**5. Conclusions**

In view of the fact that the preliminary concerns arose about environmental chemicals or toxins and declining sperm counts, there has been an explosion of research in this area. The initial 'environmental oestrogen' hypothesis has been superseded by a more refined definition of EDCs. It is now accepted that there are a plethora of ways in which the environmental chemicals can potentially act on the endocrine as well as male reproductive systems. Though supportive data must need to determine whether human male reproductive health is declining or not. However; the hypothesis of a 'testicular dysgenesis syndrome' is an important advancement and may aid our understanding of the underlying aetiology of these disorders. Within the reproductive tract, the male is exquisitely vulnerable to the effects of anti-androgens during development due the dependence on the synthesis and action of androgens for the masculinization of the male reproductive tract. The ability of phthalates to suppress androgen synthesis during development and to induce testicular dysgenesis together with cryptorchidism and hypospadias has close parallels with human TDS. However, the crucial question regarding whether the level of environmental chemicals is sufficient to impact on human male reproductive health remains unanswered, although advances will be made from studying the effects of multi-component EDC mixtures in both in vitro and in vivo test systems. Moreover, it has been observed that in wildlife, there is a increasing rates of testicular cancer, to the debate regarding trends in sperm counts, there has been increasing concern that hazardous substances in the environment adversely affect male reproductive health. The ultimate benefits of this chapter that should serve as a framework for future studies to improve our knowledge in this area. By better defining the problems, learning about the mechanisms responsible for adverse effects, and developing panels of relevant biomarkers, we will make progress toward preventing future adverse effects on male reproductive health.
