Environmental Health Perspectives Volume
103, Supplement 6, September 1995
[Citation
in PubMed]
How Should Federal Policy Reflect Recent Research in the Area of Intrauterine
Exposure to Environmental Hazards?
J. Routt Reigart
Department of Pediatrics, Medical University of South Carolina, Charleston,
South Carolina
Abstract
Present policy neither evaluates nor adequately protects the fetus from
the effects of intrauterine exposure to environmental hazards. Some examples
are intrauterine lead and methylmercury exposure and intrauterine PCB exposures.
A sound policy based on a few basic principles can be developed to protect
the fetus from harm from intrauterine exposures. -- Environ Health Perspect
103(Suppl 6):143-145 (1995)
Key words: environmental policy, intrauterine exposure, fetus,
lead, mercury, PCBs
This article was presented at the Symposium on Preventing
Child Exposures to Environmental Hazards: Research and Policy Issues held
18-19 March 1994 in Washington, DC.
Address correspondence to Dr. J. Routt Reigart, Department
of Pediatrics, Medical University of South Carolina, 171 Ashley Avenue,
Charleston, SC 29425-3302. Telephone (803) 792-2114. Fax (803) 792-9223.
Introduction
While intrauterine exposure to environmental hazards has many similarities
to postuterine exposure, it is important in formulating policy to keep in
mind some obvious but important differences between these two exposure periods.
The most obvious yet most important fact is that intrauterine exposure can
only occur through exposure of the mother. The implications of this are
many and complex. Clearly, the mother's environment and behavior are important
determinants of the exposure of the fetus. The mother's environment encompasses
both recent and present exposure to toxicants and other environmental hazards.
A clear and difficult example of this is fetal exposure to lead. While it
is clear that fetal blood lead measured by cord blood lead determinations
approximates maternal blood lead (1), it is not clear to what extent
maternal blood lead during pregnancy reflects current exposure versus mobilization
of lead from bone stores as a function of pregnancy. Protection of the fetus
from this exposure may require prevention of both current and prior exposure.
Since very low levels of maternal lead are necessary to prevent fetal injury,
it may well be that prevention of fetal exposure to lead may require lifetime
maintenance of very low levels of lead in the mother. This would require
aggressive prevention of childhood exposure as well as markedly stricter
regulation of occupational exposure of adults. An active research agenda
in the area of fetal lead exposure is presently supported by the National
Institute of Environmental Health Sciences (NIEHS) and includes studies
in adult pregnant humans and nonhuman primates. The question to be asked
in this context is: Should policy await complete research in this area,
or should action be taken immediately to monitor parental and fetal exposure?
The example of methylmercury exposure and its effect on the fetus presented
in this issue present further policy dilemmas in this area (2). Since
a primary source of methylmercury exposure of parents and thus the fetus
is parental eating of contaminated fish, particularly large predatory fish,
policy should be directed toward limiting ingestion of such contaminated
fish by adults, particularly women of childbearing age. However, such policy
confronts several difficult limitations. First, the primary source of mercury
may not be controllable. In fact, much environmental mercury is not a product
of human activity and therefore is extraordinarily difficult to control.
Certainly every effort should be made to control industrial and refuse contamination;
such efforts can decrease environmental mercury contamination but will not
remove naturally occurring mercury sources. Second, monitoring contamination
of fish requires an aggressive and extensive program, as there may be very
large differences in contamination of fish over very small geographic areas.
For instance, one freshwater lake may have fish with high levels of methylmercury,
while another in the same state or county may have fish with much lower
levels of contamination. Similarly, marketplace monitoring will have little
effect on consumption of contaminated fish that come to the table without
passing through the marketplace. Finally, though laws, regulations, or warning
notifications may decrease consumption of contaminated fish by sport fishermen,
such actions have little effect on persons who consume fish caught for subsistence.
In fact, subsistence fishing, with the risk of methylmercury, PCB, and
other exposures, represents a major issue related to environmental justice.
It is particularly those of low socioeconomic status and ethnic minorities
who are most likely by custom or socioeconomic status to rely on potentially
contaminated fish for subsistence.
An additional problem requiring consideration in our desire to protect
the fetus from environmental hazards is the needs and rights of the mother.
Some of the neurotoxic effects on the fetus related to maternal environmental
exposures may be considered entirely related to the behavior of the mother.
Some examples of these exposures include maternal use of tobacco products,
drug use, and ethanol ingestion. These types of behavior may be considered
voluntary, though many mothers may be addicted to an extent that they cannot
control their behavior. How should federal policy attempt to prevent such
behavior? This issue is beyond the scope of this workshop but presents an
important concern for policy on both the federal and local government levels.
A more direct concern for this conference is the issue of parental workplace
exposure. In those workplace situations where the fetus is equally or more
susceptible to the exposure than the adult, protection requires actions
aimed at protecting the fetus that may appear excessive for protection of
the adult worker. Again, good examples of this are lead, mercury, and some
chemicals. In such a context, there are only two possible interventions.
First, women could be excluded from such hazardous workplaces. Obviously,
such a policy has important implications regarding the rights of those excluded
from the workplace. Alternatively, the workplace can be made sufficiently
safe to protect the fetus, even though this level of protection may be more
than is necessary to protect adult workers. While this form of policy clearly
is the more protective of the rights and prerogatives of the adult worker,
it is far more difficult and expensive to achieve.
Prevention of exposures that are not primarily a function of behavior
such as occupation, substance abuse, and ethnic custom presents a somewhat
different challenge. In such cases it may not be necessary to limit choice
of occupation, alter ethnic customs, or alter addictive behaviors. However,
the challenge of policy may still be formidable. Limitation of parental
exposure to airborne lead has been accomplished largely by eliminating lead
from gasoline. However, further reduction of parental exposure, which is
largely a function of residual lead-based paints and contaminated soils
and dusts, is a far more difficult and costly process. Similarly, limitation
of exposure to farm and industrial chemicals often has been an extraordinarily
difficult policy task. As our population and resultant use of chemicals
increase, control of exposure to such agents becomes increasingly difficult.
It is unfortunate that such chemical exposures disproportionately affect
persons of low socioeconomic status and ethnic minorities. This greater
effect on relatively disenfranchised populations often has led to inadequate
attention by policymakers to the plight of these adversely affected populations.
Recommendations
In light of these considerations, several specific recommendations can
be made to guide policy decisions. These recommendations seem to me to be
reasonable standards by which to judge the regulatory process.
Policy Should Follow the Science
It is clear that some risks, specifically carcinogenic and water contamination,
are overvalued by the public and some policymakers. On the other hand, neurodevelopmental
risks such as exposure to lead, methylmercury, and PCBs often are underestimated
by the public and in public policy. Only when these toxicants are found
in water or are thought to be carcinogens do they stimulate high-level public
concern. While the political process requires public support to develop
and implement policy, we as scientists must improve the level of public
understanding of the actual risks to children from these toxicants and the
relative impacts of various health end points and routes of exposure on
our children. It seems incongruous that there is enormous public concern
over 20 parts per billion of lead in first draw water of some homes (especially
when many occupants of these homes rarely drink water or offer it to their
children), while contamination of dusts and soils to thousands of parts
per million by lead-based paint contamination often arouses little or no
public support for lead-based paint abatement efforts. While it is certainly
appropriate to reduce lead in water to the lowest level possible, it is
even more desirable to reduce direct and indirect exposure to lead-based
paints. Education of the public and legislators in the science is necessary
to enact appropriate public policy.
While Policy Clearly Should Be Based on Science, the Science Should
Not Serve as a Barrier to Timely Policy
Often the public interest requires action in the absence of complete
science. In particular, actions often can be adequately justified using
animal models in the absence of complete human data. Dead or damaged animals
often should be sufficient to justify action to protect humans, particularly
the fetus and young infant. It is not necessary for sound public policy
to require dead or severely damaged infants prior to acting to protect the
fetus from environmental hazards. Also, human neurobehavioral data may allow
action in the absence of complete mechanistic understanding. For example,
the intrauterine effects of lead are probably real based on behavioral studies
in the first years after birth, but our understanding of the mechanism(s)
for this effect is limited. This limited understanding should not deter
efforts to decrease intrauterine lead exposure. Nor should incomplete data
on methylmercury effects or mechanisms delay action to decrease intrauterine
exposure to this toxicant.
Policy Should Be Goal-directed and Reasonably Consistent
All Government Policy Should Specifically Identify the Fetus and
Newborn as Potentially Vulnerable and Susceptible Hosts. Regulatory
policies should evaluate toxicants specifically for their risks to the fetus
and newborn. In light of the vulnerability of the developing nervous system
of the fetus, specific concern for neurodevelopmental outcomes should be
an intrinsic part of the evaluation and regulatory processes. As the productivity
of our population is largely determined by its neurodevelopmental capability,
neurodevelopmental risk should be the most important of the outcomes evaluated
in this process. It should always be remembered that the two primary tasks
of infancy and childhood are growth and development and that development
is the more susceptible of these tasks to injury from environmental hazards.
Intrauterine environmental injuries can and do affect both of these tasks.
Government policy should specifically and explicitly protect the most susceptible
segments of the population, who are the fetus and the infant.
Government Policy Should Recognize that the Fetus and Newborn Differ
Biologically from Adults. It is not possible with any degree of
assurance to extrapolate from adults to children. It is true that some environmental
hazards affect the fetus less than adults, and some affect the fetus more.
Similarly, some toxicants are concentrated by the fetus, while others do
not reach the fetus at all due to placental protection. For example, as
noted previously in this session, lead seems to equilibrate with maternal
lead, while methylmercury seems to concentrate in the fetus above maternal
levels. In addition, the processes of development of the nervous system
of the fetus, as outlined by Dr. Tilson at this workshop, are quite different
from maintenance of the mature nervous system of the adult. Therefore, effects
on this fetal development must differ both qualitatively and quantitatively
from effects on the mature nervous system. We must demand that these effects
be specifically assessed and addressed in the regulatory process to protect
our children.
Decisions Must Be Made That Protect the Fetus and the Newborn.
However, these policies may be directed specifically to the fetus
(such as limiting lead exposure only for women of childbearing age and pregnant
women) or to the population as a whole sufficient to protect the fetus and
newborn (e.g., limiting lead exposure of all men and women equally to protect
the fetus, even though this protection may be excessive for the general
population). The policy that seems most protective of the fetus without
infringing on the rights of adult women is to decrease the exposure of the
total population sufficiently to protect the fetus. Though this may be quite
difficult, particularly in the workplace, it seems the most defensible approach
on social and ethical bases.
Policy Should Ensure the Safety of the Population
Testing, evaluation, registration, and control of environmental hazards,
particularly environmental toxicants, should reflect specific concern for
the fetus and the newborn. Specifically, it is reasonable and appropriate
to require testing based on neurodevelopmental effects upon the fetus. In
addition, regulation of these hazards should reflect our best understanding
at the time of the risk to the fetus from such environmental exposures.
While it may be true that subsequent research may show that we have been
overcautious, it is preferable to err on the side of safety to the fetus
rather than to recognize after many years that we have allowed unnecessary
injury to occur.
Policies Should Reflect Parental Differences That May Differentially
Affect the Fetus
In particular, differences in habitation, occupation, location, and ethnicity
have major impacts on exposure of the fetus to toxic substances. Also, diet
and health of the mother dependent or independent of the above factors have
major impacts on fetal exposure to toxicants. All our citizens should be
allowed to live in environmentally safe environments. Policy should not
allow the influence of more affluent and influential segments of the public
coupled with a "not in my back yard" attitude to subject less
affluent segments of our population to hazards considered unacceptable to
the rest. Also, all occupations should be provided a level of environmental
safety sufficient to protect the fetus. It is not acceptable for some occupations
to be intrinsically hazardous and thus to subject the worker and the fetus
to unnecessary risk. It is not appropriate, either, to require that some
populations accept major cultural alterations to protect themselves and
their children from environmental hazards.
Federal Research Agenda Should Work to Fill Gaps in Our Knowledge
Of major interest are the changes that occur in maternal biokinetics
during pregnancy and determinants of placental transport and fetal accumulation
of toxicants. The example of the metals lead and mercury illustrates this
area of concern and need for increased information. While it appears likely
that methylmercury accumulates in the fetus preferentially, the determinants
of this accumulation are not clear, nor are potential methods to prevent
such accumulation; likewise with lead accumulation in the fetus. Many mothers
today have large stores of lead in stable pools, particularly bone. There
are virtually no data, however, as to the extent to which this lead is mobilized
and transported to the fetus. Also, there is little evidence as to the timing
of such transport, though it would seem likely that it would occur preferentially
during the latter period of gestation when mineralization of the fetus is
most active. Little is known of the kinetics of absorption and distribution
of lead in the pregnant woman related to current exposure. Improvements
in such information could be quite useful in efforts to protect the fetus
from intrauterine lead neurotoxicity.
In addition to biokinetics, evidence is lacking relating to the specific
effects that toxicants have on development of the nervous system in utero.
Specific information regarding toxic effects on morphogenesis, synaptogenesis,
and biochemical development of the fetal nervous system could be invaluable
in assessing and preventing the neurodevelopmental damage occurring with
intrauterine exposure to toxicants.
There is a need for improved methods to detect and measure intrauterine
developmental toxicity. Methods that do not require developmental measurement
or cross-species extrapolation would markedly improve our ability to assess
and regulate intrauterine exposure to developmental toxicants. Such methods
presently seem far in the future but could be predicted as a realistic outcome
of basic research into the precise mechanisms of toxicant injury to the
developing nervous system.
Finally, federal research could do much to provide a framework in behavioral
research that might allow alteration of behavior that results in injury
to the fetus. Obviously, such research and interventions must be conducted
in a culturally sensitive fashion to allow improved outcomes for the fetus
without being destructive of the rights of parents.
Conclusions
It appears clear from this workshop that our ability to protect the fetus
from neurodevelopmental environmental injury is presently very limited.
Limitations exist in all areas. We are limited in our understanding and
limited regarding a consensus on the basic principals of fetal protection.
We are limited by a lack of understanding and resolve on the part of policymakers
regarding extension of suitable and adequate protection to the fetus. Despite
these limitations, we owe it to our unborn children, and to all children,
to provide an environment that will allow full realization of their intrinsic
potential. We must not lose sight of this duty as we proceed in the scientific
and regulatory arenas.
REFERENCES
1. Rabinowitz MB, Needleman HL. Temporal changes in the
lead concentrations of umbilical cord blood. Science 216:1429-1431 (1982).
2. Gilbert SG, Grant-Webster KS, Burbacher TM. Neurobehavioral
effects of prenatal methylmercury exposure. Environ Health Perspect 103(Suppl
5):000-000 (1995).
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