Mouse Study Hints at How Air Pollution Might Impact a Mammal’s Sperm
A study in mice has identified a possible way in which air pollution might impact male fertility among mammals.
It’s not yet clear if the results extend to humans, but the mouse model suggests breathing fine particulate matter smaller than or equal to 2.5 micrometres (PM2.5) is linked to inflammation in the brain and reduced sperm count.
Recently, research has shown air pollution has a dangerous and deadly impact on human health, inducing changes in our lungs, our hearts, and maybe even our brains. The reproductive system is likely no exception, but how it is impacted is still unclear.
At the moment, some parts of the world are undoubtedly experiencing an infertility crisis. The sperm counts of men in Western nations, for instance, have halved in the last few decades. What is still in doubt, however, is what is driving these changes.
Numerous studies among animals and humans have found a link between air pollution and a decrease in sperm production.
Air pollution is, therefore, a leading culprit in the infertility crisis, but while some animal studies have found PM2.5 exposure is marked by testicular inflammation, others have found no such signs.
In these cases, something else must be driving the loss of sperm, and the new research on mice suggests it could be in our brains.
Similar to previous research, when healthy mice were exposed to PM2.5 in the ambient air, they showed lower sperm counts and significant inflammation in a part of the brain known as the hypothalamus.
This is a region of the forebrain that connects to the pituitary gland and gonadal glands, an axis that impacts our hormone production and the reproductive system.
When special mice were bred without a key marker of inflammation in the hypothalamus, called Inhibitor Kappa B Kinase 2 (IKK2 for short), the authors found the animals coped much better with the physiological impacts of air pollution. The sperm impairment seen in normal mice seemed to have been halted.
“All these findings strongly support the hypothesis of a causal role of hypothalamic inflammation in the impairment of sperm production by PM2.5 exposure,” the authors argue, “thereby providing a deep mechanistic insight into this mounting public health concern induced by PM2.5 exposure.”
The current research on mice is some of the strongest evidence we have to date on how air pollution impacts mammalian reproduction. But we are still a long way from figuring out the mechanism in humans or coming up with a solution.
“Our findings showed that the damage due to air pollution – at least to the sperm count – could be remedied by removing a single inflammation marker in the brains of mice, suggesting that we may be able to develop therapies that could prevent or reverse the damaging effects of air pollution on fertility,” explains Zhekang Ying, who studies the health effects of air pollution at the University of Maryland.
The team hopes their findings will have an impact, not just on fertility research going forward but also on how inflammation in the hypothalamus from air pollution might impact our heart and lung health as well. The research is long overdue.
The study was published in Environmental Health Perspectives.