Prenatal cocaine exposure (PCE), theorized in the 1970s, occurs when a pregnant woman uses cocaine including crack cocaine and thereby exposes her fetus to the drug. Babies whose mothers used cocaine while pregnant supposedly have increased risk of several different health issues during growth and development and are colloquially known as crack babies.
PCE is very difficult to study, because it rarely occurs in isolation; usually it coexists with a variety of other factors, which may confound a study's results. Pregnant mothers who use cocaine often use other drugs in addition, may be malnourished and lacking in medical care, are at risk of violence, and may neglect their children. Children with PCE in foster care may experience problems due to unstable family situations. Factors such as poverty that are frequently associated with PCE have a much stronger influence on children's intellectual and academic abilities than does exposure to cocaine in isolation. Thus, researchers have had difficulty in determining which effects result from PCE and which result from other factors in the children's histories.
PCE is associated with premature birth, birth defects, attention deficit hyperactivity disorder, and other conditions. The effects of cocaine on a fetus are thought to be similar to those of tobacco, and are less severe than those of alcohol. No scientific evidence has shown a difference in harm to a fetus between crack and powder cocaine.
No specific disorders or conditions have been found to result from people whose mothers used cocaine while pregnant. PCE appears to have little effect on infant growth. Studies focusing on children six years and younger have not shown any direct, long-term effects of PCE on language, growth, or development as measured by test scores.
In the media "Crack baby" (or "cocaine baby" and "crack kid") was a term coined to describe children who were exposed to crack cocaine as fetuses, which emerged in the US during the 1980s and 1990s amid a crack epidemic. Early studies reported that people who had been exposed to crack in utero would be severely emotionally, mentally, and physically disabled; this belief became common in the scientific and lay communities. Fears were widespread that a generation of cocaine-exposed children was going to put severe strain on society and social services as they grew up. Later studies failed to substantiate the findings of earlier ones that PCE has severe disabling consequences; these earlier studies had been methodologically flawed (e.g., with small sample sizes and confounding factors). Scientists have come to understand that the findings of the early studies may have been overstated.
Historical context
During the 1980s and 1990s, a surge occurred in the use of crack cocaine in US cities: the crack epidemic. During this time, fears arose throughout the country that PCE would create a generation of youth with severe behavioral and cognitive problems. Early studies in the mid-1980s reported that cocaine use in pregnancy caused children to have severe problems, including cognitive, developmental, and emotional disruption. These early studies had methodological problems, including small sample size, confounding factors such as poor nutrition, and use of other drugs by the mothers. The results of the studies, though, sparked widespread media discussion in the context of the new war on drugs. For example, a 1985 study that showed harmful effects of cocaine use during pregnancy created a huge media buzz. The term "crack baby" resulted from the publicity surrounding crack and PCE.
Media reports commonly emphasized that babies who had been exposed to crack in utero would never develop normally. The children were reported to be inevitably destined to be physically and mentally disabled for their whole lives.
Babies exposed to crack in utero were written off as doomed to be severely disabled, and many were abandoned in hospitals. They were expected to be unable to form normal social bonds. Experts foresaw the development of a "biological underclass" of born criminals who would prey on the rest of the population. Crime rates were predicted to rise when the generation of crack-exposed infants grew up (instead, they dropped). The children were predicted to be difficult to console, irritable, and hyperactive, putting a strain on the school system. Charles Krauthammer, a columnist for The Washington Post wrote in 1989, "[t]heirs will be a life of certain suffering, of probable deviance, of permanent inferiority." The president of Boston University at the time, John Silber, said, "crack babies ... won't ever achieve the intellectual development to have consciousness of God." These claims of biological inferiority played easily into existing class and racial biases. Reporting was often sensational, favoring the direst predictions and shutting out skeptics.
Reporting on the effects of PCE may have been affected by publication bias, a disproportionate publication of studies indicating more severe outcomes as the crack epidemic emerged. Scientific studies that reported PCE to have significant effects were more likely to be published than those that did not. Between 1980 and 1989, 57% of studies showing cocaine has effects on a fetus were accepted by the Society for Pediatric Research, compared with only 11% of studies showing no effects. Findings that other factors such as prematurity were behind symptoms that cocaine-exposed babies showed did not "fit within the narrative of what had become a national scare" and were given less attention. Ideas about severe effects of PCE may have been more readily embraced because they "fit in with cultural stereotypes".
At the time, the proposed mechanism by which cocaine harmed fetuses was as a stimulant— cocaine was predicted to disrupt normal development of parts of the brain that dealt with stimulation, resulting in problems such as bipolar disorder and attention deficit disorder. Reports from the mid-1980s to early '90s raised concerns about links between PCE and slowed growth, deformed limbs, defects of the kidneys and genitourinary and gastrointestinal systems, neurological damage, small head size, atrophy or cysts in the cerebral cortex, bleeding into the brain's ventricles, and obstruction of blood supply in the central nervous system.
After the early studies that reported that PCE children would be severely disabled, came studies that purported to show that cocaine exposure in utero has no important effects. Almost every prenatal complication originally thought to be due directly to PCE was found to result from confounding factors such as poor maternal nutrition, use of other drugs, depression, and lack of prenatal care. More recently, the scientific community has begun to reach an understanding that PCE does have some important effects, but that they are not as severe as was predicted in the early studies. The effects of PCE are subtle, but they exist. Most people who were exposed to cocaine in utero are normal or close to it.
Pathophysiology
Cocaine, a small molecule, can cross the placenta into the bloodstream of the fetus. In fact, it may be present in a higher concentration in the amniotic fluid than it is in the mother's bloodstream. The skin of the fetus can absorb the chemical directly from the amniotic fluid until the 24th week of pregnancy. Cocaine can also show up in breast milk and affect the nursing baby. The severity of effects depends on how much of the drug is used, how often, and the stage in the development of the fetus.
Cocaine prevents the reuptake of the neurotransmitters dopamine, serotonin, and norepinephrine. Thus, they stay in the synapse longer, causing excitement of the sympathetic nervous system and evoking a stress response.Volpe 2008, p.1025 The euphoria experienced by cocaine users is thought to be largely due to the way it prevents these neurotransmitters from being reabsorbed by the presynaptic neuron that released it.
Use of cocaine during pregnancy can negatively affect both the mother and the fetus, but how it affects the fetus is poorly understood. Three main mechanisms of cocaine exposure can harm a fetus, by altering brain chemistry, altering the expression of certain genes, and the constriction of blood vessels. The neurotransmitters affected by cocaine are involved in the development of the fetus's brain, so the drug may affect fetal development directly by altering the development of the brain's monoaminergic system. The most important way cocaine affects fetal development is by binding to dopamine receptors. Cocaine decreases a fetus's ability to synthesize and release dopamine and increases the density of dopamine receptors on the surfaces of neurons.
Another possible mechanism by which cocaine harms the fetus may be in part by interfering with blood supply to the uterus.Aronson 2008, pp. 512–14 Cocaine causes vasoconstriction (narrowing of blood vessels) in both mother and fetus, which can cause hypoxia in the fetus. Constricting blood vessels causes tissues to receive insufficient blood flow, killing cells, but this effect is less pronounced with cocaine than with nicotine. The reduction in blood flow to the uterus limits the delivery of oxygen and nutrients to the fetus. Cocaine also constricts the blood vessels in the fetus, which is potentially linked to slowed fetal growth and abnormal development of the genitourinary, cardiovascular, digestive, and musculoskeletal systems.
Cocaine causes changes in the mother's blood pressure that are thought to be the cause of strokes in the fetus; one study found that 6% of cocaine-exposed infants had had one or more strokes. Such prenatal strokes may be the cause of neurological problems found in some cocaine-exposed infants after birth.
Blood vessel contraction can also cause premature labor and premature birth. Cocaine has also been found to enhance the contractility of the tissue in the uterus, another factor that has been suggested as a possible mechanism for its contribution to increased prematurity rates. Increased contractility of the uterus may also be behind the increased likelihood of placental abruption (the placenta tearing away from the uterine wall), which some findings have linked with PCE.
Diagnosis Cocaine use during pregnancy can be discovered by asking the mother, but sometimes women will not admit to having used drugs. Mothers may lie for fear of prosecution or having their children taken away, but even when they are willing to tell the truth, their memories may not be very accurate. Determining the purity of the drug they have taken also may not be possible. More reliable methods for detecting cocaine exposure involve testing the newborn's hair or meconium (the infant's earliest stool). Hair analysis, however, can give false positives for cocaine exposure, and a newborn may not have enough hair to test. The newborn's urine can be tested for cocaine and metabolites, but it must be collected as soon as possible after birth. It is not known how long after exposure the markers will still show up in a newborn's urine. The mother's urine can also be tested for drugs, but it cannot detect drugs used too far in the past or determine how much or how often the drugs were used. Tests cannot generally detect cocaine use over a week prior to sample collection. Mothers are more honest about cocaine use when their urine is also tested, but many users still deny it. Both maternal and neonatal urine tests can give false negatives.
Effects and prognosis As of 2014, studies had returned widely varying reports of the effects of PCE; some claimed the physical disabilities are severe and generalized, others find specific effects, and others none at all.
Timing