Penises are shrinking, and more boys are being born with genital defects, two Melbourne scientists claim.
They think chemicals in plastics are to blame.
Their controversial stance is based on studies of animals exposed to the chemicals, as well as human data they say shows rates of hypospadia – a penis birth defect causing a range of functionality problems – have doubled in Australia.
“Exposure to these chemicals, this is the No.1 reproductive issue for men,” says Associate Professor Andrew Pask, who leads a lab at Melbourne University researching male reproduction.
However, government regulators say the best-available science shows these chemicals are not having an effect on humans. Other experts say a link is possible but that the evidence is a long way from settled.
Some plastics can release chemicals, known as endocrine disruptors, that can mimic human sex hormones. In animal studies, exposure when pregnant can have profound effects on an animal’s offspring, including infertility, undescended testes and hypospadia.
There is no strong evidence about what they do to humans.
But we all have observable levels in our blood because they are so common in everyday life. Dr Pask points to several chemicals that may have an effect on humans: BPA, phthalates (both used in plastics), parabens (used in toothpastes and beauty products) and atrazine (herbicide).
Despite a large number of studies overseas, Dr Pask and his Melbourne University colleague Dr Mark Green believe they are Australia’s only scientists studying the chemicals’ effect on male reproduction.
A 2007 study found the rate of severe hypospadia had almost doubled between 1980 and 2000 in Western Australia, with one in 118 male babies born with the birth defect. A Victorian study from 1998 reported similar findings. But a review of studies around the world reported the data was too inconsistent to draw strong conclusions.
A small French study in 2015 found a “strong” link between exposure to endocrine-disrupting chemicals during pregnancy and hypospadia, as did another in Italy.
“No one likes to talk about this. Often parents don’t even like to tell their kids they had it – it gets surgically repaired but often the surgeries don’t work very well,” says Dr Pask.
“When it’s doubling, it cannot be genetic defects – it takes years for that to spread through a population. So we know it has to be environmental in origin.”
Pask also points to studies showing exposure to EDCs that mimic the female sex hormone oestrogen can shorten penis length. However there is no population-level data to back this claim.
Hypospadia causes the urethra, which is supposed to exit at the the tip of the penis, to do so anywhere from the shaft to the scrotum, causing a range of functionality problems including difficulty urinating.
In his lab, Dr Pask says it is remarkably easy to give a baby mouse hypospadia: infuse the pregnant mother’s drinking water with atrazine (his findings have not yet been published).
In animals, the damage intensifies over subsequent generations, he says. It becomes particularly acute by the third generation. “Humans have been exposed to these since the 1950s, so about two generations,” says Dr Green.