Mercury and Pregnancy

Bellinger, David C.

doi:10.1002/bdra.23219

Cited by 8 publications

(6 citation statements)

References 25 publications

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“…Contamination of mercury occurs primarily through the consumption of contaminated seafood and rice grown in contaminated waters. It is actively transported across the placenta and impairs fetal neurodevelopment [6, 7].…”

Section: Introductionmentioning

confidence: 99%

The Concentration of Micronutrients and Heavy Metals in Maternal Serum, Placenta, and Cord Blood: A Cross-Sectional Study in Preterm Birth

Irwinda

Wibowo

Putri

2019

Journal of Pregnancy

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Background Preterm birth is still a global burden particularly in Indonesia. The suboptimal concentration of certain micronutrients and heavy metals is hypothesized to play a role in the mechanism of preterm birth. Objective This study aimed to analyze the micronutrients and heavy metals concentrations between subjects with term and preterm birth. Design A cross-sectional study was conducted during January–June 2017 in Cipto Mangunkusumo Hospital and Budi Kemuliaan Hospital, Jakarta, Indonesia. Subjects were divided into term and preterm birth groups. The measured outcomes were maternal serum, placental, and blood cord concentration of zinc, copper, iron, selenium, manganese, mercury, lead, AtRA, and 25(OH)D. Results A total of 51 pregnant women participated in this study. Term group had higher concentration of maternal serum AtRA (0.22 ± 0.07 ng/mL versus 0.12 ± 0.03 ng/mL, p <0.001), higher placental concentration of manganese {0.99 (0.38 – 1.78) μg/g versus 0.42 ± 0.18 μg/g, p <0.001}, iron (252.16 ± 170.61 μg/g versus 78.45 ± 51.73 μg/g, p <0.001), copper {2.96 ± 1.80 μg/g versus 1.62 (0.70 – 3.88) μg/g, p 0.019}, zinc {58.34 (27.88 – 124.05) μg/g versus 28.41 (1.46 – 137.69) μg/g, p 0.011}, selenium (0.31 ± 0.31 ng/g versus 0.14 ± 0.20 ng/g, p 0.024), AtRA {21.7 ± 10.69 ng/g versus 0.7 (0.42 – 5.10) ng/g, p <0.001}, and 25(OH)D {75.84 ± 45.12 ng/g versus 18.00 (5 – 88) ng/g, p <0.001}, lower placental concentration of mercury (0.20 ± 0.17 ng/g versus 20.47 ± 41.35 ng/g, p 0.019) and lead (0.02 ± 0.01 ng/g versus 0.81 ± 1.43 ng/g, p 0.009), and higher cord blood concentration of copper {32.20 (16.30 – 69.60) μg/dL versus 20.60 (5.80 – 53.30) μg/dL, p 0.006} and AtRA (0.16 ± 0.04 versus 0.07 ± 0.01, p <0.001). Conclusion Preterm birth is associated with lower concentrations of micronutrients which play a role in antioxidant mechanism, as well as higher concentration of mercury and lead.

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Section: Introductionmentioning

confidence: 99%

The Concentration of Micronutrients and Heavy Metals in Maternal Serum, Placenta, and Cord Blood: A Cross-Sectional Study in Preterm Birth

Irwinda

Wibowo

Putri

2019

Journal of Pregnancy

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“…This is somewhat surprising since there is vast literature on the developmental neurotoxicity that indicates an inverse association between chemical exposure and child neurodevelopment (Bellinger 2014 for an updated review). Extensive evidence also shows that some environmental agents alter developmental programming via changes in gene expression or imprinting that do not result in malformations but in functional deficits that become apparent later in life.…”

mentioning

confidence: 99%

Early-Life Toxic Insults and Onset of Sporadic Neurodegenerative Diseases—an Overview of Experimental Studies

Tartaglione

Venerosi

Calamandrei

2015

Current Topics in Behavioral Neurosciences

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The developmental origin of health and disease hypothesis states that adverse fetal and early childhood exposures can predispose to obesity, cardiovascular, and neurodegenerative diseases (NDDs) in adult life. Early exposure to environmental chemicals interferes with developmental programming and induces subclinical alterations that may hesitate in pathophysiology and behavioral deficits at a later life stage. The mechanisms by which perinatal insults lead to altered programming and to disease later in life are still undefined. The long latency between exposure and onset of disease, the difficulty of reconstructing early exposures, and the wealth of factors which the individual is exposed to during the life course make extremely difficult to prove the developmental origin of NDDs in clinical and epidemiological studies. An overview of animal studies assessing the long-term effects of perinatal exposure to different chemicals (heavy metals and pesticides) supports the link between exposure and hallmarks of neurodegeneration at the adult stage. Furthermore, models of maternal immune activation show that brain inflammation in early life may enhance adult vulnerability to environmental toxins, thus supporting the multiple hit hypothesis for NDDs' etiology. The study of prospective animal cohorts may help to unraveling the complex pathophysiology of sporadic NDDs. In vivo models could be a powerful tool to clarify the mechanisms through which different kinds of insults predispose to cell loss in the adult age, to establish a cause-effect relationship between "omic" signatures and disease/dysfunction later in life, and to identify peripheral biomarkers of exposure, effects, and susceptibility, for translation to prospective epidemiological studies.

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“…Since then, however, some studies have found measurable damage to infants' brain development in mothers exposed to lower levels of mercury. Several scientists and advocates specializing in mercury damage have concluded that the EPA's safe level is too lax to protect the developing fetus, and recommendations have been made that the EPA lower its mercury exposure level by 50 to 75% [ 67 , 68 ].…”

Section: Recommendations To Minimize Human Mercury Exposurementioning

confidence: 99%

Sources and Toxicity of Mercury in the San Francisco Bay Area, Spanning California and Beyond

Kolipinski

Subramanian

Kristen

et al. 2020

Journal of Environmental and Public Health

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This report synthesizes and evaluates published scientific literature on the environmental occurrence and biomagnification of mercury with emphasis on the San Francisco Bay Area (SFBA), California. Mercury forms various compounds, well known for their toxicity in humans and environmental ecosystems. Elemental mercury is transported and distributed by air, water, and sediments. Through the metabolic processes of algae and bacteria, mercury is converted into organic compounds, such as methylmercury (MeHg), which then bioaccumulates up through trophic levels. In fish, it is found primarily in skeletal muscle, while in humans, the primary target organs are the brain and kidneys. Health concerns exist regarding bioaccumulation of mercury in humans. This paper reviews the known anthropogenic sources of mercury contamination, including atmospheric deposition through aerial transport from coal burning power plants, cement production, and residual contaminants of mercury from gold mining, as well as mercury-containing waste from silver amalgams emitted from dental offices into waterways. Although tools exist for measuring mercury levels in hair, breast milk, urine, blood, and feces in humans, current diagnostic tools are inadequate in measuring total mercury load, including deposited mercury in tissues. Additionally, insufficient attention is being paid to potential synergistic impacts of mercury interaction with multipliers such as lead, cadmium, and aluminum. We provide specific data on methylmercury concentrations at different trophic levels, followed by recommendations for reducing the level of mercury in the SFBA in order to protect the health of humans and other species.

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Mercury and Pregnancy

Cited by 8 publications

References 25 publications

The Concentration of Micronutrients and Heavy Metals in Maternal Serum, Placenta, and Cord Blood: A Cross-Sectional Study in Preterm Birth

The Concentration of Micronutrients and Heavy Metals in Maternal Serum, Placenta, and Cord Blood: A Cross-Sectional Study in Preterm Birth

Early-Life Toxic Insults and Onset of Sporadic Neurodegenerative Diseases—an Overview of Experimental Studies

Sources and Toxicity of Mercury in the San Francisco Bay Area, Spanning California and Beyond

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