Correlations between mercury concentrations in umbilical cord tissue and other biomarkers of fetal exposure to methylmercury in the Japanese population

Abstract

Methylmercury (MeHg) is one of the most risky substances to affect humans through fish consumption, and the fetus is known to be in the most susceptible group. Our objective in this study is to examine the relationships of total mercury (THg) and MeHg concentrations between umbilical cord tissue and other tissues as biomarkers of fetal exposure to MeHg in the Japanese population. In total, 116 paired samples were collected in three Japanese districts, the Tsushima Islands, Fukuoka City, and Katsushika ward of metropolitan Tokyo. THg was measured for hair and THg and MeHg were measured in cord tissues, maternal blood, and cord blood. The relationships among tissues in Hg concentrations were similar among districts. Therefore, we analyzed the relationships using all the samples. More than 90% of Hg in cord tissue, cord blood, and maternal blood was MeHg. THg and MeHg in cord blood was about two times higher than in maternal blood. A strong correlation was found between THg and MeHg in cord tissue. The cord tissue THg and MeHg showed a strong correlation with cord blood Hg, which is recognized as the best biomarker for fetal exposure to MeHg. The findings of this study indicate the significance of cord tissue THg and MeHg as biomarkers for fetal exposure to MeHg at parturition.

Introduction

Fetuses are known to be a high-risk group for methylmercury (MeHg) exposure because of the high susceptibility of the developing brain itself (Choi, 1989; Sakamoto et al., 1993; World Health Organization (WHO), 1990). Moreover, MeHg easily crosses the blood–placenta barrier, accumulating more in the fetus than the mother (Choi, 1989; Sakamoto et al., 2002, Sakamoto et al., 2004; Stern and Smith, 2003; WHO, 1990). Therefore, the effect of MeHg exposure on pregnant women is an important issue for elucidation, especially in Japanese and some other populations that consume much fish and sea mammals (Grandjean, 1997, Grandjean, 2005; Myers et al., 1995a, Myers et al., 1995b, Myers et al., 2003; National Research Council (NRC), 2000; WHO, 1990).

The epidemic called “Minamata disease” is well known as the first instance on record of severe MeHg poisoning caused by manmade environmental pollution, which occurred mainly among fishermen and their families in and around Minamata City. It originated from the consumption of large amounts of fish and shellfish contaminated with MeHg discharged from a chemical plant (Irukayama and Kondo, 1966). The principal symptoms included neurological disorders such as sensory disorders, cerebellar ataxia, contraction of the visual field, hearing impairments, and disequilibrium (Takeuchi et al., 1962). The first patient was reported in 1953, and the number of patients rapidly increased after 1955. Up to the present, more than 2000 people have been certified to have Minamata disease. Furthermore, many fetuses exposed to MeHg through the placenta of the exposed mother showed severe cerebral-palsy-like symptoms, while their mothers had mild or no manifestation of the poisoning (Harada, 1978). Outbreaks of the typical fetal-type Minamata disease occurred during 1955–1959 when the mercury pollution appears to have been most severe, judging from the incidence of patients (Harada, 1978) and the MeHg concentration in the preserved umbilical cords of inhabitants of the area (Nishigaki and Harada, 1975). During the period, a deceased male birth ratio associated with increased male fetal death was observed in Minamata City pollution, indicating its severity and widespread distribution (Sakamoto et al., 2001). This landmark epidemic was the first to bring worldwide attention to the high risk of fetal exposure to MeHg.

Thereafter, large prospective cohort studies were conducted in the Seychelles (Myers et al., 1995a, Myers et al., 1995b, Myers et al., 2003) and the Faroe Islands (Grandjean, 1997, Grandjean, 1999, Grandjean, 2005), where fish or sea mammal consumption is high. Though the MeHg exposure level was similar in these studies, different conclusions were reached (NRC, 2000). The exposure level in the epidemic in Minamata is thought to have been much higher than in those studies. Therefore, the study of Minamata disease is still very important, and it will provide more obvious health effect information by using recently developed neurological test batteries. Fortunately, Japanese people have a custom of preserving a small piece of the dried umbilical cord tissue as a birth memento in a wooden or plastic box deep inside a chest of drawers. MeHg in the tissue will not be reduced by microorganisms, because it is completely dried. By measuring the Hg concentrations in this preserved dry cord sample, we can estimate the individual MeHg exposure level at birth. Grandjean et al. (2005) revealed that cord tissue Hg as well as cord blood Hg was useful as a predictor of the effect of fetal exposure to MeHg. However, the preserved cord tissues had often been treated with mercurochrome at the period when cut off at parturition. The mercurochrome can easily dissociate into Hg ions in the solution and the ions act as a disinfectant. Then the cord tissue treated with mercurochrome shows a very high Hg concentration when total mercury (THg) is measured. Accordingly, we need to measure not THg but MeHg in the preserved cord tissue in Japan, especially in the samples treated back in those days. Some studies (Akagi et al., 1998; Nishigaki and Harada, 1975) have revealed exposure of the fetus to MeHg in the Minamata area by measuring it in the preserved cord tissue. The present study investigates the relationships between THg and MeHg in cord tissue and the relationships between other biomarkers of fetal exposure to MeHg in the Japanese population to evaluate the significance of the Hg concentrations in cord tissue.