Sl. No. Methods of Assessment: 1. Testosterone (T) , Prolactin, LH, FSH, and Inhibin-B concentrations. 2. Semen volume and pH. 3. Sperm density/Sperm count. 4. Sperm morphology and morphometry 5. Sperm motility (% of motile and velocity), Sperm viability (Vital stain and Hyper Osmotic Swelling (HOS)). 6. Sperm function assays (Acrosome reaction, Hemizona assay of sperm binding and sperm penetration assay). 7. Sperm genetic analysis (Sperm chromatin stability assay, Comet assay. Assessment of chromosomal aneuploidy and Nuclear microdeletions). 8. Marker chemicals from accessory glands (Epididymis is represented by glycerylphosphorylcholine, Seminal vesicles by fructose, and the Prostate gland by zinc). 9. Nocturnal penile measurements. 10. Personal reproductive history (Pubertal development, Paternity (Pregnancy timing and outcomes), Sexual functions (Erection, Ejaculation, Orgasm and

Table 2. Assessment of Male Reproductive Capacity in Humans (Moline et al., 2000).

evaluating marker chemicals secreted by each respective gland (Schrader, 1997). For example, the epididymis is represented by glycerylphosphorylcholine, the seminal vesicles by fructose, and the prostate gland by zinc. Measures of semen pH and volume provide additional general information on the nature of seminal plasma, reflecting post testicular effects. A toxicant or its metabolite may act directly on accessory sex glands to alter the quantity or quality of their secretions. Alternatively, the toxicant may enter the seminal plasma and affect the sperm or may be carried to the site of fertilization by the sperm and affect the ova or conceptus. The presence of toxicants or their metabolites in seminal plasma can be analyzed using atomic absorption spectrophotometry or gas chromotography/mass spectrometry. Impact on the neuroendocrine system is another mechanism whereby toxicants can disturb the male reproductive system. To establish the extent of endocrine dysfunction, hormone levels can be measured in blood and urine. The profile recommended by NIOSH to evaluate endocrine dysfunction associated with reproductive toxicity consists of assessing serum concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone, and prolactin (Schrader, 1997). Because of the pulsatile secretion of LH, testosterone, and to a much lesser extent FSH, and the variability in the evaluation of reproductive hormones, it is recommended that three blood samples be drawn at set intervals in the early morning and the results pooled or averaged for clinical assessment. In epidemiologic field studies, however, multiple blood samples are impractical and may decrease participation rates. Alternatively, LH and FSH can be measured in urine, providing indices of gonadotropin levels that are relatively unaffected by pulsatile secretion. However, if an exposure can affect hepatic metabolism of sex steroid hormones (Apostoli et al., 1996), urinary measures of excreted testosterone metabolite (androsterone) or estradiol metabolite (estrone-3-glucuronide) are not recommended. Moreover, future assessment of reproductive hormones may extend to inhibin, activin, and follistatin, polypeptides that are

Libido)).

secreted primarily by the gonads and that act on the pituitary to increase (activin) or decrease (inhibin and follistatin) FSH synthesis and secretion. Within the gonads, these peptides regulate steroid hormone synthesis and may also directly affect spermatogenesis. Ongoing studies are investigating the utility of serum inhibin-B level as an important marker of Sertoli cell function and *in utero* developmental toxicity (Jensen et al., 1997). Other indicators of central nervous system toxicity are reported alterations in sexual function, including libido, erection, and ejaculation. There is not much literature on occupational exposures causing sexual dysfunction in men (Schrader, 1997); however, there are suggestions that lead, carbon disulfide, stilbene, and cadmium can affect sexual function. These outcomes are difficult to measure because of the absence of objective measures and because sexual dysfunction can be attributed to and affected by psychologic or physiologic factors (Schrader, 1997).
