On Sat, 11 Nov 2000, Cheryl A. Rickabaugh wrote:
> Tips Folks:
>
> I'm working on a text project and a reviewer has suggested including crack
> babies in the discussion of teratogens and prenatal development. If I recall
> correctly this topic was discussed on this list fairly recently with much of
> the thread devoted to (I believe) myths about crack babies.
>
> I do _not_ want to re-energize this discussion, but have been unable to
> access the archives though I've been trying for close to a week and my
> PsychInfo search has been disappointing. I would be very grateful if anyone
> w/authoritative knowledge and/or references could contact me back channel.
> I'm facing a deadline of only a matter of a few days.
It's no fun if I have to do it privately. So here's a public
response. First, some of the articles I have from our previous
discussion. Next, two new ones that look interesting from a quick
PubMed search. I find the comparison between smoking (acceptable)
and cocaine (not) of particular ironic interest, as it is for the
societal effects of alcohol (legal) compared with pot (not). Is
there such a thing as cultural or societal hypocrisy?
A major part of Neurotoxicology and Teratology, 15, 1993 is on
the myth of crack babies.
Coles, C. (1993). Saying "goodbye" to the "crack baby".
Neurotoxicology and Teratology, 15, 290-292
Woods, N. et al (1998). Pygmalion in the cradle: observer bias
against cocaine-exposed infants. Developmental and behavioral
pediatrics, 19, 283--
Frank, D. et al (1993). Children exposed to cocaine prenatally:
pieces of the puzzle, N&T, 298-300
Hutchings, D. (1993) The puzzle of cocaine's e ffects following
maternal use during pregnancy. N&T, 281-286
Chasnoff, I. (1993). Missing pieces of the puzzle, N&T, 287-288
Also
Lyons, P. (1998). The construction of the crack babies phenomenon
as a social problem. American Journal of Orthopsychiatry, 68,
313--
--1994. smoking cigarettes may do developing fetus more harm than
ingesting cocaine, some experts say. Journal of the American
Medical Assoc , 271, 576--
Azar, B. (1997). Researchers debunk the myth of the "crack baby"
APA Monitor, Dec 28 [should be available on-line]
>From PubMed
Health Care Women Int 1997 Jan-Feb;18(1):31-41
Biological markers and social differentiation: crack babies and
the construction of the dangerous mother.
Litt J, McNeil M
Department of Sociology, Iowa State University, Ames 50011, USA.
[EMAIL PROTECTED]
Crack mothers-particularly African American and Latina women-have
been constructed as maternal villains who actively and
permanently damage their offspring. Many women have been arrested
or lost parental rights to their children because of child
neglect charges. Despite this panic, recent medical and legal
research indicates that reports of damage to the fetus have been
greatly exaggerated. This article examines the ongoing questions
in medical publications about crack babies. The authors connect
the search for biological markers of cocaine use during pregnancy
to a new cultural conception of a bio-underclass. The conclusion
considers medical developments and controversies in the broader
context of class and racial divisions and reproductive politics
in the United States.
: J Pharmacol Exp Ther 1998 Jun;285(3):931-45
Fetal nicotine or cocaine exposure: which one is worse?
Slotkin TA
Department of Pharmacology and Cancer Biology, Duke University
Medical Center, Durham, North Carolina, USA.
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.
-Stephen
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Stephen Black, Ph.D. tel: (819) 822-9600 ext 2470
Department of Psychology fax: (819) 822-9661
Bishop's University e-mail: [EMAIL PROTECTED]
Lennoxville, QC
J1M 1Z7
Canada Department web page at http://www.ubishops.ca/ccc/div/soc/psy
Check out TIPS listserv for teachers of psychology at:
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