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 |