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Article

Toxic effect of lead on human sper
effect matozoa: A
spermatozoa:
study among pigment factor y workers
factory

and low antioxidant profile along with N. Naha,
increase incidence of sperm
Abstract A. R. Chowdhury1
Occupational lead exposure caused male reproductive abnormality and sperm membrane Department of
lipid per oxidation was prevalent after
impairment, but information on spermatozoa activity, Physiology, College of

occupational lead exposure.[10,11] The
Medical Sciences,
motility, and maturation is limited. In the above
positive correlation between heavy
Chitwan, Nepal, India;
perspective, spermatozoa morphology, motility, activity, 1
Industrial Toxicology
and nutritional status in lead exposed workers (7–15 years metal lead and cadmium in the Division, Regional
exposure) were assessed. Low sperm velocity, gross, and seminal plasma of oligo, astheno, Occupational Health
forward progressive motility with high stationary motile teratospermia group was found by Center (E), (ICMR),
spermatozoa revealed lowering of sperm cell activity after Kasperczyk et al.[12] Kolkata, India
exposure (P < 0.001), which was supported by higher
The gradual decline of semen
seminal fructose and reduced sperm ATPase activity. For correspondence:

cholesterol with decreasing sperm
Lowering of seminal plasma total protein with concomitant AR Chowdhury,

count was also evidenced from the
increase in free amino acid was prevalent as exposure Deputy Director (Sr.
Grade), Regional
earlier study.[13] Lowering of seminal
increased (P < 0.001), suggesting disturbance in cellular
Occupational Health
plasma fructose was observed in
nutritional status. Prolonged liquefaction time, reduced
Center (E), Indian
normal subjects when compared with
semen volume, viscosity, seminal plasma protein,
Council of Medical
fructose, and cholesterol level among workers indicated
accessory sex gland dysfunction after occupational lead azoospermic patients as reported by Research, Block-DP,

exposure (P < 0.001). Deterioration of sperm density and Srivastava et al.[14], but Videla et al. Sector-V, Salt Lake
reported contradictory result in case
Kolkata – 700091,
morphology was associated with high blood and semen
of normal, azoo, and oligo spermic
India. E-mail:
lead of workers (P < 0.001) leading to infertility without
subjects, suggesting the failure of
amalrc2001@yahoo.co.in
altering FSH, LH, and testosterone level.
germinal line of testis were possible
only when the infection or androgen
deficiency was prevalent. [15]
Key words: Blood lead, Lead exposed workers, Semen
biochemistry, Semen lead, Sperm morphology
Interference of inorganic lead to the
hypothalamic–pituitary–gonadal axis,
semen characteristics, and accessory
INTRODUCTION gland function was prevailed among
the working population [16-18], while
The diminution of semen quality due to occupational exposure some other reports revealed
of heavy metals is a major health concern in the globe.[1-3] significant decrease in human semen
Lead exposure and moderate lead absorption produces quality after lead exposure without
alteration in fertility with decreased production in altering the reproductive hormone
spermatozoa in the battery factory workers probably due to level. [19-21] However, very little
the direct toxic effect of lead on germinal epithelium of testis information is available on sperm
during spermatogenesis.[4-6] Sperm velocity and morphology motility, activity, and maturation in
were necessary for fertility potential of the persons [7] and case of lead exposed factory workers.
significant reduction in total motile sperm proportion, forward Therefore, the present study was
progression, and sperm kinetics as well as abnormality of carried out to compare the
sperm structures was predominant after exposure.[8,9] Blood morphology, nutritional status,
lead level was also inversely correlated with sperm count motility, and activity of spermatozoa
and viability.[9] Reduction in sperm motility, count, density, between lead exposed pigment factory

Indian Journal of Occupational and Environmental Medicine - December 2005 - Volume 9 - Issue 3 118
Naha N, et al: Toxic effect of lead on human spermatozoa

workers and nonoccupationally exposed control subjects. RESULTS

MATERIALS AND METHODS [Table 1] showed the distribution of subjects according to the
questionnaire. Majority of the subjects of groups I (18.75%),
The study was conducted in lead based pigments factories in II (19.35%), and III (16.12%) were in the age of 35 years. The
Kolkata. Prior to study, the clearance was obtained from the mean age for group I was found to be 36.13±1.06 years, while
ethical committee (ICMR, Government of India). In this cross- that for group II was 36.61±0.95 years, and 37.16±1.05 years
sectional study 50 nonoccupationally exposed control subjects for group III. All the subjects belonged to lower strata (100%)
(group I) and 95 exposed workers of active reproductive age, according to modified Kuppuswamy ’s socio-economic
55±5 kg weight and 160±5 cm height were randomly classification.[34] There was no reproductive disease history
selected. They were divided into two groups depending on among the working and control population, but infertility was
duration of exposure: (1) low exposed group with 7–10 years significantly high among the working population (40%,
exposure for 8 h/day (Group II: n = 30) and (2) high exposed n = 38). Smoking, alcohol consumption, and use of gutkha/
group for 8 h/day exposure over a period of more than 10– panparag as well as minor electric shock during working were
15 years (Group III: n = 50). Using interview technique as predominant among the battery factory workers of groups II
a tool for data collection, detail information of the subjects and III in comparison with the matched control subjects
were recorded on the predesigned proforma that includes age, (group I).
educational level, socio-economic status, working schedule,
duration of exposure, use of protective devices, smoking, and [Table 2] described the semen profile of the subjects according
other addiction history, marital status, and number of to extent of occupational lead exposure after adjusting for
children, use of contraceptive devices, history of disease of the confounding factors namely age, socio-economic status,
the individual subjects, and his family. Semen samples were duration of exposure, smoking habits, use of alcohol, and
collected from the subjects of the three groups in a clean, gutkha/panparag as well as absteinence period. Seminal
dry, sterilized, wide mouth, well stopper glass vial by viscosity was significantly decreased in-group III compared
masturbation after 2–5 days of abstinence. [22] One part of with group I (P < 0.001), but not in-group II. Prolonged
semen was stored at -20°C in lead free storage vial for lead liquefaction, reduced semen volume, and sperm density was
content analysis. About 2 ml of morning, fasting, venous blood predominant in both the exposed groups with respect to
was also stored at -20°C in lead free EDTA vial for metal control and in between the two exposed groups (P < 0.001).
analysis. Physical characteristics of semen was analyzed Control and low exposed subjects were normospermic and
after liquefaction of the sample.[23] Sperm density, motility with high exposed subjects were hypospermic and oligospermic
four different grades, sperm head morphology, and in nature as per the reference value.[23] Seminal cholesterol
corresponding morphometry was measured at
Table 1: Profiles of lead exposed workers and control
4 0 0 ´ magnification (Model: CH20i, Olympus, India). [22] subjects based on questionnaire data
Sperm velocity track was determined following the standard
Evaluating factors Control group I Exposed groups II and III
laboratory technique [24] using nomogram.[25] After liquefaction,
Participation rate 34.48% (n = 50) 65.52% (n = 95)
whole semen was centrifuged at 800 g for 10 min and seminal
Socio-economic status * Lower (100%) Lower (100%)
plasma was separated. Seminal plasma total protein [26], Married + 100% 100%
fructose [27], free amino acid [28], and cholesterol [29] were Issueless, reported fertility Nil 4% (Consult with physician)
measured spectrophotometrically (model: DU 64, Beckman problem
Typhoid Nil 17% (Within 25 years age)
spectrophotometer, USA). Serum level of FSH[30], LH[31], and Chicken pox Nil 16% (Within 31–45 years
testosterone[32] were assayed following the standard protocol age)
as supplied through the respective ELISA kits. Lead was Gastritis 10% 33% (3–4 years back)
Electric shock Nil 16% (2–3 years back)
estimated in whole blood and semen of the subjects of the Smoker 15% 83%
three groups at 283.3 nm using atomic absorption Bidi (10–15/day for 7% 50%
spectrophotometer (model: GBC AVANTA AAS, software last 10 years)
Version 1.33, Australia) attached with GF 3000 graphite Cigarette (4–5/day for 8% 33%
last 5 years)
furnace.[33] Hormone assay and metal analysis are essential Alcohol (country liquor) 2% (Occasional) 100% (Daily for 5–6 years)
for exploring the in-depth mechanism of action of lead on Gutkha/Panparag Nil 17% (5–6 pack/day for
spermatozoa of the exposed workers. The data obtained from 7–8 years)
Daddiction (Smoking Nil Nil
control and exposed groups were compared and one-way /alcohol/gutkha)
ANOVA and Scheffe’s F–test were carried out for level of
+ Wives not taken any pill. Their male counterparts never used any contraceptive
significance following the computer based statistical software devices.
SPSS, Version 10.0 for Windows (SPSS Inc. USA). * According to modified Kuppuswamy’s socio-economic classification. n = sample size.

119 Indian Journal of Occupational and Environmental Medicine - December 2005 - Volume 9 - Issue 3
Naha N, et al: Toxic effect of lead on human spermatozoa

Table 2: Semen profile (mean ± SE) of the subjects after occupational lead exposure
Parameters Group I Group II Group III
Liquefaction time (min) 15 ± 0.88 (10) 24.35 ± 0.56 † (20) 33.76 ± 0.97 †, * (25)
Seminal viscosity (mm) 2.46 ± 0.15 (15) 2.04 ± 0.18 ‡ (15) 1.53 ± 0.20 †, # (20)
Seminal volume (ml) 4.65 ± 0.16 (20) 2.61 ± 0.10 † (30) 1.36 ± 0.06 †, * (30)
Sperm density (million/ml) 137 ± 7.20 (30) 74.70 ± 2.44 † (40) 28.97 ± 1.94 †, * (30)
Seminal plasma total protein (mg/ml) 84.03 ± 2.09 (22) 30.30 ± 1.94 † (30) 9.17 ± 0.75 †, * (16)
Seminal plasma free amino acid (mg/ml) 12.51 ± 0.90 (31) 26.97 ± 0.96 † (31) 54.28 ± 2.03 †, * (17)
Seminal plasma cholesterol (mg/ml) 4.52 ± 0.39 (15) 1.93 ± 0.12 † (30) 0.65 ± 0.04 †, * (35)
Seminal plasma fructose (mg/ml) 0.48 ± 0.05 (31) 1.38 ± 0.04 † (30) 2.89 ± 0.21 †, * (15)
† P < 0.001.
‡ nonsignificant at P < 0.05 (compared with group I).
* P < 0.001.
# nonsignificant at P < 0.05 (compared with group II). Number in the parenthesis indicates sample size of individual in each group.

and fructose content were varied significantly (P < 0.001) groups I and III (P < 0.01) and between groups II and III
after exposure and seminal plasma total protein and free (P < 0.001), taper head spermatozoa between groups I and
amino acid exhibited reciprocal relationship (P < 0.001). II and between groups I and III (P < 0.001) as well as
Seminal plasma total protein was decreased by 64% in group acrosome defected spermatozoa between groups I and III
II and 89% in group III with concomitant 2.2-fold rise of free (P < 0.01) were predominant after occupational lead
amino in group II and 4.3-fold rise in group III workers with exposure. Spermatozoa with amorphous head were
respect to group I control subjects. About 2.9-fold increase of significantly increased among the three experimental groups
seminal fructose in-group II and 6-fold increase in-group III (P < 0.02: between groups I and II; P < 0.001: between
was also observed. groups I and III; P < 0.001: between groups II and III),
whereas normal sperm head percentage was decreased
Gross morphological abnormality of spermatozoa was significantly (P < 0.001) of the same comparable groups.
significantly higher in both the exposed groups with respect Sperm head morphometry (six subtypes) of lead exposed
control (P < 0.001). Although abnormality of low exposed workers (groups II and III) and control subjects (group I) were
group was slightly higher than the reference value, but both varied nonsignificantly (P < 0.05) as shown in [Figure 2].
the low exposed group (44.54 ± 0.57) and high exposed group
(60.04 ± 1.53) was teratospermic in nature and the control Sperm velocity was significantly decreased in groups II and
group value (33.75 ± 1.09) was within the normal range.[23] III subjects when compared with group I and also in between
The present study also showed that total sperm head, mid the two exposed groups (P < 0.001). The decrement ratio of
piece, and tail abnormalities was increased significantly sperm velocity in groups I (76.01±3.36), II (24.57±2.15), and
(P < 0.001) after exposure. The classification of human III (5.31±0.52) was about 15: 5: 1. The sperm velocity of
spermatozoa according to head abnormalities and its relation control subjects was considered as ‘velocity group I category’
to the occupational lead exposure was shown in [Figure 1]. as per the nomogram [25], whereas low exposed subjects
represented the ‘velocity groups II and III category’, and
Significant increase of double head spermatozoa between ‘velocity groups IV and V category’ was restricted for high

Figure 1: Variations of the human sperm head abnormalities after occupational lead exposure

Indian Journal of Occupational and Environmental Medicine - December 2005 - Volume 9 - Issue 3 120
Naha N, et al: Toxic effect of lead on human spermatozoa

Figure 2: Variations of the human sperm head morphometry after Figure 4: Correlation of human sperm velocity and motility grade
occupational lead exposure after occupational lead exposure

in group III than in group II with respect to group I, while SM
was increased by 1.1-fold of the same comparable group. The
decrement ratio of gross and FP motility in groups I–III was
about 2.6: 1.9: 1 and 2.5: 1.8: 1, respectively, whereas the
increment ratio of SM spermatozoa of the same comparable
groups was approximately 1: 1.9: 3. The increment ratios for
MM (1: 1.6:2.3) and CM (1: 1.4: 2.1) spermatozoa were more
or less same. This study also showed that gross sperm
motility and FP of all the three groups was much lower than
the respective reference values.[23]

[Table 3] represented the hormonal profile of the subjects
after occupational lead exposure. Although serum FSH, LH,
and testosterone level was decreased nonsignificantly
Figure 3: Sperm velocity track of the subjects after occupational
(P < 0.05) in the three study groups, but all the values were
within the reference range as per the ELISA kits.[30-32]
lead exposure

exposed subjects. In our study sperm velocity was decreased
by 25% in-group III than in group II with respect to group I. [Table 4] described the body burden of lead according to extent
Figure 3 represented the sperm velocity track of 20 individuals of exposure at work place. Lead concentration in whole blood
from the three experimental groups and simultaneously the and semen was increased significantly in both the exposed
velocity category of each study group. groups and also between the two exposed groups (P < 0.001).
The increment of blood lead was 1.9-fold in group II and 3.9-
The present study exhibited a correlation between sperm fold in group III with respect to group I, whereas 2.7-fold, and
velocity and motility grade after occupational lead exposure, 4.6-fold were the increment of semen lead of the two exposed
where sperm velocity, gross, and forward progressive (FP) groups (groups II and III), respectively.
motility varied proportionately (P < 0.001) and stationary
motile (SM), moderate motile (MM) and circular motile (CM) DISCUSSION
spermatozoa established the inverse relationship (P < 0.001)
in respect of duration of lead exposure [Figure 4]. Gross sperm The present study showed deterioration in sperm density and
motility and FP was decreased by 37% and 33%, respectively, motility in the lead exposed pigment factory workers with

Table 3: Serum hormone profile (mean ± SE) of the subjects after occupational lead exposure
Parameters Group I Group II Group III
Serum FSH(mIU/ml) 2.69 ± 0.35 (12) 2.58 ± 0.56 ‡ (12) 2.16 ± 0.29 ‡, # (12)
Serum LH (mIU/ml) 5.14 ± 0.68 (12) 4.27 ± 0.73 ‡ (12) 3.9 ± 0.49 ‡, # (12)
Serum testosterone (ng/ml) 5.24 ± 0.69 (12) 4.83 ± 0.35 (12) 4.59 ± 0.37 (12)
‡ nonsignificant at P < 0.05 (compared with group I).
# nonsignificant at P < 0.05 (compared with group II). Number in the parenthesis indicates sample size of individual in each group.

121 Indian Journal of Occupational and Environmental Medicine - December 2005 - Volume 9 - Issue 3
Naha N, et al: Toxic effect of lead on human spermatozoa

Table 4: Body burden of lead (mean ± SE) of the subjects after occupational lead exposure
Parameters Group I Group II Group III
Blood lead (mg/dl) 7.22 ± 0.40 (5.08–9.42) n = 1 0 13.62 ± 0.78 † (10.72–16.71) n = 1 0 28.29 ± 1.55 †, * (22.42–38.30) n = 1 0
Semen lead (mg/dl) 3.99 ± 0.43 (2.39–5.96) n = 1 0 10.85 ± 0.24 † (10.05–12.26) n = 1 0 18.30 ± 0.63 †, * (15.18–20.77) n = 1 1
† P < 0.001 (compared with group I).
* P < 0.001 (compared with group II). Number in the parenthesis indicates the range of the parameters. n = sample size of individual parameter in each group.

high prevalence of sperm head abnormality in comparison quality and fertility (40% workers have fertility problem)
with the nonoccupationally exposed matched control subjects without affecting the serum FSH, LH, and testosterone level,
of same socio-economic status. This observation was in which are in corroboration with the previous finding, [19-21] but
corroboration with the earlier observations of Roy Chowdhury at the same time contradictory to others results.[16-18]
et al.[35,36] These pigment factory workers exposed to lead
fumes and dust during their work, which caused adverse In our study deterioration of sperm quality and fertility
effects on sperm morphology and density.[3,4,6] Morphological potential of the subjects were associated with high lead
abnormalities of spermatozoa were also depended on the concentration in whole blood and semen of the workers in
duration and nature of exposure.[2,19] respect of duration of exposure. Xuezhi showed that lead
exposure caused prolonged liquefaction time, low volume,
Fructose is the main energy source for spermatozoa motility sperm count, viability, and retarded sperm activity in male
[37]
and sperm velocity is the average velocity of all workers with high blood lead level,[38] which is similar to the
spermatozoa in one sample,[23] therefore, both are related with observation of Apostoli et al.[1] and Kasperczyk et al.[12]
sperm motility grade leading to sperm activity. Lowering of Semen lead was higher in the infertile men than the fertile
sperm velocity, gross motility, and FP with concomitant rise group and low semen lead level was the indicator of low
of SM were prevalent in the lead exposed pigment factory industrial exposure.[39] Moderate lead exposure also caused
workers of high seminal plasma fructose level, which reduction in sperm characteristics among the factory
indicated retarded sperm activity might be due to lead induced workers.[17]
alteration of normal fructolysis. This observation showed
similarities with the earlier findings.[8-10] The present finding Therefore, in conclusion it can be pointed out that lead may
was also in corroboration with the previous observation by cross the blood testis barrier and affect spermatozoa of the
showing diminution of sperm ATPase activity after exposed population leading to accessory gland dysfunction,
occupational lead exposure leading to low sperm motility.[35] morphological abnormality, high seminal fructose in
As increase amount of free amino acid depends on the oligospermic exposed workers, [14-15] disturbance in cellular
degradation of protein present in the system,[28] therefore, nutritional status, and energy-dependant processes like
lowering of seminal plasma total protein with concomitant
sperm production and motility leading to reduced sperm
rise of free amino acid in pigment factory workers with
count, retarded sperm activity, and infertility. Smoking habits,
respect to control subjects indicated that lead may alter the
addiction to alcohol, gutkha, etc. may be the added factors in
protein metabolism and subsequently increase the amino acid
lead toxicity, [40] whereas minor electric shock, typhoid,
level, suggesting disturbance in cellular nutritional status,
gastritis, pox, and the age of the subjects did not show any
necessary for cell survival, and proper function.
correlation after exposure.[41]
Low volume, viscosity, prolonged liquefaction time, and
ACKNOWLEDGMENT
deviation of the seminal fructose, cholesterol, and protein
content among the lead exposed pigment factory workers in
We acknowledge DST (Government of West Bengal) for
the present study indicated the alteration of normal secretary
financial support and ROHC (E), ICMR, Kolkata for infra
activity of seminal vesicle and prostate after occupational lead
structural facilities. The authors are grateful to Dr. B. Manna,
exposure. Previous study reported that 95% of ejaculatory
NICED (ICMR), Kolkata for his contribution on statistical
volume comes from these two accessory sex glands and
analysis of data. Thanks are due to all the donors without
alteration of normal liquefaction associated with low viscosity,
whose cooperation the study would have been completed.
indicating deficiency of liquefying agent due to low prostatic
secretary activity. [23] Thus the present study suggesting
REFERENCES
probable dysfunction of accessory gland seminal vesicle and
prostate after toxic insult of lead at work place. 1. Apostoli P, Kiss P, Porru S, Bonde JP, Vanhoorne M. Male reproduc-
tive toxicity of lead in animals and humans. ASCLEPIOS study group.
The present study showed significant decline in human sperm Occup Environ Med 1998;55:364-74.

Indian Journal of Occupational and Environmental Medicine - December 2005 - Volume 9 - Issue 3 122
Naha N, et al: Toxic effect of lead on human spermatozoa

2. Alexander BH, Checkoway H, van Netten C, Muller CH, Ewers TG, 20. Assenato G, Paci C, Baser ME, Molinini R, Candela RG, Altamura
Kaufman JD, et al. Semen quality of men employed at a lead smelter. BM, et al. Sperm count suppression without endocrine dysfunction in
Occup Environ Med 1996;53:411-6. lead-exposed men. Arch Environ Health 1987;42:124-7.
3. Robins TG, Bornman MS, Ehrlich RI, Cantrell AC, Pienaar E, Vallabh 21. Gennart JP, Bernard A, Lauwerys R. Assessment of thyroid, testes,
J, et al. Semen quality and fertility of men employed in a South Afri- kidney and autonomic nervous system function in lead exposed work-
can lead acid battery plant. Am J Indus Med 1997;32:369-76. ers. Int Arch Occup Env Hlth 1992;64:49-57.
4. Lancranjan I, Popescu HI, Gavanescu O, Klepsch I, Serbanescu M. 22. WHO Laboratory Manual for The Examination of Human Semen &
Reproductive ability of workmen occupationally exposed to lead. Arch Sperm-Cervical Mucus Interaction. 4 th edn. Cambridge University
Environ Health 1975;30:396-401. Press, 1999.
5. Roy CA, Rao RV, Gautam AK, Kashyap SK. Functional changes of 23. In: Hafez ESE. editor. Techniques of human andrology. Amsterdam:
testes in lead induced rats. Indus Health 1987;25:55-62. North Holland Publishing Co. 1977;147-78, 266.
6. Bonde JPE, Kolstad H. Fertility of Danish battery workers exposed to 24. Bartak J. Sperm velocity test in clinical practice. Int J Fertil
lead. Int J Epidemiol 1997;26:1281-8. 1971;16:107.
7. Sallam HN, Ezzeldin F, Sallam A, Agameya AF, Farrag A. Sperm ve- 25. Hyne J. A quick calculation of the velocity of spermatozoa. Int J Fertil
locity and morphology, female characteristics and the hypo osmotic 1965;7:345.
swelling test as predictors of fertilization potential: experience from 26. Lowry OH, Rosenbrough NJ, Farrel AL, Randall RJ. Protein measure-
the IVF model. Int J Fertil Womens Mmed 2003;48:88-95. ment with the folin phenol reagent. J Biol Chem 1951;193:265-75.
8. Viskum S, Rabjerg L, Jorgensen PJ, Grandjean P. Improvement in se- 27. Foreman D, Gayler L, Evans E, Trella C. A modification of Roe proce-
men quality associated with decreasing occupational lead exposure. dure for determination of fructose in tissue with increased specificity.
Am J Ind Med 1999;35:257-63. Anal Biochem 1973;56:589-90.
9. Rosa MD, Zarrilli S, Paesano L, Carbone U, Boggia B, Petretta M, et 28. Sushilkumar, Dalal B, Bhan VM. Host preference on the basis of bio-
al. Traffic pollutants affect fertility in men. Hum Reprod 2003;18:1055- chemical profiles of the grubs of Mexican beetle Zygograma biocolorata
61. Pallister. Weed news 1995;2:6-8.
10. Rhemrev JP, Vermeidan JP, Hoenen GR, De Bruijne JJ, Rekers- 29. Zlatkis A, Zak B, Boyle GJ. Serum cholesterol estimation by ferric
Mombarg LT, Bast A. Progressively motile human spermatozoa are chlortide method. J Lab Clin Med 1953;41:486-90.
well protected against in vitro lipid peroxidation imposed by reduced 30. Odell WD, Parlow AF, Cargille CM, Ross GI. Radioimmunioassay for
oxidative stress. Andrologia 2001;33:151-8. human FSH: physiological studies. J Clin Invest 1968;47:2551-62.
11. Jiun YS, Hsien LT. Lipid peroxidation in workers exposed to lead. 31. Saxena BB, Demura H, Gandy HM, Peterson RE. Radioimmunoassay
Arch Env Hlth 1994;49:256-9. of FSH and LH in plasma. J Clin Endocrinol Metab 1968;28:519-34.
12. Kasperczyk A, Kasperczyk, S, Dziwisz M, Birkuer E, Walecko C, 32. Joshi UM, Shah HP, Sudhana SP. A sensitive and specific enzyme im-
Winiarska H, et al. Lead and cadmium concentration in human semen. munoassay for serum testosterone. Steroids 1979;34:35-46.
Ginekol Pol 2002;73:449-53. 33. Sinclair D, Chapple G. GBC AA application 1988; p. 12.
13. Das RP, Roy S, Poddar AK. Cholesterol and ascorbic acid in semen 34. In: Mahajan BK, Gupta MC, editors. Text book of preventive and so-
under varied clinical conditions. J Popul Res 1976;3:9-15. cial medicine. 2nd edn. Jaypee Publishers; 1995. p. 135-6.
14. Srivastava A, Chopra SK, Dasgupta PR. Biochemical analysis of hu- 35. Naha N, Roy S, Guha T, Roy Chowdhury A. Lead induced changes in
man seminal plasma I. Fructose, ascorbate, cholesterol, adenosine tri- seminal constituents of workers from battery and paint factories in
phosphatase and lactic dehydrogenase. Andrologia 1983;15:431-5. Kolkata. Indian Biologist 2003;35:41-8.
15. Videla E, Blanco AM, Galli ME, Fernandez-Collazo E. Human semi- 36. Roychowdhury A, Gautam AK. Alteration of human sperm and other
nal biochemistry: fructose, ascorbic acid, citric acid, acid phosphatase seminal constituents after lead exposure. Ind J Physiol Alld Sci
and their relationship with sperm count. Andrologia 1981;13:212-4. 1995;49:58-73.
16. Ng TP, Goh HH, Ng YL, Ong HY, Ong CN, Chia KS et al. Male endo- 37. In: Johnson AD, Vandemark NL, editors. The testis. New York: Aca-
crine functions in workers with moderate exposure to lead. Br J Ind demic Press; 1970.
Med 1991;48:485-91. 38. Xuezhi J, Youkin L, Yilan W. Studies of lead exposure on reproductive
17. Cullen MR, Kaye RD. Endocrine and reproductive dysfunction in men system: a review work in China. Biomed Environ Sci 1992;5:266-75.
associated with inorganic lead intoxication. Arch Env Hlth 39. Saaranen M, Suistomaa U, Kantola M, Saarikoski S, Vanha-Perttula T.
1984;39:434-9. Lead, magnesium, selenium and zinc in human seminal fluid: com-
18. Winder C. Lead, reproduction and development. Neurotoxicol parison with semen parameters and fertility. Hum Reprod 1987;2:475-
1993;14:303-17. 9.
19. Telisman S, Cvitkovic P, Jurasovic J, Pizent A, Gavella M, Rocic B. 40. Joffe JM. Influence of drug exposure of the father on perinatal out-
Semen quality and reproductive endocrine function in relation to come. Clin Perinatol 1979;6:21-36.
biomarkers of lead, cadmium, zinc and copper in men. Environ Health 41. Check JH, Shanis B, Bollendorf A, Adelson H, Breen E. Semen char-
Perspect 2000;108:45-53. acteristics and infertility in aging. Arch Androl 1989;23:275-7.

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