Annex C. 

Controlled Human Exposure Studies 

Table C-1. Cardiovascular effects. 

Study Pollutant Exposure Findings 

Reference: Barregard et al. 

(2006, 091381) 

Subjects: 13 healthy adults 

Gender: 6 M/7 F 

Age: 20-56 yr 

Wood smoke 

Particle Size: 

Session 1: GMD 42 nm; 

Session 2: GMD 112 nm 

Particle Number/Count: 

Session 1: 180,000/cm3; 

Session 2: 95,000/cm3

Concentration: 

Session 1: median: 

279 μg/m3

; 

Session 2: median 

243 μg/m3

 

Subjects exposed in two groups for 4 h to 

filtered air, followed a wk later by a 4-h 

exposure to wood smoke. Exposures 

conducted with two 25-min periods of light 

exercise. Other measured combustion 

products: 

Session 1: NO2 (0.08 ppm), CO (13 ppm), 

formaldehyde (114 μg/m3

), acetaldehyde 

(75 μg/m3), benzene (30 μg/m3), 

1,3-butadiene (6.3 μg/m3

); 

Session 2: NO2 (0.09 ppm), CO (9.1 ppm), 

formaldehyde (64 μg/m3), acetaldehyde 

(40 μg/m3

), benzene (20 μg/m3), 

1,3-butadiene (3.9 μg/m3

). 

Time to analysis: Immediately following 

exposure as well as 3 and 20 h postexposure. 

Statistically significant increase in plasma 

factor VIII 20 h post wood smoke exposure 

relative to filtered air. The factor VIII/von 

Willebrand ratio in plasma was increased with 

wood smoke relative to filtered air at 0, 3, and 

20 h post-exposure. Wood smoke exposure 

increased the urinary excretion of free 

8-iso-prostaglandin2α relative to clean air 20 h 

post-exposure (n = 9). These findings were 

more pronounced in session 1 than session 2 

(similar mass concentration but higher number 

concentration in Session 1). 

Reference: Beckett et al. 

(2005, 156261) 

Subjects: 12 healthy adults 

Gender: 6 M/6 F 

Age: 23-52 yr 

Ultrafine and fine zinc oxide 

Particle Size: UF: 

<0.1 μm; Fine: 0.1-1.0 μm 

Particle Number/Count: 

UF: 4.6 × 107/cm3; Fine: 1.9 

× 105

/cm3

Concentration: 500 μg/m3 

Subjects exposed via mouthpiece for 2 h 

during rest to filtered air, ultrafine, and fine 

zinc oxide in a randomized crossover study 

design. Exposures were separated by at least 

3 wk. 

Time to analysis: Immediately following 

exposure and 3, 6, 11, 23, and 24 h after 

exposure. 

Exposure to ultrafine and fine zinc oxide did 

not affect HRV (time and frequency domain 

parameters) relative to clean air immediately 

following exposure, or at 3, 6, 11, and 23 h 

post-exposure. Exposure did not affect blood 

pressure through 24 h post-exposure. No 

effects of exposure to either fine or ultrafine 

zinc oxide observed on factor VII, von 

Willebrand factor (vWf), tissue plasminogen 

activator (t-PA), or fibrinogen. No effect of 

exposure observed on peripheral blood cell 

counts or levels of pro-inflammatory cytokines. 

Reference: Blomberg et al. 

(2005, 191991) 

Subjects: 15 older adults 

(former smokers) with COPD 

Age: 56-72 yr 

DE 

Concentration: 300 μg/m3 

Subjects exposed for 1 h with intermittent 

exercise to DE and filtered air in a randomized 

crossover study design. 

Time to analysis: 6 and 24 h post-exposure. 

DE was not observed to affect blood levels of 

C-reactive protein, fibrinogen, D-Dimer, 

prothrombin factor 1-2, or von Willebrand 

factor activity at 6 and 24 h post-exposure. 

Reference: Brauner et al. 

(2007, 091152) 

Subjects: 29 healthy adults 

Gender: 20 M/9 F 

Age: 20-40 yr 

Urban traffic particles 

 

Particle Number/Count: 

6-700nm: 10,067/cm3

Concentration: PM2.5: 

9.7 μg/m3

; PM10-2.5: 12.6 μg/m3

Subjects exposed to urban traffic particles and 

filtered air for 24 h with and without two 

90-min periods of light exercise in a 

randomized crossover study design. 

Concentrations of NOX and NO were low and 

did not differ between filtered and unfiltered 

exposures. CO concentrations were higher 

with filtered air (0.35 and 0.41 ppm), while O3

concentrations were lower with filtered air 

(12.08 and 4.29 ppb). 

Time to analysis: 6 and 24 h after the start of 

exposure. 

An increase in DNA strand breaks and 

formamidopyrimidine-DNA glycosylase sites in 

peripheral blood mononuclear cells were 

observed after 6 and 24 h of exposure to urban 

particulates. The particle concentration at the 

57nm mode was shown to be the major 

contributor to these effects. 

 

Note: Hyperlinks to the reference citations throughout this document will take you to the NCEA HERO database (Health and 

Environmental Research Online) at http://epa.gov/hero. HERO is a database of scientific literature used by U.S. EPA in the process of 

developing science assessments such as the Integrated Science Assessments (ISA) and the Integrated Risk Information System (IRIS). 

December 2009 C-1 
Study Pollutant Exposure Findings 

Reference: Brauner et al. 

(2008, 156293) 

Subjects: 42 healthy older 

adults (21 couples) 

Age: 60-75 yr 

Indoor air particles 

Particle Number/Count: 

10-700 nm: 10,016/cm3

Concentration: Coarse: 

9.4 μg/m3

; Fine: 12.6 μg/m3

Exposures consisted of two 48 h periods in 

the home of each subject with or without the 

use of a HEPA filter (randomized crossover 

design). HEPA filters reduced coarse 

concentration from 9.4 to 4.6 μg/m3

, and fine 

concentration from 12.6 to 4.7 μg/m3. 

Concentrations of NO2 did not differ between 

the 2 sessions (20 ppb). 

Time to analysis: After the completion of 

each 48 h session. 

The use of HEPA filters significantly improved 

microvascular function (p = 0.04) after 48 h 

(reactive hyperemia-peripheral arterial 

tonometry). Microvascular function was 

assessed using a scoring system representing 

the extent of reactive hyperemia. The 

reduction in PM concentration through the use 

of HEPA filters did not significantly affect blood 

pressure following the 48-h exposures. 

Lowering PM concentration did not significantly 

affect inflammatory response markers in 

peripheral venous blood (IL-6, TNF-α, 

C-reactive protein, plasma amyloid A). 

Reference: Brauner et al. 

(2008, 191966) 

Subjects: 29 healthy adults 

Gender: 20 M, 9 F 

Age: M avg 27 yr, F avg 

26 yr 

Urban traffic particles 

Particle Number/Count:

11,600/cm3

Concentration: PM2.5: 

10.5 μg/m3

; PM10-2.5: 

13.8 μg/m3

 

Subjects exposed to urban traffic particles and 

filtered air for 24 h with and without two 

90-min periods of light exercise in a 

randomized crossover study design. 

Concentrations of NOX and NO were low and 

did not differ between filtered and unfiltered 

exposures. CO concentrations were higher 

with filtered air, while O3 concentrations were 

lower with filtered air. 

Time to analysis: 6 and 24 h after the start of 

exposure. 

Exposure to urban traffic particles was not 

observed to affect microvascular function 

(digital peripheral artery tone) at 6 or 24 h after 

the start of exposure. No difference in various 

blood markers of coagulation, inflammation, or 

protein oxidation (e.g., fibrinogen, platelet 

count, CRP, IL-6, TNF- α) were demonstrated 

between particle and filtered air exposure. 

Reference: Carlsten et al. 

(2007, 155714) 

Subjects: 13 healthy adults 

Gender: 11 M/2 F 

Age: 20-42 yr 

DE 

2002 Cummins B-series 

diesel engine (6BT5.9G6, 

5.9 L) operating at load 

Concentration: Fine PM: 

100, 200 μg/m3

Subjects exposed for 2 h at rest to filtered air 

and each of the two DEPs concentrations in a 

randomized crossover study design. 

Exposures were separated by at least 2 wk. 

Other diesel emissions measured: NO2 (10-35 

ppb), CO (0.7-1.8 ppm). 

Time to analysis: 3, 6, and 22 h after the 

start of exposure. 

No statistically significant changes in 

plasminogen activator inhibitor-1 (PAI-1), vWf, 

D-dimer, or platelet count observed 3, 6, or 

22 h following exposure to DE relative to 

filtered air. Non-statistically significant 

increases in D-dimer, vWf, and platelet count 

were observed at 6 h following the start of 

exposure (4 h post-exposure). No 

diesel-induced increase in C-reactive protein 

observed relative to filtered air in peripheral 

venous blood at 1 or 20 h post-exposure. 

Reference: Carlsten et al. 

(2008, 156323) 

Subjects: 16 adults with 

metabolic syndrome 

Gender: 10 M/6 F

Age: 25-48 yr 

DE 

2002 Cummins B-series 

diesel engine (6BT5.9G6, 

5.9 L) 

Concentration: Fine PM: 

100, 200 μg/m3

Subjects exposed for 2 h at rest to filtered air 

and each of the two DE particle 

concentrations in a randomized crossover 

study design. Exposures were separated by at 

least 2 wk. Other diesel emissions measured: 

NO2 (30 ppb), NO (1.69 ppm), CO (0.65 ppm).

Time to analysis: 3, 7, and 22 h after the 

start of exposure. 

At 5 h after the end of diesel exposure (fine 

particulate concentration 200 μg/m3

), the 

authors observed a significant decrease in vWf 

in peripheral venous blood. No other changes 

in thrombotic markers (vWf, D-dimer, PAI-1) 

were observed at either concentration between 

1 and 20 h post-exposure. 

Reference: Danielsen et al. 

(2008, 156382) 

Subjects: 13 healthy adults 

Gender: 6 M/7 F 

Age: 20-56 yr 

Wood smoke 

Particle Size: 

Session 1: GMD 42 nm; 

Session 2: GMD 112 nm 

Particle Number/Count: 

Session 1: 180,000/cm3; 

Session 2: 95,000/cm3

Concentration: 

Session 1: median: 

279 μg/m3

; 

Session 2: median 

243 μg/m3

Subjects exposed in two groups for 4 h to 

filtered air, followed a wk later by a 4-h 

exposure to wood smoke. Exposures 

conducted with two 25-min periods of light 

exercise. Other measured combustion 

products: 

Session 1: NO2 (0.08 ppm), CO (13 ppm), 

formaldehyde (114 μg/m3

), acetaldehyde 

(75 μg/m3), benzene (30 μg/m3), 

1,3-butadiene (6.3 μg/m3

); 

Session 2: NO2 (0.09 ppm), CO (9.1 ppm), 

formaldehyde (64 μg/m3), acetaldehyde 

(40 μg/m3

), benzene (20 μg/m3), 

1,3-butadiene (3.9 μg/m3

). 

Time to analysis: 3 and 20 h post-exposure. 

Exposure to wood smoke increased the mRNA 

levels of hOGG1 in PBMCs relative to filtered 

air 20 h after exposure. DNA strand breaks 

were shown to decrease in PBMCs 20 h after 

wood smoke exposure. 

Reference: Devlin et al. 

(2003, 087348) 

Subjects: 10 healthy older 

adults 

Gender: 7 M/3 F 

Age: Avg 66.9 yr 

Fine CAPs (Chapel Hill, NC) 

Concentration: Mean: 

40.5 μg/m3

, Range: 

21.2-80.3 μg/m3

Exposures conducted for 2 h at rest to filtered 

air and CAPs in a randomized crossover 

study design. 

Time to analysis: Immediately following 

exposure and 24 h post-exposure. 

CAPs exposure resulted in statistically 

significant reductions (p <0.05) in time domain 

(PNN50) and frequency domain (HF power) 

parameters relative to clean air immediately 

following exposure. These relative decreases 

were still apparent 24 h after exposure (p 

<0.08). 

December 2009 C-2 
Study Pollutant Exposure Findings 

Reference: Fakhri et al. 

(2009, 191914) 

Subjects: 50 adults (40 

healthy, 10 asthmatic) 

Gender: 24 M/26 F 

Age: 19-48 yr 

Fine CAPs (Toronto) 

Concentration: 127 ± 

62 μg/m3 with and without 

co-exposure to O3 (114 ± 

ppb) 

Exposures conducted through a facemask 

which covered the subject’s nose and mouth. 

Subjects were exposed to CAPs, O3, CAPs + 

O3 and filtered air for 2 h at rest in a 

randomized crossover study design. 

Time to analysis: Every 30 min during 

exposure, with the final measurement made 

immediately prior to the end of the exposure. 

Exposure to CAPs or O3, alone or in 

combination, resulted in no significant changes 

in HRV or blood pressure relative to filtered air. 

However, a negative concentration response 

relationship was reported between CAPs 

concentration with co-exposure to O3 and 

SDNN, rMSSD, HF power and LF power 

(statistically significant for LF power). Diastolic 

blood pressure was observed to increase with 

exposure to CAPs + O3, but not with either 

pollutant alone. There was no difference in 

response between asthmatics and healthy 

subjects. 

Reference: Frampton et al. 

(2006, 088665) 

Subjects: 16 asthmatic 

adults, 40 healthy adults 

Gender: Asthmatics: 

8 M/8 F, Healthy: 20 M/20 F 

Age: 18-40 yr 

Ultrafine EC 

Particle Size: CMD ~25 nm

Particle Number/Count: 

10 μg/m3: ~2.0 × 106/cm3; 

25 μg/m3

: ~7.0 × 106/cm3; 

50 μg/m3

: ~10.8 × 106/cm3

Concentration: 10, 25, and 

50 μg/m3

Study conducted using a randomized 

crossover design with 2-h exposures. 

Asthmatics (n = 16) exposed to filtered air and 

10 μg/m3

. 12 healthy adults exposed to filtered 

air and 10 μg/m3

 at rest; 12 healthy adults 

exposed to filtered air, 10 and 25 μg/m3

 with 

intermittent exercise; 16 healthy adults 

exposed to filtered air and 50 μg/m3

 with 

intermittent exercise. Exposures were 

conducted via mouthpiece. 

Time to analysis: Immediately following 

exposure as well as 3.5, 21, and 45 h postexposure. 

No effect of ultrafine particle exposure on 

leukocyte counts or leukocyte expression of 

adhesion molecules observed in healthy 

subjects exposed at rest to 10 μg/m3

. Among 

healthy adults exposed to ultrafine carbon 

during exercise, monocyte expression of 

adhesion molecules CD54 and CD18 

decreased relative to filtered air immediately 

following exposure. An ultrafine 

particle-induced decrease in PMN expression 

of CD18 was also observed 0-21 h 

post-exposure. Expression of CD11b on 

monocytes and eosinophils was reduced 

following exposure to ultrafine particles in 

exercising asthmatics 0-21 h post-exposure. A 

decrease in total leukocyte count was 

observed following ultrafine particle exposure 

in exercising healthy and asthmatic subjects. 

Reference: Gong et al. 

(2004, 087964) 

Subjects: 13 older adults 

with COPD, 6 healthy older 

adults 

Gender: COPD: 5 M/8 F, 

Healthy: 2 M/4 F 

Age: COPD: avg 68 yr, 

Healthy: avg 73 yr 

Fine CAPs (Los Angeles) 

Particle Size: 85% of mass 

between 0.1 and 2.5 μm 

Concentration: Mean: 

194 μg/m3, Range: 

135-229 μg/m3

Exposures to CAPs and filtered air 

(randomized crossover) for 2 h with 

intermittent light exercise (four 15-min 

periods). Exposures were separated by at 

least 2 wk. 

Time to analysis: Immediately following 

exposure as well as 4 and 22 h postexposure. 

SDNN shown to decrease following CAPs 

exposure relative to filtered air in healthy older 

adults (4-22 h post-exposure). No 

CAPs-induced changes in HRV were observed 

in older adults with COPD. Ectopic heart beats 

were observed to increase slightly with CAPs 

relative to filtered air among healthy subjects, 

but decreased among subjects with COPD. 

Exposure to CAPs did not affect platelet or 

white blood cell count, or levels of fibrinogen, 

vWF, or factor VII. 

Reference: Gong et al. 

(2004, 055628) 

Subjects: 12 adult 

asthmatics, 4 healthy adults 

Gender: Asthmatics: 

4 M/8 F, Healthy: 2 M/2 F 

Age: Asthmatics: avg 38 yr, 

Healthy: avg 32 yr 

Coarse CAPs (Los Angeles) 

Particle Size: 80% of mass 

between 2.5 and 10 μm, 

20% of mass <2.5 μm 

Concentration: Mean: 

157 μg/m3

, Range: 

56-218 μg/m3

Exposures to CAPs and filtered air 

(randomized crossover) for 2 h with 

intermittent light exercise (four 15-min 

periods). Exposures were separated by at 

least 2 wk. 

Time to analysis: Immediately following 

exposure as well as 4 and 22 h postexposure. 

SDNN shown to decrease following CAPs 

exposure relative to filtered air in healthy 

adults (4-22 h post-exposure). Decrease in 

PNN50 also observed in healthy adults at 4 h 

post-exposure. No CAPs-induced decreases in 

HRV demonstrated in asthmatics. 

Reference: Gong et al. 

(2008, 156483) 

Subjects: 14 adult 

asthmatics, 17 healthy adults 

Gender: Asthmatics: 

9 M/5 F, Healthy: 5 M/12 F 

Age: Asthmatics: 34 ± 12 yr, 

Healthy: 24 ± 8 yr 

Ultrafine CAPs (Los 

Angeles) 

Particle Number/Count: 

145,000/cm3, Range 

39,000-312,000/cm3

Concentration: Mean100 μg/m3

, Range13-277 μg/m3

Subjects exposed for 2 h during intermittent 

exercise (15-min periods) to both CAPs and 

filtered air in random order. The first 7 

subjects underwent whole body exposure, 

while the remaining subjects were exposed 

through a facemask. Facemask exposures 

had higher particle counts but lower particle 

mass than whole body exposures. Exposures 

were separated by at least 2 wk. 

Time to analysis: Immediately following 

exposure as well as 4 and 22 h postexposure. 

Relative to filtered air, exposure to ultrafine 

CAPs resulted in a transient decrease in LF 

power 4 h post-exposure. This effect of CAPs 

on HRV was not influenced by health status. 

CAPs exposure was not observed to affect any 

other measures of HRV, blood pressure, or 

blood markers of inflammation or coagulation. 

There were no differences in response 

observed between facemask and whole body 

exposures. 

December 2009 C-3 
Study Pollutant Exposure Findings 

Reference: Graff et al. 

(2009, 191981) 

Subjects: 14 healthy adults 

Gender: 8 M/6 F

Age: 20-34 yr 

Coarse CAPs (Chapel Hill, 

NC) 

Concentration: 89 

± 49.5 μg/m3

 (estimated 

inhaled dose ≈ 67% of 

measured particle mass) 

Subjects exposed for 2 h with intermittent 

exercise (15-min periods) to coarse CAPs and 

filtered air in a randomized crossover design. 

Exposures were separated by at least 2 mos. 

Time to analysis: 0-1 and 20 h postexposure. 

At 20 h post-exposure, tPA was observed to 

decrease by 32.9% from baseline (preexposure) per 10 μg/m3

 increase in CAPs 

concentration (p = 0.01). D-dimer 

concentration decreased 11.3% per 10 μg/m3

, a change of marginal statistical significance (p 

= 0.07). No other coarse CAPs-induced 

changes in blood biomarkers of coagulation 

(e.g., vWF, factor VII, plasminogen, fibrinogen, 

or PAI-1) or inflammation (e.g., CRP) were 

observed. At 20 h post-exposure, overall HRV 

(SDNN) was shown to decrease by 14.4% 

relative to pre-exposure measurements per 

10 μg/m3

 increase in CAPs concentration. No 

other changes in HRV were observed following 

exposure to coarse CAPs. 

Reference: Huang et al. 

(2003, 087377) 

Subjects: 38 healthy adults 

Gender: 36 M/2 F 

Age: Avg 26.2 ± 0.7 yr 

Fine CAPs (Chapel Hill, NC) 

Concentration: 

23.1-311.1 μg/m3

Subjects exposed to CAPs (n = 30) or filtered 

air (n = 8) for 2 h with intermittent exercise 

(subjects did not serve as their own controls). 

Component data of CAPs was available for 37 

of the 38 subjects. 

Time to analysis: 18 h after exposure. 

The increase in blood fibrinogen following 

exposure to fine CAPs reported by Ghio et al. 

(2000, 012140) was shown to be associated 

with copper, zinc, and vanadium content in the 

CAPs. 

Reference: Larsson et al. 

(2007, 091375) 

Subjects: 16 healthy adults 

Gender: 10 M/6 F 

Age: 19-59 yr 

Traffic particles (road 

tunnel) 

 

Particle Size: PM2.5, PM10; 

PM2.5 mass constituted 

~36% of PM10 mass 

Particle Number/Count: 

20-1,000 nm: 1.1 × 105/cm3, 

< 100 nm: 0.85 × 105/cm3 

Concentration: PM2.5- 

46-81 μg/m3

; PM10- 

130-206 μg/m3

Exposures were conducted for 2 h with 

intermittent exercise in a room adjacent to a 

busy road tunnel. Study used a randomized 

crossover design with each subject also 

exposed to normal air (control). Exposures 

were separated by 3-10 wk. No exposures to 

filtered air were conducted. Other traffic 

emissions measured: NO (874 μg/m3

), NO2

(230 μg/m3), CO (5.8 μg/m3 reported, likely 

5.8 mg/m3

). 

Time to analysis: 14 h post-exposure. 

No change in plasma levels of fibrinogen or 

PAI-1 observed 14 h post-exposure. 

Reference: Lucking et al. 

(2008, 191993) 

Subjects: 20 healthy adults 

Gender: M 

Age: 21-44 yr 

DE 

Protocol 1 (n=8): idling 

Deutz diesel engine 

(F3M2011, 2.2 L, 500 rpm) 

using gas oil 

Protocol 2 (n=12): idling 

Volvo diesel engine (TD45, 

4.5 L, 4 cylinders, 680 rpm) 

using Gasoil E10 

Particle Number/Count: 

Protocol 1: 1.2 × 106/cm3; 

Protocol 2: 1.26 × 106

/cm3

Concentration: Protocol 1: 

348 μg/m3, Protocol 2: 

330 μg/m3

 

In both protocols, exposures were conducted 

with intermittent exercise (15-min periods) to 

DE and filtered air in a randomized crossover 

design with exposures separated by at least 

one wk. 

Protocol 1 (n=8): Exposures conducted for 2 

h. Other diesel emissions measured: NOX

(0.58 ppm), NO2 (0.23 ppm), NO (0.36 ppm), 

CO (3.54 ppm), total hydrocarbon (2.8 μg/m3

). 

Time to analysis: 6 h post-exposure. 

Protocol 2 (n=12): Exposures conducted for 

1h. Other diesel emissions measured: NOX

(2.78 ppm), NO2 (0.62 ppm), NO (2.15 ppm), 

CO (3.08 ppm), total hydrocarbon 

(1.58 μg/m3

). 

Time to analysis: 2 and 6 h post-exposure. 

Thrombus formation was observed to increase 

with diesel 2 and 6 h post-exposure using an 

ex vivo perfusion chamber. Both plateletneutrophil and platelet-monocyte aggregates 

increased relative to filtered air 2 h following 

exposure to diesel (only evaluated in Protocol 

2). Plasma concentrations of soluble CD40L 

were also observed to increase with diesel. 

Exposure to diesel was not shown to affect 

total leukocyte, monocyte, or platelet counts. 

Reference: Lund et al. 

(2009, 180257) 

Subjects: 10 healthy adults 

Gender: 4 M/6 F 

Age: 18-40 yr 

DE 

Idling Cummins diesel 

engine (5.9 L) using 

commercial No. 2 fuel 

Particle Size: MMAD 

0.10 μm 

Concentration: 100 μg/m3

Subjects exposed for 2 h with intermittent 

exercise (15-min periods) to DE and filtered 

air in a randomized crossover study design. 

Other diesel emissions measured: NOX (4.7 

ppm), NO2 (0.8 ppm), CO (2.8 ppm), total 

hydrocarbons (2.4 ppm). 

Time to analysis: 30 min and 24 h postexposure. 

Exposure to diesel resulted in an increase 

in MMP-9 plasma concentration and activity as 

well as an increase in endothelin-1 plasma 

concentration at both 30 min and 24 h postexposure. 

December 2009 C-4 
Study Pollutant Exposure Findings 

Reference: Lundback et al. 

(2009, 191967) 

Subjects: 12 healthy adults 

Gender: M 

Age: 21-30 yr 

DE 

Idling Volvo diesel engine 

(TD45, 4.5 L, 4 cylinders, 

680 rpm) using Gasoil E10 

Particle Number/Count: 

1.26 × 106/cm3 

Concentration: 330 μg/m3

Subjects exposed for 1 h with intermittent 

exercise (15-min periods) to DE and filtered 

air in a randomized crossover study design. 

Exposures were separated by at least one wk. 

Other diesel emissions measured: NOX (2.78 

ppm), NO2 (0.62 ppm), NO (2.15 ppm), CO 

(3.08 ppm), total hydrocarbon (1.58 μg/m3

). 

Time to analysis: 10, 20, 30, and 40 min 

post-exposure. 

Diesel-induced increase in arterial stiffness 

(increases in augmentation pressure and 

augmentation index, as well as decrease in 

time to wave reflection) observed at 10 and 20 

min post-exposure using radial artery pulse 

wave analysis. No effect of diesel observed on 

carotid-femoral pulse wave velocity which was 

assessed 40 min post-exposure, but not at 

earlier time points. No effect of diesel observed 

on blood pressure 10-30 min post-exposure. 

Reference: Mills et al. 

(2005, 095757) 

Subjects: 30 healthy adults 

Gender: M 

Age: 20-38 yr 

DE 

Idling 1991 Volvo diesel 

engine (TD45, 4.5 L, 4 

cylinders, 680 rpm) 

Particle Number/Count: 

1.2 × 106/cm3 

Concentration: 300 μg/m3 

Subjects exposed for 1 h with intermittent 

exercise (15-min periods) to DE and filtered 

air in a randomized crossover study design. 

Exposures were separated by two wk. Other 

diesel emissions measured: NO2 (1.6 ppm), 

NO (4.5 ppm), CO (7.5 ppm), total 

hydrocarbon (4.3 ppm), formaldehyde 

(0.26 μg/m3

). 

Time to analysis: 2-4 h post-exposure for 15 

subject; 6-8 h post-exposure for the other 15 

subjects. 

Forearm blood flow increase (induced by 

bradykinin, acetylcholine, and sodium 

nitroprusside) was attenuated by DE 2 and 6 h 

post-exposure. A 6 mmHg increase in diastolic 

blood pressure (p = 0.08) 2 h following 

exposure to DE was observed relative to 

filtered air control. Bradykinin-induced release 

of t-PA was attenuated by diesel exposure 6 h 

post-exposure. DE did not affect the release of 

t-PA 2 h post-exposure. No diesel-induced 

changes in serum IL-6 or TNF-α observed 6 h 

post-exposure. 

Reference: Mills et al. 

(2007, 091206) 

Subjects: 20 older adults 

with prior myocardial 

infarction 

Gender: M 

Age: 60 ± 1 yr 

DE 

Idling 1991 Volvo diesel 

engine (TD45, 4.5 L, 4 

cylinders, 680 rpm) using 

low sulfur gas-oil E10 

Particle Size: Median 

particle diameter 54 nm, 

Range 20-120 nm 

Particle Number/Count: 

1.26 × 106/cm3

Concentration: 300 μg/m3

Subjects exposed for 1 h with intermittent 

exercise (15-min periods) to DE and filtered 

air in a randomized crossover study design. 

Exposures were separated by at least two wk. 

Other diesel emissions measured: NOX (4.45 

ppm), NO2 (1.01 ppm), NO (3.45 ppm), CO 

(2.9 ppm), total hydrocarbon (2.8 ppm). 

Time to analysis: During exposure and 6-8 h 

post-exposure. 

A greater increase in exercise induced 

ST-segment depression and ischemic burden 

was observed during exposure to DE than 

clean air. No diesel-induced effects on 

vasomotor dysfunction observed 6 h 

post-exposure. Bradykinin-induced release of 

t-PA was attenuated by diesel exposure 

relative to filtered air 6 h post-exposure. Effect 

of diesel on t-PA release was not evaluated at 

earlier times post-exposure. No diesel-induced 

changes in blood leukocyte counts or serum 

C-reactive protein 6 h post-exposure. 

Reference: Mills et al. 

(2008, 156766) 

Subjects: 12 adults with 

coronary heart disease, 12 

healthy adults 

Gender: M 

Age: CHD: 59 ± 2 yr, 

Healthy: 54 ± 2 yr 

Fine CAPs (Edinburgh, 

Scotland, UK) 

Particle Size: Mean 

1.23 μm 

Particle Number/Count: 

99,400/cm3 

Concentration: 

190 ± 37 μg/m3

Exposures conducted for 2 h with intermittent 

exercise. Subjects exposed to CAPs and 

filtered air using a randomized crossover 

design with exposures separated by at least 2 

wk. 

Time to analysis: 2, 6-8, and 24 h postexposure. 

CAPs exposure had no significant effect on 

vascular function in healthy adults or adults 

with coronary heart disease 6-8 h 

post-exposure (i.e., no change in forearm 

blood flow as assessed using venous 

occlusion plethysmography). The authors 

attributed this lack of response to a low 

concentration of combustion-derived particles. 

Small increase in blood platelet and monocyte 

concentration observed following CAPs 

exposure. Exposure to CAPs did not affect 

serum CRP concentration or total leukocyte or 

neutrophil count. 

Reference: Peretz et al. 

(2007, 156853) 

Subjects: 5 healthy adults 

Gender: M 

Age: 20-31 yr 

DE 

2002 Cummins B-series 

diesel engine (6BT5.9G6, 

5.9 L); operating at 75% of 

rated capacity 

Concentration: Fine PM 

50, 100, 200 μg/m3

 

Subjects exposed for 2 h at rest to filtered air 

and each of the three DE particle 

concentrations in a randomized crossover 

study design. Exposures were separated by at 

least 2 wk. Other diesel emissions measured, 

200 μg/m3

 exposure: NO2 (23 ppb), NO (1.75 

ppm), CO (1.58 ppm). 

Time to analysis: 6 and 22 h after the start of 

exposure. 

PBMC expression of 10 genes involved in the 

inflammatory response were observed to be 

significantly affected by exposure to DE at the 

highest concentration tested (8 upregulated, 2 

downregulated) 6 h after the start of exposure. 

The expression of 4 genes (1 upregulated, 3 

downregulated) associated with the 

inflammatory response showed significant 

changes 22 h after diesel exposure. PBMC 

expression of 5 genes involved in the oxidative 

stress pathways showed significant changes at 

6 h after the start of diesel exposure at the 

highest concentration tested (4 upregulated, 1 

downregulated). 7 genes involved in the 

oxidative stress pathways showed significant 

changes at 22 h following exposure (4 

upregulated, 3 downregulated). 

December 2009 C-5 
Study Pollutant Exposure Findings 

Reference: Peretz et al. 

(2008, 156854) 

Subjects: 17 adults with 

metabolic syndrome, 10 

healthy adults 

Gender: Metabolic 

syndrome: 11 M/6 F, 

Healthy: 8 M/2 F 

Age: Metabolic syndrome: 

20-48 yr, Healthy: 20-42 yr 

DE 

2002 Cummins B-series 

diesel engine (6BT5.9G6, 

5.9 L) using No. 2 undyed 

on-highway fuel; operating 

at 75% of rated capacity 

Particle Size: Median 

particle diameter 1.04 μm 

Concentration: Fine PM 

100, 200 μg/m3

Subjects exposed for 2 h at rest to both 

concentrations of DE as well as filtered air in a 

randomized crossover design. Exposures 

were separated by at least 2 wk. Other diesel 

emissions measured, 100 μg/m3

 exposure: 

NO2 (16.5 ppb), NO (0.96 ppm), CO (0.51 

ppm); 200 μg/m3

 exposure: NO2 (24.7 ppb), 

NO (1.54 ppm), CO (0.89 ppm). 

Time to analysis: Immediately following 

exposure (within 30 min post-exposure) and 

3 h from the start of exposure. 

Exposure to 200 μg/m3

 elicited a statistically 

significant decrease in brachial artery diameter 

relative to filtered air immediately following 

exposure. A smaller decrease in brachial artery 

diameter was also observed following 

exposure to DE at 100 μg/m3

. Plasma levels of 

endothelin-1 were observed to increase 

following DE exposure (200 μg/m3

). The 

observed effects were more pronounced in 

healthy subjects than in subjects with 

metabolic syndrome. DE did not affect 

endothelium-dependent flow-mediated 

dilatation. No effect of DE on blood pressure 

was demonstrated immediately following 

exposure. 

Reference: Peretz et al. 

(2008, 156855) 

Subjects: 13 adults with 

metabolic syndrome, 3 

healthy adults 

Gender: Metabolic 

syndrome: 8 M/5 F, Healthy: 

3 M/0 F 

Age: Metabolic syndrome: 

31-48 yr, Healthy: 24-39 yr 

DE 

2002 Cummins B-series 

diesel engine (6BT5.9G6, 

5.9 L) using No. 2 undyed 

on-highway fuel; operating 

at 75% of rated capacity 

Concentration: Fine PM 

100, 200 μg/m3

Subjects exposed for 2 h at rest to both 

concentrations of DE as well as filtered air in a 

randomized crossover design. Exposures 

were separated by at least 2 wk. Other diesel 

emissions measured, 100 μg/m3

 exposure: 

NO2 (20.6 ppb), NO (0.95 ppm), CO (0.47 

ppm); 200 μg/m3

 exposure: NO2 (28.3 ppb), 

NO (1.63 ppm), CO (0.74 ppm). 

Time to analysis: 1, 3, 6, and 22 h from the 

start of exposure. 

Exposure to 200 μg/m3

 increased HF power 

and decreased the LF/HF ratio 1h 

post-exposure; however, this effect was not 

consistent across subjects. No effect of DE 

was observed at later time points. Subjects 

with metabolic syndrome did not experience 

greater changes in HRV than healthy subjects. 

Reference: Power et al. 

(2008, 191982) 

Subjects: 5 adults with mildto-moderate allergic asthma 

Gender: 1 M/4 F

Age: 28-51 yr 

Carbon and ammonium 

nitrate particles 

Concentration: 

With co-exposure to 0.2ppm 

O3: 255 μg/m3, 

Without co-exposure to 

0.2ppm O3: 313 μg/m3

Subjects exposed for 4 h with intermittent 

exercise (30-min periods) to filtered air, 

particles, and particles + O3 in a crossover 

study design. Exposures were separated by at 

least 3 wk. 

Time to analysis: 3 h 40 min from the start of 

exposure. 

Time and frequency domain HRV parameters 

were not affected by particle exposure relative 

to filtered air. However, exposure to particles 

with O3 resulted in a significant decrease in 

SDNN as well as changes to both high and low 

frequency power normalized to the difference 

between total and very low frequency power. 

Reference: Routledge et al. 

(2006, 088674) 

Subjects: 20 older adults 

with coronary artery disease, 

20 healthy older adults 

Gender: CAD: 17 M/3 F, 

Healthy: 10 M/10 F 

Age: CAD: 52-74 yr, 

Healthy: 56-75 yr 

Ultrafine carbon 

Particle Size: <10-300 nm; 

mode at 20-30 nm 

Concentration: Ultrafine 

carbon: 50 μg/m3

; SO2: 200

ppb 

Exposures conducted (head dome system) to 

filtered air, ultrafine carbon, SO2, and ultrafine 

carbon + SO2 for 1 h at rest using a 

randomized crossover study design. 

Time to analysis: Immediately following 

exposure as well as 3 and 23 h postexposure. 

No PM-induced changes in HRV observed 

among subjects with coronary artery disease. 

Among healthy subjects, small increase in 

HRV (RR, SDNN, rMSSD, and LF power) 

demonstrated immediately post-carbon 

exposure. Relative to filtered air control, 

exposure to ultrafine carbon did not 

significantly affect blood pressure in healthy 

adults or adults with coronary artery disease 

0-3 h post-exposure. Exposure to ultrafine 

carbon, either alone or with SO2, did not affect 

plasma levels of fibrinogen or D-dimer at 3 or 

23 h post-exposure. Exposure to ultrafine 

carbon did not affect peripheral blood 

leukocyte count or C-reactive protein levels 3 

or 23 h post-exposure. 

Reference: Rundell and 

Caviston (2008, 191986) 

Subjects: 15 healthy college 

athletes 

Gender: M 

Age: Avg 19.5 yr 

Gasoline emissions 

2.5 hp gasoline engine 

running 10 s each min 

during exposure and in the 

min prior to exposure 

Particle Size: PM1.0 

Particle Number/Count: 

Trial 1: 336,730 ± 

149,206/cm3

; 

Trial 2: 396,200 ± 

82,564/cm3

 

Subjects were exposed twice to both clean air 

and dilute gasoline exhaust during 6-min 

periods of maximal exercise on a cycle 

ergometer. Clean air exposures occurred first 

and were separated by 3 days. Gasoline 

exhaust exposures were also separated by 3 

days, with the first occurring 7 days after the 

second clean air exposure. Other emissions 

measured: CO (6.3 ± 3.4 ppm). 

Time to analysis: 6 min 

There was no difference in total work done (kJ) 

between the clean air exposures or between 

the clean air exposures and the first exposure 

to gasoline exhaust. However, the second 

gasoline exhaust exposure was demonstrated 

to significantly decrease work accumulated 

over the 6min exercise period compared with 

either of the other exposure conditions (p < 

0.01). 

December 2009 C-6 
Study Pollutant Exposure Findings 

Reference: Samet et al. 

(2007, 156940) 

Subjects: Ultrafine CAPs: 

20 healthy adults, Coarse 

CAPs: 14 healthy adults 

Gender: Ultrafine CAPs: 

11 M/9 F, Coarse CAPs: 

8 M/6 F 

Age: Ultrafine CAPs: 

18-35 yr, Coarse CAPs: 

18-35 yr 

CAPs (Chapel Hill, NC) 

Particle Size: Ultrafine 

0.049 ± 0.009 μm; Coarse 

3.59 ± 0.58 μm 

Concentration: Ultrafine 

47.0 ± 20.2 μg/m3

; Coarse 

89.0 ± 49.5 μg/m3

Preliminary report comparing effects of 

controlled exposures to coarse, fine, and 

ultrafine CAPs among healthy adults (3 

separate studies). A randomized crossover 

design was used in evaluating effects of 

coarse CAPs (n=14) and ultrafine CAPs 

(n=20) relative to filtered air following 2-h 

exposures with intermittent exercise. Results 

compared with previous study of controlled 

exposure to fine CAPs (Chapel Hill, NC) 

where subjects did not serve as their own 

controls (Ghio et al., 2000, 012140). 

Time to analysis: 0-20 h post-exposure. 

Statistically significant decrease in SDNN 

observed 20 h following exposure to coarse 

CAPs relative to filtered air. Subjects in the 

high ultrafine CAPs group experienced a 

decrease in SDNN based on an analysis of 

24 h ambulatory Holter monitoring relative to 

filtered air. Fine CAPs did not significantly 

affect HRV. Increased levels of D-dimer 

observed 18 h following exposure to ultrafine 

CAPs. No CAPs-induced changes in plasma 

factor VII, plasminogen, fibrinogen, PAI-1, vWf, 

or t-PA. No CAPs-induced changes in 

C-reactive protein levels were observed. 

Reference: Samet et al. 

(2009, 191913) 

Subjects: 19 healthy adults 

Gender: 10 M/9 F 

Age: 18-35 yr 

Ultrafine CAPs (Chapel Hill, 

NC) 

Particle Size: < 0.16 μm 

Particle Number/Count: 

120,662 ± 48,232 

particles/cm3

 

Concentration: 49.8 ± 

20 μg/m3

Subjects exposed for 2 h with intermittent 15 

periods of exercise to UF CAPs and filtered 

air using a randomized crossover study 

design. 

Time to analysis: Immediately following 

exposure and 1 and 18 h post-exposure. 

UF CAPs exposure resulted in an increase in 

plasma concentrations of D-dimer both 

immediately following exposure (20.6% 

increase per 105

 particles/cm3) as well as 18 h 

post-exposure (18.2% increase per 105

particles/cm3

). Plasma concentration of PAI1 

also increased with UF CAPs, although this 

increase was not statistically significant (24% 

increase, p = 0.1). No UF CAPs-induced 

changes observed in plasma concentrations of 

tPA, vWF, CRP, fibrinogen, plasminogen, 

or Factor VII. HF and LF power were both 

observed to increase with UF CAPs exposure 

relative to filtered air at 18 h post-exposure 

(41.8% and 36%, respectively, per 105

particles/cm3

 increase in UF CAPs). UF CAPs 

expressed as mass concentration was not 

observed have a statistically significant effect 

in HF total power. UF CAPs was not observed 

to affect time domain measures of HRV over 

24 h. The QT interval was shown to decrease 

both immediately following and at 18 h post 

exposure (not statistically significant 

immediately following exposure). 

Reference: Shah et al. 

(2008, 156970) 

Subjects: 16 healthy adults 

Age: 26.9 ± 6.9 yr 

Ultrafine EC 

Particle Number/Count: 

10.8 ± 1.7 × 106 /cm3

Concentration: 50 μg/m3

Exposures conducted via mouthpiece for 2 h 

with intermittent exercise to filtered air and 

ultrafine carbon in a randomized crossover 

study design. 

Time to analysis: Immediately following 

exposure as well as 3.5, 21, and 45 h postexposure. 

Exposure to ultrafine carbon attenuated peak 

forearm blood flow after ischemia relative to 

filtered air 3.5 h post-exposure. Venous nitrate 

levels were significantly lower at 21 h following 

exposure to UF carbon compared with filtered 

air exposure. PM exposure was not observed 

to affect blood pressure relative to filtered air at 

times 0-45 h post-exposure. 

Reference: Tornqvist et al. 

(2007, 091279) 

Subjects: 15 healthy adults 

Gender: M 

Age: 18-38 yr 

DE 

Idling 1991 Volvo diesel 

engine (TD45, 4.5 L, 4 

cylinders, 680 rpm) 

Concentration: 300 μg/m3

Subjects exposed for 1h with intermittent 

exercise (15-min periods) to DE and filtered 

air in a randomized crossover study design. 

Exposures were separated by at least two wk. 

Other diesel emissions measured: NOX (4.44 

ppm), NO2 (0.82 ppm), NO (3.62 ppm), total 

hydrocarbon (2.21 ppm). 

Time to analysis: 24 h post-exposure. 

DE was observed to significantly attenuate 

endothelium-dependent vasodilation 24 h 

post-exposure. Endothelium-independent 

vasodilation was not affected by diesel 

exposure. Exposure to DE did not affect blood 

pressure relative to filtered air 24 h after 

exposure. DE significantly increased plasma 

levels of IL-6 and TNF-α 24 h following 

exposure. Exposure to diesel resulted in an 

increase in total antioxidant capacity of plasma 

relative to filtered air 24 h post-exposure. 

Reference: Urch et al. 

(2004, 055629) 

Subjects: 24 healthy adults 

Gender: 14 M/10 F 

Age: 35 ± 10 yr 

Fine CAPs (Toronto) 

Concentration: 150 μg/m3

(range 101-257 μg/m3

) with 

120 ppb O3 

Exposures conducted through a facemask 

which covered the subject’s nose and mouth. 

Subjects were exposed to CAPs + O3 and 

filtered air for 2 h at rest in a randomized 

crossover study design. Exposures were 

separated by at least 2 days. 

Time to analysis: Immediately following 

exposure. 

CAPs + O3 exposure resulted in a significant 

decrease in brachial artery diameter 

immediately post-exposure (Brook et al., 2002, 

024987), which was demonstrated to be 

associated with both the organic and EC

fractions of the CAPs. 

December 2009 C-7 
Study Pollutant Exposure Findings 

Reference: Urch et al. 

(2005, 081080) 

Subjects: 23 healthy adults 

Gender: 13 M/10 F 

Age: 32 ± 10 yr 

Fine CAPs (Toronto); 

Concentration: 150 μg/m3

(range 102-214 μg/m3) with 

120 ppb O3 

Exposures conducted through a facemask 

which covered the subject’s nose and mouth. 

Subjects were exposed to CAPs + O3 and 

filtered air for 2 h at rest in a randomized 

crossover study design. 

Time to analysis: Every 30 min during 

exposure, with the final measurement made 

immediately prior to the end of the exposure. 

An increase in diastolic blood pressure of 6 

mmHg was observed at the end of CAPs + O3

exposure, which was statistically different from 

the change in blood pressure experienced 

during exposure to filtered air (1 mmHg). This 

effect was associated with the organic fraction 

of PM2.5. 

Reference: Zareba et al.

(2009, 190101) 

Subjects: 24 healthy adults

Gender: 12 M/12 F 

Age: 18-40 yr

Ultrafine EC 

Particle Size: Count 

median diameter 25 nm

Particle Number/Count: 

2×106/cm3 (10 μg/m3), 

7×106

/cm3 (25 μg/m3)

Concentration: 10 μg/m3

; 

25 μg/m3

Protocol 1 (n=12, 6 M/6 F): Subjects exposed 

to 10 μg/m3 UF carbon and filtered air for 2 h 

at rest in a randomized crossover design. 

Exposures were separated by at least 2 wk. 

Protocol 2 (n=12, 6 M/6 F): Subjects exposed 

to 10 μg/m3

, 25 μg/m3, and filtered air for 2 h 

with intermittent exercise (15-min periods) in a 

restricted randomized crossover design (all 

subjects exposed to 10 μg/m3 before 

25 μg/m3). Exposures were separated by at 

least 2 wk. 

Time to analysis (both protocols): 

Immediately following exposure and 3.5 and 

21 h post-exposure.

Exposure to 10 μg/m3 at rest resulted in no 

change in HRV frequency domain parameters 

relative to filtered air exposure. Time domain 

parameters were observed to increase slightly 

with UF carbon exposure (10 μg/m3

 at rest), 

however, only the increase in rMSSD was 

statistically significant (p = 0.032). Some 

trends toward less shortening of QT interval, 

increase in ST segment, and increase in 

variability of repolarization (variability of T 

wave complexity) were observed with 

exposure to 10 μg/m3

 at rest, none of which 

were statistically significant. 

In Protocol 2, exposure to 10 μg/m3

 UF carbon 

was observed to slightly increase HRV time 

domain parameters as was demonstrated in 

Protocol 1. However, this was not observed at 

the higher concentration (25 μg/m3

). As with 

exposure at rest, exposure to UF carbon 

during exercise was observed to affect 

repolarization (reduction in QT duration and 

increase in T-wave amplitude), although this 

effect was not statistically significant.

 

December 2009 C-8 
Table C-2. Respiratory effects. 

Reference Pollutant Exposure Findings 

Reference: Alexis et al. 

(2006, 154323) 

Subjects: 9 healthy adults 

Gender: 3 M/6 F 

Age: 18-35 yr 

Coarse fraction particles 

(Chapel Hill, NC) 

Heat-treated (biologically 

inactive) and non-heated 

particles 

Particle Size: MMAD 5 μm 

Concentration: 0.65 mg per 

subject 

Subjects were administered heat-treated 

PM10-2.5, non-heated PM10-2.5, and 0.9% saline 

(control) via nebulization in a randomized 

crossover study design. Exposures were 

separated by at least 1 wk. 

Time to analysis: 2-3 h post-inhalation. 

Both heat-treated and non-heated coarse PM 

were observed to increase neutrophil counts in 

induced sputum 2-3 h post-inhalation. Biologically 

active PM (non-heated) induced an increase 

expression of macrophage TNF-α mRNA, eotaxin, 

and immune surface phenotypes on 

macrophages (mCD14, CD11b/CR3, and 

HLA-DR). 

Reference: Barregard et al. 

(2008, 155675) 

Subjects: 13 healthy adults 

Gender: 6 M/7 F 

Age: 20-56 yr 

Wood smoke 

Particle Size: 

Session 1: geometric mean 

diameter 42 nm, Session 2: 

geometric mean diameter 112 

nm 

Particle Number/Count: 

Session 1: 180,000/cm3; 

Session 2: 95,000/cm3

Concentration: Session 1: 

median 279 μg/m3

; Session 2: 

median 243 μg/m3 

Subjects exposed in two groups for 4 h to filtered 

air, followed a wk later by a 4-h exposure to 

wood smoke. Exposures conducted with two 

25-min periods of light exercise. Other measured 

combustion products: 

Session 1: NO2 (0.08 ppm), CO (13 ppm), 

formaldehyde (114 μg/m3

), acetaldehyde 

(75 μg/m3

), benzene (30 μg/m3), 1,3-butadiene 

(6.3 μg/m3); 

Session 2: NO2 (0.09 ppm), CO (9.1 ppm), 

formaldehyde (64 μg/m3

), acetaldehyde 

(40 μg/m3), benzene (20 μg/m3), 1,3-butadiene 

(3.9 μg/m3

). 

Time to analysis: Immediately following 

exposure as well as 3 and 20 h post-exposure. 

Relative to filtered air, exposure to wood smoke 

was observed to increase levels of eNO 3 h 

post-exposure. Serum Clara cell protein 

increased 20 h after wood smoke exposure. 

Wood smoke was observed to increase levels of 

malondialdehyde in breath condensate 

immediately after as well as 20 h post-exposure. 

Effects of wood smoke on eNO and 

malondialdehyde levels were similar between the 

two sessions of wood smoke exposure. However, 

serum Clara cell protein was significantly 

increased with wood smoke in session 1 (higher 

particle count) but not in session 2. 

Reference: Bastain et al. 

(2003, 098690) 

Subjects: 18 nonsmoking 

adults with positive allergy 

skin test to short ragweed 

Gender: 7 M/11 F 

Age: 18-38 yr 

DEP 

Isuzu diesel engine, 4 cylinder, 

4JB1 

Concentration: 0.3 mg in 

200 μl saline 

Subjects underwent nasal provocation challenge 

(intranasal spray) with allergen and either DEP or 

placebo (saline) in a randomized crossover study 

design. Challenges were separated by 30 days. 

This protocol was then repeated 30 days after 

the last exposure. 

Time to analysis: 24 h post-exposure and 4 and 

8 days after exposure. 

DEP significantly increased allergic responses to 

short ragweed. Relative to allergen + placebo, 

allergen + DEP increased allergen specific IgE 

4days following exposure, and increased IL-4 1 

day post-exposure. The enhancement of allergic 

response with DEP was observed to be 

reproducible within subjects. 

Reference: Beckett et al. 

(2005, 156261) 

Subjects: 12 healthy adults 

Gender: 6 M/6 F 

Age: 23-52 yr 

Ultrafine and fine zinc oxide 

Particle Size: UF: 

<0.1 μm; Fine: 0.1-1.0 μm 

Particle Number/Count: UF: 

4.6 × 107

/cm3; Fine: 1.9 × 

105

/cm3

Concentration: 500 μg/m3

Subjects exposed via mouthpiece for 2 h during 

rest to filtered air, ultrafine, and fine zinc oxide in 

a randomized crossover study design. 

Exposures were separated by at least 3 wk. 

Time to analysis: 11 and 24 h after exposure. 

No changes observed in neutrophil count in 

induced sputum. No PM (zinc oxide)-induced 

changes in respiratory symptoms observed 

0-24 h post-exposure. 

Reference: Behndig et al. 

(2006, 088286) 

Subjects: 15 healthy adults 

Gender: 8 M/7 F 

Age: 21-27 yr 

DE 

Idling 1991 Volvo diesel 

engine (TD45, 4.5 L, 4 

cylinders, 680 rpm) 

Particle Size: PM10; majority 

of PM mass made up of 

particles < 1 μm in diameter 

Concentration: 100 μg/m3

Exposures conducted for 2 h with intermittent 

exercise to both DE and filtered air in a 

randomized crossover design. Exposures were 

separated by at least 3 wk. Other diesel 

emissions measured: NOX (1.8 ppm), NO2 (0.4 

ppm), NO (1.3 ppm), CO (10.4 ppm), total 

hydrocarbons (1.3 ppm). 

Time to analysis: 18 h post-exposure. 

Exposure to DE increased neutrophil and mast 

cell numbers in bronchial mucosa at 18 h 

post-exposure. Neutrophils, IL-8, and 

myeloperoxidase observed to increase in 

bronchial lavage fluid following exposure relative 

to filtered air. No inflammatory response observed 

in the alveolar compartment. Exposure to DE 

increased urate and reduced glutathione 

bronchoalveolar lavage at 18 h post-exposure. 

Reference: Blomberg et al. 

(2005, 191991) 

Subjects: 15 older adults 

(former smokers) with COPD 

Age: 56-72 yr 

DE 

Concentration: 300 μg/m3 

Subjects exposed for 1 h with intermittent 

exercise to DE and filtered air in a randomized 

crossover study design. 

Time to analysis: 6 and 24 h post-exposure. 

DE was not observed to affect levels of Clara cell 

protein in peripheral blood at 6 and 24 h postexposure. 

December 2009 C-9 
Reference Pollutant Exposure Findings 

Reference: Bosson et al. 

(2007, 156286) 

Subjects: 16 healthy adults 

Gender: 7 M/9 F 

Age: 20-28 yr 

DE 

Idling Volvo diesel engine 

Concentration: PM 

300 μg/m3

 followed by 

exposure to filtered air or 0.2 

ppm O3

Subjects exposed to DE for 1 h followed 5 h later 

by a 2-h exposure to either filtered air or O3 (0.2 

ppm) using a randomized crossover study 

design. All exposures were conducted with 

subjects engaged in intermittent exercise. 

Time to analysis: 18 h after second exposure 

(filtered air or O3). 

The percentage of neutrophils and concentration 

of myeloperoxidase in induced sputum (18 h 

post-O3/air exposure) was significantly higher 

following diesel + O3 than diesel + air. 

Reference: Bosson et al. 

(2008, 196659) 

Subjects: 14 healthy adults 

Gender: 9 M/5 F 

Age: 21-29 yr 

DE 

Idling 1991 Volvo diesel 

engine (TD45, 4.5 L, 4 

cylinders) 

Concentration: PM 

300 μg/m3 or filtered air 

followed by exposure to 0.2 

ppm O3

Subjects exposed to DE or filtered air for 1h 

followed 5 h later by a 2-h exposure to O3 (0.2 

ppm) using a randomized crossover study 

design. All exposures were conducted with 

subjects engaged in intermittent exercise. Other 

diesel emissions measured: NO2 (0.51 ppm), NO 

(1.65 ppm), total hydrocarbons (1.18 ppm). 

Time to analysis: 24 h after the start of the initial 

exposure. 

Neutrophil and macrophage numbers in bronchial 

wash were significantly increased 16 h following 

O3 exposure when preceded by exposure to 

diesel, compared to O3 exposure preceded by 

exposure to filtered air. 

Reference: Brauner et al. 

(2009, 190244) 

Subjects: 29 healthy adults 

Gender: 20 M, 9 F 

Age: M avg 27 yr, F avg 26 yr 

Urban traffic particles 

Particle Size: PM2.5, PM10-2.5

Particle Number/Count: 6-

700 nm: 10,067/cm3

Concentration: PM2.5: 

9.7 μg/m3

, PM10-2.5: 12.6 μg/m3

Subjects exposed to urban traffic particles and 

filtered air for 24 h with and without two 90-min 

periods of light exercise in a randomized 

crossover study design. Concentrations of NOX

and NO were low and did not differ between 

filtered and unfiltered exposures. CO 

concentrations were higher with filtered air (0.35 

and 0.41 ppm), while O3 concentrations were 

lower with filtered air (12.08 and 4.29 ppb). 

Time to analysis: 2.5, 6, and 24 h after the start 

of exposure. 

Epithelial membrane integrity and blood-gas 

barrier permeability, assessed using pulmonary 

clearance of 99mTc-labeled diethylenetriamine 

pentaacetic acid (DTPA), was observed to 

increase with exercise, but was not affected by 

exposure to urban particles (2.5 h of exposure). 

Exposure to urban particles was not shown to 

affect plasma or urine concentration of Clara cell 

16 protein at 6 and 24 h after the start of 

exposure. No relationship between exposure and 

pulmonary function was observed at 2.5 h. 

Reference: Gilliland et al. 

(2004, 156471) 

Subjects: 19 adults with 

allergic rhinitis and positive 

skin test to ragweed, GSTM1 

(14 null, 5 present); GSTT1 (9 

null, 10 present); GSTP1 

codon 105 variants (13 I/I, 6 

I/V, 0 V/V) 

Gender: 7 M/12 F 

Age: 20-34 yr 

DEP 

Isuzu diesel engine, 4 cylinder, 

4JB1 

Concentration: 0.3 mg DEP 

in 300 μL saline 

Subjects were challenged intranasally with 

allergen and placebo (saline) as well as allergen 

plus DEP in saline in a randomized crossover 

design. Challenges were separated by at least 6 

wk. 

Time to analysis: 10 min, 24 h, and 72 h postchallenge. 

Subjects who were GSTM1 null or homozygous 

for GSTP1 I105 wild-type allele experienced 

significantly greater increase in nasal IgE and 

histamine with diesel plus allergen compared to 

subjects with functional GSTM1 or who were 

heterozygous for GSTP1 I/V(105). 

Reference: Gong et al. 

(2004, 087964) 

Subjects: 13 older adults with 

COPD, 6 healthy older adults 

Gender: COPD: 5 M/8 F, 

Healthy: 2 M/4 F 

Age: COPD: avg 68 yr, 

Healthy: avg 73 yr 

Fine CAPs (Los Angeles) 

Particle Size: 85% of mass 

between 0.1 and 2.5 μm 

Concentration: Mean: 

194 μg/m3

, Range: 

135-229 μg/m3

 

Exposures to CAPs and filtered air (randomized 

crossover) for 2 h with intermittent light exercise 

(four 15-min periods). Exposures were separated 

by at least 2 wk. 

Time to analysis: Immediately following 

exposure as well as 4 and 22 h post-exposure. 

No CAPs-induced respiratory symptoms 

observed in healthy older adults or older adults 

with COPD at 0, 4, or 22 h post-exposure. 

Exposure to CAPs did not significantly affect FVC 

or FEV1. CAPs exposure caused a decrease in 

arterial oxygen saturation immediately following 

exposure which was more pronounced in healthy 

older adults than in older adults with COPD. 

Exposure to CAPs was not observed to affect the 

levels of white blood cells, columnar epithelial 

cells, IL-6, or IL-8 in induced sputum. 

Reference: Gong et al. 

(2004, 055628) 

Subjects: 12 adult 

asthmatics, 4 healthy adults 

Gender: Asthmatic: 4 M/8 F, 

Healthy: 2 M/2 F 

Age: Asthmatic: avg 38 yr, 

Healthy: avg 32 yr 

Coarse CAPs (Los Angeles) 

Particle Size: 80% of mass 

between 2.5 and 10 μm, 20% 

of mass <2.5 μm 

Concentration: Mean: 

157 μg/m3

; Range: 

56-218 μg/m3

Exposures to CAPs and filtered air (randomized 

crossover) for 2 h with intermittent light exercise 

(four 15-min periods). Exposures were separated 

by at least 2 wk. 

Time to analysis: Immediately following 

exposure as well as 4 and 22 h post-exposure. 

No effect of CAPs exposure on spirometry or 

arterial oxygen saturation was observed 0, 4, or 

22 h post-exposure. No respiratory symptoms 

reported 0-22 h post-exposure in either healthy or 

asthmatic adults. Sputum cell counts at 22 h postexposure did not differ between CAPs and filtered 

air. 

December 2009 C-10 
Reference Pollutant Exposure Findings 

Reference: Gong et al. 

(2005, 087921) 

Subjects: 18 older adults with 

COPD, 6 healthy older adults 

Gender: COPD: 9 M/9 F, 

Healthy: 2 M/4 F 

Age: COPD: avg 72 yr, 

Healthy: avg 68 yr 

Fine CAPs (Los Angeles) 

Concentration: CAPs: 

200 μg/m3; NO2: 0.4 ppm 

Each subject was exposed to CAPs, NO2, CAPs 

+ NO2, and filtered air for 2 h with intermittent 

exercise. Exposure order was not fully 

counterbalanced as NO2 exposures were 

conducted after the majority of the CAPs and 

filtered air exposures had been completed. 

Exposures were separated by at least 2 wk. 

Time to analysis: Immediately following 

exposure as well as 4 and 22 h post-exposure. 

Exposure to CAPs was observed to decrease 

maximal mid-expiratory flow and arterial oxygen 

saturation relative to filtered air 4-22 h 

post-exposure. This response was more 

pronounced in healthy older adults than in older 

adults with COPD. Concomitant exposure to NO2

did not enhance the response. No other 

respiratory responses (symptoms, spirometry, 

sputum cell counts) were affected by exposure to 

CAPs. 

Reference: Gong et al. 

(2008, 156483) 

Subjects: 14 adult 

asthmatics, 17 healthy adults 

Gender: Asthmatics: 9 M/5 F, 

Healthy: 5 M/12 F 

Age: Asthmatics: 34 ± 12 yr, 

Healthy:24 ± 8 yr 

Ultrafine CAPs (Los Angeles) 

Particle Number/Count: 

145,000/cm3, Range 39,000-

312,000/cm3

Concentration: Mean: 

100 μg/m3

, Range: 

13-277 μg/m3

 

Subjects exposed for 2 h during intermittent 

exercise (15-min periods) to both CAPs and 

filtered air in random order. The first 7 subjects 

underwent whole body exposure, while the 

remaining subjects were exposed through a 

facemask. Facemask exposures had higher 

particle counts but lower particle mass than 

whole body exposures. Exposures were 

separated by at least 2 wk. 

Time to analysis: Immediately following 

exposure as well as 4 and 22 h post-exposure. 

No significant differences in respiratory symptoms 

observed between filtered air and ultrafine CAPs 

exposures. Individuals exposed to higher particle 

counts tended to experience greater symptoms 

with CAPs than with filtered air. An ultrafine 

CAPs-induced decrease in arterial oxygen 

saturation (0.5%) was observed at 0, 4, and 22 h 

post-exposure. A decrease in FEV1 (2%) was also 

observed 22 h post-exposure relative to filtered 

air. Responses were not significantly different 

between healthy and asthmatic adults. CAPs 

exposure was not observed to affect total sputum 

cell counts or cytokine levels. There were no 

differences in response observed between 

facemask and whole body exposures. 

Reference: Graff et al. (2009, 

191981) 

Subjects: 14 healthy adults 

Gender: 8 M/6 F 

Age: 20-34 yr 

Coarse CAPs (Chapel Hill, 

NC) 

Concentration: 89 

± 49.5 μg/m3 (estimated 

inhaled dose ≈ 67% of 

measured particle mass) 

Subjects exposed for 2 h with intermittent 

exercise (15-min periods) to coarse CAPs and 

filtered air in a randomized crossover design. 

Exposures were separated by at least 2 mos. 

Time to analysis: 0-1 and 20 h post-exposure. 

Pulmonary function (FVC, FEV1, and carbon 

monoxide diffusing capacity) was not affected by 

exposure to coarse CAPs either immediately 

following exposure or 20 h post-exposure. A 

significant increase in percent PMNs (10.7% 

increase per 10 μg/m3

 coarse CAPs) was 

observed in BAL fluid 20 h post-exposure. 

Percent monocytes in BL fluid were slightly 

decreased at 20 h post-exposure (2.0% decrease 

per 10 μg/m3

 CAPs; p = 0.05). Total protein in 

BAL fluid was also observed to decrease 

following CAPs exposure (1.8% decrease per 

10 μg/m3

 CAPs). Markers of inflammation in BAL 

and BL fluids including IL-6, IL-8, and PGE2 were 

not affected by exposure to coarse CAPs. 

Reference: Huang et al. 

(2003, 087377) 

Subjects: 38 healthy adults 

Gender: 36 M/2 F 

Age: Avg 26.2 ± 0.7 yr 

Fine CAPs (Chapel Hill, NC) 

Concentration: 

23.1-311.1 μg/m3

Subjects exposed to CAPs (n = 30) or filtered air 

(n = 8) for 2 h with intermittent exercise (subjects 

did not serve as their own controls). Component 

data of CAPs was available for 37 of the 38 

subjects. 

Time to analysis: 18 h after exposure. 

The increase in bronchoalveolar lavage fluid 

neutrophils observed by Ghio et al. (2000, 

012140) following exposure to fine CAPs was 

shown to be associated with iron, selenium, and 

sulfate content of the CAPs. 

Reference: Kongerud et al. 

(2006, 156656) 

Subjects: 17 asthmatic 

adults, 46 healthy adults 

Gender: Asthmatics6 M/11 F, Healthy- 24 M/22 F 

Age: Asthmatics: avg 23 yr, 

Healthy: avg 26 yr 

DEP 

NIST 1650, heavy duty diesel 

engine 

Concentration: Untreated 

and treated with 0.1 ppm O3

(48 h); 300 μg per nostril 

DEP (with and without O3 pre-treatment) were 

intranasally instilled, using the saline vehicle as 

control. Subjects did not serve as their own 

controls (not a crossover design). 

Time to analysis: 4 and 96 h post-instillation. 

Exposure to DEP was not observed to alter 

markers of inflammation in nasal lavage fluid 

(e.g., cell counts, IL-8, IL-6) at 4 or 96 h 

post-instillation. 

Reference: Larsson et al. 

(2007, 091375) 

Subjects: 16 healthy adults 

Gender: 10 M/6 F 

Age: 19-59 yr 

Traffic particles (road tunnel) 

Particle Size: PM2.5, PM10; 

PM2.5 mass constituted ~36% 

of PM10 mass 

Particle Number/Count: 20-

1,000 nm: 1.1 × 105/cm3, < 

100 nm: 0.85 × 105

/cm3 

Concentration: PM2.5- 

46-81 μg/m3

; PM10- 

130-206 μg/m3

Exposures were conducted for 2 h with 

intermittent exercise in a room adjacent to a busy 

road tunnel. Study used a randomized crossover 

design with each subject also exposed to normal 

air (control). Exposures were separated by 

3-10wks. No exposures to filtered air were 

conducted. Other traffic emissions measured: 

NO (874 μg/m3

), NO2 (230 μg/m3), CO (5.8 μg/m3

reported, likely 5.8 mg/m3). 

Time to analysis: 14 h post-exposure. 

An increase in bronchoalveolar lavage fluid cell 

number, lymphocytes, and alveolar macrophages 

were observed 14 h after road tunnel exposure 

relative to control. Traffic particulate exposure 

was not shown to effect cytokine or adhesion 

molecule expression in bronchial tissues. 

Respiratory symptoms were reported to increase 

during exposure to road tunnel air relative to 

pre-exposure symptom ratings. Exposure to road 

tunnel air was not shown to affect lung function. 

December 2009 C-11 
Reference Pollutant Exposure Findings 

Reference: Mudway et al. 

(2004, 180208) 

Subjects: 25 healthy adults 

Gender: 16 M/9 F 

Age: 19-42 yr 

DE 

Idling 1991 Volvo diesel 

engine (TD45, 4.5 L, 4 

cylinders, 680 rpm) 

Concentration: PM10

100 μg/m3

Subjects exposed to DE and filtered air for 2 h 

with intermittent exercise (15-min periods) in a 

randomized crossover design. Exposures were 

separated by at least 3 wk. Other diesel 

emissions measured: NO2 (0.2 ppm), NO (0.6 

ppm), CO (1.7 ppm), total hydrocarbons (1.4 

ppm), formaldehyde (43.5 μg/m3

). 

Time to analysis: 1 h after the start of exposure, 

immediately following exposure, and 6 h postexposure. 

DE caused mild throat irritation in some subjects 

and a significant increase in airways resistance 

(Raw) during or immediately following exposure. 

No changes in FEV1 or FVC were observed 

following exposure to diesel. Neutrophil numbers 

in the bronchial airways tended to increase 

following exposure to DE; however, this increase 

was highly variable between subjects and did not 

reach statistical significance. Exposure to DE did 

not affect levels of SOD or malondialdehyde in 

the airways. An increase in levels of ascorbate 

and GSH in nasal lavage fluid was observed 6 h 

following exposure to DE. 

Reference: Pietropaoli et al. 

(2004, 156025) 

Subjects: 16 asthmatic 

adults, 40 healthy adults 

Gender: Asthmatic: 8 M/8 F, 

Healthy: 20 M/20 F 

Age: 18-40 yr 

Ultrafine EC 

Particle Size: CMD ~25 nm 

Particle Number/Count: 

10 μg/m3: ~2.0 × 106/cm3; 

25 μg/m3

: ~7.0 × 106/cm3; 

50 μg/m3

: ~10.8 × 106/cm3

Concentration: 10, 25, and 

50 μg/m3

Study conducted using a randomized crossover 

design with 2-h exposures. Asthmatics (n = 16) 

exposed to filtered air and 10 μg/m3

. 12 healthy 

adults exposed to filtered air and 10 μg/m3

 at 

rest; 12 healthy adults exposed to filtered air, 10 

and 25 μg/m3

 with intermittent exercise; 16 

healthy adults exposed to filtered air and 

50 μg/m3

 with intermittent exercise. Exposures 

were conducted via mouthpiece. 

Time to analysis: Immediately following 

exposure as well as 3.5, 21, and 45 h postexposure. 

No PM-induced changes in eNO or cell counts, 

IL-6, or IL-8 in induced sputum were observed in 

any of the protocols 21 h following exposure. 

Ultrafine carbon was not observed to increase 

respiratory symptoms in any of the study 

protocols. Healthy adults experienced an ultrafine 

PM-induced reduction in maximal mid-expiratory 

flow and CO diffusing capacity relative to filtered 

air 21 h following exposure. 

Reference: Pourazar et al. 

(2005, 088305) 

Subjects: 15 healthy adults 

Gender: 11 M/4 F 

Age: 21-28 yr 

DE 

Idling Volvo diesel engine 

Particle Number/Count: 4.3 

× 106

/cm3 

Concentration: PM10

300 μg/m3

Subjects exposed to DE and filtered air for 1 h 

with intermittent exercise (randomized crossover 

study design). Other diesel emissions measured: 

NO2 (1.6 ppm), NO (4.5 ppm), CO (7.5 ppm), 

total hydrocarbons (4.3 ppm), formaldehyde 

(0.26 mg/m3

). 

Time to analysis: 6 h post-exposure. 

Exposure to DE significantly increased nuclear 

translocation of NF-κB, AP-1, phosphorylated 

p38, and phosphorylated JNK in bronchial 

epithelium 6 h post-exposure. 

Reference: Pourazar et al. 

(2008, 156884) 

Subjects: 15 healthy adults 

Gender: 11 M/4 F 

Age: 21-28 yr 

DE 

Idling Volvo diesel engine 

Particle Number/Count: 4.3 

× 106/cm3

Concentration: PM10

300 μg/m3

 

Subjects exposed to DE and filtered air for 1 h 

with intermittent exercise (randomized crossover 

study design). Other diesel emissions measured: 

NO2 (1.6 ppm), NO (4.5 ppm), CO (7.5 ppm), 

total hydrocarbons (4.3 ppm), formaldehyde 

(0.26 mg/m3

). 

Time to analysis: 6 h post-exposure. 

Exposure to DE observed to enhance epidermal 

growth factor receptor (EGFR) expression in 

bronchial epithelium 6 h post-exposure. 

Reference: Riechelmann 

et al. (2004, 180120) 

Subjects: 30 healthy adults 

Gender: 11 M/19 F 

Age: 22-32 yr 

Urban dust 

NIST SRM 1649a 

Concentration: 150, 

500 μg/m3

Subjects exposed to both concentrations of 

urban dust (nose only exposure system) as well 

as filtered air for 3h at rest in a randomized 

crossover design. Exposures were separated by 

at least 1 wk. 

Time to analysis: 30 min, 8 h, and 24 h postexposure. 

An increase in nasal secretion (nasal cytology) of 

IL-6 and IL-8 were observed 24 h after exposure 

to 500 μg/m3

 urban dust. 

Reference: Samet et al. 

(2007, 156940) 

Subjects: Ultrafine CAPs: 20 

healthy adults, Coarse CAPs: 

14 healthy adults 

Gender: Ultrafine CAPs: 

11 M/9 F, Coarse CAPs: 

8 M/6 F 

Age: 18-35 yr 

CAPs (Chapel Hill, NC) 

Particle Size: Ultrafine: 

0.049 ± 0.009 μm, Coarse: 

3.59 ± 0.58 μm 

Concentration: Ultrafine: 

47.0 ± 20.2 μg/m3

, Coarse: 

89.0 ± 49.5 μg/m3

Preliminary report comparing effects of controlled 

exposures to coarse, fine, and ultrafine CAPs 

among healthy adults (3 separate studies). A 

randomized crossover design was used in 

evaluating effects of coarse CAPs (n=14) and 

ultrafine CAPs (n=20) relative to filtered air 

following of 2-h exposures with intermittent 

exercise. Results compared with previous study 

of controlled exposure to fine CAPs (Chapel Hill, 

NC) where subjects did not serve as their own 

controls (Ghio et al., 2000, 012140) 

Time to analysis: 0-20 h post-exposure. 

As was shown with fine CAPs, exposure to 

coarse CAPs increased the percentage of 

neutrophils in bronchoalveolar lavage fluid 20 h 

following exposure. Unlike fine CAPs, coarse 

CAPs did not increase the percent of monocytes 

in bronchoalveolar lavage fluid. Ultrafine CAPs 

were not shown to affect any markers of 

pulmonary inflammation in bronchoalveolar 

lavage fluid 18 h after exposure. No 

CAPs-induced changes in lung function were 

observed. 

Reference: Samet et al. 

(2009, 191913) 

Subjects: 19 healthy adults 

Gender: 10 M/9 F 

Age: 18-35 yr 

Ultrafine CAPs (Chapel Hill, 

NC) 

Particle Size: < 0.16 μm 

Particle Number/Count: 

120,662 ± 48,232 

particles/cm3

Concentration: 49.8 ± 

20 μg/m3

Subjects exposed for 2 h with intermittent 15 

periods of exercise to UF CAPs and filtered air 

using a randomized crossover study design. 

Time to analysis: Immediately following 

exposure and 1 and 18 h post-exposure. 

No effect of UF CAPs observed on pulmonary 

function immediately following exposure or 18 h 

post-exposure. IL-8 in BAL fluid was observed to 

increase with UF CAPs 18 h post-exposure. UF 

CAPs was not shown to alter any other 

inflammatory markers in BAL fluid. 

December 2009 C-12 
Reference Pollutant Exposure Findings 

Reference: Schaumann et al. 

(2004, 087966) 

Subjects: 12 healthy adults 

Gender: 4 M/8 F 

Age: Avg 27 ± 2.5 yr 

Fine PM 

Collected (filter) from 

industrialized and 

non-industrialized areas in 

Germany 

Concentration: 100 μg per 

subject 

Bronchoscopic instillation of particles collected 

from both areas was conducted in contralateral 

lung segments for each subject. 

Time to analysis: 24 h post-instillation. 

Particles collected from the industrialized area 

(transition metal-rich) increased the percentage of 

monocytes and oxidant radical generation in 

bronchoalveolar lavage fluid 24 h after exposure 

compared with PM containing less metal. 

Reference: Stenfors et al. 

(2004, 157009) 

Subjects: 15 asthmatic 

adults, 25 healthy adults 

Gender: Asthmatic: 10 M/5 F, 

Healthy: 16 M/9 F 

Age: Asthmatic: 22-52 yr, 

Healthy:19-42 yr 

DE 

Volvo diesel engine 

Concentration: PM10

108 μg/m3

Subjects were exposed for 2 h with intermittent 

exercise to DE and filtered air using a 

randomized crossover study design. Other diesel 

emissions measured: NO2 (0.7 ppm). 

Time to analysis: 1 h after the start of exposure, 

immediately following exposure, and 6 h postexposure. 

DE was observed to increase neutrophilia and 

IL-8 in bronchial lavage fluid among healthy 

subjects 6 h after exposure. Among asthmatic 

subjects, exposure to DE did not cause an 

increase in inflammatory markers. No dieselinduced change in pulmonary function was 

observed during or immediately following 

exposure. 

Reference: Tunnicliffe et al. 

(2003, 088744) 

Subjects: 12 asthmatic 

adults, 12 healthy adults 

Gender: Asthmatics: 7 M/5 F, 

Healthy: 5 M/7 F 

Age: Asthmatics: avg 35.7 yr, 

Healthy: avg 34.5 yr 

Aerosols of ammonium 

bisulfate and sulfuric acid 

Particle Size: MMD 0.3 μm 

Concentration: 200, 

2,000 μg/m3

Subjects were exposed for 1 h at rest to 

ammonium bisulfate (low and high 

concentrations), sulfuric acid (low and high 

concentrations) and filtered air in a randomized 

crossover design. Exposures were separated by 

at least 2 wk and were conducted using a head 

dome exposure system. 

Time to analysis: Immediately following 

exposure as well as 5.5-6 h post-exposure. 

Neither ammonium bisulfate nor aerosolized 

sulfuric acid were observed to affect lung function 

or respiratory systems following exposures to 200 

or 2,000 μg/m3

 among healthy or asthmatic 

adults. Exposures to ammonium bisulfate at both 

concentrations resulted in a significant increase in 

eNO in the asthmatic subjects. 

Table C- 3. Central nervous system effects. 

Reference Pollutant Exposure Findings 

Reference: Cruts et al. 

(2008, 156374) 

Subjects: 10 healthy 

adults 

Gender: M 

Age: 18-39 yr 

DE 

Idling Volvo diesel engine 

(TD45, 4.5 L, 4 cylinders, 680 

rpm) 

Particle Number/Count: 1.2 

× 106

/cm3

Concentration: 300 μg/m3

Subjects were exposed to DE and filtered air for 

1 h at rest in a randomized crossover study 

design. Exposures were separated by 2-4 days. 

Other diesel emissions measured: NO2 (1.6 ppm), 

NO (4.5 ppm), CO (7.5 ppm), total hydrocarbons 

(4.3 ppm). 

Time to analysis: From onset of exposure until 

1 h post-exposure. 

Exposure to DE was observed to significantly 

increase the median power frequency (MPF) in 

the frontal cortex during exposure, as well as in 

the hour following the completion of the 

exposure. 

December 2009 C-13 
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