Suchergebnisse

Lead poisoning is the most common disease of environmental origin in the United States today. Adult lead poisoning results primarily from exposure by inhalation in the workplace. Pediatric lead poisoning results principally from the ingestion of lead from environmental media, including paint chips, dust, soil, drinking water, ceramics, and medications. Lead is toxic to many organ systems, among them developing erythrocytes, the kidneys, and the nervous system. Lead-induced toxicity to the central nervous system causes delayed development, diminished intelligence, and altered behavior. In young children, this effect has been demonstrated convincingly to occur at blood lead levels between 10 and 20 micrograms per dl. The Centers for Disease Control and Prevention has recommended that a blood lead level of 10 micrograms per dl or higher be considered evidence of increased lead absorption, and the National Academy of Sciences has concurred in that recommendation. Unresolved issues in need of further study include the frequency of screening young children for lead, the question of whether women should be offered screening for lead before conceiving a pregnancy, the role of x-ray fluorescence analysis in assessing lead in bone, and the appropriate legislative response of the United States government to lead-based paint abatement.

In this study of the phenomenon of lead poisoning in children, the various approaches that several cities have employed to combat the problem are discussed. Several suggestions for dealing with the situation are proposed. These include educational programs, followup reports, legislation, and research.

The incidence of secondary poisoning was determined by using radio-telemetry
to assess the survival of 68 ferrets and 21 cats on two treatment sites and
one control site in the dry tussock grasslands of New Zealand. The treatment
sites were aerially poisoned with 1080-coated carrot baits (0.02%
wt/wt) to control rabbits. The control site was not poisoned. Ferrets and
cats were monitored at two-weekly intervals for at least 1 month before, and 2
months after the poison operations. Muscle samples from ferrets and cats that
died within 50 days of poisoning on the treatment sites were assayed for 1080.
In all, 7–11% (n = 28) of ferrets on one site and
8–15% (n = 26) of ferrets at the other site apparently
died of secondary 1080 poisoning. Natural mortality rates of ferrets were
46–81% per annum. While we have evidence that secondary poisoning
of cats does occur, we monitored insufficient numbers of cats to reliably
estimate mortality rates.
Declines in predator numbers are commonly observed after rabbit poisoning.
This study indicates that secondary poisoning contributes to these declines.

For some neurotoxic chemicals, neurobehavioral effects are now considered to be among the most sensitive end points yet detected, particularly if exposures occur during critical windows of vulnerability. Chemically induced problems with perception and cognitive ability in children can be hard to identify; teasing them out of a host of genetic and sociocultural influences is a difficult task. Today, most data on environmentally relevant neurobehavioral effects in children are concentrated in three chemicals: lead, methylmercury, and polychlorinated biphenyls. But mounting evidence of the neurobehavioral effects of chemicals along with growing public concern over pediatric mental health problems such as attention deficit/hyperactivity disorder dictates that scientists and legislators improve test methods, explore mechanisms, and develop appropriate strategies for risk assessment and policy making.