VOC sampling locations table for Ground Zero area, Jan 2002

NYC 9/11 Public Portal Document

environmentally relevant PM samples in rodents. Rats to WTC PMjj. It is known that some asthmatic were intratracheally instilled with 2.5 mg (~8.3 mg/kg) of individuals are hyperresponsive to nonspecific irritants various emission source and urban ambient air PM such as cold dry air (Anderson and Daviskas, 2000) or samples (Costa and Dreher, 1997), a dose about twice as cigarette smoke (Bonham et al., 2001). This high, based on body weight, as the 100 pg WTC PM2.5 subpopulation is likely to be at high risk for development dose in mice (~4 mg/kg). Oil fly ashes and urban ambient of dust-induced airways obstruction (Donaldson et al., air PM samples (including a ROFA similar to the one used 2000; Peden, 2001; Nel et al., 2001). Very few studies in the present study and NIST 1649a) induced strong have been published regarding the effects of alkaline neutrophilic responses 24 hr after exposure, while aerosols on pulmonary function in asthma. One study biochemical markers of lung injury were lower in the reported that inhalation of high concentrations of an urban air PM samples compared with the oil fly ash alkaline aerosol (pH 9.8 to 10.3) had no significant effect samples. ROFA at this dose induced airway on irritant symptoms or specific airways resistance in mild hyperresponsiveness in rats which persisted at least 4 days, asthmatic patients (Eschenbacher, 1991). However, this and was greater than that observed in an urban ambient air aerosol was composed of a simple mixture of sodium PM sample (Pritchard et al., 1996). The fact that WTC carbonate, sodium bicarbonate, and sodium hydroxide. PM2.5 induced a significantly greater degree of airway The chemical composition of the alkaline (pH 8.88 to hyperresponsiveness in mice than ROFA, which is used as 10.00) WTC PMj j is much more complex and interactions a toxic positive control particle in many studies, suggests of numerous chemical species may be associated with a very significant respiratory effect of a relatively high development of airway hyperresponsiveness to dose exposure to WTC PM2 5. methacholine or other bronchoconstrictors. Some people were exposed acutely to high How does the dose of 100 jJ-g WTC PMj s, which concentrations of dust in the WTC disaster, and caused bronchiolar inflammation and airway subsequently developed wheezing or symptoms ofsensory hyperresponsiveness in mice, relate to exposure of people irritation, such as cough and irritation of the nose and at the WTC site? Because inflammation was observed throat. These effects resemble, in some respects, the mainly in the airways, and airway hyperresponsiveness is reactive airways dysfunction syndrome (RADS). RADS mainly due to dysfunction of airway smooth muscle can occur after single or multiple high-level occupational (Fredberg, 2000), the dose metric which is probably most exposures to an irritating vapor, fume, or smoke (Gautrin relevant is dose per surface area of the tracheobronchial et al., 1999). Effects can occur within minutes or hours (TB) region of the respiratoiy tract. The TB region is after exposure, and include cough, dyspnea, and wheezing. defined as the airways (excluding the nasal (head) region) Clinical tests can show airways obstruction, persistent from the trachea down to the terminal bronchioles airway hyperresponsiveness, and inflammation. The (Overton et al., 2001). Therefore, to assess the risks of recovery process appears to be dependent on the initial exposure in people, the concentrations of WTC PM2 5 in degree of injury. The effects of a high dose exposure to air which could produce doses per TB surface area in WTC PM2.5 in mice (100 pg) appear to mimic at least humans equivalent to that in mice should be calculated. some ofthese responses, especially the significant increase These WTC PM2 5 concentrations may be estimated (Table in airway hyperresponsiveness to Meh. It is important to 22) using the following assumptions: 1) The mouse note that WTC PM2 5-induced pulmonary inflammation, alveolar pulmonary surface area can be estimated from an although significantly greater than in control mice, was not allometric equation based on body weight (Jones and as robust as one might expect in a realistic animal model Longworth, 1992), and the TB surface area is very small of RADS. However, the degree to which inflammation in comparison to the alveolar surface area (Overton et al., and airway hyperresponsiveness are associated in RADS 2001); 2) Oropharyngeal aspiration bypasses the mouse is not clear (Gautrin et al., 1999). Examination of other nose and spreads the dose of WTC PM2 5 evenly over the time points would be necessary to determine the TB and pulmonary alveolar surface areas of the mouse persistence of WTC PM-induced airway lung; 3) The human TB dose per surface area, selected to hyperresponsiveness in mice and its similarity to RADS. match the mouse dose per surface area, does not clear from Close examination of the data suggested that the lung in the time frame of exposure to WTC PM2 5 (an individual mice within the outbred CD-I strain vary in 8-hour work shift was selected); and 4) The model of the sensitivity to the effects of WTC PM25. Certain fraction of inhaled PM2.5 (model particles with MMAD = individuals within the human population may also have 1, CTg = 2.5, and density = 1 g/cc) deposited in the TB particular susceptibility to the hazards posed by exposure region (Freijer et al., 1999) assumes a reference 30 year-

45

NYC-WTC_000149188