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#544 - Statement on Immune Toxins, 30-Apr-1997

[Here we present, verbatim, a consensus statement about toxic chemicals
and the immune system written by 18 scientists[1] and published in the
summer of 1996.[2] The scientists met at a workshop in Racine,
Wisconsin, February 10-12, 1995, to discuss the issue "because of the
pervasive contamination of the environment by compounds... [having] the
potential to disturb the immune system of wildlife and humans....
introduced into the environment by human activity...."[2] The statement
is not easy reading, so we have added a few clarifications and
commentaries of our own inside square brackets.]

Consensus Statement

The following consensus was reached by participants[1] at the workshop.

A) We are certain of the following--

A competent immune system is essential for health.

Experimental lab studies demonstrate that certain synthetic chemicals
affect the immune system (e.g., aromatic hydrocarbons; carbamates [a
class of pesticides]; heavy metals [for example, mercury];
organohalogens [for example, many chlorine-containing compounds];
organophosphates [a class of pesticides]; organotins [chemicals
containing tin and carbon atoms]; oxidant air pollutants, such as ozone
and nitrogen dioxide; and polycyclic aromatic hydrocarbons [often
produced by combustion of coal, oil, gasoline, garbage, medical
waste]). These effects are manifested as alterations in the immune
system that may lead to a decreased quality of life. These alterations
include immune modulation [changes in the immune system] expressed as
an increase or decrease in measured immune parameters [for example, the
number of T cells or B cells in blood], hypersensitivity, and
autoimmunity.

[In other words, from experiments on laboratory animals, it is known
with certainty that many classes of common chemicals can change the
immune system and can cause hypersensitivity and autoimmune diseases.
In humans, hypersensitivity is often expressed as an allergic reaction.
[3,pgs.81-106] Autoimmune diseases include diabetes, multiple
sclerosis, rheumatoid arthritis, lupus, and a dozen other diseases.
[3,pg.123]]

Changes in the characteristics of the immune system in humans and
certain wildlife species have been associated with both therapeutic and
environmental exposure to synthetic chemicals, e.g., diethylstilbestrol
(DES), dioxin, polychlorinated biphenyls (PCBs).

Impairment of the immune system can result from alterations in the
development [before and shortly after birth or hatching] of the immune
system and may be long-lasting. The effects may not be manifested at
hatching or birth and may not be expressed until the animal or human
reaches adulthood.

Life-long capacity for immune response [i.e., healthy functioning of
the immune system] is determined early in development, during prenatal
and early postnatal development in mammals and prehatching and early
posthatching development in egg-laying species.

Alterations in the developing and mature immune systems may not be
recognized as an adverse health effect until long after the exposure.

Some wildlife and human populations are exposed to elevated levels of
certain synthetic chemicals.

The widespread exposure of populations of humans and wildlife to many
man-made chemicals has made it difficult, if not impossible, to find
control populations that have no exposure level. True control
populations for human and wildlife epidemiological studies are thus
lacking. [In other words, we are all now exposed to many chemicals that
can change our immune systems, so it is not possible to find a "control
group" of people who have truly healthy, unaffected immune systems that
can be studied.]

B) We estimate with confidence that--

Certain synthetic chemicals, such as those listed above, released or
reintroduced into the environment act upon the developing and mature
immune systems in humans and other vertebrates.

Prenatal and early postnatal mammals and the immature and early life
stages of amphibians, reptiles, fishes, and birds are likely to be the
most vulnerable life stages to immunomodulation [changes in the immune
system].

Vulnerability upon exposure varies among gender, species, and stages of
the life cycle. In addition to embryos, fetuses, and the newborn,
children, the very old, and certain populations (e.g., chronically ill,
poorly nourished, HIV positive) are also likely to be more at risk.
[Naturally, this makes it difficult to study the effects of chemicals
on the immune system because the effects vary greatly, depending on the
stage of life of the person or animal being studied.]

In certain instances, humans and wildlife are experiencing immune
alterations. Data suggest that immune alterations seen in wild animals
and humans are consistent with those produced by synthetic chemicals
identified as immunotoxic in studies with laboratory animals.

Immunotoxic effects expressed in individuals could therefore be
expressed at the population level thus affecting biodiversity at the
community or ecosystem level. [In other words, so many individuals
might be affected that entire populations could have their immune
systems degraded.]

Immune system effects reported in wildlife, in parallel with IN VITRO
[test tube] and IN VIVO [living animal] experimental studies, support
the possibility for qualitative prediction of human effects.

Current predictive capability for immunomodulation is limited to
identification of qualitative changes not quantitative changes.

C) Based on our current understanding we predict--

Certain synthetic chemicals can cause alterations of the developing
immune system.

Alterations in immunologic function whether occurring prenatally or
embryologically or later in life can translate into altered host
resistance and susceptibility to disease, including autoimmune disease.
Disease patterns are thus likely to be affected by immune modulation
induced by immunological toxicants.

D) There are uncertainties in our understanding because--

More needs to be learned about how the immune system develops.

Few well-controlled human or wildlife ecoepidemiological studies that
document immune modulation [immune system changes] have been completed.

The lack of sensitive tests and the uncertainty about exposure have
been impediments in many of these studies. Exposure is well known for
some wildlife studies.

Information on exposure is limited. Little is known about the effects
of long-term, low-level exposure.

Little is known about the effects of exposure to chemical mixtures.
Most published studies use single agents when testing for the effects
of environmental exposure. The specific components of environmental
mixtures are rarely defined.

The pharmacokinetics of many immunotoxic compounds in target organs is
understood in experimental animals but not in humans and wildlife.
[Pharmacokinetics refers to the precise details, at the level of the
cell, of how chemicals affect living things.]

Data are lacking about the persistence of the effects of
immunomodulators.

For regulatory purposes, the current lack of knowledge about the
mechanisms leading to immunomodulation makes cause-and-effect linkages
extremely difficult.

Uncertainty exists about whether the right questions have been asked
concerning the mechanisms of immune modulation.

E) Our judgment is that--

The potential exists for widespread immunotoxicity in humans and
wildlife species because of the worldwide lack of appropriate
protective standards. This is based on documented immune effects from
high-level exposure, plus a large amount of anecdotal data on humans
and wildlife, and strong experimental animal data.

Although exposure is widespread, it varies from region to region and
individual to individual. Based on anecdotal information, it is
presumed that exposure is greater in Eastern Europe and the former
Soviet Union and especially in developing countries because of lack of
adequate environmental regulations and enforcement.

The lack of human epidemiological studies in the developing world makes
it impossible to determine the scale of immune modulation and/or
autoimmune disease among these populations. The consequences of
chemical exposure in developing countries may be severe because of
multiple confounders such as poverty, malnutrition, and poor medical
care. The consequences will be difficult to identify because of the
lack of adequate control cohorts.

The risk of exposure to known immunomodulators is sufficient to warrant
regulatory approaches that would limit exposure. [In other words, we
already know enough to justify taking regulatory action.]

F) To improve our predictive capacity--

More basic research is needed on the development of the immune system
of diverse animal species and the factors that drive its maturation and
senescence [loss of power with age]. Further study is needed to
understand the mechanistic role of synthetic chemicals in the
alteration of these processes.

Priority needs to be given to developing assays [tests] predictive of
disease resistance for a variety of species. It is important to know
how immune modulation affects increased prevalence of infectious
diseases among humans and wildlife.

More emphasis must be placed on developmental immunotoxicology. This
can be accomplished through collaborative research efforts to
standardize protocols, share specimens, and to develop inexpensive,
rapid biomarkers of immunotoxicity. The use of the Internet and other
online systems to apprise researchers of planned and ongoing
experiments will increase collaborative opportunities.

Models based on "real world" situations (dose, duration of exposure,
timing) that include metabolism, pharmacokinetics, route of exposure,
and target effects in a number of indicator species should be developed
for extrapolation to humans and other species.

Ecoepidemiological criteria that include dose-response, time order
(exposure precedes effect), specificity, strength of association,
coherence, and predictability combined with laboratory validation are
needed to improve the level of certainty in epidemiological studies.

More epidemiological research among susceptible populations, especially
in developing countries, is needed. [End of consensus statement.]

--Peter Montague (National Writers Union, UAW Local 1981/AFL-CIO)

=====

[1] Authors of the statement include: Dr. John B. Barnett, Department
of Microbiology and Immunology, West Virginia University, Morgantown,
West Virginia; Dr. Theo Colborn, World Wildlife Fund, Washington, D.C.;
Dr. Michael Fournier, Laboratoire de Rescherche en Toxicologie de
l'Environnement, Universite du Quebec, Montreal, Quebec, Canada; Dr.
John Gierthy, Department of Environmental Health and Toxicology, State
University of New York, Albany, N.Y.; Dr. Keith Grasman, Department of
Biological Sciences, Wright State University, Dayton, Ohio; Dr. Nancy
Kerkvliet, Department of Agricultural Chemistry, Oregon State
University; Corvallis, Oregon; Mr. Garet Lahvis, University of
Maryland, School of Medicine, Baltimore, Md.; Dr. Michael Luster,
Environmental, Immunological, and Neurobiological Section, National
Institute of Environmental Health Sciences, Research Triangle Park,
North Carolina; Dr. Peter McConnachie, Immunotransplant Lab, Southern
Illinois University, School of Medicine, Springfield, Illinois; Dr. J.
Peterson Myers, W. Alton Jones Foundation, Charlottesville, Va.; Dr.
A.D.M.E. Osterhaus, Erasmus University, Rotterdam, The Netherlands; Dr.
Robert Repetto, World Resources Institute, Washington, D.C.; Dr.
Rosalind Rolland, World Wildlife Fund, Washington, D.C.; Dr. Louise
Rollins-Smith, Vanderbilt University, Nashville, Tenn.; Dr. Ralph
Smialowicz, U.S. Environmental Protection Agency, Research Triangle
Park, North Carolina; Dr. Michael Smolen, World Wildlife Fund,
Washington, D.C.; Dr. Sarah Walker, University of Missouri, Department
of Internal Medicine, Columbia, Mo.; Dr. David Watkins, University of
Wisconsin, Medical School, Madison, Wisconsin.

[2] "Statement of the Work Session on Chemically-Induced Alterations in
the Developing Immune System: The Wildlife/Human Connection,"
ENVIRONMENTAL HEALTH PERSPECTIVES Vol. 104 Supplement 4 (August, 1996),
pgs. 807-808.

[3] William R. Clark, AT WAR WITHIN; THE DOUBLE-EDGED SWORD OF IMMUNITY
(New York: Oxford University Press, 1995).

Descriptor terms: immune system; toxic heavy metals; mercury;
pesticides; carbamates; organophospates; organochlorines;
organohalogens; tin; ozone; nitrogen dioxide; air pollution; pahs; des;
pcbs; dioxin; development; wildlife; developing countries;