VOC sampling locations table for Ground Zero area, Jan 2002

NYC 9/11 Public Portal Document

building materials (e.g., calcium, silicon, iron, and sulfate) in PM particles, to PM of either fine or coarse size containing marked elevations of certain metals, or to fine PM containing usual combinations of silicon coagulated with metals or other toxic materials. Lioy et al. directed notable attention to indoor dust loadings of lead as posing potential chronic health risks. The possible contributions of certain other metals (e.g., nickel, chromium) found in settled dusts or airborne PM to irritative symptoms also need further evaluation. The discussions below for lead, nickel, and chromium contain more information on the possible bases for concern with these particular metals. The issue of potentially greater toxicity being associated with unusually increased quantities of very fine or ultrafine particles present in airborne PM also needs to be evaluated further.

Some newly available findings fi-om the laboratory toxicity studies of WTC-derived dusts may offer insights into potential health responses associated with exposures on September 11 to WTC-derived materials in the initial WTC building collapse dust cloud and later exposures to WTC-particles deposited indoors. ORD NHEERL scientists analyzed chemical and toxicological properties of PM2.5 derived from the collapsed WTC buildings (EPA, 2002c; McGee et al., 2002; Gavett et al., 2002). Deposited dust samples were collected from sites within a half-mile of Ground Zero on September 11 and 12 and size-separated to collect the PM2 5 fraction. Gavett et al. (2002) evaluated responses of young adult female mice to bolus doses of WTC-derived PM2 5 dusts administered by intratracheal instillation directly into the lungs and to 5-hour inhalation exposures to WTC PM25. On the basis of the overall pattern of results obtained, Gavett et al. observed both a small degree of pulmonary inflammation in response to WTC dust, which was distinctly less compared with exposure to residual oil fly ash (ROFA), and some notable increases in airway hyperresponsiveness to methacholine, a nonspecific bronchoconstricting agent, greater than that observed in mice exposed to ROFA or other PM samples. These effects may be interpreted as being consistent with reports of airway hyperresponsiveness and irritant responses in people exposed to high concentrations of WTC- derived dusts. Whereas the mild pulmonary inflammation in mice diminished fi-om 1 to 3 days after exposure, the airway hyperresponsiveness appeared to persist longer.

These results suggest possible limited, short-term lung inflammation effects fi-om exposures to high concentrations of WTC dust (as may have occurred mainly on September 11) or possible long-term airway hyperresponsiveness that might portend more prolonged sensitivities and irritative symptoms for persons experiencing extended high-level exposures to WTC-derived dusts indoors. Gavett et al. (2002) estimated the human exposure equivalent of the doses that led to these responses in mice, and calculated an 8-hour exposure at moderate activity level to a concentration of 425 pg/m’ using a multiple-path particle deposition model (Ferijer et al., 1999). Individuals who are especially sensitive to inhalation of dusts, such as asthmatics, might experience these effects at lower concentrations over more prolonged periods of exposure. As mentioned previously, it is likely that persons caught in the initial dust/smoke cloud could have been exposed to PM2 5 concentrations in excess of 1000 pg/m’. However, a dose equivalent to a human exposure of 130 pg/m’ over 8 hours caused no significant effects in the mice, suggesting that most healthy people would not be expected to respond to this moderately high exposure level with any adverse respiratory responses (EPA, 2002c; Gavett et al., 2002).

DRAFT-DO NOT QUOTE OR CITE 41 October 2002

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