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Industrial Health 2003, 41, 55–62
*To whom correspondence should be addressed.
Review Article
Effect of Occupational Exposures on Male Fertility:
Literature Review
Einat K. SHEINER
1
, Eyal SHEINER
2
*, Rachel D. HAMMEL
4
,
Gad POTASHNIK
3
and Refael CAREL
1
1
Department of Occupational Medicine,
2
Department of Obstetrics and Gynecology,
3
Fertility & In-Vitro Fertilization Unit,
1–4
Faculty of Health Sciences, Soroka University Medical Center, Ben-Gurion University of the Negev, Beer-
Sheva, Israel
Received September 17, 2002 and accepted January 14, 2003
Abstract: The present review was aimed to determine the influence of working conditions,
occupational exposures to potential chemical and physical reproductive toxic agents and psychological
stress during work on male fertility. Significant associations were reported between impaired semen
parameters and the following chemical exposures: metals (lead, mercury), pesticides
(dibromochlorophane, 2,4-dichlorophenoxyacetic acid), ethylene glycol ethers and estrogens. The
following physical exposures were shown to deteriorate sperm parameters: radiation (both ionized
and microwaves) and heat. Psychological distress has another important contribution to infertility.
Several studies indicated that stress has a negative impact on sperm parameters. Occupational
parameters should be an important part of history taking among patients attending infertility clinics.
Key words: Male infertility, Occupational exposures, Psychological stress
Introduction
Problems of the human reproductive tract lead to a variety
of undesired outcomes such as complete or partial infertility;
spontaneous abortion, including early undiagnosed
miscarriage; teratogenic insults and birth defects; mutation
development and genetic defects; cancers in progeny (i.e.
diethylstilbestrol, DES); as well as growths in the
reproductive tract and breasts. In the U.S., one in seven
married couples suffers from fertility problems. Spontaneous
abortion occurs in approximately 10–20% of clinically
identified pregnancies. Of live births, around 7% are born
with low birth weights, and 3% suffer from significant birth
defects. Developmental delay is diagnosed with a high
prevalence in the early years of life
1)
.
In an attempt to prevent or to explain these phenomena,
many couples turn to their health care providers with
questions about the influence of workplace exposures on
the abovementioned conditions. The answers to these
questions are complicated due to the lack of information on
causality and on the multi-factorial nature of the problem;
absence or scarcity of data on the thousands of chemicals
used industrially; and the unclear influence of lifestyle,
previous health status, use of medications, and psychological
factors on reproductive success.
In every clinical investigation of a fertility problem, an
extensive evaluation must be performed on the health status
and possible outside influences in both partners. In the
evaluation of reproductive injury in the male, it is important
to include the following
2)
:
56
EK SHEINER et al.
Industrial Health 2003, 41, 55–62
1. Urological evaluation including the existence of
abnormal anatomy, genetic causes, endocrinologic
disturbance, and varicocele.
2. History of testicular trauma, surgery, or mumps.
3. Heat exposure: heat stroke, tight underwear, hot baths,
or work conditions requiring extended periods of sitting,
extended travel, or work in the heat (see details to come).
4. Extreme allergic reaction.
5. Drug dependence, alcohol use, or heavy smoking.
6. Use of medications such as cimetidine, spironolactone,
nitrofuran, sulfasalazine, erythromycin, tetracycline,
anabolic steroids, chemotherapeutic agents, alpha-
blockers, pentolamine, methyldopa, guanethidine and
reserpine.
7. Frequency of sexual relations: For most couples,
intercourse every 36 hours around the time of ovulation
should optimize the conditions for conception.
8. Exposure to environmental and industrial toxins.
Evidence has shown a considerable and continuous decline
in the quality of sperm over the past fifty years. The increase
in environmental pollution in industrial countries in recent
decades raises questions about the extent of the contribution
of environmental and industrial factors to this decline
3, 4)
.
At the National Institute for Occupational Safety and
Health Registry, approximately 104,000 chemical and
physical agents existing in workplaces are listed. The toxicity
of most of these materials is not known or has only been
partially studied
5)
.
In humans, exposure to some of these agents may cause
cancer, reproductive and developmental disturbances,
neurological and immunological sequellae and other damage.
The effects on fertility and development may directly
influence couples planning pregnancy, especially considering
the fact that exposure to some materials during critical points
of fetal development may directly affect the fetus in its adult
life, and even generations to come.
There are many reasons for the lack of information on
the influence of occupational exposure to chemical and
physical materials. Animal studies generally test the health
effects of a single factor. This standard approach makes it
difficult to come to a conclusion about the interactions of
different factors. Furthermore, animal studies generally do
not investigate long-term effects or those difficult to identify,
such as developmental delay. Epidemiological studies in
humans often provide limited and imprecise information
regarding exposure or health outcomes. Other limiting factors
stem from a lack of governmental support for the study and
a lack of accessibility to the exposure data, particularly in
developing countries. The missing data is filled in by the
industrial organizations supporting the investigations, which
could lead to inaccuracy in the study design and in
interpretation of results
6)
. Another known limitation is the
technical difficulty in obtaining repeated semen samples from
healthy employees in order to pursue this type of investigation
in the workplace
7)
.
The earliest report of occupational exposure related to
fertility was done by the English doctor Percivall Pott in
1775, and described the high incidence of skin cancer of
the testicles in chimney sweeps. This observation led to
the publication of safety guidelines requiring the bathing of
these workers
8)
. Currently, the main known categories of
occupational agents and factors affecting fertility include:
heavy metals; solvents; pesticides and other agricultural
chemicals; estrogens; exposure to physical agents such as
radiation; heat; and professions which involve a combination
of negative factors such as welding and driving
9)
.
Exposure to Chemical Agents (Table 1)
Metals
One of the first materials to be demonstrated as detrimental
to fertility was lead. An increase in the level of lead in blood
tests in men was linked to an amplified risk of miscarriage
in a case-control study from Finland
10)
. Another Finnish
study provided support for the existence of a connection
between occupational exposure of the father to lead and birth
defects in children
11)
. Analysis of sperm counts in lead
workers showed a decrease in sperm count, as well as
decreased motility and lifespan of sperm, in direct relation
to the level of lead in the blood
12)
. A non-significant longer
time-to-pregnancy interval within subjects exposed to high
levels of lead was documented by Apostoli et al.
13)
. On the
basis of animal studies, alterations in sperm chromatin
stability or epigenetic effects may serve as possible
mechanisms causing reduced fertility
14)
. Concentrations of
lead and cadmium in semen samples of subjects with
abnormal semen parameters as compared to
normozoospermic patients did not differ
15)
. On the contrary,
Telisman et al.
16)
concluded that even moderate exposures
to lead (blood lead < 400 microg/L) and cadmium (blood
cadmium < 10 microg/L) can significantly reduce human
semen quality without conclusive evidence of impairment
of male reproductive endocrine function.
In laboratory animals, high levels of hexavalent chromium
cause testicular atrophy and decrease in sperm count. In
human studies, it has been found that exposure to chromium
is significant in welders. Diminished sperm quality among
welders has been demonstrated in a number of studies
17, 18)
,
57
OCCUPATION & MALE FERTILITY
but has not been definitively linked to exposure to chromium.
As such, this profession is linked generally with occupational
exposures affecting fertility (see details which follow). A
biological theory exists stating a direct influence of lead
and chromium on the structure of sperm, involving a partial
exchange with zinc, which is an important ingredient of sperm
that makes it heat-resistant
9)
. Exposure to copper has even
been shown to be linked to a decreased sperm count and to
be a cause of terato- and asthenozoospermia
9)
.
Pesticides
In 1977, it was reported that a group of men working in a
pesticide plant in California had experienced a decreased
birth rate in recent years [19]. The plant dealt at that time
with the production of an agricultural pesticide called
Dibromochloropropane (DBCP). A similar report was
published a year later in Israel by Potashnik et al.
20)
about
workers in a pesticide plant who came in contact with the
same material. This report demonstrated the suppressive
effect of DBCP on human spermatogenesis
20)
. In a follow-
up of the workers exposed to this material, it became clear
that the agent could cause permanent azoospermia
21)
.
Potashnik and Porat
21)
investigated testicular function among
15 employees in the DBCP plant in a 17-year follow-up
study. An improvement in the sperm count with exposure
cessation was observed within 36–45 months in one third of
the azoospermic men, and in one half of the oligospermic
men, with no improvement expected beyond that time frame.
Additionally, the insult was accompanied by an increase in
gonadotropin levels and a decrease in testosterone levels.
Tielemans et al.
22)
reported reduced in vitro fertilization rates
with paternal pesticide exposure. Other chemicals used in
agriculture, such as ethylene di-bromide and carbaryl were
linked to a decline in sperm function and in male fertility.
Moreover, an increased risk of spontaneous abortion was
found among wives of workers exposed to pesticides
23)
.
Industrial chemicals (Solvents)
Materials of the ethylene glycol ether variety, particularly
2-methoxyethanol (2-ME) and 2-ethoxyethanol (2-EE),
represent an important group of organic solvents found in
paints, dyes and thinners, as well as many other uses. Studies
in laboratory animals have demonstrated damage by 2-ME
and 2-EE to male fertility and to the physical and aesthetic
structure of offspring
24, 25)
. Cherry et al.
26)
found a significant
association between intensity of exposure to solvents and
clinical findings of less than 12 × 10
6
motile sperm (Odds
ratios (ORs) were 2.07 (95% confidence interval (95% CI)
1.24 to 3.44) for moderate exposure and 3.83 (95% CI 1.37
to 10.65) for high exposure to solvents). Kurinczuk and
Clarke
27)
investigated exposure to solvents among infertile
men attending hospital clinics. Compared with fertile
controls, the infertile men were 1.73 times (95%CI 1.26–
2.38) more likely to work with solvents. The authors
concluded that workers with solvents were at an increased
risk of presenting with infertility, although it was not mediated
through effects on standard measures of sperm quality. While
investigating the relationship between occupational styrene
exposure and male fecundity, a non-significant reduced
fecundity was observed for the styrene-exposed workers
(fecundity ratio 0.79, 95% CI 0.59–1.05). However, the
authors concluded that it is unlikely that styrene exposure
has a direct effect on male fertility
28)
.
De Celis et al.
29)
investigated whether occupational
exposure to hydrocarbons has adverse effects on the semen
quality. Damage to the spermatogenic process resulting from
Table 1. Occupational chemical agents with possible adverse effect on male fertility
Substance Effect Ref
Metals Lead Spontaneous abortions, Birth defects 10, 11, 12, 16
Decreased sperm count
Cadmium Reduced sperm quality 16
Chromium Testicular atrophy 17, 18
Decreased sperm count 9
Copper Decreased sperm count 9
Pesticides DBCP Decreased sperm count, Azoospermia 21, 22
Ethylene di-bromide Decreased sperm function 23
Carbaryl Decreased sperm function 23
Solvents Ethylene glycol ether, Hydrocarbon Decreased sperm function 24, 25, 26, 27, 29, 30
Phthalate esters Anti-fertility effects, Decreased sperm function 31, 32, 33
Estrogens Decreased sperm counts 34, 35
58
EK SHEINER et al.
Industrial Health 2003, 41, 55–62
hydrocarbon exposure was demonstrated by an increased
rate of abnormalities in the semen of exposed workers as
compared with unexposed controls. Thus, it seems that there
is a clear association between solvent exposure and impaired
semen parameters
30)
.
Results of past animal studies have indicated the anti-fertility
effects of phthalate esters and even possible mutagenic effects
at very high doses
31)
. Moreover, preliminary results indicated
that antifertility effects occurred with as little as three
subcutaneous doses of 1 ml/kg each, with a dose-dependent
effect. Likewise, a continuous breeding protocol in CD-1
mice was utilized to examine the reproductive toxicity of
phthalate esters. Reproductive function was evaluated during
the cohabitation period by measuring number of litters per
pair, live pups per litter, and pup weight. Both di-n-pentyl
phthalate (DPrP) and di-n-propyl phthalate (DPP) were toxic
to the reproductive system as evidenced by a complete
inhibition of fertility and reduced fertility. Toxicity of DPP
had a strong component of both male and female reproductive
systems, whereas DPrP was more toxic to the female than
the male reproductive system. In addition, DPP and DPrP
treatment was associated with decreased testis and epididymis
weights, decreased epididymal sperm concentration, and
elevated seminiferous tubule atrophy
32)
. However, human
exposure data suggests that humans produce very low levels
of the monoester from an environmental exposure to the diester.
Thus, the likelihood of any reproductive toxicity via oral
exposure appears extremely rare
33)
.
Estrogens
Estrogens and estrogen derivatives are found in use in
the pharmaceutical industry (oral contraceptive pills and,
in the past, DES—diethylstilbestrol), DDT, chlordecone, and
phytoestrogens (mainly in soy beans). It is known that
estrogen derivatives affect the development of sertoli cells
in the testicles. These cells secrete hormones that regulate
the production of sperm, the descent of the testicles into the
scrotum, and urethral development
6)
. Synthetic estrogen,
DES, which was used from the 1940’s to the 1970’s in the
treatment of threatened abortions and the prevention of
miscarriages, was discovered to be a factor in decreased
sperm counts and testicular cancer in boys born to treated
mothers. The effect of estrogens on adult males is less clear,
but there are reports of hormone imbalance in men who work
in the oral contraceptive industry
34)
, and of a decrease in
sperm count in workers with chlordecone poisoning
35)
.
Exposure to Physical Agents
Ionizing and non-ionizing radiation
The effect of ionizing radiation on spermatogenesis has
been investigated extensively in the laboratory, and human
data exists as well. In the 1970’s, in the U.S., prisoners
volunteered to be subjected to x-rays of their testicles in a
study that aimed to determine the effect of radiation on
spermatogenesis
36)
. The results showed that a dose of 0.11
Gy causes a meaningful suppression of sperm count, and
that radiation of 3–5 Gy leads to permanent sterility. In an
investigation of sperm parameters in people who worked in
the clean-up of the Chernobyl nuclear disaster, significant
changes were found in the population exposed to more than
100 mSv
37)
. Damage to sperm quality has also been described
following long-term exposure to microwaves
38)
.
Heat
Active production of sperm requires a temperature about
3–4°C lower than normal body temperature. This fact is
supported by the decreased sperm count seen in pathologies
such as varicocele and cryptorchidism, as well as in cases
of prolonged sauna exposure and in paralyzed patients
restricted to wheelchairs
39, 40)
. The effect of chronic
occupational exposure to high temperatures has been
examined, in addition to in the welding profession, in the
ceramics industry
41)
. Impairment of spermatogenesis has
been found in a high prevalence among professional drivers,
as well
42, 43)
. Velez de la Calle et al.
44)
investigated infertility
risk factors in a French military population and found heat
exposure as an independent risk factor for male infertility
(OR 4.5, 95%CI 1.9–10.6), using a multivariate analysis.
Compound exposures
Occupational exposures do have a negative impact on
the male reproductive system, but sometimes it is difficult
to isolate a single insult. An insult to spermatogenesis has
been proven, for example, among professional drivers
42, 43)
,
who are exposed to the products of fuel consumption, noise,
vibration, emotional stress, physical load on the pelvic organs,
and increased temperature in the pelvis because of prolonged
sitting. Another example is that of welders, who are exposed
to heat, solvents, heavy metals and noise. As previously
stated
17, 18)
, theories exist about the diminished sperm quality
in welders, but the weight of each associated factor in the
impairment has not yet been established. As such, there are
many methodological problems in these studies.
59
OCCUPATION & MALE FERTILITY
Psychological factors
There is no doubt that infertility status is linked to
psychological disturbances and emotional stresses in both
partners
45)
. From the physiological point of view there is a
connection between psychological stress and levels of cortisol,
prolactin, progesterone and testosterone
46)
. Psychological stress
can represent part of the etiology of infertility [Psychogenic
Hypothesis], and can also be a result of the infertility itself
[Psychological Consequences Hypothesis]. The hypothesis
of stress as a lone factor in the etiology of infertility has been
rejected by the majority of studies; however, the evidence
that it stands as an additional, independent factor is growing.
Stoleru, et al.
47)
, in a prospective study in 63 couples that
began shortly after they stopped using contraceptives, showed
that a number of psychological factors separated the couples
that did conceive within a year from those that did not. In
another prospective study
48)
, the same group of researchers
attempted to distinguish between psychological factors leading
to infertility (Psychogenic Hypothesis) and those that stem
from fertility problems (Psychological Consequences
Hypothesis). For a period of 13 months, the researchers
followed couples whose fertility status was not known
beforehand and couples with known fertility problems. The
investigators concluded that in women, the parameters
checking integration between the desire for a child and
sexuality/sexual problems, reflected a reaction to fertility status
(that is to say, a result in favor of the Psychological
Consequences Hypothesis). In men, however, the same
parameters represented etiological factors in infertility (in other
words, a cause—in favor of the Psychogenic Hypothesis).
The majority of studies concentrate on the influence of
emotional stress on various aspects of female fertility, but a
number of studies exist that deal with the relationship between
male stress and fertility status. In a study of 28 couples,
Slade et al.
49)
found that decreased mood and low self-esteem
in husbands was responsible for pregnancy outcomes 3 years
later. The connection between sperm quality and pressure
situations was examined by Harrison et al.
50)
. In a study of
500 men whose partners underwent IVF treatments, it was
found that their sperm quality was lower during the treatment
cycles than at other times. While the study did not examine
stress directly, they did suggest the possibility that during
pressuring psychological situations (in this case, the stress
related to IVF treatments), sperm quality may be adversely
affected. Clarke et al.
51)
also showed that the sperm quality
of 40 men whose partners underwent IVF treatment dropped
in the time surrounding the return of the embryos to the
mother’s uterus. In this study, an evaluation was made of
specific psychological changes, and a relationship was proven
between these changes and lower quality of sperm. Further
support for the theory that there is a relationship between
psychological stress and lower sperm quality parameters
comes from the work of Giblin et al.
52)
. This group followed
28 healthy volunteers and examined sperm samples and
emotional stress every two weeks for one half year. Increased
stress was found in an inverse relation with sperm parameters
of semen volume and percent of normal morphological shapes.
An additional angle, less documented in the literature, is
the subject of emotional pressures in the workplace and their
influence on fertility. The limited attention given to the topic
of psychological stresses at work is partially explained by
the difficulty in separating between sources of emotional
stress at work and outside work. In a case-control study
performed at Soroka University Medical Center, men coming
for evaluation and treatment at the fertility clinics for a male/
female/combined fertility problem were examined
53)
. The
Fig. 1. Significantly higher stress (burnout) parameters among patients with male
infertility as compared to the controls (p<0.05 for all variables; adopted from Sheiner
et al. J Occup Envir Med 2002; 44: 1093–9).
Burnout
Tension
Listlessness
Cognitive weariness
4
3.5
3
2.5
2
1.5
1
0.5
0
Case Control
60
EK SHEINER et al.
Industrial Health 2003, 41, 55–62
participants were asked to complete a questionnaire including
sociodemographic, medical and occupational details, as well
as a questionnaire about pressure, burnout and satisfaction
at work. The average of the burnout grades were considerably
higher among workers with a background of male infertility
compared to the control group (Fig. 1). The most obvious
difference was observed in the parameter of cognitive
weariness. So, it appears that workplace stresses do have
an adverse effect on fertility.
Conclusion
In conclusion, the knowledge existing today regarding
the influence of chemical, physical and emotional factors
on male fertility is limited. The main categories known to
adversely affect male fertility include heavy metals, solvents,
pesticides and other agricultural materials, radiation, heat
and welding. In recent decades, the industrial world has
become inundated with an ever-increasing number of
chemical and physical agents about whose toxicity in general,
and toxicity on the male reproductive system, very little is
known. Psychological stress, in addition to being a result
of infertility problems, can also be a cause for decreased
fertility. Expanding knowledge about materials and
exposures that could adversely affect male fertility has great
importance in maintaining a worker’s health, his family life,
and the health of his progeny. In addition, learning about
exposures that could negatively impact the male reproductive
system is particularly important because of the relatively
short time period before the damage becomes evident (in
contrast to, for example, cancer). As such, protecting workers
from exposures that could impact their fertility will generally
protect them from other negative health effects, which could
ultimately result from such exposures.
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