Health Assessment Document for Diesel Emissions - NSCEP | US ...

1 S. typhimurium were inconclusive because of the high mortality rates in the controls. The mice
2 exposed to diesel exhaust did not exhibit an enhanced mortality when challenged with the
3 influenza virus. Hatch et al. ( 1985) found no changes in the susceptibility of mice to Group C
4 Streptococcus sp. infection following intratracheal injection of 100 !J.g ofDPM suspended in
· 5 unbuffered saline.
6 Hahon et al. (1985) assessed virus-induced mortality, virus multiplication with
7 concomitant interferon (IFN) levels (lungs and sera), antibody response, and lung histopathology
8 in mice exposed to diesel exhaust prior to infectious challenge with Aa/PR/8/34 influenza virus.
9 Weanling mice were exposed to the diesel exhaust containing 2 mg/m 3 DPM for 7 h/day, 5
10 days/week. In mice exposed for 1, 3, and 6 mo, mortality was similar between the exposed and
11 control mice. In mice exposed for 3 and 6 mo, however, there were significant increases in the
12 percentage of mice having lung consolidation, higher virus growth, depressed interferon levels,
13 and a fourfold reduction in hemagglutinin antibody levels; these effects were not seen after the
14 1-mo exposure.
15 The effects of diesel exhaust on the pulmonary defense mechanisms are determined by
16 three critical factors related to exposure: the concentrations of the pollutants, the exposure
17 duration, and the exposure pattern. Higher doses of diesel exhaust as determined by an increase
18 in one or more of these three variables have been reported to increase the numbers of AMs,
. .
19 PMNs, and Type II cells in the lung, whereas lower doses fail to produce such changes. The
20 single most significant contributor to the impairment of the pulmonary defense mechanisms
21 appears to be an excessive accumulation ofDPM, particularly as particle-laden aggregates of
22 AMs. Such an accumulation would result from an increase in deposition and/or a reduction in
23 clearance. The deposition of particles does not appear to change significantly following
24 exposure to equivalent diesel exhaust doses over time. Because of the significant nonlinearity in
25 particle accumulation between low and high doses of diesel exhaust exposure, coupled with no
. -
26 evidence of increased particle deposition, an impairment in one or more of the mechanisms of
27 pulmonary defense appears to be responsible for the DPM accumulation and subsequent
28 pathological sequelae. The time of onset of pulmonary clearance impairment was dependent
29 both on the magnitude and on the duration of exposures. For example, for rats exposed for
30 . 7 h/day, 5 days/week for 104 weeks, the concentration needed to induce pulmonary clearance
31 impairment appears to lie between 0.35 and 2.0 mg/m 3 D:PM.
32
33 5.1.2.3.5. Effects on the immune system. The effects of diesel exhaust on the immune system
· 34 of guinea pigs were investigated by Dziedzic {1981 ). Exposures were to 1.5 mg/m 3 DPM for 20
35 hlday, 5.5 days/week for up to 8 weeks. There was no effect of diesel exposure when compared
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