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Human Reproduction Vol.21, No.9 pp. 2201–2208, 2006 doi:10.1093/humrep/del181
Advance Access publication June 14, 2006.
© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved.
2201
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Mini Review—Developments in Reproductive Medicine
Health issues and the environment—an emerging paradigm for providers
of obstetrical and gynaecological health care
Stephen J.Genuis
Department of Obstetrics and Gynecology, University of Alberta, Edmonton, Alberta, Canada
E-mail: sgenuis@ualberta.ca
Although ongoing study is required to winnow environmental ideology from scientific fact, existing evidence from
recent research demonstrates a definitive link between chemical toxicants and potential health sequelae, including
congenital affliction and gynaecological disorders. Amid media clamour of health risk and biological peril associated
with various environmental toxicants, a spectrum of responses has emerged: some have embraced the environmental
cause, some have summarily dismissed it as piffle and perhaps the majority has remained disinterested. Although
journals devoted to toxicological and environmental health concerns have become prominent in academia with volu-
minous numbers of scientific reports being published, there has been limited exploration of the relationship between
contemporary chemical exposure and reproductive medical issues in mainstream obstetrics and gynaecology litera-
ture. Providers of obstetrical and gynaecological health care need to acquire knowledge of taking an exposure his-
tory, instruction in details of precautionary avoidance, skills to provide preconception care and necessary tools to
investigate and manage patients with toxicant exposure.
Key words: congenital anomalies/endocrine disrupting chemicals/environmental health/human exposure assessment/toxicology
What you don’t know has power over you;
knowing it brings it under your control, and
makes it subject to your choice. Ignorance
makes real choice impossible.
Abraham Maslow
There are many opinions, beliefs and urban legends about the
risks of various environmental exposures and insufficient
research to conclusively establish fact from fancy on many
related issues. Although advocates have staged demonstrations
and press conferences to draw attention to the plight of the
environment, some writers and commentators, at times radiat-
ing a smug sense of cerebral superiority, have allegedly
debunked fanatical activists who rant about environmental pol-
lutants. Credible scientific study is emerging, however, which
raises disquieting evidence about the potential for environmen-
tal toxicants to profoundly affect the health and well-being of
individuals at all stages of life—from the microscopic embryo
within the amniotic sac to the toddler on the playground; from
the child in a classroom to the robust adolescent and from the
young adult in the workplace to the senior in a nursing home.
In this article, recent research exploring the impact of adverse
exposure on reproductive health will be surveyed, and recom-
mendations for integration into obstetrical and gynaecological
care will be discussed.
A historical perspective on chemical exposure
Medical professionals have long been aware of the importance
of various chemicals in the day-to-day functioning of the human
organism. The study of human biochemistry, a requirement for
medical students, involves the exploration of myriad biochemi-
cal reactions that constitute the basis for the functioning of the
human species. With the objective of ameliorating human suffer-
ing, medical pharmacology includes the study of how therapeu-
tic agents interact and modify human biochemistry in
dysfunctional states. Toxicology, on the contrary, involves the
pursuit of understanding how, where and which chemical agents
adversely affect inherent biochemistry and endeavours to corre-
late exposure to specific toxicants with consequent morbidity
and mortality. The recognition that numerous toxicants with a
wide variety of chemical structures have the potential to
adversely affect biochemical functioning is well documented.
The revered Hippocratic Oath, crafted as a template for ethi-
cal practice in medicine, was conceived in an era when toxic
chemical tonics of bribed medical practitioners were frequently
used to poison unsuspecting political or business rivals.
Hippocrates admonished practitioners to avoid using their
practical skills of chemical intervention to inflict injury or
harm. Centuries later, the familiar phrase ‘mad as a hatter’
arose from the observation of individuals occupationally
exposed to mercury, a well-recognized heavy metal toxicant
(Fraser-Moodie, 2003). In the production of felt hats, once
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popular in North America and Europe, a mercury compound
was applied to the animal fur—as well as direct ingestion by
licking the brushes, the fumes of this compound were conse-
quently inhaled by hatters working in poorly ventilated work-
shops. These labourers often developed a sequence of
symptoms including trembling (known as ‘Hatter’s Shakes’),
slurred speech, loss of co-ordination, irritability, anxiety,
depression and various personality changes which cumula-
tively became known as the ‘Mad Hatter Syndrome’.
Examples of the impact of various toxic agents are also evi-
dent in literature relating to gestational exposures. In
Minamata, a small factory town ∼570 miles southwest of
Tokyo, a petrochemical and plastics manufacturing company
dumped an estimated 27 tons of mercury compounds into the
Minamata Bay between 1932 and 1968. Thousands of people
whose diet included fish from the bay developed symptoms of
mercury poisoning, and numerous neonates succumbed from
diffuse central nervous system (CNS) damage following in
utero mercury exposure (Satoh, 2003).
The problem of limb defects in offspring of some mothers
receiving thalidomide to manage hyperemesis is another well-
known example of potential damage resulting from gestational
toxicant exposure (McBride, 2004). Furthermore, the diethyl-
stilboestrol (DES) tragedy highlighted the potential for delayed
sequelae with toxicant exposure. After the administration of
this estrogenic agent in pregnancy to diminish miscarriage risk,
exposed offspring realized increased rates of reproductive dys-
function, certain cancers as well as (according to some
research) long-term psychiatric and psychosexual changes
(Ehrhardt et al., 1985; Saunders, 1988; Meyer-Bahlburg et al.,
1995; Swan, 2000; Palmer et al., 2002)—effects not readily
apparent at birth.
Contemporary regulations regarding pharmaceuticals and
safety precautions for selected chemical agents have resulted,
in part, as a response to disastrous outcomes resulting from
adverse exposures. The current safety recommendations
regarding the instillation of carbon monoxide detectors
(Runyan et al., 2005), the removal of lead from paint and
gasoline (American Academy of Pediatrics, 1987), the restric-
tion of polychlorinated biphenyl (PCB) use in industry
(Carpenter, 1998), the discontinuation of asbestos insulation in
construction (Robinson et al., 2005) and numerous other exam-
ples attest to the recent recognition of toxicant hazards. Yet,
many health professionals in clinical practice, including spe-
cialists in reproductive medicine, have not fully considered the
potential impact of contemporary chemical exposure on the
health and well-being of their patients (Kilpatrick et al., 2002;
Marshall et al., 2002).
Over the last half-century, more than 75 000 new synthetic
chemicals have been introduced, some of which are in wide-
spread daily use (Berkson, 2000). Unlike pharmaceutical regu-
lation, an ‘innocent until proven guilty’ approach remains in
effect for novel chemical agents used for non-medicinal pur-
poses—whereby proof of safety is generally not required
before the widespread dissemination of these agents. As a res-
ult, individuals are routinely exposed to various chemical com-
pounds through inhalation, ingestion, dermal application,
surgical and dental implants and vertical transmission. Consid-
ering historical precedent, it is not a quantum leap to con-
sider that among the vast assortment of synthetic chemicals,
some and perhaps many of these compounds may pose a
health risk. In fact, emerging research correlates exposure to
several chemicals with adverse health outcomes. As some
environmental health research has direct application to
obstetrical and gynaecological health care, a brief introduc-
tion to environmental medicine will be followed by an
exploration of toxicant research specifically related to repro-
ductive health.
Overview of human exposure medicine
Health care related to adverse exposure, sometimes referred to
as environmental medicine, seeks to understand health prob-
lems that arise as a result of the interaction between people and
adverse determinants in their environment. According to recent
analyses, potential sources of toxicant exposure are ubiquitous:
various foods contain toxic substances including contaminated
breast milk (Schecter et al., 2003), some baby food (Schecter
et al., 2002) and routine foodstuffs (Robbins, 2001; Genuis,
2005); adverse chemical agents may be inhaled in many
homes, schools and workplaces (Kilburn, 1998, 2004) and
various personal care products and industrial solutions provide
dermal exposure to chemical toxicants (Harte
et al., 1991;
Rapp, 2004).
Although small exposures may seem insignificant and harm-
less, some chemical agents bioaccumulate within the human
body and have the potential to eventually reach levels where
clinical illness may ensue. Cumulative exposure from various
sources has resulted in the Centers for Disease Control (CDC),
finding that the average American child and adult have accu-
mulated numerous toxicants in their bodies (Centers for Dis-
ease Control, 2005). At levels measuring in parts per trillion
and parts per billion, inherent hormones such as insulin and
estradiol (E
2
) are bioactive on cells and tissues; exposure to
some toxic chemicals also appears to have bioactive impact at
seemingly minuscule levels (Welshons et al., 2003).
Toxicants remaining within maternal circulation have the
potential to affect metabolic activity and also account for the
vertical transmission of numerous synthetic chemicals often
found in contemporary neonates (Environmental Working
Group, 2005). Although individual toxicants have distinct
properties, many eventually deposit and become stored within
various tissues including bone and fat. Through hormonal
mechanisms such as leptin release, fat cells have significant
impact on human metabolism, but it remains to be established
how stockpiled toxicants affect the physiology of adipose tis-
sue. There is evidence, however, that some toxicants induce
insulin resistance (Alonso-Magdalena et al., 2006) and thus
may play a significant role in the pathogenesis of myriad
chronic afflictions (Cordain et al., 2003). Research continues
to uncover various pathophysiological mechanisms whereby
chemical agents effect injury.
Mechanisms of toxicity
Chemical compounds can adversely affect cells and tissues
through several differing mechanisms. In addition to causing
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2203
direct cellular damage to cell membranes or various intracellu-
lar components, xenobiotics (foreign chemicals) can also alter
communication between cells and thus disrupt cellular and tis-
sue regulation. There is much attention to a pathophysiological
mechanism entitled endocrine disruption or hormone deception
whereby various agents, referred to as endocrine disrupting
chemicals (EDCs) or hormone disruptors, act by direct or indi-
rect action to mimic, stimulate, antagonize, alter or displace the
action of natural hormones (Colborn et al., 1993; Brevini et al.,
2005). As a result, EDCs may disrupt routine physiological
messages from cells and tissues by interference with produc-
tion, release, metabolism, binding, action or the elimination of
inherent hormones (National Research Council, 1999). Dys-
regulation of myriad inherent physiological processes such as
fetal development, routine homeostasis and intellectual func-
tioning may ensue.
EDCs from various sources—from plastics in teething toys
to household cleaners, from industrial by-products to pesticides
in food and from personal cosmetics to occupational sol-
vents—can infiltrate the endocrine system of unsuspecting
individuals and alter hormonal production and physiology. As
‘a wide range of hormone-dependent organs (pituitary gland,
hypothalamus, reproductive tract) are targets of EDCs disrupt-
ing effect’ (Brevini et al., 2005), the mechanics of intricate and
finely tuned inherent signals may be disturbed, potentially
causing developmental changes or health problems, the extent
of which is currently under investigation. Although toxicants
potentially cause damage in various ways, hormone disruption
is a common mechanism by which adverse agents alter the
development and functioning of the human organism.
Establishing adverse exposure as causality of disease
Vociferous claims that insufficient proof exists to establish a
link between common chemical exposure and harm as well as
protestations by some industry that the benefits and expediency
of chemical use outweigh the risks have contributed to confu-
sion regarding chemical toxicity. With the gold standard of
randomized controlled trials (RCTs) in mind, some health per-
sonnel allege lack of proper evidence and remain reluctant to
accept that widespread chemical exposure may be the aetiolog-
ical source of much contemporary affliction. When studying
environmental toxicants, there are, most assuredly, distinct
challenges in conclusively demonstrating direct causative links
with adverse health outcomes.
RCTs are precluded in toxicology assessment because it is
unethical to deliberately expose individuals to potentially toxic
chemicals. The allegation that clinical trials are the only objec-
tive and credible means in medicine to establish efficacy of an
intervention or causality of disease is, however, a myth. Just as
it would be farsical to require RCT confirmation to establish
the efficacy of parachutes ‘to prevent death and major trauma
related to gravitational challenge’ (Smith and Pell, 2003), RCT
evidence is not required to reasonably correlate adverse expo-
sure with adverse outcomes; other research methodologies can
be effective instruments to establish causality of disease. There
are, however, other challenges in conclusively demonstrating
causative links.
Individuals have differing genetic vulnerabilities and may
exhibit differing manifestations to the same exposure—thus
making it difficult to link the outcome with a specific expo-
sure. With variability in effect combined with potentially long
lags between exposure and outcome, index of suspicion may
be low and correlation hard to conclusively prove. A major
breakthrough with the understanding of toxicants and lag
times, however, became evident following the DES tragedy:
agents can have long-term sequelae without immediate detri-
mental impact or obvious side effects. Furthermore, individu-
als often have multiple exposures with the bioaccumulation of
varying chemicals in the body (Centers for Disease Control,
2005)—rendering it difficult to link a single specific outcome
with a single specific exposure (Hauser et al., 2005).
With several confounding variables and logistical challenges
clouding the outcome of toxicant research, some clinicians
have remained sceptical of environmental medicine. Recently,
however, a number of credible case–control reports, prospec-
tive cohort studies and other research work have suggested a
causative link between various agents and serious health
sequelae. In fact, reproductive abnormalities such as infertility
(Greenlee et al., 2003; Claman, 2004), recurrent miscarriage
(Sugiura-Ogasawara et al., 2005), preterm birth (Latini et al.,
2003) as well as various types of cancer (Harte et al., 1991; Ma
et al., 2002; Warner et al., 2002; Ekbom et al., 2003), neuro-
logical afflictions (Gorell et al., 1998), endocrine disturbances
(Berkson, 2000), immune system irregularities (Baccarelli
et al., 2002; Forawi et al., 2004), developmental problems
(Siddiqi et al
., 2003) and several other maladies have been cor-
rel
ated in some cases with exposure to toxic agents.
Reference values for toxicants
Many agencies and individuals involved in industry and public
health have come to rely on so-called reference levels for vari-
ous chemicals—the predicted daily human exposure dose
alleged to be able to occur without deleterious effects during a
lifetime. Doses of environmental chemicals asserted to be
‘safe’, however, are based on many assumptions and are typi-
cally derived from animal experiments where the presumed
safe dose was never actually tested. Various concerns have
been raised with the current construct of safe exposure levels.
Many chemical agents are relatively new, and safety testing
has never been performed; accordingly, reference values have
not been established. Furthermore, because human exposure
medicine is a comparatively new field with incomplete recog-
nition of the totality of adverse effects, existing values may be
inaccurate for many reasons including the following: (i) cur-
rent safety levels frequently reflect testing of a one-time expo-
sure and do not incorporate bioaccumulation and repeated
exposures; (ii) animals commonly used in toxicology testing
may have inherent detoxification mechanisms not present in
people, thus invalidating the application of animal research to
humans (Rat Genome Sequencing Project Consortium, 2004);
(iii) there can be immense variability in individual response to
exogenous chemical agents that may not be adequately
accounted for when determining reference values; (iv) in addi-
tion to the impact of single exposures, contact with multiple
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agents may facilitate synergism of toxicity; (v) analysis of
endocrine responses is not part of conventional toxicological
assessment and is often omitted (Welshons et al., 2003) and
(vi) vested interests frequently have input into determining
threshold levels for toxicants (Ziem and Castleman, 1989).
In addition, reference values are based on adult research not
fetal impact—in utero is a time in the life cycle when there is a
particular propensity to respond adversely to chemical agents
(Environmental Working Group, 2005; U.S. Environmental
Protection Agency, 2005). The immature fetal liver is not suffi-
ciently efficient at detoxifying contaminants particularly dur-
ing organogenesis and early gestation: the result is rapid fetal
bioaccumulation. Furthermore, with higher unbound fractions
of bioactive toxicants because of low levels of binding pro-
teins, with undeveloped excretion pathways (e.g. pollutants
excreted in urine are recycled into the nose and mouth as amni-
otic fluid), with high toxicant concentrations by weight in the
small fetus (compared with mother), with rapidly developing
organs and with an immature and more permeable blood–brain
barrier and a proportionately larger brain, there is a much
longer half-life of toxicant in the fetus with a greater target-
tissue dose and greater access to the CNS (Birnbaum and
Fenton, 2003; Makri et al., 2004; Barton et al., 2005). The
developing fetus is at particular risk for untoward chemical
damage—a reality not usually represented in reference values.
In view of fetal vulnerability, a recent study of cord blood
samples taken by the American Red Cross revealing that the
average sample contained 287 toxicants (including heavy met-
als, various pesticide gasoline by-products and fire retardants)
(Environmental Working Group, 2005) has raised serious con-
cern about the individual and public health sequelae of in utero
pollution via vertical transmission. The concomitant statistics
that many pregnancies are terminated for congenital anomalies,
that ∼3% of offspring in America are born with a major birth
defect (Arias et al., 2003), that the incidence of paediatric can-
cer is on the rise (Birnbaum, 2005), that ∼17% of children experi-
ence developmental disorders (Boyle et al., 1994; Needham
et al., 2005) and that an estimated 1 in 12 children and teens has
a chronic disability (Cohn, 2002) [some of these problems
already having been linked to known environmental exposures
(Branum et al., 2003; Needham et al., 2005)] have resulted
in the rising attention to prenatal sensitivity to low levels of
toxicants.
Obstetrical concerns related to adverse exposure
With recognition that the placenta does not act as an effective
filter against many exogenous chemical agents, the teratogenic
effect of selected toxicants has become an issue of increasing
concern in modern-day obstetrics and gynaecology. For
example, alcohol use in pregnancy, referred to as ‘the drink
that lasts a lifetime’, has gathered much attention as the aetiol-
ogy of fetal alcohol spectrum disorder—a range of life-long
developmental, physical and neuropsychiatric disabilities.
Cocaine abuse and exposure to other street drugs have also
been associated with adverse fetal outcomes. Recently, how-
ever, published research has linked obstetrical and paediatric
problems with adverse exposure to various household and
industrial toxicants during pregnancy. Exploration of a few
studies highlights the concern.
In 1999, the Journal of the American Medical Association
published an article regarding pregnancy outcome following
maternal exposure to organic solvents (Khattak et al., 1999).
With the recognition that innumerable women of childbearing
age are exposed to these agents, this prospective controlled
observational study was designed to explore a potential link
between fetal outcome and gestational exposure to organic sol-
vents. Pregnant women occupationally exposed to solvents
were matched to comparable pregnant women exposed to a
recognized non-teratogenic agent. In addition to increased rates
of miscarriage, solvent-exposed women were 13 times more
likely to have children with major cardiovascular and CNS
malformations, leading the authors to conclude that ‘occupa-
tional exposure to organic solvents during pregnancy is associ-
ated with an increased risk of major fetal malformations’
(Khattak et al., 1999).
The DES experience of long-term deleterious sequelae with-
out obvious birth defect has been noted with several other pre-
natal exposures. For example, an important study published in
the Journal of Epidemiology and Community Health (Knox,
2005) endeavoured to retest previous findings that most child-
hood cancer is instigated by prenatal exposure to various toxic
inhalants. The study explored a potential link between the birth
addresses of chi
ldren who succumbed to childhood cancer in
Great Britain over a 15-year period and the location of high
atmospheric emissions of different chemical agents. Signifi-
cant correlation between birth proximity with sites of industrial
use of specific chemical agents was confirmed, and the authors
concluded that the maternal inhalation of such toxicants was
causally related to fatal paediatric cancer in progeny.
Numerous other studies have linked various toxic chemical
exposure during pregnancy with myriad afflictions including
psychiatric illness and behavioural problems (Vreugdenhil et al.,
2002; Sorensen et al., 2003), respiratory disease (McKeever
et al., 2002; Miller et al., 2004), neurological disorders
(Gilbertson, 2004) and genital abnormalities (Steinhardt,
2004; Swan et al., 2005). Researchers have recently demon-
strated, for example, a highly significant relationship between
maternal exposure to phthalates (a family of compounds used
widely in plastics and personal care products) and alterations in
the development of male genitalia (Swan et al., 2005). Further-
more, fetal developmental alterations may not only affect the
fetus directly exposed, but the impact may continue through
multiple generations (Anway et al., 2005). Animal research has
recently demonstrated that toxicant exposure during gestation
is able to alter gene regulation and expression by epigenetic
changes, an alteration which may persist through successive
generations (Anway et al., 2005).
As well as physical alterations, toxic chemicals have the poten-
tial to affect the psyche of developing individuals. Although it
may be evident that men and women biologically differ, a major
determinant in that difference, both physically and psychologi-
cally, is the intricate hormonal balance of parts per billion and
parts per trillion of androgens and estrogens present during
embryonic and fetal development. The introduction of EDCs
(sometimes referred to as gender benders) at critical times of
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fetal maturation has the potential, according to various
researchers, to affect gender attributes and psychosexual out-
come as well as genital formation (Ehrhardt et al., 1985;
Saunders, 1988; Collaer and Hines, 1995; Meyer-Bahlburg
et al., 1995; Berkson, 2000; Rapp, 2004; Steinhardt, 2004;
Swan et al., 2005).
In review, recent medical and scientific literature suggests
that toxicant exposure during gestation—a time when fetal
cells are rapidly proliferating and differentiating into specific
tissues and organs—may have serious implications for the
health and well-being of the developing child, with repercus-
sions for families, societies and public health care systems.
Although obstetric sequelae resulting from toxicant exposure is
a recognized concern, adverse environmental exposures through-
out life may also be a determinant of some non-maternity diffi-
culties presenting to the practicing gynaecologist.
Gynaecologic concerns related to toxicant exposure
Although understanding of female endocrine and gynaecologic
response to adverse influences is still in its relative infancy,
recent scientific literature is beginning to elucidate a possible
connection between adverse toxicants and several gynaecolog-
ical disturbances including bleeding irregularities, precocious
puberty, polycystic ovary syndrome (PCOS), subfecundity,
infertility, recurrent miscarriage, ovarian failure and more
(Falsetti and Eleftheriou, 1996; Berkson, 2000; Cordain et al.,
2003; Drbohlav et al., 2004; Mlynarcikova et al., 2005; Sugiura-
Ogasawara et al., 2005; Tsutsumi, 2005). Some recent investiga-
tion of toxicants related to gynaecological outcome has centred
on the prominent role of exogenous estrogen and androgen
modifiers in male and female physiology (Cotton, 1994;
McLachlan, 2001).
In couples presenting with infertility, for example, male
reproductive dysfunction or altered sperm production may be
the result of prenatal toxicant exposure (Main et al., 2006) or
post-natal interaction with environmental or occupational
EDCs which alter testosterone metabolism (Quinn et al., 1990;
Egeland et al., 1994; Claman, 2004). Furthermore, it is well
recognized that intact estrogen physiology is required for
female embryonic development, breast maturation and
puberty, normal sexual response, pregnancy as well as healthy
vascular, heart and bone function. Anything that disrupts the
normal physiology of estrogen—by mimicking or antagonizing
the effects of E
2
—may facilitate reproductive dysfunction
and disorders such as endometriosis (Dubeyl et al., 2000;
Tsutsumi, 2005).
Endometriosis and toxicants
With prevalence rates of 10–20% of American women,
endometriosis frequently causes chronic pelvic pain and infer-
tility, accounting for incalculable suffering as well as about
half-a-million surgical procedures in the United States annu-
ally. This increasingly common disorder in industrialized
countries (Koninckx, 1999) may afflict very young women and
often occurs in geographic clusters. Koninckx et al. (1994), for
example, found that in addition to having the world’s highest
incidence of endometriosis, Belgian women also sustain
inordinately high concentrations of dioxin (a potent disruptor
of estrogen metabolism) in their breast milk. Furthermore,
various researchers have found high rates of endometriosis in
animals as well as in individuals exposed to EDCs (Cummings
et al., 1996; Osteen and Sierra-Rivera, 1997; Rier and Foster,
2002).
On the basis of these initial observations, work has been
done to confirm suspicions that human endometriosis may res-
ult from toxic exposure (Rier and Foster, 2003; Louis et al.,
2005). A recent case–control study by Heilier et al. (2005), for
example, assessed the level of estrogenic EDCs as well as syn-
thetic chemicals that operate via other response mechanisms in
hospitalized women who were subdivided into groups accord-
ing to diagnosis. By linear regression analysis and the stand-
ardization of variables, the researchers noted a significant
association between the body burden of EDCs in participants
and the finding of adenomyosis and endometriosis (Heilier
et al., 2005). Furthermore, a cohort study investigating the
relation between the fetal environment and endometriosis
recently found a significant increase in laparoscopically con-
firmed endometriosis in women previously exposed to estro-
gen-disrupting DES in utero (Missmer et al., 2004).
In view of preliminary data on potential gynaecological out-
comes as well as on documented obstetric and paediatric
sequelae associated with toxicant exposure, it is important to
explore measures that might prevent and ameliorate illness for
women and their offspring.
Clinical considerations
Despite compelling evidence that some chemical exposures
may have adverse sequelae, there is insufficient proof to
directly establish safety or harm for many of the thousands of
chemicals in everyday use. How should clinicians approach the
issue of environmental toxicants?
As most human activity involves a certain degree of risk, it
is important to consider the risk–benefit ratio when providing
clinical advice about any health determinant, including the
benefits and risks associated with the use of and exposure to
specific chemicals. As the in utero peril to the fetus from toxi-
cants is manifest, it is recommended that pregnant patients
adhere to the ‘Precautionary Principle’ (Wingspread statement
on the Precautionary Principle, 1998) whereby individuals are
educated regarding potential toxic exposures and then imple-
ment a concerted effort to avoid them. Patients should acquire
a thorough understanding of how and where toxic exposure
occurs and develop a plan to avoid adverse contact. Accord-
ingly, physicians need to be educated about chemical toxicants
to transmit this important information to patients.
Medical practitioners in all clinical spheres need to incorpo-
rate exposure evaluation as a routine component of patient
assessment (Ott, 1995; Needham et al., 2005; Ozkaynak et al.,
2005). To determine potential exposure, past and present, we
can use a human exposure questionnaire as an instrument to
help in the diagnosis and education of patients. Various assess-
ment instruments are available in the scientific literature (Rea,
1997; Miller and Prihoda, 1999; Steele and Fawal, 2000) and
from medical organizations (Marshall, 2002).
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To assess the ‘body burden’ of contaminants, some organi-
zations such as the CDC have performed screening toxicant
panels (Centers for Disease Control, 2005)—this type of labo-
ratory investigation can provide definitive evidence of bioac-
cumulation. Such screening, however, is usually confined to
research and is not frequently used in clinical practice thus far.
Major drawbacks to blood testing include exorbitant expense
as well as frequent false-negative reporting because many toxi-
cants are sequestered within storage sites such as fat and thus
not adequately reflected in blood samples.
The process of expelling chemical residue from the body is
often referred to as detoxification, a process performed in great
part by the liver in conjunction with excretion through routes
such as stool, urine, exhaled breath and perspiration. Utilization
of specific physical modalities to facilitate toxicant expulsion
from the body is not a new concept: Hippocrates used solari-
ums, religious groups used fasting, aboriginal groups used
sweat lodges and hot baths, Egyptians used body wraps, spe-
cific eastern European groups have used Turkish baths and
some Scandinavian cultures have employed saunas and steam
baths—all of which allegedly enhance the mobilization of
stored metabolic and exogenous toxicants. There has been
recent work attempting to utilize biochemical interventions and
physical modalities to facilitate and enhance the body’s inherent
detoxification mechanisms (Schnare et al., 1982, 1984; Kilburn
et al., 1989; Shields et al., 1989; Tretjak et al., 1990; Rea et al.,
1996; Baker, 1997; Rea, 1997; Berkson, 2000). Although pre-
liminary data suggest clinical improvement after detoxification
interventions, this evolving area has not been adequately stud-
ied or reported in mainstream medical and toxicology literature
(Kilburn, 2004); further research needs to be undertaken to
establish definitive evidence-based recommendations.
Conclusion
If individuals and the public are properly educated about chem-
ical toxicants, they will be empowered with the choice to make
decisions to protect themselves and their offspring; without
knowledge, the choice is precluded. As official advocates for
reproductive care in the community, women’s health physi-
cians have the distinctive opportunity to assist individual
patients as well as to proactively engage in public health edu-
cation relating to the impact of adverse exposure. With appro-
priate knowledge and skills of exposure assessment,
precautionary avoidance and potential therapeutic options, pro-
viders of obstetrical and gynaecological health care may be
able to prevent congenital anomalies and ameliorate the life
situation for many women.
Acknowledgements
Special thanks to the anonymous associate editor at Human Reproduc-
tion who provided invaluable suggestions for the final draft.
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Submitted on January 29, 2006; resubmitted on March 18, 2006, April 21,
2006; accepted on April 28, 2006
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