Review of the Air Quality Criteria Document for Particulate Matter

Mortality6-6 Line 25-26. “Statistically independent” is unclear here. Like for effects due to infectiousillnesses, respiratory and cardiovascular causes can be difficult to entangle, and can becaused by the same insult.6-9 Line 26. It would seem that harvesting could be more readily addressed in the context of“identifiable PM episodes” than the typical time-series studies in which only day-to-dayvariability in concentration is studied. Is it being suggested that low level exposure mayhave a different lag profile?6-40 Line 14. Should be “88" cities.6-42 Line 5-6. On p.6-7, the reported reasonable range of effects from the 1996 CD isestimated to be 2.5-5.0% increase per 50 mcg/m 3 . The 2.3% increase estimated inNMMAPS II is outside this range and therefore, strictly, not consistent. As noted, therewere studies by 1996 showing statistically significant effects that were smaller than 2.5%(e.g., 1.8%), but that is not relevant. See also p.6-49 (line 19) and p.6-76 (line 3).6-43 Line 6-7. We do not know from NMMAPS II whether a different tack to trying toaccount for gaseous pollutant effects (see above) on the PM estimates would havereached different conclusions.6-44 Line 20-26. In the 10-Cities studies, the attempt to control for gaseous pollutant effectsis severely hampered by lack of power (see point 3 above).6-59 Line 26. This should be Table 6-3 rather than 6-1.6-61 Table 6.3. The “single pollutant models” heading is confusing, since this includes 2-pollutant model findings.6-62 Line 6. This should be Table 6-4 rather than 6-3.6-78 The threshold discussion here is premature, since no studies presenting data on thresholdshave been presented up to this point.6-92 Why is a 20 mcg/m 3 increment used for both PM 2.5 and PM 15 ?6-101 It is not clear why these studies of mortality in children and on development (IUGR)(6.2.3.4) are included in a section on purported long-term effects on mortality, nor why atime-series study (Loomis p.6-104) is included. I would argue with the descriptor“likely” (p.6-103, line 5).Morbidity6-125 Line 14. This is not strictly a subset of the 88 cities, I believe (e.g., Boulder?).6-139 The Seaton study (line 26) also found a reduction in hemoglobin concentration inassociation with PM.6-141 I would not consider the data on blood viscosity as “highly suggestive” (line ), given thenegative findings of several other studies including the more recent Seaton study (1999).6-141 Line 9. It should be noted that effects at longer lags are often not investigated.4-143 Line 25 to p.6-172. The point that the single “best” lag represents the most valid effectestimate, based on it being biased high but countered by not reflecting the full impact ofmultiple lags, is ingenious but nevertheless nonsense.6-173 Line 8. Power for Edinburgh for hospitalization counts (but not for mortality) should beadequate.6-175. Line 16. Why is the Sheppard study particularly “unique”?6-176. Line 13-17. The effects of acid aerosol and PM should not be compared on a mcg permcg basis.6-176 Line 3. Asthma ER visit studies that complicate the argument about fine PM hereinclude Lipsett 1997 from Coachella Valley on coarse PM and Chapela (year?) fromMexico City in which no PM effects were detected.Interpretation6-216 Line 25. Have some studies really looked at cardiac symptoms?6-226 The argument that SO 2 cannot be a confounder of PM because it is part of the causalpathway is wrong in most settings. If the point that is being made that we have effects ofthe host of pollutants together from similar sources (for example, summer haze), then thisA - 15