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Epidemiologic Notes and Reports Lead Poisoning Associated with Intravenous-Methamphetamine Use -- Oregon, 1988

Between August 1 and September 6, 1988, 14 cases of non-A, non-B (NANB) hepatitis were reported in Marion County, Oregon, to the Oregon Health Division (OHD) by the county health department and private physicians. Previously, an average of less than one case per month was reported in the county. During the same period, OHD learned that eight intravenous-methamphetamine users (IVMUs) in Oregon thought to have NANB hepatitis had also been recently diagnosed with lead poisoning. A statewide media campaign describing the lead poisoning outbreak was conducted to alert IVMUs, physicians, and county health departments. In addition, OHD implemented a reporting system for suspected and confirmed lead poisoning cases.

A suspected case of IVMU-associated lead poisoning was defined as three or more of the following symptoms in an IVMU: abdominal pain, nausea, vomiting, lower back and leg pains, weakness, weight loss, and anorexia. A confirmed case was defined as seronegativity for both acute hepatitis A and acute hepatitis B and a blood-lead level of greater than or equal to 40 ug divided by L (1.93 umol/L) and/or an erythrocyte protoporphyrin (EP) level of greater than or equal to 60 ug divided by L (1.06 umol/L) in an IVMU.

In 1988, 37 suspected and 14 confirmed cases were reported to OHD; in 1989, no suspected or confirmed cases have been reported. Clinical evaluation for lead poisoning was completed for 19 suspected cases. In six, blood-lead levels were less than 25 ug divided by L (1.21 umol/L); the other 13 had blood-lead levels of greater than or equal to 40 ug divided by L, and/or EP levels of greater than 60 ug divided by L. One person with an uncertain history of methamphetamine use was asymptomatic but had a blood-lead level of 87 ug divided by L (4.2 umol/L).

The 14 confirmed case-patients ranged in age from 24 to 36 years (mean: 27.1; median: 29); 11 were male. Except for one person who had onset in March 1988, onset of symptoms occurred between July 20 and August 17, 1988. The most common symptoms were abdominal pain, vomiting, constipation, nausea, and weakness; duration of symptoms ranged from 3 weeks to 6 weeks. Blood-lead levels ranged from 49 ug divided by L to 513 ug divided by L. Analysis of an illicit methamphetamine sample provided by one of the patients with confirmed lead poisoning detected 60% lead by weight. Reported by: DB Chandler, PhD, RL Norton, MD, Oregon Health Science Univ Poison Center, Portland; KW Kauffman, J Gordon, PhD, LR Foster, MD, State Epidemiologist, Health Div, Oregon Dept of Human Resources. Div of Environmental Hazards and Health Effects, Center for Environmental Health and Injury Control, CDC.

Editorial Note

Editorial Note: This report has two important clinical and public health implications. First, lead poisoning may not be diagnosed if physicians do not have a high index of suspicion, especially for illness in persons not usually considered to be at risk for lead poisoning. Second, illicit products may be grossly contaminated with poisonous substances. Products manufactured in clandestine laboratories have caused substantial mortality and morbidity (e.g., parkinsonism in drug users exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-contaminated meperidine analogs (1) and toxic-oil syndrome following use of contaminated rapeseed oil (2)).

Acute lead poisoning from IV exposure to lead has been previously reported (1-3); some of these cases resulted from illicit methamphetamine use. In the Oregon outbreak, the total number of IVMUs affected by lead-contaminated methamphetamine was probably greater than reported because the case definition excluded IVMUs with blood-lead levels less than 40 ug divided by L. In addition, the population at risk (i.e., IVMUs) is difficult to study; almost half the suspected cases were lost to follow-up, and many exposed or ill persons probably did not identify themselves to health-care providers.

The clustering of cases within a 1-month period suggests a point-source epidemic. Whether contamination of the methamphetamine with lead-containing material was deliberate or a result of inadequate processing is unknown. However, lead acetate is a reagent in the manufacture of phenyl-2-propanone, a precursor of methamphetamine in the amalgam process.

Most of the Oregon patients had only slightly elevated SGOT levels (median: 124 IU/L). However, elevations of bilirubin (median: 2.4 mg divided by L) and marked increases in SGOT levels in some of these persons are unusual in lead poisoning. Particularly because IV-drug use is the most commonly identified risk factor reported by persons with NANB hepatitis (4,5), some of these patients may have had either acute or chronic NANB hepatitis of viral etiology in addition to lead poisoning. Alternatively, these abnormalities in SGOT and bilirubin may have resulted from exposure to solvents used to manufacture the methamphetamine. Physicians should be aware that acute lead poisoning can have many signs and symptoms similar to those of NANB hepatitis and that illicit methamphetamine can contain substantial amounts of lead (3).

During the outbreak, the OHD notified health-care providers that any NANB hepatitis case should be reviewed for possible lead poisoning. Because there have been no indications of a continuing problem, no further actions have been taken.


  1. Ruttenber AJ, Garbe PL, Kalter HD, et al. Meperidine analog exposure in California narcotics abusers: initial epidemiologic findings. In: Markey SP, Castagnoli N, Trevor AJ, Kopin IJ, eds. MPTP: a neurotoxin producing a Parkinsonian syndrome. Orlando: Academic Press, 1986:339-53.

  2. World Health Organization. Toxic oil syndrome: mass food poisoning in Spain--report of a WHO meeting, Madrid 21-25 March 1983. Copenhagen: World Health Organization Regional Office for Europe, 1984:1-2.

  3. Allcott JV, Barnhart RA, Mooney LA. Acute lead poisoning in two users of illicit methamphetamine. JAMA 1987;258:510-1.

  4. Alter MJ, Hadler SC, Francis DP, Maynard JE. The epidemiology of non-A, non-B hepatitis in the United States. In: Dodd RY, Barker LF, eds. Infection, immunity, and blood transfusion. New York: Alan R. Liss, 1985:71-9.

  5. CDC. Hepatitis surveillance report no. 52. Atlanta: US Department of Health and Human Services, Public Health Service, 1989:25-7.

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