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MARIJUANA

Fetal Risk Summary

Marijuana (cannabis; hashish) is a natural substance that is smoked for its hallucinogenic properties. (One marijuana cigarette is commonly referred to as a “joint.”) Hashish is a potent concentrated form of marijuana. The main psychoactive ingredient, delta-9-tetrahydrocannabinol (D-9-THC, THC), is also available in a commercial oral formulation (dronabinol) for use as an antiemetic agent. Natural preparations of marijuana may vary widely in their potency and, except for the commercial preparation, no standardization exists either for the THC content or for the presence of contaminants. Only the commercially available oral formulation can be legally used in the United States.

The use of marijuana by pregnant women is common. Most investigators have reported incidences of 3%–16% (1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16 and 17). Other researchers have proposed that even these figures represent underreporting, especially in the 1st month when pregnancy may not be suspected (18,19 and 20). Because of the illicit nature of marijuana, many women will simply not admit to its use (4,8). Data from the Ottawa Prenatal Prospective Study in Canada indicated that 20% of their patients used marijuana during the year before pregnancy, with the incidence declining to about one-half this figure after the women knew they were pregnant (13). In addition, heavy marijuana usage (more than five joints/week or the use of hashish), when compared with alcohol or nicotine usage, was the least reduced of the three agents during pregnancy (21).

Even though the usage of marijuana by pregnant women is common, the effects of this usage on the pregnancies and the fetuses are still unclear. Part of this problem is attributable to the close association between marijuana, alcohol, nicotine, other abuse drugs, and lifestyles that may increase perinatal risk (1,2 and 3,6,7). Separating the effects of these agents by statistical methods becomes a major task of almost all studies. The results of this separation have produced sufficient data, however, to allow classification of the major concerns surrounding exposure to marijuana during pregnancy. These concerns are as follows: Placental passage of D-9-THC Pregnancy complications Length of gestation Quality and duration of labor Effect on maternal hormone levels Fetal or newborn complications In utero growth retardation Congenital anomalies Neurobehavioral complications in newborn Induction of leukemia in childhood D-9-THC and a metabolite, 9-carboxy-THC, cross the placenta to the fetus at term (4,22). Data for other periods of gestation and for other metabolites are not available. A 1982 study found measurable amounts of 9-carboxy-THC, but not THC, in two cord blood samples but did not quantify the concentrations (4). In a study of 10 women who daily smoked up to five marijuana cigarettes, maternal serum samples were drawn 10–20 minutes before corresponding cord blood samples (22). The time interval between last exposure and sampling ranged from 5–26 hours. This is well beyond the time of peak THC levels that occur 3–8 minutes after beginning to smoke (23). Maternal levels of THC were below the limit of sensitivity (0.2 ng/mL) in five samples and ranged from 0.4 to 6 ng/mL in the others. Measurable cord blood concentrations of THC were found in three samples and varied between 0.3 and 1.0 ng/mL. The maternal plasma:cord blood ratios for these three samples were 2.7, 4, and 6. The metabolite, 9-carboxy-THC, was measured in all maternal and cord blood samples, ranging between 2.3 and 125 ng/mL and 0.4 and 18 ng/ml, respectively. Plasma:cord blood ratios for the metabolite varied from 1.7 to 7.8.

Marijuana-induced complications of pregnancy are controversial, with different studies producing conflicting results. One of these areas of controversy involves the effect of marijuana on length of gestation. A 1980 prospective study of 291 women found no relationship between maternal use of marijuana and gestational length (3). Similar results were reported from two studies, one in 1982 involving 1,690 women (24) and one in 1989 with 1,226 women (25). Of interest, marijuana use by the women in the later study was confirmed with urine assays (25). A significantly (p<0.001) shorter gestational period was found in 1,246 users in a retrospective study of 12,424 pregnancies, but this difference disappeared when the data were controlled for nicotine exposure, demographic characteristics, and medical and obstetric histories (9).

In contrast to the above reports, three groups of investigators have associated regular marijuana use with shorter gestations (1,10,14) and one group with longer gestations (26). In 36 women using marijuana two or more times/week, 9 (25%) delivered prematurely, a rate much higher than the 5.1% for users of marijuana one time or less/week and the 5.6% for nonusers (1). Investigation of 583 women who delivered single live births, a continuation of the 1980 study mentioned above, now revealed that heavy use of marijuana (more than five marijuana cigarettes/week) was significantly (p=0.008) associated with a reduction of 0.8 week's gestational length after adjustment for the mother's prepregnancy weight (10). A total of 84 women (14.4%) used marijuana in this population, 18 of whom were classified as heavy users. A large prospective study of 3,857 pregnancies ending in singleton live births found that regular marijuana use (two to three times/month or more) was associated with an increased risk of preterm (<37 weeks) delivery for white women but not for nonwhite women (14). For the 122 regular white users, 8.2% delivered prematurely compared with 3.8% of 105 occasional users (one marijuana cigarette or less/month) and 4.0% of 2,778 nonusers. In the nonwhite groups, the incidences of shortened gestation for the 86 regular, 53 occasional, and 706 nonusers were 10.5%, 11.3%, and 8.8%, respectively. In a population of lower socioeconomic status women, the total amount of marijuana used during pregnancy was positively correlated with an average 2 days' prolongation of gestation (26). However, the authors of this study noted that their evidence for a longer gestational period was weak in terms of magnitude.

A second pregnancy complication examined frequently is the effect of marijuana on the quality and duration of labor. No association between marijuana and duration of labor, including precipitate labor and the type of presentation at birth, was found in the Ottawa Prenatal Prospective Study (3,5,8) or in another study (26). In contrast, other investigators found a significant difference (p<0.01) in precipitate labor (<3 hours total) between users (29%) and nonusers (3%) (4,27). Although not significant, 31% of users (11 of 35) had prolonged, protracted, or arrested labor as compared with 19% (7 of 36) nonusers (4,27). Because of the dysfunctional labor, 57% of the newborn infants in the user group had meconium staining vs 25% among nonusers (p=0.05), a situation that probably resulted in the observation that 41% of newborn infants of users required resuscitation compared with 21% of infants of nonusers. Adjustment of the data for race, income, smoking, alcohol use, and first physician visit did not change the findings. A second study by these latter investigators using a different group of patients produced similar results in the incidence of dysfunctional labor, precipitate labor, and meconium staining, but the differences between users and nonusers were not significant (7).

In nonhuman primates, marijuana disrupts the menstrual cycle by inhibiting ovulation through its effects on the pituitary trophic hormones (luteinizing hormone and follicle-stimulating hormone), prolactin, and resulting decreases in estrogen and progesterone levels (16). Tolerance to these effects has been reported (16). Similar effects have been observed in human clinical studies (16).

Thirteen pregnant women, who were regular users of marijuana (once/month to four times/day), were matched with controls (28). No effect of this exposure was measured on the levels of human chorionic gonadotropin (hCG), pregnancy-specific b-1-glycoprotein, placental lactogen, progesterone, 17-hydroxyprogesterone, estradiol, and estriol.

Concerns with the fetal complications arising from maternal marijuana use center around the effects on in utero growth retardation, structural anomalies, and neurobehavioral complications in the newborn infant. A recent report has now indicated that induction of leukemia in childhood must also be considered. As with pregnancy complications, conflicting reports are common.

Data of the Ottawa Prenatal Prospective Study indicated no significant reduction in birth weight or head circumference (after adjustment for other factors) in babies of marijuana users (3,5,8,10,13). Compared with infants of nonusers, birth weight actually increased by an average of 67 g in irregular users (one marijuana cigarette/week or less) and 117 g in moderate users (two to five/week), whereas heavy use (more than five/week) was associated with a nonsignificant reduction of 52 g (10). Other studies have observed no effect on growth after adjustment of their data (1,7,9,26,29). However, in one study, a reduction of 0.55 cm in infant length, but not head circumference, was correlated with maternal use of three marijuana cigarettes/day in the 1st trimester (26). Use during the remainder of pregnancy or the total amount smoked during pregnancy did not significantly affect the infants' length or head circumference.

Positive correlations with reduced in utero growth (after adjustment) have been reported by a number of researchers. In one study, use of less than three joints/week was associated with a decrease in birth weight of 95 g compared with that of controls, and use of three or more cigarettes/week was associated with a reduction of 139 g (24,30). Both weight reductions were significant (p<0.01). Some of these same researchers published a related study in 1989 involving Boston-area women enrolled in an investigation between 1984 and 1987 (25). Their findings indicated that marijuana use during pregnancy, when confirmed by positive urine assays, was independently associated with impaired fetal growth, and that the effects of cocaine abuse were additive but not synergistic (25). However, they could not demonstrate a cause-and-effect relationship with marijuana because of other factors, such as the markedly elevated blood levels of carbon monoxide that occur with marijuana use (blood carboxyhemoglobin levels after smoking marijuana are about 5 times those observed after smoking tobacco) (25). Of 1,226 mothers who were studied, 331 (27%) used marijuana during gestation as determined by history and positive urine assay. Only 278 (84%) of these would have been detected by history alone. After controlling for potentially confounding variables (e.g., tobacco, alcohol, opiates, certain diseases, and obstetric factors), infants of marijuana users with positive urine assays (N=202) were compared to infants of nonusers (N=895) and found to have statistically significant differences in birth weight (reduction of 79 g; p=0.04) and length (reduction of 0.52 cm; p=0.02). Head circumference was reduced by 0.19 cm but the difference was not significant (p=0.15). The birth weight and length measurements did not differ statistically if only self-reported marijuana use was considered, demonstrating the importance of a biologic marker in studies involving this drug.

Another study, conducted from 1975 to 1983 in two phases, found decreased birth weight only in the second phase (17). The two phases, involving 1,434 and 1,381 patients, respectively, differed primarily in their assessment of marijuana use early in pregnancy. In the first phase, 9.3% used marijuana, with consumption of two to four joints/month associated with a significant increase in birth weight. No trend was observed with more or less frequent use. The second phase, with 10.3% users, found weight reductions in all classifications of marijuana exposure: 127 g for two to three joints/week, 143 g for four to six joints/week, and 230 g for daily use (17). The authors speculated that the difference between the groups may have been related to the use of other abuse drugs (e.g., cocaine) or changes in the composition or contaminants of marijuana. Regular use (two to three times/month or more) of marijuana was correlated with an increased risk of low-birth-weight (<2500 g) and small-for-gestational-age (SGA) infants in whites only in a 1986 study (14). Compared with 3,490 nonusers, in whom the risks of low-birth-weight and SGA infants were 2.7% and 4.9%, respectively, regular use (N=122) was associated with rates of 8.2% and 12.5%, respectively. In 845 nonwhites, no differences between users and nonusers were observed. Examination of 462 infants, 16% of whom were exposed to marijuana and alcohol during early gestation, found a significant correlation between maternal marijuana use and decreased body length at 8 months of age (11). Body weight and head circumference were not significantly affected.

In three case reports on the same five infants, low birth weight (all <2500 g) with reduced head circumference and length were observed (31,32 and 33). Two of the infants were premature (<37 weeks). The mothers of these infants smoked 2–14 marijuana cigarettes/day during pregnancy, with one also using alcohol, cocaine, and nicotine, and two others using nicotine.

Animal research in the 1960s and 1970s yielded inconclusive evidence on the teratogenicity of marijuana and its active ingredients unless high doses were used in certain species (34,35,36 and 37). In humans, most investigators and reviewers have concluded either that marijuana does not produce structural defects or that insufficient data exist to reach any conclusion (1,13,25,26,29,38,39,40,41,42,43,44,45,46,47,48 and 49). However, one reviewer cautioned that marijuana-induced birth defects could be rare and easily missed (48), and another observed that marijuana could potentiate known teratogens by lowering the threshold for their effects (42). A previously mentioned study that used urine assays to document marijuana exposure found that the drug was not associated with minor (either singly or as a constellation of three) or major congenital anomalies (25).

Because marijuana use is so common in women during pregnancy, and because of its frequent association with alcohol and other abuse drugs, it is not surprising that a number of studies and case reports have described congenital malformations in infants whose mothers were smoking marijuana. With some exceptions, the majority of these investigators did not attribute the observed defects to marijuana, but they are chronicled here mainly for a complete record.

Frequent References have described the combined maternal use of marijuana and lysergic acid diethylamide (LSD) in cases ending with poor fetal outcome. A 1968 report described an infant with right terminal transverse acheiria (absence of hand) (50). The mother had taken LSD early in gestation before she knew she was pregnant. She had also smoked marijuana throughout the pregnancy and had taken a combination product containing dicyclomine, doxylamine, and pyridoxine for 1st trimester nausea. A second infant with a terminal transverse deficit, who was also exposed to the two hallucinogens, was described in 1969 (51). The defect involved portions of fingers of the left hand. Syndactyly of the right hand with shortened fingers and talipes equinovarus of the left foot were also present. A critique of these case reports and others concluded that the defects in the two infants may have been caused by amniotic band syndrome (52). Complete exstrophy of the bladder, epispadias, widely separated pubic rami, and bilateral inguinal hernias were observed in a newborn exposed to LSD, marijuana, and mephentermine (53). Marijuana was allegedly used only twice by the mother. In another case, a female infant with multiple anomalies compatible with trisomy 13 with D/D translocation was delivered from a 22-year-old mother who had last used LSD 9 months before conception (54). The mother used marijuana, barbiturates, and amphetamines throughout gestation and, presumably, before conception. The authors speculated that the defect may have been caused by LSD-induced damage of maternal germ cells before fertilization. A 1972 case report described an infant with multiple eye and central nervous system defects consisting of brachycephaly with widely separated sutures, bilateral cephalohematomas, a right eye smaller than the left, a possible cataract, and multiple brain anomalies (55). The mother had taken marijuana, LSD, and other drugs throughout pregnancy. In a study of 140 women using LSD and marijuana followed through 148 pregnancies, 8 of 83 liveborn infants had major defects, as did 4 of 14 embryos examined after induced abortion (56). The incidence of defects in this sample is high (8.1%), but many of the women were using multiple other abuse drugs and had lifestyles that probably were not conducive to good fetal health. Two other reports involving the combined use of marijuana and LSD with resulting adverse fetal outcomes do not appear to have any relationship to either drug (57,58). One of these involved a report of six cases of persistent ductus arteriosus, one of which was exposed to marijuana in utero (57). The history of maternal marijuana use was coincidental. The second case described an infant who died at 2.5 months of age of a bilateral in utero cerebral vascular accident and resulting porencephaly (58). The mother had used marijuana, LSD, alcohol, and other abuse drugs, including cocaine. This latter drug was thought to be the causative agent.

In one of two fatal cases of congenital hypothalamic hamartoblastoma tumor, an infant exposed to marijuana also had congenital heart disease and skeletal anomalies suggestive of the Ellis-von Creveld syndrome (i.e., chondroectodermal dysplasia syndrome) (59). In addition to marijuana, the mother had used cocaine and methaqualone during early pregnancy, but the authors did not attribute the defects to a particular agent. In a report of an infant with a random pattern of amputations and constrictions consistent with the amniotic band sequence, the mother's occasional use of marijuana was coincidental (60).

In contrast to the above case reports, in which marijuana use during the pregnancies was apparently not related to fetal outcome, two studies have reported possible associations with the drug (9,24), and one case report found defects similar to those reported in one of the studies (31,32 and 33). However, in both studies, marijuana usage in pregnancy was poorly quantified (9). Additionally, a third study observed severe minor facial defects only in the offspring of heavy users (61). In a study of 1,690 mother-child pairs, women who smoked marijuana, but who only drank small amounts of alcohol, were 5 times more likely than nonusers to deliver an infant with features compatible with the fetal alcohol syndrome (see Ethanol) (24). The relative risk for this defect in marijuana users was 12.7 compared with 2.0 in nonusers. In a series of case reports, five infants were described with congenital defects suggestive of the fetal alcohol syndrome (31,32 and 33). In addition to daily marijuana use by the mothers, one used alcohol, cocaine, and nicotine; two used nicotine only; and two denied the use of other drugs (31). In a large study involving 12,424 women of whom 1,246 (10%) used marijuana during pregnancy, a crude association between one or more major malformations and marijuana usage was discovered; no association was found with minor malformations (9). Logistic regression was used to control confounding variables, and although the odds ratio (1.36) was suggestive, the association between marijuana and the defects was not significant. The third study compared 25 marijuana users with 25 closely matched nonusing controls in a search for minor anomalies (61). Infants were examined at a mean age of 28.8 months. No relationship between the drug use and minor malformations was found, but the authors could not exclude the existence of a possible relationship at birth since some minor anomalies disappear with age. Of interest, three infants had severe epicanthal folds, three had true ocular hypertelorism, and all were the offspring of heavy (more than five joints/week) users (61).

Strabismus was diagnosed in 24% (7 of 29) of the infants delivered from mothers maintained on methadone throughout pregnancy in a 1987 report (62). This percentage was approximately 4–8 times the expected incidence of the eye defect in the general population. Two (29%) of the seven infants were also exposed in utero to marijuana vs. three (14%) of the nonaffected infants. Although use of other abuse drugs was common, the authors attributed the eye condition to low birth weight and, possibly, an unknown contribution from methadone. However, in the Ottawa Prenatal Prospective Study, 35% of the marijuana-exposed infants compared with 6% of the controls had more than one of the following eye problems: myopia, strabismus, abnormal oculomotor functioning, or unusual discs (p<0.008) (13). The examiner was blinded to the prenatal histories of the infants.

Significant alterations in neurobehavior in offspring of regular marijuana users were noted in the Ottawa Prenatal Prospective Study (3,5,13,15). After adjustment for nicotine and alcohol use, in utero exposure to marijuana was associated with increased tremors and exaggerated startles, both spontaneous and in response to minimal stimuli (13,15). Decreased visual responses, including poorer visual habituation to light, were also observed in these infants. In addition, a slight increase in irritability was noted. In early data from the Ottawa group, a distinctive shrill, high-pitched, cat-like cry, reminiscent of the cry considered to be symptomatic of drug withdrawal, was heard from a large number of the offspring of regular users (3). No differences were noted between exposed and nonexposed infants in terms of lateralization, muscle tone, hand-to-mouth behavior, general activity, alertness, or lability of states (3). On follow-up examinations, the abnormalities in neonatal neurobehavior apparently did not result in poorer performance on cognitive and motor tests at 18 and 24 months (13). The investigators cautioned that they were unable to determine whether the follow-up results were truly indicative of a return to normal or were related to insensitivity of the available tests (13). A 1984 report examining maternal drinking and neonatal withdrawal found that marijuana use had no effect on the signs of withdrawal in their patients (63). In another study, no increase in startles, tremors, or other neurobehavioral measures at birth was noted in exposed infants (26). Marijuana exposure also had no effect on muscle tone. Evaluation at 1 year of age found no significant differences in growth or in mental and motor development between infants exposed in utero to either none or varying amounts of the drug (26).

The development of leukemia in children exposed to marijuana during gestation has been suggested in a 1989 report (64). In a multicenter study conducted between 1980 and 1984 by the Childrens Cancer Study Group, in utero marijuana exposure was significantly related to the development of acute nonlymphoblastic leukemia (ANLL). Of the 204 cases that were analyzed, marijuana use was found in 10 mothers, only one of whom used other (LSD) mind-altering drugs. An 11th case mother used methadone. Only 1 of the 203 closely matched healthy controls was exposed to abuse drugs. The 10-fold risk induced by marijuana exposure was statistically significant (p=0.005). The mean age of ANLL diagnosis was significantly younger in the exposed children than in nonexposed children: 37.7 months vs 96.1 months, respectively (p=0.007). Based on the French-American-British system of classification, the morphology of the leukemias also differed significantly, with 70% of the exposed cases presenting with monocytic (M5) or myelomonocytic (M4) morphology compared with 31% of the nonexposed cases (p=0.02). Additionally, only 10% of the exposed children had M1 or M2 (myelocytic) morphology vs 58% of the nonexposed children (p=0.02). The authors were able to exclude reporting bias but could not exclude the possibility that the association was related to other factors, such as the presence of herbicides or pesticides on the marijuana.

Early concerns (65,66) that marijuana-induced chromosomal damage could eventually lead to congenital defects have been largely laid to rest (39,48,49). The clinical significance of any drug-induced chromosomal abnormality is doubtful (48). Finally, heavy marijuana use in males has been associated with decreased sperm production (16,66). However, the clinical significance of this finding has been questioned since there is no evidence that the reduction in sperm counts is related to infertility (16,66).

In summary, the use of marijuana in pregnancy has produced conflicting reports on the length of gestation, the quality and duration of labor, fetal growth, congenital defects, and neurobehavior in the newborn. These effects have been the subject of a number of reviews (16,35,36,38,39,40,41 and 42,45,46,47,48 and 49,67,68). Research using urine assays to document maternal marijuana use indicates that the drug is associated with reduced fetal growth (weight and length) but not with gestational length (25). Moreover, this growth retardation is independent of the effects of cocaine, with the effects being additive rather than synergistic. The possible association of in utero marijuana exposure with ANLL in children should be a major concern of any woman who chooses to use this drug during pregnancy. No pattern of malformations has been observed that could be considered characteristic of in utero marijuana exposure. In most studies, the use of marijuana is closely associated with the use of nicotine and alcohol, and the abuse of other drugs, both prescription and illicit, occurs frequently. In addition, failure to account for the varying concentrations of D-9-THC contained in the natural product, the presence of contaminants, and the underreporting of maternal marijuana use could very well have changed the findings of many studies. Based on this information, it is probable that some of the effects observed in offspring of marijuana users are the result of a combination of such factors as drug use, lifestyles, socioeconomic status, maternal diseases and nutrition, and other unidentified elements. The effects on fetal growth and the reported association with childhood leukemia may be caused by marijuana or by factors closely related to the use of the drug. Additional research, especially long-term studies on exposed infants, is required before final conclusions can be reached.

Breast Feeding Summary

D-9-Tetrahydrocannabinol (D-9-THC; THC), the main active ingredient of marijuana (cannabis, hashish), is excreted into breast milk (26,42,69,70). Analysis of THC and two metabolites, 11-hydroxy-THC and 9-carboxy-THC, were conducted on the milk of two women who had been nursing for 7 and 8 months and who smoked marijuana frequently (69). A THC concentration of 105 ng/mL, but no metabolites, was found in the milk of the woman smoking one pipe of marijuana daily. In the second woman, who smoked seven pipes/day, concentrations of THC, 11-hydroxy-THC, and 9-carboxy-THC were 340 ng/mL, 4 ng/mL, and none, respectively. The analysis was repeated in the second mother, approximately 1 hour after the last use of marijuana, using simultaneously obtained samples of milk and plasma. Concentrations (in ng/mL) of the active ingredient and metabolites in milk and plasma (ratios shown in parenthesis) were 60.3 and 7.2 (8.4), 1.1 and 2.5 (0.4), and 1.6 and 19 (0.08), respectively. The marked differences in THC found between the milk samples was thought to be related to the amount of marijuana smoked and the interval between smoking and sample collection. A total fecal sample from the infant yielded levels of 347 ng of THC, 67 ng of 11-hydroxy-THC, and 611 ng of 9-carboxy-THC. Because of the large concentration of metabolites, the authors interpreted this as evidence that the nursing infant was absorbing and metabolizing the THC from the milk. In spite of the evidence that the fat-soluble THC was concentrated in breast milk, both nursing infants were developing normally.

In animals, THC decreases the amount of milk produced by suppressing the production of prolactin and, possibly, by a direct action on the mammary glands (42). Although data on this effect are not available in humans, maternal marijuana use does not seem grossly to affect the nursing infant (26). In 27 infants evaluated at 1 year of age, who were exposed to marijuana via the milk, compared with 35 nonexposed infants, no significant differences were found in terms of age at weaning, growth, and mental or motor development (26).

Although no adverse effects of marijuana exposure from breast milk have been reported, follow-up of these infants is inadequate. At the present time, the long-term effects of this exposure are unknown and additional research to determine these effects, if any, is warranted (70). The American Academy of Pediatrics considers the use of marijuana during breast feeding to be contraindicated (71).

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