Letters

Disorders of spermatogenesis in Finland

BMJ 1997; 314 doi: https://doi.org/10.1136/bmj.314.7086.1042 (Published 05 April 1997) Cite this as: BMJ 1997;314:1042

Is this a period effect, and if so, why?

  1. Michael Joffe, Senior lecturer in public healtha
  1. a Imperial College School of Medicine at St Mary's, Norfolk Place, London W2 1PG
  2. b Department of Forensic Medicine, PO Box 40, SF-00014, University of Helsinki, Finland
  3. c School of Medicine, University of Tampere, Finland

    Editor—Jarkko Pajarinen and colleagues report a dramatic deterioration in spermatogenesis between 1981 and 1991 at necropsy in middle aged Finnish men who died suddenly.1 The rate of abnormality seems extremely high, even in 1981. Could this be explained by, for example, the different fixatives used or by varying delay between death and necropsy? Have similar findings been reported in other comparable studies?

    The authors discuss the discrepancy between their findings and the evidence that sperm concentration has not declined in Finland up to as recently as 1994.2 The explanation given, that blocked seminiferous tubules together with normal spermatogenesis can coexist with an impaired sperm count, cannot account for observations that are the other way around. What could be relevant, however, are differences in age distribution and in location within Finland.

    Assuming that these findings can be accepted as real, a key question is whether they are due to a cohort effect or a period effect. A cohort effect corresponds to an exposure in early life that led to a permanent defect. A period effect results from an acute or chronic exposure that occurred, or at least had its effect, between 1981 and 1991. Pajarinen and colleagues could have investigated this by analysing each of their cross sectional studies by age (allowing for a possible “normal” background deterioration): a cohort effect would predict that older men had better spermatogenesis, whereas a chronic period effect would predict the reverse as older men would have been exposed for more years. If both effects were present they would tend to counterbalance one another. An acute period effect would predict no relation with age, unless susceptibility varied with age.

    On the face of it, the steep rise in arrested spermatogenesis would suggest an acute period effect–that is, a sudden event that occurred between the two studies. One possibility is the Chernobyl accident of 1986, during which Finland received an appreciable dose of radiation; the peak radiation dose in southern Finland occurred somewhat to the east of Helsinki.3 A slight rise in congenital malformations showing a dose-response relation4 was reported in Finland after the accident.3 Although the external dose was small, certain substances, such as plutonium and indium, are actively taken up by the adult testis5 and could cause appreciable damage by emitting high energy radiation.

    References

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    Author's reply

    1. Jarkko Pajarinen, Doctorb,
    2. Pekka J Karhunen, Professorc
    1. a Imperial College School of Medicine at St Mary's, Norfolk Place, London W2 1PG
    2. b Department of Forensic Medicine, PO Box 40, SF-00014, University of Helsinki, Finland
    3. c School of Medicine, University of Tampere, Finland

      Editor—Michael Joffe presents an interesting hypothesis of a possible association between deteriorating spermatogenesis in Finland and the Chernobyl accident in 1986. We do not think that radiation could entirely explain our finding, however, as most of our necropsy data came from the Helskini area, which avoided the peak of radiation. The hypothesis does, however, raise new questions which should be considered in future investigations.

      The incidence of normal spermatogenesis (56%) in our series correlates well with another study which reported normal spermatogenesis in 50% of cases.1 In addition, our series included heavy drinkers, in whom there is a high incidence of disorders of spermatogenesis.1 2 3 This significantly decreased the mean incidence of normal spermatogenesis in our series. Interestingly, when moderate drinkers were analysed in the 1981 series normal spermatogenesis was found in four out of five men. The role of alcohol consumption in the deterioration of spermatogenesis was not, however, included in our study.

      To allow for confounding from the various types of fixation methods we assessed the effects of certain fixatives on spermatogenesis in a previous study.2 Formalin caused detachment of germinal epithelium in seminiferous tubules, making the scoring of spermatogenesis to some extent more difficult. Neither formalin nor Bouin's solution had an effect on the state of spermatogenesis. Recently, we investigated the effects of fixation on testes with an identical state of spermatogenesis. No association was observed between testicular morphology and the type of fixative solution (unpublished data). In addition, we do not think that the slight difference of 0.3 days (3.5 in 1981 v 3.8 in 1991) between death and necropsy could explain the difference between the two series; reasons other than technical might explain this finding.

      As we pointed out in our article, blockage of seminiferous tubules has been observed in several oligospermic men, suggesting an inconsistency between semen analysis and state of spermatogenesis.4 The total sperm reserve is unlikely to be completely depleted after one ejaculation.5 A slight deterioration in spermatogenesis, such as partial spermatogenic arrest, could produce enough spermatozoa to make a comparison with normal spermatogenesis difficult, especially if analysis was performed after a period of abstinence, during which sperm reserves become replenished. If semen analysis was performed at more frequent intervals differences in spermatogenesis might become more apparent.

      References

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      4. 4.
      5. 5.
      View Abstract

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