Letter re: "Cyclosiloxanes produce fatal liver and lung damage in mice".

indicates that this compound exhibits toxicity comparable to these other agents." Conventional toxicity tables (8,9) comparing LD50 values show that the ip LD for sodium chloride is 4 g/kg. Thus, ordinary table salt is more toxic than either CS-D4 or breast implant distillate! To further put this into perspective relative to silicone breast implants, it would take about two 660-pound breast implants in an average size women to achieve a dose equivalent to the LD50 reported for CS-D4 by Lieberman et al. (1). This is based on the unrealistic assumption that all of the CS-D4 in an implant would be released at one time. The histopathologic findings reported by Lieberman et al. (1) are an enigma. Tables 2 and 3 in their paper show the reported histopathologic changes and average grade of the reported lesions for implant distillate and CS-D4, respectively. The findings reported in these tables are clearly not dose related. For example, in Table 2 (1), the highest incidence (3 of 6 animals) of extensive necrosis was produced by the lowest dose (3.5 g/kg), which had the lowest incidence (1 of 6 animals) of individual cell necrosis. Conversely, a dose of 35 g/kg had a 1-of-6 incidence of extensive necrosis and a 5-of-6 incidence of individual cell necrosis. Further, the increases reported by Lieberman et al. (1) for the three liver enzymes (Figure 3A and B) are minimal, relative to the high doses administered , and do not appear to be dose related. There is no indication in the figures that the observed values are statistically significantly different from control. Statistical significance is difficult to determine from examination of the figures because of the tremendous variability and the fairly consistent or uniform response across all the doses. The observation in this study that death of the animals occurred 5-8 days after the ip injections of either distillate or CS-D4 indicates that death was not due to a direct toxic effect of the test materials. The delayed deaths are consistent with an infectious process probably related to the quality of the test material or to a highly inflammatory process related to the route and volume of test material administered with a resultant peritonitis. It is perplexing that Lieberman et al. (1) apparently did not perform a microbiologic assessment on the test material or the animals at necropsy to rule out an infectious process. Certainly the apparent increase in free …