Review of the Air Quality Criteria Document for Particulate Matter

studies, and is presented as observation time after instillation. Seventh, no PM size is listed forthe Hamada study. Eighth, what word is “alveotis” supposed to be in the description of theKodavanti et al. 2000b study? Finally, were the deposited doses the same for instillation andinhalation in the Watkinson et al. study?P 8-18, Table 8-5: First, give age and gender of subjects for each study. Second, in theCreutzenberg et al. study, does “retention increased” mean that clearance slowed, or simply thatthe lung burden increased? If that is the only reported effect, why bother to list the study?P 8-19, L 1010: What were the lengths of the exposures cited in the paragraph. As a generalprincipal, exposures need to be described by concentration, pattern, and length in order to beplaced in context by the reader. Concentration alone isn’t an adequate description of anexposure.P 8-23, L 7: If by “injected” you mean instilled, then use “instilled” as is done elsewhere.P 8-23, L 19: The important issue is not whether biologicals can “account” for the PM effects,the important issue is whether they might contribute to the effects. It’s not a credible propositionthat any single PM feature or type can “account” for the effects.P 8-24, Table 8-6: First, if the PM concentration and size aren’t known in the Cormier et al.study, and the only particle description is “swine building”, what is the study doing in the table?We apparently have no idea what the exposure was or what part particles might have played inthe effects. Second, in the Elder et al. study, does the 100 :g/m 3 refer to the carbon, theendotoxin, or both? Third, was there no estimate of PM concentration in the Rose et al. study?Overall, the poor characterization of exposures in the studies in this table renders most of thempretty useless for understanding the respiratory effects of bioaerosols. Aren’t there any reportsof effects of airborne pollen? Those are also bioaerosols.P 8-26, Table 8-7: First, are “OTT” “MSH” defined somewhere? Second, why give themonocrotaline dose in the Costa & Dreher study – that isn’t given for other monocrotalinereferences. Third, the location & time of collection of the CAPs should be given. Fourth, is“FOFA” something different than “ROFA”? Fourth, the gender & age of subjects should begiven. Finally, the Minami et al. paper is a ridiculous citation. Both the experimental design andthe interpretation are absurd. They injected undefined material into the jugular vein until theanimals died, and noted that the heart acted up before death. You could do the same with tapwater! This is an excellent example of the fact that not all published papers are worth includingin this document. You can publish almost anything, but that doesn’t mean that all publicationscontain meaningful information.P 8-29, L 6: Here and elsewhere, the author’s name is “Muggenburg”, not “Muggenberg”.P 8-31, L 15-19: It is noted that there was little pulmonary effect in the dogs, but also thatlavage neutrophils were doubled. That apparent conflict needs more explanation.P 31, L 21: “Indice” should be “index”.P 8-31, L 26: “Suggests” should be “suggested”.P 8-31, L 26-28: This sentence doesn’t make sense. Why do you call an increase in T-wavealternans an “anti-arrhythmic” effect?P 8-32, L 6-19: This paragraph is confusing, and suggests that the author must be confusedabout these dog studies. It notes that Muggenberg (sic) found results in dogs exposed to ROFAthat contrast with Godleski’s results in dogs exposed to CAPs. That’s an “apples and oranges”A - 26