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Lack of evidence that essential oils affect puberty

Authors:

Abstract

Lavender (Lavandula angustifolia) and tea tree (Melaleuca alternifolia) essential oils have been linked to endocrine disruption manifested as pre-pubertal breast development in children. The link is casual and based on weak in vitro data suggesting the oils have estrogenic activity. More work is required to explain the in vitro results. Any link, casual or causal, between lavender or tea tree oil product use and the pre-pubertal breast development has public health, regulatory, ecotoxicological and/or commercial consequences. It is worth considering that the chemical constituents of lavender and tea tree essential oils are not unique to those oils. They are found in hundreds of other essential oils. If these two oils did possess estrogenic activity, then it is likely that other essential oils would also have estrogenic activity by virtue of the constituents they share with lavender and tea tree oil. Each year thousands of tonnes of essential oils are ubiquitously ingested by and applied to humans and other animals in products such as foods, beverages, personal care products and pharmaceutical agents. Consequently, it is important that the nature of any link between essential oils and endocrine disruption be clarified.
Reproductive
Toxicology
44
(2014)
50–51
Contents
lists
available
at
ScienceDirect
Reproductive
Toxicology
j
ourna
l
ho
me
pa
g
e:
www.elsevier.com/locate/reprotox
Letter
to
the
Editor
Lack
of
evidence
that
essential
oils
affect
puberty
Dear
Sir,
The
review
by
Fisher
and
Eugster
[1]
due
to
be
published
in
Reproductive
Toxicology
repeats
the
putative
link
between
the
essential
oils
of
lavender
and
tea
tree
and
breast
development
stating:
“Other
examples
of
naturally
occurring
endocrine
disruptors
include
lavender
oil,
tea
tree
oil
and
fennel,
all
of
which
have
been
linked
to
breast
development
in
prepubertal
children
pre-
sumably
due
to
estrogenic
effects.”
Here
the
authors
have
referred
to
the
2007
paper
by
Henley
et
al.
[2].
They
have
linked
essential
oils
to
endocrine
disruption
by
referring
to
gynecomastia
and/or
to
in
vitro
estrogenic
activity,
without
also
referring
to
other
studies
that
suggest
otherwise.
The
review
“summarises
the
current
understanding
of
the
major
environmental
influences
on
pubertal
timing,
focusing
on
factors
for
which
the
most
scientific
evidence
exists”
[1].
Knowledge
in
the
field
is
growing
steadily
and
recently
published
data
on
lavender
oil
provide
compelling
evidence
that
lavender
oil
is
not
estrogenic
[3].
In
this
study,
lavender
oil
at
dosages
of
20
or
100
mg/kg
was
not
active
in
a
rat
uterotrophic
assay,
the
gold-standard
in
vivo
assay,
with
no
evidence
of
estrogenic
activity
shown.
While
tea
tree
oil
has
not
yet
been
tested
in
vivo,
in
a
report
on
the
oil
by
the
European
Commission’s
Scientific
Committee
on
Consumer
Products
(now
the
Scientific
Committee
on
Consumer
Safety)
[4],
the
committee
commented:
“Since
the
hormonal
active
ingredients
of
Tea
Tree
Oil
were
shown
not
to
penetrate
the
skin,
the
hypothesized
correlation
of
the
finding
of
3
cases
of
gynecomastia
to
the
topical
use
of
Tea
Tree
Oil
is
considered
implausible.”
The
implausibility
of
tea
tree
oil
having
any
estrogenic
effect
is
further
supported
by
Tisserand’s
review
[5]
of
the
estrogenic
activ-
ity
of
clary
sage
in
which
he
notes
that
according
to
Anstead
et
al.
[6]
and
Blair
et
al.
[7]
phenolic
structure
is
important
for
estro-
genicity,
as
is
the
presence
of
a
second
ring.
This
does
not
rule
out
other
mechanisms
of
xenoestrogenic
action
such
as
metabolic
activation
[8–10]
or
epimutations
after
developmental
exposure
[11,12].
However,
none
of
this
negates
the
fact
that
a
putative
link
[2]
has
been
made
and
is
being
overstated
and
perpetuated.
Since
the
Henley
et
al.
article
was
published,
it
has
been
cited
more
than
170
times
(Google
Scholar,
accessed
16
September
2013)
to
ref-
erence
the
estrogenic
or
endocrine
disrupting
activity
of
lavender
and/or
tea
tree
oils
without
the
benefit
of
additional
data.
DOI
of
original
article:
http://dx.doi.org/10.1016/j.reprotox.2013.03.012.
Case
reports
are
a
very
useful
means
of
identifying
possible
links
between
product
exposure
and
detrimental
biological
effects.
How-
ever,
they
are
not
definitive
in
their
own
right.
The
co-incidence
of
oil
exposure
and
endocrine
disruption,
manifested
as
breast
devel-
opment,
has
not
been
demonstrated
to
be
causal.
The
cause
of
the
pre-pubertal
gynecomastia
has
not
been
identified
and
tea
tree
and
lavender
oils
have
not
been
definitively
identified
as
endocrine
disrupting
compounds.
Both
tea
tree
(Melaleuca
alternifolia)
and
lavender
(Lavandula
angustifolia)
oils
have
a
long
history
of
appar-
ently
safe
use
[13,14].
Tisserand
has
previously
postulated
[15]
that
phthalates
may
have
contributed
to
the
endocrine
effect
noted
by
Henley
et
al.
[2].
Tisserand
[15]
also
noted:
“The
composition
of
the
essential
oils
tested
is
not
given,
nor
is
any
other
information
about
them,
apart
from
the
supplier.
Since
they
do
not
appear
to
be
organically
grown,
biocide
con-
tent
is
a
possibility.”
Since
no
compositional
data
on
the
lavender
or
tea
tree
oils
was
provided
in
the
original
paper
[2],
the
presence
or
absence
of
xenoestrogenic
contaminants
such
as
plasticisers,
pesticides
or
herbicides
is
unknown.
Conclusions
about
the
estrogenic
activity
of
the
oils
are
not
possible
without
these
data.
The
absence
of
tea
tree
oil
exposure
by
two
of
the
three
reported
cases
[2]
also
argues
against
a
causative
role
for
tea
tree
oil
and
a
number
of
publications
questioned
the
purported
link
between
gynecomastia
and
the
two
essential
oils
at
the
time
[16–20].
Any
link,
casual
or
causal,
between
lavender
or
tea
tree
oil
prod-
uct
use
and
the
development
of
pre-pubertal
gynecomastia
has
public
health,
regulatory,
ecotoxicological
and/or
commercial
con-
sequences.
It
is
worth
considering
that
the
chemical
constituents
of
lavender
and
tea
tree
essential
oils
are
not
unique
to
those
oils
[21–23].
They
are
found
in
hundreds
of
other
essential
oils.
If
these
two
oils
did
possess
estrogenic
activity,
then
it
is
likely
that
other
essential
oils
would
also
have
estrogenic
activity
by
virtue
of
the
constituents
they
share
with
lavender
and
tea
tree
oil.
Each
year
thousands
of
tonnes
of
essential
oils
are
ubiquitously
ingested
by
and
applied
to
humans
and
other
animals
in
products
such
as
foods
[24],
beverages
[25,26],
personal
care
products
and
pharmaceuti-
cal
agents.
Consequently,
it
is
important
that
the
nature
of
any
link
between
essential
oils
and
endocrine
disruption
be
clarified.
This
may
be
achieved
by
continued
research
into
the
safety
and
efficacy
of
the
oils
funded
by
industry
and
independent
sources
combined
with
ongoing
surveillance
of
reports
of
adverse
effects
by
industry
and
regulatory
authorities.
Finally,
a
recent
revisiting
of
the
existing
literature
on
the
in
vitro
and
in
vivo
estrogenic
activity
of
essential
oils
has
led
one
of
the
authors
(CFC)
to
suggest
an
alternative
hypothesis.
It
may
be
that
a
large
proportion
of
the
in
vitro
results
suggesting
that
essential
oils
and/or
their
components
are
estrogenic,
are
false
pos-
itive
results.
Commonly
utilised
disposable
laboratory
plasticware,
such
as
the
96-well
polystyrene
plastic
trays
in
which
the
tests
for
http://dx.doi.org/10.1016/j.reprotox.2013.09.010
0890-6238/©
2014
Elsevier
Inc.
All
rights
reserved.
Letter
to
the
Editor
/
Reproductive
Toxicology
44
(2014)
50–51
51
estrogenic
activity
are
often
performed,
contains
many
xenoestro-
genic
compounds
including
phthalates
and
nonylphenols
that
may
leach
into
the
test
system,
especially
in
the
presence
of
essential
oils
which
have
solvent
properties.
The
use
of
disposable
labora-
tory
plasticware
may
be
confounding
the
results,
a
phenomenon
that
has
been
reported
in
the
past
[27,28].
This
needs
testing
and
it
is
worth
noting
that
Henley
et
al.
used
polystyrene
plates
(Korach
K,
personal
communication).
Closing
remarks
go
to
Fisher
and
Eugster
[1]
who
rightly
point
out
that
more
research
is
“needed
to
address
the
question
of
what
environmental
factors
affect
puberty
and
how
we
can
best
eliminate
relevant
exposures
with
the
goal
of
maximising
the
health
and
well-being
of
today’s
children
and
future
generations
to
come.”
Conflict
of
interest
In
the
past,
C.F.
Carson
has
received
research
grants
and/or
con-
sulting
fees
from
the
Australian
Government
and/or
from
industry
for
research
about
essential
oils.
R.
Tisserand
is
a
shareholder
of
First
Natural
Brands,
which
owns
Tisserand
Aromatherapy.
T.
Larkman
is
CEO
of
the
Australian
Tea
Tree
Industry
Association
(ATTIA
Ltd),
an
Australian
based
not-for-profit
organisation
formed
in
1986
as
the
peak
body
to
promote
and
represent
the
interests
of
the
Australian
tea
tree
industry.
Transparency
document
The
Transparency
document
associated
with
this
article
can
be
found
in
the
online
version,
at
http://dx.doi.org/10.1016/
j.reprotox.2013.09.010.
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Christine
F.
Carson
School
of
Pathology
&
Laboratory
Medicine
(M504),
The
University
of
Western
Australia,
35
Stirling
Hwy,
Crawley,
WA
6009,
Australia
Robert
Tisserand
407
Park
Road,
Ojai,
CA
93023,
USA
Tony
Larkman
ATTIA
Ltd.,
PO
Box
903,
Casino,
NSW
2470,
Australia
Corresponding
author
at:
ATTIA
Ltd.,
PO
Box
903,
Casino,
NSW
2470,
Australia.
Tel.:
+61
2
4017
1336;
fax:
+61
7
5604
1629.
E-mail
addresses:
christine.carson@uwa.edu.au
(C.F.
Carson),
robert@roberttisserand.com
(R.
Tisserand),
tlarkman@attia.org.au
(T.
Larkman)
28
June
2013
Available
online
17
February
2014
... I am concerned by the conclusions in this paper by Ramsay et al (1) and in particular the statement "…that physicians are aware that lavender oil (LO) and tea tree oil (TTO) possess endocrine-disrupting chemical (EDC) activities that should be considered in the evaluation of premature breast development in girls and gynecomastia in boys and adult men" when there remains reasonable doubt that it is indeed the essential oils (EOs) that are causing the EDC activity observed. An alternative hypothesis postulated by Carson et al (2) was cited and discussed, however the experimental work described to address this may be insufficient to dismiss the hypothesis. ...
... Earlier speculation raised questions regarding an earlier report (8) as to whether the properties of an oil in general could dissolve BPA analogs from the plastic assay plates and, therefore, elicit the detected hormonal activity (56). We addressed this concern by conducting additional experiments with corn and soybean oil alongside LO and TTO. ...
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