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Acute Poisoning Following Exposure to an Agricultural Insecticide -- California

In 1984, 1,156 workers were documented to have had possible pesticide-related illnesses in California. Twenty of the 274 workers exposed to field residues had systemic reactions, one of which was related to exposure to Phosdrin (mevinphos), an organophosphate insecticide (1). Although only one systemic reaction to mevinphos was reported among California field workers for each of the years 1982-1984, a 1981 incident involved over 30 workers and is reported below.

At 7 a.m. on April 23, 1981, 44 farm workers entered a field in the Salinas Valley of California to harvest a crop of iceberg lettuce. By 9 a.m., several workers experienced dizziness, visual disturbances, headache, nausea, and eye irritation. At 11 a.m., a field supervisor reported that, at 5 a.m. the same morning, despite a cancellation order sent the previous day, the field had been sprayed with mevinphos.

Thirty-one field workers and three agricultural officials who had been inspecting the harvested lettuce were seen at a local hospital for evaluation and treatment. Tests for plasma cholinesterase were performed. Two workers were hospitalized for observation and treatment of respiratory difficulties. Two others had plasma cholinesterase levels below the lower limit of normal. The remaining workers disrobed, were "hosed down" with water, and after redressing, were instructed to wash their clothes when they got home; none was advised against returning to work the following day.

The next day, several workers were unable to return to work because of continuing symptoms. A union representative arranged for further examinations at a second hospital; 29 workers were examined and tested for cholinesterase activity. One was hospitalized because of bradycardia.

Investigators from the National Institute for Occupational Safety and Health (NIOSH), in collaboration with investigators from the second hospital, conducted an investigation beginning April 24 during the acute phase of this episode (2). They interviewed the 29 workers who reported symptoms and signs, including eye irritation (76%), headache (48%), visual disturbances (48%), dizziness (41%), nausea (38%), fatigue (28%), chest pain or shortness of breath (21%), skin irritation (17%), fasciculation of the eyelids (10%), fasciculation of muscles in the arm (7%), excessive sweating (7%), and diarrhea (7%). Twenty-two (76%) of the workers reported three or more symptoms or signs.

Levels of plasma cholinesterase and red blood cell (RBC) cholinesterase were determined for all 29 workers on April 24; no result was below the lower limit of normal. When the workers returned 6 days later for follow-up examinations, tests for cholinesterase were again performed. The mean plasma cholinesterase level for the group had increased by 5 Michel units; 2 weeks later, when 26 workers were tested a third time, the mean plasma cholinesterase level had increased by another 14 Michel units. These increases were found to be statistically significant.

Periodic examinations over the next 12 weeks also included tests for cholinesterase. For 27 workers, followed for at least 8 weeks each, investigators attempted to estimate presumptive "baseline" levels of plasma- and RBC-cholinesterase levels by averaging the results of the previous two tests. Comparing these derived "baseline" levels retrospectively with the values determined during the acute phase of the episode, it was possible to estimate an average depression of cholinesterase activity. The average depression for plasma cholinesterase was 15.6%, and for RBC cholinesterase, 5.6%. These estimated depressions were presumed to be caused by the exposure to mevinphos. For both plasma cholinesterase and RBC cholinesterase, the estimated depression was greater among workers reporting four or more signs or symptoms than among those reporting fewer than four, but this difference was not statistically significant. Cholinesterase activity appeared to return to the estimated "baseline" levels within 2 weeks after the exposure to mevinphos. Reported by J Midtling, MD, A Velasco, MD, C Clements, MD, P Barnett, Natividad Medical Center, Salinas, RJ Jackson, MD, DC Mengle, MS, Epidemiological Studies Section, Health Protection Div, California Dept of Health Svcs; Hazard Evaluations and Technical Assistance Br, Div of Surveillance, Hazard Evaluations, and Field Studies, National Institute for Occupational Safety and Health, CDC.

Editorial Note

Editorial Note: Organophosphates inhibit the enzyme, cholinesterase; toxic effects from exposure to organophosphates are believed due to a consequent increase of the neurotransmitter, acetylcholine, in the nervous system. The antidotes are atropine, which blocks the effects of acetylocholine, and Protopam Chloride (pralidoxime chloride), which "reactivates" acetylcholinesterase (3). Humans have two cholinesterases, RBC cholinesterase (or "true cholinesterase") and plasma cholinesterase (or "pseudocholinesterase"), which are generated in the liver.

Symptoms following moderate exposure to organophosphates include headache, dizziness, weakness, nausea and vomiting, fasciculations of eyelids and skin, blurred vision (due to pupillary constriction), and sweating. More severe exposures may cause abdominal cramps, muscular tremors, hypotension, bradycardia, dyspnea, and, ultimately, death from respiratory paralysis (4). The chronic health effects of exposure to the organophosphate residues have not been fully investigated (5,6), but are currently under study by NIOSH (7).

Acute poisoning due to organophosphate insecticides is diagnosed by a history of exposure and the appearance of typical signs and symptoms; the diagnosis is assisted by a favorable response to a test dose of atropine. Poisoning is confirmed by laboratory tests that demonstrate a depression (usually 25% or more) in cholinesterase activity. Because plasma cholinesterase is generated in the liver and may be affected by any factor that alters normal liver function, it is considered more labile than RBC cholinesterase. Hence, RBC cholinesterase, which measures the same enzyme that is active in nerve tissue, is the preferred index of toxic effects. During recovery from a toxic inhibition of cholinesterase, RBC cholinesterase is regenerated more slowly than plasma cholinesterase (8).

The prevalence of signs and symptoms among the 29 workers studied was not recorded beyond the day after exposure to mevinphos. These workers may have intensified their exposure by redonning clothing contaminated with pesticide residue. The pattern of increasing postexposure cholinesterase values seen among these workers suggests that they experienced significant depressions of cholinesterase soon after exposure, despite acute-phase test results within the normal range. In turn, this suggests that, in the absence of previously measured baseline values for cholinesterase, the results of tests after possible toxic exposures must be interpreted with caution. Exposures to organophosphates can produce significant toxicity even though laboratory results of postexposure tests fall within the normal range. Thus, when workers with possible exposure to organophosphates present with symptoms, such as those described, and do not have previously established baseline values for cholinesterase activity, test results in the low or middle portion of the range of laboratory normal values should not rule out the presence of significant toxicity. Preexposure baseline levels should be established for each worker expected to be frequently exposed to organophosphates or their residues.

The rate of decrease in cholinesterase levels is thought to correlate more directly with symptoms than is the amount of the depression. Because moderate exposure on a continuing basis produces a cumulative effect, continuous moderate exposures may cause the cholinesterase level to gradually fall; a sudden, unexplained onset of symptoms may occur when the cholinesterase level falls below a "threshold" in the worker. Thus, symptomatic workers, and those with a demonstrated depression of cholinesterase activity, are at increased risk if they continue to work in jobs exposing them to cholinesterase inhibitors before they have fully recovered (9). State health officials have estimated that as few as 1% of the residue-induced illnesses among California field workers are reported (5).


  1. California Department of Food and Agriculture, Worker Health and Safety Branch. Summary of reports from physicians of illnesses that were possibly related to pesticide exposure during the period January 1-December 31, 1984, in California. Occupational Injury Report (HS1304). Sacramento, California: Department of Food and Agriculture, April 1985.

  2. National Institute for Occupational Safety and Health. Health hazard evaluation report no. HETA 81-301-1467. Cincinnati, Ohio: National Institute for Occupational Safety and Health, 1984.

  3. Moss M. Pesticides. In: Rom, WN, ed. Environmental and occupational medicine. Boston, Massachusetts: Little, Brown, and Co., 1983:555-6.

  4. U.S. Environmental Protection Agency. Recognition and management of pesticide poisonings, 3rd ed. Washington, DC: U.S. Environmental Protection Agency, 1982. (EPA publication no.

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