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TENTH INTERIM REPORT OF THE SUBCOMMITTEE ON ACUTE EXPOSURE GUIDELINE LEVELS 5 Major Issues In general, the document should have a discussion of the analytical procedures, sterilizer type, and sterilant used. Historically, ethylene oxide was mixed with halons when it was used in hospital sterilizers. Some of the sterilizers also used steam to supplement the process. Another issue is the use of water aspiration to draw a vacuum. These factors are important because a common method of monitoring EtO in workplace air is infrared absorption. If halon was also used, the best wavelength for analysis of EtO is also the region for IR absorption of halon. The common solution is to move to an analytical wavelength where water is an interferent; this then becomes an analytical problem with water aspiration, steam, and any other source of water, but this is generally not a problem in dental laboratories where pure EtO (no halon) is dispensed from a disposable cartridge. A portable GC or FTIR eliminates these analytical problems. The subcommittee questions the statement that reported EtO concentrations measured at the floor were significantly higher than those measured closer to the source. While pure EtO is more dense than air, at concentrations that are in the range of parts per million, there is very little difference in density, and normal room air eddy currents mix the EtO; that mixing precludes any concentration gradients. Summary, 6th paragraph. The subcommittee understands the discussion that the mechanism of action is the same; however, wide range exists in lethal concentration of 660 ppm for death in female mice to 13,349 in rabbits with no effect. These observations seem to argue for a greater interspecies uncertainty factor or a more comprehensive discussion of the factors which explain these marked differences. Section 4.1. Expand the PBPK discussion. The subcommittee believes that the NAC used those data as rationale for stating later that humans are less susceptible to the adverse health consequences of inhaled EtO, as compared with laboratory rodents. Section 6.3, 2nd paragraph. Is a disturbance in gluthione-S-transferase activity associated with EtO developmental toxicity? If not, the justification for the intraspecies UF of 3 does not hold if the AEGL-2 is based upon the developmental toxicity study of Snellings. The subcommittee understands that the NAC followed the SOP manual for assigning the 10-min AEGL-2 the same value as the 30-min AEGL-2. However, the text is not clear in that it is acceptable to go to a 30-min or 1-hr AEGL from a 10-min exposure and from 8-hr to 30-min but not from 4-hr to 30-min? At what point in the SOP manual is this practice addressed? Section 7.3. Why was the Jacobson study used here and not the Nachreiner study? Section 7.2 points out the latter is a good study and that Jacobson used an unspecified rat strain. Section 7.3, 2nd paragraph. Use the PBPK discussion to support and explain the interspecies uncertainty factor. Section 8.2. The discussion of ERPG-3 requires refinement, as these are AEGL-2 effects. What study did the ERPG Committee use that the NAC did not or discounted? Figure 1. This is not a convincing figure, as it is essentially a straight line through two points.
