function. Mercury exposure could have a long-lasting effect on cardiac parasympathetic activity and some evidence has shown that mercury exposure might affect heart rate variability, particularly early exposures in children. The mechanism by which mercury produces toxic effects on the cardiovascular system is not fully elucidated, but this mechanism is believed to involve an increase in oxidative stress. The exposure to mercury increases the production of free radicals, potentially because of the role of mercury in the Fenton reaction and a reduction in the activity of antioxidant enzymes, such as glutathione peroxidase. In this review we report an overview on the toxicity of mercury and focus our attention on the toxic effects on the cardiovascular system.