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

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----- N \0 00 VI I 0'1 N tJ § I I tJ 0 z 0 -....::l (") tri 0 ::0 0 c::: 0 ....::l t'I1 Table 5-11. Effects of chronic exposures to diesel exhaust on. serum chemistry of laboratory animals Exposure Particles C x T CO N0 2 S0 2 Species/sex period (mg/m 3 ) (mg·h/m 3 ) (ppm) (ppm) (ppm) Effects Study Rat, F344, M,F Hamster,. Syrian, M,F Rat, F344/JcL, M, F Rat, F344; Hamster, Syrian Cat inbred, M 7 h/day 5 days/week 104 weeks 7-8 h/day 5 days/week 75 weeks 16 h/day 6 days/week 130 weeks 16 h/day 5 days/week 104 weeks 8 h/day 7 days/week 124 weeks 'Light-duty engine. bHeavy-duty engine.
1 serum enzymes in the control versus the exposed female rats appear to be a random event among 2 these aged subjects. The incidence of age-related disease, such as mononuclear cell leukemia, 3 can markedly affect such enzyme levels, seriously compromising the usefulness of a comparison 4 to historical controls. The serum sodium values of 144 versus 148 mmol/L in control and 5 exposed rats, respectively, although statistically different, would have no biological import. 6 The increased serum enzyme activities, aJkaline phosphatase, SGOT, SGPT, garnma- 7 glutamyl transpeptidase, and decreased cholinesterase activity suggest an impaired liver; 8 however, such an impairment was not established histopathologically (Heinrich et al., 1982; 9 Research Committee for HERP Studies, 1988; Brightwell et al., 1986). The increased urea 10 nitrogen, electrolyte levels, and gamma globulin concentration and reduction in total blood 11 proteins are indicative of impaired kidney function. Again there was no histopathological con:fir- 12 mation of impaired kidneys in these studies. 13 Clinical chemistry studies suggest impairment of both liver and kidney functions in rats 14 and hamsters chronically exposed to high concentrations of diesel exhaust. The absence of 15 histopathological confirmation, the appearance of such effects near the end of the lifespan of the 16 laboratory animal, and the failure to find such biochemical changes in cats exposed to a higher 17 dose, however, tend to discredit the probability of hepatic and renal hazards to humans exposed 18 at atmospheric levels of diesel exhaust. 19 20 5.1.2.3.9. Effects on microsomal enzymes.· Several studies have examined the effects of diesel 21 exhaust exposure on microsomal enzymes associated with the metabolism and possible 22 activation of xenobiotics, especially polynuclear aromatic hydrocarbons. These studies are 23 summarized in Table 5-12. Lee et al. ( 1980) measured the activities' of aryl hydrocarbon 24 hydroxylase (AHH) and epoxide hydrase (EH) in liver, lung, testis, and prostate gland of adult 25 male rats exposed to 6.32 mg/m 3 DPM 20 h/day for 42 days, Maximal significant AHH activities 26 (pmol/min/mg microsomal protein)occurred at different times during the exposure period, and 27 differences between controls and exposed rats, respectively, were as follows: prostate 28 0.29 versus 1.31, lung 3.67 versus 5.11, and liver 113.9 versus 164.0. There was no difference in 29 AHH activity in the testis between exposed and control rats. Epoxide hydrase activity was not 30 significantly different from control values for any of the organs tested. 31 Pepelko and Peirano (1983) found no statistical differences in liver microsomal 32 cytochrome P448-450 levels and liver microsomal AHH between coritrol and diesel-exposed 33 mice either at 6 and 8 mo of exposure. Small differences were noted in the lung microsomal 34 AHH activities, but these were believed to be artifactual differences, due to increases in 2/1198 5-63 DRAFT --DO NOT CITE OR QUOTE
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DRAFT DO NOT CITE OR QUOTE Health A
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CONTENTS (continued) 2.5.1. Volatil
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CONTENTS (continued) 11.2.1. H.fl.Z
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LIST OF TABLES (continued) 2-14. Me
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PREFACE This draft health assessmen
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AUTHORS, REVIEWERS, AND CONTRIBUTOR
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l. INTRODUCTION 1 Diesel engines ar
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1 achieved by using specific solven
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Nitro-PAH• Table 2-10. Concentrat
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1 pollutants depends on the amount
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1 For the simplest alkoxy radicals,
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1 2 3 4 5 6 7 8 9 10 11 12 13 H ON0
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1 conditions (Pitts et al., 1985c )
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Table 2-14. Mean particle, gas, and
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1 sample collection. There was no b
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1 of downtown Los Angeles (Arey et
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1 exposures. This is a complex ques
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1 Dunstan, TDJ; Mauldin, RF; Jinxia
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1 Lipkea, WH; DeJoode, AD; Christen
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1 Pitts, JN, Jr; Sweetman, JA; Ziel
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1 NOTE TO READERS CHAPTER3 2 Becaus
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1 volume basis (Table 4-1 ). This i
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1 Pritchard (1989), utilizing data
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1 4.3.3.3. Potential Mechanisms for
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1 not accurately reflect the actual
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1 Lee, PS; Chan, TL; Hering, WE. (1
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1 one-half units up to 3, strong (O
Page 148: Study Ulfvarson et a!. (1987) Batti
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Page 163: 1 control]). Heinrich et al. (1986a
Page 174: 1 Heinrich et al. ( 1986a; see also
Page 185: 1 thoracic area at subsequent times
Page 189: 1 with matched controls for the num
Page 201: 1 In related studies, Navarro et al
Page 210: 1 Mauderly et al. (1987b) evaluated
Page 216 and 217: 1 pattern of adverse effects on res
Page 218: 1 DPM concentrations) that resulted
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Page 226 and 227: 1 Klosterkotter, W; Blinemann, G. (
Page 228 and 229: 1 Misiorowski, RL; Strom, KA; Vosta
Page 232: 1 Wright, ES. (1986) Effects of sho
Page 235: 1 Studies showing these effects are
Page 238: 1 exposure level. In the 0.3 5 mg/m
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1 to derive the RfC. The discussion
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1 The BMC values are the lower 95%
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Table 6-5. Results of benchmark con
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1 U.S. Environmental Protection Age
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1 the latter, 16 were classified as
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1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
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1 burdens of the NMRI mice after 12
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1 with four to seven rings), which
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1 five daily doses of2,000 f...lg.
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1 occupations. The observed absence
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1 occupations). Analysis was conduc
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1 the confined space of a truck cab
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1 The corresponding odds ratios for
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1 Approximately 20,000 miners are e
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1 bladder cancer was found in Canad
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1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
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1 Kaplan, I. (1959) Relationship of
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9. MUTAGENICITY 1 Since 1978, more
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1 the presence of heritable translo
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1 9.5. REFERENCES 2 3 "Barfknecht,
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1 U.S. Environmental Protection Age
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1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
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1 inconsequential in rats relative
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1 response. cell injury, or cell pr
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1 Caution must be exercised in extr
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1 Rister, M: Baehner, RL. ( 1977) E
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1 The potency of the other diesel e
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Table 11-2. Incidence of lung tumor
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Table 11-5. Unit risk estimates per
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1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
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1 to reflect the potency of several
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1 Huisingh. J; Bradow, R; Jungers,
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1 particles are fine and ultrafine
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1 are available. Exposure is most o
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1 · some of which can be informed
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1 For example, in a recent meta-ana
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1 nonthreshold-mutagen driven MOA.
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1 that their developing pulmonary a
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1 impacts. Use of these measures re
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2/1198 Appendix A Experimental Prot
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APPENDIX A. EXPERIMENTAL PROTOCOL A
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2/1198 Appendix B Alternative Model
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1 d: Dose of organics, mg/cm 2 of l
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Table B-4. Comparison of observed t
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1 uncertainties below). Based on th
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1 B.lO. RFERENCES 2 3 Bohning D., A
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1 and 2 m.(t) = (y2i - YI/exp[Ap)a/
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1 C.l. INTRODUCTION 2 As discussed
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1 For mouth breathing: 2 (DF)H . =
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TABLE C-1. LUNG MODEL FOR RATS AT T
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TABLE C-3. RATIO OF PULMONARY SURFA
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