Polychlorinated biphenyls (PCBs) in San Francisco Bay.

San Francisco Bay is facing a legacy of polychlorinated biphenyls (PCBs) spread widely across the land surface of the watershed, mixed deep into the sediment of the Bay, and contaminating the Bay food web to a degree that poses health risks to humans and wildlife. In response to this persistent problem, water quality managers are establishing a PCB total maximum daily load (TMDL) and implementation plan to accelerate the recovery of the Bay from decades of PCB contamination. This article provides a review of progress made over the past 15 years in managing PCBs and understanding their sources, pathways, fate, and effects in the Bay, and highlights remaining information needs that should be addressed in the next 10 years. The phaseout of PCBs during the 1970s and the 1979 federal ban on sale and production led to gradual declines from the 1970s to the present. However, 25 years after the ban, PCB concentrations in some Bay sport fish today are still more than ten times higher than the threshold of concern for human health. Without further management action it appears that the general recovery of the Bay from PCB contamination will take many more decades. PCB concentrations in sport fish were, along with mercury, a primary cause of a consumption advisory for the Bay and the consequent classification of the Bay as an impaired water body. Several sources of information indicate that PCB concentrations in the Bay may also be high enough to adversely affect wildlife, including rare and endangered species. The greater than 90% reduction in food web contamination needed to meet the targets for protection of human health would likely also generally eliminate risks to wildlife. PCB contamination in the Bay is primarily associated with industrial areas along the shoreline and in local watersheds. Strong spatial gradients in PCB concentrations persist decades after the release of these chemicals to Bay Area waterways. Through the TMDL process, attention is being more sharply focused on the PCB sources that are controllable and contributing most to PCB impairment in the Bay. Urban runoff from local watersheds is a particularly significant pathway for PCB entry into the Bay. Significant loads also enter the Bay through Delta outflow (riverine input). Recent studies have shown that erosion of buried sediment is occurring in large regions of the Bay, posing a significant problem with respect to recovery of the Bay from PCB contamination because the sediments being eroded and remobilized are from relatively contaminated buried sediment deposits. In-Bay contaminated sites are likely also a major contributor of PCBs to the Bay food web. Dredged material disposal, wastewater effluent, and atmospheric deposition are relatively minor pathways for PCB loading to the Bay. Priority information needs at present relate to understanding the sources, magnitude of loads, and effectiveness of management options for urban runoff; the regional influence of in-Bay contaminated sites; remobilization of PCBs from buried sediment; historic and present trends; in situ degradation rates of PCBs; reliable recovery forecasts under different management scenarios; the spatial distribution of PCBs in soils and sediments; and the biological effects of PCBs in interaction with other stressors. The slow release of pollutants from the watershed and the slow response of the Bay to changes in inputs combine to make this ecosystem very slow to recover from pollution of the watershed. The history of PCB contamination in the Bay underscores the importance of preventing persistent, particle-associated pollutants from entering this sensitive ecosystem.

Investigation of cerebrospinal fluid neuropeptides in idiopathic senile dementia.

Thyrotrophin-releasing hormone and gonadotrophin-releasing hormone were measured in lumbar CSF from patients with idiopathic senile dementia, cerebral tumours and spinal disc lesions. Somatostatin was also measured in lumbar CSF from patients with dementia and patients with other neurological disorders, but the numbers involved were much smaller. The levels of these neuropeptides were significantly reduced in the patients with senile dementia. These results suggest a possible involvement of hpothalamic neuropeptides in idiopathic senile dementia.

Neuroblastoma in adults.

Two cases of neuroblastoma are described in patients who were both more than 25 years old when their symptoms first appeared. The behaviour of this tumour appears less aggressive in adults than in children, but the cases presented illustrate its resistance to chemotherapy and radiotherapy, and surgery is suggested as the first line of treatment in adults, even if the growth cannot be removed completely.