Due to their ability to mimic the action of sex hormones, endocrine disruptors have long been suspected of having a negative impact on human fertility. A recent study has just confirmed that an action of these disruptors decreases the production of testosterone and thus interferes with the fetal development of the human testicles.
Several studies carried out in recent years suggest a marked decrease in male fertility. For example, a French team recently reported that the average sperm concentration of men aged 18 to 70 has dropped by around 33% over the past 15 years, and that this drop was accompanied by a similar reduction in the number sperm with normal morphology. The magnitude of this reduction, as well as the rapidity with which it has occurred, raises the worrying possibility that environmental factors are affecting the male reproductive system and may be contributing to the rise in infertility cases observed over the past few decades in industrialized countries.
Bisphenol A, phthalates and bromine compounds affect sperm quantity and quality
The main environmental factor pointed to is a group of compounds called “endocrine disruptors”. As their name suggests, these molecules have the ability to interfere with the normal functioning of the hormonal system and thus cause adverse effects in an organism or its offspring.
Among the endocrine disruptors most likely to affect fertility, bisphenol A, phthalates and brominated compounds are the most important. These molecules are indeed present in a host of industrial products (plastics, cosmetics, tin cans, household products and flame retardants, among others) and can partially dissolve to be subsequently absorbed by the human body. 90% of the population of Western countries is regularly in contact with bisphenol A and that this molecule can be detected in various biological fluids, including semen. Some studies have reported that men who have higher levels of BPA in their urine were more likely to have low sperm count and therefore lower quality sperm.
Testicular cancer, infertility, undescended testicle in infants
One of the most worrying aspects of endocrine disruptors is their potential to act directly on the fetus and affect the development of the reproductive system from the outset. For example, it is possible that the marked increase in the incidence of testicular cancer as well as cryptorchidism (undescended testicle at birth) observed in recent years is linked, at least in part, to developmental anomalies caused by endocrine disruptors.
Recent results suggest that these abnormalities could be caused by a disturbance of the endocrine function of the testicles. By exposing fetal testicles to low concentrations of bisphenol A (2 micrograms per liter), the researchers observed a notable decrease in the secretion of testosterone, the hormone essential for the production of spermatozoa, as well as levels of the protein INSL3 , involved in the descent of the testes during development. These results confirm that certain endocrine disruptors can directly affect human testicular development and that this effect could contribute to the reduction of male fertility.
Its environment to the eye
Until now, efforts to reduce exposure to bisphenol A have mainly focused on plastics intended for use by children (baby bottles, for example). In light of these observations, some are of the opinion that pregnant women should also pay particular attention to these molecules by avoiding, for example, products contained in polycarbonate containers or even in certain cans. Using glass containers to reheat food in the oven or microwave is also preferable. Beyond the foods we eat, some of the molecules present in our immediate environment can therefore influence the maintenance of our health or the development of diseases.
Roland M et al. Decline in semen concentration and morphology in a sample of 26,609 men close to general population between 1989 and 2005 in France. Hmm. Repr. ; 28: 462-470.
N’tumba-Byn T et al. Differential effects of bisphenol a and diethylstilbestrol on human, rat and mouse fetal Leydig cell function. PLoS One. 7:e51579.