Exposure to high phthalate levels delays puberty.

Jul 21, 2009

Noriega N, KL Howdeshell, J Furr, CR Lambright, VS Wilson, and LE Gray Jr. Pubertal administration of DEHP delays puberty, suppresses testosterone production and inhibits reproductive tract development in male Sprague-Dawley and Long-Evans rats. Toxicological Sciences doi:10.1093/toxsci/kfp129.


Male rats reach puberty later and have skewed hormone levels after exposure to high concentrations of a plastics chemical.

A chemical used to soften plastics postpones puberty in two different breeds of male rats when exposed to the highest levels tested. The rats exposed to lower levels of the phthalate (pronounced THAL-ate) entered puberty at the right time.

Other studies have shown that higher – but not lower – doses of phthalates delay puberty in male rats.

Phthalates are a class of chemicals used in plastic household products – like vinyl flooring and shower curtains – and personal products, such as toys and make-up. The phthalate studied in this research, called DEHP, is mostly used to make PVC plastic pliable. This special property makes DEHP common in medical devices, like the tubing used in IVs in neonatal intensive care units.

Phthalates are considered endocrine disruptors because of they can prevent androgen hormone effects. As antiandrogens, the chemicals are thought to inhibit androgen hormones, such as testosterone.

The researchers tested a wide range of DEHP levels in two different strains of rats and compared when the animals from the differen test groups hit puberty. The doses used – 10, 100, 300 and 900 milligrams per kilogram of rat body weight – are much higher than levels measured in people.

In this sophisticated, two-part study, the authors raised two breeds of rats and fed them one of the four doses of DEHP every day, starting when they were weaned at 22 days old, and continuing until either puberty or adulthood. Other rats did not eat DEHP and acted as controls.

Researchers examined the rats at puberty and as adults. They analyzed blood for hormone levels, evaluated gonads (prostate, seminal vesicles, testes and epididymides) for proper development and weighed the organs (liver, kidney and adrenal glands), which are sometimes affected by DEHP. They also compared how much testosterone was made by the testes in the SD rats during and after puberty.

In both breeds of rats, the highest exposure to DEHP delayed puberty. But there were differences. The Long Evans (LE) rats took longer to complete puberty than did the Sprague Dawley (SD) rats. Puberty was slowed in LE rats dosed with the top two concentrations tested and delayed in SD rats only if they were given the highest levels of DEHP. That delay was accompanied by decreased testosterone production by the testis.

The two breeds differed in the way DEHP affected their sexual development; most effects were seen at the two highest doses and in the SD rats. Sperm count declines were more dramatic in the SD breed, as was abnormal testes growth that lasted into adulthood.

The differences in how the two rat strains responded to the chemical are most likely due to differences in biology – that DEHP may affect the male reproductive system differently in each strain – and not just to random chance, the authors suggest.

It is possible that looking at a diverse population, such as many rat strains or humans, would reveal some who are very sensitive to DEHP and some who are very resistant to DEHP. The challenge now is to continue to identify who is sensitive, how little DEHP can harm them and what kind of harm that is.