Our Stolen Futurea book by Theo Colborn, Dianne Dumanoski, and John Peterson Myers



This mouthful of a title, below, may deflect casual readers from very important results. Don't let it.


Gray, LE, C Wolf, C Lambright, P Mann, M Price, RL Cooper and J Ostby. 1999. Administration of potentially antiandrogenic pesticides (procymidone, linuron, iprodione, chlozolinate, p,p'-DDE, and ketoconazole) and toxic substances (dibutyl- and diethylhexyl phthalate, PCB 169, and ethane dimethane sulphonate) during sexual differentiation produces diverse profiles of reproductive malformations in the male rat. Toxicology and Industrial Health. 15:94-118.

Gray et al. establish definitively that endocrine disruption occurs through interaction with androgen receptor, that multiple compounds are antiandrogens, and that their interaction can produce a diversity of impacts on the developing male reproductive tract.

These results are important for several reasons.

  • They reinforce the fact that endocrine disruption is not just about estrogens and estrogenicity.
  • They demonstrate that systematic search though compounds in current use not yet identified as endocrine disruptors yields positive results... this search is just beginning, and the number revealed here suggests there will be many more.
  • They show that the same compound can have multiple impacts on multiple components of the reproductive tract.

Among the results:

  One of the endpoints Grey et al. measured was the percentage of male pups born with hypospadias (right). Males in the control group never had hypospadias.

Diethylhexyl phthalate (DEHP) proved to be highly toxic to the reproductive system of male offspring in transgenerational studies (in which the pregnant female was exposed and effects measured in her offspring). "DEHP induced high levels of testicular and epididymal abnormalities, including atrophy and agenesis. A striking effect of DEHP was noted in 8-day old pups. Several males from different litters displayed hemorrhagic testes that were visible by gross examination of the inguinal region. Obviously, the testis is a direct target of DEHP during perinatal life."

Treatment by procymidone demasculinized and feminized (two separate effects) the male rat offsprings in a manner nearly identical to that seen with vinclozolin. The effects included permanent nipples and hypospadias. Procymidone was more potent than p,p'-DDE, the parent compound of which (DDT) has been banned since 1976.

The collection of effects seen in offspring treated by PCB 169 is similar but more pronounced than exposures caused by TCDD (dioxin). Several aspects of this work indicate that PCB 169 is not functioning as an antiandrogen but instead is working through interaction with the Ah receptor, as does TCDD.

Gray et al. also determined the percentage of male pups born with areolas (left). Males in the control group never had areolas.  






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