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The Problem With D4

Editor’s note: The Department of Ecology is updating a landmark Washington state program that requires makers of kids’ products to report the use of certain chemicals in clothes, toys, other things kids use.

Most of the program changes Ecology is considering would add chemicals to the reporting requirement, giving consumers and policymakers much needed information on chemicals in kids’ products. However the agency is also considering removing the chemical D4 (octamethylcyclotetrasiloxane) from the reporting requirement despite strong evidence this chemical disrupts the endocrine system and has been reported over 2000 times in kids’ products, like footwear, bibs, baby changing mats, teethers, and pacifiers.

We asked Katie Pelch, Senior Scientist at The Endocrine Disruption Exchange (TEDX), to explain why TEDX supports continued reporting of the endocrine-disrupting chemical.

What is the evidence of D4 causing endocrine disruption?

D4 is used as an intermediate chemical in the production of silicone polymers. Under the current rules, manufacturers have filed over 2,300 reports of D4 in children’s products since 2008. D4 has been shown to behave like an estrogen in rats and mice using the uterotrophic assay, a common toxicological test that measures a chemical’s estrogenicity based on its ability to increase the weight of a rodent’s uterus. Three studies examined D4 across different species (rats and mice), strains (F-344 and Sprague Dawley rats), and exposure paradigms (oral and inhalation routes; juvenile or ovariectomized adults) and all reported that D4 increased the uterine weight in exposed animals. They also showed that D4 increased epithelial cell height, another estrogen-like response that contributes to the increased uterine weight following exposure. These results were blocked by the potent anti-estrogen ICI.

Recently, one study reported that D4 did not increase uterine weight in the uterotrophic assay, possibly due to the fact that D4 was injected subcutaneously. Chemicals are often metabolized differently based on how they enter the body, whether through the food, through inhalation, or via an injection. D4 is known to have route-specific differences in pharmacokinetics, thus this is a possible explanation for the different findings. Importantly, though, the authors of this study concluded that D4 was estrogenic because it induced the expression of estrogen-responsive genes in vivo and in vitro.

More importantly, D4 consistently causes fetal loss in rats, reducing the number of live pups born. While the mechanisms responsible for fetal loss have not been completely worked out, there is some evidence that it is due to disrupted luteinizing hormone signaling rather than the estrogenicity of the chemical. While mechanisms for complex biological processes like maintenance of pregnancy are difficult to discern, the lack of a clear mechanism does not deter from the fact that an adverse outcome has occurred.

How can people concerned about harmful chemicals in kids’ products help?

D4 clearly has the potential to act as an endocrine disruptor and a reproductive toxicant, as demonstrated by independent academic, government, and industry scientists. The single negative uterotrophic assay should not carry more weight than previous positive findings from other scientists and the consistent reporting of fetal loss should not be ignored. Click here to tell Ecology to keep D4 on the list.