OBJECTIVES. This work was undertaken to determine whether there are any chronic neurological sequelae to acute organophosphate pesticide poisoning. METHODS. California surveillance data were used in a study of neurological function among 128 men poisoned by organophosphate pesticides in California from 1982 to 1990 and 90 referents. Tests included a neurological physical examination, 5 nerve conduction tests, 2 vibrotactile sensitivity tests, 10 neurobehavioral tests, and 1 postural sway test. RESULTS. After correcting for confounding, the poisoned group performed significantly worse than the referent group on two neurobehavioral tests (sustained visual attention and mood scales). When the data were restricted to men with documented cholinesterase inhibition (n = 83) or to men who had been hospitalized (n = 36), the poisoned subjects also showed significantly worse vibrotactile sensitivity of finger and toe. Significant trends of increased impairment were found with increased days of disability on a wide spectrum of tests of both central and peripheral nerve function. CONCLUSIONS. While these findings are limited by low response rates and by small sample sizes for specific pesticides, this study was based on a large surveillance database and is the largest study to date of the chronic effects of organophosphate pesticide poisoning. The evidence of some long-term effects of poisoning is consistent with two prior studies.
Central giant cell granulomas (CGCGs) are jaw tumors of unknown origin that often exhibit an aggressive, though unpredictable, clinical course. The purpose of this study was to determine the immunoprofile of the mononuclear cells that seem to be responsible for the biologic behavior of these tumors. Numbers of cells in cell cycle were also determined and compared in clinically aggressive and non-aggressive CGCGs. Sixteen aggressive and 12 non-aggressive CGCGs were immunohistochemically stained with antibodies to CD34, CD68, factor XIIIa, alpha-smooth muscle actin, prolyl 4-hydroxylase, Ki-67, and p53 protein. Cell populations and numbers of cells in cell cycle were determined through microscopic quantitative assessment. CD34-positive cells were limited to support vessels. CD68-positive mononuclear cells constituted a small population of cells in all tumors. With two exceptions, factor XIIIa-positive cells were rarely seen. Alpha-smooth muscle actin staining was present in approximately half the tumors, and occasionally large numbers of positive cells were seen. Most mononuclear cells were positive for fibroblast-associated antigen. No phenotypic differences were detected between aggressive and non-aggressive tumors. P53 protein did not appear to be overexpressed in CGCGs. Ki-67 staining showed that only mononuclear cells were in cell cycle, and that there were no differences between aggressive and non-aggressive tumors. We conclude that CGCGs are primarily fibroblastic (and myofibroblastic) tumors in which macrophages appear to play a secondary role. Tumor cells show no differentiation toward endothelial cells or macrophage-related dendrocytes (factor XIIIa). Cellular phenotypes and numbers of cells in cell cycle are similar in both aggressive and non-aggressive tumors.
Sixty-five farmers reported on pesticide use and the signs and symptoms of acute pesticide poisoning when using two different plant protection strategies: in 2003 using chemical controls and in 2004 using an approach to Integrated Pest Management (IPM) based on an ecological analysis of the field conditions. Exposure to organophosphates was confirmed as a serious risk factor for occupational poisoning. The adoption of IPM reduced the use of pesticides and halved the incidence of acute pesticide poisoning. Overall, the pesticide use spectrum shifted towards lower WHO Hazard Classes. A reduction of adverse health effects was attained through a reduction in exposure to toxic pesticides and behavioural changes. Given that other strategies to reduce the rate of acute poisoning have proven ineffective, interventions aiming to minimize pesticide poisoning in India and in other developing countries with similar rural conditions should focus on restricting the use of highly toxic compounds and educating farmers on IPM.
A group of 31 lettuce harvesters exposed to the organophosphate pesticide mevinphos presented to a local emergency room with moderate cholinergic symptoms and eye and skin irritation, with 22 of the subjects (76%) reporting three or more symptoms. None had baseline cholinesterase values, and plasma cholinesterase activity for all but two workers was above the lower limit of the laboratory normal range. None of the workers received antidotes and all were released for return to work. Twenty-nine workers sought additional care when symptoms persisted, and were followed by the investigators until 12 weeks after exposure. Plasma and red blood cell (RBC) cholinesterase increased until 14 days after exposure. Plasma cholinesterase was estimated to have been inhibited by an average of 15.6% (p less than 0.01), and RBC cholinesterase by 5.6% (p less than 0.01). These findings support the utility of sequential postexposure plasma cholinesterase analyses in confirmation of suspect organophosphate-induced illness when baseline values are not available.
Human biomonitoring investigations have provided data on a wide array of chemicals in blood and urine and in other tissues and fluids such as hair and human milk. These data have prompted questions such as a) What is the relationship between levels of environmental chemicals in humans and external exposures? b) What is the baseline or “background” level against which individual levels should be compared? and c) How can internal levels be used to draw conclusions about individual and/or population health? An interdisciplinary panel was convened for a 1-day workshop in November 2004 with the charge of focusing on three specific aspects of biomonitoring: characteristics of scientifically robust biomonitoring studies, interpretation of human biomonitoring data for potential risks to human health, and communication of results, uncertainties, and limitations of biomonitoring studies. In this report we describe the recommendations of the panel.
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