Nonatherosclerotic vascular changes may also mediate the effect of smoking on
genital function. The vasoconstrictive effects of nicotine in Cigarette smoke may impair
the complicated vascular processes involved in erection (Benowitz 1988). This may
be due in part to disturbances of prostaglandin production in the vascular endothelium
or to an enhancement of platelet aggregation noted by several investigators (Nadler,
Velasco, Horton 1983: Alster et al, 1986: Taylor etal. 1987: Lassila etal. 1988: Jeremy
etal. 1986: FitzGerald, Oates, Nowak 1988: Chapter 6).

Finally. hormonal effects of cigarette smoking could alter sexual responsiveness and
spermatogenesis. Alterations in the secretion of luteinizing hormone releasing hor-
mone (Moss, Riskind, Dudley 1979) or catecholamines (Patra, Sanyal, Biswas 1979:
Klaiber and Broverman 1988) are two such possibilities, but disturbances in sex
hormones, particularly low testosterone or high estradiol. have been suggested more
often. In general, men who smoke cigarettes have similar or higher testosterone levels
than nonsmokers; thus, it is difficult to associate low testosterone with sexual dysfunc-
tion among men who smoke (Briggs 1973: Shaarawy and Mahmoud 1982: Andersen,
Semezuk, Tabor 1984; Handelsman et al. 1984: Deslypere and Vermeulen 1984:
Vermeulen and Deslypere 1985: Vogt, Heller, Boreili 1986; Barrett-Connor and Khaw
1987; Dai et al. 1988: Lichtenstein et al. 1987; Meikle et al. 1987: Klaiber and
Broverman 1988), The adrenal androgens (i.€.. androstenedione.
dehydroepiandrosterone, and dehydroepiandrosterone sulfate) are elevated in male
smokers (Barrett-Connor, Khaw. Yen 1986; Barrett-Connor and Khaw 1987; Dai et al.
1988). Aromatization of these hormones may explain the elevated levels of estradiol
among males who currently smoke (Entrican, Mackie. Douglas 1978: Lindholm et al.
1982: Klaiber, Broverman, Dalen 1984: Barrett-Connor and Khaw 1987; Lichtenstein
et al. 1987; Dai et al. 1988; Klaiber and Broverman 1988). Elevations in circulating
estrogens may interfere with spermatogenesis and sexual behavior (Klaiber and Brover-
man 1988); such an explanation remains speculative.

Several studies have suggested that the estradiol and testosterone levels of former
smokers are comparable with those of never smokers (Deslypere and Vermeulen 1984:
Vogt, Heller, Borelli 1986; Barrett-Connor and Khaw 1987; Lichtenstein et al. 1987),
This observation implies that smoking cessation is likely to reverse any effect mediated
by disturbances of these hormones. Alternatively, former smokers may have had a
lower total dose. Androstenedione and dehydroepiandrosterone sulfate levels may be
modestly higher in former smokers compared with those of never smokers (Barrett-
Connor, Khaw, Yen 1986; Barrett-Connor and Khaw 1987: Lichtenstein et al. 1987),
However, the relevance of these findings to sexual capabilities is unlikely to be
significant. These hormones appear to have little intrinsic potency, and are important
because of their capacity for conversion to more active hormones such as testosterone
and estradiol (Baxter and Tyrrell 1987).

Sexual Activity and Performance

Surveys of the relationship between smoking and frequency of sexual episodes
(intercourse or masturbation) have generally found smokers to be as sexually active as
nonsmokers. In two studies of elderly men, sexual activity in smokers was comparable |

40]
with that of nonsmokers (Tsitouras, Martin, Harman 1982: Diokno. Brown, Herzog
1990): in a cross-sectional study of younger men. no differences were indicated ( Vogt,
Heller. Borelli 1986). Adolescent smokers are more sexually active than nonsmokers
(Russell 1971; Malcolm and Shephard 1978). In contrast, Cendron and Vallery-Mas-
son (1971), in studying 70 men older than age 45, found that those who reported
smoking between ages 25 to 40 also reported being less sexually active at those ages
than those who denied smoking. Overall, it appears that the relation between current
cigarette smoking and the level of male sexual activity is not very strong. Among
younger males, personality differences between smokers and nonsmokers may
dominate any adverse physiologic effects (Russell 1971).

If, as the aforementioned studies suggest, current smokers (or ever smokers) are
similar in sexual habits to never smokers, then no differences would be expected for
former smokers. Vogt, Heller, and Borelli (1986) evaluated 239 healthy male volun-
teers aged 19 to 40 without genital abnormalities or diseases and taking no medications.
The study results indicated that the 36 former smokers among them were comparable
with both never smokers and current smokers in sexual activity (Vogt, Heller, Borelli
1986).

Impotence. the inability to maintain an erection sufficient for intercourse. has been
more extensively investigated in relation to smoking. Among treated hypertensives
aged 40 to 64, cigarette smokers were more likely to report impotence. although the
differences were modest and not statistically significant (Biihler et al. 1988). A
statistically significant association was reported among men undergoing radiation
therapy for prostatic cancer (Goldstein et al. 1984). However. in both studies. poten-
tially important covariates, such as alcohol intake and age. were not considered. Two
other studies of men undergoing impotence evaluation indicated a high prevalence of
smoking and suggested an association between smoking with impotence (Virag.
Bouilly, Frydman 1985: Condra et al. 1986). Unfortunately, neither study included a
sexually functional control group. and both studies based their conclusions on ques-
tionable comparisons of the smoking rate in their clinic patients with that of the general
population. Vogt. Heller, and Borelli (1986) studied a group of young volunteers
without selecting for impotence. These investigators found that smokers reported more
difficulties with decreased libido and erection than nonsmokers (Vogt. Heller. Borelli
1986). This analysis did not consider former smokers separately.

An acute effect of smoking on sexual performance is suggested by a study of smokers
monitored while viewing erotic films (Gilbert. Hagen, D'Agostino 1986). The succes-
sive smoking of 2 cigarettes high in nicotine content significantly impaired the rate of
penile diameter change compared with that observed after smoking | cigarette or eating
candy. However, the clinical relevance of these observations is unknown because frank
impotence was not studied.

An important clinical measurement in the evaluation of impotence is the PBI. which
indicates the systolic blood pressure in the penis divided by systolic blood pressure in
the arm. A low value is considered to be evidence of compromise of the penile blood
supply. a factor which may interfere with erection. Several studies of men undergoing
evaluation of impotence reported an association between smoking and low PBI Jacobs
etal. 1983: Condra et al. 1986: Bornman and Du Plessis 1986: DePalma et al. 1987).

402
Among impotent diabetics, evidence of nocturnal erections was found less in smokers
compared with nonsmokers, thus suggesting an increased risk of vascular compromise
in smokers (Takahashi and Hirata 1988). However. other studies of impotent men have
not reported differences between smokers and nonsmokers in vascular measurements
(Wabrek et al. 1983; Virag, Bouilly, Frydman 1985; Kaiser et al. 1988). Most of these
investigations did not consider covariates such as alcohol use, although one study
suggested that smoking in isolation had little effect and that an association of smoking
with an abnormal PBI may be due to the association of smoking with other arterial risk
factors (Virag, Bouilly, Frydman 1985),

In many of the studies relating smoking and impotence, the investigators did not
distinquish nonsmokers as ex-smokers or never smokers. However. two investigations
considered former smokers separately (Table 15), Wabrek and associates (1983)
studied 120 men who were referred to a hospital-based erectile dysfunction program.
The percentage of former smokers was approximately the same among men with
impaired, borderline, and normal PBI. Condra and colleagues (1986) reported on 178
patients also referred for impotence. Former smokers were not separated for analysis.
but this study suggests that the PBI for ex-smokers is more normal than in current
smokers (Condra et al. 1986). However, neither study considered important covariates,
such as age and alcohol use (Wabrek et al. 1983: Condra et al. 1986).

Two recent investigations considered the effect of smoking cessation on impotence.
Forsberg and colleagues (1979) noted that two smoking men who were impotent
improved their functioning after smoking cessation at the same time that measures of
penile blood flow improved. However. it is not clear how these two men were selected
for this study. and control subjects were lacking. Elist. Jarman. and Edson (1984)
reported on the treatment of 60 impotent men. Twenty nonsmokers were treated with
the vasodilator isoxsuprine, and 40 smokers were either advised to stop smoking or
advised to stop smoking and also given isoxsuprine. There was no mention of
randomization, and there was no untreated control group. Similar proportions im-
proved whether given isoxsuprine, convinced to stop smoking. or both (Elist, Jarman,
Edson 1984).

Animal data have not elucidated the relation between smoking and either sexual
activity or impotence. Soulairac and Soulairac (1972) studied the sexual activity of
male rats given either a 0.6 mg/kg or a 1.2 mg/kg dose of nicotine subcutaneously. The
sexual activity of the rats after the nicotine administration was compared with that
before treatment. Sexual activity was markedly increased with the 0.6 mg/kg dose. and
at 1.2 mg/kg there was trembling and twitching and no sexual behavior for 2 to 3 hours.
In contrast, exposure to smoke from | cigarette has been shown to interfere with the
physiology of erection in male dogs (Juenemann et al. 1987).

In summary, the level of sexual activity does not appear to be affected by cigarette
smoking. Cigarette smoking may be associated with impaired male sexual perfor-
mance. Among impotent men, smokers are more likely to have an underlying vascular
problem. These associations have been more commonly noted in groups already at high
tisk of impotence, such as hypertensives and diabetics. However. these associations
have not been consistently observed, and the positive findings may be due to the
association of smoking with other factors such as alcohol use. Moreover, because the

403
TABLE 15.—Sexual performance among male former smokers

 

 

Reference Studs population Findings Comments
Vogt. Heller. Obe Volunteers No differences in sexual No consideration
(1984) activiy between former. of covariates

current. and never smokers

Wabrek et al. Impotent patients Propartion of former smokers No consideration
(1983) similar in men with of covariates
abnormal. impaired. and
normal PBI

Condra et al. Impotent patients Indications that former No consideration
(1986) smokers had more normal of covariates
PBI than current smokers

Forsberg et al. Impotent patients Two smokers improved No controls
(1979) sexual performance after
smoking cessation

Elist. Jarman, Edson Impotent patients Smoking cessation improved No untreated and
(1984) sexual performance as well controls
as vasodilator

 

NOTE, PBl=penile brachial inde,

studies of PBI are generated entirely in referral populations. it is unclear if these findings
can be generalized. Because of limited and uncontrolled data: no conclusions can be
drawn regarding sexual performance or PBI among former smokers.

Sperm Density and Quality

Measurements of sperm density. morphology. and motility are commonly used
assessments of sperm quality (Rogers and Russell 1987). Over 20 studies huve dealt
with the relation of cigarette smoking to sperm density. motility, and morphology
(Viczian 1968a: Schirren and Gey 1969: Campbell and Harrison 1979: Vogel. Brover-
man. Klaiber 1979: SteKhun 1980: Nebe and Schirren 1980: Evans et al. 1981: Godfrey
1981: Rodriguez-Rigau. Smith. Steinberger 1982: Shaarawy and Mahmoud 1982:
Buiatti etal. 1984: Andersen, Semezuk. Tabor 1984: Nordenson, Abramsson, Duchek
1984: Handelsman etal. }984: Hoidas et al. 1985: Kulikauskas. Blaustein. Ablin 1985;
Ablin 1986: Rantala and Koskimtes 1987: Vogt. Heller, Borelli 1986: Klaiber et al.
1987: Dikshit. Buch, Mansur 1987; Saaranen etal. 1987; Klaiberand Broverman 1988:
Saaranen et al. 1989: Rut. Oldereid. Purvis 1989; Marshburn, Sloan, Hammond 1989:
Oldereid et al. 1989). Table 16 summarizes the findings of those studies that reported
mean values for smokers and nonsmokers. In most studies, men smoking cigarettes
had lower sperm density, although many of these studies indicated differences that were
not statistically significant. The smokers’ average sperm density was at least 80 percent
that of the nonsmokers. In several studies sperm morphology or motility was impaired

404
in smokers compared with nonsmokers. but this was a less consistent finding. Few
studies have considered the spermatic chromosomal characteristics of smokers com-
pared with nonsmokers. Nordenson, Abramsson. and Duchek (1984) found smokers
to have more chromosome breaks than nonsmokers. but Oldereid and coworkers (1989)
reported no differences in DNA condensation as assessed by flow cytometry.

Although differences in mean values of any of these measurements suggest an effect
of smoking. the most relevant parameter may be the percentage of smokers and
nonsmokers who exhibit deficiencies in sperm density. morphology. or motility.
Several researchers have investigated the relative risk of azoospermia (no sperm in the
ejaculate) or oligospermia (reduced number of sperm) in smokers versus nonsmokers
or never smokers (Table 17). Although the range of relative risks is wide. there is a
clear pattern of increased risk among smokers. However, the clinical significance of
oligospermia is uncertain. Most studies have used one ejaculate per man, although the
within-man coefficient of variation can be as much as 60 percent (Schenker etal. 1988).

The available information suggests that current smoking is related to low sperm
density. However, these data are limited. Many studies investigated men visiting
infertility clinics, limiting generalization. Moreover, if male smokers with poor sperm
quality are most likely to attend these clinics, selection biases may distort the results.
Also, many of these studies were relatively informal. Few of the studies accounted for
potentially confounding factors such as alcohol use and age. Less than half of the
studies documented that a period of sexual abstinence was required for subjects before
giving the sperm sample, and few of the studies analyzed multiple semen specimens as
some authorities recommend (Zaneveld and Jeyendran 1988). Most studies have a
small number of subjects. and their statistical power is limited for this reason. In some
of the studies, it is not clear whether former smokers were included in the smoker or
nonsmoker group.

A few studies investigated ex-smokers (Table 18). One was a case-control study of
male infertility in Italy (Buiatti et al. 1984). The cases were azoospermic or oli gosper-
mic men being treated for infertility at the University of Florence. Controls were
University outpatients who had normal sperm counts. There were no significant
differences between smoking categories in the percentage of men with low sperm
counts. Vogt. Heller, and Borelli (1986) evaluated 239 male volunteers. Among
former smokers (those who had smoked for at least | year and those who had stopped
smoking for at least | year). percent normal spermatozoa. percent young forms, percent
old forms, and percent degenerate forms were comparable with those of never smokers.
Stekhun (1980) reported that 42 percent of former smokers had oligospermia compared
with 18 percent of never smokers. Schirren and Gey (1969) reported that three men
with low sperm density and motility showed substantial increases in these parameters
3 to 6 months after smoking cessation. However, there were no controls defined in this
analysis. Because of the limitations of the four studies. no conclusions are possible
regarding the effects of smoking cessation on sperm quality in humans.

Animal studies have not been particularly informative. In some studies. rodents that
were heavily exposed to nicotine or cigarette smoke demonstrated testicular atrophy.
but this has not been a general finding (Larson, Haag. Silvette 1961: Larson and Silvette
1968: Dontenwill et al. 1973b: Essenberg. Fagan. Malerstein 1951: Thienes 1960:

405
TABLE 16.—Sperm quality among smokers and nonsmokers

 

Ratio of measure among smokers

Study population
' to that among nonsmokers

(number of

 

/ honsmokers/number of Sperm @ Normal‘ Motile
Reference smokers) density sperm sperm Comments
Viezian Obstetrics clinic 0.82 0,90 0.77 No decrease in
(1968a) (smokers only ) (50/120) sperm density with
increasing amounts
smoked: controls
were fertile men
Vogel. Broverman. — Unstated 0.60" NS 0.87"
Klaiber (39/17)
(1979)
Nebe and Schirren Andrology clinic 1.01 _— _—
(1980) (455/451)
Evans et al. Subfertility clinic — 0.92" -~ Smokers and
(1981) (43/423) nonsmokers
matched on sperm
density
Godfrey Infertility clinic — 0,94 — Oligospermic” men
(1981) (74f75) omitted
(<b x 10°/mL)
Spira et al. Vasectomy candidates 01.75" 0.94 0.93"
(1981) (173/122)
Infertility clinic 0.86 0.91" 0.97
(228/292)
Rodriguez-Rigau, Infertility chnic 0.95 1.00 1.00
Smith, Steinberger (101/58)
(1982)
Shaarawy and Volunteers 0.93 0.69" 0.67" All subjects were
Mahmoud (1982) (20/25) fertile
Andersen, Semezuk, Infertility clinic (86/137) 0.99 1.07 1.08 10 azoospermic”
Tabor (1984) smokers omitted
from analssis
Handelsman Semen donors (71/23) 0.67 0.98 0.93"
etal. (1984)
Kulikauskas, Fertility clinic (135/103) 0.43" £.00 0.78"
Blaustein.
Ablin (1985)
Rantala and Infertility clinic (50/60) 0.90 0,98 0.95 Oligospermic” men
Koskimies omitted (<1 x
(1987) 10°mL
Vogt. Heller. Borelli Volunteers OR 1° 1.01 0.99
(1986) (52/150)

406
TABLE 16.—Continued

 

Ratio of measure among

Study population smokers to that among nonsmokers

 

 

(number of

nonsmokers/number of Sperm % Normal ‘% Motile
Reference smokers) density sperm sperm Comments
Saaranen Infertility clinic 0.81 1.00 0.97 Azoospermic’ men
etal. (1987) (110/54) omitted
Klaiber et al. Paid volunteers (90/60) 0.77" 0,98 0.89"
(1987)

Males from infertile 0,52" 0.04 0.80"

couples (43/51)
Dikshit. Buch. Infertility clinic 0.96 0.99 1Ol
Mansuri (1987) (288/219)
Klaiber and Volunteers 0.93 1.02 0.97
Broverman (1988) (21/22)
Saaranen etal. Semen donors O.83 0.95 1.01
(1989) and fertile men (32/28)
Marshburm, Sloan, Infertility clinic 0.92 0,99 0.94
Hammond (1989) (294/152)
Rui, Oldereid. Infertility clinic L.17 1.05 0,96 Azoospermic™ men
Purvis (1989) (203/147) omitted
Eftendy and Krause Infertility clinic 1.13 1.06 1.12

(1987) (61/31)

 

"Statistically significant difference (p<0.05) between smokers and nonsmokers
b :

Ohgospermia is a low sperm count.
‘ a .

Azoospermia is the absence of sperm.

Thompson et al. 1973: Patra, Sanyal, Biswas 1979: Biswas and Patra 198t). Some
studies have noted a disturbance of spermatogenesis. a decrease in the interstitium, or
a destruction of the seminiferous epithelium (Larson, Haag. Silvette 1961: Larson and
Silvette 1968: Essenberg. Fagan. Malerstein 1951: Viczian 1968b: Wyrobeck and
Bruce 1975; Biswas and Patra 1981: Alwachi et al. 1986; El-Sayad et al. 1987). The
results may depend on the duration and dose of exposure. as well as on the ages at which
exposure takes place. Moreover, the relevance to humans of the large doses given to
the animals is uncertain. None of these investigations considered spermatogenesis after
exposure ended: thus. few conclusions may be drawn regarding the effect of cessation
of exposure even within the limitations of the animal studies.

407
TABLE 17,—Fstimated relative risk of azoospermia or oligospermia among
smokers versus nonsmokers or never smokers

 

Study population

 

(number of Estimated
nonsmokers/ relative risk in
Reterence number of smokers) Contrast smokers Comments
Schirren and Gey — Andrology clinic Azoospermia: 1.2
(1969) (S80/1377) smokers vs. nonsmokers
Oligospermia: smokers 1.2 Oligospermia not
vs. nonsmokers defined
Campbell and Fertility clinic Oligospermia 1.6" Azoospermic men
Harrison (1979; (119/134) 1<40 x 10°%mL): omitted
smokers vs. nonsmokers
Stekhun Not stated (33/105) — Oligospermia; current 3.2 Oligospermia not
(1980) smokers vs. never defined
smokers
Rodriguez-Rigau. Fertility clinic Oligospermia: 0.9
Smith, Steinberger (101/58) (<20 x 10°%/mL3:
(L9R2) current smokers vs.
nonsmokers
Buiatti et al. Fertility clinic Oligospermia 1.0
(1984) (80/135) (<20. 10%mL):
smokers vs.
nonsmokers
Andersen, Fertility clinic Azoospermia: current oot
Semezuk. (86/147) smokers vs. nonsmokers
Tabor (1984)
Ablin (1986) Not stated Oligospermia 2.9"
(135/238) (<40 x 10"/mL):
smokers vs. nonsmokers
Vogt. Heller. Volunteers Oligospermia (<1 x oo
Borelli (1986) (52/150) 10°/mLy: current
smokers vs. never
smokers
Avoospermia: °°
current smokers vs.
never smokers
Klaiber et al. Volunteers with Oligospermia (<20 x °°
(1987) Vanicocele 1o°'%mL
Cd1/9) current smokers \s,
never smokers
Volunteers without ~~ Oligaspermia (<20 x 1.3
varicocele tO"mL»: current
(79/61) smokers vs. never
smokers
Ferthity clinic with — Oligospermia (<20 x 77

408

Vareocele (8/21)

fh
10°/mL): current
smokers vs. never
smokers
TABLE 17.—Continued

 

Study population

 

(number of Estimated
nonsmokers/ relative risk in
Reference number of smokers) Contrast smokers Comments
Klaiber et al. Fertility clinic Oligospermia (<20 x LS
(1987) without varicocele 10°/mL); current
(continued) (35/30) smokers vs, never
smokers
Dikshit, Buch, Fertility clinic Oligospermia (<20 x 1.2

Mansuri (1987)

(219/288)

6
10°/mL)}: current
smokers vs. never
smokers

Azvoospermia: current
smokers vs. never
smokers

 

NOTE: Azoospermia is the absence of sperm: oligospermia is a low sperm count.

“Estimated relative risk statistically significantly (p<0.05) different from 1.0.

TABLE 18.—Sperm quality among former smokers

 

 

Reference Study population Findings Comments
Schirren andGey — Andrology Smoking cessation improved sperm No control
(1969) patients density and motility in 3 smokers
Stekhun (1980) Not stated Former smokers had RR of 2.3 for Oligospermia not

Buiatti et al.
(1984)

Vogt, Heller,
Borelli (1986)

Male partners of
infertile couples

Healthy volunteers

oligospermia

defined

No difference between current, former,
and never smokers in prevalence of

azoo-/oligospermia

No difference between current. former,
and never smokers in sperm

morphology

No consideration
of covariates

 

NOTE: RRe=relative risk.

409
tN

Nd

CONCLUSIONS

- Women who stop smoking before becoming pregnant have infants of the same

birthweight as those born to never smokers.

Pregnant smokers who stop smoking at any time up to the 30th week of gestation
have infants with higher birthweight than do women who smoke throughout
pregnancy. Quitting in the first 3 to 4 months of pregnancy and abstaining
throughout the remainder of pregnancy protect the fetus from the adverse effects of
smoking on birthweight.

Evidence from two intervention trials suggests that reducing daily cigarette con-
sumption without quitting has little or no benefit for birthweight.

Recent estimates of the prevalence of smoking during pregnancy. combined with an
estimate of the relative risk of low birthweight outcome in smokers, suggest that 17
to 26 percent of low birthweight births could be prevented by eliminating smoking
during pregnancy: in groups with a high prevalence of smoking (e.g.. women with
less than a high school education), 29 to 42 percent of low birthweight births might
be prevented by elimination of cigarette smoking during pregnancy.

. Approximately 30 percent of women who are cigarette smokers quit after recogni-

tion of pregnancy. with greater proportions quitting among married women and
especially among women with higher levels of educational attainment.

Smoking causes women to have natural menopause | to 2 years early. Former
smokers have an age at natural menopause similar to that of never smokers.

410
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CHAPTER 9
SMOKING, SMOKING CESSATION, AND
OTHER NONMALIGNANT DISEASES

425