MERCURY:  Neurotoxicity and Molecular Effects of Methylmercury
Source: Pavia and "Salvatore Maugeri" Foundation, Pavia, Italy; and 2 Karolinska
Institute, Stockholm, Sweden

Abstract
The neurotoxicity of high levels of methylmercury (MeHg) and the high susceptibility of the developing brain are well established both in humans and experimental animals. Prenatally poisoned children display a range of effects varying from severe cerebral palsy to subtle developmental delays. Still unknown is the lowest dose that impairs neurodevelopment.

In the adult, MeHg poisoning is characterized by damage to discrete anatomical areas of the brain, such as the visual cortex and the granule layer of the cerebellum, axon degeneration associated with secondary myelin disruption of the sensory branch of the peripheral nerve with preservation of the motor branch.

Overt signs and symptoms may take weeks or months before they become manifest. Such effects include constriction of the visual field and other visual abnormalities, sensory impairment of the extremities cerebellar ataxia, hearing loss, muscle weakness, tremor, and mental deterioration.

For the child, the immature central nervous system (CNS) is extremely sensitive to MeHg neurotoxicity and the fetal brain may be affected even if the mother shows no signs of poisoning.

Unlike focal damage in adults, the developing brain shows a diffuse and wide-spread damage. High-dose exposure may result in cerebral palsy, blindness, deafness, and severe mental retardation.

LEAD:  Lifetime Exposure to Environmental Lead and Children's Intelligence at 11-13 Years: The Port Pirie Cohort Study
Source: J Appl Toxicol. 1999 May-Jun;19(3):167-72.
Shilu Tong,Peter Baghurst, Anthony McMichael, Michael Sawyer, Jane Mudge,

Division of Human Nutrition, Commonwealth Scientific Industrial Research Organisation, Australia, Department of Epidemiology and Population Sciences, London School of Hygiene and Tropical Medicine, London Women's and Children's Hospital, Adelaide, Australia

Abstract
Objective: To examine the association between environmental exposure to lead and children's intelligence at age 11-13 years, and to assess the implications of exposure in the first seven years of life for later childhood development.

Design: Prospective cohort study.
Subjects: 375 children born in or around the lead smelting town of Port Pirie, Australia, between 1979 and 1982.
Main outcome measure: Children's intelligence quotient (IQ) measured at 11-13 years of age.

Results: IQ was inversely associated with both antenatal and postnatal blood lead concentrations. Verbal, performance, and full scale IQ were inversely related to blood lead concentration with no apparent threshold. Multivariate analyses indicated that after adjustment for a wide range of confounders, the postnatal blood lead concentrations (particularly within the age range 15 months to 7 years) exhibited inverse associations with IQ. Strong associations with IQ were observed for lifetime average blood lead concentrations at various ages. The expected mean full scale IQ declined by 3.0 points (95% confidence interval 0.07 to 5.93) for an increase in lifetime average blood lead concentration from 0.48 to 0.96 µmol/l (10 to 20 µg/dl).

Conclusions: Exposure to environmental lead during the first seven years of life is associated with cognitive deficits that seem to persist into later childhood.