Comment on behalf of the British Andrology Society on a report that dog sperm quality has declined over the last 26 years and its implications for human health. (Environmental chemicals impact dog semen quality in vitro and may be associated with a temporal decline in sperm motility and increased cryptorchidism” by Lee et al. Scientific Reports, 6:31281, 2016)
Back in 1992, a paper was published making the surprising claim that human sperm counts had declined by 50% over the last 50 years. This generated a great deal of public interest, even though the report itself was heavily criticised for methodological defects by some scientists. Since then, numerous papers have been published on the general topic of men’s reproductive health but without any clear consensus as to what could be doing us harm.
Now, Lee et al. report that the quality of dog sperm has declined significantly over the last 26 years and that cases of undescended testes have increased in number, along with some alterations in male:female sex mortality ratios. Crucially, because all the data were collected by one lab, using consistent protocols and with careful checks on accuracy, most of the criticisms made of the 1992 human study do not apply.
In an attempt to understand these findings, testicular and sperm samples from the dogs and samples of widely-used dog foods were analysed for the presence of common environmental contaminants, some of which are known to damage reproductive function. Detectable levels of many of these were found in both dog tissues and dog food and when a couple were tested on sperm, one of them was able to induce the same effect on sperm as had been found in the dogs at fairly comparable concentrations to average levels found in the dog testes.
All this suggests a potential problem for dog fertility, possibly as a result of compounds to which they are exposed through their environment. And since dogs live in close proximity to humans and show similar susceptibility to certain reproductive diseases, should we be concerned that the same could be true for humans? In fact there are a number of key differences between the dog and human evidence.
Of most concern regarding human semen quality is the alleged decline in sperm numbers. However, there was no evidence of such a decline in the dogs. The principal effect seen in the dogs was on the forward motility of sperm. It is of a magnitude and consistency to be a cause for concern as regards dogs’ reproductive health but the lack of an effect on sperm numbers does suggest a mechanistic difference between the two species.
The increase in undescended testis in the dogs reflects increases that are reported by some in humans. However, the human data are still debated because it is not clear whether the reports of changes in incidence actually reflect changes in detection rates.
The best evidence of an adverse effect on the reproductive health of men is a steady increase in the rate of testicular cancer in almost every country with cancer registry data. It is now widely accepted not only that this is a real phenomenon but that the origin of much testicular cancer appears to lie in early development, as a result of abnormalities induced in very early germ cells. However, there is no consensus yet as to what may be causing such abnormalities. Lee et al. cite other studies showing a similar temporal increase in testicular cancer incidence in dogs but their own study was not set up to detect this.
The correlation between the presence of environmental toxins in both dog foods and reproductive tissues and the adverse effects on reproductive health is intriguing. It is particularly noteworthy that the compound the authors tested on sperm in vitro and found similar effects to those observed in vivo has also been reported by others as being present in human semen, where it was associated with the same effect on sperm forward motility as found in the dogs. This potential link with humans merits further study but it should be pointed out that this is an effect operating in adults, whereas the best evidence for induced testicular pathology occurring in humans (the testicular cancer data discussed above) primarily relates to events occurring in the womb.
Dog sperm then may be susceptible to toxins found in dry and tinned dog foods. Fortunately that is not eaten by humans so further data are required on the levels of these toxins in the human diet. However, there are so many potentially reprotoxic and indeed beneficial compounds both normally present and as contaminants that effects are difficult to determine. We ourselves have undertaken dietary studies on human sperm. In one of these, there was an effect of male age on sperm DNA damage (in healthy non-smokers) but it was also found that micronutrient intake was associated with improved sperm DNA quality in older men. In another, independent of age, men with substantial daily caffeine consumption had increased sperm DNA damage associated with double-strand DNA breaks. DNA damage in sperm can be converted to chromosomal aberrations and gene mutations after fertilization, increasing the risks of developmental defects and genetic diseases among offspring. Both of the compounds tested by Lee et al. also caused DNA strand break damage in dog sperm.
The paper by Lee et al. presents very useful and novel data showing that reproductive health in dogs may be declining and that this may be associated with dietary contaminants. As with all the best research, it also raises more questions and begs further study into whether these contaminants could be having an effect on humans at relevant doses. We do not yet have sufficient data to make firm conclusions about the relevance of Lee et al.’s findings to humans.
Martin Brinkworth & Diana Anderson
University of Bradford
On behalf of the BAS Committee