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. 2018 Jul 1;15(7):1380. doi: 10.3390/ijerph15071380

Table 2.

Summary of in vivo studies on health effects of PM2.5.

Health Effects Animal Models PM2.5 Dosage Methods of PM2.5 Treatment Study Findings and/or Conclusion Reference
Respiratory diseases C57BL/6 mice 5 and 15 μg/mouse Instillation Low doses of PM2.5 may simulate histological and functional changes in lung tissue, but do not impact oxidative stress and inflammations. Acute PM2.5 exposure enhances pulmonary oxidative stress, inflammatory responses, and deteriorated pulmonary impedance. [106]
6 h/day, 5 days/week for 5, 14, and 21 days Inhalation PM2.5 induces MCP-1 and neutrophils levels in pulmonary inflammation. [107]
6.25 mg/kg/day, once a day for 3 days Instillation ACE2 deficiency enhances inflammatory responses and tissue remodeling through p-STAT3 and p-ERK1/2 signaling pathways in PM2.5-induced acute lung injury. [108]
2.5, 5, and 10 mg/kg/mouse Instillation Acute PM2.5 exposure triggered the Th2-mediated immune response and leads to locally and systemically acute inflammations in mice. [109]
Wistar rats 0.3, 1.0, and 3.0 μg /mL Instillation PM2.5 upregulates endothelin A receptors and endothelin B receptors, and are associated with JNK and p38 pathways and MEK1/2 and p38 pathways in rat bronchi. [110]
0.4 mg/mL/rat Inhalation PM2.5 can significantly enhance changes of Cyclin-dependent kinase 2 and p53 in the early phase, cyclin B and Cell Cycle Controller 2 in mid-term, and p21 in long-term exposure. [111]
8 mg/rat Instillation PM2.5 exposure significantly induces the expression level of SOD, IL-6 and IL-8, and neutrophil under cold stress. [112]
0.3, 0.75, 2, and 5 mg/rat Instillation PM2.5 can induce the inflammation response and reduce the phagocytic activity of alveolar macrophages, resulting in lung injuries in female rats. [113]
0.375, 1.5, 6.0, and 24.0 mg/kg (body weight) Inhalation PM2.5-induced pathological injury is related to ROS production, mitochondrial fusion–fission dysfunction, mitochondrial lipid peroxidation, and abnormal cellular homeostasis [114]
0.1, 0.5, 2.5, and 7.5 mg/kg Intraperitoneal instillation Maternal PM2.5 may upregulate the epithelial-mesenchymal transition ion through the TGF-β/Smad3 signaling pathway in postnatal pulmonary dysfunction. [115]
Cardiovascular dysfunction Balb/c mice 10 mg/kg Instillation PM2.5 increases T helper 17-mediated viral replication, perforin response, and imbalance of MMP-2/TIMP-1 in virus-induced myocarditis. [123]
10 mg/kg Instillation PM2.5 induces T regulatory cells (Treg) responses in virus-induced myocarditis. [124]
0.3 mg/mouse Instillation PM2.5 exposure induces HO-1, ET-1, Cyp1A1, Cyp1B1 myeloperoxidase, and Hsp70 levels of lung and heart. [125]
Apoe(-/-) mice 6 h/day, 5 days/week for 6 months Inhalation Ni and P of PM2.5 may correlate with heart rate and heart rate variability. Long-range transported PM2.5 may positively associate with heart rate and negatively with heart rate variability. [126]
3, 10, and 30 mg/kg Instillation PM2.5 can significantly enhance malondialdehyde and reduce heart rate variability in atherosclerosis. [127]
24 h/day, 7 days/week, for 2 months Inhalation PM2.5 can upregulate the visfatin to activate the inflammation, oxidative stress and accelerate the atherosclerosis. [128]
6 h/day, 5 days/week for 3 months Inhalation PM2.5 induces CD36-dependent 7-ketocholesterol accumulation in macrophages on the progression of atherosclerosis. [129]
Kkay mice 6 h/day, 5 day/week for 8 weeks Inhalation IKK/NFκB pathway also plays a critical role in mediating PM2.5-related cardiovascular impairment in a type 2 diabetes mellitus mice model. [130]
Wistar rats 0.2, 0.8, and 3.2 mg/rat Instillation PM2.5 alone exposure induces inflammation, endothelial function, and ANS injuries, and ozone potentiated these effects induced by PM2.5. [131]
SD rats 10 h/day for 4 or 5 consecutive days Inhalation PM2.5 exposure depresses cardiovascular system with diet-induced metabolic syndrome. [132]
0.375, 1.5, 6, and 24 mg/kg Instillation PM2.5 induces oxidative stress, inflammation, and calcium homeostasis disorder, resulting in mitochondrial damage. [133]
0, 0.3, 1, and 3 mg/mL for 24 h Instillation PM2.5 induces the endothelin B and endothelin A receptor upregulation via the MEK/ERK1/2 pathway in rat coronary arteries. [134]
10 mg/mL/day for 7 days Nasal Inoculation PM2.5 might exaggerate neurobehavioral alterations that are associated with astrocytes activation and inflammatory reactions in ischemic stroke of SD male rats. [135]
Diabetes mellitus C57BL/6 mice 6 h/day, 5 days/week for 10 months Inhalation Chronic PM2.5 exposure enhances gene expression, mitochondrial alterations, and oxidative stress in brown and white adipose tissues. [141]
6 h/day, for 9 or 30 consecutive days Inhalation PM2.5 induces NF-κB-related inflammasome activation and vascular insulin resistance leads to peripheral blood and bone marrow endothelial progenitor cells level recovery. [142]
6 h/day, 5 days/week for 10 months Inhalation Chronic PM2.5 exposure induces macrophage infiltration and Unfolded Protein Response in white adipose tissue. [143]
6 h/day, 5 days/week for 17 weeks Inhalation PM2.5 enhances insulin resistance through regulation of hepatic lipid metabolism, visceral adipose tissue inflammatory responses, and glucose utilization in skeletal muscle through both CCR2-dependent and -independent pathways in HFD-fed mice. [144]
B6.129SF2/J mice 5 μg/day/mouse for 12 weeks Instillation PM2.5 promotes [eHsp72]/[iHsp70] and the cell stress response, leading to an increased risk of metabolic dysfunction and type 2 diabetes mellitus in HFD-fed mice [145]
SD rats 24 h/day, 7 days/week, for 16 weeks. Inhalation PM2.5 exposure significantly elevates the levels of glycated hemoglobin A1c, IL-6, and fibrinogen, which lead to the deterioration of tubular injury, glomerulosclerosis, aortic medial thickness, and focal myocarditis in the kidney and heart. [146]
5 h/day for 3 days Inhalation PM2.5 exposure increases the angiotensin/bradykinin systems, immune, and antioxidant imbalance in early kidney damage. [147]
3 and 30 μg/mouse Instillation Long-Term PM2.5 increases blood pressure by inhibition of the D1 receptor through regulation of the G protein-coupled receptor, kinase 4 [148]
15 mg/kg, cumulative dose is 30 mg/kg Instillation PM2.5 reduces levels of GSH-Px and induced malondialdehyde, resulting in an oxidative response and inflammation in the pancreas, and pancreatic GLUT2 levels declined. [149]
Allergic sensitization NC/Nga mice Supernatant fraction: 50 μg; precipitate fraction: 200 μg Nasal Inoculation PM2.5 can enhance airway hyperresponsivness in mice through an inflammasome activation and synergistic action of insoluble and soluble fractions of PM2.5. [155]
Balb/c mice 1, 10, and 100 μg/mouse Instillation PM2.5 can synergize with allergens to exacerbate the progression of asthma via activation of the Th2-related immune response. [156]
100 μg/mouse Intraperitoneal injection PM2.5 and formaldehyde co-exposure can induce oxidative stress to significantly exacerbate allergic asthma via the transient receptor potential vanilloid 1 pathway. [157]
10, 31.6, or 100 µg/mouse Instillation PM2.5 exacerbates allergic airway inflammation via thymic stromal lymphopoietin activation. [158]
33.3 µg/mouse Instillation PM2.5 and allergens from dust mites enhance the hyper-responsiveness of the airway through the activation of T-helper cell type 17 activation. [159]
Guinea pig 1.1 ± 0.2 kg/chamber Inhalation Acute PM2.5 exposure with aluminum hydroxide in sensitized animals enhances the specific-hyperresponsiveness and eosinophilic and neutrophilic airway inflammation in allergic asthma. [160]