Between fathers and fetuses - the social construction of male reproduction and the politics of fetal harm

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

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 asWlius 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 priorities of research are deWned; in editorial rooms, where reporters decide which news warrants coverage and what slant to take on stories; and in courts and legislatures, where decisions are made regarding the deWnition of and culpability for social problems

This chapter examines the cultural characterizations of sperm and male reproduction in science, news stories and public policy, all of which have

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shielded men from culpability for fetal health problems (A more detailed discussion of the rise of the concept of fetal rights and fetal protectionism can

be found in Daniels, 1993.) After a brief discussion of the social construction

of maternity and paternity, I analyse the symbols of the ‘crack baby’, ‘preg-nant addict’ and ‘absent father’ as central to public discourse on fetal harm, particularly in the US Finally, I explore the range of complex questions about biological gender diVerence generated by the politics of fetal risks, and the problematic nature of the idea of individual causality in discussions of fetal harm

Social constructions of maternity and paternity

In Western industrial cultures, notions of masculinity have been historically associated with the denial of men’s physical vulnerabilities and bodily needs, which are instead projected onto the maternal body Debates over fetal harm have been constituted by the analytically distinct and antithetical categories

of male virility and vulnerability Men were assumed either to be invulnerable

to harm from the toxicity of drugs, alcohol and environmental and occupa-tional hazards, or to be rendered completely infertile by any vulnerability to risk In particular, sperm that crossed the line from virile to vulnerable by being damaged by reproductive toxins were assumed to be incapable of fertilization And the converse operated as well – men not rendered infertile

by their toxic exposures were assumed to be immune from any other form of reproductive risk (such as genetic damage)

Social constructions of maternity, by contrast, have beenWrmly aligned 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 selecProtec-tively 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.)

‘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-tallyXawed 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 drug use on newborn infants

The limitations of the study were never reported Instead, the press picked

up and exaggerated ChasnoV’s Wndings, often reporting that 375 000 babies were born every year ‘addicted to cocaine’ (Brody, 1988: p 1; Stone, 1989:

p 3) As the distinctions between drug use and abuse collapsed, the reported numbers of crack babies exploded By 1990, news stories reported that one out of every ten children was born ‘addicted to crack cocaine’ or damaged by women’s use of drugs (Daniels, 1993) By 1993, nine inXuential national daily newspapers in the United States had run more than 197 stories on pregnancy

and cocaine addiction alone (including the New York Times, Wall Street Journal, Washington Post, Christian Science Monitor, Los Angeles Times, Chicago Tribune, Boston Globe, Atlanta Constitution /Atlanta Journal and USA Today).

The mindset created by this public discourse encouraged physicians, nurses and social workers to attribute many serious problems experienced by infants at birth to the use of drugs or alcohol by the child’s mother, particu-larly in low-income inner-city neighbourhoods

Symptoms associated with ‘crack babies’ ranged from very speciWc condi-tions that could, in fact, be tied to maternal drug use (such as drug with-drawal symptoms) to low birth weight, small head circumference, irritability, respiratory problems, gastrointestinal problems and diarrhoea – conditions that could easily be caused by poor nutrition or a host of environmental factors (For a complete discussion of the symptoms associated with fetal cocaine exposure, see Zuckerman, 1991: pp 26–35.) More highly controlled studies estimated that approximately 41 000 babies were born annually in the

US with clear symptoms of drug-related health problems (such as drug withdrawal symptoms), a far cry from the 375 000, presented by NAPARE, as exposed to drugs in the womb (Dicker and Leighton, 1990) The results of these studies were never reported by the national press, just as the press rarely reports research showing little or no association between moderate drug and

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 ofWndings 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 toWnd 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 charges against women, prosecutors continue to bring criminal charges against women they suspect of drug or alcohol use during pregnancy To date, almost all of these cases have been brought against African–American women (Paltrow, 1992) (However, it is diYcult to calculate total numbers, since so many women are charged by local prosecutors who do not report their cases to any central national source.)

What has been the response of state and federal public health agencies to women and fetal health? Public health departments have produced warning labels on wine, beer, and liquor bottles and cigarette packages, together with

an avalanche of public notices about pregnancy and alcohol consumption in restaurants and bars Such labels stigmatize women by perpetuating assump-tions that only women are vulnerable to risk and that women, therefore, are the primary source of fetal harm Men are left entirely out of the frame as social attention focuses exclusively on the maternal–fetal nexus

By implying women’s ignorance or ill intentions, public health warnings aimed at pregnant women legitimate an atmosphere that encourages public retribution against women, by focusing exclusively on individual behaviour and not on the social and political causes of low birth weight, fetal birth defects or other health problems Retribution is invited by the fact that public health warnings aimed at men (e.g for heart disease, high blood pressure, cigarette smoking and steroid use) focus on behaviours that cause harm to

self, whereas messages aimed at women focus exclusively on women’s harm

to others (the fetus).

One New Jersey public health advertisement displays an image of a preg-nant woman holding a drink and warns, ‘A pregpreg-nant woman never drinks alone’ (N.J Perinatal Cooperative, 1993) Yet a pregnant woman also never drinks in isolation from the eVects of her home, her job and her physical, social and political environment Even symptoms speciWc to drug or alcohol abuse, such as drug withdrawal symptoms or fetal alcohol syndrome, are 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

oxide If she works in a laundrette or dry cleaners, she might be exposed to solvents, cleaners or excessive heat If she works in a factory, she might be required to do heavy lifting, or she might be exposed to toxic chemicals and the dust of heavy metals If she lives in a low-income neighbourhood, she is likely to be exposed to lead from outdated plumbing or in the dust from old paint (Massachusetts Coalition for Occupational Safety and Health, 1992) But drawing fathers into the circle of causality, essential to a deconstruc-tion of the symbol of the pregnant addict, has proved more diYcult Both metaphorically and literally, fathers were absent from virtually all of the news stories on fetal health and addiction The absence of fathers in news reports of crack babies was made easier to believe by the racial subtext of the story: African–American women are often characterized as abandoned, single mothers – women dangerously unconstrained by nuclear family relations The absent father came to represent not only men’s physical distance from the out-of-wedlock child but also men’s distance from fetal harm

Virile fathers and the ‘all or nothing’ sperm theory

Embedded in scientiWc research and newspaper and magazine stories were further assumptions about male reproduction that posed serious barriers to the father/fetal connection ScientiWc literature on reproductive toxicity has traditionally dismissed the links between paternal use of drugs and alcohol (or exposure to occupational or environmental toxins) and harm to fetal health, because it was assumed that damaged sperm were incapable of

fertilizing eggs Indeed, male reproductive success was de Wned as the ability to

penetrate an egg Because penetration was the measure of normality, those sperm that succeeded were assumed to be healthy By deWning male repro-ductive health along the principles of this ‘all or nothing’ theory, most scientiWc studies until the late 1980s dismissed the possibility that defective sperm could contribute to fetal health problems The ‘all or nothing’ theory was based on certain culturally imbued assumptions about the reproductive process As Emily Martin has so well documented, scientists characterized the egg as the passive recipient and the sperm as conqueror in the process of 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 reproducreproduc-tive 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)

Scientists who did try to pursue the father–fetal connection, such as Gladys Friedler at Boston University – who was theWrst 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 theWrst studies linking environmental exposures to male reproductive harm The cultural construc-tion of male reproducconstruc-tion 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 ‘aXurry 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 there had, in fact, been a 42 per cent decline in sperm count over the past 50 years, from 113 to 66 million per millilitre of semen (Carlsen et al., 1992) While this was far from the 20 million generally assumed to be the minimum for male fertility, it raised concern lest the downward trend should continue Remarkably, in searching for a cause, scientistsWrst focused on the fashion shift from boxer shorts to jockey shorts Heat kills sperm, and because jockey shorts hold the testicles close to the body, they might decrease sperm production The researchers also suspected increased sexual activity Men who engage in frequent sex have lower sperm counts than men who wait a number of days between sexual encounters After controlling for both prom-iscuity levels and discounting the ‘jockey shorts’ thesis, the Copenhagen researchers found an association between the increase in testicular cancer in key countries and substantial sperm-count declines They speculated that the aetiology of both could be found in exposures to environmental toxins (Carlsen et al., 1992) Although still concentrating on male fertility, rather than on potential links between paternal exposure and fetal harm, the Copenhagen study did suggest that sperm might be more vulnerable to hazards than previously assumed, and that more research was needed on the potential links between toxic exposures and male reproductive health prob-lems But the links between paternal exposures and fetal health problems would not fully emerge until the assumption that damaged sperm were incapable of fertilization was thrown into question by a larger shift in the dominant paradigm of fertility and reproduction, a shift generated by the development of the ‘seductive egg’ theory

The ‘seductive egg’ theory

The ‘seductive egg’ theory originated from research on sea urchins Unlike mammalian reproduction, sea urchins engage in ‘external fertilization’ – sperm are released into the ocean, where they must locate eggsXoating free in the sea Scientists explained sperm’s ability toWnd eggs of the same species by postulating that eggs release a substance or ‘chemical signal’ that attracts sperm (Shapiro, 1997: p 293) This process of sperm ‘chemotaxis’ was then extended to research on human reproduction

In 1991, research conWrmed that sperm swam toward the Xuid surround-ing the egg when isolated in test tubes (Ralt et al., 1991) Major science magazines reported the news with titles such as ‘Does Egg Beckon Sperm

When Time Is Right?’ (Science, April 1991), ‘Eggs Urge Sperm to Swim Up and See Them’ (New Scientist, April 1991) and ‘Do Sperm Find Eggs Attract-ive?’ (Nature, May 1991) As Science News recharacterized the process of

fertilization, ‘A human egg cell does not idle languidly in the female repro-ductive tract, like some Sleeping Beauty waiting for a sperm Prince Charming

to come along and awaken it for fertilization Instead, new research indicates that most eggs actively beckon to would-be partners, releasing an as-yet-unidentiWed chemical to lure sperm cells’ (Ezzell, 1991: p 214)

Emily Martin has noted that scientists confronted with this new evidence

in the late 1980s vacillated between a model that emphasized the egg as seductress and the more mutual paradigm of sperm–egg fusion (Martin, 1991) In either case, the sperm takes on a less aggressive role in the process of fertilization The fusion model is devoid of (most of ) the human agency imparted to eggs and sperm in traditional descriptions, opting instead for a characterization that relies on a simple chemical process

Changing characterizations of the process of fertilization thus created a new context (valid or not) for research supporting the link between paternal exposures and fetal harm Yet a mutual picture of procreation did not necessarily lessen women’s culpability for fetal harm In the ‘aggressive egg’ model, women were once again at fault for seducing if not ‘bad men’, then at least ‘bad sperm.’ While potentially drawing men into the circle of causality with women, cultural constructions embedded in scientiWc magazines and newspaper stories continued to lay the blame at women’s door Yet by 1991, growing evidence had clearly implicated men in fetal health problems

The evidence of male-mediated developmental toxicology

Male reproductive exposures are now strongly suspected of causing not only infertility but also miscarriage, low birth weight, congenital abnormalities, cancer, neurological illness and other childhood health problems (Davis et al., 1992: p 289) Studies of male reproductive health and toxicity have

concentrated primarily on the eVects of occupational and environmental exposures of men and less on the eVects of what scientists refer to as men’s

‘lifestyle factors’, such as drinking, smoking, or drug use (Davis et al., 1992; Colie, 1993; Friedler, 1993; Olshan and Faustman, 1993)

Because adult males continuously produce sperm throughout their lives, the germ cells from which sperm originate are continuously dividing and developing Sperm take approximately 72 days to develop to maturity, and then move for another 12 days through the duct called the epididymis, where they acquire the ability to fertilize an egg During this developmental process, sperm may be particularly susceptible to damage from toxins because cells that are dividing are more vulnerable to toxicity than cells that are fully developed and at rest, as are eggs in the female reproductive system Abnor-mal sperm may still be capable of fertilizing an egg because speed may be more important than size or shape, as was suggested in the earliest article on this subject (Moore, 1989)

Some of the earliest epidemiological research studied the eVects of radi-ation exposures on the children born to men who survived the atomic bombs

at Nagasaki and Hiroshima However, few associations were found between paternal exposures and childhood health problems, possibly due to the fact that so few men conceived children in the six months after the bombing, when the exposure eVects of radiation were at their strongest (Yoshimoto, 1990; Olshan and Faustman, 1993) A number of events triggered studies of male reproduction during the 1970s and 1980s Vietnam veterans concerned about the eVects of the herbicide Agent Orange called for studies on links between male exposures during the war and childhood diseases of their

oVspring A 1980 study of more than 500 men indicated that men who showed signs of toxic exposure to dioxin (TCDD) in Agent Orange had twice the incidence of children with congenital anomalies than men without symptoms (Stellman and Stellman, 1980: p 444) Other studies also showed increased rates of spinal malformation, spina biWda, congenital heart defects and facial clefting in the children of Vietnam veterans Later studies, however, failed to conWrm these Wndings Controversy persists over the paternal–fetal

eVects of the herbicide, no doubt fuelled in part by the legitimacy and liability implications of positive associations for the US government (Colie, 1993:

p 6)

In 1977, men working at an Occidental Chemical plant in Lathrop, Califor-nia noticed a pattern of sterility among their co-workers In the 1950s, the company had actually funded research on the carcinogenicity and reproduc-tive eVects of the pesticide produced there, DBCP (dibromochloropropane), but had quietly shelved the research afterWndings demonstrated associations between DBCP exposures and reproductive eVects in laboratory animals (Robinson, 1991: pp xiii–xv) Later studies conWrmed that the men’s sterility was linked to their DBCP exposure, and the chemical was banned from

further use in the US By 1980, researchers had documented not only sterility but also increases in spontaneous abortion resulting from paternal exposure

to DBCP (Kharrazi, Patashnik, and Goldsmith, 1980) Seventeen studies have now evaluated the impact of pesticides and herbicides on male reproduction and paternal–fetal health (Olshan and Faustman, 1993: p 195)

Other studies have analysed the eVects of occupational exposures on paternal–fetal health, with many Wnding signiWcant associations between paternal exposures and fetal health problems Toluene, xylene, benzene, TCE, vinyl chloride, lead, and mercury have all been associated with spontaneous abortion Paints, solvents, metals, dyes and hydrocarbons have been asso-ciated with childhood leukaemia and childhood brain tumours (summarized

in Olshan and Faustman, 1993: p 196) In analyses by occupation, janitors, mechanics, farm workers and metal workers have been reported to have an excess number of children with Down’s syndrome (Olshan and Faustman, 1993: p 196) One study of 727 children born with anencephaly found correlations for paternal employment as painters (Colie, 1993: p 7) Painters and workers exposed to hydrocarbons have also been shown to have higher rates of children with childhood leukaemia and brain tumours (Savitz and Chen, 1990) More than 30 studies have examined the relationship between paternal occupation and childhood cancer (Olshan and Faustman 1993:

p 197)

There are problems with many of these studies, although the diYculties apply to both men and women It is diYcult, for instance, to specify the nature of exposures to toxic substances at work It is also diYcult to get a sample size large enough to provide conclusive results, especially for condi-tions that are typically rare in children And, as in all epidemiological studies,

it is diYcult to control for confounding factors, such as the eVects of multiple chemical exposures and alcohol or drug use However, whilst the problem of confounding variables is common to all epidemiological studies of reproduc-tive toxicity, for cultural reasons scientists are more acutely aware of method-ological caveats when studying men For instance, studies of paternal eVects are routinely criticized for not controlling for maternal exposures, while studies on women virtually never control for the exposures of fathers Studies

on men’s occupational and environmental exposures rarely control for men’s use of drugs or alcohol Studies that do focus on the eVects of lifestyle factors

on men’s reproduction are criticized for not controlling for men’s workplace exposures, while studies of women and drug use do not control for women’s occupational exposures

The biological processes of male-mediated teratogenicity have also been examined through clinical studies on animals and studies of the eVect of toxic exposures directly on sperm All of the problems of confounding variables associated with epidemiological research can be avoided by conducting animal studies The earliest studies of the eVects of illicit drugs, for instance,