" DISCLAIMER: The ILO does not take responsibility for content presented on this web portal that is presented in any language other than English, which is the language used for the initial production and peer-review of original content. Certain statistics have not been updated since the production of the 4th edition of the Encyclopaedia (1998)."

Saturday, 19 February 2011 00:00

Male Reproductive System and Toxicology

Written by
Rate this item
(1 Vote)

Spermatogenesis and spermiogenesis are the cellular processes that produce mature male sex cells. These processes take place within the seminiferous tubules of the testes of the sexually mature male, as shown in Figure 1. The human seminiferous tubules are 30 to 70 cm long and 150 to 300 mm in diameter (Zaneveld 1978). The spermatogonia (stem cells) are ppositioned along the basement membrane of the seminiferous tubules and are the basic cells for the production of sperm.

Figure 1. The male reproductive system


Sperm mature through a series of cellular divisions in which the spermatogonia proliferate and become primary spermatocytes. The resting primary spermatocytes migrate through tight junctions formed by the Sertoli cells to the luminal side of this testis barrier. By the time the spermatocytes reach the membrane barrier in the testis, the synthesis of DNA, the genetic material in the nucleus of the cell, is essentially complete. When the primary spermatocytes actually encounter the lumen of the seminiferous tubule, these undergo a special type of cell division which occurs only in germ cells and is known as meiosis. Meiotic cellular divison results in the splitting up of the chromosomes pairs in the nucleus, so that each resulting germ cell contains only a single copy of each chromosome strand rather than a matched pair.

During meiosis the chromosomes change shape by condensing and becoming filamentous. At a certain point, the nuclear membrane which surrounds them breaks down and microtubular spindles attach to the chromosomal pairs, causing them to separate. This completes the first meiotic division and two haploid secondary spermatocytes are formed. The secondary spermatocytes then undergo a second meiotic division to form equal numbers of X- and Y-chromosome bearing spermatids.

The morphological transformation of spermatids to spermatozoa is called spermiogenesis. When spermiogenesis is complete, each sperm cell is released by the Sertoli cell into the seminiferous tubule lumen by a process referred to as spermiation. The sperm migrate along the tubule to the rete testis and into the head of the epididymis. Sperm leaving the seminiferous tubules are immature: unable to fertilize an ovum and unable to swim. Spermatozoa released into the lumen of the seminiferous tubule are suspended in fluid pproduced primarily by the Sertoli cells. Concentrated sperm suspended within this fluid flow continuously from the seminiferous tubules, through slight changes in the ionic milieu within the rete testis, through the vasa efferentia, and into the epididymis. The epididymis is a single highly coiled tube (five to six metres long) in which sperm spend 12 to 21 days.

Within the epididymis, sperm progressively acquire motility and fertilizing capacity. This may be due to the changing nature of the suspension fluid in the epididymis. That is, as the cells mature the epididymis absorbs components from the fluid including secretions from the Sertoli cells (e.g., androgen binding protein), thereby increasing the concentration of spermatozoa. The epididymis also contributes its own secretions to the suspension fluid, including the chemicals glycerylphosphorylcholine (GPC) and carnitine.

Sperm morphology continues to transform in the epididymis. The cytoplasmic droplet is shed and the sperm nucleus condenses further. While the epididymis is the principal storage reservoir for sperm until ejaculation, about 30% of the sperm in an ejaculate have been stored in the vas deferens. Frequent ejaculation accelerates passage of sperm through the epididymis and may increase the number of immature (infertile) sperm in the ejaculate (Zaneveld 1978).


Once within the vas deferens, the sperm are transported by the muscular contractions of ejaculation rather than by the flow of fluid. During ejaculation, fluids are forcibly expelled from the accessory sex glands giving rise to the seminal plasma. These glands do not expel their secretions at the same time. Rather, the bulbourethral (Cowper’s) gland first extrudes a clear fluid, followed by the prostatic secretions, the sperm-concentrated fluids from the epididymides and ampulla of the vas deferens, and finally the largest fraction primarily from the seminal vesicles. Thus, seminal plasma is not a homogeneous fluid.

Toxic Actions on Spermatogenesisand Spermiogenesis

Toxicants may disrupt spermatogenesis at several points. The most damaging, because of irreversibility, are toxicants that kill or genetically alter (beyond repair mechanisms) spermatogonia or Sertoli cells. Animal studies have been useful to determine the stage at which a toxicant attacks the spermatogenic process. These studies employ short term exposure to a toxicant before sampling to determine the effect. By knowing the duration for each spermatogenic stage, one can extrapolate to estimate the affected stage.

Biochemical analysis of seminal plasma pprovides insights into the function of the accessory sex glands. Chemicals that are secreted primarily by each of the accessory sex glands are typically selected to serve as a marker for each respective gland. For example, the epididymis is represented by GPC, the seminal vesicles by fructose, and the prostate gland by zinc. Note that this type of analysis pprovides only gross information on glandular function and little or no information on the other secretory constituents. Measuring semen pH and osmolality provide additional general information on the nature of seminal plasma.

Seminal plasma may be analysed for the presence of a toxicant or its metabolite. Heavy metals have been detected in seminal plasma using atomic absorption spectrophotometry, while halogenated hydrocarbons have been measured in seminal fluid by gas chromatography after extraction or protein-limiting filtration (Stachel et al. 1989; Zikarge 1986).

The viability and motility of spermatozoa in seminal plasma is typically a reflection of seminal plasma quality. Alterations in sperm viability, as measured by stain exclusion or by hypoosmotic swelling, or alterations in sperm motility parameters would suggest post-testicular toxicant effects.

Semen analyses also can indicate whether production of sperm cells has been affected by a toxicant. Sperm count and sperm morphology provide indices of the integrity of spermatogenesis and spermiogenesis. Thus, the number of sperm in the ejaculate is directly correlated with the number of germ cells per gram of testis (Zukerman et al. 1978), while abnormal morphology is probably a result of abnormal spermiogenesis. Dead sperm or immotile sperm often reflect the effects of post-testicular events. Thus, the type or timing of a toxic effect may indicate the target of the toxicant. For example, exposure of male rats to 2-methoxyethanol resulted in reduced fertility after four weeks (Chapin et al. 1985). This evidence, corroborated by histological examination, indicates that the target of toxicity is the spermatocyte (Chapin et al. 1984). While it is not ethical to intentionally expose humans to suspected reproductive toxicants, semen analyses of serial ejaculates of men inadvertently exposed for a short time to potential toxicants may provide similar useful information.

Occupational exposure to 1,2-dibromochloropropane (DBCP) reduced sperm concentration in ejaculates from a median of 79 million cells/ml in unexposed men to 46 million cells/ml in exposed workers (Whorton et al. 1979). Upon removing the workers from the exposure, those with reduced sperm counts experienced a partial recovery, while men who had been azoospermic remained sterile. Testicular biopsy revealed that the target of DBCP was the spermatogonia. This substantiates the severity of the effect when stem cells are the target of toxicants. There were no indications that DBCP exposure of men was associated with adverse pregnancy outcome (Potashnik and Abeliovich 1985). Another example of a toxicant targeting spermatogenesis/spermiogenesis was the study of workers exposed to ethylene dibromide (EDB). They had more sperm with tapered heads and fewer sperm per ejaculate than did controls (Ratcliffe et al. 1987).

Genetic damage is difficult to detect in human sperm. Several animal studies using the dominant lethal assay (Ehling et al. 1978) indicate that paternal exposure can produce an adverse pregnancy outcome. Epidemiological studies of large populations have demonstrated increased frequency of spontaneous abortions in women whose husbands were working as motor vehicle mechanics (McDonald et al. 1989). Such studies indicate a need for methods to detect genetic damage in human sperm. Such methods are being developed by several laboratories. These methods include DNA probes to discern genetic mutations (Hecht 1987), sperm chromosome karyotyping (Martin 1983), and DNA stability assessment by flow cytometry (Evenson 1986).

Figure 2. Exposures positively associated with adversely affecting semen quality


Figure 2 lists exposures known to affect sperm quality and table 1 provides a summary of the results of epidemiological studies of paternal effects on reproductive outcomes.

Table 1. Epidemiological studies of paternal effects on pregnancy outcome

Reference Type of exposure or occupation Association with exposure1 Effect
Record-based population studies
Lindbohm et al. 1984 Solvents Spontaneous abortion
Lindbohm et al. 1984 Service station + Spontaneous abortion
Daniell and Vaughan 1988 Organic solvents Spontaneous abortion
McDonald et al. 1989 Mechanics + Spontaneous abortion
McDonald et al. 1989 Food processing + Developmental defects
Lindbohm et al. 1991a Ethylene oxide + Spontaneous abortion
Lindbohm et al. 1991a Petroleum refinery + Spontaneous abortion
Lindbohm et al. 1991a Impregnates of wood + Spontaneous abortion
Lindbohm et al. 1991a Rubber chemicals + Spontaneous abortion
Olsen et al. 1991 Metals + Child cancer risk
Olsen et al. 1991 Machinists + Child cancer risk
Olsen et al. 1991 Smiths + Child cancer risk
Kristensen et al. 1993 Solvents + Preterm birth
Kristensen et al. 1993 Lead and solvents + Preterm birth
Kristensen et al. 1993 Lead + Perinatal death
Kristensen et al. 1993 Lead + Male child morbidity
Case-control studies
Kucera 1968 Printing industry (+) Cleft lip
Kucera 1968 Paint (+) Cleft palate
Olsen 1983 Paint + Damage to central nervous system
Olsen 1983 Solvents (+) Damage to central nervous system
Sever et al. 1988 Low-level radiation + Neural tube defects
Taskinen et al. 1989 Organic solvents + Spontaneous abortion
Taskinen et al. 1989 Aromatic hydrocarbons + Spontaneous abortion
Taskinen et al. 1989 Dust + Spontaneous abortion
Gardner et al. 1990 Radiation + Childhood leukaemia
Bonde 1992 Welding + Time to conception
Wilkins and Sinks 1990 Agriculture (+) Child brain tumour
Wilkins and Sinks 1990 Construction (+) Child brain tumour
Wilkins and Sinks 1990 Food/tobacco processing (+) Child brain tumour
Wilkins and Sinks 1990 Metal + Child brain tumour
Lindbohmn et al. 1991b Lead (+) Spontaneous abortion
Sallmen et al. 1992 Lead (+) Congenital defects
Veulemans et al. 1993 Ethylene glycol ether + Abnormal spermiogram
Chia et al. 1992 Metals + Cadmium in semen

1 – no significant association; (+) marginally significant association; + significant association.
Source: Adapted from Taskinen 1993.

Neuroendocrine System

The overall functioning of the reproductive system is controlled by the nervous system and the hormones pproduced by the glands (the endocrine system). The reproductive neuroendocrine axis of the male involves principally the central nervous systems (CNS), the anterior pituitary gland and the testes. Inputs from the CNS and from the periphery are integrated by the hypothalamus, which directly regulates gonadotrophin secretion by the anterior pituitary gland. The gonadotrophins, in turn, act principally upon the Leydig cells within the interstitium and Sertoli and germ cells within the seminiferous tubules to regulate spermatogenesis and hormone production by the testes.

Hypothalamic–Pituitary Axis

The hypothalamus secretes the neurohormone gonadotrophin releasing hormone (GnRH) into the hypophysial portal vasculature for transport to the anterior pituitary gland. The pulsatile secretion of this decapeptide causes the concomitant release of luteinizing hormone (LH), and with lesser synchrony and one-fifth the potency, the release of follicle stimulating hormone (FSH) (Bardin 1986). Substantial evidence exists to support the presence of a separate FSH releasing hormone, although none has yet been isolated (Savy-Moore and Schwartz 1980; Culler and Negro-Vilar 1986). These hormones are secreted by the anterior pituitary gland. LH acts directly upon the Leydig cells to stimulate synthesis and release of testosterone, whereas FSH stimulates aromatization of testosterone to estradiol by the Sertoli cell. Gonadotropic stimulation causes the release of these steroid hormones into the spermatic vein.

Gonadotrophin secretion is, in turn, checked by testosterone and estradiol through negative feedback mechanisms. Testosterone acts principally upon the hypothalamus to regulate GnRH secretion and thereby reduces the pulse frequency, primarily, of LH release. Estradiol, on the other hand, acts upon the pituitary gland to reduce the magnitude of gonadotrophin release. Through these endocrine feedback loops, testicular function in general and testosterone secretion specifically are maintained at a relatively steady state.

Pituitary–Testicular Axis

LH and FSH are generally viewed as necessary for normal spermatogenesis. Presumably the effect of LH is secondary to inducing high intratesticular concentrations of testosterone. Therefore, FSH from the pituitary gland and testosterone from the Leydig cells act upon the Sertoli cells within the seminiferous tubule epithelium to initiate spermatogenesis. Sperm production persists, although quantitatively reduced, after removing either LH (and presumably the high intratesticular testosterone concentrations) or FSH. FSH is required for initiating spermatogenesis at puberty and, to a lesser extent, to reinitiate spermatogenesis that has been arrested (Matsumoto 1989; Sharpe 1989).

The hormonal synergism that serves to maintain spermatogenesis may entail recruitment by FSH of differentiated spermatogonia to enter meiosis, while testosterone may control specific, subsequent stages of spermatogenesis. FSH and testosterone may also act upon the Sertoli cell to stimulate production of one or more paracrine factors which may affect the number of Leydig cells and testosterone production by these cells (Sharpe 1989). FSH and testosterone stimulate protein synthesis by Sertoli cells including synthesis of androgen binding protein (ABP), while FSH alone stimulates synthesis of aromatase and inhibin. ABP is secreted primarily into the seminiferous tubular fluid and is transported to the proximal portion of the caput epididymis, possibly serving as a local carrier of androgens (Bardin 1986). Aromatase catalyses the conversion of testosterone to estradiol in the Sertoli cells and in other peripheral tissues.

Inhibin is a glycoprotein consisting of two dissimilar, disulphide-linked subunits, a and b. Although inhibin preferentially inhibits FSH release, it may also attenuate LH release in the presence of GnRH stimulation (Kotsugi et al. 1988). FSH and LH stimulate inhibin release with approximately equal potency (McLachlan et al. 1988). Interestingly, inhibin is secreted into the spermatic vein blood as pulses which are synchronous to those of testosterone (Winters 1990). This probably does not reflect direct actions of LH or testosterone on Sertoli cell activity, but rather the effects of other Leydig cell products secreted either into the interstitial spaces or the circulation.

Prolactin, which is also secreted by the anterior pituitary gland, acts synergistically with LH and testosterone to promote male reproductive function. Prolactin binds to specific receptors on the Leydig cell and increases the amount of androgen receptor complex within the nucleus of androgen responsive tissues (Baker et al. 1977). Hyperprolactinaemia is associated with reductions of testicular and prostate size, semen volume and circulating concentrations of LH and testosterone (Segal et al. 1979). Hyperprolactinaemia has also been associated with impotency, apparently independent of altering testosterone secretion (Thorner et al. 1977).

If measuring steroid hormone metabolites in urine, consideration must be given to the potential that the exposure being studied may alter the metabolism of excreted metabolites. This is especially pertinent since most metabolites are formed by the liver, a target of many toxicants. Lead, for example, reduced the amount of sulphated steroids that were excreted into the urine (Apostoli et al. 1989). Blood levels for both gonadotrophins become elevated during sleep as the male enters puberty, while testosterone levels maintain this diurnal pattern through adulthood in men (Plant 1988). Thus blood, urine or saliva samples should be collected at approximately the same time of day to avoid variations due to diurnal secretory patterns.

The overt effects of toxic exposure targeting the reproductive neuroendocrine system are most likely to be revealed through altered biological manifestations of the androgens. Manifestations significantly regulated by androgens in the adult man that may be detected during a basic physical examination include: (1) nitrogen retention and muscular development; (2) maintenance of the external genitalia and accessory sexual organs; (3) maintenance of the enlarged larynx and thickened vocal cords causing the male voice; (4) beard, axillary and pubic hair growth and temporal hair recession and balding; (5) libido and sexual performance; (6) organ specific proteins in tissues (e.g., liver, kidneys, salivary glands); and (7) aggressive behaviour (Bardin 1986). Modifications in any of these traits may indicate that androgen production has been affected.

Examples of Toxicant Effects

Lead is a classic example of a toxicant that directly affects the neuroendocrine system. Serum LH concentrations were elevated in men exposed to lead for less than one year. This effect did not progress in men exposed for more than five years. Serum FSH levels were not affected. On the other hand, serum levels of ABP were elevated and those of total testosterone were reduced in men exposed to lead for more than five years. Serum levels of free testosterone were significantly reduced after exposure to lead for three to five years (Rodamilans et al. 1988). In contrast, serum concentrations of LH, FSH, total testosterone, prolactin, and total neutral 17-ketosteroids were not altered in workers with lower circulating levels of lead, even though the distribution frequency of sperm count was altered (Assennato et al. 1986).

Exposure of shipyard painters to 2-ethoxyethanol also reduced sperm count without a concurrent change in serum LH, FSH, or testosterone concentrations (Welch et al. 1988). Thus toxicants may affect hormone production and sperm measures independently.

Male workers involved in the manufacture of the nematocide DBCP experienced elevated serum levels of LH and FSH and reduced sperm count and fertility. These effects are apparently sequelae to DBCP actions upon the Leydig cells to alter androgen production or action (Mattison et al. 1990).

Several compounds may exert toxicity by virtue of structural similarity to reproductive steroid hormones. Thus, by binding to the respective endocrine receptor, toxicants may act as agonists or antagonists to disrupt biological responses. Chlordecone (Kepone), an insecticide that binds to oestrogen receptors, reduced sperm count and motility, arrested sperm maturation and reduced libido. While it is tempting to suggest that these effects result from chlordecone interfering with oestrogen actions at the neuroendocrine or testicular level, serum levels of testosterone, LH and FSH were not shown to be altered in these studies in a manner similar to the effects of oestradiol therapy. DDT and its metabolites also exhibit steroidal properties and might be expected to alter male reproductive function by interfering with steroidal hormone functions. Xenobiotics such as polychlorinated biphenyls, polybrominated biphenyls, and organochlorine pesticides may also interfere with male reproductive functions by exerting oestrogenic agonist/antagonist activity (Mattison et al. 1990).

Sexual Function

Human sexual function refers to the integrated activities of the testes and secondary sex glands, the endocrine control systems, and the central nervous system-based behavioural and psychological components of reproduction (libido). Erection, ejaculation and orgasm are three distinct, independent, physiological and psychodynamic events which normally occur concurrently in men.

Little reliable data are available on occupational exposure effects on sexual function due to the problems described above. Drugs have been shown to affect each of the three stages xof male sexual function (Fabro 1985), indicating the potential for occupational exposures to exert similar effects. Antidepressants, testosterone antagonists and stimulants of prolactin release effectively reduce libido in men. Antihypertensive drugs which act on the sympathetic nervous system induce impotence in some men, but surprisingly, priapism in others. Phenoxybenzamine, an adrenoceptive antagonist, has been used clinically to block seminal emission but not orgasm (Shilon, Paz and Homonnai 1984). Anticholinergic antidepressant drugs permit seminal emission while blocking seminal ejection and orgasm which results in seminal plasma seeping from the urethra rather than being ejected.

Recreational drugs also affect sexual function (Fabro 1985). Ethanol may reduce impotence while enhancing libido. Cocaine, heroin and high doses of cannabinoids reduce libido. Opiates also delay or impair ejaculation.

The vast and varied array of pharmaceuticals that has been shown to affect the male reproductive system pprovides support for the notion that chemicals found in the workplace may also be reproductive toxicants. Research methods that are reliable and practical for field study conditions are needed to assess this important area of reproductive toxicology.



Read 7714 times Last modified on Tuesday, 11 October 2011 20:45


Part I. The Body
Cardiovascular System
Digestive System
Mental Health
Musculoskeletal System
Nervous System
Renal-Urinary System
Reproductive System
Respiratory System
Sensory Systems
Skin Diseases
Systematic Conditions
Part II. Health Care
Part III. Management & Policy
Part IV. Tools and Approaches
Part V. Psychosocial and Organizational Factors
Part VI. General Hazards
Part VII. The Environment
Part VIII. Accidents and Safety Management
Part IX. Chemicals
Part X. Industries Based on Biological Resources
Part XI. Industries Based on Natural Resources
Part XII. Chemical Industries
Part XIII. Manufacturing Industries
Part XIV. Textile and Apparel Industries
Part XV. Transport Industries
Part XVI. Construction
Part XVII. Services and Trade
Part XVIII. Guides

Reproductive System Additional Resources

Click the Button below to view additional resources for this topic.


Reproductive System References

Agency for Toxic Substance and Disease Registry. 1992. Mercury toxicity. Am Fam Phys 46(6):1731-1741.

Ahlborg, JR, L Bodin, and C Hogstedt. 1990. Heavy lifting during pregnancy–A hazard to the fetus? A prospective study. Int J Epidemiol 19:90-97.

Alderson, M. 1986. Occupational Cancer. London: Butterworths.
Anderson, HA, R Lilis, SM Daum, AS Fischbein, and IJ Selikoff. 1976. Household contact asbestos neoplastic risk. Ann NY Acad Sci 271:311-332.

Apostoli, P, L Romeo, E Peroni, A Ferioli, S Ferrari, F Pasini, and F Aprili. 1989. Steroid hormone sulphation in lead workers. Br J Ind Med 46:204-208.

Assennato, G, C Paci, ME Baser, R Molinini, RG Candela, BM Altmura, and R Giogino. 1986. Sperm count suppression with endocrine dysfunction in lead-exposed men. Arch Environ Health 41:387-390.

Awumbila, B and E Bokuma. 1994. Survey of pesticides used in the control of ectoparasites on farm animals in Ghana. Tropic Animal Health Prod 26(1):7-12.

Baker, HWG, TJ Worgul, RJ Santen, LS Jefferson, and CW Bardin. 1977. Effect of prolactin on nuclear androgens in perifused male accessory sex organs. In The Testis in Normal and Infertile Men, edited by P and HN Troen. New York: Raven Press.

Bakir, F, SF Damluji, L Amin-Zaki, M Murtadha, A Khalidi, NY Al-Rawi, S Tikriti, HT Dhahir, TW Clarkson, JC Smith, and RA Doherty. 1973. Methyl mercury poisoning in Iraq. Science 181:230-241.

Bardin, CW. 1986. Pituitary-testicular axis. In Reproductive Endocrinology, edited by SSC Yen and RB Jaffe. Philadelphia: WB Saunders.

Bellinger, D, A Leviton, C Waternaux, H Needleman, and M Rabinowitz. 1987. Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development. New Engl J Med 316:1037-1043.

Bellinger, D, A Leviton, E Allred, and M Rabinowitz. 1994. Pre- and postnatal lead exposure and behavior problems in school-aged children. Environ Res 66:12-30.

Berkowitz, GS. 1981. An epidemiologic study of preterm delivery. Am J Epidemiol 113:81-92.

Bertucat, I, N Mamelle, and F Munoz. 1987. Conditions de travail des femmes enceintes–étude dans cinq secteurs d’activité de la région Rhône-Alpes. Arch mal prof méd trav secur soc 48:375-385.

Bianchi, C, A Brollo, and C Zuch. 1993. Asbestos-related familial mesothelioma. Eur J Cancer 2(3) (May):247-250.

Bonde, JPE. 1992. Subfertility in relation to welding–A case referent study among male welders. Danish Med Bull 37:105-108.

Bornschein, RL, J Grote, and T Mitchell. 1989. Effects of prenatal lead exposure on infant size at birth. In Lead Exposure and Child Development, edited by M Smith and L Grant. Boston: Kluwer Academic.

Brody, DJ, JL Pirkle, RA Kramer, KM Flegal, TD Matte, EW Gunter, and DC Pashal. 1994. Blood lead levels in the US population: Phase one of the Third National Health and Nutrition Examination survey (NHANES III, 1988 to 1991). J Am Med Assoc 272:277-283.

Casey, PB, JP Thompson, and JA Vale. 1994. Suspected paediatric poisoning in the UK; I-Home accident surveillance system 1982-1988. Hum Exp Toxicol 13:529-533.

Chapin, RE, SL Dutton, MD Ross, BM Sumrell, and JC Lamb IV. 1984. The effects of ethylene glycol monomethyl ether on testicular histology in F344 rats. J Androl 5:369-380.

Chapin, RE, SL Dutton, MD Ross, and JC Lamb IV. 1985. Effects of ethylene glycol monomethyl ether (EGME) on mating performance and epididymal sperm parameters in F344 rats. Fund Appl Toxicol 5:182-189.

Charlton, A. 1994. Children and passive smoking. J Fam Pract 38(3)(March):267-277.

Chia, SE, CN Ong, ST Lee, and FHM Tsakok. 1992. Blood concentrations of lead, cadmium, mercury, zinc, and copper and human semen parameters. Arch Androl 29(2):177-183.

Chisholm, JJ Jr. 1978. Fouling one’s nest. Pediatrics 62:614-617.

Chilmonczyk, BA, LM Salmun, KN Megathlin, LM Neveux, GE Palomaki, GJ Knight, AJ Pulkkinen, and JE Haddow. 1993. Association between exposure to environmental tobacco smoke and exacerbations of asthma in children. New Engl J Med 328:1665-1669.

Clarkson, TW, GF Nordberg, and PR Sager. 1985. Reproductive and developmental toxicity of metals. Scand J Work Environ Health 11:145-154.
Clement International Corporation. 1991. Toxicological Profile for Lead. Washington, DC: US Department of Health and Human Services, Public Health Service Agency for Toxic Substances and Disease Registry.

——. 1992. Toxicological Profile for A-, B-, G-, and D-Hexachlorocyclohexane. Washington, DC: US Department of Health and Human Services, Public Health Service Agency for Toxic Substances and Disease Registry.

Culler, MD and A Negro-Vilar. 1986. Evidence that pulsatile follicle-stimulating hormone secretion is independent of endogenous luteinizing hormone-releasing hormone. Endocrinology 118:609-612.

Dabeka, RW, KF Karpinski, AD McKenzie, and CD Bajdik. 1986. Survey of lead, cadmium and flouride in human milk and correlation of levels with environmental and food factors. Food Chem Toxicol 24:913-921.

Daniell, WE and TL Vaughn. 1988. Paternal employment in solvent related occupations and adverse pregnancy outcomes. Br J Ind Med 45:193-197.
Davies, JE, HV Dedhia, C Morgade, A Barquet, and HI Maibach. 1983. Lindane poisonings. Arch Dermatol 119 (Feb):142-144.

Davis, JR, RC Bronson, and R Garcia. 1992. Family pesticide use in the home, garden, orchard, and yard. Arch Environ Contam Toxicol 22(3):260-266.

Dawson, A, A Gibbs, K Browne, F Pooley, and M Griffiths. 1992. Familial mesothelioma. Details of seventeen cases with histopathologic findings and mineral analysis. Cancer 70(5):1183-1187.

D’Ercole, JA, RD Arthur, JD Cain, and BF Barrentine. 1976. Insecticide exposure of mothers and newborns in a rural agricultural area. Pediatrics 57(6):869-874.

Ehling, UH, L Machemer, W Buselmaier, J Dycka, H Froomberg, J Dratochvilova, R Lang, D Lorke, D Muller, J Peh, G Rohrborn, R Roll, M Schulze-Schencking, and H Wiemann. 1978. Standard protocol for the dominant lethal test on male mice. Arch Toxicol 39:173-185.

Evenson, DP. 1986. Flow cytometry of acridine orange stained sperm is a rapid and practical method for monitoring occupational exposure to genotoxicants. In Monitoring of Occupational Genotoxicants, edited by M Sorsa and H Norppa. New York: Alan R Liss.

Fabro, S. 1985. Drugs and male sexual function. Rep Toxicol Med Lettr 4:1-4.

Farfel, MR, JJ Chisholm Jr, and CA Rohde. 1994. The long-term effectiveness of residential lead paint abatement. Environ Res 66:217-221.

Fein, G, JL Jacobson, SL Jacobson, PM Schwartz, and JK Dowler. 1984. Prenatal exposure to polychlorinated biphenyls: effects on birth size and gestational age. J Pediat 105:315-320.

Fenske, RA, KG Black, KP Elkner, C Lee, MM Methner, and R Soto. 1994. Potential exposure and health risks of infants following indoor residential pesticide applications. Am J Public Health 80(6):689-693.

Fischbein, A and MS Wolff. 1987. Conjugal exposure to polychlorinated biphenyls (PCBs). Br J Ind Med 44:284-286.

Florentine, MJ and DJ II Sanfilippo. 1991. Elemental mercury poisoning. Clin Pharmacol 10(3):213-221.

Frischer, T, J Kuehr, R Meinert, W Karmaus, R Barth, E Hermann-Kunz, and R Urbanek. 1992. Maternal smoking in early childhood: A risk factor for bronchial responsiveness to exercise in primary-school children. J Pediat 121 (Jul):17-22.

Gardner, MJ, AJ Hall, and MP Snee. 1990. Methods and basic design of case-control study of leukemia and lymphoma among young people near Sellafield nuclear plant in West Cumbria. Br Med J 300:429-434.

Gold, EB and LE Sever. 1994. Childhood cancers associated with parental occupational exposures. Occup Med .

Goldman, LR and J Carra. 1994. Childhood lead poisoning in 1994. J Am Med Assoc 272(4):315-316.

Grandjean, P and E Bach. 1986. Indirect exposures: the significance of bystanders at work and at home. Am Ind Hyg Assoc J 47(12):819-824.
Hansen, J, NH de-Klerk, JL Eccles, AW Musk, and MS Hobbs. 1993. Malignant mesothelioma after environmental exposure to blue asbestos. Int J Cancer 54(4):578-581.

Hecht, NB. 1987. Detecting the effects of toxic agents on spermatogenesis using DNA probes. Environ Health Persp 74:31-40.
Holly, EA, DA Aston, DK Ahn, and JJ Kristiansen. 1992. Ewing’s bone sarcoma, paternal occupational exposure and other factors. Am J Epidemiol 135:122-129.

Homer, CJ, SA Beredford, and SA James. 1990. Work-related physical exertion and risk of preterm, low birthweight delivery. Paediat Perin Epidemiol 4:161-174.

International Agency for Research on Cancer (IARC). 1987. Monographs On the Evaluation of Carcinogenic Risks to Humans, Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs. Vol. 1-42, Suppl. 7. Lyon: IARC.

International Labour Organization (ILO). 1965. Maternity Protection: A World Survey of National Law and Practice. Extract from the Report of the Thirty-fifth Session of the Committee of Experts on the Application of Conventions and Recommendations, para. 199, note 1, p.235. Geneva:ILO.

——. 1988. Equality in Employment and Occupation, Report III (4B). International Labour Conference, 75th Session. Geneva: ILO.

Isenman, AW and LJ Warshaw. 1977. Guidelines On Pregnancy and Work. Chicago: American College of Obstetricians and Gynecologists.

Jacobson, SW, G Fein, JL Jacobson, PM Schwartz, and JK Dowler. 1985. The effect of intrauterine PCB exposure on visual recognition memory. Child Development 56:853-860.

Jensen, NE, IB Sneddon, and AE Walker. 1972. Tetrachlorobenzodioxin and chloracne. Trans St Johns Hosp Dermatol Soc 58:172-177.

Källén, B. 1988. Epidemiology of Human Reproduction. Boca Raton:CRC Press

Kaminski, M, C Rumeau, and D Schwartz. 1978. Alcohol consumption in pregnant women and the outcome of pregnancy. Alcohol, Clin Exp Res 2:155-163.

Kaye, WE, TE Novotny, and M Tucker. 1987. New ceramics-related industry implicated in elevated blood lead levels in children. Arch Environ Health 42:161-164.

Klebanoff, MA, PH Shiono, and JC Carey. 1990. The effect of physical activity during pregnancy on preterm delivery and birthweight. Am J Obstet Gynecol 163:1450-1456.

Kline, J, Z Stein, and M Susser. 1989. Conception to birth-epidemiology of prenatal development. Vol. 14. Monograph in Epidemiology and Biostatistics. New York: Oxford Univ. Press.

Kotsugi, F, SJ Winters, HS Keeping, B Attardi, H Oshima, and P Troen. 1988. Effects of inhibin from primate sertoli cells on follicle-stimulating hormone and luteinizing hormone release by perifused rat pituitary cells. Endocrinology 122:2796-2802.

Kramer, MS, TA Hutchinson, SA Rudnick, JM Leventhal, and AR Feinstein. 1990. Operational criteria for adverse drug reactions in evaluating suspected toxicity of a popular scabicide. Clin Pharmacol Ther 27(2):149-155.

Kristensen, P, LM Irgens, AK Daltveit, and A Andersen. 1993. Perinatal outcome among children of men exposed to lead and organic solvents in the printing industry. Am J Epidemiol 137:134-144.

Kucera, J. 1968. Exposure to fat solvents: A possible cause of sacral agenesis in man. J Pediat 72:857-859.

Landrigan, PJ and CC Campbell. 1991. Chemical and physical agents. Chap. 17 in Fetal and Neonatal Effects of Maternal Disease, edited by AY Sweet and EG Brown. St. Louis: Mosby Year Book.

Launer, LJ, J Villar, E Kestler, and M de Onis. 1990. The effect of maternal work on fetal growth and duration of pregnancy: a prospective study. Br J Obstet Gynaec 97:62-70.

Lewis, RG, RC Fortmann, and DE Camann. 1994. Evaluation of methods for monitoring the potential exposure of small children to pesticides in the residential environment. Arch Environ Contam Toxicol 26:37-46.

Li, FP, MG Dreyfus, and KH Antman. 1989. Asbestos-contaminated nappies and familial mesothelioma. Lancet 1:909-910.

Lindbohm, ML, K Hemminki, and P Kyyronen. 1984. Parental occupational exposure and spontaneous abortions in Finland. Am J Epidemiol 120:370-378.

Lindbohm, ML, K Hemminki, MG Bonhomme, A Anttila, K Rantala, P Heikkila, and MJ Rosenberg. 1991a. Effects of paternal occupational exposure on spontaneous abortions. Am J Public Health 81:1029-1033.

Lindbohm, ML, M Sallmen, A Antilla, H Taskinen, and K Hemminki. 1991b. Paternal occupational lead exposure and spontaneous abortion. Scand J Work Environ Health 17:95-103.

Luke, B, N Mamelle, L Keith, and F Munoz. 1995. The association between occupational factors and preterm birth in US nurses’ survey. Obstet Gynecol Ann 173(3):849-862.

Mamelle, N, I Bertucat, and F Munoz. 1989. Pregnant women at work: Rest periods to prevent preterm birth? Paediat Perin Epidemiol 3:19-28.

Mamelle, N, B Laumon, and PH Lazar. 1984. Prematurity and occupational activity during pregnancy. Am J Epidemiol 119:309-322.

Mamelle, N and F Munoz. 1987. Occupational working conditions and preterm birth: A reliable scoring system. Am J Epidemiol 126:150-152.

Mamelle, N, J Dreyfus, M Van Lierde, and R Renaud. 1982. Mode de vie et grossesse. J Gynecol Obstet Biol Reprod 11:55-63.

Mamelle, N, I Bertucat, JP Auray, and G Duru. 1986. Quelles mesures de la prevention de la prématurité en milieu professionel? Rev Epidemiol Santé Publ 34:286-293.

Marbury, MC, SK Hammon, and NJ Haley. 1993. Measuring exposure to environmental tobacco smoke in studies of acute health effects. Am J Epidemiol 137(10):1089-1097.

Marks, R. 1988. Role of childhood in the development of skin cancer. Aust Paediat J 24:337-338.

Martin, RH. 1983. A detailed method for obtaining preparations of human sperm chromosomes. Cytogenet Cell Genet 35:252-256.

Matsumoto, AM. 1989. Hormonal control of human spermatogenesis. In The Testis, edited by H Burger and D de Kretser. New York: Raven Press.

Mattison, DR, DR Plowchalk, MJ Meadows, AZ Al-Juburi, J Gandy, and A Malek. 1990. Reproductive toxicity: male and female reproductive systems as targets for chemical injury. Med Clin N Am 74:391-411.

Maxcy Rosenau-Last. 1994. Public Health and Preventive Medicine. New York: Appleton-Century-Crofts.

McConnell, R. 1986. Pesticides and related compounds. In Clinical Occupational Medicine, edited by L Rosenstock and MR Cullen. Philadelphia: WB Saunders.

McDonald, AD, JC McDonald, B Armstrong, NM Cherry, AD Nolin, and D Robert. 1988. Prematurity and work in pregnancy. Br J Ind Med 45:56-62.

——. 1989. Fathers’ occupation and pregnancy outcome. Br J Ind Med 46:329-333.

McLachlan, RL, AM Matsumoto, HG Burger, DM de Kretzer, and WJ Bremner. 1988. Relative roles of follicle-stimulating hormone and luteinizing hormone in the control of inhibin secretion in normal men. J Clin Invest 82:880-884.

Meeks, A, PR Keith, and MS Tanner. 1990. Nephrotic syndrome in two members of a family with mercury poisoning. J Trace Elements Electrol Health Dis 4(4):237-239.

National Reasearch Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: National Academy Press.

——. 1993. Pesticides in the Diets of Infants and Children. Washington, DC: National Academy Press.

Needleman, HL and D Bellinger. 1984. The developmental consequences of childhood exposure to lead. Adv Clin Child Psychol 7:195-220.

Nelson, K and LB Holmes. 1989. Malformations due to presumed spontaneous mutations in newborn infants. New Engl J Med 320(1):19-23.

Nicholson, WJ. 1986. Airborne Asbestos Health Assessment Update. Document No. EPS/600/8084/003F. Washington, DC: Environmental Criteria and Assessment.

O’Leary, LM, AM Hicks, JM Peters, and S London. 1991. Parental occupational exposures and risk of childhood cancer: a review. Am J Ind Med 20:17-35.

Olsen, J. 1983. Risk of exposure to teratogens amongst laboratory staff and painters. Danish Med Bull 30:24-28.

Olsen, JH, PDN Brown, G Schulgen, and OM Jensen. 1991. Parental employment at time of conception and risk of cancer in offspring. Eur J Cancer 27:958-965.

Otte, KE, TI Sigsgaard, and J Kjaerulff. 1990. Malignant mesothelioma clustering in a family producing asbestos cement in their home. Br J Ind Med 47:10-13.

Paul, M. 1993. Occupational and Environmental Reproductive Hazards: A Guide for Clinicians. Baltimore: Williams & Wilkins.

Peoples-Sheps, MD, E Siegel, CM Suchindran, H Origasa, A Ware, and A Barakat. 1991. Characteristics of maternal employment during pregnancy: Effects on low birthweight. Am J Public Health 81:1007-1012.

Pirkle, JL, DJ Brody, EW Gunter, RA Kramer, DC Paschal, KM Flegal, and TD Matte. 1994. The decline in blood lead levels in the United States. J Am Med Assoc 272 (Jul):284-291.

Plant, TM. 1988. Puberty in primates. In The Physiology of Reproduction, edited by E Knobil and JD Neill. New York: Raven Press.

Plowchalk, DR, MJ Meadows, and DR Mattison. 1992. Female reproductive toxicity. In Occupational and Environmental Reproductive Hazards: A Guide for Clinicians, edited by M Paul. Baltimore: Williams and Wilkins.

Potashnik, G and D Abeliovich. 1985. Chromosomal analysis and health status of children conceived to men during or following dibromochloropropane-induced spermatogenic suppression. Andrologia 17:291-296.

Rabinowitz, M, A Leviton, and H Needleman. 1985. Lead in milk and infant blood: A dose-response model. Arch Environ Health 40:283-286.

Ratcliffe, JM, SM Schrader, K Steenland, DE Clapp, T Turner, and RW Hornung. 1987. Semen quality in papaya workers with long term exposure to ethylene dibromide. Br J Ind Med 44:317-326.

Referee (The). 1994. J Assoc Anal Chem 18(8):1-16.

Rinehart, RD and Y Yanagisawa. 1993. Paraoccupational exposures to lead and tin carried by electric-cable splicers. Am Ind Hyg Assoc J 54(10):593-599.

Rodamilans, M, MJM Osaba, J To-Figueras, F Rivera Fillat, JM Marques, P Perez, and J Corbella. 1988. Lead toxicity on endocrine testicular function in an occupationally exposed population. Hum Toxicol 7:125-128.

Rogan, WJ, BC Gladen, JD McKinney, N Carreras, P Hardy, J Thullen, J Tingelstad, and M Tully. 1986. Neonatal effects of transplacental exposure to PCBs and DDE. J Pediat 109:335-341.

Roggli, VL and WE Longo. 1991. Mineral fiber content of lung tissue in patients with environmental exposures: household contacts vs. building occupants. Ann NY Acad Sci 643 (31 Dec):511-518.

Roper, WL. 1991. Preventing Lead Poisoning in Young Children: A Statement by the Centers for Disease Control. Washington, DC: US Department of Health and Human Services.

Rowens, B, D Guerrero-Betancourt, CA Gottlieb, RJ Boyes, and MS Eichenhorn. 1991. Respiratory failure and death following acute inhalation of mercury vapor. A clinical and histologic perspective. Chest 99(1):185-190.

Rylander, E, G Pershagen, M Eriksson, and L Nordvall. 1993. Parental smoking and other risk factors for wheezing bronchitis in children. Eur J Epidemiol 9(5):516-526.

Ryu, JE, EE Ziegler, and JS Fomon. 1978. Maternal lead exposure and blood lead concentration in infancy. J Pediat 93:476-478.

Ryu, JE, EE Ziegler, SE Nelson, and JS Fomon. 1983. Dietary intake of lead and blood lead concentration in early infancy. Am J Dis Child 137:886-891.

Sager, DB and DM Girard. 1994. Long term effects on reproductive parameters in female rats after translactional exposure to PCBs. Environ Res 66:52-76.

Sallmen, M, ML Lindbohm, A Anttila, H Taskinen, and K Hemminki. 1992. Paternal occupational lead exposure and congenital malformations. J Epidemiol Community Health 46(5):519-522.

Saurel-Cubizolles, MJ and M Kaminski. 1987. Pregnant women’s working conditions and their changes during pregnancy: A national study in France. Br J Ind Med 44:236-243.

Savitz, DA, NL Sonnerfeld, and AF Olshaw. 1994. Review of epidemiologic studies of paternal occupational exposure and spontaneous abortion. Am J Ind Med 25:361-383.

Savy-Moore, RJ and NB Schwartz. 1980. Differential control of FSH and LH secretion. Int Rev Physiol 22:203-248.

Schaefer, M. 1994. Children and toxic substances: Confronting a major public health challenge. Environ Health Persp 102 Suppl. 2:155-156.

Schenker, MB, SJ Samuels, RS Green, and P Wiggins. 1990. Adverse reproductive outcomes among female veterinarians. Am J Epidemiol 132 (January):96-106.

Schreiber, JS. 1993. Predicted infant exposure to tetrachloroethene in human breastmilk. Risk Anal 13(5):515-524.

Segal, S, H Yaffe, N Laufer, and M Ben-David. 1979. Male hyperprolactinemia: Effects on fertility. Fert Steril 32:556-561.

Selevan, SG. 1985. Design of pregnancy outcome studies of industrial exposures. In Occupational Hazards and Reproduction, edited by K Hemminki, M Sorsa, and H Vainio. Washington, DC: Hemisphere.

Sever, LE, ES Gilbert, NA Hessol, and JM McIntyre. 1988. A case-control study of congenital malformations and occupational exposure to low-level radiation. Am J Epidemiol 127:226-242.

Shannon, MW and JW Graef. 1992. Lead intoxication in infancy. Pediatrics 89:87-90.

Sharpe, RM. 1989. Follicle-stimulating hormone and spermatogenesis in the adult male. J Endocrinol 121:405-407.

Shepard, T, AG Fantel, and J Fitsimmons. 1989. Congenital defect abortuses: Twenty years of monitoring. Teratology 39:325-331.

Shilon, M, GF Paz, and ZT Homonnai. 1984. The use of phenoxybenzamine treatment in premature ejaculation. Fert Steril 42:659-661.

Smith, AG. 1991. Chlorinated hydrocarbon insecticides. In Handbook of Pesticide Toxicology, edited by WJ Hayes and ER Laws. New York: Acedemic Press.

Sockrider, MM and DB Coultras. 1994. Environmental tobacco smoke: a real and present danger. J Resp Dis 15(8):715-733.

Stachel, B, RC Dougherty, U Lahl, M Schlosser, and B Zeschmar. 1989. Toxic environmental chemicals in human semen: analytical method and case studies. Andrologia 21:282-291.

Starr, HG, FD Aldrich, WD McDougall III, and LM Mounce. 1974. Contribution of household dust to the human exposure to pesticides. Pest Monit J 8:209-212.

Stein, ZA, MW Susser, and G Saenger. 1975. Famine and Human Development. The Dutch Hunger Winter of 1944/45. New York: Oxford Univ. Press.

Taguchi, S and T Yakushiji. 1988. Influence of termite treatment in the home on the chlordane concentration in human milk. Arch Environ Contam Toxicol 17:65-71.

Taskinen, HK. 1993. Epidemiological studies in monitoring reproductive effects. Environ Health Persp 101 Suppl. 3:279-283.

Taskinen, H, A Antilla, ML Lindbohm, M Sallmen, and K Hemminki. 1989. Spontaneous abortions and congenital malformations among the wives of men occupationally exposed to organic solvents. Scand J Work Environ Health 15:345-352.

Teitelman, AM, LS Welch, KG Hellenbrand, and MB Bracken. 1990. The effects of maternal work activity on preterm birth and low birth weight. Am J Epidemiol 131:104-113.

Thorner, MO, CRW Edwards, JP Hanker, G Abraham, and GM Besser. 1977. Prolactin and gonadotropin interaction in the male. In The Testis in Normal and Infertile Men, edited by P Troen and H Nankin. New York :Raven Press.

US Environmental Protection Agency (US EPA). 1992. Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders. Publication No. EPA/600/6-90/006F. Washington, DC: US EPA.

Veulemans, H, O Steeno, R Masschelein, and D Groesneken. 1993. Exposure to ethylene glycol ethers and spermatogenic disorders in man: A case-control study. Br J Ind Med 50:71-78.

Villar, J and JM Belizan. 1982. The relative contribution of prematurity and fetal growth retardation to low birth weight in developing and developed societies. Am J Obstet Gynecol 143(7):793-798.

Welch, LS, SM Schrader, TW Turner, and MR Cullen. 1988. Effects of exposure to ethylene glycol ethers on shipyard painters: ii. male reproduction. Am J Ind Med 14:509-526.

Whorton, D, TH Milby, RM Krauss, and HA Stubbs. 1979. Testicular function in DBCP exposed pesticide workers. J Occup Med 21:161-166.

Wilcox, AJ, CR Weinberg, JF O’Connor, DD BBaird, JP Schlatterer, RE Canfield, EG Armstrong, and BC Nisula. 1988. Incidence of early loss of pregnancy. New Engl J Med 319:189-194.

Wilkins, JR and T Sinks. 1990. Parental occupation and intracranial neoplasms of childhood: Results of a case-control interview study. Am J Epidemiol 132:275-292.

Wilson, JG. 1973. Environment and Birth Defects. New York: Academic Press.

——. 1977. current status of teratology-general principles and mechanisms derived from animal studies. In Handbook of Teratology, Volume 1, General Principles and Etiology, edited by JG Fraser and FC Wilson. New York: Plenum.

Winters, SJ. 1990. Inhibin is released together with testosterone by the human testis. J Clin Endocrinol Metabol 70:548-550.

Wolff, MS. 1985. Occupational exposure to polychlorinated biphenyls. Environ Health Persp 60:133-138.

——. 1993. Lactation. In Occupational and Environmental Reproductive Hazards: A Guide for Clinicians, edited by M Paul. Baltimore: Williams & Wilkins.

Wolff, MS and A Schecter. 1991. Accidental exposure of children to polychlorinated biphenyls. Arch Environ Contam Toxicol 20:449-453.

World Health Organization (WHO). 1969. Prevention of perinatal morbidity and mortality. Public Health Papers, No. 42. Geneva: WHO.

——. 1977. Modification Recommended by FIGO. WHO recommended definitions, terminology and format for statistical tables related to the perinatal period and use of a new certificate for cause of perinatal death. Acta Obstet Gynecol Scand 56:247-253.

Zaneveld, LJD. 1978. The biology of human spermatozoa. Obstet Gynecol Ann 7:15-40.

Ziegler, EE, BB Edwards, RL Jensen, KR Mahaffey, and JS Fomon. 1978. Absorption and retention of lead by infants. Pediat Res 12:29-34.

Zikarge, A. 1986. Cross-Sectional Study of Ethylene Dibromide-Induced Alterations of Seminal Plasma Biochemistry as a Function of Post-Testicular Toxicity with Relationships to Some Indices of Semen Analysis and Endocrine Profile. Dissertation, Houston, Texas: Univ.of Texas Health Science Center.

Zirschky, J and L Wetherell. 1987. Cleanup of mercury contamination of thermometer workers’ homes. Am Ind Hyg Assoc J 48:82-84.

Zukerman, Z, LJ Rodriguez-Rigau, DB Weiss, AK Chowdhury, KD Smith, and E Steinberger. 1978. Quantitative analysis of the seminiferous epithelium in human testicular biopsies, and the relation of spermatogenesis to sperm density. Fert Steril 30:448-455.

Zwiener, RJ and CM Ginsburg. 1988. Organophosphate and carbamate poisoning in infants and children. Pediatrics 81(1):121-126