Human Elimination of Organochlorine Pesticides: Blood, Urine, and Sweat Study

Abstract

Background. Many individuals have been exposed to organochlorinated pesticides (OCPs) through food, water, air, dermal exposure , and/or vertical transmission. Due to enterohepatic reabsorption and affinity to adipose tissue, OCPs are not efficiently eliminated from the human body and may accrue in tissues. Many epidemiological studies demonstrate significant exposure-disease relationships suggesting OCPs can alter metabolic function and potentially lead to illness. There is limited study of interventions to facilitate OCP elimination from the human body. This study explored the efficacy of induced perspiration as a means to eliminate OCPs. Methods. Blood, urine, and sweat (BUS) were collected from 20 individuals. Analysis of 23 OCPs was performed using dual-column gas chromatography with electron-capture detectors. Results. Various OCPs and metabolites, including DDT, DDE, methoxychlor, endrin, and endosulfan sulfate, were excreted into perspiration. Generally, sweat samples showed more frequent OCP detection than serum or urine analysis. Many OCPs were not readily detected in blood testing while still being excreted and identified in sweat. No direct correlation was found among OCP concentrations in the blood, urine, or sweat compartments. Conclusions. Sweat analysis may be useful in detecting some accrued OCPs not found in regular serum testing. Induced perspiration may be a viable clinical tool for eliminating some OCPs.

Full text

Research Article
Human Elimination of Organochlorine Pesticides:
Blood, Urine, and Sweat Study
Stephen J. Genuis,1,2 Kevin Lane,3and Detlef Birkholz1
1University of Alberta, Edmonton, AB, Canada T6G 2R7
2University of Calgary, Calgary, AB, Canada T2N 4N1
3Department of Chemistry, e King’s University, Edmonton, AB, Canada T6B 2H3
Correspondence should be addressed to Stephen J. Genuis; sgenuis@shaw.ca
Received  June ; Revised  September ; Accepted  September 
Academic Editor: Alex Boye
Copyright ©  Stephen J. Genuis et al. is is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
Background. Many individuals have been exposed to organochlorinated pesticides (OCPs) through food, water, air, dermal expo-
sure, and/or vertical transmission. Due to enterohepatic reabsorption and anity to adipose tissue, OCPs are not eciently elimi-
nated from the human body and may accrue in tissues. Manyepidemiological studies demonstrate signicant exposure-disease rela-
tionships suggesting OCPs can alter metabolic function and potentially lead to illness. ere is limited study of interventions to facil-
itate OCP elimination from the human body. is study explored the ecacy of induced perspiration as a means to eliminate OCPs.
Methods. Blood, urine, and sweat (BUS) were collected from  individuals. Analysis of  OCPs was performed using dual-column
gas chromatography with electron-capture detectors. Results. Various OCPs and metabolites, including DDT, DDE, methoxychlor,
endrin, and endosulfan sulfate, were excreted into perspiration. Generally, sweat samples showed more frequent OCP detection
than serum or urine analysis. Many OCPs were not readily detected in blood testing while still being excreted and identied in
sweat. No direct correlation was found among OCP concentrations in the blood, urine, or sweat compartments. Conclusions.Sweat
analysis may be useful in detecting some accrued OCPs not found in regular serum testing. Induced perspiration may be a viable
clinical tool for eliminating some OCPs.
1. Introduction
Organochlorinated compounds have been used globally for
many years as solvents, fumigants, and insecticides. In the
s,SwisschemistandNobelPrizerecipientPaulMuller
rst discovered that the most well-known organochlorine
agent dichlorodiphenyltrichloroethane (DDT) had signi-
cant insecticide properties []. Since then, this pest control
agent has been utilized around the world to prevent the
transmission of many vector-born diseases including malaria
and typhus []. Alongside DDT, several other organochlo-
rinated pesticides (OCPs) were subsequently developed and
were also utilized to control various pests. With unfolding
toxicological research, however, evidence of potential human
health risks associated with exposure to these agents began
to appear. Like many OCPs, it was eventually conrmed that
DDT elicited toxic eects that harmed nontarget species,
bioaccumulated in the animal food chain, and had a very
slow rate of environmental degradation. As a result, the use
of DDT was eventually banned in the United States in 
[].
DuetotheabilityofOCPstoaccumulateinbody
tissues, their long half-life of elimination from the body, and
emerging evidence of potential toxicity to human health,
many countries throughout the world went on to ban many
of the agents within the OCP family []. e sequelae of
the OCP experiment, however, continue to linger as human
contamination with these chemical compounds is still evi-
dent throughout the globe. Various factors are contributing
to this reality, including the following: (i) the ongoing use of
OCPs in some countries, (ii) the persistence of these agents
within the environment and within the human body, (iii) the
widespread use of international travel resulting in potential
OCPexposurewhenvisitingorrelocatingtojurisdictions
Hindawi Publishing Corporation
BioMed Research International
Volume 2016, Article ID 1624643, 10 pages
http://dx.doi.org/10.1155/2016/1624643

BioMed Research International
T : Organochlorine pesticide groupings based on chemical
structure.
Group Constituents
(i) DDT and analogues
DDT
DDE
DDD
Methoxychlor
(ii) Hexachlorobenzene Hexachlorobenzene
(iii) Hexachlorocyclohexane 𝛼-HCH, 𝛽-HCH, 𝛿-HCH, and
𝛾-HCH
(iv) Cyclodiene
Endosulfan I and endosulfan II
Heptachlor
Aldrin
Dieldrin
Endrin
(v) Chlordecone, Kelevan, and
Mirex
Chlordecone, Kelevan, and
Mirex
(vi) Toxaphene Toxaphene
whereOCPsarestillused,(iv)theglobalexchangeof
potentially contaminated foodstus originating from juris-
dictions where OCPs are still used, and (v) the potential for
vertical transmission of OCPs from contaminated mothers
to ospring during pregnancy and lactation []. As a result,
OCPs continue to be found in individuals and population
groups, including infant children. Individuals contaminated
with OCP compounds remain at risk for adverse health
consequences and some will potentially pass on these agents
to subsequent generations through vertical transmission.
From a clinical perspective, the question remains about
how to assess and manage people who have health issues
related to xenobiotic contamination [–]. As many persis-
tent toxicants including OCPs can sequester and accrue in
tissues rather than remaining in the blood compartment [],
biomonitoring for such chemical agents through unprovoked
blood and urine analysis does not necessarily reect the
actual body burden of these chemicals []. Furthermore, as
persistent organochlorine compounds have been associated
with myriad health risks, it might be possible to diminish the
risk of adverse health sequelae and transgenerational spread
ofOCPsifmeanswereidentiedtofacilitateeliminationof
theseagentsfromthehumanbodyaltogether.
Existing medical literature suggests that elimination of
organochlorine compounds and other persistent chemical
agentsfromthehumanbodycanhavesignicantclinical
benet in ameliorating health problems [–]. Accordingly,
the value of establishing inter ventions to facilitate elimination
oftoxicchemicalagentsisthusapparent.Inthisresearch
study, we provide an overview of literature linking some
OCPs with potential human health eects, we endeavor to
demonstrate that routine blood testing for OCPs may be
inadequate for biomonitoring body burdens, and we provide
evidence that transdermal depuration through perspiration
facilitates elimination of various OCP compounds.
2. Background
OCPs are lipophilic contact insecticides; they have low
vapour pressures and slow rates of environmental degrada-
tion. ese properties make them highly penetrable, long
lasting, and extremely eective pesticide agents []. ese
properties also contribute to bioaccumulation within the
humanorganismbythereadyabsorptionintothebodyand
subsequent deposition into adipose tissue. Like medications,
the toxicity of OCPs is related to pharmacokinetics, bioavail-
ability,andthemoleculartopologywhichis,inturn,related
to their molecular size, volatility, and lipophilicity. ese
factors determine the absorption, distribution, metabolism,
excretion, and toxicity (ADMET) of each chemical agent.
Additionally, toxicity also depends on the age, nutritional
status, and innate detoxication capacity of the host as
well as the frequency, intensity, and nature of the toxic
exposures []. Based on their chemical structures, OCPs
canbegroupedintocategories(Table).Similarchemical
structures within each group account for the similar chemical
properties and comparable ADMET outcomes.
Uptake of OCPs into the human body may occur by
ingestion, by inhalation, by vertical transmission, or by
transdermal mechanisms. In addition, exposure to OCPs
in combination with other pollutants, like inorganic toxic
elements, may facilitate an additive or synergistic eect [].
An interesting study of  adults over the age of  years,
for example, reported signicantly higher mortality levels in
smokersinthendorrdtertileofOCPbloodlevelsbutnot
among smokers in the lowest tertile of exposure [].
In clinical practice, patients presenting with the sequelae
of toxicant exposures are oen challenging and misdiagnosed
as “they will seldom present with a history of toxic exposure;
their symptoms are multisystem and multifactorial; and the
ndings of the physical exam may provide little conrmation
of the intake” []. Additionally, there is limited research
on the full long-term impact of OCPs and other accrued
toxicantswithinthehumanbody.Asaresultoftheunfolding
health problems associated with bioaccumulation of adverse
agents [, ] and the likelihood of vertical transmission
[] and potential transgenerational impact [], however,
there is emerging attention to the development of eective
interventions to facilitate elimination of toxic compounds
[, ].
To date, it has been realized that organochlorine insecti-
cides exert pathobiological impact including carcinogenicity,
neurotoxicity, hormone disruption, and other toxic eects
[, –]. Some studies have linked OCP exposure to
signicantly higher rates of cancers of the breast, liver,
testicles, and lung, as well as sarcoma and non-Hodgkin’s
lymphoma [, ]. OCP exposure has also been linked to
higher rates of endometriosis in women [] and increased
risk for diabetes and obesity [–], as well as higher risk for
neurological disorders like Parkinson’s disease [, ]. Stud-
ies with children and adolescents have linked OCP exposure
to neurological and psychiatric sequelae including abnormal
reexes, reduced cognitive development, depression, and
behavioral problems []. e potential to prevent and/or
treat such conditions by identifying individuals with a body

BioMed Research International 
burden of these chemical agents, and then treating them to
facilitate elimination of their accrued load of toxicants, is
worthy of exploration and further research.
2.1. Biochemical and Pathophysiological Mechanisms of Harm.
Although designed as acute neurotoxins, OCPs have been
found to dysregulate human metabolic processes through
several dierent pathways. ese pathophysiological mech-
anisms include mitochondrial damage [, ], oxidative
stress [], cell death [], endocrine disruption [], and
epigenetic modication [, ]. As discussed, there is also
evidence that concomitant contamination with OCPs along
with other toxic chemical agents may exhibit synergistic
eects [].
Additionally, OCPs also exhibit synaptic dysregulation by
altering the cation channels (e.g., sodium) at the synapse in
nerve cells []. Although this eect establishes their ecacy
against insect pests, the similarity between organismal synap-
tic cation channels between species results in nonspecicity
and inadvertent harm to nontarget organisms []. Another
potential pathway of harm is the recently established mech-
anism entitled “toxicant induced loss of tolerance” (TILT)
[]. is pathophysiologic mechanism resulting in human
multimorbidity is characterized by a toxicant burden (e.g.,
persistent OCPs) resulting in impaired tolerance and hyper-
sensitivity []. When triggered by an antigenic incident from
the environment (e.g., pollen, chemical agent, or food), an
immune response ensues potentially producing antibodies
and proinammatory cytokines. A multisystem response
resulting in a condition entitled “Sensitivity Related Illness”
(SRI) is oen the result []. Unfolding research continues
to expound on various pathophysiological mechanisms of
damage to the human organism.
2.2. Human Exposure. ere is mounting evidence that indi-
viduals and population groups are currently being exposed to
a multitude of dierent types of chemical toxicants, some of
which may accrue within the body. e Centers for Disease
Control, for example, recently released a study conrming
accrualofmultiplepollutantsinmostAmericanadultsand
children []. In a similar nation-wide epidemiological study
in Canada, Health Canada also reported on an assortment of
stockpiled chemical toxicants within the general population
[].
An issue of particular concern is fetal and early life
exposure to xenobiotics at critical times of development as
a result of maternal exposure and bioaccumulation [].
Although OCPs were not specically measured, a recent
cord-blood study revealed an accumulation of various tox-
icants in neonates at birth []. Studies on OCPs within
lactating women have conrmed OCP levels in some women
that exceed Health Canada’s tolerable daily intake (TDI)
guidelines []. e potential clinical sequelae of such accrual
within reproductive-aged women can be seen, for example,
in a large observational study examining specic OCP expo-
sures (dicofol and endosulfan) []. is research suggests
a correlation of increased risk of autistic spectrum disorder
based on the distance between maternal residence and the
location of pesticide application []. Such emerging work
on gestational and lactational exposures led to the recent
“Special Communication” by the International Federation
of Obstetrics and Gynecology [] (an organization which
oversees much of the maternity care throughout the world)
in an eort to bring global attention to the reality of
widespread vertical transmission of toxicants and the myriad
pediatric health problems resulting from maternal xenobiotic
pollution.
Although restrictive policies have been implemented for
OCP usage in many jurisdictions, these agents continue to
be found within individuals and population groups. is
is, as discussed, due to continued usage in some areas of
the world, vertical transmission to ospring, and persistence
within the human organism. Why do they persist? Following
exposure, OCP compounds are dechlorinated and conjugated
in the liver where biliary excretion is the main mechanism
for elimination. However, organochlorine compounds are
reabsorbed to some degree in the enterohepatic circulation
and this recycling phenomenon accounts for the persistence
within the human body [].
As a result of such persistence and the lipophilic nature
of OCPs, these chemical agents tend to store and bioaccu-
mulate in adipose tissues. Although the complete range of
toxicity relating to OCP exposure and bioaccumulation is
not fully understood and remains somewhat controversial,
many adverse sequelae have been linked to exposure to such
agents as previously mentioned. Accordingly, interventions
arerequiredtoassistinfacilitatingeliminationofOCPs,
in order to prevent or overcome adverse clinical sequelae
resulting from the potential physiological disruption caused
by the enduring presence of these toxicants.
us far, there has been limited work on interventions
to facilitate elimination of OCPs [, –]. Schnare et
al.examinedtheuseofinducedperspirationasameans
to expedite elimination of PCBs, PBBs, and OCPs [].
eir work conrmed that enhanced mobilization and excre-
tion via induced perspiration reduced the body burden of
hexachlorobenzene (HCB) and  polychlorinated biphenyl
congeners []. Removal of organochlorine compounds has
also been facilitated by specic interventions which interrupt
the enterohepatic circulation [, , ]. e main purpose of
this study is to determine whether induced perspiration can
be used clinically to facilitate decorporation of the range of
both parent OCPs as well as their metabolites.
3. Materials and Methods
3.1. Participant Recruitment. Nine males and  females with
mean ages of . ±. years and . ±. years,
respectively, were recruited to participate in this study aer
appropriate ethical approval was received from the Health
Research Ethics Board of the University of Alberta.  partic-
ipants were patients with various clinical conditions and 
were otherwise healthy adults. Participants with health issues
were recruited from the rst author’s clinical practice by
invitation and both healthy and sick individuals were selected
as samples of convenience by availability, desire to participate,
and ease of contact. Each participant in the study provided
informed consent and volunteered to give one  mL

BioMed Research International
T : Participant demographics and general clinical characteristics.
Participant Gender Age Clinical diagnosis Technique used for sweat collection
 M  Diabetes, obesity, hypertension Exercise
 F  Rheumatoid arthritis Steam sauna
 M  Addiction disorder Steam sauna
 F  Bipolar disorder Steam sauna
 F  Lymphoma Steam sauna
FFibromyalgia Steamsauna
 F  Depression Steam sauna
 F  Chronic fatigue Infrared sauna
 F  Diabetes, fatigue, obesity Steam sauna
 M  Chronic pain, cognitive decline Exercise
 M  Healthy Exercise
 M  Healthy Infrared sauna
 M  Healthy Infrared sauna
 F  Healthy Infrared sauna
 M  Healthy Infrared sauna
 F  Healthy Infrared sauna
 F  Healthy Infrared sauna
 M  Healthy Infrared sauna
 M  Healthy Infrared sauna
 F  Healthy Infrared sauna
random sample of blood, one sample of rst morning urine,
and one  mL sample of sweat. Demographic and clinical
characteristics of all research participants are provided in
Table .
3.2. Samples Collection. All blood samples were collected at
one DynaLIFE laboratory site in Edmonton, Alberta, Canada,
with vacutainer blood collection equipment (BD Vacutainer,
Franklin Lakes, NJ , USA) using -gauge stainless
steel needles which were screwed into the “BD Vacutainer
One-Use Holder” (REF ). e  mL glass vacutainer
was directly inserted into the holder and into the back
end of the needle. is process and the use of glass blood
collection tubes were used to prevent contamination. Blood
was collected directly into plain  mL glass vacutainer tubes,
allowed to clot, and aer  minutes were centrifuged for 
minutes at , revolutions per minute (RPM). Aer serum
was separated o, samples were picked up by ALS laboratories
(about  kilometres from the blood collection site) for storage
pending analysis. When received at ALS, serum samples were
transferredtomLglassvialsandstoredinafreezerat−∘C,
pending transfer to the analytical laboratory.
For urine collection, participants were instructed to
collect a rst morning midstream urine sample directly into
a provided  mL glass jar container with Teon-lined lid
onthesamedaythatbloodsampleswerecollected.Urine
samples were delivered by the participants directly to ALS
laboratories, Edmonton. Samples were transferred to  mL
glassvialsandstoredinafreezerat−∘C, pending transfer.
For sweat collection, participants were instructed to
collect perspiration from any site on their body directly into
theprovidedmLglassjarcontainerwithTeon-lined
lid, by placing the jar against their prewashed skin (with
toxicant-free soap, water, and nonplastic brush) when actively
sweating or by using a stainless steel spatula against their skin
to transfer perspiration directly into the glass jar. Stainless
steel, made up primarily of iron, chromium, and nickel, was
chosen as it is the same material as the needles used in
standard blood collections and is reported not to o-gas
orleachatroomorbodytemperature.Allbutoneofthe
participants (/) provided  mL of sweat. Each of the
glass bottles used for sampling in this study was provided by
ALS laboratories and had undergone extensive cleaning and
rinsing. e containers were deemed appropriate for sweat
collection with negligible risk of contamination: laboratory-
grade phosphate-free detergent wash; acid rinse; multiple hot
and cold deionized water rinses, oven dried, capped, and
packed in quality-controlled conditions.
Sweat was collected within  week before or aer collect-
ing the blood and urine samples. No specications were given
as to how long sweating had commenced before collection.
 participants collected sweat inside a dry infrared sauna;
collectedsweatinsideasteamsauna,andcollected
sweat during and immediately aer exercise; no specic
instruction was given regarding the type or location of
exercise. Participants were educated about the research and
wereaskedtometiculouslyavoidexposuretoanypotential
sources of toxicants around the time of collection. Sweat was
delivered by the participants directly to ALS laboratories.
Samples were transferred to  mL glass vials and stored in
a freezer at −∘C, pending analysis. No preservatives were
usedinthejarsprovidedforsweatandurinecollectionnor
in the serum storage vials.

BioMed Research International 
T : Organochlorine pesticides analyzed.
Group Parent Metabolite
DDT and analogues DDT
Methoxychlor
DDE, DDD
NA
Hexachlorobenzene Hexachlorobenzene NA
Hexachlorocyclohexane 𝛼-BHC, 𝛽-BHC, 𝛿-BHC, and
𝛾-BHC NA
Cyclodiene
Endosulfan I, endosulfan II Endosulfan sulfate
Aldrin Dieldrin
Endrin Endrin ketone
Endrin aldehyde
Heptachlor Heptachlor epoxide
cis-chlordane, trans-chlordane trans-nonachlor
Chlordecone∗,Kelevan
∗,andMirex Mirex NA
Tox a p h e n e ∗
∗Did not test for this specic compound in this study.
3.3. Laboratory Method Description. Of the  categories of
OCPs,  were analyzed (Table , toxaphene was not included
in this study). Organochlorine pesticide concentrations of
parent and metabolite compounds were analyzed using
dual-column gas chromatography with electron-capture
detectors (GC-ECD). A pair of surrogate standards, tetra-
chlorometaxylene (TCMX) and decachlorobiphenyl (DCB),
were used to monitor the performance of the method.
e methodology for determining the selected organo-
chlorine pesticides was as follows. Serum samples were
weighed into glass tubes (g) and mL of methanol was
added to the serum samples. Sweat and urine samples were
weighedintoglasstubes(g)andmLofmethanolwas
added to each of the samples. Serial extraction of the bioactive
compounds was performed on serum, sweat, and urine
samples  times by adding  mL of an ethyl ether :hexane
solution ( : , v/v) and removing the supernatant via centrifu-
gation. e extract was then put through a sodium sulfate
column to dry. e resulting extracts were combined and
concentrated to  mL and put through a  g, % deactivated
orisil column. Florisil was used to eliminate coeluting
chlorophenols. External standard calibration was used for
quantication. Method blanks were used to ensure quality
control, water and calf serum samples. Instrument detection
limits were determined to be . 𝜇g/kg. Pentachloroni-
trobenzene (PCNB) was added to the extracts as an internal
standard and the samples were analyzed by dual-column gas
chromatography with electron-capture detectors (DB- and
DB-).
4. Results and Discussion
e results of the study can be found in Tables  and .
e parent OCP compounds showed dierential detection
(Tables (a)–(c)) and compounds detected in at least one
participant’s serum sample include aldrin, DDT, endosulfan I
and endosulfan II, heptachlor, mirex, hexachlorobenzene, 𝛼-
HCH, 𝛽-HCH, and 𝛾-HCH. Endrin, 𝛿-HCH, and methoxy-
chlor were not detected in any of the participant’s serum
samples. e parent compounds detected in at least one
participant’s urine sample include aldrin, DDT, endosulfan I
and endosulfan II, endrin, mirex, 𝛾- HCH, and methoxychlor.
Heptachlor, 𝛼-HCH, 𝛽-HCH, 𝛿-HCH, and hexachloroben-
zene were not detected in any participant’s urine sample. All
of the parent compounds except the isomers of hexachloro-
cyclohexane were detected in at least one participant’s sweat
sample.
e metabolite compounds also showed dierential
detection. e metabolite compounds detected in at least
one participant’s serum sample include DDE, endrin ketone,
endrin aldehyde, and heptachlor epoxide. e metabolites,
DDD, endosulfan sulfate, and dieldrin, were not detected in
any serum samples. e metabolite compounds detected in
at least one participant’s sweat sample include DDE, DDD,
endosulfan sulfate, dieldrin, and endrin ketone. Neither
endrin aldehyde nor heptachlor epoxide was detected in any
sweat samples. e metabolite compounds detected in at
least one participant’s urine sample include DDD, endosulfan
sulfate, dieldrin, endrin aldehyde, and heptachlor epoxide.
e metabolites DDE and endrin ketone were not detected
in any urine samples.
Of the parent compounds, DDT, methoxychlor, and
endrin as well as the metabolites DDE, DDD, and endo-
sulfan sulfate appear to be readily excreted into sweat as
they are found in over half of the participants examined
(Table ). Additionally, with the exception of DDE, these
OCPs were not readily detected in blood testing while still
being excreted and identied in sweat. is may indicate
that these OCP compounds are stored and sequestered in
tissues, not evident in blood testing, but are mobilized and
excreted during perspiration. In contrast, endosulfan I was
almost exclusively detected in urine samples of over half of
the participants (Table ). Collectively, the ndings suggest
that these participants have been commonly exposed to DDT,
methoxychlor, endrin, and endosulfan I and are also carrying
a body burden of the metabolites DDE, DDD, and endosulfan
sulfate.

BioMed Research International
T : (a) Distribution of parent compounds in serum (SE), sweat (SW), and urine (U) (𝜇g/kg). (b) Distribution of parent compounds in
serum (SE), sweat (SW), and urine (U) (𝜇g/kg). (c) Distribution of parent compounds in serum (SE), sweat (SW), and urine (U) (𝜇g/kg).
(a)
SE
Aldrin
SW
Aldrin
U
Aldrin
SE
DDT
SW
DDT
U
DDT
SE
Endosulfan
I
SW
Endosulfan
I
U
Endosulfan
I
𝑛∗ 
Mean∗∗ — . — — . — — — .
Median∗∗ — . — — . — — — .
Std. Dev.∗∗ — . — — . — — — .
Range .–. .–. .–. .–. .–. .–. . . .–.
∗𝑛represents the number of participants with a detectable amount of the OCP from the  total participants examined.
∗∗For matrices having fewer than  individuals with detectable OCP levels, the mean, median, and standard deviation measurements were not provided.
(b)
SE
Endrin
SW
Endrin
U
Endrin
SE
Heptachlor
SW
Heptachlor
U
Heptachlor
SE
Mirex
SW
Mirex
U
Mirex
𝑛∗     
Mean∗∗ — . — . — — — — —
Median∗∗ — . — . — — — — —
Std. Dev.∗∗ — . — . — — — — —
Range — .–. . .–. . — .–. .–. .–.
∗𝑛represents the number of participants with a detectable amount of the OCP from the  total participants examined.
∗∗For matrices having fewer than  individuals with detectable OCP levels, the mean, median, and standard deviation measurements were not provided.
(c)
SE
Methoxychlor
SW
Methoxychlor
U
Methoxychlor
SE
Hexachlorobenzene
SW
Hexachlorobenzene
U
Hexachlorobenzene
𝑛∗   
Mean∗∗ — . — . — —
Median∗∗ — . — . — —
Std. Dev.∗∗ — . — . — —
Range — .–. .–. .–. . —
∗𝑛represents the number of participants with a detectable amount of the OCP from the  total participants examined.
∗∗For matrices having fewer than  individuals with detectable OCP levels, the mean, median, and standard deviation measurements were not provided.
Most of the compounds examined were detected in
less than half of the participants regardless of the matrix
(Table ). is likely reects a reduced exposure level to
these compounds. However, hexachlorobenzene, heptachlor,
and endrin ketone were detected in at least % of par-
ticipants and were all predominantly detected in serum
samples (Table ). Although some compounds were detected
in participant urine, these levels typically occurred around
the limit of detection and at much lower levels than either
serum or sweat analysis. With the exception of endosulfan I,
this suggests that urine analysis is not reliable as an analytic
tool to measure the body burden of these compounds.
e partitioning of these compounds in the body seems
to be related to their lipophilicity. With the exception of
endosulfan I and its metabolite endosulfan sulfate, all of the
compoundsdetectedinoverhalfoftheparticipantshave
log 𝐾ow values above  (Table ). is indicates that they are
highlylipophilicandfatsolubleandareexpectedtosequester
in fat tissue. In comparison to the compounds found
predominantly in sweat, hexachlorobenzene and heptachlor
have reportedly similar degrees of lipophilicity but were
predominantly found in blood (Tables (a)–(c)). erefore,
these ndings may suggest that lipophilicity is not the only
factor aecting the partitioning of these compounds.
ere are limitations to the study and to interpretation
of the results. ere has been discussion in lay circles that
diering means of thermal depuration by varying types of
sauna (such as infrared sauna versus steam sauna), exercise,
or other perspiration induction activities may result in
dierences in excretion rates through skin. is study did not
have an adequate data set to control for potential dierences
in the excretion of the range of OCPs between usages of far-
infrared sauna, regular sauna, or exercise. Several other issues
may impact the reliability and reproducibility of perspiration
analysis that were not considered including body site of
sampling, timing of collection while perspiring, dierences
in skin characteristics between individuals, temperature and
humidity of the surroundings, and factors such as diet,

BioMed Research International 
T : Percentage of individuals with detection of organochlorine
pesticides within serum, sweat, and urine (𝑛=20).
Serum Sweat Urine
,󸀠-DDT   
,󸀠-DDE   
,󸀠-DDD   
Methoxychlor   
Endosulfan I   
Endosulfan sulfate   
Endrin   
Aldrin   
Dieldrin   
trans-nonachlor   
BHC (hexachlorobenzene)   
𝛼-BHC   
𝛽-BHC   
𝛿-BHC   
𝛾-BHC   
Endosulfan II   
Endrin ketone   
Endrin aldehyde   
Heptachlor epoxide   
Heptachlor   
cis-chlordane   
trans-chlordane   
Mirex   
pharmaceutical intake, and supplement use. Accordingly,
attempts to accurately quantify the relative amount of toxi-
cantsreleasedintoperspirationarelimited.
Areas for future research in relation to induced perspi-
ration might include an examination of (i) dierences in
rates of excretion into perspiration of assorted xenobiotics
from diverse sites in the body, (ii) whether there is diurnal
variation in the toxicant content of perspiration, (iii) whether
hydration status aects the xenobiotic concentration of per-
spiration, (iv) dermal reabsorption potential of toxicants aer
perspiration, and (v) the release of xenobiotics in those in
fasting states compared to those without caloric restriction.
5. Conclusion
As DDT, DDE, DDD, methoxychlor, endosulfan sulfate, and
endrin appear to be readily excreted into sweat, induced
perspiration appears to be a potential clinical tool to diminish
the body burden of these agents. With the exception of
DDE, however, these agents are not readily detected in blood
testing. is suggests that common blood analysis may not
truly represent the body burden of these compounds. As
the routine use of unprovoked blood testing may thus be
inadequate for biomonitoring body burdens of OCPs, there
may be clinical advantages to the induction of perspiration
through methods like sauna and/or exercise in order to
collect samples for biomonitoring and diagnosis of many
retained OCP compounds.
T : Octanol/water partition coecient of key OCPs [–].
Compound log 𝐾ow
Aldrin .
Endrin .
Endosulfan I .
Endosulfate .
p,p󸀠-DDT .
p,p󸀠-DDE .
p,p󸀠-DDD .
Methoxychlor .
Heptachlor .
Hexachlorobenzene .
In conclusion, the previous four papers in this “blood,
urine, and sweat (BUS)” series have demonstrated that
induced perspiration is eective at facilitating the removal of
manytoxicelementsaswellasvariousorganiccompounds,
but not all [–]. is OCP study provides evidence that
transdermal depuration through perspiration facilitates elim-
ination of some parent and metabolite OCP compounds, but
not all. While the absolute amount of each OCP compound
released into sweat may be small according to this data, an
average adult may sweat more than one liter per hour during
exercise. Under thermal stress, maximal rates of sweating may
be as high as two to four liters/hour []; and sweating rates
for “acclimatized” people who regularly use saunas may be as
high as two liters/hour []. Accordingly, regular sessions of
induced perspiration should be considered cumulatively as a
potentialclinicalmodalitytodiminishbodyburdensofmany
xenobiotics, including OCP compounds.
Additional Points
Key Findings
(a) DDT and/or its metabolite(s) were found in nearly
every participant regardless of age suggesting that
exposure is very common.
(b) Nearly all organochlorine pesticide (OCP) parent
compounds and several metabolites were detected in
perspiration suggesting that sweating may be eca-
cious in diminishing the body burden of many of
these toxicants.
(c) ere were some parent OCPs, such as endosulfan I
and hexachlorobenzene, and some metabolites, such
as endrin ketone and heptachlor, that were not readily
excreted into perspiration.
(d) Lipophilicity appeared to be a major factor inuenc-
ing the ecacy of transdermal OCP elimination but
not the exclusive determinant.
(e) Only endosulfan I appeared to be predominantly
detected in urine suggesting that urine analysis has
limited value in detection of retained OCPs.

BioMed Research International
Competing Interests
ere is no conict of interests regarding the publication of
this paper.
Acknowledgments
anks are due to Dr. Peter Mahay and the Department
of Chemistry at e King’s University for their thoughtful
assistance in this work.
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