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Maternal and Paternal Recreational Drug Use and Sudden Infant Death Syndrome
Hillary Klonoff-Cohen, PhD;
Phung Lam-Kruglick, MA
Arch Pediatr Adolesc Med. 2001;155:765-770.
ABSTRACT
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Objective To determine whether maternal or paternal use of cocaine, opiates, or
marijuana during conception and pregnancy and postnatally increases the risk
of sudden infant death syndrome (SIDS) during the first year of the infant's
life. This is an important issue and may prove useful in further decreasing
the rate of SIDS.
Methods A case-control study was conducted consisting of 239 infants who died
of SIDS in southern California between 1989 and 1992, and 239 healthy infants
who were matched on the basis of birth hospital, date of birth, age, and sex.
Specific drug use at the period of conception, during pregnancy and breastfeeding,
and in the presence or vicinity of the infant was ascertained by telephone
for the white, African American, Hispanic, Asian American, and Pacific Islander
case and control fathers and mothers.
Results Maternal recreational drug use during pregnancy was not associated with
the risk of SIDS after adjusting for maternal smoking during pregnancy (adjusted
odds ratio [OR] = 2.0; 95% confidence interval [CI], 0.6-6.5). There were
statistically significant differences between case and control fathers' use
of marijuana during conception (OR = 2.2; 95% CI, 1.2-4.2; P = .01), during pregnancy (OR = 2.0; 95% CI, 1.0-4.1; P = .05), and postnatally (OR = 2.8; 95% CI, 1.1-7.3; P = .04) and the risk of SIDS, while adjusting for paternal smoking
and alcohol use.
Conclusions There was no association between maternal recreational drug use and
SIDS. Paternal marijuana use during the periods of conception and pregnancy
and postnatally were significantly associated with SIDS. The role of paternal
psychoactive drug use, especially the relationship between marijuana and SIDS,
is an understudied area; however, before any definitive role for the father
can be confirmed, these findings should be investigated and replicated in
future studies.
INTRODUCTION
MATERNAL substance abuse may be present in 11% of all pregnancies.1 Maternal use of opiates, stimulants, and sedative
tranquilizers has been linked in previous studies to subsequent sudden infant
death syndrome (SIDS) in offspring,2 although
the incidence rate and exact mechanisms are unknown. Approximately 2996 infants
died of SIDS in 1997 (77.2 per 100 000 live births) in the United States,
making it the third-leading cause of death in infants aged 1 week to 12 months.3
OPIATE USE AND SIDS
The possible connection between maternal opiate use during pregnancy
and subsequent SIDS in offspring has been suggested anecdotally by Kahn et
al4 and Pierson et al,5
in studies of SIDS deaths from heroin and methadone,6, 7, 8, 9
and in studies of cocaine-exposed infants.6, 7, 8, 9, 10
In the largest study, Chavez et al11 reported
17 SIDS deaths out of 688 live births to drug-using mothers (eg, methadone,
heroin, cocaine, and amphetamines). Among opiate-exposed neonates, the risk
of SIDS has been shown to relate to the severity of drug withdrawal, which
correlates with the degree of maternal drug use. No study to date has fully
and comprehensively separated the effects of opiates from other potential
confounders including prenatal care, prematurity, low birth weight, and socioeconomic
class.
The National Institute of Child Health and Human Development SIDS Cooperative
Epidemiological Study12 reported a 2-fold increase
in SIDS risk (P<.001) with illicit drug use during
pregnancy, after controlling for birth weight and African American background.
Although maternal substance abuse was not rigorously defined, the findings
were most relevant to opiate use.
COCAINE USE AND SIDS
In the 1980s, cocaine use in its freebase form ("crack") overtook heroin
as the main drug problem in the United States13;
however, the causal relationship between cocaine use during pregnancy and
SIDS remains unclear. Two studies suggest an increased risk of dying of SIDS
when exposed to cocaine in utero.14, 15
Chasnoff et al14 reported a 15% incidence rate
of SIDS (n = 10) among 66 infants of mothers who had used cocaine during pregnancy
compared with 4% among infants whose mothers used opiates. The finding of
8.8 SIDS deaths per 1000 infants born to cocaine-using mothers in this group
was similar to Davidson-Ward et al's16 reported
incidence of 8.4 SIDS deaths per 1000 live births to cocaine-using mothers
in Los Angeles County, California. Durand et al15
studied the SIDS rate for cocaine-exposed hospital-born infants; they noted
that unrecognized maternal drug abuse may have occurred in the control group.
In contrast, the prospective study by Bauchner et al17
found no increased risk of SIDS among infants exposed to cocaine in utero
in a larger group of 175 infants and 821 controls, using maternal interview
and urine toxicologic tests on multiple occasions. The study by Fulroth et
al18 revealed that of 368 infants with documented
exposure to cocaine, none died of SIDS. Lounsbury et al19
indicated that intrauterine exposure to cocaine did not predispose to SIDS.
Fares et al20 performed a meta-analysis of
10 published studies and reported a combined odds ratio [OR] of 3.9 (95% confidence
interval [CI], 3.0-5.0) for SIDS in infants exposed to cocaine vs all illicit
drugs; when the comparison group consisted of drug-free controls, the OR was
4.1. However, after controlling for concurrent use of other drugs, SIDS was
not specific for cocaine but for intrauterine exposure to drugs in general.
MARIJUANA AND SIDS
One study addressed the effects of maternal marijuana use and SIDS.
Ostrea et al21 determined that there was an
increase in the OR for SIDS among drug-positive infants exposed to all drugs,
including marijuana (OR = 1.5; 95% CI, 0.46-5.01). For those infants exposed
to cocaine (OR = 1.9; 95% CI, 0.58-6.20) and opiates (OR = 2.3; 95% CI, 0.66-7.76),
there was an association with SIDS; however, the CIs were wide and included
the OR of 1. Ostrea et al concluded that "prenatal drug exposure in infants
was not associated with an increase in the incidence of SIDS during the first
2 years of life."
Conflicting results among these studies may be due to small sample sizes,
inability to document maternal and paternal drug use (including variations,
type, dose, duration, and timing during conception and pregnancy), failure
to differentiate between prenatal and postnatal drug exposure, and absence
and/or inadequate adjustment of potential confounders (eg, socioeconomic status,
prematurity, low birth weight, and prenatal care).4, 5, 6, 7, 8, 9, 10, 14, 15, 16, 17, 18, 19, 20, 21
To our knowledge, no other studies have investigated paternal substance
use, including marijuana, during pregnancy and conception, nor have any studies
examined maternal recreational drug use during the period of conception.
SUBJECTS AND METHODS
HYPOTHESIS
The objective of this study was to investigate whether maternal and/or
paternal recreational drug use (cocaine, opiates, or marijuana) during the
periods of conception and pregnancy and postnatally (ingested through breastfeeding
and/or passively inhaled in the home) increased the risk of SIDS within a
racially diverse group. This is a secondary analysis of a previously published
article on passive tobacco smoking22 and SIDS;
a detailed description of the methodology of that study appears elsewhere.23
STUDY SAMPLE
A total of 400 eligible cases were initially identified from death certificates
located in the health departments of southern California. One hundred of these
case parents were untraceable despite tremendous effort to locate this transient
population by implementing 14 strategies that have been described previously.24 Hence, matching control parents for the 100 case
parents were not chosen from the corresponding birth hospitals. During the
study period, 300 cases and 260 controls were interviewed; this was before
the height of the publicity on SIDS and its correlation with sleep position.
Overall, there was a 70% response rate (560 of 800). After couples with missing
recreational drug data were dropped and matching was implemented, a total
of 239 cases and 239 matched controls were retained for this analysis.
This study sample consisted of 239 white, African American, Hispanic,
and Asian American infants who had died of SIDS and 239 control infants born
between January 1989 and December 1992 in 5 counties in southern California
(San Diego, San Bernardino, Riverside, Orange, and Los Angeles Counties).
All SIDS diagnoses were based on an autopsy data sheet and final autopsy report.
A SIDS death was defined as a death occurring between 1 week and 1 year of
age, with a diagnosis of SIDS confirmed by autopsy. Contact was made with
parents of infants who had died of SIDS approximately 6 to 12 months after
the infant's death, to comply with the requirements of the Committee on Human
Subjects regarding observance of the grief period.
Control infants were randomly selected from all eligible live births
from the same 110 birth hospitals of the case infants, and were additionally
matched to the case by date of birth, sex, and race. The medical records department
at each hospital contacted the control parents by mail to maintain confidentiality.
On average, control parents were contacted 3 to 6 months after the case interview.
All study infants were required to be free of pulmonary, cardiac, or
neurologic complications and metabolic disturbances. Unautopsied deaths were
excluded.
INTERVIEW
A telephone interview examined sociodemographic characteristics and
the timing and frequency of use of cigarettes, alcohol, and recreational substances
for both case and control parents. Detailed maternal and paternal recreational
drug histories were obtained from the mother and father (if possible), including
the time frame and frequency of substance use. The period of conception was
defined as the interval between the last menstrual period and the confirmation
of a positive pregnancy test by the physician. "Postnatally" included recreational
drug exposure from 2 sources: during breastfeeding, or smoking marijuana in
the presence or vicinity of the infant, which may passively expose the infant
to this drug. Other substances (tobacco, alcohol, and over-the-counter and
prescription medications) used during the specified periods were also recorded.
Complete paternal and maternal medical histories, labor and delivery complications,
and neonatal characteristics were primarily obtained from the interview and
medical records and verified with obstetric and pediatric records. The time
span of responses for the control parents was limited to the life span of
the case infants (eg, if a case infant lived for 6 months, the matched control's
history would coincide to 6 months).
This study was approved by the Institutional Review Boards of all hospitals
involved and the University of California, San Diego, Committee on Human Subjects.
STATISTICAL ANALYSES
Conditional logistic regression was used to examine the relationship
between SIDS and marijuana or other drug use by the mother and father during
conception, pregnancy, and infancy. Potential confounders (maternal or paternal
tobacco smoking, alcohol use, age, level of education, infant medical conditions
at birth, low birth weight, sleep position, and bed sharing) were identified
from previous literature and stratified analyses. Confounders were included
in the final models if they changed the magnitude of association between SIDS
and drug exposure by at least 15%. Multiplicative interactions (eg, between
maternal and paternal drug use or between drug and tobacco or alcohol use)
were assessed through significance testing. Stata 5.0 statistical software
(Stata Corp, College Station, Tex) was used for all analyses.
RESULTS
MATERNAL RECREATIONAL DRUG USE DURING CONCEPTION AND PREGNANCY AND
POSTNATALLY
Marijuana predominated as the drug of choice among the mothers. As indicated
in Table 1, SIDS outcome was not
significantly associated with maternal marijuana use during conception (defined
as the interval between the last menstrual period and medical confirmation
of pregnancy) or pregnancy or postnatally.
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Table 1. Timing of Maternal Recreational Drug Use (Excluding Marijuana)
and Marijuana Use and Risk of Sudden Infant Death Syndrome, Unadjusted and
Adjusted Conditional Logistic Regression Results*
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Other recreational drugs used by the mother included cocaine, crack,
crystal, amphetamine, methamphetamine, and speed; cocaine was the most commonly
used drug. Of the 28 women who used recreational drugs other than marijuana
during pregnancy, 42% used cocaine (n = 6 cases, 6 controls), 7% used crack
(n = 2 cases, 0 controls), 11% used crystal (n = 2 cases, 1 control), 21%
used methamphetamine (n = 5 cases, 1 control), 11% used speed (n = 3 cases,
0 controls), and 7% used another drug (n = 1 case, 1 control).
Maternal drug use during pregnancy was significantly associated with
SIDS in univariate analysis; the unadjusted OR was 3.5 (95% CI, 1.2-10.6; P = .03). However, after adjusting for potential risk factors
associated with socioeconomic status (poverty) including maternal alcohol
use during pregnancy, maternal age and level of education, low infant birth
weight, medical conditions at birth (eg, jaundice, apnea, fever, or meconium
aspiration), sleep position, and bed sharing, the OR was no longer statistically
significant (OR = 1.94; 95% CI, 0.6-6.5). To maintain power, fewer variables
were entered into the model. Maternal tobacco smoking during pregnancy was
the only potential confounder. Although adjusting for this factor reduced
the OR to 2.0 (95% CI, 0.6-6.5; P = .25), it was
not statistically significant. The effect of recreational drug use while breast-feeding
could not be assessed because few women reported using recreational drugs
during this period (n = 3). There was no association between SIDS and maternal
recreational drug use during the period of conception using multivariate analyses.
Dose-response effects could not be calculated because of the small sample
of drug users as well as missing information for frequency, duration of use,
and quantity.
PATERNAL RECREATIONAL DRUG USE DURING CONCEPTION AND PREGNANCY AND
POSTNATALLY
Marijuana also predominated as the drug of choice among the fathers.
As indicated in Table 2, paternal
marijuana use during all periods (conception, pregnancy, and infancy) was
significantly associated with SIDS outcome in both univariate and multivariate
models. The ORs for marijuana use were 2.2 (95% CI, 1.2-4.2; P = .01) during conception, 2.0 (95% CI, 1.0-4.1; P = .05) during pregnancy, and 2.8 (95% CI, 1.1-7.3; P = .04) postnatally (eg, smoking in the presence or vicinity of the
infant), while simultaneously adjusting for paternal postnatal tobacco smoking
and/or alcohol use during conception. Although the unadjusted and adjusted
ORs were very similar, smoking and alcohol were important confounders that
had to be adjusted for in the analyses. For example, the OR for paternal marijuana
use during conception decreased to 1.8 while adjusting for only smoking, but
increased to 2.7 while adjusting for only alcohol use. The OR while adjusting
for both smoking and alcohol use was 2.2, which was identical to the unadjusted
result. Adjustment for other potential risk factors, including paternal age
or education level, low infant birth weight, medical conditions at birth,
sleep position, and bed sharing did not alter the ORs.
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Table 2. Timing of Paternal Recreational Drug Use (Excluding Marijuana)
and Marijuana Use and Risk of Sudden Infant Death Syndrome, Unadjusted and
Adjusted Conditional Logistic Regression Results*
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Other recreational drugs used by the father included cocaine, speed,
methamphetamine, amphetamine, heroin, phencyclidine, lysergic acid diethylamide,
crystal, and mushrooms; cocaine was the second most commonly used drug among
the fathers. Of the 44 men who used recreational drugs other than marijuana
during conception, 59% used cocaine (n = 14 cases, 12 controls). After adjusting
for alcohol use, the OR for paternal recreational drug use (excluding marijuana)
during conception was 1.9 (95% CI, 1.0-3.7; P = .06).
Because men who used drugs may also have indulged in smoking or alcohol
consumption, multiplicative interactions were evaluated between paternal drug
use and paternal smoking and drinking. These interactions were not statistically
significant (P = .95). Furthermore, interactions
between maternal and paternal recreational drug use were not statistically
significant (P = .80); the magnitude of association
and significance were dominated by paternal drug use when both maternal and
paternal variables were entered into the same model. Hence, ORs were higher
and P values were lower for men than for women.
COMMENT
Substance abuse among women and their partners during periods of conception
and pregnancy may contribute to SIDS, a national perinatal health problem.
Recreational drugs have been implicated as a risk factor for SIDS, although
findings have not been consistent.2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15
In this study, the number of mothers who reported using drugs during conception
or pregnancy was small, and therefore, we had little power to detect statistically
significant associations.
Other studies have reported that maternal recreational drug use plays
a role in SIDS; however, they generally ascertained substance exposure prospectively
prior to the SIDS event, rather than retrospectively. Almost a decade ago,
a meta-analysis25 of 20 articles on the association
between maternal recreational drug exposure and SIDS found a nonstatistically
significant OR of 3.67 (95% CI, 0.93-14.2) for women using multiple drugs,
including cocaine, compared with drug-free controls.
In our study, maternal recreational drug use was not a risk factor for
SIDS when potential risk factors associated with poverty and lack of education
were included (maternal alcohol use during pregnancy, maternal age and level
of education, low birth weight, medical conditions at birth, sleep position,
and bed sharing); these factors did not act as confounders in our data. Interestingly,
maternal smoking during pregnancy was the overwhelming confounder; adjusting
for this factor reduced the OR from 3.5 (95% CI, 1.2-10.6, unadjusted model)
to 2.0 (95% CI, 0.6-6.5). Few studies have looked at potential confounders,
and only 1 study adjusted for smoking,26 even
though maternal tobacco smoking during pregnancy is a well-documented risk
factor. The high association that other studies reported between drug use
and SIDS may be due to the possibility that women who used drugs during pregnancy
also smoked. This was confirmed by Blair et al,26
who stated, "Maternal use of illegal drugs became nonsignificant in the multivariate
model after adjustment for maternal and paternal smoking."
In the current study, the risk of SIDS was approximately 2 times higher
for men who used recreational drugs (excluding marijuana) during conception
compared with those who did not, although these findings were of borderline
significance (OR = 1.9; P = .06). To our knowledge,
no other studies have examined paternal drug use during this period. However,
Blair et al26 reported that paternal use of
all illegal drugs after the infant's birth remained significant in the multivariate
model for SIDS (adjusted OR = 4.68; 95% CI, 1.56-14.05). In addition, we believe
that our study is the first to examine marijuana use by the father during
the periods of conception and pregnancy and postnatally. When multivariate
analyses were conducted and an adjustment was made for the father's tobacco
smoking and alcohol consumption during conception, there was an association
between paternal marijuana use and SIDS during conception (OR = 2.2; P = .01), during pregnancy (OR = 2.1; P = .05), and postnatally (OR = 3.3; P = .04).
These tentative results may be biased because it is unknown how often and
for how long the fathers smoked marijuana in the proximity of the pregnant
mothers or infants, although this fact does not negate the potential role
of this drug at the time of conception. Hence, whether a father's drug use
plays a significant role in SIDS needs to be extensively explored and replicated
in future studies.
We found an association between SIDS and paternal marijuana use during
all periods, whereas this was not the case with maternal use. This may be
due to the larger number of men who smoked marijuana (compared with very few
women) or to the greater amount, frequency, and duration of their use. Finally,
men may not be aware that their lifestyle habits affect pregnancy outcomes.
A potential limitation of this study was ascertainment bias for the
100 untraceable cases, with the possibility that they were the heaviest drug
users. Furthermore, the drug histories were based primarily on self-report
because recreational drug use is rarely noted in medical records. No maternal
or infant drug screening was conducted. Although the ideal way of addressing
this issue would be direct documentation of drug use collected prospectively,
the number of mothers and infants, length of time, and cost required to obtain
a large enough sample would be prohibitive. In our study, telephone interviews
occurred 6 to 12 months after the infant's death. Recall bias and reliability
of sensitive and confidential information could be questionable. Because of
societal pressures and the stigma surrounding substance use during pregnancy
and postnatally, underreporting by both men and women could have been a potential
problem. Both case and control parents may have resisted the truthful reporting
of drug use. If this occurred equally, nondifferential bias classification
would have resulted, and estimates would have been biased toward nonsignificance.
Parents of infants who died of SIDS reported exposure up until 2 years previously,
whereas control parents had no reason to spend so much time reviewing the
exposure. If the case parents remembered more accurately, perhaps out of guilt,
this could have resulted in an association between drug use and SIDS.27 To reduce recall bias, a drug history was obtained
with a structured interview (which had been pilot tested) in a nonthreatening
environment, which has reportedly improved the rate of maternal admission
to illicit drug use.1 To ensure valid and reproducible
reporting for both case and control parents, great attention was devoted to
the interview technique, questionnaire design, sensitivity of information,
and data collection methods (eg, wording, chronological order of questions,
and use of memory probes).
The advantages of this study were that patient inclusion was based on
disease and not drug status, the study design was adequate to assess polydrug
use (eg, tobacco, alcohol, and drugs), both maternal and paternal drug consumption
were factors in intrauterine and postnatal exposure to drugs (through breastfeeding
and passively), and multivariate analyses were conducted.
Whether or not a true relationship exists, direct and oblique references
linking SIDS to maternal substance use appear in both scientific and lay literature.
An increasing number of SIDS deaths list maternal drug use on death certificates.2 In the future, it is necessary to test the relationship
between all recreational drugs and SIDS in a much larger study sample; to
further separate the different types of drugs by frequency, quantity, and
timing for different racial groups of mothers and fathers; to use biochemical
measures (eg, hair, nail clippings, or meconium) to validate self-reporting;
to clarify physiologic and pathophysiologic mechanisms; and to determine if
there are variations in neonatal growth parameters.
AUTHOR INFORMATION
Accepted for publication February 2, 2001.
This research was supported by grants 1KT 0038 and 2KT 0063 from the
Tobacco-Related Disease Research Program, Office of the President, University
of California, Oakland, Calif.
The authors wish to thank Melissa Tan, BS, for her expert technical
assistance.
From the Department of Family and Preventive Medicine, University of
California, San Diego.
Corresponding author and reprints: Hillary Klonoff-Cohen, PhD, Department
of Family and Preventive Medicine, Division of Epidemiology, University of
California, San Diego, 9500 Gilman Dr, 0607, La Jolla, CA 92093-0607.
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