title: Regional differences and temporal trends in male reproductive health disorders: semen quality may be a sensitive marker of environmental exposures.
abstract: The decline in semen quality has been the subject of an animated debate. A recent prospective study now irrefutably shows a decline in semen quality in men from Finland, a country that previously boasted good semen quality. Semen quality has, in some countries, reached a level where a considerable fraction of young men are at risk of fertility problems. Impaired semen quality, testicular cancer, cryptorchidism and hypospadias are risk factors for each other, and the testicular dysgenesis syndrome (TDS) has been put forward to explain the observations. This syndrome implies that the four disease entities share the same patho-physiological etiology caused by disturbed testicular development in early fetal life. It seems likely that the rapid rise in TDS-associated conditions can, at least partly, be explained by environmental factors. Animal studies provide strong evidence that manmade chemicals can disrupt the hormone dependent pathways responsible for fetal gonadal development, subsequently leading to TDS-like symptoms. In humans, fetal exposure to endocrine disrupting substances may play a role, although genetic factors are probably also involved. Recent studies indicate that exposure to endocrine disrupters also in adulthood may affect semen quality and reproductive hormones. Causal relationships are inherently difficult to establish in humans, and a clear connection between the disorders and specific toxicants has not been established. It seems likely that the cumulative effects of various low-dose exposures to endocrine disrupters in our environment are responsible for the adverse effects in the male reproductive system. Semen quality may be the most sensitive marker of adverse environmental exposures, and we suggest that standardized surveillance studies of semen quality are continued or initiated to monitor the combined effects of various preventive actions.
authors.affiliation: University Department of Growth and Reproduction, Rigshospitalet, Section 5064, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. loa.nordkap@rh.regionh.dk
authors.forename: Loa
authors.initials: L
authors.lastname: Nordkap
authors.forename: Ulla Nordström
authors.initials: UN
authors.lastname: Joensen
authors.forename: Martin
authors.initials: M
authors.lastname: Blomberg Jensen
authors.forename: Niels
authors.initials: N
authors.lastname: Jørgensen
mesh_terms: D000818:Animals; D015415:Biomarkers; D003456:Cryptorchidism / Q000139:chemically induced / Q000453:epidemiology; D052244:Endocrine Disruptors / Q000633:toxicity*; D004781:Environmental Exposure; D005060:Europe / Q000453:epidemiology; D006059:Gonadal Dysgenesis / Q000139:chemically induced / Q000453:epidemiology / Q000473:pathology; D006801:Humans; D007021:Hypospadias / Q000139:chemically induced / Q000453:epidemiology; D007248:Infertility, Male / Q000139:chemically induced / Q000453:epidemiology; D008297:Male; D009017:Morbidity; D060728:Reproductive Health; D055101:Semen Analysis; D013736:Testicular Neoplasms / Q000139:chemically induced / Q000453:epidemiology
chemical_list: D015415:Biomarkers; D052244:Endocrine Disruptors