Environmental Medicine, Part
1: The Human Burden of Environmental Toxins and Their Common Health
Effects
by Walter J. Crinnion, ND
Abstract
Chemical compounds ubiquitous in our food, air, and
water are now found in every person. The bioaccumulation of these
compounds in some individuals can lead to a variety of metabolic and
systemic dysfunctions, and in some cases outright disease states. The
systems most affected by these xenobiotic compounds include the immune,
neurological, and endocrine systems. Toxicity in these systems can lead to
immune dysfunction, autoimmunity, asthma, allergies, cancers, cognitive
deficit, mood changes, neurological illnesses, changes in libido,
reproductive dysfunction, and glucose dysregulation. Chemicals and their
effects on these systems are reviewed in this article. Subsequent articles
in this series will focus on therapeutic regimens to combat the toxic
effects of these and other compounds. (Altern Med Rev 2000;5(1):52-63)
Environmental Toxic Load
The twentieth century, with its promise of "Better Living Through
Chemistry," brought a host of chemical toxin-related illnesses, often
referred to as environmental illness. Recent articles in the medical
literature have shown the rate of cancers not associated with smoking are
higher for those born after 1940 than before, and that this increase in
cancer rate is due to environmental factors other than smoking.1
New medical diagnoses include sick (closed) building syndrome,2,3
and multiple chemical sensitivity (MCS),4-6
both of which are known to be related to overexposure to environmental
contaminants. The primary action of the major pesticide classes and
solvents is to disrupt neurological function.7,8
In addition to being neurotoxic, these compounds are profoundly toxic to
the immune and endocrine systems.9-11 The
adverse health effects are not limited only to those systems, as these
compounds can cause a variety of dermatological, gastrointestinal,
genitourinary, respiratory, musculoskeletal, and cardiological problems as
well.12
Our environment is currently flooded with chemicals that are present in
our air, water, and food. Since 1976 the U.S. Environmental Protection
Agency (EPA) has been conducting the National Human Adipose Tissue Survey
(NHATS). NHATS is an annual program that collects and chemically analyzes
a nationwide sample of adipose tissue specimens for the presence of toxic
compounds. The objective of the program is to detect and quantify the
prevalence of toxic compounds in the general population. Specimens are
collected from autopsied cadavers and elective surgeries from all regions
of the country. In 1982 the EPA expanded beyond their normal list to look
for the presence of 54 different environmental chemical toxins. Their
results were astounding. Five of these chemicals – OCDD (a dioxin) and
four solvents: styrene,1
,4-dichlorobenzene, xylene, and ethylphenol – were found in 100 percent of
the samples
(see Table
1). The quantitative ranges of these five compounds were also
alarming. OCDD levels ranged from 19-3,700 ng per gram of fat, styrene
8-350 ng/g, 1,4-dichlorobenzene 12-500 ng/g, xylene 18-1,400 ng/g, and
ethylphenol 0.4-400 ng/g. These alone would give each person a total toxic
burden ranging from 57.4-6,350 ng of toxins per gram of fat.
Another nine chemicals were found in 91-98 percent of all samples,
including such toxins as benzene, toluene, chlorobenzene, ethylbenzene,
one furan, three dioxins, and DDE. DDE is formed by a partial
dechlorination of DDT, which can occur in the human body within six months
of exposure to DDT. It also occurs in nature, but studies vary as to the
t1/2 of DDT in the environment. Previously the t1/2 of DDT was thought to
be two years, but recent findings in Yakima, Washington indicate it may be
decades in certain circumstances. Upon degradation, DDT becomes DDE or
DDD.
In addition, PCBs were found in 83 percent of all samples and beta-BHC
in 87 percent, yielding a total of 20 toxic compounds found in 76 percent
or more of all samples. Seventy-six percent of individuals had as much as
25,704 ng of total toxic compounds per gram of fat.
Additional studies yielded similar results. A CDC study of 5,994
persons aged 12-74 years found 99.5 percent had p,p-DDE at serum levels
equal to or greater than 1 part per billion (ppb), in a range of 1-379
ppb.14 A study of adipose levels taken
from autopsies of older subjects who had been Texas residents showed the
presence of p,p-DDE, dieldrin, oxychlordane, heptachlor epoxide, and
para-BHC in 100 percent of samples.15 A
study of four-year-old children in Michigan revealed the presence of DDT
in 70 percent, PCB in 50 percent, and PBB in 21 percent.16
Nursing was the primary source of exposure for these individuals. These
ongoing assessments have shown quite clearly it is not a question of if we
are carrying a burden of toxic xenobiotic compounds, it is a question of
how much and how they affect our health.
Sources of Environmental Toxins
Multiple chemical load comes from daily exposure to chemical compounds
in our indoor and outdoor air, food, and water. The EPA's TEAM study
documented the following chemicals to be "ubiquitous" in the air:
p-xylene, tetrachloroethylene, ethylbenzene, benzene,
1,1,1-trichloroethane, and o-xylene. Those listed as "often present" were:
chloroform, carbon tetrachloride, styrene, and p-dichlorobenzene.17
This study found air samples taken with a monitor attached to the study
individuals had higher levels of chemicals in the personal air space over
a 24-hour period than what was recorded in outdoor air samples. These
elevated personal and breath levels were more directly attributable to
indoor air pollution. However, researchers noted persons who visited a
service station or dry cleaner, smoked, or drove a vehicle had elevated
personal exposure and breath levels of solvents. They also found certain
occupations, such as painting or working in chemical or plastic
manufacturing plants resulted in higher exposure levels.
Testing for chemical residues on food, which is routinely done
throughout the world, consistently reveals multiple contaminants. The most
comprehensive testing in the United States is the ongoing FDA Total Diet
Survey.18 While the Total Diet Survey
looks for the presence of many different chemicals, their findings of
chlorinated pesticides are alarming. DDE was found in 100 percent of
samples of raisins, spinach (fresh and frozen), chili con carne (beef and
bean), and beef. Ninety-three percent of American processed cheese,
hamburger, hot dogs, bologna, collards, chicken, turkey, and ice cream
sandwiches contained DDE. DDE was found in 87 percent of lamb chops,
salami, canned spinach, meatloaf, and butter, and in 81 percent of samples
of cheddar cheese, pork sausage, hamburger, white sauce, and creamed
spinach. Of all items sampled, 42 had DDE in 63 percent or more of all
samples. Foods with the highest concentration of DDE, in descending order,
were: fresh or frozen spinach (mean concentration 0.0234 ppm), butter
(mean concentration 0.0195 ppm), collards (0.0126 ppm), pork sausage
(0.0124 ppm), lamb chops (0.0113 ppm) and canned spinach (0.0109 ppm).
Since DDT and DDE have been banned for use in this country since 1972, it
is likely some of this contamination is from produce imported from other
countries where these chemicals are still used
(See Table
2).
Unless these volatile pesticides, such as DDT and toxaphene, get
trapped in the soil, tree bark, or other stable materials, they can begin
a wind-driven leapfrogging around the globe. The more volatile the
chemical, the faster it enters the air and the less readily it enters the
fat of plants or animals it contacts
(See Table
3). DDT is less volatile and tends to stay longer where it lands.
Volatile chemicals applied in tropical regions evaporate into the
atmosphere and then condense in cooler climates. As the ambient
temperature falls, the compound becomes less volatile, slowing the spread
of the compound. In other words, if two forests were exposed to identical
amounts of a volatile pesticide, trees in the colder climate would become
more heavily contaminated.
This global leapfrogging may account for the results of a study on the
diet of arctic indigenous women. The diets of two groups of women (from
the eastern and western Canadian Arctic) were found to be very high in
organochlorine compounds (OCCs). The primary sources of these compounds
were the meat and blubber of ringed seal, walrus, mattak, and narwhal, as
well as caribou, whitefish, inconnu, trout, and duck.19 Since these OCCs
were transported in the air, they landed in the arctic, but due to the low
temperature were unable to volatilize again.
Adverse Immune Effects of Environmental Pollutants (Immunotoxicity)
Environmental chemicals have a wide range of effects on immune system
function, ranging from decreased cell-mediated immunity (with a decrease
in ability to fight infections and tumors) to increased sensitivity
(allergy) and autoimmunity.11,19,20 Among
the OCCs, DDT has been found to have the following effects on the immune
system: reduced killing capacity of polymorphs, reduced number of plasma
responder cells, increased degranulation of mast cells, leukopenia,
decreased phagocytic ability, changes in the spleen, thymus, and lymph
glands, variation in complement, and disturbances in fetal and perinatal
immune regulation. Similar effects have also been found from exposure to
chlordanes (used as termiticides in the United States and Canada until
1978, when they were banned for home use; they are still used on certain
crops and in some seed treatment) and hexachlorobenzene (HCB – a
chlorinated pesticide used as a fungicide, and also found in chlorinated
solvents such as perchloroethylene used in dry cleaning). Studies of
thousands of patients at the Environmental Health Center in Dallas have
shown that persons with two or more OCCs present in their serum have some
form of immunotoxicity.21
Chemicals produced by combustion, the polycyclic aromatic hydrocarbons
(PAH), have similar depressing effects on the immune system, including:
decreased T-cell-dependent antibody response, decreased splenic activity,
diminished T-cell effector functions, suppression of T-cytotoxic
induction, depressed natural killer cell activity, as well as being highly
carcinogenic.22 Organophosphate
pesticides, which are not as biologically persistent as OCCs, are also
toxic to the immune system. They have been found to cause decreased
percentages of CD4 and CD5 cells, increased number and percentages of CD26
cells, increased incidence of atopy and antibiotic sensitivity, and high
rates of autoimmunity. This elevation in autoimmunity is reflected by high
levels of antibodies to smooth muscle, parietal cells, brush border,
thyroid, and myelin, in addition to elevated ANA.23
Similar immunosuppression has also been found for organotins and heavy
metals.22
The mode of exposure to a pesticide appears to have an effect on the
persistence of immunotoxicity, as demonstrated by two polybrominated
biphenyl (PBB) mass exposures. One exposure took place in Taiwan, when
rice bran cooking oil was contaminated with PBBs. This oil was used for
cooking and the persons who used it were found to have immune system
abnormalities. One year after exposure, these persons were found to have
decreased concentration of IgM and IgA (with normal IgG), low T-suppresser
cells, low B-cells, and suppression of delayed hypersensitivity to recall
antigens. When rechecked two years after exposure, the above indices had
returned to normal. This was not the case in Michigan, where a massive PPB
exposure occurred in 1973-74. During that time period a PBB-containing
flame retardant called "Firemaster" was inadvertently sold as an animal
feed called "Nutrimaster." This mistake was devastating to both the
livestock and the humans who raised them and consumed their products.
Exposed individuals were found to have lower levels of circulating
T-lymphocytes and reduced lymphoproliferation response, resulting in
reduced cell-mediated immunity. These individuals also had a high
prevalence of persistent skin, neurological, and musculoskeletal symptoms.24
These changes have persisted on all subsequent studies, which seems to
indicate that when these toxins are concentrated in the food chain before
reaching humans, their effect can be longer lasting.
The development of autoimmunity has been linked with chemical exposure
as well. The notion of chemically-induced autoimmune states is not new,
since many chemicals are known to induce the onset of systemic lupus
erythematosis (SLE). Some chemicals, including formaldehyde and other
volatile organic compounds, are thought to induce tissue-specific
autoimmune reactions by acting as haptens. These low molecular weight
molecules bind to various tissues in the body, making a new antigenic
combination. The immune system then produces antibodies to this new
combination, which can attack the parent tissue with or without the
chemicals being present. Chemically-exposed individuals often present with
elevated antibodies to certain body tissues, including anti-myelin,
anti-parietal, anti-brush border, and anti-smooth muscle antibodies.25
A study of 298 patients with exposure to industrial chemicals showed the
following abnormalities:26
a. NK activity – chemically exposed patients when compared to controls
show either very low activity or very high activity.
b. Lymphocyte blastogenic response to T-cell mitogens (PHA, CONA) and
B-cell mitogens were 30-45 percent lower than controls.
c. Elevated IgG and IgM levels against formaldehyde, trimellitic
anhydride, phthalic anhydride, and benzene. These levels were usually
higher in persons with elevated T4/T8 ratios, noted in almost 15 percent
of the exposed patients.
d. Autoantibodies against their own tissue.
For a good review of the numerous studies on the immunotoxicity of
pesticides, the author recommends the book, Pesticides and the Immune
System; The Public Health Risks, published by World Resources Institute,
in Baltimore, MD. For a broader view of toxin-related autoimmunity, refer
to the papers developed for the Workshop on Linking Environmental Agents
to Autoimmune Diseases.27
Toxin-Associated Cancers
As mentioned earlier, the Davis study1 revealed men born in the 1940s
had twice the cancer incidence as those born from 1888-1897, even when
smoking was factored out. Women born in the 1940s had 50 percent more
total cancers; with 30 percent more cancer not linked to smoking in white
women.
Three studies have shown elevated levels of OCCs in adipose tissue of
breast cancer patients as compared to controls. The chemicals found in
higher amounts in the malignant persons were: DDT, DDE, PCBs, and
hexachlorocyclohexane (HCH – also known as lindane, Kwell shampoo, or BHC,
a chlorinated pesticide commonly used to treat lice infestations).28
-30Not only are these compounds higher in the adipose tissue
of breast cancer patients, but they are actually found in higher levels in
malignant tissue than in adjacent healthy tissue. These studies indicate
that breast tissue concentrates OCCs more than adipose stores in other
body locations. Serum levels of OCCs have also been associated with
increased risk of breast cancer. Elevated levels of DDE and PCB in the
serum can result in a four-fold increased risk of breast cancer,31
although other studies have not found such a correlation between breast
cancer and serum pesticide levels.32,33
The epidemiological association between chemical exposure and childhood
cancers has also been examined
(see Table
4). In one study, 45 childhood brain cancer patients were compared to
85 friend controls. A significant positive association was found between
brain cancer and exposure to No-Pest Strips, termite treatment, Kwell
Shampoo (lindane), flea collars on pets, diazinon use in the garden or
orchard, and the use of herbicides in yards (odds ratio [OR] 6.2). When
compared to 108 cancer controls, a significant positive association was
found between brain cancer and home pesticide bombs, termite treatment,
pet flea collars, and garden use of insecticides, carbaryl, and
herbicides.34
Several other studies have found 2,4-D (a common weed killer) use
around the home was associated with soft tissue sarcomas (OR 4.0).35
Having No-Pest Strips in the home was associated with leukemia (OR 3.0);
insecticide use in the home was associated with brain tumors for ages <20
(OR 2.3); household pesticide use was associated with leukemia (OR 4.0);
garden pesticide use with leukemia (OR 5.6); and, household insecticide
use with non-lymphocytic leukemia (OR 3.5).
For adults the use of chlorophenoxy acid herbicides (such as 2,4-D) has
been strongly associated with increased incidence of lung cancer, stomach
cancer, leukemia, Hodgkin's lymphoma (two studies found a five-fold risk),
non-Hodgkin'[s lymphoma (NHL – five to six-fold increased risk), and soft
tissue sarcomas (many studies have shown a five to seven-fold increased
risk, and one review study reported a 40-fold increased risk).36
2,4-D gained notoriety from its combination with 2,4,5-T to form a mixture
known as Agent Orange. 2,4-D is commonly used by municipalities and states
as a spray on roadways and right-of-ways to inhibit weed growth. It can be
purchased at home stores for home lawn care and is often applied by
chemical lawn care companies. It contains several dioxin contaminates and,
in the author's opinion, is toxic to animals, children, and adults. One
study showed Kansas farmers using herbicides 20+ days per year have six
times the risk of developing lymphoma and soft tissue sarcomas compared to
non-exposed individuals. Those who mixed and applied herbicides and were
exposed 20+ days per year were eight-times as likely to contract NHL.
Other factors associated with increased risk of NHL from 2,4-D exposure
are: (a) increased period of time of exposure;
(b) not using protective equipment;
(c) using backpack or hand sprayers;
(d) employing tractor mounted or mist blower sprayer; and
(e) aerial spraying of herbicides.
Hematological Malignancies
Several studies have associated exposures to solvents with acute
myelogenous leukemia, multiple myeloma, and other forms of leukemia. A
retrospective cohort study of 14,457 workers exposed to trichloroethylene
between 1952 and 1953 showed mortality was raised for multiple myeloma and
NHL in white women.37 In a Finnish study,
workers exposed to 1,1,1-trichloroethylene showed increased cancers of the
cervix and lymphohematopoietic tissues. After 10 years (from first
personal measurement) increased rates of pancreatic cancer and NHL were
seen. At a 20-year follow-up, increased multiple myeloma and cancer of the
nervous system were found. Workers exposed to trichloroethylene showed
(after a 20-year follow-up) an increase in rates of cancers of the
stomach, liver, prostate, and lymphohematopoietic tissues.38
A review article by Fleming and Timmeney revealed there have been 280
cases of aplastic anemia associated with pesticide exposure reported in
the literature. The majority of these cases were young (average age 34)
with a short latency (mean, five months) and had a history of occupational
exposure to pesticides.39 Another study
which examined the cancer risk for painters showed an increased incidence
of multiple myeloma (OR 1.95, 95% CI), bladder tumors (OR 1.52, 95% CI),
as well as kidney and other urothelial tumors (OR 1.45, 95% CI).40
A Swedish study of 275 confirmed multiple myeloma diagnoses found a clear
association between farming and multiple myeloma, with exposure to
chlorophenoxy acid herbicides (2,4-D) and DDT being prime risk factors.41
Neurotoxicity
Most of the major classes of pesticides are neurotoxins by design;
i.e., they kill pests by attacking the nervous system. OCCs affect the
nerve by disrupting ion flow along the axon. Organophosphate pesticides,
which were developed from nerve gas research, and carbamates affect
acetylcholinesterase, resulting in excessive acetylcholine levels in
synapses. Solvents, some of which were originally used as anesthetics,
dampen the propagation and transmission of electrical impulses along nerve
axons. These agents produce various forms of toxic encephalopathy (acute
or chronic, selective or diffuse toxic encephalopathies), as
neuronopathies, axonopathies, myelin-opathies, or vasculopathies.
Neuronopathies can be diffuse or selective, depending on whether
specific neurons are affected, or if the damage is more broadly spread
throughout the nervous system. The target site of toxic agents producing
neuronopathies is the nerve cell body, with the consequence of either
axonal or dendritic breakdown
(See Table
5).
An example of a neurotoxin causing diffuse neuronopathy is
methylmercury, which has been found to preferentially damage the granule
cells of layer IV in the visual cortex, granule cells in the granular
layer of the cerebellum, and sensory neurons of the dorsal root ganglia.22
This results in neuronal degeneration progressing to necrosis with axonal
dystrophy and demyelination. Another example is aluminum, which has been
found to cause fatal dialysis encephalopathy following 3-7 years of
intermittent dialysis. Although brain aluminum levels were elevated, there
was no evidence of neurofibrillary tangles in these patients, indicating
the presence of aluminum alone is insufficient to lead to senile dementia
of the Alzheimer's type.
The neuronopathies can also be selective, affecting only certain
neurons. Examples of agents causing selective neuronopathies include
doxorubicin (Adriamycin), which affects the dorsal root ganglia;
cisplatin, which affects sensory neurons; and manganese (metal fume
fever), which produces a Parkinson-like syndrome. Manganese-induced damage
is found in the substantia nigra, globus pallidus, and caudate nucleus,
with depletion of dopamine and serotonin levels. Symptoms begin as
psychiatric changes, followed by impaired motor activity with muscle
rigidity and tremors. Parkinsonism can also be caused by MPTP, an illicit
synthetic opioid derivative.42 This
compound can cause sudden Parkinson-like symptoms after exposure. MPTP is
metabolized in monoamine oxidase (MAO)-containing tissues to MPP+, the
ultimate neurotoxin to MAO-containing tissues. MPP+ is selectively toxic
to substantia nigra cells, effectively knocking out dopamine production.43
The area of the axon affected differentiates axonopathies. The proximal
axon is different in its ability to initiate action potentials and
synthesize protein. Damage to this part of the axon is referred to as
proximal axonopathy, and is the type of damage seen in amyotrophic lateral
sclerosis (ALS). Proximal axonopathies are often caused by volatile
organic compounds (halomethane, methylene chloride, carbon tetrachloride,
and butane), all of which decrease the excitability of the neuron by
stabilizing membranes and decreasing ion flux. Distal axonopathies have
been shown to be caused by a variety of compounds, including acrylamide (a
polymerizing agent used to strengthen paper), which primarily affects
sensory fibers. Carbon disulfide (a solvent for fats and lacquers and for
extraction of oil from olives, palmstones, and other oil-bearing fruits),
affects sensory and motor fibers. Hexacarbon solvents lead to multifocal
distal progressive sensory-motor axonopathy with giant axonal swelling;
paranodal demyelination of swollen axons occurs frequently with exposure
to these solvents. Organophosphate pesticides (parathion, malathion,
diazinon, etc.) destroy available acetylcholinesterase by phosphorylation,
which is irreversible (unless an antidote is given within 24 hours).
Exposures may be additive and the effects can last until more
acetylcholinesterase is synthesized. Carbamates (carbaryl, sevin,
aldicarb) carbamylate the acetylcholinesterase, which is reversible since
it is not a stable bond and can be hydrolyzed easily.
Myelinopathies are caused by organotins, which are used as stabilizers
in plastic polymers and catalysts in silicon and epoxy curing. They are
also used in wood and textile preservation as fungicides, bactericides,
and insecticides. Examples of organotins are TET and TMT. Hexachlorophene
(HCP), added to soap for antimicrobial action, also causes myelin damage.
It is readily absorbed through intact skin and mucus membranes, and like
TET and TMT can cause blurred vision and muscular weakness, progressing to
paralysis. The optic nerve is particularly susceptible to HCP and to
particular solvents such as ingested methanol and ethanol, inhaled
trichloroethylene, toluene, CS2, and benzene. Other solvents can lead to
specific myelinopathies; for example, the trigeminal nerve is especially
sensitive to trichloroethylene (found in dry cleaning fluid). Hearing loss
is commonly caused by toluene, styrene, xylene, and trichloroethylene,
which cause myelin damage to the vestibulocochlear nerve. Other toxins,
such as carbon monoxide and Cuprisone (a copper-chelating agent used in
the treatment of Wilson's disease), are examples of toxins affecting the
maintenance of myelin.
Endocrine Toxicity
In addition to the well-documented estrogenic effects of OCCs, actual
damage to the endocrine organs can also occur. The most common symptoms of
toxic damage to the endocrine system are:
(a) sleep disturbances or changes in energy level or mood;
(b) alterations in weight, appetite and bowel function;
(c) sexual interest and function change; in females any menstrual
change;
(d) changes in temperature perception, sweating, or flushing; and
(e) alteration of hair growth and skin texture.
With the exception of reproductive effects, most of these endocrine
symptoms occur only after immunological and/or neurological symptoms are
already present.
Aliphatic solvents, such as n-hexane, cause necrosis of zona
fasciculata and zona reticularis of the adrenals, where glucocorticoids
are produced. OCCs and carbamates have demonstrated histological changes
to these areas in animal models.22,44
Cadmium and carbon tetrachloride have both been shown to cause
non-specific inhibition of steroidogenesis. Occupational lead workers
showed decreased secretion of glucocorticoids (17-hydroxy) and androgenic
steroids (17-keto). In these persons, the lesion was apparently at the
hypothalamus/pituitary level, because a normal ACTH response was found
with stimulation.22 Dioxins and mirex
(used to treat fire ants) caused direct suppression of glucocorticoid
synthesis, resulting in hypoglycemia.45
The thyroid is not immune to environmental toxins, as many chemicals
can cause a reduction of both T4 and T3 levels. Inducers of hepatic
cytochrome P450, such as phenobarbitol, benzodiazepines, calcium-channel
blockers, steroids, retinoids, chlorinated hydrocarbons, and
polyhalogenated biphenyls can lead to reduction in T4. Phenobarbitol and
PCBs (found in 83 percent of NHATS samples, ranging up to 1,700 ng/g) have
both been shown in animal models to increase the activity of hepatic
UDP-glucuronyl transferase, leading to increased bile flow and biliary
excretion of tyrosine-glucoronide. Feeding PCB to rats produced a
dose-dependent significant reduction in serum T4 levels, along with marked
hypertrophy and hyperplasia of thyroid follicular cells compared to
controls. Rats exposed to soil, dust, and air extracts of landfill
containing the dioxins TCDD, PCDD, and PCB showed reduced total serum T4
in a dose-response relationship.46
Animals fed a diet of fish from the Great Lakes have also exhibited
thyroid dysregulation.47
Depressed thyroid function has been correlated with exposure to lead,
carbon disulfide, and PBBs. It appears the decrease in thyroid hormone
secretion in lead workers is secondary to problems with the hypothalamus.
In Michigan, PBB-exposed persons showed non-goitrogenic thyroid
dysfunction. PCBs are structurally similar to thyroid hormones (both are
polyhalogenated compounds with two phenolic rings), allowing them to
interact with thyroid hormone receptors, binding proteins, and transport
systems. Depending on the dose and the congener, they could either
facilitate or impede thyroid-hormone-directed gene regulation.
Hydroxylated PCBs (PCBs that have undergone phase-I biotransformation)
have actually been shown to bind to transthyrethrin (serum binding
protein) with a higher affinity than thyroid hormones. They can change the
kinetics of thyroid hormone transport within the circulatory system or
across target-cell membranes and exhibit T3-like or anti-T3-like
properties. They can also interfere with the intracellular production of
T3. For infants exposed to PCBs this can have a devastating effect on
neurological and anatomical development.48
In addition to causing reduced functioning, some compounds such as
polycyclic hydrocarbons, nitrosamines, and other compounds can initiate
thyroid carcinogenesis. A common component of permanent hair dye
preparations, 2,4-diaminoanisole sulfate (2,4-DAAS), when fed at high
doses caused a 58-percent incidence of thyroid neoplasm in male rats and
42-percent incidence in females, compared to 7-8 percent in controls.22
The effects of environmental chemicals, especially the estrogenic OCCs,
are well documented. While many were found to be estrogenic, when combined
their estrogenicity can increase as much as 1,600 times. Some combinations
also cause previously non-estrogenic compounds to become estrogenic.49
The facts about environmental estrogens have been cogently discussed in
Coburn, Dumanski, and Myers' recent book, Our Stolen Future.50
There are also non-estrogenic toxic effects of OCCs on male and female
reproduction. High levels of OCCs in the serum have been strongly linked
to infertility, stillbirths, and miscarriages.51
Urban air pollution has been associated with reduced male fertility.52
While there appears to be a worldwide decline in the sperm levels of
males,53 organic farmers have very high
sperm density.54 This gives rise to the
theory that exposure to environmental chemicals will lower sperm levels,
and avoidance of such chemicals may help return the levels to normal.
There have been multiple studies on sperm counts related to one
agricultural OCC, dibromochloropropane (DBCP). Exposure to DBCP can lead
to azospermia and severe oligospermia.55
This effect on fertility may be only associated with DBCP or it may serve
as a model for other OCC-induced spermatogenesis problems.
Summary
Humans are now struggling under a burden of multiple environmental
toxins. For many individuals, this is not from workplace exposure, but
from simply living in a polluted world. Some individuals appear to be less
able to clear the daily chemical exposure from the body than others,
leading to a total load of toxins that exceeds the ability of the body to
adapt. When the toxic load reaches this point, damage to certain organ
systems can occur. The major organ systems affected are the immune,
neurological, and endocrine systems. Immunotoxicity may be the major
factor in the increasing rates of asthma, allergies, cancers, and chronic
viral infections. Neurological toxicity can affect cognition, mood, and
cause chronic neurological illnesses. Endocrine toxicity can affect
reproduction, menses, libido, metabolism, stress-handling ability, glucose
regulation, and other important functions. While this all seems
overwhelming, there are ways to approach these problems. Subsequent
articles in this series on environmental medicine will address chemical
classes and what can be done to help deal with their toxic effects.
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