Prenatal cocaine exposure

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Prenatal cocaine exposure (PCE), theorized in the 1970s, occurs when a pregnant woman uses 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.[1]

"Crack baby" was a term coined to describe children who were exposed to

sample sizes and confounding factors). Scientists have come to understand that the findings of the early studies may have been overstated.[2] Commentators have characterized the phenomenon as a moral panic.[3][4]

No specific disorders or conditions have been found to result for people whose mothers used cocaine while pregnant.[5] Studies focusing on children of six years and younger have not shown any direct, long-term effects of PCE on language, growth, or development as measured by test scores.[6] PCE also appears to have little effect on infant growth.[7] However, 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.[8] No scientific evidence has shown a difference in harm to a fetus between crack and powder cocaine.[9]

PCE is very difficult to study because it very rarely occurs in isolation; usually it coexists with a variety of other factors, which may confound a study's results.[6] Thus, studies have failed to clearly show that PCE has negative cognitive effects, partly because such effects may be due to concurrent factors.[10] Pregnant mothers who use cocaine, often use other drugs in addition, or they may be malnourished and lacking in medical care. Children in households where cocaine is abused are at risk of violence and neglect, and those 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.[11] Thus, researchers have had difficulty in determining which effects result from PCE and which result from other factors in the children's histories.

Historical context

The US government published posters like this one in the 1980s and 1990s to warn people away from crack.

During 1980s and 1990s, a surge occurred in use of crack

War on Drugs.[16][1] For example, a 1985 study that showed harmful effects of cocaine use during pregnancy created a huge media buzz.[15][17] The term "crack baby" resulted from the publicity surrounding crack and PCE.[18]

Media reports commonly emphasized that babies who had been exposed to crack in utero would never develop normally.[14][18] The children were reported to be inevitably destined to be physically and mentally disabled for their whole lives.[2] Babies exposed to crack in utero were written off as doomed to be severely disabled, and many were abandoned in hospitals.[19] They were expected to be unable to form normal social bonds.[14] Experts foresaw the development of a "biological underclass" of born criminals who would prey on the rest of the population.[17][19][20] Crime rates were predicted to rise when the generation of crack-exposed infants grew up (instead, they dropped).[19] The children were predicted to be difficult to console, irritable, and hyperactive, putting a strain on the school system.[7] 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."[17][19] 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."[19][20] 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.[20]

Powder (left) and crack cocaine (right)

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.[21] Scientific studies that reported PCE to have significant effects were more likely to be published than those that did not.[22] 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.[23] 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.[24] Ideas about severe effects of PCE may have been more readily embraced because they "fit in with cultural stereotypes".[24]

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

cysts in the cerebral cortex, bleeding into the brain's ventricles, and obstruction of blood supply in the central nervous system.[21]

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.[19] 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.[25] More recently, the scientific community has begun to reach an understanding that PCE does have some important effects, but that they are not severe as was predicted in the early studies.[19] The effects of PCE are subtle but they exist.[21][26][27] Most people who were exposed to cocaine in utero are normal or close to it.[14]

Pathophysiology

Cocaine is a small enough molecule to pass across the placental barrier into the bloodstream of the fetus.[28]

Cocaine, a small molecule, is able to cross the placenta into the bloodstream of the fetus.[28][29] In fact, it may be present in a higher concentration in the amniotic fluid than it is in the mother's bloodstream.[30] The skin of the fetus is able to absorb the chemical directly from the amniotic fluid until the 24th week of pregnancy.[30] Cocaine can also show up in breast milk and affect the nursing baby.[30][31] The severity of effects depends on how much of the drug is used, how often, and the stage in the development of the fetus.[32]

Cocaine prevents the

presynaptic neuron that released it.[33][1][22]

Use of cocaine during pregnancy can negatively affect both the mother and the fetus,[23] but the ways in which it affects the fetus are poorly understood.[25] 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.[1] The neurotransmitters affected by cocaine are involved in the development of the fetus's brain,[32] so the drug may affect fetal development directly by altering the development of the brain's monoaminergic system.[34] The most important way cocaine affects fetal development is by binding to dopamine receptors.[14]

Another possible mechanism by which cocaine harms the fetus may be in part by interfering with blood supply to the uterus.

musculoskeletal systems.[32]
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.[30] Such prenatal strokes may be the cause of neurological problems found in some cocaine-exposed infants after birth.[7] Blood vessel contraction can also cause
premature labor and premature birth.[18] 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.[35] 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.[23]

Diagnosis

Cocaine use during pregnancy can be discovered by asking the mother, but sometimes women will not admit to having used drugs.

Effects and prognosis

Studies have returned widely varying reports of the effects of PCE; some claim the physical disabilities are severe and generalized, others find specific effects, others none all.[1] The timing of the dose of the drug is an important determinant of outcome, in addition to how much is used, for how long, and what kind of care is rendered after birth.[1] Drug use in the first trimester is the most harmful to the fetus in terms of neurological and developmental outcome.[40] The effects of PCE later in a child's life are poorly understood; little information is available about the effects of in utero cocaine exposure on children over the age of five.[6] Some studies have found PCE-related differences in height and weight, while others have not; these differences are generally either small or are gone by the time children are of school age.[6] Much is still not known about what factors may exist to aid children who were exposed to cocaine in utero.[25] Whether the effects of PCE are increased once children reach adolescence is unknown, as is whether the neural rewiring that occurs during this developmental period attenuates the effects.[22] A review of 27 studies performed between 2006 and 2012 found that cognitive development was mildly to moderately affected in PCE adolescents, but how important these effects were in practical terms was unclear.[22]

Unlike

fetal alcohol syndrome, no set of characteristics has been discovered that results uniquely from cocaine exposure in utero.[25] Cocaine exposure in utero may affect the structure and function of the brain, predisposing children to developmental problems later, or these effects may be explained by children of crack-using mothers being at higher risk for domestic violence, deadbeat parenting, and maternal depression.[6] When researchers are able to identify effects of PCE, they are typically small.[25]

Pregnancy and birth

Premature baby

Studies have found after controlling for other factors that some effects are present in pregnancies involving cocaine:

spontaneous abortion with cocaine use.[17] Cocaine reduces the appetite and has been linked with reduced maternal weight gain during pregnancy; in addition, constriction of the blood vessels may further limit supply of nutrients to the fetus.[41]
Using cocaine while pregnant also heightens the chances of maternal and fetal vitamin deficiencies,
sudden infant death syndrome;[21] however, by itself, cocaine exposure during fetal development has not subsequently been identified as a risk factor for the syndrome.[42] Some PCE children experience hypertonia (excessive muscle tone),[43] and reduced reflexes and motor function have been found in babies four to six weeks old.[22]

While newborns who were exposed prenatally to drugs such as

barbiturates or heroin frequently have symptoms of drug withdrawal (neonatal abstinence syndrome), this does not happen with babies exposed to crack in utero; at least, such symptoms are difficult to separate in the context of other factors such as prematurity or prenatal exposure to other drugs.[18]

Mental, emotional, and behavioral outcomes

Studies have shown small deficits in behavioral, cognitive, attention, emotional, and language function in PCE infants, children, and adolescents,[22] but other studies attribute findings of negative effects on cognitive development to confounding factors.[10] Studies suggest that the environment in which a child grows up makes a more important contribution to outcome in cognitive, behavioral, and other outcomes than does the cocaine exposure itself.[11] School performance is mildly affected in older children.[29] In IQ studies, cocaine-exposed children do not appear to score lower than others.[1] Although PCE is correlated with low IQ scores, scientists generally believe that PCE alone does not cause this effect; rather, it is more likely due to associated factors.[11] In school-aged and younger children, PCE does not appear in studies to predispose children to poorer intellectual performance.[6] Poor performance on IQ tests could actually be due to trouble with sustaining attention if the tests fail to account for this factor separately.[10]

Cocaine causes impaired growth of the fetus's brain, an effect that is most pronounced with high levels of cocaine and prolonged duration of exposure throughout all three trimesters of pregnancy.[43] Prenatal cocaine exposure has been found to affect the cognitive performance of individuals and affect speech and language development, behavior, physical and cognitive growth, and function. The more of the substance the fetus is exposed to the more of an effect it can have on the overall development as well as running the risk of being fatal to the fetus during the prenatal stage(s) of pregnancy. The effects of cocaine uses can cause for there to be an increased chance of the baby being born premature, affecting the body weight, height and the growth of the organs and brain due to the premature state of the baby as well as the impact of the harmful substances the baby was exposed to. This can have effects on other areas such as brain development, being exposed to a stimulant such as cocaine can cause damage and issues in development over time. In behavior, cognition, memory, grasping of information, and attention are areas that are common struggles for children that were exposed to cocaine in the womb. These effects are seen in individuals reaching the age of 10 and older. Long-term studies have shown that there are alterations made in the structure and function of the brain occur when exposed to these drugs with cause change in the behaviors of the individual over time and they develop and grow. All of the effects physically and cognitively all vary for each individual based on their level of exposure to the drug, the gestational timing of the infant as it develops, determine some physical effect that might have occurred and the care they receive after being born.[1] Studies that use neuroimaging such as magnetic resonance imaging (MRI) and FMRI have shown differences in brain structure of PCE children, for example in the cerebral cortex and limbic system.[1] Those PCE children who had slowed brain growth as fetuses are at higher risk for impaired brain growth and motor, language and attention problems after they are born.[43] Studies have found that children exposed to cocaine during fetal development experience problems with language, behavior, development, and attention.

attention deficit disorder,[15] and a link has been found between the disorder itself and PCE.[45]
Mild deficits in language have been found in older PCE children.[29] Language development is impaired, possibly into late adolescence, but adolescents up to age 17 may improve their receptive language skills.[1]

Evidence suggests that in utero cocaine exposure leads to problems with behavior and sustained attention, possibly by affecting parts of the brain that are vulnerable to toxins during fetal development.[6] School-age PCE children have been found to have trouble regulating their behavior and sustaining their attention.[10] Children who had been exposed to high levels of cocaine in utero show poorer behavioral inhibition than those with lower levels of exposure or unexposed children.[11] The changes in behavior and attention caused by PCE are measurable by standardized scales;[43] however these behavioral effects seem to be mild.[15] Children exposed to cocaine in the first trimester are less sociable, more withdrawn, and show more anxious and depressed behaviors.[1] Those exposed to higher doses of cocaine have been reported to show aggressive and disruptive behaviors.[1] PCE girls are seven times more likely to have delinquent behavioral problems, but PCE boys are no more likely than other boys.[45] Studies from the 2000s and 2010s are conflicted on whether PCE adolescents are at greater risk for use of drugs such as cocaine, alcohol, and marijuana.[22] A 2010 study found that PCE adolescent girls were have anxiety than their non-exposed peers.[22]

Physical outcomes

Slowed growth is well documented in fetuses, but it is not as clear whether older children remain smaller or catch up to their peers.

neuroendocrine system, but more study is needed to determine whether it does and what the effects are.[22]

A review of the literature reported that cocaine use causes

congenital defects between 15 and 20% of the time; however another large-scale study found no difference in rates of birth anomalies in PCE and non-PCE infants.[46] It has been suggested that some birth defects could be due to cocaine's disruption of blood vessel growth.[46]
Most PCE-related congenital defects are found in the brain, heart,
genitourinary tract, arms and legs.[46]
Cocaine use by pregnant mothers may directly or indirectly contribute to defects in the formation of the
congestive heart failure.[33] Genital malformations occur at a higher-than-normal rate with PCE.[46]
The liver and lungs are also at higher risk for abnormalities.
skull has three lobes, the brain is deformed, and hydrocephalus occurs, is also associated with PCE.[47] Like birth defects, small head size, and stroke are risks in PCE.[48]

Epidemiology

Of all cocaine users, women of childbearing age comprise 15–17%.[29] An estimated 0.6 to 3% of pregnant women in the developed world use cocaine.[5][14] A 1995 survey in the US found that between 30,000 and 160,000 cases of prenatal exposure to cocaine occur each year.[49] By one estimate, in the US 100,000 babies are born each year after having been exposed to crack cocaine in utero.[35] An estimated 7.5 million PCE children are living in the US.[14] Pregnant women in urban parts of the US and who are of a low socioeconomic status use cocaine more often.[34] However, the real prevalence of cocaine use by pregnant women is unknown.[25][11]

Legal and ethical issues

Women have been prosecuted for using crack while pregnant.

The harm to a child from PCE has implications for public policy and law. Some US states have pressed charges against pregnant women who use drugs, including

trimester of pregnancy was sentenced to prison for eight years when her child was born with cocaine metabolites in its system.[40] The Supreme Court of South Carolina upheld this conviction.[40] As of 2013, all but one of the women prosecuted in the US for drug use while pregnant have won their cases on appeal.[50]

From 1989 to 1994, in the midst of public outcry about cocaine babies, the Medical University of South Carolina tested pregnant women for cocaine, reporting those who tested positive to the police.[51] The US Supreme Court found the policy to be unacceptable on constitutional grounds in 2001.[51] Some advocates argue that punishment for crack-using pregnant women as a means to treat their addiction is a violation of their right to privacy.[40] According to studies, fear of prosecution and having children taken away is associated with a refusal to seek prenatal care or medical treatment.[15]

Some nonprofit organizations aim to prevent PCE with

sterilization—an approach which has led to public outcry from those who consider this practice to be eugenics.[52]

Social stigma

Children who were exposed to crack prenatally faced social stigma as babies and school-aged children; some experts say that the "crack baby" stigma was more harmful than the PCE.[17] Teachers were affected by these cultural stereotypes; such biases may have negatively affected the educational experiences of children thus stigmatized.[53] Teachers who knew that specific children had been exposed to crack in utero may have expected these children to be disruptive and developmentally delayed.[42] Children who were exposed to cocaine might be teased by others who knew of the exposure, and problems these children had might be misdiagnosed by doctors or others as resulting from PCE when they may really have been due to factors like illness or abuse.[13]

The social stigma of the drug also complicated studies of PCE; researchers labored under the awareness that their findings would have political implications.[13] In addition, the perceived hopelessness of 'crack babies' may have caused researchers to ignore possibilities for early intervention that could have helped them.[7] The social stigma may turn out to be a self-fulfilling prophecy.[54]

Research

Confounding factors

A number of the effects that had been thought after early studies to be attributable to prenatal exposure to cocaine are actually due partially or wholly to other factors, such as exposure to other substances (including

marijuana) or to the environment in which the child is raised.[46]

PCE is very difficult to study because of a variety of factors that may confound the results: pre- and postnatal care may be poor; the pregnant mother and child may be

third trimester.[22] Drug use by mothers puts children at high risk for exposure to toxic or otherwise dangerous environments, and PCE does not present much risk beyond these risk factors.[6] PCE is clustered with other risk factors to the child, such as physical abuse and neglect, domestic violence, and prenatal exposure to other substances.[46] Such environmental factors are known to adversely affect children in the same areas being studied with respect to PCE.[34]
Most women who use cocaine while pregnant use other drugs too; one study found that 93% of those who use cocaine or opiates also use tobacco, marijuana, or alcohol.[10] When researchers control for use of other drugs, many of the seeming effects of cocaine on head size, birth weight, Apgar scores, and prematurity disappear.[10]

Addiction to any substance, including crack, may be a risk factor for child abuse or neglect.[42] Crack addiction, like other addictions, distracts parents from the child and leads to inattentive parenting.[18] Mothers who continue to use drugs once their babies are born have trouble forming the normal parental bonds, more often interacting with their babies with a detached, unenthusiastic, flat demeanor.[55] Conversely, low-stress environments and responsive caregiving may provide a protective effect on the child's brain, potentially compensating for negative effects of PCE.[22] Many drug users do not get prenatal care, for a variety of reasons including that they may not know they are pregnant.[40] Many crack addicts get no medical care at all and have extremely poor diets, and children who live around crack smoking are at risk of inhaling secondary smoke.[18] Cocaine using mothers also have a higher rate of sexually transmitted infections such as HIV and hepatitis.[21]

In some cases, it is not clear whether direct results of PCE lead to behavioral problems, or whether environmental factors are at fault.[6] For example, children who have caregiver instability may have more behavioral problems as a result, or it may be that behavioral problems manifested by PCE children lead to greater turnover in caregivers.[6] Other factors that make studying PCE difficult include unwillingness of mothers to tell the truth about drug history, uncertainty of dosages of street drugs[37] and high rates of attrition (loss of participants) from studies.[34]

Animal models

One way to address problems with uncertainty about cocaine's effects due to confounding factors is to use animal models; these allow experimenters to study the effects at specific doses and times.[56] Studies have used mice, other rodents, rabbits, and primates.[14] However, differences between species' physiology and

teratogenic in animals may not be in humans and vice versa.[57] Animals cannot be used to measure differences in abilities such as reasoning that are only found in humans.[57]
Animal studies in various species have found that cocaine impacts brain structure, function, and chemistry, and causes long-term changes at the molecular, cellular, and behavioral levels.[1] Animal Model Studies have shown that cocaine has the ability to cross the placenta and the blood brain barrier in the body. This is yet another example of the damage that can be done that can impact and effect the brain and body function and health overall. While the animal model is not as reliable for certain tests because we function differently, this test in particular gives us the idea of the level of damage that can be cause to the fetus of a pregnant women using cocaine during her pregnancy.[1] In research studies on pregnant rats, injected cocaine did less damage to cells than injected nicotine, and more recovery occurred between doses.[10] Adult rats that were exposed to cocaine prenatally have deficits in learning, memory, and motor skills, and may have abnormalities in dopamine processing.[55] Animal research has also shown that offspring of males that used cocaine while their sperm were forming may go on to have abnormalities later in life.[1]

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Bibliography

External links