Fetal Nicotine or Cocaine Exposure: Which One is Worse?
Abstract
Despite extensive adverse publicity, tobacco use continues in approximately 25% of all pregnancies in the United States, overshadowing illicit drugs of abuse, including cocaine. The societal cost of maternal smoking is seen most readily in underweight newborns, in high rates of perinatal morbidity, mortality and Sudden Infant Death Syndrome and in persistent deficits in learning and behavior. We have designed animal models of nicotine exposure to prove that nicotine itself is a neuroteratogen, thus providing a causative link between tobacco exposure and adverse perinatal outcomes. In particular, nicotine infusion paradigms that, like the transdermal patch used in man, produce drug exposure without the confounds of other components of tobacco or of episodic hypoxic-ischemic insult, have enabled a mechanistic dissection of the role played by nicotine in fetal brain damage. Nicotine targets specific neurotransmitter receptors in the fetal brain, eliciting abnormalities of cell proliferation and differentiation, leading to shortfalls in the number of cells and eventually to altered synaptic activity. Because of the close regulatory association of cholinergic and catecholaminergic systems, adverse effects of nicotine involve multiple transmitter pathways and influence not only the immediate developmental events in fetal brain, but also the eventual programming of synaptic competence. Accordingly, defects may appear after a prolonged period of apparent normality, leading to cognitive and learning defects that appear in childhood or adolescence. Comparable alterations occur in peripheral autonomic pathways, leading to increased susceptibility to hypoxia-induced brain damage, perinatal mortality and Sudden Infant Death. Identifying the receptor-driven mechanisms that underlie the neurobehavioral damage caused by fetal nicotine exposure provides a rational basis for decisions about nicotine substitution therapy for smoking cessation in pregnancy. In contrast to the effects of nicotine, animal models of crack cocaine use in pregnancy indicate a more restricted spectrum of effects, a reflection of differences both in pharmacokinetics and pharmacodynamics of the two drugs. Notably, although cocaine, like nicotine, also targets cell replication, its effects are short-lived, permitting recovery to occur in between doses, so that the eventual consequences are much less severe. To some extent, the effects of cocaine on brain development resemble those of nicotine because the two share cardiovascular actions (vasoconstriction) that, under some circumstances, elicit fetal hypoxia-ischemia. In light of the fact that nearly all crack cocaine users smoke cigarettes, the identification of specific developmental effects of cocaine may prove difficult to detect. Although scientists and the public continue to pay far more attention to fetal cocaine effects than to those of nicotine or tobacco use, a change of focus to concentrate on tobacco could have a disproportionately larger impact on human health.
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Neuronal damage and cell loss involving apoptosis genes intensify after birth even after nicotine exposure stops.
“Neuronal damage and cell loss involving the activation of genes associated with apoptosis intensify in the postnatal period despite the discontinuation of nicotine exposure.”
From Developmental toxicity of nicotine: A transdisciplinary synthesis and implications for emerging tobacco products (2017) · cites this paper as [59]
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- Authors
- Slotkin, T. A.
- Affiliations
- Duke Medical Center (US)
- Corresponding author
- Slotkin, Theodore A.
- ORCID
- Slotkin, Theodore A.
- Venue
- The Journal of Pharmacology and Experimental Therapeutics
- Publisher
- Elsevier BV
- Published
- 1998-06
- Volume
- 285
- Issue
- 3
- Pages
- 931-945
- ISSN
- 0022-3565 (ISSN-L)
- OpenAlex
- W2136699448
- Cited by
- 676
- References
- 8
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 1 · 2023: 8 · 2022: 11 · 2021: 12 · 2020: 8 · 2019: 10 · 2018: 19 · 2017: 16 · 2016: 24 · 2015: 27 · 2014: 25 · 2013: 23 · 2012: 31
- FWCI
- 27.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Pharmacology and Experimental Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- PubMed
- Funders
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD 09713, R01HD009713)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Keywords
- prenatal nicotine exposure, maternal smoking, fetal brain development, cholinergic receptors, catecholaminergic system, synaptic development, perinatal mortality, sudden infant death syndrome, hypoxia-ischemia, smoking cessation during pregnancy, nicotine patch, cell proliferation and differentiation
- MeSH terms
- Cocaine, Female, Embryonic and Fetal Development, Fetus, Ganglionic Stimulants, Humans, Infant Mortality, Infant, Newborn, Infant, Newborn, Diseases, Nicotine, Pregnancy, Prenatal Exposure Delayed Effects, Receptors, Nicotinic, Risk Factors, Smoking, Sudden Infant Death, Neurotransmitter Agents, Dopamine Uptake Inhibitors, Substance-Related Disorders
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