Mercury exposure during pregnancy could increase fetal and infant growth rates

Mercury exposure during pregnancy could increase fetal and infant growth rates

Today we are surrounded by man-made chemicals, both those that are introduced intentionally and those that inadvertently contaminate the environment as a result of their use in other applications.

Lernen: Auswirkungen der Quecksilberbelastung auf die fötale Körperbelastung und ihre Assoziation mit dem Wachstum von Säuglingen. Bildnachweis: SciePro/Shutterstock

Endocrine disrupting chemicals (EDCs) are of particular concern, particularly when exposure occurs in fetal life. A new study looks at fetal growth rates linked to mercury exposure.

introduction

Many EDCs are fatty substances, including mercury, which has been reported to correlate with metabolic syndrome. It was recently revealed that mercury levels in the blood of women living in South Korea are approximately 4.5 g/L, which is quite high compared to the 0.65–1.35 μg/L and ~9 ng/g reported in women in the US and Japan respectively.

Mercury exposure occurs primarily through the consumption of fish, particularly in the form of methylmercury (MeHg). This is an organic mercury compound that accumulates in fish flesh. When taken by pregnant women, it can cross the placenta and accumulate in the fetus.

For this reason, the Korean Ministry of Food and Drug Safety has set limits for fish consumption during pregnancy, including fish such as mackerel and cod, of which 400g is the upper limit per week, as well as shark and tuna, with a recommended intake of only 100g per week.

In the current study, published in Environmental research The researchers used a physiologically based pharmacokinetic (PBPK) model to calculate the predicted concentration of MeHg in a given organ over time. It uses the pharmacokinetics of the substance (absorption, distribution, metabolism and excretion). [ADME]) as well as intensity and route of exposure.

This model can also help estimate the integrated exposure dose. Mathematically predicting the amount of Hg in the pregnant woman's body allows for reverse dosimetry, leading to an estimate of the internal dose of the chemical.

In this study, researchers tried to find out the Hg exposure to the fetus due to transplacental absorption and how this affected fetal growth. Data come from the Children's Health and Environmental Chemicals in Korea (CHECK) study, which began in January 2011 and ended in December 2012.

This included approximately 330 pregnant women who attended several university hospitals in South Korea with their newborns at the time of birth. Blood and urine samples from pregnant women as well as umbilical cord and placenta samples were tested for MeHg along with first urine and meconium. Additionally, expressed breast milk and the infant's hair were collected on day 30.

The measured Hg value was applied to the model, and the exposure amount was calculated after adjusting for fetal growth and an increase in maternal blood, rich tissue, and fat compartments during pregnancy. The amount of Hg that crosses the placenta to accumulate in the fetal plasma was calculated to achieve the Hg burden of the fetal body.

What did the study show?

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The geometric mean (GM) birth weight was 3.3 kg for boys and 3.2 kg for girls, respectively. The GM-Hg concentration in maternal Hg and cord blood was ~4.5 and ~7.4 μg/L, respectively, measured in just over a hundred paired samples. The former is like the Human Biomonitoring-1 (HBM-1) value and indicates that Hg exposure during pregnancy needs to be moderated in the affected individual.

In contrast, placenta and meconium concentrations increased to 9.0 and 36.9 ng/g, respectively. Infant hair samples (n=25) showed a GM of ~440 ng/g. Therefore, Hg levels in meconium and cord blood were higher than those in maternal blood, confirming the results of previous studies.

Fetal tissues, including placenta, umbilical cord blood, meconium, and infant hair, are all enriched in Hg compared to maternal blood, with hair samples having concentrations 20 to 174 times higher than in maternal blood.

While 95% of the mothers had Hg blood concentrations below 8.7 μg/L, the corresponding value in 95% of the newborn cord blood samples was 17.2 μg/L. In comparison, cord blood MeHg levels were estimated to be 13.4 or less in 95% of samples. In contrast, only 5% of cord blood samples had MeHg values ​​below 4.

Overall, Hg levels in this study were lower than suggested in Japanese or Singaporean studies, but higher than those in the United States or Canada.

Therefore, the calculated fetal body burden of MeHg in this cohort ranged from 26.3 to 86.9 mg. Five rounds of follow-up assessed postnatal cord blood Hg concentrations, with 75% of values ​​below 9.6 μg/L.

Exposure during fetal life affected neonatal length at birth, showing a positive correlation with cord blood Hg. This is true even after accounting for maternal characteristics, including body mass index (BMI). However, head circumference and birth showed no such correlation.

Postnatal growth was not statistically associated with cord blood Hg levels. Nevertheless, trends for rapidly increasing weight gain were observed for both sexes in the high-exposure group after six months of life. This indicates that, in addition to individual constitution, age, weaning practices and child behavior, Hg levels influence weight gain.

The presence of lead could also influence these results, with increased length and weight reported to be linearly related to cord blood lead concentrations. When lead and Hg exposure were implemented into the mixed model, no association with length or weight was observed.

What are the effects?

Previous studies have failed to agree on the association between Hg exposure and growth rates, with some reporting an increase and others reporting a decrease. This study also establishes the importance of the presence of Hg in the diet, but data on the nature of its importance still need to be collected.

However, the fact that Hg exposure has negative effects on the fetus makes it necessary to establish upper limits for such exposure during pregnancy.

The Environmental Protection Agency (EPA) has already established a reference dose of 0.1 μg/kg/day for MeHg, which is sufficient to prevent adverse effects from such exposure for a lifetime.

A previous study by the same authors showed that Hg exposure is associated with hyperlipidemia and elevated liver enzymes, probably due to its ability to inhibit the breakdown of oxidized lipids that are toxic to the host. However, this is accompanied by induced oxidative stress and systemic inflammation, which influence the buildup of abnormal fat cells.

Further research with specific information, such as fish nutrition after birth and concurrent exposure to other environmental pollutants, is needed to clarify and generalize the relationship between Hg and growth.”

Reference:

• Lee, S. et al. (2022). Auswirkungen der Quecksilberbelastung auf die fötale Körperbelastung und ihre Assoziation mit dem Wachstum von Säuglingen. Umweltforschung. doi: https://doi.org/10.1016/j.envres.2022.114780. https://www.sciencedirect.com/science/article/abs/pii/S0013935122021077

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