Buchholz U, Mermin J, Rios R, Casagrande TL, Galey F, Lee M, Quattrone A, Farrar J, Nagelkerke N, Werner SB. An Outbreak of Food-Borne Illness Associated With Methomyl-Contaminated Salt. JAMA. 2002;288(5):604-610. doi:10.1001/jama.288.5.604
Author Affiliations: Epidemic Intelligence Service, Epidemiology Program Office, Centers for Disease Control and Prevention, Atlanta, Ga (Drs Buchholz and Mermin); Fresno County Department of Community Health, Fresno, Calif (Messrs Rios and Casagrande); University of California, Davis (Dr Galey); California Department of Food and Agriculture, Sacramento (Dr Lee); California State Department of Health Services, Berkeley and Sacramento (Drs Quattrone, Farrar, and Werner); and the National Institute for Public Health and the Environment, Bilthoven, the Netherlands (Dr Nagelkerke). Dr Buchholz is now at the Robert Koch-Institut, Berlin, Germany; Dr Mermin is now at the Global AIDS Program, National Center for HIV, STD, and TB Prevention, Centers for Disease Control and Prevention; Mr Rios is now at the Merced County Department of Public Health, Merced, Calif; and Dr Galey is now at the University of Wyoming, Laramie.
Context On January 5, 1999, the California Department of Health Services was
notified of the repeated occurrence (December 21, 1998, and January 2, 1999)
of gastrointestinal tract illness among patrons at a Thai restaurant in central
Objective To identify the source of the outbreak.
Design Case-control study; microbiological and toxicological laboratory testing
of samples of food, stool, and vomitus.
Setting Thai food restaurant in central California.
Participants Patrons of the restaurant. A case (n = 107) was defined as dizziness,
nausea, or vomiting occurring in a person who ate at the restaurant between
December 20, 1998, and January 2, 1999, with onset of symptoms within 2 hours
of eating. A control (n = 169) was a person who ate at the restaurant during
the same period but reported no symptoms.
Main Outcome Measures Odds ratios (ORs) of illness associated with food exposures; ORs of
shifts during which illness occurred associated with certain cooks; laboratory
Results The median latency period was 40 minutes from beginning eating to first
symptom and was 2 hours to onset of diarrhea. The median duration of symptoms
was 6 hours. Twenty-six persons (24%) visited the emergency department or
were treated by a physician; no person required hospitalization. Patients
reported nausea (95%), dizziness (72%), abdominal cramps (58%), headache (52%),
vomiting (51%), chills (48%), and diarrhea (46%). Fifty-one cases (48%) included
dizziness, lightheadedness, or a feeling of disequilibrium as the initial
symptom. Illness was statistically associated with several foods and ingredients,
but no single dish or ingredient explained a substantial number of cases.
The analysis of food exposures included salt added by cooks, as estimated
by using the amount of salt in the recipe for each dish and the amount of
each dish eaten by respondents. This association was stronger with increasing
levels of salt: ORs for illness among persons who consumed more than 0.42
to 0.84, more than 0.84 to 1.25, and more than 1.25 tsp of salt added to foods
in the kitchen were 1.9 (95% confidence interval [CI], 0.6-5.7), 3.0 (95%
CI, 1.0-8.8), and 4.0 (95% CI, 1.3-13.5) compared with persons who consumed
less than 0.42 tsp (P value for trend = .004). Methomyl,
a highly toxic carbamate pesticide, was identified in a sample of vomitus
(20 ppm) and in salt taken from containers in the storeroom (mean, 5600 ppm)
and the stovetop (mean, 1425 ppm). The oral toxic dose causing illness in
50% of those exposed to methomyl was estimated to be 0.15 mg/kg of body weight
(estimated range, 0.09-0.31 mg/kg of body weight). The presence of cook A
was associated with shifts during which cases of illness occurred (OR, 10.4;
95% CI, 1.2-157.4).
Conclusion This outbreak of gastrointestinal illness was associated with the consumption of food seasoned with
methomyl-contaminated salt. To allow rapid assessment for further
investigational and control measures by health officials, physicians
should report suspected outbreaks of illness to public health
departments, however trivial the symptoms or cause may seem.
On December 21, 1998, the Fresno County Health Department in California was notified of 8 persons who developed nausea, vomiting, and dizziness within
2 hours of eating at a local Thai restaurant. Although several persons were
treated at emergency departments, no one was hospitalized, and ill persons
recovered in less than 1 day. The Fresno County Health Department inspected
the restaurant and obtained several food samples for laboratory studies. Low
levels of Bacillus cereus were found in one sample
of cooked duck. A stool sample collected from one patient was negative for Campylobacter, Shigella, and Salmonella.
Twelve days later (January 2, 1999), 11 persons reported illness after
eating at the same restaurant. The intervals to onset, symptoms, and duration
were similar to those of the illnesses reported the previous week. The restaurant
closed voluntarily. The Fresno County Health Department interviewed ill patrons,
inspected the restaurant again, and obtained additional food samples. Initial
case findings in emergency departments of Fresno County hospitals identified
3 additional patients with similar symptoms and exposure history. On January
5, 1999, the California Department of Health Services was asked to assist
with the investigation.
We conducted a case-control study of customers. For persons who ate
at the restaurant between December 20, 1998, and January 2, 1999, a case of
restaurant-associated illness was defined as dizziness, nausea, or vomiting,
with onset of symptoms within 2 hours of eating. Controls were persons who
ate at the restaurant on the same days that cases of illness were reported
but who did not report illness themselves. By telephone, we administered a
questionnaire to cases and controls regarding demographic information, food
and beverages consumed, quantity consumed, and clinical symptoms following
the meal. We requested from the main chef the quantity of common ingredients,
including salt, typically added to each dish. The main chef ensured quality
and uniformity of food preparation by training new cooks personally for an
extended period and habitually supervising the preparation of all dishes served
We calculated the amount of salt consumed per person for the dishes
prepared at the restaurant by multiplying the amount of salt estimated to
have been added by the main chef in each dish by the proportion of the dish
that was consumed, as reported by study subjects. We then added the salt quantities
for all dishes eaten by each person. For trend analysis, we created 4 categories
of equal intervals (<0.42, >0.42 to 0.84, >0.84 to 1.25, and >1.25 tsp
of salt). Odds ratios (ORs) for illness among persons with different levels
of salt exposure were compared by using the Mantel-Haenszel χ2
test and P value for trend. For the association of
dichotomous exposures and illness, we calculated ORs and their 95% confidence
intervals (CIs). For the difference between the means in 2 groups, we used
the t test.
After the restaurant reopened, we counted the number of customers for
3 days and added their total charges to arrive at an average estimate of money
spent per customer, which was $11.62. We knew the gross income for the restaurant
for all days between December 20, 1998, and January 2, 1999. For example,
on January 2, 1999, the total was $1239.36. The number of customers was thus
estimated as the ratio of those gross incomes divided by $11.62. For January
2, 1999, this estimate was 107 ($1239.36/$11.62). Because of the intense media
publicity and short latency period, we assumed that there were no cases that
we did not identify. Attack rates for all days were calculated as the number
of known cases divided by the estimated total number of customers.
The restaurant was open for lunch and dinner on all days between December
20, 1998, and January 2, 1999, except December 25, 1998, and January 1, 1999.
Restaurant staff were assigned to work lunch, dinner, or both shifts. It was
unknown which cook prepared dishes for particular customers. However, to investigate
the potential association between particular employees and illness, an exposure
was defined as the presence or absence of an individual cook during a shift
and an outcome regarding whether a case occurred during that shift.
The owners of the restaurant were interviewed extensively about cooking
practices, ingredients of menu items, and employees. Because reported symptoms
were similar on December 21, 1998, and January 2, 1999, we considered the
possibility of an intentional outbreak. We therefore interviewed all employees
about not only food preparation but also possible conflicts among employees
or with the restaurant owners. We visited the restaurant and observed the
preparation of dishes. We collected information on pest-control measures and
obtained and catalogued 80 food samples from the restaurant.
Agricultural-grade methomyl is a white crystalline solid with a slight
sulfurous odor.1 It is packaged in 8-ounce,
red-and-white, foil-lined bags and manufactured by a single company in the
United States. This highly toxic agricultural pesticide is designated a class
1 chemical by the Environmental Protection Agency and was identified in a
sample of vomitus.1 Methomyl is classified
as a restricted-use pesticide because of its high toxicity to humans. Because
it can be legally purchased and used in Fresno only by users registered with
the office of the Fresno County Agricultural Commissioner, we asked the commissioner's
office to compare the names and addresses of restaurant staff with their list
of registered users.
The Public Health Laboratory at the Fresno County Health Department,
the West Coast Analytical Service, the California Veterinary Diagnostics Laboratory
of the University of California, Davis, and the California Department of Food
and Agriculture Laboratory tested food and water samples and a specimen of
vomitus for one or more of the following: bacterial pathogens, including Bacillus cereus and Staphylococcus aureus; emetine (ipecac); metals, minerals, and anions; boron; nitrate and
nitrite; organic molecules; detergent; mycotoxins (trichothecenes: DON, T2,
and DAS); glutamate and γ-aminobutyric acid; biogenic amines (cadaverine
and putrescine); and organophosphates and carbamates, including methomyl.
A sample of salt was specifically analyzed for methomyl from the bulk container
in the storeroom and the stovetop container by using liquid chromatography/mass
spectrophotometry. In addition, crystals from the storeroom salt were separated
by using carbon tetrachloride and floating crystals analyzed via high-performance
To estimate the toxic dose of methomyl associated with illness in 50%
of those exposed (TD50), we used data from January 2, 1999, the
last day before the restaurant was closed and the day samples of salt were
obtained. First, we determined the concentration of methomyl in the stovetop
sample of salt (a small container from which cooks added salt directly to
the food) that reflected concentrations placed into dishes on January 2. Second,
using the total number of diners on January 2, 1999 (n = 107), we modeled
the TD50 through logistic regression. Third, we divided the obtained
value of the TD50 by the average of the estimated body weight of
customers to obtain an estimate of the TD50 per kilogram of body
weight. Fourth, to indicate the variance in our estimate, we conducted a sensitivity
The proportion of each dish that was eaten was reported by 58 persons
who dined on January 2, 1999. The number of teaspoons of salt added routinely
by chefs to each dish was multiplied by the number of grams of salt per teaspoon
(5 g/tsp). Laboratory tests determined the methomyl concentration in the stovetop
salt sample. Because dishes were cooked an average of 2 to 3 minutes, we tested
the degradation of methomyl in boiling water for 3 minutes; 80% of methomyl
remained. We therefore calculated the total amount of methomyl ingested by
each person by multiplying 80% of the concentration of methomyl per gram of
salt by the amount of salt that was added in the kitchen and consumed by each
We identified 40 persons from the case group and 38 controls who had
eaten at the restaurant on January 2, 1999. The actual number of patrons who
were not ill was assumed to be 67 (107 estimated customers—40 cases).
The probability of identifying a control was 0.57 (38/67).
We developed a logistic regression model to calculate the probability
of becoming a case as a function of the dose of methomyl ingested and weighted
each case with 1 and each control with 1.76 (67/38) because 1 control represented
1.76 persons who were not ill. If we denote M as the dose of methomyl consumed,
the logistic model can be written as intercept + β (M) × dose = logodds (case). When the dose is TD50, the logodds
(case) becomes 0. After further algebraic conversions, the TD50
can be calculated by the formula TD50 = –intercept/β(M).
We estimated each person's weight with known age through the application
of weight by age charts. For January 2, we knew the age of 45 persons. We
calculated the weight-adjusted TD50 by dividing the estimated TD50 by the average estimated weight of the customers on January 2, 1999.
We conducted sensitivity analyses regarding the calculated TD50 by varying several factors: weight of customers between the median
(57.1 kg) and the mean (60.0 kg); proportion of methomyl that remained after
cooking (between 50% and 100%); and relationship of the number of cases to
the number of controls (between 1:1 and 1:1.76).
We examined restaurant invoices and obtained shipment and distribution
information from the salt distributor. We also asked the salt producer for
information on salt production and quality-control procedures.
The restaurant employed 12 cooks, 10 wait staff, and 2 dishwashers who
sometimes helped with preparing vegetables. Generally, all employees ate food
from the restaurant at the end of their shifts. The dishes were prepared differently
for cooks and wait staff. Usually, 2 dishes were prepared in a large quantity
for each group; however, the cooks' dishes contained fish sauce instead of
salt. The cooks were Laotian, and wait staff were either Thai or American.
Meals for employees were usually prepared by a single cook, frequently the
Although the owners indicated occasional problems with their cooks,
staff denied conflicts with the owners, even when interviewed privately. Staff
reported occasional tensions between cooks and wait staff. The restaurant
owners described an incident in July 1998 when the tires of their car and
one waitress's car were slashed.
We conducted 317 interviews. Of the persons interviewed, 132 reported
illness, and 107 met the case definition and had a known onset of illness.
Of the 185 persons who did not report illness, 16 were excluded because their
day of dining was unknown or they visited the restaurant on a day for which
no illness was reported, leaving 169 controls. No restaurant staff met the
case definition. Sixty-one percent of cases and 60% of controls were female.
Cases were more likely to be adults (>17 years of age) than were controls
(OR, 3.5; 95% CI, 1.2-12.6). The median (range) age of cases and controls
was 31 years (4-70 years) and 36 years (2-83 years), respectively (P = .53). Five children became ill.
The median interval from food consumption to illness was 40 minutes
(range, 5-120 minutes), and the median duration of symptoms was 6 hours (range,
1-168 hours). The median interval from the start of the meal until onset of
diarrhea was 2 hours. Of 107 cases, 102 (95%) reported nausea; 76 (72%), dizziness;
62 (58%), abdominal cramps; 56 (52%), headache; 54 (51%), vomiting; 51 (48%),
chills; 49 (46%), diarrhea; 15 (14%), fever; 8 (7%), weakness; 9 (8%), lightheadedness;
2 (2%), tingling; 2 (2%), blurry vision; and 2 (2%), sweating. The following
symptoms were mentioned once for each: fatigue, excessive salivation, droopy
eyelids, drowsiness, feeling drunk, dry mouth, eye pain, hives, and numb extremities.
The initial symptom was reported as dizziness, lightheadedness, or the feeling
of disequilibrium by 51 patients (48%), as nausea by 28 (26%), and as abdominal
cramps or pain by 15 (14%). To an open-ended question on the taste of the
food, case patients gave a variety of answers: bitter (n = 4), sweet (n =
2), bland (n = 3), salty (n = 2), sour (n = 2), uncooked (n = 2), foul (n
= 1), metallic (n = 1), "like MSG" (n = 1), rancid (n = 1), spicy (n = 1),
and tart (n = 1). Twenty-six persons (24%) visited the emergency department
or were treated by a physician. Diagnoses of food poisoning, gastroenteritis,
diarrhea, and acute gastritis were made. No biological sample was taken in
the emergency department or by physicians. There were no hospitalizations
Cases occurred sporadically between December 20, 1998, and January 2,
1999 (Figure 1). The estimated total
number of customers varied between 83 (December 20, 1998) and 153 (December
27, 1998). The estimated attack rates between December 20, 1998, and January
2, 1999, varied between 0% (on December 22, 24, 28, and 29) and 38% on January
2, 1999. No other outbreaks or cases of a similar illness were reported to
the California Department of Health Services or the Fresno County Health Department
during 1998 or 1999.
Approximately 100 dishes were available on the restaurant menu. Illness
was associated with consumption of several dishes, but no single dish accounted
for case numbers sufficient to explain the outbreak. We found the strongest
association between illness and eating ground meat (indefinite OR; 95% CI
[lower limit], 1.5), duck (OR, 10.0; 95% CI, 1.2-462.0), chicken coconut soup
(OR, 9.0; 95% CI, 2.3-49.0), and garlic chicken (OR, 7.7; 95% CI, 1.5-74.0).
However, among these, none accounted for more than 15 (14%) cases.
Because no specific dish could account for the majority of cases, we
examined the association between illness and specific ingredients. Consumption
of chili oil (OR, 3.2; 95% CI, 1.5-7.1), lime leaf (OR, 2.4; 95% CI, 1.3-4.3),
and lemon grass (OR, 2.4; 95% CI, 1.2-4.5) was associated with illness, but
even these could not account for more than 34 (32%) cases. Consuming any of
the vegetarian dishes appeared protective (OR, 0.3; 95% CI, 0.1-0.7), as did
consumption of any appetizer (OR, 0.5; 95% CI, 0.3-0.9) and any of the rice
dishes (OR, 0.6; 95% CI, 0.3-1.1).
Salt, glutamate, and sugar were added to almost all dishes. Whereas
glutamate and sugar were uniformly distributed among dishes, salt was not.
The 4 dishes most associated with illness—ground meat, duck, chicken
coconut soup, and garlic chicken—contained between 1 and 2 tsp of salt.
The majority of appetizers and vegetarian dishes, which were protective for
illness, contained less than 1 tsp of salt. In addition, 3 customers did not
consume any salt added by cooks in the kitchen, and none of them reported
illness. To further evaluate the association between salt consumption and
illness, we examined the odds of reporting illness at different levels of
exposure to salt added to foods in the kitchen (Figure 2). There was an estimated dose response: the association
between cases and exposure to salt estimated to have been added to foods in
the kitchen became stronger with increasing levels of salt exposure. Odds
ratios of persons who consumed more than 0.42 to 0.84, more than 0.84 to 1.25,
and more than 1.25 tsp of salt added to foods in the kitchen were 1.9 (95%
CI, 0.6-5.7), 3.0 (95% CI, 1.0-8.8), and 4.0 (95% CI, 1.3-13.5) in comparison
with those of persons who consumed 0.42 tsp or less (P
value for trend = .004). Adults ate a median of 1.0 and children a median
of 0.4 tsp of salt added to foods in the kitchen (P<.001).
Presence of employees during shifts was known from December 21, 1998,
through January 2, 1999, the dates during which 106 of the 107 cases occurred.
The presence of only one cook (cook A) was associated with illness among customers
(OR, 10.4; 95% CI, 1.2-157.4). This cook was present when 73 (69%) of 106
cases became ill. Cooks A and B were present during 16 (80%) of the 20 shifts,
when 104 (98%) of the 106 cases occurred.
The restaurant contained a small kitchen. Condiments for seasoning were
maintained on a table close to the cooks and included vinegar, oyster sauce,
red wine, soy sauce, and chili oil. Small plastic containers of salt, sugar,
and glutamate, filled from the storeroom, were also kept on the stovetop for
use in food preparation. These small containers were refilled approximately
every 2 days.
Sugar, salt, and glutamate were stored in large bulk containers in the
storage room. No enamelware or earthenware was used, except 2 pots for preparation
of curry dishes. Neither pot had glazing. The cooks reported no recent change
in cooking practices. Dishes were made fresh for each customer, and almost
nothing was precooked and reheated. The one exception was sticky rice, which
was usually prepared the day before and then stored in the refrigerator. The
table salt for customers was placed in tabletop shakers, and these were refilled
directly from a retail-purchased container that was maintained in the dining
area. This salt had a different source than did the storeroom salt that was
used in the kitchen for food preparation.
Methomyl was not used by the pest control company hired by the restaurant
to perform biweekly treatments. The last visit by the company was on December
15, at which time hydroprene and acephate were sprayed.
The database of the Fresno County Agricultural Commissioner identified
one registered user of methomyl who lived at the same apartment complex as
cook A and another registered user who was a relative of cook B. In 2001,
Fresno County had a population of 799 407, with 2809 (0.4%) registered
The one stool sample collected did not yield Campylobacter,
Shigella, or Salmonella. Bacillus cereus was not identified in abnormal levels in any food item.
The sample of vomitus tested negative for emetine (ipecac). The food and water
samples were within nontoxic levels of the metals tested. Rice was negative
for mycotoxins (trichothecenes). Neither nitrate nor nitrite was found in
the vomitus sample, and the screen for potentially toxic organic compounds
identified only γ-tocopherol. Among the samples tested for glutamate,
there were 2 (chili with fish sauce with 17.4 mg/mL and soy sauce with 28
mg/mL) that had slightly elevated levels; the salt and sugar samples did not
contain glutamate. Samples tested for cadaverine, putrescine, and tyramine
were within levels that were unlikely to cause adverse effects. The extended
organophosphate screen of the vomitus sample did not detect measurable levels
of any compound tested, while the extended carbamate screen detected methomyl.
The samples that tested positive for methomyl contained the following concentrations:
salt from the storeroom container (measured in 2 laboratories), 4800 ppm and
6400 ppm (mean, 5600 ppm); salt from the stovetop container (measured in 2
laboratories), 1200 ppm and 1650 ppm (mean, 1425 ppm); curry chicken, 305
ppm; chicken coconut soup, 52 ppm; garlic chicken, 34 ppm; chili oil, 28 ppm;
Thai salsa, 26 ppm; rice, 19 ppm; duck, 20 ppm; vomitus, 20 ppm; glutamate
from the storeroom container, 8 ppm; and sugar from the stovetop container,
Microscopic examination of the storeroom salt revealed 2 types of crystals,
1 resembling sodium chloride (common table salt) and 1 resembling methomyl
(Figure 3). High-performance liquid
chromatography analyses of the second type of crystal confirmed the presence
of methomyl in purities between 65% and 100%.
For January 2, 1999, we calculated the TD50 as 8.6 mg of
methomyl. The average estimated weight of customers was 57.1 kg, resulting
in a TD50 of 0.15 mg/kg of body weight. In the sensitivity analysis,
the TD50 ranged from 0.09 to 0.31 mg/kg of body weight.
According to restaurant invoices, the salt in the storeroom came directly
from the distributor's warehouse in 11.3-kg bags. The distributor sold about
500 bags weekly to customers in the area. The salt producer shipped salt bags
in his own vans directly to the distributor's warehouse, where the bags were
not repacked. No methomyl-containing products were purchased, stored, or shipped
by the distributor or the salt producer. Drivers routinely checked bags and
culled any wet or torn bags immediately. The ponds from which the salt was
generated were protected from runoff contamination. In addition, the production
process prevented the inclusion of substances other than sodium chloride (99.95%)
and water (0.03%). The company distributed more than 8000 tons of salt monthly
throughout the United States, and no similar incidents were reported in 1998
Using the results of this investigation, the Fresno Police Department
initiated a criminal investigation that is ongoing. Extensive interviews of
restaurant staff and others have been conducted by the department. To date,
no arrests have been made.
Clinical, epidemiologic, and laboratory evidence suggests that the outbreak
described in this report was associated with consumption of foods containing
methomyl-contaminated salt at a restaurant. Estimated doses of methomyl were
sufficient to cause symptoms but not hospitalization or death.
We were unable to identify how contamination could have occurred unintentionally.
First, reports from the salt producer and distributor indicate little to no
possibility for contamination at production or distribution. In addition,
no similar outbreaks were reported, making widespread contamination during
production or distribution unlikely. Second, different pesticides were used
for routine administration at the restaurant, methomyl is a restricted agricultural
pesticide, the salt bags purchased at the time were substantially different
in size and color than the bags in which methomyl is sold, and the extent
of contamination by methomyl found in the salt would make unintentional contamination
Some circumstantial and epidemiologic evidence raised the possibility
of intentional contamination by restaurant personnel. The owners described
tensions with and among staff and an incident of slashed vehicle tires. Easy
access to the storeroom container of salt was limited to employees and owners
of the restaurant. Through the connection with a relative, cook B had ready
access to methomyl, although he was not a registered user. It is important
that another registered user lived at the same apartment complex as cook A,
since he was the only cook who was significantly associated with the shifts
during which illness occurred.
The variance in the proportion of ill customers on different days of
the outbreak could be due to a number of factors. First, the storeroom container
could have been contaminated just one time, most likely on December 20, 1998.
If that dose of methomyl was not homogeneously mixed, the stovetop container
could have had varying concentrations of methomyl from day to day through
being refilled from random parts of the storage container (refilling occurred
on average every 2 days). Second, the storage container or perhaps even the
stovetop container could have been contaminated repeatedly, although we believe
the latter possibility is less likely because the perpetrator risked being
observed at some point. Third, and in combination with any of the possibilities
above, there could have been perhaps intentionally exaggerated variation in
the amounts of salt added to dishes by cooks. Because we did not know which
cook prepared the dish for which person, we could not assess the association
of the cooks with cases.
No cook or wait staff reported illness. Cooks usually prepared their
own meal and used fish sauce instead of salt because of ethnic food preference.
However, food for the wait staff was cooked with salt. They usually ate a
common dish that was prepared for them in a big bowl, mostly by the owner
herself. Because methomyl breaks down rapidly under high temperature and the
common dish for wait staff had perhaps been cooked longer because of the larger
quantity, extended heat exposure may have reduced methomyl in the dish for
wait staff to nontoxic levels. Alternatively, staff may have been reluctant
to report illness for fear of retribution.
This outbreak indicates that persons who ingest low levels of carbamate
in food may present with symptoms that resemble mild gastrointestinal illness
caused by bacterial or viral pathogens. Classic muscarinic effects, such as
lacrimation, salivation, and bronchospasm, were uncommonly reported. However,
dizziness was the first symptom in almost half of the cases, and the early
onset of diarrhea, within only 2 hours of food consumption, hinted at a toxic
origin rather than an infectious agent. Reports of salivation, even if infrequent,
should raise suspicion of potential intoxication with a cholinesterase inhibitor.
Initially, we were unable to identify a toxin that could adequately
explain the symptoms in this outbreak. A preliminary laboratory screening
for organic toxic compounds was essentially negative. It was only after careful
reexamination of symptoms, negative findings for more common toxins, and knowledge
that food-borne outbreaks of chemical origin in Thailand were frequently associated
with insecticide contamination, most commonly methomyl,2
that we proceeded to test specifically for organophosphates and carbamates.
This outbreak provided an unusual opportunity to estimate the dose of
ingested methomyl that was associated with illness. To do these calculations,
we had to make several assumptions. First, we assumed an equal concentration
of the salt within the stovetop container. Second, we assumed that cooks actually
added as much salt as was indicated by the chef. Third, we assumed that the
cooking time was relatively constant among dishes and cooks. Fourth, we assumed
that the weight of the customers was in line with national weight by age charts.
Fifth, we assumed that the proportion of cases among the unidentified customers
from January 2, 1999, was not higher than among the identified customers.
Nevertheless, we believe that our estimate is valid, and sensitivity analysis
showed that the extremes differ by a factor of less than 4. We estimated the
TD50 to be 8.6 mg, or 0.15 mg/kg of body weight, with an estimated
range of 0.09 to 0.31 mg/kg of body weight. In comparison, the oral lethal
dose (LD50) necessary to kill half of exposed male rats is 17 mg/kg.3 The lethal dose of a fatal human episode of methomyl
poisoning has been reported to be 12 to 15 mg/kg, an approximately 40- to
170-fold higher exposure than that experienced by restaurant customers.4
To our knowledge, this is the first large outbreak of chemical food
poisoning with probable intentional background reported in the United States.
Acts of intentional contamination with chemicals may cause substantial damage
and be difficult to recognize and control. For example, among all food-borne
outbreaks reported to the Centers for Disease Control and Prevention between
1993 and 1997, 88% of those with an incubation time of less than 6 hours never
had an etiology identified (M. Young, written communication, March 2000).
We relied initially on screening tests that did not focus on pesticides. It
was difficult and time consuming to find a laboratory willing and able to
do more specific tests for pesticides, including methomyl. Ultimately, it
was not until 4 months into the investigation that we identified the responsible
toxic agent. The rapid identification of a toxic agent, just like the identification
of a biological organism, is critical to investigations, including criminal
investigations. Strengthening laboratory and public health capacity to recognize
and control toxin-related outbreaks, perhaps through a network of competent
laboratories such as those developed for biological agents, is an important
component in the process of improving our public health surveillance and response