Today, artificial chemicals are all around us.
EDCs, which disrupt the hormones and cause birth defects in babies, are particularly concerning. A new study examines the effects of mercury exposure on fetal growth.
Introduction
EDCs include mercury, which is known to be associated with metabolic syndrome. Recently it has come to light that the blood mercury levels in women living in South Korea are about 4.5 g/L, which is quite high relative to the 0.65–1.35 μg/L and ~9 ng/g reported in women in the USA and Japan, respectively.
Mercury exposure is the main concern. via Fish consumption, particularly in the form MeHg (methylmercury) This organic mercury compound can build up in fish flesh. This mercury compound can pass through the placenta and accumulate in the fetus if it is ingested during pregnancy.
Because of this, the Korea Ministry of Food and Drug Safety set limits on fish consumption during pregnancy. This includes fish like mackerel and fish like cod. The upper limit is 400g per week. There are also recommendations for shark and tuna intakes of 100g each week.
The current study was published by Environmental Research, the researchers used a physiologically-based pharmacokinetic (PBPK) model to calculate the predicted concentration of MeHg in a given organ with time. It uses the substance’s Pharmacokinetics (the absorption and distribution, metabolism and elimination) to do so. [ADME]) and the intensity and route of exposure.
This model can also assist in estimating the total exposure dose. Reverse dosimetry is a mathematical method that predicts the amount Hg in a pregnant woman’s blood. This allows them to estimate the internal dose.
Researchers sought to determine the effect of transplacental Hg absorption on fetal growth and the impact this had on the burden of Hg found in the fetus. The data came from the Children’s Health and Environmental Chemicals in Korea (CHECK) study that began in January 2011 and ended in December 2012.
There were approximately 330 mothers who attended several South Korean universities with their infants when they were born. The blood and urine of pregnant women, as well as the umbilical cord or placental samples, were tested for MeHg. On day 30, the infant’s hair and expressed breast milk were also collected.
After adjusting for factors such as fetal growth, maternal blood loss, richly-supplied tissues and fat compartments, the measured Hg level was applied on the model. Calculating the amount of Hg passing through placenta to accumulate in the fetal blood was done to determine the fetal Hg body burden.
What did the study reveal?
The geometric mean (GM), birth weight for both boys and girls was 3.3 and 3.2 kilograms, respectively. The GM Hg concentration in maternal and cord blood Hg was ~4.5 and ~7.4 μg/L, respectively, measured in just over a hundred paired samples. The first value is similar to the HBM-1 (human biomonitoring-1) value. It indicates that Hg should be reduced during pregnancy.
Contrary to this, the meconium and placental levels reached 9.0 and 36.9 mg/g, respectively. A GM of 440 ng/g was found in infant hair samples (n=25). According to earlier studies, Hg levels in cord blood and meconium were higher than those in maternal blood.
The fetal tissues (including placentas, cord blood, meconium and infant hair) are all rich in Hg, with hair samples showing concentrations between 20-174 times those of maternal blood.
While 95% of the mothers had blood Hg concentrations below 8.7 μg/L, the corresponding level in 95% of neonate cord blood samples was 17.2 μg/L. The MeHg levels in cord blood were at least 13.4 for 95% of samples. However, less than 5% of cordblood samples had MeHg levels below 4.
The overall Hg level was lower than the Japanese and Singapore studies suggested, but higher than those reported in Canada or the USA.
The calculated fetal MeHg body burden was therefore between 26.3 and 86.9 mg. Five rounds of follow-up assessed postnatal Hg concentrations in cord blood, with 75% of values being below 9.6 μg/L.
Exposure during fetal life had an impact on newborn length at birth. This correlation was positive with cord blood Hg. This holds true regardless of maternal characteristics (BMI, body mass index) or maternal characteristics. Head circumference and birth did not show a correlation.
The statistical association between cord blood Hg levels and postnatal growth was not significant. However, the high-exposure group showed a trend for rapid weight gains after six months of living for both sexes. This shows that Hg levels can have an impact on weight gain, regardless of individual constitution, age and weaning practices.
These findings may also be affected by lead exposure. According to some reports, an increase in length and weight is linearly related to cord blood lead concentrations. The mixed model did not show any relationship between lead and Hg exposure.
What are the implications?
Previous studies did not agree on the relationship between Hg and growth rates. Some reported an increase, while others reported a decrease. This study also confirms the importance of Hg in diet, although data on its nature remain to be collected.
Hg can cause harm to the fetus so it is necessary to limit Hg in pregnancy.
The Environmental Protection Agency (EPA) has already set a reference dose of 0.1 μg/kg/day for MeHg, sufficient to avoid adverse effects over a lifetime of such exposure.
A previous study by the same authors found Hg exposure to be associated with hyperlipidemia and increased liver enzymes. This was probably due to Hg’s ability inhibit the breakdown oxidized fats that can be toxic to the host. The induced oxidative stress and systemic inflammation that accompany this can cause abnormal fat cell formation.
To clarify and expand the relationship between Hg growth and growth, further research is needed with more specific information such as fish diets after birth and co-exposures to environmental contaminants..”
