44 96
Duration and
intensity of
the
smoking habit was associated
with
an
increased
risk
of
ED.
Among
former
smokers,
the
risk
of
ED
significantly
decreased, with
an
increase
in
the
number of years since the patient quit smoking
[22]. Austoni
et
al
evaluated
16
724
subjects
and
showed
a
dose
and
duration–response
effect
of
smoking
on
ED.
ORs
of
ED
for
current
smokers were 1.1
(95% CI,
0.7–1.6), 1.7
(95% CI,
1.2–2.3), and 1.6
(95% CI, 1.3–2.0)
for
<
10 yr, 10–20 yr, and
>
20
yr,
respectively,
compared with
never
smokers.
Also,
former
smokers had
a duration–response
effect of
smoking
on ED with ORs of 1.0
(95% CI, 0.6–1.7), 1.2
(95% CI, 0.8–1.8),
and
2.0
(95% CI,
1.3–2.0)
for
<
10
yr,
10–20
yr,
and
>
20
yr,
respectively,
compared with
never
smokers
[6] .3.3.
The
role
of
passive
smoking
on
erectile
dysfunction
Evidence
exists
that
secondhand
(passive)
smoking
increases
the
risk
of
heart
disease
(by
approximately
30%)
and
adversely
affects
vascular
function.
Despite
the
fact
that
the
dose
of
smoke
delivered
to
active
smokers
is
100
times
than
that
delivered
to
a
passive
smoker,
the
relative
risk
of
CVD
for
active
smokers
is
1.78
compared
with 1.31
for passive
smokers.
In many
cases,
the
effects of
even brief
(minutes
to hours) passive
smoking are nearly as
large as
those
from chronic active smoking. Passive smoking
leads
to
68–86%
of
the
risk
of
light
smoking,
depending
on
the
level
of
secondhand
smoke
exposure
[23].
To date
very
few
data
regarding
the
role
of
passive
smoking
on
ED
development
are
available. A
recent
report
addressing
this
issue
derives
from
the
Boston
Area
Community
Health
survey.
This
study
demonstrated
that,
although
the
association
between
passive
smoking
and
ED
is
not
statistically
significant,
the
magnitude
of
the
effect
of
passive
smoking
is
comparable with
10–19
pack-years
of
smoking exposure
[24]. Previously published data
from
the
Massachusetts
Male
Aging
Study
also
showed
that
men
exposed
to
passive
smoking
double
the
risk
of
developing
ED
over
a
9-yr
follow-up
period
[4].
Bivalacqua et al
recently determined
the effect of passive
cigarette
smoke
on
erectile
function
in
vivo,
molecular
mechanisms
involved
in
penile
vascular
function,
and
erectile
function
and
penile
molecular
signaling
in
the
presence
of
phosphodiesterase
type
5
inhibitor
therapy.
The
results
of
their
study
showed
that
short-term
exposure
to
secondhand
smoke
impairs
erectile
function
through
excessive
penile
ROS,
signaling
an
iNOS
activity. Decreased
penile
constitutive NOS
activity may
be
attributable
to
the
decreased
eNOS
activity
resulting
from
increased
oxidative
stress. Sildenafil therapy restored NOS activity and decreased
ROS
signaling,
resulting
in
improved
erectile
function
[25] .Overall,
these
results
suggest
that,
although
the
in-
creased
risk
in ED with passive
smoking
is
small,
long-term
chronic
exposure
to
passive
smoking
may
have
adverse
effects
on
erectile
function.
3.4.
Smoking
cessation
and
erectile
function
recovery
Only
a
few
studies have
investigated
the
effects
of quitting
smoking
on
erectile
function.
Guay
et
al were
the
first
to
measure nocturnal penile
tumescence and rigidity using
the
RigiScan
portable
home monitor
in
10 male
smokers.
All
patients
had
smoked
for
at
least
30
pack-years
and were
smoking
1
pack
of
cigarettes
per
day.
Two
nights were
monitored: For
the
first night,
the patients had not
stopped
smoking;
for
the
second
night,
the
patients
had
stopped
smoking
for
24 h.
In
addition,
four men
were monitored
after cessation of
smoking and wearing nicotine patches
for
1 mo.
Rigidity
activity
units
and
tumescence
activity
units
were
recorded.
Results
showed
significant
improvement
24 h after
smoking cessation
for both of
these
indices. More
interestingly,
the
results
relative
to
the
four men who were
assessed
1
mo
later
while
adhering
to
a
daily
21-mg
nicotine
transdermal
patch
regimen
indicated
a
trend
for
continued
improvement
[26] .Similarly,
Sighinolfi
et
al
showed
a
significant
improvement
in
penile
blood
flow
24–36 h
after
smoking
discontinuation
in
a
sample
of
20
heavy
smokers
affected with
ED
[27].
In
a
prospective
comparative
study
conducted
on
118
former
smokers
and
163
current
smokers,
Pourmand
et
al
assessed
whether
stopping
smoking
can
improve ED
in
smokers. After 1 yr of
follow-up,
the
ED
status
improved
in
25%
of
former
smokers but
in none of
the
current
smokers; 2.5% of
former
smokers and 6.8% of
current
smokers had a deterioration
in
ED.
Former
smokers
had
a
significantly
better
ED
status
after
the
follow-up
(
p
= 0.009).
Among
former
smokers,
patients with
advanced
ED
and
those who were
older
had
less
improvement
[28].
More
recently,
the
association
between
smoking
cessa-
tion
and
an
improvement
in
men’s
sexual
health
was
demonstrated
in
another
prospective
study.
Participants
were
aged
23–60
yr,
smoked
at
least
15
cigarettes
per
day
for a minimum of 5
consecutive years, had no
self-reported
sexual
dysfunction
before
smoking
onset,
and
received
an
8-wk
nicotine
transdermal
patch
treatment.
Study
results
showed
that
successful
quitters,
compared
with
unsuccessful quitters, presented significantly greater penile
tumescence
at
follow-up
(4
wk
after
nicotine
patch
discontinuation),
but
there
were
no
differences
at
mid-
treatment
(while
using
a
high-dose
nicotine
patch).
The
overall
pattern
of
results was
similar
to
previous
studies
showing
that
smoking
cessation
leads
to
significant
improvements
in
penile
blood
flow,
as
well
as
rigidity
and
tumescence.
Interestingly,
results
suggested
for
the
first
time
that
cessation-induced
improvements
in
sexual
health were
attributable
primarily
to
nicotine
elimination
(as
evidenced by between-group differences
in physiologic
outcome measures
at
follow-up when
successful
quitters
were
nicotine
and
smoke
free),
rather
than
tobacco
smoke
discontinuation
alone
[29].
As
reported
in
the
study
from
Chew et al, among
former smokers, the age-adjusted odds of
ED were
significantly higher 6–10 yr
following
cessation of
smoking
than
<
5 or
>
10 yr. These patterns of ED
in
former
smokers suggest that there may be a
latent
interval between
active
smoking
and
symptomatic
ED,
involving
a
process
initially
triggered
by
smoking
[10].
Table 2presents
a
detailed
overview
of
the
characteristics,
outcomes,
and
covariates of studies assessing
the
risk of smoking cessation
and
erectile
function
recovery.
E U R O P E A N
U R O L O G Y
F O C U S
1
( 2 0 1 5
)
3 9 – 4 6
44