This study was designed to examine the environmental exposure of surface- and groundwater pollution in remote mountainous regions of northern Vietnam. In 2008, we monitored the loss of four commonly applied pesticides (imidacloprid, fenitrothion, fenobucarb, dichlorvos) from paddy rice farming systems to a receiving stream on the watershed scale and quantified groundwater pollution. For the entire monitoring period, runoff loss of pesticides from the watershed was estimated to range between 0.4% (dichlorvos) and 16% (fenitrothion) of the total applied mass. These losses were correlated well with the octanol–water partition coefficient and water solubility of pesticides (r2 = 0.78–0.99). In the groundwater collected from eight wells, all target pesticides were frequently detected. Maximum measured concentrations were 0.47, 0.22, 0.17, and 0.07 µg L−1 for fenitrothion, imidacloprid, fenobucarb, and dichlorvos, respectively. Our results strongly indicate that under the current management practice pesticide use in paddy fields poses a serious environmental problem in mountainous regions of northern Vietnam.
❑ Respiratory failure is the usual cause of death after acute poisoning by cholinesterase-inhibiting pesticides.
severe poisoning may include coma, pulmonary edema, ataxia, toxic psychosis (manifested as confusion or bizarre behavior), dyspnea, fasciculations, bradycardia, cardiac dysrhythmias, and weakness or paralysis. The actual cholinergic symptomatology may depend somewhat on the route of exposure and the balance between nicotinic (organophosphate pesticides) and muscarinic receptors (organophosphate and carbamate pesticides). (See Table 1, page 8.) The symptoms of carbamate poisoning typically are less severe and of shorter duration than those of organophosphate poisoning.
Poisoning due to chronic exposure to cholinesterase-inhibiting insecticides may not be readily apparent because the symptoms are sometimes nonspecific and resemble other illnesses such as influenza, heat exhaustion, alcohol toxicity, or simple fatigue. Also the history of exposure may not be particularly remarkable in such cases. Repeated absorption of organophosphates at subacute concentrations may cause persistent anorexia, weakness, and malaise (“orange-picker’s flu”), a condition seen in farm workers engaged in crop spraying. Certain neurobehavioral effects may persist after chronic exposure, as well as after acute toxicoses.
Despite the lack of distinct symptomatology, it is important to aggressively investigate all suspected cases of chronic pesticide poisoning because such a case may represent a sentinel event, indicating a workplace hazard or other populations at risk. In some states, failure to report a pesticide-related illness can result in a fine. (Check with your state health department.)
A combination of history, physical examination, and laboratory tests will provide the most appropriate approach to diagnosing pesticide-related illnesses.
Direct Biologic Indicators
❑ Analysis of blood and urine for direct evidence of organophosphate or carbamate exposure is valuable, but usually is available only from reference laboratories.
Detection of intact organophosphate or carbamate compounds in blood is usually not possible except during or soon after exposure. In general, cholinesterase-inhibiting pesticides do not remain unhydrolyzed in the blood more than a few minutes or hours, unless the quantity absorbed is large or the hydrolyzing liver enzymes are inhibited.
The metabolites of organophosphates (i.e., the corresponding alkyl phosphates) and the unique metabolites of N-methyl carbamates can often be detected in the urine up to 48 hours after exposure. The appearance of these urinary metabolites can demonstrate