There is global concern over significant threats from a wide variety of environmental hazards to which children face. Large-scale and long-term birth cohort studies are needed for better environmental management based on sound science. The primary objective of the Japan Environment and Children’s Study (JECS), a nation-wide birth cohort study that started its recruitment in January 2011, is to elucidate environmental factors that affect children’s health and development.

Arsenic toxicity is a global health problem affecting many millions of people. The main source of exposure is drinking water contaminated by natural geological sources. Current risk assessment is based on the recognized carcinogenicity of arsenic, but neurotoxic risks have been overlooked. In 1955, an outbreak of arsenic poisoning occurred among Japanese infants, with more than 100 deaths. The source was contaminated milk powder produced by the Morinaga company. Detailed accounts of the Morinaga dried milk poisoning were published in Japanese only, and an overview of this poisoning incident and its long-term consequences is therefore presented. From analyses available, the arsenic concentration in milk made from the Morinaga milk powder is calculated to be about 4–7 mg/L, corresponding to daily doses slightly above 500 μg/kg body weight. Lower exposures would result from using diluted milk. Clinical poisoning cases occurred after a few weeks of exposure, with a total dose of about 60 mg. This experience provides clear-cut evidence for hazard assessment of the developmental neurotoxicity. At the present time, more than 600 surviving victims, now in their 50s, have been reported to suffer from severe sequelae, such as mental retardation, neurological diseases, and other disabilities. Along with more recent epidemiological studies of children with environmental arsenic exposures, the data amply demonstrate the need to consider neurotoxicity as a key concern in risk assessment of inorganic arsenic exposure.

Lead Toxicity: Does the Critical Level of Lead Resulting in Adverse Effects Differ between Adults and Children?: Katsuyuki Murata, et al. Department of Environmental Health Sciences, Akita University School of MedicineObjectives: The Scientific Committee on Neurotoxicology and Psychophysiology and the Scientific Committee on the Toxicology of Metals of the International Commission on Occupational Health in 2006 recommended that the standard for blood lead (BPb) levels be reduced to 30 µg/dl for industrial workers and 5 µg/dl for children. To examine whether the critical level of lead producing adverse effects truly differs between workers and children, we provided an overview of studies addressing the critical level of lead in workers, together with a perspective on lead toxicity in children.Data sources and extraction: In 25 reports published in English with keywords of “benchmark dose (BMD),” “lead” and “humans,” only five studies proved to be relevant to lead toxicity. Four more studies with figures illustrating significant relationships between lead and neurotoxic outcomes were selected.Data synthesis: Based on data from previous reports using a BMD approach, the critical organ of lead in workers was thought to be the nervous system and the critical BPb level (number‐weighted mean) was between 10.7 and 17.5 µg/dl. The neurotoxic effects of lead exposure at such levels seemed reversible. The BPb level at which lead‐associated intellectual deficits occurred in children was as low as the critical level of BPb (below 5 µg/dl) for inhibited heme synthesis in workers.Conclusions: The neurotoxic effects of lead in workers appear to be initiated at BPb levels below 18 µg/dl, which are somewhat higher than the critical level of lead neurotoxicity in children. Each national institute for risk management should take evidence‐based preventive action against subclinical lead poisoning in workers, as well as in children.

The main chemical forms of mercury are elemental mercury, inorganic divalent mercury, and methylmercury, which are metabolized in different ways and have differing toxic effects in humans. Among the various chemical forms of mercury, methylmercury is known to be particularly neurotoxic, and was identified as the cause of Minamata disease. It bioaccumulates in fish and shellfish via aquatic food webs, and fish and sea mammals at high trophic levels exhibit high mercury concentrations. Most human methylmercury exposure occurs through seafood consumption. Methylmercury easily penetrates the blood-brain barrier and so can affect the nervous system. Fetuses are known to be at particularly high risk of methylmercury exposure. In this review, we summarize the health effects and exposure assessment of methylmercury as follows: (1) methylmercury toxicity, (2) history and background of Minamata disease, (3) methylmercury pollution in the Minamata area according to analyses of preserved umbilical cords, (4) changes in the sex ratio in Minamata area, (5) neuropathology in fetuses, (6) kinetics of methylmercury in fetuses, (7) exposure assessment in fetuses.