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Heroin-Related Deaths -- District of Columbia, 1980-1982

In the period January 1980-December 1982, 266 deaths occurred in the District of Columbia because of intravenous heroin use (Figure 1).* These deaths represented a substantial increase in numbers beginning in the second quarter of 1979. The median age of all decedents for this 2-year period was 30 years; 93% were black, and 82% were male. These deaths constituted 96% of all deaths due to abuse of narcotics in the District of Columbia during the study period; they clustered significantly in the spring and summer, on Friday and Saturday, and from 6 p.m. through 12 midnight. The median age at which the decedents in this group first used heroin was 19. Analyses of heroin preparations sold on the street indicated that quinine was the only other pharmacologically active substance consistently present in packages of heroin associated with these heroin-related deaths (HRDs).

A comparison was made of autopsy data for persons whose deaths were classified as HRDs and data for a control group consisting of persons who died of natural or traumatic causes (including homicide and suicide) in the same time period and had measurable concentrations of morphine in their blood at autopsy.** Seventy-three percent of persons whose deaths were classified as HRDs and 32% of controls had measurable concentrations of ethanol in blood; 50% of the former and 15% of the latter had concentrations greater than 100 mg/dl. The median concentration of morphine in blood for HRDs at autopsy was 0.03 mg/dl, compared with 0.01 for controls.

Analyses of risk factors during the study period (Table 1) indicated that persons with HRDs were 22 times as likely to have blood ethanol levels greater than 100 mg/dl than levels equal to or less than 100 mg/dl and 15 times as likely to have blood morphine concentrations equal to or greater than 0.02 mg/dl than to have levels of less than 0.02 mg/dl. Analysis of the case-control data showed that the presence of a single, recent needle-injection site or a single track area was significantly associated with a higher risk of HRD than were multiple sites or track areas (p 0.05).

The parameters of deaths among HRDs by quarter year, weight of heroin and quinine in street packages, and price of heroin were used in a multiple linear regression model for an interval that included both endemic and epidemic periods (1976-1982). Analysis indicated a positive association between HRDs and the quarterly average amount of heroin and quinine in street packages, as well as between HRDs and the quarterly average concentration of heroin (percentage dry weight); the same analysis indicated an inverse association between HRDs and the price (dollars/milligram of pure heroin) of heroin.

The above positive association between quinine and HRDs is also supported by pharmacologic data. Doses of quinine estimated from concentrations in street preparations ranged from 98 mg to 314 mg. For a 10-second injection, dose rates would range between 10 mg/sec and 131 mg/sec, 59-182 times the currently recommended maximum therapeutic dose rate for quinine dihydrochloride (1). Reported by JL Luke, MD, Chief Medical Examiner, Office of the Chief Medical Examiner, ME Levy, MD, Public Health Svcs Administrator, Office of the Commissioner of Public Health, District of Columbia; Morals Div, Metropolitan Police Dept, District of Columbia; Div of Epidemiology and Statistical Analysis, National Institute on Drug Abuse; Office of Intelligence, Drug Enforcement Administration; Chronic Diseases Div, Center for Environmental Health, CDC.

Editorial Note

Editorial Note Epidemiologic features of HRD in previous epidemics have been described (2-4). Investigators have attributed these deaths to the high concentration of heroin in street preparations and to a loss of tolerance to heroin. Relatively little is known about why epidemics of HRDs occur, whether particular groups are at high risk for a fatal overdose at such times, or how demographic and toxicologic variables differ during epidemics from those at other times. The 1981 population-based HRD mortality rate of 17.4/100,000 population for the District of Columbia is the highest ever reported in the medical literature. Results from the case-control study described above and the magnitude of morphine concentrations in blood indicate that the pharmacologic effects of heroin played a major role in this epidemic (i.e., on the basis that minimum lethal blood morphine concentration may range from 0.02-0.04 mg/dl and because heroin-related decedents in this study were 15 times more likely than controls to have blood morphine concentrations of 0.02 mg/dl or greater). In addition, analysis of case-control data showed elevated concentrations of morphine in urine and bile significantly more often (p 0.05) among controls than among members of the case group, indicating that the case group used heroin less chronically than did the controls (6-8). Likewise, the case-control data clearly establish that the combination of ethanol and heroin elevate the risk for a fatal overdose--a point that has not been emphasized in past analyses of these epidemics (3,5). The acute effects of blood ethanol appear more prominent than the chronic effects, since liver pathology does not significantly increase the risk of HRD after the confounding influence of blood ethanol is removed.

The data from the District of Columbia study also suggest that the lack of tolerance to heroin is a risk factor for death from overdose, but that this lack may be due to sporadic use of the drug in combination with ethanol rather than to an addict's resumption of frequent heroin use after a period of abstinence. These data differ from earlier study results that suggest that HRD epidemics are related to the fluctuating strength of heroin sold on the street. The association between quinine and HRDs also conflicts with past reports and merits further consideration (2,8,9).

Although the mechanisms for the epidemiologically identified risk factors have not been firmly established, the data from the District of Columbia study support the adoption of public health education measures aimed at reducing heroin-related mortality. The following recommendations should be considered for use by public health care providers:

  1. Heroin users should be continually reminded of the

well-documented elevation in the risk for death associated with using heroin in any context, using heroin after a period of postaddiction abstinence, and using heroin for recreational (nonaddictive) purposes.

2) The risk of combining heroin use with ethanol ingestion should be made clear to all heroin users. Addiction treatment programs should also address the problem of substituting addiction to ethanol for addiction to heroin, methadone, or other drugs. Heroin addicts under treatment who have problems with ethanol abuse should be treated for both drug problems.

3) Measures should be considered to decrease the ready availability of quinine. Heroin users should also be apprised of the potential risks involved when quinine is used as a diluent in preparations of heroin.


  1. American Medical Association. AMA drug evaluations. 4th ed. New York: John Wiley & Sons, 1980:1390.

  2. DuPont RL, Greene MH. The dynamics of a heroin addiction epidemic. Science 1973;181:716-22.

  3. Greene MH, Luke JL, DuPont RL. Opiate "overdose" deaths in the District of Columbia I. Heroin-related fatalities. Medical Annals of D.C. 1974;43:175-81.

  4. Zimney EL, Luke JL. Narcotic-related deaths in the District of Columbia: 1971-1979. J Forensic Sci 1981;26:462-9.

  5. Cherubin C, McCusker J, Baden M, et al. Epidemiology of death in narcotic addicts. Am J Epidemiol 1972;96:11-22.

  6. Christopoulos GN, Kirch ER. Isolation and identification of morphine from postmorteum tissues. J Chromatogr 1972;65:507-19.

  7. Sapira JD. The narcotic addict as a medical patient. Am J Med 1968;45:555-88.

  8. Garriott JC, Sturner WQ. Morphine concentrations and survival periods in acute heroin fatalities. N Engl J Med 1973;289:1276-8.

  9. Abramson DH. Bigeminy and heroin intoxication. NY State J Med 1972;72:2888-90.

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