Indirect sources of mercury poisoning in the Iraqi epidemic.

Secondary sources of intoxication with methylmercury poisoning other than home-made bread were explored. Mercury levels in various food items were below 0.05 mg/kg.Over 30 000 specimens of meat and internal organs of sheep were analysed because of the strong suspicion that the animals had been fed treated barley. It was found that 6-12% of the specimens analysed contained more than 0.5 mg/kg of mercury. Consumption of meat did not appear to constitute a danger of intoxication during the outbreak.

An outbreak of organomercury poisoning among Iraqi farmers.

An outbreak of organomercury poisoning due to the consumption of treated grain by farmers and their families occurred in Iraq in 1971-72. A total of 6530 cases were admitted to hospital and of these 459 died. However, there were many more with minor symptoms of poisoning who consulted outpatient departments. This outbreak constituted the largest poisoning epidemic ever recorded. No age was exempt and no pronounced sex difference was apparent. The latent period of up to 60 days between dosage and the onset of symptoms was probably the major factor contributing to the size of the epidemic. Measures taken to limit the outbreak are outlined.

Epidemiology of organomercury poisoning in Iraq. I. Incidence in a defined area and relationship to the eating of contaminated bread.

A survey was carried out in a defined area in rural Iraq where there had been many cases of organomercury poisoning following the consumption of bread contaminated by mercury, in order to determine the true incidence of the disorder. The results were compared with those obtained from a similar rural area from which few cases had been reported. A questionnaire was used to determine the amount of contaminated bread eaten and the frequency of symptoms; a simple clinical examination was performed and blood and hair samples were collected for estimation of total mercury concentration. Of 700 people over the age of 5 years in the high-exposure area, 66% admitted to having eaten contaminated bread, while none of the 864 persons in the low exposure area had done so. The mean period during which contaminated bread was eaten was 32 days, but some people had eaten it for as long as 3 months. A mean of 121 loaves was eaten, the maximum being 480 loaves. For the mean number of loaves the intake of methylmercury was likely to have been between 80 mg and 250 mg, but the people who had consumed the largest amount of contaminated bread may have ingested up to 1 000 mg of methylmercury over a 3-month period. Of those with signs of alkylmercury poisoning at the time of the survey, 80% had eaten more than 100 loaves, and 53 (71%) out of 75 persons who had eaten more than 200 loaves showed some evidence of poisoning.The incidence rate for poisoning was estimated at 271 per 1 000; this figure includes a mortality rate of 59 per 1 000, 32 per 1 000 cases with severe disability, 41 per 1 000 cases with mild or moderate disability and 138 per 1 000 cases with only subjective evidence of poisoning at the time of the study.

Epidemiology of organomercury poisoning in Iraq. II. Relationship of mercury levels in blood and hair to exposure and to clinical findings.

In the survey described by Al-Mufti et al. (see page 23) blood and hair samples were analysed for total mercury by modified atomic absorption spectrophotometry. The hair samples were divided into 2.5-cm segments and analysed consecutively. The mean blood levels were 34 ng/ml and 7 ng/ml, respectively in those who had and those who had not eaten contaminated bread.Corresponding mean maximum hair mercury values were 136 mug/g and 5 mug/g, respectively. Hair mercury values provided a better discrimination between different categories of exposure than blood mercury values at the time the survey was performed, some months after the end of the outbreak. Those persons who had not eaten contaminated bread but who lived in the area of high exposure had hair mercury values between the values of those who had eaten and those who had not eaten contaminated bread and who lived in the area of low exposure. Sequential estimation of mercury in 2.5-cm segments of hair in women gave information on the period of accumulation of mercury more than 1 year before the time of collection of the samples. It was possible to show an approximate relationship between the maximum hair mercury value and the amount of contaminated bread eaten. The match between the blood mercury level and the severity of poisoning was poor, owing to the length of time that had elapsed between the onset of poisoning and the sampling. With hair mercury, while the group results showed a good relation to the severity of poisoning, in individual cases the match was less good, especially in those persons where an insufficient length of hair was available for analysis. Biological variation in sensitivity to methylmercury was also likely to have been an important factor.

Epidemiology of organomercury poisoning in Iraq. III. Clinical features and their changes with time.

Three categories of mercury poisoning were defined in the survey described by Al-Mufti et al. (see page 23) and the age-specific incidence rates for these are given. Persons with physical signs consistent with a diagnosis of organomercury poisoning were allocated to categories of severe disability or mild/moderate disability. However, the largest category consisted of persons who had symptoms but no readily elicitable physical signs at the time of the survey. These symptoms followed a consistent pattern with paraesthesia involving the lips and/or circumoral region or trunk and difficulty with walking, described as weakness or unsteadiness of the legs, and in some cases repeated falls, forming the most commonly occurring symptom complex. Mean maximum hair mercury levels differentiated this group very clearly from the group with no symptoms of mercury poisoning. Very few people in the area of low exposure complained of such symptoms; where they did occur they were less well related to the time of the outbreak and showed little tendency to improve. Most people reported improvement in their symptoms by the time of the survey, with more improvement in some symptoms than in others. However, it is not known whether those people with symptoms only at the time of the survey had had at an earlier stage mild signs which had cleared. It was thought unlikely that further substantial improvement would occur in those persons with disability at the time of the survey.