Neonatal hair test for cocaine:Toronto experience

Gideon Koren, MD FRCPC; Julia Klein, MSC

July, 1997

In large US cities, an estimated 10% to 45% of women cared for at teaching hospitals use cocaine during pregnancy.^1,2 Between June 1990 and December 1991, we conducted a prevalence study of cocaine use during pregnancy in one inner-city and two suburban metropolitan Toronto hospital nurseries and found 37 of 600 (6.25%) infants tested positive for cocaine.³ In metropolitan Toronto, the number of newborns affected by their mothers' drug use is steadily increasing.⁴

Cocaine and its metabolites cross the placenta and have been shown to be associated with increased perinatal and neonatal risks.^3,5-8 In utero cocaine exposure has been ascertained by interviewing mothers (self-report) and screening the urine of mothers, neonates, or both.

Because it can provide a cumulative and temporal account of exposure, hair is being used as a biological matrix for detecting adults' cocaine consumption and neonates' in utero exposure. Cocaine and its metabolites are embedded into the hair shaft and remain there for the life of the hair. Hair analysis has been used to confirm self-reported cocaine use and to study the prevalence of cocaine use among pregnant women in the Toronto area.^3,5 In our recent population-based study, we showed that taking the mother's history and doing urine tests did not detect most cases of intrauterine exposure to cocaine, but that hair analysis indicated exposure in almost all cases.³

Diagnosis of intrauterine exposure to cocaine often helps explain perinatal and neonatal complications and identifies addicted mothers who might not be able to provide, or might need help in providing, an acceptable level of neonatal care. Because the hair with which neonates are born grows during the last 3 months of pregnancy, a positive neonatal hair test shows that a mother was consuming the drug long after she knew she was pregnant.

Since the neonatal hair test for cocaine was established in 1989⁵ and its use as a research tool for ascertaining the prevalence of use in the Toronto area was confirmed,³ physicians, hospital nurseries, and social welfare agencies (eg, Children's Aid) have increasingly requested analysis of neonatal hair to corroborate or refute clinical suspicion of cocaine use during pregnancy when urine test results were negative. This report should help establish the sensitivity of clinical suspicion of in utero exposure to cocaine as validated by hair testing. The hypothesis underlying this research was that use of the hair test in cases of clinical suspicion but negative urine test results would yield a substantially higher prevalence rate than expected in the general population.

Between October 1991 and April 1995, we analyzed hair samples from 192 neonates and four mother-infant pairs. Among the neonatal hair samples provided for analysis, 10 did not contain sufficient hair to analyze for cocaine metabolites, but 55 (30%) of the remaining 182 samples tested positive for the cocaine metabolite benzoylecgonine (Table 1). Most samples (72%) were sent from hospital nurseries and clinics. The rest were sent from social welfare agencies and privately practising physicians.

There are obvious shortcomings in the accuracy of self-reported cocaine use during pregnancy. Fear of legal consequences and embarrassment at admitting illicit substance use lead to underreporting. While some debate the justification of routine neonatal screening for illicit drugs, most health professionals agree that clinical suspicion of such exposure should be confirmed or denied by a sensitive and accurate test. Before our study, clinicians could not validate their nonspecific clinical suspicions and neonates with the very serious diagnosis of in utero drug exposure went home without appropriate management and follow up.

Of the samples referred to us by health professionals because of clinical suspicions, about 30% yielded positive results, a 5.5-fold higher prevalence than that found in population-based research.³ This difference (5.5% vs 30.0%) was highly significant (P < 0.0001) and means that the hair test was used efficiently and was justified overall. The decision to collect a sample is usually prompted by history and clinical presentation (Table 2) and is based on nonspecific criteria because in utero exposure to cocaine is not a phenotypic syndrome.

Concentrations of benzoylecgonine in neonatal hair were significantly higher (4.37 ± 12.5ng/mg of hair) in this cohort than they were in our previous population-based study (1.82 ± 7.08ng/mg) (P = 0.0001), indicating that when clinical suspicions prompt physicians to test neonatal hair, a subgroup of heavy cocaine users, who probably are at higher perinatal risk, is detected.

The high proportion of positive samples referred by social welfare agencies is consistent with clustering of high-risk cases. Agency staff are privy to background information that could heighten suspicion of cocaine use. A dimension most relevant to social welfare cases is the medicolegal implication of ensuring proper care of children who have been exposed to cocaine in utero. Custody of these children is often subject to legal intervention. Hair analysis has been used to corroborate or refute claims of intrauterine exposure to cocaine. A case of a mother who was referred on two separate occasions showed that repeated hair analysis can prove changes in cocaine use over time.

Whether all newborns should be screened for exposure to cocaine is continually under debate. The complex relationships between maternal and fetal rights and the extremely heterogenous views on drug testing in western societies make it unlikely that routine screening will ever take place. Our results suggest strongly that it might be sufficient to test suspected cases based on nonspecific signs of cocaine exposure and not take on the enormous cost and ethical-legal liabilities inherent in universal testing.

Because neonatal hair grows during the last trimester of pregnancy, positive results of a neonatal hair test show that the mother was using cocaine long after pregnancy was recognized and, therefore, probably was addicted. Confirmation of in utero exposure to cocaine might allow for earlier intervention to ensure proper care for both baby and mother. Both mother and infant should be closely followed with postnatal care, supportive counseling, contraceptive counseling, public health nurse visits, and training in parenting skills.⁹ Evidence shows that interventions such as home visits benefit children's early development.¹⁰

References

1. Volpe JJ. Effect of cocaine use on the fetus. N Engl J Med 1992;327:399-407.
2. Osterloh JD, Lee BL. Urine drug screening in mothers and newborns. Am J Dis Child 1989;143:791-3.
3. Forman R, Klein J, Meta D, Barks J, Greenwald M, Koren G. Maternal and neonatal characteristics following exposure to cocaine in Toronto. Reprod Toxicol 1993;7:619-22.
4. Metro Toronto Research Group on Drug Use in Metropolitan Toronto. Drug use in metopolitian Toronto. Toronto: Metro Toronto Department of Health; 1995. p. 51.
5. Graham K, Koren G, Klein J, Schneiderman J, Greenwald M. Determination of gestational cocaine exposure by hair analysis. JAMA 1989;262:3328-30.
6. Zuckerman B, Frank D, Hingson R, Amaro H, Levenson S, Kayne H, et al. Effects of maternal marijuana and cocaine use on fetal growth. N Engl J Med 1989;320:762-8.
7. Chasnoff IJ, Burns KA, Burns WJ. Cocaine use in pregnancy: perinatal morbidity and mortality. Neurobehav Toxicol Teratol 1987;9:291-5.
8. Frank DA, Zuckerman BS, Amaro H, Aboagye K, Bauchner H, Cabral H, et al. Cocaine use during pregnancy: prevalence and correlates. Pediatrics 1988;82:888-95.
9. Levy M, Koren G. Obstetric and neonatal effects of drugs of abuse. Emergency aspects of drug abuse. Emerg Clin North Am 1990;8:633-52.
10. Black MM, Nair P, Kight C, Wachtel R, Roby P, Schuler M. Parenting and early development among children of drug-abusing women: effects of home intervention. Pediatrics 1994;94:440-8.

Table 1. Samples testing positive for cocaine exposure

SOURCE	NO. OF SAMPLES REFERRED	NO. OF SAMPLES TESTING POSITIVE (%)*	POSITIVE SAMPLES AS A PROPORTION OF ENTIRE SAMPLE %*
Children's Aid	17	9 (56)	5
Hospital nurseries	1382	36 (27)	20
Primary care physicians	22§	6 (30)	3
Unknown	15	4 (29)	2
TOTAL	192	55	30

*Calculation does not include samples insufficient for testing.
One sample was insufficient for testing.
Six samples were insufficient for testing.
§Two samples were insufficient for testing

Table 2. Causes of clinical suspicion of cocaine exposure

• History of maternal drug use
• History indicating drug use (eg, blurred speech)
• Signs of needle marks
• Intrauterine growth retardation (baby weighed less than third percentile for age)
• Placental abruption
• Intracranial hemorrhages
• Unexplained changes in arousal and sleep patterns of infants
• Low birth weight infants
• Neonatal seizures
• Sexually transmitted diseases in neonates