{'fraction_non_alphanumeric': 0.015648854961832062, 'fraction_numerical': 0.0007633587786259542, 'mean_word_length': 5.392682926829268, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Lead and neurobehavioral development in gulls: a model for understanding effects in the laboratory and the field.

Animals, including humans, are increasingly exposed to a variety of environmental chemicals that can cause adverse developmental neurobehavioral effects. Most studies either examine effects in the laboratory, or report levels in wild animals, but the relationship between dose, tissue levels and effects are seldom examined in one system. Establishing this relationship is particularly important for endocrine disruptors because of the current controversies regarding impacts on both humans and wildlife. In this paper we synthesize results from a 10-year research program that uses the herring gull chick as a model to examine the relationship between dose, tissue levels, and response to lead in both the laboratory and the wild; and compare levels that cause deficits to those that occur in wild populations of a number of birds. The laboratory studies show that lead affects several aspects of neurobehavioral development in herring gull chicks. There are critical periods for the effects of lead on neurobehavioral development; and there are dissociations: different behaviors have different critical periods. Response latency may be affected most when exposure occurs at one age, while accuracy of response may be affected more at a different age of exposure. Further, there is not necessarily a correlation between impairment and the recovery trajectory. The field experiments show that there are similar lead-induced neurobehavioral deficits in the wild as occur in the laboratory. However, there were important differences: recovery occurred sooner in the field compared to the laboratory; parents partially compensated for the behavioral deficits and succeeded in getting surviving chicks to a similar fledging weight as control chicks, and although survival was decreased in lead-injected chicks in the wild, it was not as low as predicted because of the protective behavior of their parents. These impairments resulted in decreases in survival, which reduced overall fledging rates for a population with lead exposure. Data on exposure levels, as indicated by lead levels in feathers of birds worldwide, suggest that some birds are at risk of neurobehavioral impairment from exposure to lead. Although the neurobehavioral deficits are subtle, and difficult to prove using only wild populations, the data from the field experiments with herring gulls clearly indicate that the deficits occur. This providers a model for studying the neurobehavioral effects of any chemicals on wild populations.