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Prenatal cocaine exposure

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Jan 9, 2022

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]

Medical syndrome
Further information: Neonatal withdrawal

“Crack baby” was a term coined to describe children who were exposed to crack (freebase cocaine in smokable form) as fetuses; the concept of the crack baby emerged in the US during the 1980s and 1990s in the midst of a crack epidemic.[2] Other terms are “cocaine baby” and “crack kid”. 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.[2] Fears were widespread that a generation of crack babies 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.[2]

No specific disorders or conditions have been found to result for people whose mothers used cocaine while pregnant.[3] 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.[4] PCE also appears to have little effect on infant growth.[5] 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.[6] No scientific evidence has shown a difference in harm to a fetus between crack and powder cocaine.[7]

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.[4] Thus, studies have failed to clearly show that PCE has negative cognitive effects, partly because such effects may be due to concurrent factors.[8] 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.[9] Thus, researchers have had difficulty in determining which effects result from PCE and which result from other factors in the children’s histories.

. . . Prenatal cocaine exposure . . .

The US government published posters like this one in the 1980s and ’90s to warn people away from crack.

During 1980s and 1990s, a surge occurred in use of crack cocaine in US cities:[10] 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.[11][12] Early studies in the mid-1980s reported that cocaine use in pregnancy caused children to have severe problems, including cognitive, developmental, and emotional disruption.[13] These early studies had methodological problems, including small sample size, confounding factors such as poor nutrition, and use of other drugs by the mothers.[13] The results of the studies, though, sparked widespread media discussion in the context of the new War on Drugs.[14][1] For example, a 1985 study that showed harmful effects of cocaine use during pregnancy created a huge media buzz.[13][15] The term “crack baby” resulted from the publicity surrounding crack and PCE.[16]

Media reports commonly emphasized that babies who had been exposed to crack in utero would never develop normally.[12][16] 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.[17] They were expected to be unable to form normal social bonds.[12] Experts foresaw the development of a “biological underclass” of born criminals who would prey on the rest of the population.[15][17][18] Crime rates were predicted to rise when the generation of crack-exposed infants grew up (instead, they dropped).[17] The children were predicted to be difficult to console, irritable, and hyperactive, putting a strain on the school system.[5]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.”[15][17] 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.”[17][18] 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.[18]

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.[19] Scientific studies that report that PCE has significant effects may be more likely to be published than those that do not.[20] 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.[21] 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.[22] Ideas about severe effects of PCE may have been more readily embraced because they “fit in with cultural stereotypes”.[22]

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.[2] 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.[19]

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.[17] 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.[23] 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.[17] The effects of PCE are subtle but they exist.[19][24][25] Most people who were exposed to cocaine in utero are normal or close to it.[12]

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