Skip to main content

Table 1 Main health outcome findings and brief details of methodology from reviewed publications

From: Controlled human exposure to diesel exhaust: results illuminate health effects of traffic-related air pollution and inform future directions

Study

Nominal PM concentration of DE exposures (μg/m3)

Concurrent exposures

Participant characteristics

Main findings

Primary topic

Cosselman et al. [12]

PM2.5 = 200

Antioxidant

Healthy

Acute DE exposure associated with oxidative changes in healthy volunteers

DE significantly decreased GSH/GSSG ratio and significantly increased IL-6 mRNA

Antioxidant pre-treatment did not significantly attenuate DE effect on GSH/GSSG ratio, and non-significantly decreased DE effect on IL-6 mRNA

Oxidative stress and antioxidants

Carlsten et al. [13]

PM2.5 = 300

Antioxidant

Healthy

Asthmatics

Antioxidant supplementation decreased baseline airway hyperresponsiveness in hyperresponsive subjects

DE exposure significantly increased airway hyperresponsiveness in hyperresponsive subjects

DE-induced increase hyperresponsiveness was attenuated by antioxidant supplementation

Oxidative stress and antioxidants

Yamamoto et al. [14]

PM2.5 = 300

Antioxidant

Asthmatics

Acute DE exposure causes changes in systemic miRNAs

DE associated changes in miR-144 may be mediated by oxidative stress

Oxidative stress and antioxidants

Pettit et al. [15]

PM2.5 = 300

None

Healthy

DE exposure was associated with changes in expression of genes linked to oxidative stress, protein degradation, and coagulation pathways

Oxidative stress and antioxidants

Allen et al. [16]

PM2.5 = 200

None

Metabolic syndrome

DE exposure did not induce changes in markers of oxidative stress or systemic antioxidant response in subjects with metabolic syndrome

Oxidative stress and antioxidants

Peretz et al. [17]

PM2.5 = 50, 100, 200 (multi-concentration crossover)

None

Healthy

DE exposure associated with changes in gene expression in peripheral blood mononuclear cells

Genes associated with oxidative stress and inflammatory pathways are involved

Oxidative stress and antioxidants

Pourazar et al. [18]

PM10 = 300

None

Healthy

DE exposure activated transcription factors associated with oxidative stress, inducing increased production of proinflammatory cytokines

Oxidative stress and antioxidants

Mudway et al. [19]

PM10 = 100

None

Healthy

Airway inflammation nor antioxidant depletion was observed in airways 6 h post DE exposure

Reduced glutathione was increased in bronchial and nasal airways at 6 h post-DE exposure

DE demonstrated oxidative activity in vitro

Oxidative stress and antioxidants

Blomberg et al. [20]

PM = 300

None

Healthy

DE exposure increased ascorbic acid concentration in nasal lavage

DE exposure did not affect antioxidant concentrations in plasma, BW, or BAL

DE exposure did not affect malondialdehyde nor protein carbonyl concentrations in plasma or BAL

Oxidative stress and antioxidants

Jiang et al. [21]

PM2.5 = 300

None

Asthmatics

DE exposure induced changes in DNA methylation at CpG sites located in genes related to inflammation and oxidative stress, and in miRNA

Systemic inflammation

Xu et al. [22]

PM1 = 300

46 dB or 75 dB traffic noise

Healthy

DE exposure associated with symptoms of irritation and decreased peak expiratory flow

DE exposure increased inflammatory markers (peripheral blood monocyte and leukocyte counts, serum IL-6)

Systemic inflammation

Channell et al. [23]

PM = 100

None

Healthy

DE or NO2 exposure increases circulating proinflammatory factors

Plasma from DE or NO2 exposed volunteers induced inflammatory response in human endothelial cells

Systemic inflammation

Rabinovitch et al. [24]

PM2.5 = 300

None

Asthmatics

DE exposure associated with changes in CysLTR1 methylation and expression

CysLTR1 may be involved in mechanistic pathway of DE-related lung function decline in asthmatics

Respiratory

Ryu et al. [25]

PM2.5 = 300

Allergen

Atopic + airway hyperresponsive

Atopic + airway normally responsive

Short term exposure to allergen + DE alters lung immune regulatory proteins

Whole DE associated with decreased allergen-induced levels of SPD in airways

Particle depletion restored allergen-induced increase in SPD

Respiratory

Wooding et al. 2020[26]

PM2.5 = 300

None

Healthy never-smokers

Ex-smokers without COPD

Mild-moderate COPD

DE exposure increased neutrophil extracellular traps in lung

DE exposure increased peripheral neutrophil activation in COPD patients

COPD patients may be more susceptible to inflammation post DE exposure

Respiratory

Mookherjee et al. [27]

PM2.5 = 300

Allergen

Atopic + airway hyperresponsive

Atopic + airway normally responsive

Co-exposure to DE and allergen associated with protein changes in lung not detected with DE mono-exposure or allergen alone

Respiratory

Clifford et al. [28]

PM2.5 = 300

Allergen

Atopic, non-asthmatic

Asthmatics

In bronchial epithelium, allergen mono-exposure, DE mono-exposure, or DE + allergen co-exposure induced changes at 7 CpG sites at 48 h post exposure

Exposure to allergen and DE separated by 4 weeks associated with changes in over 500 CpG sites

Changes modified by which exposure occurred first

Respiratory

Kramer et al. [29]

PM2.5 = 300

Allergen

Atopic + airway hyperresponsive

Atopic + airway normally responsive

Co-exposure to DE + allergen may cause protective changes in lung adiponectin

Protective response not observed after allergen mono-exposure or in participants with baseline airway hyperresponsiveness

Respiratory

Carlsten et al. [30]

PM2.5 = 300

Allergen

Atopic + airway hyperresponsive

Atopic + airway normally responsive

DE enhanced allergen-induced increases airway eosinophils, IL-5, and eosinophil cationic protein in atopic volunteers

GSTT1 null genotype significantly associated with enhanced IL-5 response

Respiratory

Hosseini et al. [31]

PM2.5 = 300

Allergen

Atopic + airway hyperresponsive

Atopic + airway normally responsive

In atopic volunteers, allergen + DE co-exposure increased CD4, IL-4, CD138, and neutrophil elastase in respiratory submucosa

Allergen + DE co-exposure did not change eosinophils or mast cells

Respiratory

Behndig et al. [32]a

PM10 = 100

None

Healthy

Mild asthmatics

Moderate asthmatics

Allergic rhinitics, non-asthmatic

DE exposure did not affect markers of proliferation and apoptosis in in the bronchial epithelium of asthmatics, allergic rhinitics, or healthy subjects

Respiratory

Larsson et al. [33]

PM10 = 100

None

Allergic rhinitics

DE exposure did not induce markers of neutrophilic inflammation in the airways of subjects with allergic rhinitics

DE exposure did not increase number of allergic inflammatory cells in airways

DE exposure decreased tryptase in the absence of allergic symptoms

Respiratory

Hussain et al. [34]

PM2.5 = 300

None

Asthmatics

Acute DE exposure increased airway hyperreactivity and obstruction in asthmatic subjects

DE exposure increased nitrite in exhaled breath condensate

Respiratory

Londahl et al. [35]

PM1 = 50, 300 (multi-concentration crossover)

None

Healthy

COPD

Deposited dose rate of inhaled DEP was higher in subjects with COPD compared to healthy subjects

Deposited dose rate increased with increasing disease severity

Respiratory

Behndig et al. [36]

PM10 = 100

None

Healthy

Mild asthmatics

Moderate asthmatics

DE exposure significantly increased neutrophil count, IL-6, and MPO in airways of healthy subjects

No neutrophilic inflammation observed in airways of asthmatic subjects

Respiratory

Sehlstedt et al. [37]

PM10 = 300

None

Healthy

Exposure to DE increased bronchial adhesion molecule expression and bronchoalveolar eosinophil numbers

These effects were found with DE generated from urban running conditions but not with DE from idling conditions

Respiratory

Sawant et al. [38]

PM2 = 100

NO2

Healthy

Asthmatics

Exposure to DE at 100 μg/m3 generated in this facility did not cause significant change in lung function tests

Respiratory

Bosson et al. [39]

PM = 300

O3

Healthy

DE and O3 co-exposure significantly increased sputum MPO and percentage of neutrophils compared to DE mono-exposure

MPO response was significantly associated with neutrophils and with MMP-9

Respiratory

Behndig et al. [40]

PM10 = 100

None

Healthy

DE exposure increased neutrophil and mast cell numbers in bronchial mucosa

DE exposure increased neutrophil numbers, IL-8, and MPO in bronchial lavage

These changes were not observed in alveolar lavage

Respiratory

Pourazar et al. [41]

PM10 = 300

None

Healthy

DE exposure significantly increased IL-13 in bronchial epithelium

DE exposure did not significantly affect IL-10 or IL-18 in bronchial epithelium

Respiratory

Stenfors et al. [42]

PM10 = 100

None

Healthy

Asthmatics

DE exposure increased airway resistance in both healthy and mild asthmatics

DE exposure increased airway neutrophils, leukocytes, and IL-8 in healthy subjects

DE exposure did not induce neutrophilic inflammation or exacerbate pre-existing eosinophilic inflammation in airways of asthmatic subjects

Respiratory

Nordenhall et al. [43]

PM10 = 300

None

Asthmatics

Acute DE exposure significantly increased airway hyperresponsiveness, airway resistance, and sputum IL-6 in asthmatic subjects

DE exposure did not affect sputum methylhistamine, eosinophil cationic protein, MPO, or IL-8

Respiratory

Nightingale et al. [44]

PM10 = 200

None

Healthy

Exposure to resuspended DEP did not affect pulse, BP, or lung function

DEP exposure increased sputum neutrophils, sputum MPO, and exhaled CO

DEP exposure did not affect peripheral blood inflammatory markers

Respiratory

Nordenhall et al. [45]

PM10 = 300

None

Healthy

DE exposure significantly increased sputum neutrophils, IL-6, and methylhistamine

Percentage of sputum neutrophils was significantly increased at 24 h compared to 6 h regardless of exposure condition

Respiratory

Salvi et al. [46]

PM10 = 300

None

Healthy

DE exposure increased IL-8 gene transcription and expression in bronchial tissue

DE exposure increased GRO-α expression in bronchial epithelium

DE exposure did not significantly affect transcription of IL-1b, TNF-α, IFN-y, or GM-CSF in lung

Respiratory

Salvi et al. [47]

PM10 = 300

None

Healthy

DE exposure significantly increased airway neutrophils and B lymphocytes

DE exposure increased neutrophils, mast cells, T lymphocytes, ICAM-1, and VCAM-1 in bronchial tissue

DE exposure significantly increased peripheral blood neutrophils and platelets

Respiratory

Rudell et al. [48]

n/a

None

Healthy

Lung function not affected by DE exposure

DE exposure associated with symptoms such as unpleasant smell, eye irritation, nasal irritation

Respiratory

Tousoulis et al. [49]

PM2.5 = 25

None

Healthy non-smokers

Healthy smokers

Acute DE exposure associated with adverse effects on endothelial function, vascular walls, and heart rate variability even at 24 h post-exposure

DE exposure associated with increased inflammatory markers and abnormal fibrinolytic markers

Cardiovascular

Sack et al. [50]

PM2.5 = 200

Antioxidant

Healthy

DE exposure induced acute vasoconstriction in brachial artery

Pre-treatment with antioxidant enhanced DE-induced vasoconstriction

Cardiovascular

Langrish et al. [51]b

PM10 = 300

Carbon nano-particles

Healthy

Stable CAD with previous myocardial infarction

Acute controlled exposure to air pollutants (including DE and carbon nanoparticles) did not increase the short-term risk of arrhythmia

Cardiovascular

Tong et al. [52]

PM = 100, 200, 300

(single sequence)

None

Healthy

Acute exposure to DE at 300 μg/m3 decreased brachial artery diameter, increased DBP, and induced changes in heart rate variability in GSTM1 null individuals

These cardiovascular changes were concentration dependent

Cardiovascular

Krishnan et al. [53]

PM2.5 = 200

None

Healthy

Metabolic syndrome

Acute DE exposure increased hematocrit and hemoglobin

DE exposure increased platelet count in healthy but not metabolic syndrome volunteers

Levels of IL-1β, IL-6, MPO, and endothelial activation molecules were increased post-DE exposure

Cardiovascular

Langrish et al. [54]

PM10 = 300

NO synthase inhibitor, SNP, ACh

Healthy

DE exposure increased plasma nitrite but this increase was not sufficient to compensate for excess NO consumption

BP and central arterial stiffness were increased by systemic NO synthase inhibitor post DE exposure compared to FA

Cardiovascular

Wauters et al. [55]

PM2.5 = 300

None

Healthy

Acute DE exposure attenuated vasodilation induced by ACh but not SNP

DE exposure increased ROS production in endothelial cells

Cardiovascular

Cosselman et al. [56]

PM2.5 = 200

None

Healthy

Metabolic syndrome

SBP was increased during and post DE exposure, effect not modified by metabolic syndrome

DE exposure did not significantly affect heart rate or DBP

Cardiovascular

Lund et al. [57]

PM = 100

None

Healthy

Acute exposure to DE upregulated atherosclerosis-associated factors such as MMP-9, and ET-1

Effect mediated through oxLDL-LOX-1 receptor signalling

DE exposure significantly increased plasma-soluble LOX-1

Cardiovascular

Mills et al. [58]

PM2 = 300

PM2 = 5 (particle-depleted)

Carbon nano-particles

Healthy

DE exposure increased SBP and attenuated bradykinin/ACh/SNP-induced vasodilation

Exposure to pure carbon nanoparticulate or filtered DE did not affect vasodilation

DEP but not carbon nanoparticulate attenuated vasorelaxation in vitro

Cardiovascular

Mills et al. [59]

PM = 300

None

Healthy

Stable CAD with previous myocardial infarction

Acute DE exposure did not affect heart rhythm or heart rate variability in healthy subjects or subjects stable coronary artery disease

Cardiovascular

Barath et al. [60]

PM10 = 250

None

Healthy

DE exposure impaired vasomotor function and endogenous fibrinolysis

DE generated from transient running conditions and DE from idling produced similar effects

Cardiovascular

Langrish et al. [61]

PM10 = 300

None

Healthy

DE exposure had no effect on plasma ET-1, BP, or heart rate

DE exposure increased vascular sensitivity to ET-1

DE exposure attenuated vasodilation induced by ET(A) receptor antagonism

Cardiovascular

Lund et al. [62]

PM = 100

None

Healthy

Acute DE exposure in humans significantly increased plasma ET-1 and MMP-9 expression and activity

Gasoline engine exhaust increased circulating and vascular factors associated with atherosclerosis in mice

Cardiovascular

Lundback et al. [63]

PM = 350

None

Healthy

DE exposure associated with immediate and transient increase in arterial stiffness

Cardiovascular

Carlsten et al. [64]

PM2.5 = 100, 200 (multi-concentration crossover)

None

Metabolic syndrome

In subjects with metabolic syndrome, DE exposure did not induce significant prothrombotic changes in D-dimer, vWF, and PAI-1

Cardiovascular

Lucking et al. [65]

PM = 350

None

Healthy

DE exposure increased ex vivo thrombus formation and increased in vivo platelet activation

Cardiovascular

Peretz et al. [66]

PM2.5 = 100, 200 (multi-concentration crossover)

None

Healthy

Metabolic syndrome

Acute DE exposure did not have a consistent effect on autonomic control of the heart

Cardiovascular

Peretz et al. [67]

PM2.5 = 100, 200 (multi-concentration crossover)

None

Healthy

Metabolic syndrome

Acute DE exposure at 200 μg/m3 was associated with vasoconstriction of brachial artery and effect may be dose-dependent

Exposure to DE at 200 μg/m3 increased plasma ET-1

Cardiovascular

Carlsten et al. [68]

PM2.5 = 100, 200 (multi-concentration crossover)

None

Healthy

DE exposure at 100 μg/m3 and 200 μg/m3 did not induce significant pro-thrombotic changes in D-dimer, vWF, PAI-1, or platelets

DE exposure did not significantly affect C-reactive protein

Cardiovascular

Mills et al. [69]

PM10 = 300

None

Stable CAD with previous myocardial infarction

In men with previous myocardial infarction, acute DE exposure enhanced ECG changes consistent with myocardial ischemia

DE exposure decreased acute release of endothelial tPA

Cardiovascular

Tornqvist et al. [70]

PM = 300

None

Healthy

DE exposure significantly increased plasma TNF-α and IL-6

DE exposure attenuated ACh and bradykinin-induced vasodilation

DE exposure had no effect on SNP or verapamil-induced vasodilation

Cardiovascular

Mills et al. [71]

PM = 300

None

Healthy

DE exposure attenuated bradykinin, ACh, and SNP-induced vasodilation

DE exposure attenuated bradykinin-induced increase in plasma tPA

Cardiovascular

Cliff et al. [72]

PM2.5 = 300

None

Healthy

Acute DE exposure did not affect IL-6, TNF-a, astrocytic protein S100b, neuronal cytoplasmic enzyme neuron-specific enolase, or serum brain-derived neurotrophic factor

Neurological

Cruts et al. [73]

PM = 300

None

Healthy

DE exposure significantly increased median power frequency in the frontal cortex on quantitative EEG

DE exposure was associated with general cortical stress response

Neurological

Koch et al. [74]

PM2.5 = 300

Inhaled salbutamol

Exercise-induced broncho-constriction

Acute exercise induced microvascular and macrovascular vasodilation

Vasodilatory response preserved with DE exposure

Heart rate significantly increased after DE exposure compared to FA

Exercise

Giles et al. [75]

PM2.5 = 300

None

Healthy

No acute increase in adhesion molecules and inflammatory markers in healthy volunteers during exercise + concomitant DE exposure

Exercise

Giles et al. [76]

PM2.5 = 300

None

Healthy

Exercising during DE exposure significantly increased plasma NOx compared to FA

ET-1 was significantly decreased at 2 h post-DE exposure compared to FA, effect not modified by exercise intensity

No DE-associated changes in FMD or blood pressure

Exercise

Giles et al. [77]

PM2.5 = 300

None

Healthy

Exercise associated with increased FeNO, decreased HRV, and increased plasma norepinephrine

These exercise-induced changes not modified by DE exposure

Exercise

Wauters et al. [78]

PM2.5 = 300

None

Healthy

Exercise during acute DE exposure significantly increased markers of platelet activation (P-selectin and CD63)

Acute DE exposure did not impair platelet aggregation during exercise or rest

Exercise

Wauters et al. [79]

PM2.5 = 300

Dobutamine stress

Exercise in normoxia

Exercise in hypoxia

Healthy

DE exposure during high cardiac output increased pulmonary vascular resistance and decreased distensibility of pulmonary resistive vessels

Exercise

Giles et al. [80]

PM2.5 = 300

None

Healthy

Respiratory and metabolic responses were greater during low intensity exercise compared to high intensity exercise during DE exposure

Exercise

Giles et al. [81]

PM2.5 = 300

None

Healthy

DE exposure significantly decreased exercise-induced bronchodilation

DE exposure significantly increased heart rate during exercise

DE exposure did not significantly impair performance on 20 km cycling time trial

Exercise

Li et al. [82]

PM2.5 = 300

Allergen

Atopic + airway hyperresponsive

Atopic + airway normally responsive

Changes in DNA methylation regulation enzymes are involved in response to allergen challenge

These changes are dependent on airway hyperresponsiveness, irrespective of DE exposure

Co-exposures

Wooding et al. [83]

PM2.5 = 300

PM2.5 = 20

(particle-depleted)

Allergen

Atopic + airway hyperresponsive

Atopic + airway normally responsive

Co-exposure to DE + allergen associated with impaired lung function

Impairment worse with particle depleted, NO2 enriched DE

Co-exposures

Biagioni et al. [84]

PM2.5 = 300

Allergen

Atopic + airway hyperresponsive

Atopic + airway normally responsive

In atopic volunteers, markers of allergic inflammation (SPD and MPO) are increased by allergen exposure but minimally by DE

DE decreases levels of protective protein CC16, while allergen has minimal effect

Co-exposures

Rider et al. [85]

PM2.5 = 300

Allergen

Atopic

DE or allergen exposure significantly modulate expression of miRNA and genes associated with bronchial immune responses in atopic participants

DE did not enhance allergen-associated effects at 48 h

Co-exposures

Zhang et al. 2016 [86]

PM2.5 = 300

Allergen

Atopic + airway hyperresponsive

Atopic + airway normally responsive

FEV1 was significantly decreased post DE and allergen co-exposure in GSTT1 null individuals

Post DE and allergen co-exposure, levels of an oxidative stress marker were higher in GSTT1 null individuals compared to GSTT1 present individuals

Co-exposures

Stiegel et al. [87]

PM = 300

O3

Healthy

DE and O3 co-exposure suppressed plasma IL-5, IL-12p70, IFN-γ, and TNF-α

DE and O3 co-exposure significantly decreased circulating monocytes and lymphocytes, and significantly increased neutrophils

Co-exposures

Madden et al. [88]

PM = 300

O3

Healthy

DE and O3 co-exposure decreased FEV1 in a greater than additive manner compared to DE mono-exposure and O3 mono-exposure

Co-exposures

Barath et al. [89]

PM10 = 300

O3

Healthy

DE exposure increased FeNO compared to FA

O3 exposure did not affect FeNO

Co-exposures

Bosson et al. 2008 [90]

PM10 = 300

O3

Healthy

DE exposure followed by O3 exposure increased number of bronchial neutrophils, number of bronchial macrophages, and eosinophil protein X levels

Co-exposures

Hemmingsen et al. [91]

PM1 = 300

46 dB or 75 dB traffic noise

Healthy

Exposure to DE was not associated with markers of genotoxicity, oxidative stress or inflammation in PBMC

Exposure to traffic noise was associated with markers of DNA damage

Co-exposures

Pawlak et al. [92]

PM = 100

Live attenuated influenza virus

Allergic rhinitics

In volunteers with allergic rhinitis, DE exposure prolongs eosinophil activation induced by influenza virus

DE exposure decreased markers of NK cell activation and recruitment

Co-exposures

Noah et al. [93]

PM = 100

Live attenuated influenza virus

Healthy

Allergic rhinitics

In allergic rhinitis, acute DE exposure increased eosinophil activation and increased virus quantity post inoculation with influenza virus

Co-exposures

Vieira et al. [94]

PM2.5 = 300

PM2.5 = 25 (particle-depleted)

None

Healthy

Heart failure

Compared to unfiltered DE, particle filtered DE reduced markers of endothelial dysfunction and decreased BNP in subjects with heart failure

Filtered DE

Vieira et al. [95]

PM2.5 = 300

PM2.5 = 25 (particle-depleted)

None

Healthy

Heart failure

Acute DE adversely affected markers of exercise capacity in subjects with heart failure

Particle filtered DE mitigated adverse effects of DE exposure on VO2 and O2 pulse

Filtered DE

Muala et al. [96]

PM1 = 350

PM1 = 200

(particle- depleted)

PM1 = 100 (particle- depleted)

None

Healthy

Cabin air inlet particle filter with active charcoal component reduced particulates and gaseous components of DE

Cabin filter reduced DE-associated symptoms

Filtered DE

Lucking et al. [97]

PM = 300

PM = 10 (particle- depleted)

None

Healthy

DE exposure reduced vasodilation and increased ex vivo thrombus formation

Use of particle trap increased vasodilation, reduced thrombus formation, and increased tPA

Filtered DE

Rudell et al. [98]

PM = 300

PM = 200

(particle- depleted)

PM = 100 (particle- depleted)

PM = 150 (particle- depleted)

PM = 150 (particle- depleted)

None

Healthy, not often exposed to DE

Healthy, often exposed to DE

Use of particle filter did not reduce intensity of DE-associated symptoms

Use of charcoal filter together with particle filter reduced intensity of symptoms DE-associated symptoms

Filtered DE

Rudell et al. [99]

n/a

None

Healthy

DE exposure increased neutrophils in airway lavage

DE induced migration of alveolar macrophages into airways

Use of particle trap did not significantly attenuate DE-induced effects

Filtered DE

Rudell et al. [100]

n/a

None

Healthy

DE exposure was associated with irritative symptoms and bronchoconstriction

Use of a particle trap did not significantly attenuate these DE-induced effects

Filtered DE

Gouveia-Figueira et al. [101]

PM10 = 150

None

Healthy

Biodiesel exhaust exposure was associated with changes in levels of some circulating lipid metabolites, mainly monohydroxy fatty acids

Markers and quantification of DE exposure

Gouveia-Figueira et al. [102]

PM = 150

None

Healthy

Exposure to biodiesel exhaust alters levels of biolipids in BW and BAL samples

Exposure to biodiesel exhaust significantly increased levels of PGE2, 12,13-DiHOME, and 13-HODE in BAL samples

Markers and quantification of DE exposure

Lu et al. [103]c

PM1 = 300

PM2.5 = 100

(multiple studies)

46 dB or 75 dB traffic noise

Healthy

Acute DE exposure did not significantly alter levels of urinary PAH

Markers and quantification of DE exposure

Wierzbicka et al. [104]

PM1 = 300

46 dB or 75 dB traffic noise

Healthy

DE characteristics vary greatly even at the same DEP mass concentration

Size dependent effective density prevents overestimation of lung deposited dose

Symptoms of nose and eye irritation were present

Markers and quantification of DE exposure

Rissler et al. [105]

PM10 = 50, 300 (multi-concentration crossover)

None

Healthy

Deposition of DEP was similar to spherical particles if plotted as a function of mobility diameter

Total deposited fraction of DEP is associated with tidal volume and breathing frequency

Lung deposition fractions varies greatly between subjects

Markers and quantification of DE exposure

Huyck et al. [106]

PM10 = 300

None

Healthy

Urine 1-aminopryine can be used as biomarker of DE exposure

There are two subgroups of subjects in terms of timing of 1-aminopryine excretion

Markers and quantification of DE exposure

Hubbard et al. [107]

PM2.5 = 100

None

Healthy

Polar VOC in exhaled breath condensates varied with gender and between healthy subjects

Most polar VOCs likely of endogenous source

Markers and quantification of DE exposure

Laumbach et al. [108]

PM10 = 300

None

Healthy

DE exposure significantly increased urinary 1-aminopryine

Large inter-subject variability in urine 1-aminopryine concentration and time-course of detectability

Markers and quantification of DE exposure

Sawyer et al. [109]

PM2.5 = 100

None

Healthy

DE exposure did not affect volume or total protein concentration of exhaled breath concentrates

Markers and quantification of DE exposure

Sobus et al. [110]

PM2.5 = 100

None

Healthy

Naphthalene and phenanthrene may be useful surrogates for DE concentration

Markers and quantification of DE exposure

Curran et al. [111]

PM2.5 = 300

None

Healthy

Non-significant reduction in postural stability after DE exposure

Other

Carlsten et al. [112]

PM2.5 = 100, 200 (multi-concentration crossover)

Antioxidant

Healthy

Metabolic syndrome

Controlled exposure to DE associated with mild symptoms

Majority of participants will not experience any symptoms

Blinding to DE exposure is effective

Other

Kipen et al. [113]

PM2.5 = 200

Secondary organic aerosol

Healthy

Exposure to DE or secondary organic aerosols induced decline in WBC and RBC proteasome activity

Other

Laumbach et al. [114]

PM2.5 = 300

Psychological stressor task

Healthy

DE exposure was associated with small but significant increases in symptom scores

Psychological stressor did not increase symptom severity

Other

Pleil et al. [115]

PM2.5 = 100

None

Healthy

Heat maps can be used to study existing environmental and biomarker concentrations of PAH

Other

  1. Table is organized by primary topic, then by year (most recent to least recent), then alphabetically by author. Publications categorized under “co-exposure” have been organized by type of co-exposure (eg. allergen, ozone, etc.), then by year and author as above. Target PM concentration used where available—otherwise achieved concentration used instead
  2. Ach acetylcholine, BAL bronchoalveolar lavage, BNP B type natriuretic peptide, BP blood pressure, BW bronchial wash, CAD coronary artery disease, CAP concentrated ambient particles, CC16 club cell secretory protein 16, CO carbon monoxide, COPD chronic obstructive pulmonary disease, CysLTR1 cysteinyl leukotriene receptor 1, DBP diastolic blood pressure, DE diesel exhaust, DEP diesel exhaust particles, 12,13-DiHOME 12,13-dihydroxyoctadecenoic acid, ECG electrocardiogram, EEG electroencephalogram, ET-1 endothelin-1, ET(A) endothelin receptor A, FA filtered air, FeNO fraction of exhaled nitric oxide, FEV1 forced expiratory volume in one second, FMD flow mediated dilation, GM-CSF granulocyte–macrophage colony-stimulating factor, GRO- α growth-regulated oncogene alpha, GSH/GSSG reduced to oxidized glutathione (ratio), 13-HODE 13-hydroxyoctadecadienoic acid, HRV heart rate variability, ICAM-1 intercellular adhesion molecule 1, IFN-γ interferon-gamma, IL interleukin, LOX-1 lectin-like oxidized low density lipoprotein receptor-1, miRNA microRNA, MMP-9 matrix metalloproteinase-9, MPO myeloperoxidase, NK natural killer, NO nitric oxide, NO2 nitrogen dioxide, NOx nitrite and nitrate, O2 pulse oxygen uptake per heartbeat, O3 ozone, oxLDL oxidized low density lipoprotein, PAH polycyclic aromatic hydrocarbons, PAI-1 plasmin activator inhibitor-1, PGE2 prostaglandin E2, PM particulate matter, PM1 PM with aerodynamic diameter under 1 μm, PM2 PM with aerodynamic diameter under 2 μm, PM2.5 PM with aerodynamic diameter under 2.5 μm, PM10 PM with aerodynamic diameter under 10 μm, RBC red blood cells, ROS reactive oxygen species, SBP systolic blood pressure, SNP sodium nitroprusside, SPD surfactant protein D, TNF-α tumor necrosis factor alpha, tPA tissue plasminogen activator, VCAM-1 vascular adhesion molecule 1, VO2 maximal oxygen uptake, VOC volatile organic compounds, vWF von Willebrand factor, WBC white blood cells
  3. aBehndig et al. [32] is a follow-up study to Behndig et al. [36] and Larsson et al. [33] using archived biopsies
  4. bLangrish et al. [51] uses data pooled from multiple publications, including Barath et al. [60], Cruts et al. [73], Mills et al. [59, 69, 71]
  5. cSpecimens used in Lu et al. [103] were derived from the participants in Pleil et al. [115] (EPA study), Hubbard et al. [107] (EPA study), Sobus et al. [110] (EPA study), Sawyer et al. [109] (EPA study), and Wierzbicka et al. [104] (Lund study).