Exposure to mercury during pregnancy may increase fetal and infant growth rates

Today, we are surrounded by synthetic materials, both those that are introduced on purpose and those that inadvertently pollute the environment due to their use in other materials.

Study: Effects of mercury exposure on fetal body weight and its relationship to infant growth. Image credit: SciPro/Shutterstock

Endocrine disrupting chemicals (EDCs) are of particular concern, especially when exposure occurs during fetal life. A new study examines fetal growth rates associated with mercury exposure.


Many EDCs are obesogenic, including mercury, which has been reported to be associated with metabolic syndrome. Recently, blood mercury levels in women living in South Korea have been found to be around 4.5 g/L, which is quite high compared to the 0.65–1.35 μg/L and ~9 ng/g that is reported in women in the United States and Japan, respectively.

Exposure to mercury is primary Through fish consumption, especially in the form of methylmercury (MeHg). This is an organic mercury compound that accumulates in fish flesh. When ingested by pregnant women, it can cross the placenta to accumulate in the fetus.

Korea’s Ministry of Food and Drug Safety has placed restrictions on fish consumption during pregnancy because of this, including fish such as mackerel and cod, with an upper limit of 400g per week, as well as shark and tuna, with a recommended intake of only 100g per week.

In the current study, published in Environmental studies, the researchers used a physiologically based pharmacokinetic (PBPK) model to calculate the predicted concentration of MeHg in a given organ over time. It does this by using the substance’s pharmacokinetics (absorption, distribution, metabolism and elimination [ADME]) and intensity and route of exposure.

This model can also help estimate the integrated exposure dose. Mathematical prediction of the amount of Hg in the body of a pregnant woman allows for inverse dosimetry, which leads to an estimate of the internal dose of the material.

The researchers tried, in this study, to find the burden of Hg in the fetus due to absorption through the placenta and how this affected fetal growth. The data came from the Children’s Health and Environmental Chemicals in Korea (CHECK) study, which began in January 2011 and ended in December 2012.

These included approximately 330 pregnant women who attended several university hospitals in South Korea with their newborns at birth. Blood and urine samples from pregnant women and samples from the umbilical cord and placenta were tested for MeHg, along with first urine and meconium. In addition, lost breast milk and the baby’s hair were collected on day 30.

The measured Hg level was fitted to the model and the exposure amount was calculated after correcting for fetal growth and increases in maternal blood, rich tissue and fat compartments during pregnancy. The amount of Hg passing through the placenta to accumulate in the fetal plasma was calculated as equivalent to fetal body weight Hg.

What did the study show?

The geometric mean (GM) birth weight was 3.3 kg and 3.2 kg for boys and girls, respectively. Concentrations of transgenic Hg in maternal blood and blood Hg were ∼4.5 and ∼7.4 μg/L, respectively, measured in over a hundred paired samples. The former is identical to the human biomonitoring-1 (HBM-1) value and indicates that Hg exposure during pregnancy should be targeted in the individual concerned.

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

Fetal tissue, including placenta, umbilical cord blood, meconium and infant hair, are all enriched for Hg compared to maternal blood, with hair samples showing concentrations 20-174 times higher than maternal blood.

While 95% of mothers had blood Hg levels below 8.7 μg/L, the corresponding level in 95% of neonatal blood samples was 17.2 μg/L. Relatively, cord blood MeHg levels were estimated to be 13.4 or lower for 95% of samples. In contrast, only 5% of cord blood samples had MeHg levels below 4.

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

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

Fetal exposure affected neonatal length at birth, which showed a positive correlation with cord blood Hg. This is true even after adjusting 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. However, a trend towards more rapid weight gain was observed in the high exposure group after six months of life in both sexes. This indicates that apart from individual structure, age, weaning habits and child behavior, Hg levels influence weight gain.

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

What are the consequences?

Previous studies have not agreed on the relationship between Hg exposure and growth rate, with some reporting an increase and others a decrease. This study also reveals the importance of the presence of Hg in the diet, but data on the nature of its importance remain to be collected.

However, the fact that exposure to Hg has adverse effects on the fetus makes it necessary to set an upper limit for such exposure during pregnancy.

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

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

Further studies are required with specific information, such as postnatal fish diet and co-exposure to other environmental pollutants to clarify and generalize the relationship between Hg and growth.”

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