Chlorinated Pesticides: Threats To Health and Importance of Detection

Copyright 2009 Thorne Research, Inc. All Rights Reserved. No Reprint Without Written Permission.
Alternative Medicine Review Volume 14, Number 4 2009

Page 347
Environmental
Medicine
Walter Crinnion, ND 1982 graduate of Bastyr University; practice since 1982
with a special focus on treating chronic diseases caused by environmental toxic
burden; conducts post-graduate seminars in environmental medicine; professor
and Chair of Environmental Medicine, Southwest College of Naturopathic
Medicine; contributing editor, Alternative Medicine Review
Email: [email protected]
Abstract
Although chlorinated pesticides have been mostly banned
from use in the United States, their persistent presence in
the environment poses an ongoing threat to health. Because
of the lipophilic nature of chlorinated pesticides, they are
bioaccumulative and difcult to excrete from the body. A
select group of these xenobiotics is also associated with a
wide range of health problems, identication of which would
aid in disease prevention and reversal. Ongoing research by
the Centers for Disease Control and Prevention now provides
national standards for some of these compounds, allowing
the clinician to evaluate levels in a patient. Serum samples
are easily obtained and can reveal the presence of these
xenobiotics. Eight of the most commonly found and harmful
chlorinated pesticides are reviewed in this article, along with the
most common sources of exposure and possible action steps.
(Altern Med Rev 2009;14(4):347-359)
Introduction
Multiple studies over recent decades have ex-
amined the presence of xenobiotic substances in the
blood or adipose tissue of a variety of subjects. A num-
ber of these compounds, including the chlorinated pes-
ticide dichlorodiphenyltrichloroethane (DDT) and the
industrial polychlorinated biphenyl (PCB) compounds,
are stored in the fat tissue of the body and, instead
of being easily excreted, continue to bioaccumulate
over time. A portion of these fat-soluble compounds
is passed from mother to child; thus, all new life starts
with a toxic load. Te load is increased incrementally
Chlorinated Pesticides: Treats
to Health and Importance of
Detection
Walter J. Crinnion, ND
through eating, drinking, and breathing, increasing the
total toxin burden during the aging process.
Te Environmental Working Group (EWG)
(www.ewg.org) funded and published two studies that
specically tested adults and newborns in the United
States to see how many toxins were carried. Te EWG
originally tested nine adults, none of whom worked in
industries that would ordinarily expose them to high
levels of environmental poisons.
1
Te nine adults in the
EWG study had an average of 91 of the 210 toxic com-
pounds that were tested present in serum, including an
average of 33 PCBs and four chlorinated pesticides.
Since these compounds can be passed from
mother to child, the EWG designed another study to
measure how many chemicals would be found in a ran-
dom sampling of cord blood from infants in the United
States. Te EWG newborn study looked for the pres-
ence of 413 dierent xenobiotic chemicals in the cord
blood of 10 infants born in U.S. hospitals in 2004.
2
A
total of 287 toxic compounds were found in the cord
blood samples, including 147 PCBs and 21 chlorinated
pesticides.
While these types of articles are alarming, they
do not help the clinician determine whether a patient is
carrying an abnormally high load of a particular toxin,
or whether the toxin is one that carries documented
health risk. To answer the rst question, the Centers
for Disease Control and Prevention (CDC) has been
conducting ongoing studies to identify the toxic burden
Environmental Medicine
Page 348
carried by U.S. residents. Tey have pub-
lished three reports to date that are avail-
able at http://www.cdc.gov/exposurere-
port/report.htm. When a new study is
published more compounds are added to
the list for testing. Within a few years the
number will exceed the total number of
toxins the EWG has measured, and will
include a greater number of individuals.
Not only does the CDC report
provide national normal ranges, but the
majority of these compounds are mea-
sured both as total parts per billion (ppb)
in the serum as well as a lipid-adjusted
value of ng/g of lipids.
3
Te levels re-
ported in ppb are reective of the amount
of the toxin present in the serum, mostly
found in the cholesterol and albumin frac-
tions.
4
Te lipid-adjusted value provides a
more accurate picture of the total burden
of these toxins residing in adipose tis-
sue throughout the body.
5
Te amounts
stored in adipose tissue are a result of bio-
accumulation over a lifetime.
Serum levels reect the recircula-
tion of toxins released from the adipose
tissue from lipolysis. If the individual
being tested is going through increased
lipolysis due to stress, rigorous exercise,
saunas, or weight loss, serum levels may
be higher due to increased lipolysis, as a
portion of these toxins accompanies cho-
lesterol and triglycerides released from the
bodys fat stores. Increased levels, however,
can also be reective of current exposures
either from air or food sources.
Using the lipid-adjusted value
(measuring the amount of lipids present
in the blood and adjusting the amount of
toxins to that lipid burden), an accurate
assessment of the amount of stored tox-
ins can be obtained, allowing an individual
following a cleansing protocol to monitor
progress in reducing overall burden of
these persistent and accumulating toxins.
5
Table 1 lists the most common
chlorinated pesticides found in the CDC
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Chlorinated Pesticides
Page 349
report. Also, by comparing the two values (ppb in serum
and ng/g lipids), current exposure can be more readily
determined (high in serum, but the lipid-adjusted value
shows low or no stores of this compound).
Common Findings with Serum Testing
of Chlorinated Pesticides
Close to 100 percent of all persons tested will
have p,p-dichlorodiphenyldichloroethylene (p,p-DDE)
in their serum. In a study of 5,994 individuals in Tex-
as, researchers found that increasing age, residing on a
farm, and being male increased the risk for a chlorinated
pesticide burden.
6
Te levels of p,p-DDE found in this
group are shown in Table 2.
Te CDCs reported mean levels of DDE are
1.57 ppb and 250 ng/g of lipids. One can also readily
observe from the above CDC chart that, in addition to
DDE, some individuals will also have the chlordanes
oxychlordane and trans-nonachlor. William J. Rea, MD,
at the Environmental Health Center in Dallas, has ob-
served that when individuals have more than one chlo-
rinated pesticide present in their blood, they will have
some type of immunotoxicity eect.
7
Adverse Eects of Chlorinated
Pesticides
Chlorinated pesticides as a class are insecti-
cidal primarily via the neurotoxic action of disrupting
ion ow, thus interfering with axonal transmission. Tis
leads to over-stimulation of the nerves with un controlled
neuronal discharge. Acute toxicity (poison ing) signs
and symptoms of chlorinated compounds (headache,
nausea, vomiting, hyperesthesias, irritability, confusion,
convulsions, respiratory depression, cardiac arrhyth-
mias, aplastic anemia, and porphyria cutanea tarda)
8

are rarely seen as these compounds have mostly been
banned from use since the 1980s. However, since they
are fat-soluble and tend to bioaccumulate, they can
cause a variety of health problems that often begin slow-
ly. Te eects of these compounds are most often seen
secondary to mitochondrial toxicity in the neurological,
immunological, and endocrinological systems, although
they can also aect the cardiovascular, respiratory, gas-
trointestinal, and other bodily systems.
Tese organochlorine compounds, with the
exception of dieldrin, have
been shown to induce the
function of 1A and 2B cy-
tochromes, which increases
the production of free radi-
cals and reduces glutathi-
one levels (needed to clear
phase 1 metabolites from
the body).
9
Te adverse health
eects of the specic com-
pounds listed in the discus-
sion below under each ana-
lyte are those that have been
documented in the medical
and scientic literature for that specic compound. Te
health eects across compounds can be very similar,
and many of the studies review a number of analytes
together, many of which have been found to be causative
agents.
Chlorinated Compounds with the
Greatest Documented Health Impact
Te following compounds are those associated
with the greatest amount of documented adverse health
eects in the published medical and scientic literature.
With the exception of hexachlorobenzene, they are also
the most commonly found pesticides in the CDC Tird
National Report.
Table 2. Levels of Chlorinated Pesticides in a Texas Study
6
Compound
p,p-DDE
p,p-DDT
Frequency of finding
99.5%
10.5%
Range
1 ppb up to 378.6 ppb
Organochlorine Compounds in the Serum of 5,994 Persons
Page 350
Hexachlorobenzene (HCB)
HCB is a byproduct of chemical solvents, oth-
er chlorine-containing compounds, and pesticide man-
ufacturing. Small amounts of HCB can be produced
by combustion of waste and other compounds. HCB
is an industrial byproduct of the chlor-alkali and wood
preservative industry. Hexachlorobenzene was widely
used as a pesticide until 1965, but is no longer used
commercially in the United States. HCB was also used
as a fungicide for control of mold and fungi in cereal
grains, primarily wheat. Te CDC study did not nd
HCB often enough to establish any standards, so the
presence of any level of HCB is considered abnormal
and actionable.
HCB is the only compound reviewed here not
found commonly in the CDC study, but is included in
this discussion because of its serious health eects when
present.
Exposure Sources of HCB
Te CDC estimates the average exposure to
HCB from foods is 1 mcg/kg body weight. Te foods
in which HCB was found most commonly, as a part of
the Food and Drug Administrations Total Diet Survey,
are mostly from the beef/dairy industry, with 25 per-
cent of ground beef, 66 percent of non-organic butter,
and 18 percent of American cheese samples contain-
ing HCB.
10
HCB was also found in 41 percent of lamb
chops and 50 percent of Atlantic salmon (farmed). Of
these, the highest levels were found in non-organic but-
ter. High blood levels may also be caused by industrial
exposure, such as living close to a waste facility. To help
assess these exposure sources one can utilize the data-
bases at www.scorecard.org and http://www.epa.gov/
epahome/commsearch.htm.
Adverse Health Eects from HCB
Te following is a list of the adverse health ef-
fects of HCB exposure.
Diabetes risk is increased (odds ratio [OR]
4.5) by the presence of HCB.
11
Childhood obesity is increased (OR 2.5-3.0)
with maternal serum levels of HCB.
12
Testicular cancer rates are higher in men (OR
4.4) whose mothers had high serum HCB levels.
13
Reduction of total T4 occurs with increased
levels of HCB (T4 dropped 0.32 mcg/dL per each
unit increase [in ng/mL] of HCB).
14
Increased rates of soft-tissue sarcomas and
thyroid cancers occur in persons living close to an
industry that emits HCB.
15
Porphyria with neurological manifestations
can result from HCB exposure.
16
Risk for childhood otitis media (OR 2.38) is
increased when HCB is present along with DDE.
17
Epstein Barr early antigen and risk for non-
Hodgkins lymphoma (OR 5.3 with above median
levels of HCB) increase.
18
HCB exposure may be related to increased risk
of autoimmunity (animal study evidence).
19
Chronic fatigue syndrome patients have higher
levels of HCB and/or DDE.
20
HCB can suppress gamma-interferon
production.
21
Heptachlor Epoxide (HCE)
Heptachlor and its metabolite heptachlor ep-
oxide (HCE) are chlordanes, a group of chlorinated
compounds used agriculturally until 1974 and as ter-
miticides commonly throughout North America until
1988. Bacteria in the soil, as well as the livers of hu-
mans and animals, can transform heptachlor through
cytochrome 1A1 (phase 1) to the much more toxic
and biologically persistent epoxide form. Once a house
has been treated with chlordane, the chlordanes can be
found in dust for the life of the home, contaminating
anyone living in the home who breathes the dust. Hep-
tachlor is still approved for the treatment of re ants in
underground transformers.
Exposure Sources of HCE
A major source of exposure is living in a home
built before 1988 in which chlordanes were applied in
the crawl-space under the house where the furnace or air
conditioning ducts now run. If those ducts have leaking
connections (common in older duct work), the chlor-
dane-contaminated dust can be sucked into the pipes
and distributed throughout the house. Tis can occur
no matter what grade of lter is on the furnace, because
the contamination occurs post-lter. Since heptachlor
Page 351
and HCE stick to soil and dust, another source comes
from tracking dirt into a building from outdoors. In
many areas of the country, former orchards or farmland
have been turned into housing developments. Te ar-
eas where heptachlor was used before 1974 include soil
contaminated with HCE that can make it into the dirt
and dust of the home, especially homes where shoes are
worn indoors and that have wall-to-wall carpeting to
which HCE can adhere.
Te next greatest source of exposure is through
foods, typically seafood, dairy, meats, and poultry. In
the Total Diet Survey,
10
the foods highest in heptachlor
epoxide are very similar to those in which HCB was
found. Fifty percent of the butter samples (non-organ-
ic) contained HCE. It was also found in 34 percent of
cream cheese and salmon steaks (farmed Atlantic salm-
on), 32 percent of ground beef, and 30 percent of Swiss
and cheddar cheese samples. Interestingly, 25 percent of
samples of Hubbard squash also contained HCE.
Chlordanes have been found in all studies of
breast milk in North America. Tus, children may ex-
perience transplacental transfer of chlordanes as well as
breast milk exposure.
Adverse Health Eects of HCE
Te following are adverse health eects of
HCE.
HCE is a powerful pro-oxidant and dicult to
clear through normal phase 2 detoxication.
High maternal levels of HCE lead to increased
rates of cryptorchidism in male ospring.
22
HCE has demonstrated the ability to be
an initiator, promoter, and progressor of breast
cancer.
23,24
Higher HCE blood levels increase risk of non-
Hodgkins lymphoma (third quartile levels [OR
1.82]; fourth quartile levels [OR 3.41]).
25
HCE is neurotoxic to the dopaminergic system
and may lead to increased risk for parkinsonism.
26
HCE presence, along with other chlorinated
compounds, can lead to increased risk of
atherosclerosis.
27
Oxychlordane
Oxychlordane is the major metabolite of the
various chlordane and nonachlor compounds used ag-
riculturally until 1974 and residentially until 1988. It is
found commonly in all persons living in North America
when serum levels are tested. As a human metabolite, it
has not been found in food, since it is produced by the
liver after exposure to chlordanes and nonachlors from
air, water, or food. Tis metabolite is eight times more
toxic than its parent compounds and is more bioaccu-
mulative.
28
Exposure Sources of Oxychlordane
See the above list for HCE, as all the chlor-
danes were often present together in whatever mixture
was used agriculturally or residentially.
Adverse Health Eects of Oxychlordane
Adverse health eects of oxychlordane include
the following.
Increased risk of diabetes (OR 14.7) with high
levels of oxychlordane.
29
Increased risk of non-Hodgkins lymphoma
(OR 2.68).
30
Increased risk for seminoma (testicular germ
cell tumor) (OR 1.63).
31
Increased risk of prostate cancer.
32
In vitro evidence of immunosuppression of
cell-mediated immune response to pathogens.
33
Decreased natural-killer cell ability to lyse
tumor cells.
34
Trans-Nonachlor
Trans-nonachlor is another of the major chlor-
dane compounds used agriculturally from 1953-1974
and as a termiticide until 1988.
Exposure Sources of Trans-Nonachlor
Te same exposure sources listed for the other
chlordanes also apply here. Te most likely source is ex-
posure to dirt or dust that is already contaminated with
it, especially in homes built before 1988 that have the
original ductwork still intact. Unfortunately, there were
a number of individual homeowners who chose to ap-
ply chlordane themselves, and, in these cases, chlordane
may be inside the home itself.
Page 352
Dietary sources of trans-nonachlor were sur-
prisingly few in the Total Diet Survey, with the most
frequent nding being in sweet cucumber pickles (25%
of samples), rather than dairy and beef like the other
chlordanes. Trans-nonachlor is found in most persons
tested for it.
Adverse Health Eects
Te following are adverse eects associated
with trans-nonachlor exposure.
Te adverse eects of the chlordanes are all
very similar. Many of the cancer and other adverse
health associations are found with trans-nonachlor
as well, but at diering levels of risk (dierent odds
ratios).
Exposure to trans-nonachlor results in
increased risk of obesity and diabetes, with the
highest odds ratio for diabetes of the organochlorine
compounds (OR 37.7).
29
DDE
DDE, a DDT metabolite, is the most ubiqui-
tous and abundant of the chlorinated pesticides.
6
When
DDT is produced, it consists of a combination of both
DDT and DDE. Te rate of breakdown in the envi-
ronment (in temperate climates the half-life of DDT in
soil is 20-30 years) is measured by the changing ratios
of DDE to DDT. Once in the human body, DDT is
broken down to DDE within about six months. Many
published research articles use the term DDT or total
DDT to include DDT, DDE, and DDD. Since DDE is
the most commonly found DDT compound, the main
aspects of the DDTs will be reviewed under DDE.
DDT was rst synthesized in 1874. Its pesti-
cide ability was discovered in 1939 and used in wartime
to control typhus and malaria. It was put into agricul-
tural use in the United States in 1945 and banned from
use in 1972. Production in this country, however, was
not banned so it was still manufactured and sent to
other countries, often as part of U.S. agricultural aid.
Te DDTs are found throughout the globe, including
the Arctic and Antarctic, because they have been carried
on the winds across the planet.
Te DDTs are highly lipid-soluble and are
stored in the lipid-rich tissues of the body, includ-
ing adipose tissue, the liver, and the brain. It has been
estimated that 1 ppb DDT in serum means 5-10 ppb in
brain, 47 ppb in liver, and 100-300 ppb in fat cells. DDE
has been found in all samples of breast milk around the
world. Unfortunately, the level of DDE in some of these
samples exceeds what is allowed to be sold commercial-
ly in any other milk product.
35
Exposure Sources of DDE
Te diet is the major source of exposure to
DDE/DDT. From 1986-1991, adults in the United
States consumed an average of 0.8 mcg of DDT daily.
Te largest amount of dietary DDT comes from meat,
poultry, dairy products, and sh, including sport sh.
A number of fresh-water sh advisories in certain lakes
and rivers in the United States are posted because of
DDT contamination of trout and other sh. Leafy veg-
etables often contain more DDT than other vegetables,
possibly because DDT in the air is deposited on the
leaves. Infants can be exposed by drinking breast milk.
Te most recent Total Diet Survey assessment
of DDE in food reveals that DDE is one of the most
ubiquitous toxins in foods.
10
Table 3 shows those foods
in which it was found commonly in this survey. In each
percentage grouping, the most contaminated foods are
listed rst.
A listing of the 10 foods with the highest DDE
content according to this survey are:
Catsh (farm-raised)
Butter (non-organic)
Spinach (non-organic)
Atlantic salmon (farm-raised)
American cheese
Lamb chops
Collard greens (non-organic)
Cream cheese (non-organic)
Quarter-pound cheeseburger
Cheddar cheese (non-organic)
Te other main source is DDE-contaminated
dust or dirt in a home. Tis could occur in an older
dwelling where DDT was used or in newer housing de-
velopments built on or around previously contaminated
soil. Toxic levels can also come from airborne contami-
nation when DDE/DDT is used agriculturally in other
parts of the world and makes its way across the globe
on the winds.
Page 353
Table 3. Common Food Sources of DDE
10
Catfish (farm raised)
Butter (non-organic)
Spinach (non-organic)
Salmon steaks (farmed Atlantic)
American cheese, processed
Cream cheese
Candy bar, chocolate, nougat, nuts
Quarter pound cheeseburger
Meatloaf (homemade)
Quarter pound burger
Lamb chops
Sour cream
Fast food egg, ham, biscuit breakfast
Pizza, pepperoni
Ground beef
Pizza, cheese
Collard greens, non-organic
Hot dogs
Half-and-half
Vanilla ice cream
Lasagna, beef
Cheddar cheese
Peanut butter, creamy
Baked potato, with peel (non-organic)
100%
100%
100%
100%
100%
100%
100%
98%
98%
98%
95%
93%
93%
93%
91%
90%
89%
89%
82%
80%
80%
77%
75%
73%
0.032
0.02
0.01
0.008
0.006
0.004
0.001
0.004
0.002
0.002
0.005
0.0028
0.0024
0.0012
0.002
0.0015
0.0045
0.002
0.002
0.0012
0.0008
0.003
0.0016
0.0013
Food
Percentage of samples
positive for DDE
Mean concentration
of DDE in ppm
Page 354
Sport shing is another potential source of
DDE exposure for persons who consume their catch.
State regulatory agencies periodically issue advisories
for toxic sh present in their waterways. Anyone plan-
ning on shing in a particular state, including coastal
waterways, should avail themselves of this information
before consuming the catch.
All children are exposed in utero and via breast
milk if breast fed.
Adverse Health Eects of DDE
In general, DDE causes ongoing neurological
problems (including cognitive diculties, headaches,
and depression), along with immune and endocrine
problems. Various cancers are also associated with DDE
presence. Breast cancer is not listed below because there
have been, and continue to be, published articles that do
show a correlation and others that do not. One intrigu-
ing study reported that when DDT exposure occurred
before age 14, those women have higher rates of breast
cancer.
36
Other health risks include the following:
Prenatal exposure to DDE causes hyporeexia
37

and attention problems
38
in infants. Exposure
while breastfeeding can cause delays in mental and
psychomotor development identiable at the age
of 13 months.
39
In utero exposure can also cause
impairment of cognitive skills still evident when the
infants become preschoolers.
40
Prenatal exposure to DDE, HCB, and dieldrin
increases the risk of otitis media, and higher levels
increase the risk of recurrent otitis media.
41
Prenatal DDE exposure increases the rate
of asthma in children (relative risk of 2.6 for the
highest levels of DDE).
42
DDE increases the rate of mast-cell
degranulation and increases risk of allergy and
asthma.
17,43,44
Elevated serum DDE signicantly reduces
mitogen-induced lymphocyte proliferation
response,
45
resulting in cell-mediated immune
deciency and possible increased risk of herpes
zoster.
46
DDE (and other chlorinated pesticides) are
found in higher levels in the substantia nigra in
persons with Parkinsons disease,
47
and in vitro have
been found to disrupt the transport of dopamine in
the brain.
48
DDE and HCB are associated with chronic
fatigue syndrome.
20
DDE is associated with higher rates of type 2
diabetes.
11,49
DDE is associated with a 71-percent increased
risk of developing testicular germ cell tumors.
31
Persons with above-median levels of DDE
(and other chlorinated compounds) may have
increased risk of developing pancreatic cancer,
50

and are prone to signicantly shorter survival times
should they develop the disease.
51
High DDE levels almost double the risk (OR
1.9) for endometrial cancer.
52
DDE and other environmental endocrine
disruptors have been associated with increased
rates of precocious puberty.
53
High concentration of DDE is associated
with preterm births and small-for-gestational-age
babies.
54
DDE was the most frequently found chlorinated
compound in a study of infertile females and their
male partners, with the highest residue levels being
negatively associated with fertilization.
55
DDE levels are associated with multiple
abnormalities in semen indices and sperm count,
motility, and quality.
56
DDE toxicity can lead to early menopause.
57
DDE is associated with greater risk of
endometriosis and reduced functioning of natural-
killer cells.
58
DDE exposure in utero can lead to altered
levels of thyroid hormones.
59
DDT
Refer to the above section on DDE. Te sourc-
es of DDT are similar, except DDT is present in much
smaller quantities. High DDT levels are associated
with a greatly elevated risk for liver cancer.
60
Te health
problems of DDT exposure, on the whole, are virtually
identical to those of DDE. Te main dierence is the
frequency with which DDE and DDT are found and
their respective levels. While a small amount of DDT
Page 355
is found in the adipose tissue of almost everybody, it is
rarely found in the serum. Due to the time it takes for
DDT to be metabolized to DDE in the body, detection
of DDT in the serum typically indicates current expo-
sure (probably from food sources) within the preceding
six months. In the Total Diet Survey the greatest source
of DDT was non-organic spinach.
10
Dieldrin
From the 1950s until 1970, dieldrin and a sim-
ilar compound aldrin were used extensively as insecti-
cides on crops such as corn and cotton. Tey were both
approved by the U.S. Environmental Protection Agency
in 1972 for killing termites and were used as such until
1987. Aldrin is metabolized into dieldrin after entering
the body or the environment (where sunlight and bac-
teria bring about the production of dieldrin). Dieldrin
does not break down in water and is not easily volatil-
ized to release into the air. It attaches very strongly to
soil, sediment, and dust particles, and can be taken up
by plants and stored in leaves and roots. Fish or animals
that eat dieldrin-contaminated materials store a large
amount of it in fat tissue. Animals or sh that eat other
animals have fat levels of dieldrin many times higher
because of bioaccumulation. Humans, at the top of the
food chain, are the nal repository for dieldrin.
Exposure Sources of Dieldrin
Te most common exposure to aldrin and diel-
drin occurs from contaminated foods, including sh
or shellsh from contaminated lakes or streams, root
crops, dairy products, and meats. Exposure to aldrin
and dieldrin also occurs from water, air, or contact with
contaminated soil at hazardous waste sites (check for
these at www.epa.gov). Individuals with the greatest
potential for exposure include those who live in homes
previously treated for termites using aldrin or dieldrin,
because exposure to these toxins can occur years after
they were applied.
Squash, cucumber, and zucchini plants have
the ability to take up aldrin and dieldrin from the soil,
where it accumulates in the portion we typically eat.
61

Tis is reected in the 10 foods listed in the Total Diet
Survey
10
as having the highest levels of dieldrin. Even
organic vegetables will contain high levels of these tox-
ins if grown in soil contaminated decades earlier by
aldrin or dieldrin. While these plants can be used to
remove such pesticides from the soil, it is not recom-
mended to eat or compost them. Te following are the
10 foods with the highest levels of dieldrin according to
the Total Diet Survey.
Summer squash (0.007 ppm)
Hubbard squash (0.005 ppm)
Dill cucumber pickles (0.004 ppm)
Sweet cucumber pickles (0.003 ppm)
Raw, peeled cucumbers (0.003 ppm)
Pumpkin pie (0.0024 ppm)
Atlantic salmon (0.002 ppm)
Cream cheese (0.0008 ppm)
Creamy peanut butter (0.00076 ppm)
Cheddar cheese (0.0007 ppm)
Adverse Health Eects of Dieldrin
Te following are the most signicant adverse
health eects of dieldrin exposure.
Dieldrin disrupts dopamine transport in the
brain.
48
Dieldrin increases oxidative damage in the
brain (nigrostriatal pathway),
62
and may lead to
increased rates of parkinsonism.
63
A signicant
association has also been observed between
dieldrin toxicity and already-diagnosed Parkinsons
disease.
64
Dieldrin is associated with increased rates of
hypothyroidism.
65
Dieldrin adversely aects the Leydig cells,
reducing their production of testosterone, which
could contribute to infertility.
66
Dieldrin is associated with increased rates of
lung cancer,
67
breast cancer,
68
and non-Hodgkins
lymphoma.
25
Dieldrin may increase risk of pancreatic cancer
mortality.
69
Dieldrin increases superoxide production and
causes neutrophil inammation.
70
Mirex
Mirex was used as a pesticide to control re
ants, mostly in the southeastern United States until
1978. It was used as a ame retardant additive under
the trade name Dechlorane in plastics, rubber, paint,
Page 356
paper, and electrical goods from 1959 to 1972. Mirex is
found attached to soil and dust, like many of these other
compounds.
Once in the bloodstream, mirex is carried to
many parts of the body where it is stored, mainly in fat.
Mirex is not broken down in the body by biotransfor-
mation processes.
Exposure Sources of Mirex
Te most likely way for the general population
to be exposed to mirex is by eating food, particularly
sh, taken from contaminated waters. Currently, three
states (Ohio, New York, and Pennsylvania) have issued
warnings that sh (primarily caught in Lake Ontario)
may contain mirex. Te FDAs Total Diet Survey has
not measured other foods for mirex; thus, exposure
sources are not clearly delineated.
Adverse Health Eects of Mirex
In rodents, mirex causes liver, adrenal, and
blood cancer. In humans it causes trembling, tiredness,
weakness, increased oxidative damage, and neurological
and immunological problems.
72
Most of the published
studies examining adverse health eects of mirex were
conducted while studying a number of chlorinated com-
pounds. As a single agent, it has not been well studied so
no specic articles are noted.
Te Presence of Multiple Chlorinated
Pesticides
Most of the studies referenced in this article re-
viewed multiple chlorinated compounds. Some studies
demonstrate synergism and some show adverse health
eects due to the total toxic load. Te studies that have
not shown one compound as more damaging than the
others have not been referenced here, but are readily
available on PubMed (http://www.ncbi.nlm.nih.gov/
sites/entrez?db=pubmed).
Action Steps
Te rst step is to identify exposure sources
and remediate them. Cleansing protocols can be imple-
mented to enhance the clearance of these persistent
toxins from the body. Sauna therapy and colonic irriga-
tions have been used to reduce the presence of PCBs
and chlorinated pesticides.
73
Various dietary measures
have been shown to increase normal bowel excretion of
these fat-soluble toxins. Te daily use of rice bran ber
has been documented in animal and human studies in
Japan to increase the clearance of PCBs.
73-75
Chlorophyll and chlorophyll-containing foods
have been shown to increase excretion of these fat-sol-
uble persistent toxins via the feces.
76-78
Increasing chlo-
rophyll-containing foods or daily supplementation with
chlorophyll can slowly increase the excretion of these
compounds. In addition to chlorophyll-containing
agents, polyphenols in white and green teas have been
shown to increase the excretion of fecal fat that carries
fat-soluble toxins with it.
79
In addition to increasing the
excretion of these toxins from the body, supplement-
ing with nutrient and botanical antioxidants to protect
the tissues and cells targeted by these toxic compounds
should be considered.
Summary
Chlorinated pesticides were rst used in the
1940s. Although they have now been mostly banned
from use in the United States, their typically long half-
life contributes to ongoing risk of exposure. Tey are
fat-soluble compounds dicult to eliminate from the
body and they consequently accumulate in adipose
tissue of mammalian species. Because adipose tissue
goes through daily lipolysis, a certain amount of these
xenobiotics are regularly released back into circulation.
Tese compounds can be measured in the serum and
reported both as ppb in the serum and as lipid-adjusted
amounts. Te lipid-adjusted values reect the amount
of these toxins stored in the adipose tissue and there-
fore reect total body burden. Te ppb measurements
reect the amount in circulation, either from current
exposure or daily release from adipose tissue. Te CDC
has recently provided basic reference values to help cli-
nicians interpret the reported values of these xenobiot-
ics. Of the chlorinated pesticides, heptachlor epoxide,
oxychlordane, trans-nonachlor, DDE (p,p-1), DDT
(p,p-1), dieldrin, and mirex are the most commonly
found and are associated with the greatest documented
detrimental health eects. Hexachlorobenzene has nu-
merous documented adverse health eects, although it
is not commonly found in the serum.
Many of these chlorinated pesticides are still
present in the listed food sources and can be easily
avoided. In addition to avoiding ongoing exposure to
these compounds, the addition of brown rice, rice bran
Page 357
ber, chlorophyll, and green tea to the diet can enhance
the excretion of these toxic compounds and help reduce
the total toxic burden.
Testing for these compounds permits a clini-
cian to identify persons who may need such treatments
to help prevent exacerbation of their health problems or
to reverse their health complaints.
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Alternative Medicine Review Volume 14, Number 4 2009

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