7
Between fathers and fetuses: the social
construction of male reproduction and the
politics of fetal harm
Cynthia R. Daniels
Political Science Department, Rutger University, New Brunswick, USA
In contemporary American political discourse ‘crack babies’ have been
treated as Wlius nullius – as if they had no biological fathers. With no link
between fathers and fetuses, no inheritance of harm could be attributed to the
father’s use of drugs. The absence of fathers in debates over drug addiction
and fetal harm has had profound consequences for women, for it has dictated
that women alone bear the burden and blame for the production of ‘crack
babies’.
Since at least the late 1980s, and in some cases far earlier, studies have
shown a clear link between paternal exposures to drugs, alcohol, smoking,
environmental and occupational toxins, and fetal health problems. Yet men
have been spared the retribution aimed at women. In fact, while women are
targeted as the primary source of fetal health problems, reports of male
reproductive harm often place sperm at the centre of discourse as the ‘littlest
ones’ victimized by reproductive toxins, somehow without involving their
male makers as responsible agents.
ScientiWc research linking reproductive toxins to fetal health problems
reXects deeply embedded assumptions about men and women’s relation to
reproductive biology. Critical analysis of the nature of fetal risks thus requires
not only examination of the biology of risk, but also assessment of what
Evelyn Fox Keller has called the ‘collective consciousness’ that fundamentally
shapes scientiWc inquiry on gender diVerence – a consciousness that is
constituted by ‘a set of beliefs given existence by language rather than by
bodies’ (Keller, 1992: p. 25).
In debates over fetal harm, the production of this collective consciousness
takes place in many social locations: in science laboratories, where the

with assumptions of women’s vulnerability. The science of reproductive risks
historically developed in response to women’s occupational exposures, where
it was assumed that the physical stress and toxic exposures of the workplace
would result in the degeneration of women’s reproductive systems. Protec-
tive labour law selectively exaggerated the vulnerabilities of white women to
occupational hazards and virtually ignored risks to working women of colour
(Baer, 1978; Kessler-Harris, 1982; Lehrer, 1987; Daniels, 1991, 1993). Until
well into the twentieth century, science, policy and law deeply reXected the
association of maternity with vulnerability.
The cultural associations of paternity with virility and maternity with
vulnerability formed the context within which the symbols of the ‘crack
baby’, ‘pregnant addict’ and ‘absent father’ emerged at the center of debate
over fetal hazards. (A more detailed analysis of the social and political
construction of these concepts can be found in my longer treatment of this
issue in Daniels, 1993, where I analyse the science, media, policy and law
discourses surrounding the emergence of the ideas of fetal protectionism and
fetal rights.)
114 C.R. Daniels
‘Crack babies’ and ‘pregnant addicts’
By now, the images of the crack baby and addicted mother are familiar to
anyone who has read news reports of pregnancy and addiction. In the US,
media attention began to focus in 1988 on babies aVected by maternal drug
use, with the release of a study by Dr. Ira ChasnoV, director of the National
Association for Perinatal Addiction Research and Education (NAPARE),
which reported that 375 000 babies were born every year ‘exposed to illicit
drugs in the womb’ (ChasnoV, 1989: pp. 208–10). The study was fundamen-
tally Xawed in a number of ways. ChasnoV’s sample was biased by the fact
that 34 of the 36 hospitals surveyed were public inner-city hospitals. The
study made no distinction between a single use of illegal drugs and chronic
drug addiction during pregnancy; nor did it document the actual eVects of

115Between fathers and fetuses
alcohol use and fetal health problems (Koren and Klein, 1991). There are two
stages to the ‘screening’ process by which research makes it into the press.
First, science journals review, accept or reject reports of Wndings. Koren at el.
(1989) found that professional scientiWc journals were predisposed against
reporting negative or ‘null’ associations between drug use and fetal risks.
Once scientiWc reports did begin to appear in journals, Koren and Klein
(1991) found a similar predisposition in the press against reporting negative
Wndings.
The sense of social distress created by images of addicted babies wired to
tubes in hospital incubators fed a profound need to blame. Public concern
over crack babies contains all of the characteristics of a response to plague –
fuelling the impulse of privileged populations to locate, target and contain
one group as the primary source of contamination and risk (Mack, 1991). As
Linda Singer has observed in relation to the spread of AIDS, the epidemic
‘provides an occasion and rationale for multiplying points of intervention
into the lives and bodies of populations’ (Singer, 1993: p. 117). The policy
response to the plague narrative was to Wnd a target population to blame, and
poor inner-city women were the most obvious targets. Newspaper stories
contributed to this impulse by presenting images of African–American
women as virtual monsters, snorting cocaine on the way to the delivery room
and abandoning horribly damaged babies in hospitals. In some instances,
drug use was characterized as a form of child abuse in utero, where cocaine
‘literally batters the developing child’ (see Brody, 1988: p. 1; Stone, 1989:
p. 3).
Criminal prosecutors responded to the sense of crisis by targeting pregnant
women for prosecution. By 1993, between 200 and 400 women had been
charged with fetal drug delivery, fetal abuse or manslaughter (in cases where
the pregnancy had ended in a stillbirth). Despite the fact that nearly every
case challenged in the courts has resulted in the dismissal or acquittal of

complicated by simple factors such as poor nutrition. For instance, one study
of pregnancy and alcohol use (controlling for age, smoking, drug abuse,
reproductive history, medical problems, socio-economic status and race)
found that women who consumed at least three drinks a day but ate balanced
diets experienced a rate of fetal alcohol syndrome (FAS) of only 4.5 per cent,
while women who drank the same amount and were malnourished had an
FAS rate of 71 per cent (Bingol et al., 1987). The study showed that poor
nutrition is tied directly to income – FAS is a measure not only of maternal
alcoholism but also of economic class. There has been no press coverage of
this study.
Public campaigns to ‘stem the tide of crack babies’ are clearly racialized,
primarily targeting women of colour in low-income communities. ScientiWc
research has supported the racialized nature of debate by focusing research
heavily on drugs used most commonly in poor inner cities (such as crack)
and not on substances most often abused by higher-income women (such as
prescription drugs). Public health warnings typically silhouette African–
American or Latina women; they are often produced in Spanish and directed
at inner-city neighbourhoods.
Counteracting the symbol of the pregnant addict requires breaking the
exclusive connection between pregnant women and ‘crack babies’. The circle
of causality has widened since feminist advocates started inXuencing media
coverage of the issue, and since news stories began suggesting the relation on
fetal health of the combined eVects of poverty, addiction and exposures to
workplace and environmental toxins. The precise causes of fetal health
problems are immensely complicated. A woman living in the inner city is
likely to have had little health care before she became pregnant, and also poor
antenatal care. If she is employed in a hospital, she might be exposed to
radiation, chemotherapeutic drugs, viruses or sterilizants such as ethylene
117Between fathers and fetuses
oxide. If she works in a laundrette or dry cleaners, she might be exposed to

fertilization (Martin, 1991).
The assumption that men harmed by toxic exposures would be rendered
infertile deXected research away from the connections between fathers and
fetal harm. As a result of the ‘virile sperm’ theory of conception, scientiWc
studies, until the late 1980s, focused almost exclusively on infertility as the
primary outcome of hazardous exposures and the main source of reproduc-
tive problems for men. Male reproductive health was deWned by ‘total sperm
ejaculate’, and healthy reproductive function was measured by ‘ejaculatory
performance’ – measures of volume, sperm concentration and number,
sperm velocity and motility, sperm swimming characteristics, and sperm
morphology, shape and size (Burger et al., 1989).
118 C.R. Daniels
Scientists who did try to pursue the father–fetal connection, such as Gladys
Friedler at Boston University – who was the Wrst to document a link in mice
between paternal exposure to morphine and birth defects in their oVspring in
the 1970s – had diYculty funding their research or publishing their work.
The signiWcance of Friedler’s work is that she found mutagenic eVects from
paternal exposures not only in the progeny of male mice exposed to mor-
phine and alcohol, but also in the second generation or ‘grandchildren’ of
exposed mice. In all cases, she controlled for maternal exposures so that
causality could be more clearly linked to paternal exposures (Friedler and
Wheeling, 1979; Friedler, 1985, Friedler, 1987–8).
A number of social and political events generated the Wrst studies linking
environmental exposures to male reproductive harm. The cultural construc-
tion of male reproduction was particularly evident in these early studies.
In 1979, scientiWc concern was raised by a study in Florida that docu-
mented a 40 per cent overall drop in sperm count for men over the past 50
years. Scientists responded with ‘a Xurry of sperm-count studies’ about ‘the
big drop’ (Castleman, 1993). By 1990, researchers at the University of
Copenhagen had examined 61 sperm-count studies and determined that