The First Exposure Assessment of Mercury Levels in Hair among Pregnant Women and Its Effects on Birth Weight and Length in Semarang, Central Java, Indonesia.

(1) Background: Methylmercury (MeHg) exposure during pregnancy is an important issue due to its possible adverse health effects on fetus. To contribute the development of assessment system of Hg exposure through fish consumption and health effects on children, we examined the hair Hg levels in pregnant women and birth weight and length. (2) Methods: In 2018, a cohort study was conducted on 118 pregnant women-infant pairs from six community health centers in the northern coastal area in Central Java Indonesia. Data on mothers' characteristics during pregnancy, birth outcomes, and fish consumption were collected. Total Hg concentrations were determined from hair samples. (3) Results: The median (min-max) of the maternal hair Hg level was 0.434 (0.146-8.105) µg/g. Pregnant women living in lowland areas, near the sea, showed higher hair Hg concentration and fish consumption than those in highland areas {[0.465 (0.146-8.105) vs. 0.385 (0.150-1.956) µg/g; p = 0.043] and [(85.71 (0-500.0) vs. 49.76 (0.0-428.57) g/day; p < 0.01], respectively}. The maternal hair Hg level had no association with baby's birth weight and length. (4) Conclusions: The median maternal hair Hg is at a low level and had no association with infant birth weight and length in this study subjects.

Activation of MIP-2 and MCP-5 Expression in Methylmercury-Exposed Mice and Their Suppression by N-Acetyl-L-Cysteine.

Methylmercury (MeHg) is a well-known neurotoxin of the central nervous system (CNS). Neuroinflammation is one of the main pathways of MeHg-induced CNS impairment. This study aims to investigate the expressions of IL-6, MIP-2, and MCP-5, as biomarkers in relation with MeHg-induced CNS impairment and N-acetyl-L-cysteine (NAC) treatment in mice, as well as histopathological changes of brain tissue and clinical symptom such as ataxia. Twenty male Balb/c mice, aged 8-9 weeks, were divided into 4 groups and treated with saline (control), NAC [150 mg/kg body weight (BW) day], MeHg (4 mg Hg/kg BW), or a combination of MeHg and NAC for 17 days. MeHg induced the expression of IL-6, MIP-2, and MCP-5 in the serum, with median values (those in controls) of 55.06 (9.44), 15.94 (9.30), and 458.91 (239.91) mg/dl, respectively, and a statistical significance was observed only in IL-6 expression (p < 0.05). MIP-2 and MCP-5 expressions tended to increase in the cerebrum of MeHg-treated group compared with controls; however, the difference was not statistically significant. MeHg treatment also increased IL-6 expression in the cerebellum (7.73 and 4.81 mg/dl in MeHg-treated group and controls, respectively), with a marginal significance. NAC significantly suppressed MeHg-induced IL-6 and MIP-2 expressions in the serum (p < 0.05 for both), and slightly reduced MCP-5 expression in the cerebrum. Ataxia was observed in all MeHg-treated mice after 9-day exposure as well as the decrease of intact Purkinje cells in brain tissue (p < 0.05). These findings suggest that MeHg induced neurotoxicity by elevating the expression of IL-6, MIP-2, and MCP-5 and causing ataxia symptoms, and NAC reduced MeHg-mediated effects on the CNS.