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Environmental Medicine: Integrating a Missing Element into Medical Education
POISONING OF AN URBAN FAMILY DUE TO MISAPPLICATION OF HOUSEHOLD ORGANOPHOSPHATE AND CARBAMATE PESTICIDES
Steven B.Markowitz, M.D.
Department of Community Medicine, Mt. Sinai
School of Medicine, New York, New York
ABSTRACT
A case report of an urban family who experienced excessive exposure to organophosphate and carbamate pesticides is presented. All three family members developed symptoms that were compatible with cholinesterase inhibition: headache, lightheadedness, wheezing, shortness of breath, nausea, and fatigue. Serial measurement of red blood cell and serum cholinesterases soon after exposure and during subsequent months confirmed the diagnosis of pesticide poisoning. This report demonstrates that the misapplication of pesticides commonly used in residences in urban areas can cause acute pesticide poisoning and demonstrates the usefulness of repeated measurements of cholinesterase during the post-exposure period in establishing the correct diagnosis. (Key Words: pesticides; organophosphorus compounds; residential facilities; pest control; poisoning, human.)
Address reprint requests to: Dr. Steven Markowitz, Box 1057, Mt. Sinai School of Medicine, 1 Gustave L.Levy Place, New York, NY 10029.
Copyright © 1992 by Marcel Dekker, Inc.
Reprinted with permission from Clinical Toxicology 30(2):295–303, Copyright 1992, Marcel Dekkar, Inc.
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Environmental Medicine: Integrating a Missing Element into Medical Education
INTRODUCTION
Organophosphate and carbamate pesticides have been well documented to cause acute poisoning in humans in a variety of settings (1,2). These settings include occupational exposures among pesticide applicators, manufacturing workers and farm workers; accidental inhalation, skin absorption and ingestion, especially by children; and intentional attempts at suicide (1–6).
Organophosphates and carbamates are two of the dominant classes of pesticides used for residential pest control in urban areas in the United States. Despite widespread use of these agents and considerable concern about their possible deleterious effects, especially given the large population potentially exposed, there have been few reports of urban residents made acutely or chronically ill by pesticides (5–7).
This report describes a family with clinical and laboratory evidence of acute pesticide poisoning caused by the excessive application of pesticide products used for urban residential pest control.
Environmental History
The affected family consisted of three members, a 32 year-old mother, a 35 year-old father, and their 14 year-old daughter, who were well prior to late November, 1984, when their apartment underwent commercial pesticide application for extermination of fleas. The apartment had been sprayed with unknown pesticides two times several weeks previously without the desired result and without causing illness in the family. The father reported that on November 24, 1984, a professional pesticide applicator sprayed an unknown pesticide using a tank and hose apparatus; he subsequently used eight pressurized canisters (bombs) of a specific pesticide formulation. These canisters were filled with a commercial product containing two active pesticidal ingredients: an organophosphate pesticide, dichlorvos (2,2 dichlorovinyl dimethyl phosphate), and a carbamate pesticide, propoxur (2-(1-methylethoxy) phenol methylcarbamate). Additional “inert” ingredients of the preparation were not identified. Each container was recommended to be used for 6000 cubic feet; the apartment was estimated to have a volume of 7000 cubic feet.
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Environmental Medicine: Integrating a Missing Element into Medical Education
Three hours after application of these pesticides, the father entered the apartment and saw “clouds of vapor still lingering in the air”. He covered his face with a cloth, opened the windows of the apartment, and promptly left. He returned with the mother and daughter 3–4 hours later and noted that the previously observed fog of pesticides had cleared; the apartment, however, retained a residual odor of pesticides. The family slept in the apartment that night.
Clinical History
All three family members reported experiencing the following symptoms on the following morning: burning of the throat, chest heaviness, wheezing, shortness of breath, headache, fatigue and nausea. The mother and the daughter also experienced lightheadedness. The mother additionally noted abdominal cramping and loose stools. The father went to work for 8 h, while the others stayed in the apartment. On the following day, the family moved to a local motel for 2 w, during which the apartment was reportedly cleaned twice. Details concerning the extent of cleaning are not available. The family then returned to occupy the apartment, where they noted persistence of the odor of the sprayed material.
All family members visited their personal physician four days after the pesticide application, complaining of the symptoms noted above, which had diminished somewhat during the intervening days. The results of serum and erythrocyte cholinesterase are shown in Table 1. Serum and erythrocyte cholinesterase analyses were performed by Metpath Laboratory (Teterboro, NJ) using kits supplied by Boehringer-Mannheim Diagnostics (erythrocyte cholinesterase) and Gilford (serum cholinesterase) employing a modification of the Ellman method (8).
Upon examination six weeks after initial exposure, the father reported persistence of selected symptoms including headache, fatigue and throat irritation, though these had diminished in intensity. The mother continued to complain of slight shortness of breath, chest tightness, wheezing and minimal abdominal cramping. She reported having used albuterol during the several weeks prior to her visit. The daughter’s symptoms had also decreased but she still experienced nausea, headache, sore throat, and some wheezing when in the apartment.
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Environmental Medicine: Integrating a Missing Element into Medical Education
TABLE 1 Recovery of Red Blood Cell Serum and Cholinesterase Levels
Cholinesterase Levels*
Date of Testing
11/28/84
1/8/85
2/13/85
Percent Increase**
Father
RBC
3.81
4.30
5.00
24%
Serum
2.60
7.10
6.00
57%
Mother
RBC
3.20
NA
4.20
24%
Serum
2.20
5.50
4.20
48%
Daugher
RBC
2.71
3.20
3.80
29%
Serum
0.90
4.80
3.80
76%
*normal ranges; RBC cholinesterase: 3.00–5.00 IU/mL; serum cholinesterase: 2.50–7.10 units/mL
**
The father had a history of allergic rhinitis, which occurred only during the spring. He worked as a carpenter. The mother had a past history of childhood asthma, which had abated by the age of 7. She experienced occasional wheezing as an adult, which she treated with a non-prescription bronchodilator. The child also had a history of asthma, which had not been recently active and had received albuterol from her personal physician during the current illness.
Physical examinations of all three family members were normal with the exception of minimal wheezing on forced expiration heard in the lower left lung of the mother. Pulmonary function tests performed on the two adults were also normal, except for a minimal decrease in the mother’s forced vital capacity (78% predicted).
Sequential measurements of serum and red blood cholinesterase over the three month period following the incident until mid-February 1985 are provided in Table 1. The father’s initial values of serum and erythrocyte cholinesterase were within normal limits (2.60 µ/mL and 3.81 IU/mL,
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respectively). The mother’s serum cholinesterase level was initially low, 2.20 U/mL, and her erythrocyte cholinesterase was normal at 3.20 IU/mL. The daughter had low initial values of both serum and erythrocyte cholinesterase levels (0.90 U/mL and 2.71 IU/mL, respectively). All measurements were performed by Metpath.
Repeat testing of red blood cell and serum cholinesterase on all three patients in January and February, 1985, showed significant increases in values for these tests during the intervening 6 and 11 weeks. All members of the family demonstrated a 24 to 29% increase in the erythrocyte cholinesterase from the immediate post-exposure measurement to the measurement obtained 11 weeks later. The mean increase was 26.1 % (paired t=−19.92, two tail p=.003) (9). For the serum cholinesterase, there was a 48 to 76% increase for all members in the family during the same time interval. The mean increase was 59.4% (paired t=−6.75, two tail p= .021) (9).
DISCUSSION
Diagnosis of mild to moderate organophosphate or carbamate poisoning is frequently difficult (1,10). The symptoms are non-specific and mimic other common disorders, such as viral infections. Laboratory confirmation of the diagnosis of such poisoning is, therefore, essential in all but the most severe clinical cases or in circumstances of obvious over-exposure to relevant pesticides. The clinical significance of any specific level of erythrocyte or plasma cholinesterase is measured by its percent decrease from a baseline pre-exposure level or by the degree to which the values are frankly below the established reference range (11).
Laboratory assessment of organophosphate or carbamate poisoning is complicated, however, by the relatively high inter-individual and intra-individual variability in levels of erythrocyte and serum cholinesterase. The coefficient of variation in cholinesterase between individuals is relatively high, ranging from 13% to 16% or higher for erythrocyte cholinesterase (1,12,13) and 15% to 27% for plasma cholinesterase (1,12,14).
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Intra-individual variation over time is somewhat lower. The average coefficient of intra-individual variation for plasma and erythrocyte cholinesterases in the published literature ranges from 7.6% to 11.3% (1, 15–17), though individual samples may fluctuate as much as 25% (1,17,18).
According to Gallo and Lawryk (1), if one pre-exposure cholinesterase measurement is available, then the subsequent depression of cholinesterase must be at least 20% for the plasma enzyme and 15% for the erythrocyte enzyme to reflect a significant statistical change. The percentage alterations in erythrocyte cholinesterase of 24–29% and of serum cholinesterase of 48% to 75% are higher than that expected due to normal variation.
While having pre-exposure measurements of cholinesterase levels in individuals is preferred due to the narrower intra-individual variation, they are usually not available in cases with non-occupational exposure to pesticides (11,19). In the absence of such pre-exposure measurements, sequential post-exposure measurements can be used to estimate the pre-exposure cholinesterase levels in the patients. Midtling and others described an outbreak of acute mevinphos poisoning among a group of 16 lettuce growers in California who developed symptoms compatible with organophosphate poisoning. Cholinesterase levels rose in the weeks following the outbreak of illness (4). In this report, the father had normal values initially for both erythrocyte and serum cholinesterases. Sequential measurements taken 6 and 11 weeks later, however, clearly demonstrated that the father experienced the recovery of cholinesterase levels of the same magnitude as the other two family members.
Of note is that the serum cholinesterase was more severely inhibited in these cases than the erythrocyte cholinesterase, an effect that has been previously observed with dichlorvos (20). It is possible that the recovery of the erythrocyte cholinesterase may be underestimated in this report since the interval between the first and last cholinesterase measurements was less than 12 weeks, which is the average life span of erythrocytes and the period over which a diminished level of erythrocyte cholinesterase can be expected to normalize. Serum cholinesterase, on the other hand, recovers in one to three weeks.
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Many of the symptoms experienced by the exposed persons in the present report—chest tightness, shortness of breath, headaches, lightheadedness, fatigue, nausea, and diarrhea—are compatible with the diagnosis of mild to moderate organophosphate and carbamate poisoning. Many of these same symptoms may be caused by excessive exposure to the solvent carriers that are often contained in commercial pesticide formulations. In the absence of exposure measurements or the identity of the solvents that were likely present, solvents may have contributed to the symptoms experienced. However, the level of cholinesterase inhibition strongly supports the contention that anti-cholinesterase activity was a significant factor in the complex of symptoms suffered by this family.
The persistence of symptoms, albeit attenuated, after six weeks following initial exposure is not fully explained. Since the levels of the cholinesterases had reverted to the normal range by six weeks, the symptoms that were still present at six weeks were not due to the short-term anti-cholinesterase effect of dichlorvos and propoxur. One possible explanation is that exposure to other toxins such as the solvent carriers continued, which is unlikely in view of the repeated cleaning of the apartment and the expectedly rapid volatilization of the solvents typically used as carriers. Another possible explanation is the lingering of the symptoms associated with cholinesterase inhibition, even in the absence of active inhibition. There is limited evidence of the persistence of symptoms beyond the immediate period of organophosphate poisoning (4,21), though most of the studies of persistent effects have focused on central nervous system effects rather the multi-organ symptoms that characterize acute organophosphate poisoning (22–24).
Use of pesticides in buildings and on lawns is widespread throughout the United States and represents an important means by which a large proportion of the population of the United States is potentially exposed to pesticides. Instances of organophosphate or carbamate poisoning such as described in this case report are unusual in the medical literature (5–7). This may be due to the widespread safe use of pesticides, the difficulty in diagnosing mild acute and chronic pesticide poisoning, or the general lack of
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knowledge on the part of health care providers about eliciting environmental and occupational information from patients (25). With the progressive interest in environmental health, it is likely that additional cases of environmental pesticide poisoning will be recognized, especially if a carefully elicited environmental and occupational history results in the appropriate clinical and laboratory assessment of potential cases of such poisoning.
REFERENCES
1. Gallo MA, Lawryk NJ. Organic phosphorus pesticides. In: Handbook of Pesticide Toxicology Vol 2, Hayes WJ Jr, Laws ER Jr, eds., New York: Academic Press, 1991:948.
2. Moses M. Pesticides. In: Environmental and Occupational Medicine. Rom W, ed., Boston: Little, Brown and Company, 1983:547–572.
3. Jackson RJ, Stratum JW, Goldman LR, et al. Aldicarb food poisoning from contaminated melons—California. MMWR 1986;35:254–258.
4. Midtling JE, Barnett PG, Coye MJ, et al. Clinical management of field worker organophosphate poisoning. West J Med 1985; 142:514–518.
5. Zwiener RJ, Ginsburg CM. Organophosphate and carbamate poisoning in infants and children. Pediatrics 1988;81:121–126.
6. Woody RC. The clinical spectrum of pediatric organophosphate intoxications. Neurotoxicology 1984;5:75.
7. Hodgson MJ, Parkinson DK. Diagnosis of organophosphate intoxication. N Engl J Med 1985;313:329.
8. Ellman GL, Courtney KD, Andres V, Featherstone RM. A new and rapid colorimetric determination of acetylcholinesterase activity. Biochem Pharmacol 1961;7:88–95.
9. Zar JH. Biostatistical Analysis. 2nd Ed., Englewood Cliffs, NJ: Prentice-Hall, 1984.
10. Morgan DP. Recognition and Management of Pesticide Poisonings, Fourth Ed., Washington, DC: United States Environmental Protection Agency, 1989.
11. State of California Department of Health. Epidemiological Studies Laboratory. Medical Supervision of Pesticide Workers: Guidelines for Physicians. Berkeley, California, 1988.
12. Augustinsson K. The normal variation of human blood cholinesterase activity. Acta Physiol Scand 1955;35:40–52.
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13. George PM, Abernethy MH. Improved procedure for erythrocyte cholinesterase. Clin Chem 1983;29:365–368.
14. Lewis PJ, Lowing RK, Gompertz D. Automated discrete kinetic method for erythrocyte acetylcholinesterase and plasma cholinesterase. Clin Chem 1981;27:926–929.
15. Wetstone HJ, LaMotta RV. The clinical stability of serum cholinesterase activity. Clin Chem 1965;1:370.
16. Gage JC. Blood cholinesterase values in early diagnosis of excessive exposure to phosphorous insecticides. Br Med J 1955;1:370.
17. Callaway S, Davies DR, Rutland PJ. Blood cholinesterase levels and range of personal variation in a healthy adult population. Br Med J 1951;2:812–816.
18. Fryer JH, Steel RGD, Williams HH. Cholinesterase activity levels in normal human subjects. AMA Arch Ind Health 1955;12:406–411.
19. Coye MJ, Lowe JA, Madday KT. Biological monitoring of agricultural workers exposed to pesticides: Cholinesterase activity determinations. J Occup Med 1988;28:619–627.
20. Rasmussin WA, Jensen JA, Stein WJ, Hayes WJ. Jr. Toxicological studies of DDVP for disinfection of aircraft. Aerospace Med 1963;34:594–600.
21. Tabershaw IR, Cooper WC. Sequelae of acute organic phosphate poisoning. J Occup Med 1966;8:5–20.
22. Savage EP, Keefe TH, Mounce LM, et al. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Arch Environ Health 1988;43:38–45.
23. Korsak RJ, Sato MM. Effects of chronic organophosphate pesticide exposure on the central nervous system. Clin Toxicol 1977;11:83–95.
24. Rosenstock L, Keifer M, Daniell WE, et al. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Lancet 1991;338:223–227.
25. Demers RY, Wall SJ. Occupational history taking in a family practice setting. J Med Educ 1983;58:151–153.
Representative terms from entire chapter:
serum cholinesterase
