Acceptable Levels for Ingestion of Dimethylsilanediol in Water on the International Space Station
ABSTRACT Water is recovered aboard the International Space Station (ISS) from humidity condensate and treated urine. The product water is monitored for total organic carbon (TOC). In 2010 the TOC readings indicated that a new contaminant had entered the potable water and was steadily increasing toward the TOC screening limit of 3 mg x L(-1). In a ground-based laboratory, chemists discovered that dimethylsilanediol (DMSD) was the principal new contaminant. As no standard existed for safe levels of DMSD in water, the Toxicology Office at Johnson Space Center was asked to set such a standard.
The Toxicology Office used methods developed over the past decade, in collaboration with the National Research Council Committee on Toxicology, for setting Spacecraft Water Exposure Guidelines (SWEGs). These methods require a thorough literature search and development of an acceptable concentration (AC) for each potential toxic effect, keeping in mind that the adverse effects that accompany spaceflight could increase toxicity for certain end points. Benchmark dose modeling was encouraged if sufficient data were available. The most sensitive AC becomes the driver for the SWEG.
Hematotoxicity, hepatotoxicity, and possibly neurotoxicity were the most sensitive toxicological endpoints for DMSD.
The SWEG for DMSD for 100 d of ingestion was set at 35 mg x L(-1), which is equivalent to 9 mg x L(-1) as TOC. This is well above the TOC SWEG of 3 mg x L(-1) and the peak DMSD level of processed water observed on orbit, which was 2.2 mg x L(-1) asTOC (8.5 mg x L(-10 of DMSD).
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ABSTRACT: Due to their insolubility in water and high adsorption coefficient, liquid polydimethylsiloxanes (PDMS) discharged as effluent will adsorb to particulate matter and, therefore, will become a component of sewage sludge during waste water treatment. The subsequent environmental fate of PDMS will depend on the fate of the sludge. Due to increasing practices of soil amendment with sewage sludge the principal environmental compartment receiving PDMS fluids is the soil. Degradation of PDMS is a common process taking place in many different types of soils. It occurs through a unique combination of environmental degradation processes. Initial hydrolysis of PDMS is catalysed by clay minerals, the principal component of soil. The primary hydrolysis product, dimethylsilanediol (DMSD), is then either biodegraded, or evaporated into the atmosphere, where it is subsequently oxidised in the presence of sunlight. The end products in both cases are expected to be CO2, SiO2 and H2O.Chemosphere 04/1999; 38(6):1461-8. DOI:10.1016/S0045-6535(98)00548-7 · 3.50 Impact Factor
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ABSTRACT: There are two basic mechanisms whereby chemicals produce thyroid gland neoplasia in rodents. The first involves chemicals that exert a direct carcinogenic effect in the thyroid gland and the other involves chemicals which, through a variety of mechanisms, disrupt thyroid function and produce thyroid gland neoplasia secondary to hormone imbalance. These secondary mechanisms predominantly involve effects on thyroid hormone synthesis or peripheral hormone disposition. There are important species differences in thyroid gland physiology between rodents and humans that may account for a marked species difference in the inherent susceptibility for neoplasia to hormone imbalance. Thyroid gland neoplasia, secondary to chemically induced hormone imbalance, is mediated by thyroid-stimulating hormone (TSH) in response to altered thyroid gland function. The effect of TSH on cell proliferation and other aspects of thyroid gland function is a receptor mediated process and the plasma membrane surface of the follicular cell has receptors for TSH and other growth factors. Small organic molecules are not known to be direct TSH receptor agonists or antagonists; however, various antibodies found in autoimmune disease such as Graves' disease can directly stimulate or inhibit the TSH receptor. Certain chemicals can modulate the TSH response for autoregulation of follicular cell function and thereby increase or decrease the response of the follicular cell to TSH. It is thus important to consider mechanisms for the evaluation of potential cancer risks. There would be little if any risk for non-genotoxic chemicals that act secondary to hormone imbalance at exposure levels that do not disrupt thyroid function. Furthermore, the degree of thyroid dysfunction produced by a chemical would present a significant toxicological problem before such exposure would increase the risk for neoplasia in humans.Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 01/1996; 333(1-2):131-42. DOI:10.1016/0027-5107(95)00139-5 · 4.44 Impact Factor