Table 3 Summary of respiratory and immune effects from in vivo models (17 studies)
Reference | Animal model | PM source | Dose | Route | Duration | Offspring effects |
|---|---|---|---|---|---|---|
Hamada et al. [78] | Balb/c mice | Residual oily fish ash | 50 mg/mL | Inhalation | 30 min for 5, 3, or 1 days prior to delivery | Increased airway hyperresponsiveness and elevated levels of eosinophils in BALF; histopathology showed inflammation in lungs and increased IgE and IgG1 antigen-specific antibodies; Th2-skewed immune response |
Fedulov et al. [78] | Balb/c mice | Diesel exhaust | 50 μg/mouse (DEP, CB, or TiO2) | Intranasal | Single nasal insufflation on GD14 | Airway hyperresponsiveness and airway inflammation, suggesting increased susceptibility to asthma |
Mauad et al. [53] | Balb/c mice | PM2.5 | 16.8 +/− 8.3 μg/m3 | Inhalation | 4 months (24 h/day) | Decreased surface to volume ratio; reduced inspiratory and expiratory volumes |
Corson et al. [82] | Balb/c mice | Diesel exhaust particles | Average particle concentration 1.09 mg/m3. | Inhalation | 5 times 4 days apart (before mating), then 2 times after mating | Decrease in IgE production; decrease in pulmonary eosinophils |
Sharkhuu et al. [102] | Balb/c mice | Diesel exhaust | 0, 0.8, 3.1 mg/μL | Inhalation | 10 consecutive days (4 h/day) | Number of neutrophils in BALF and splenic T cells expressing different surface markers were differentially affected by DE concentrations and sex; female offspring exposed to DE prenatally exhibited higher protein levels in the respiratory tract compared to males |
Reiprich et al. [103] | Balb/c mice | Diesel exhaust particles | 20 μg/mouse | Inhalation | GD7 to delivery (10 min 3 times/week) | Increased airway hyperresponsiveness, eosinophilic infiltration, and antigen-specific IgE production; pretreatment with N-acetylcysteine reversed asthmatic phenotype in pollutant-exposed offspring |
Thevenot et al. [72] | C57BL/6J mice or Brown-Norway rats | EPFR (DCB-230) in combustion-generated PM (0.2 μm) | 200 μg/m3 | Inhalation | 7 days (30 min/day) neonatal exposure only | Increased pulmonary pathologies and development of asthma; increased airway hyperresponsiveness |
Wang et al. [104] | C57BL/6J mice | CB-NP (unknown diameter) + MCP-230 | 50 μg/kg BW | Oropharyngeal | GD10 and GD17 (once/day) | MCP-230 exposed dams, offspring have decreased production of T helper and Tregs; Th1 and Th17 cells remained |
Manners et al. [84] | C57BL/6J mice | Diesel exhaust particles | 50 μg/mouse | Intranasal | GD3, 6, 9, 12, 15, 18 (once/day) | Increase airway inflammation and hyperresponsiveness; increase OVA-specific IgE |
Saravia et al. [73] | C57BL/6J mice | CDPM | 200 μg/m3 | Inhalation | 5 days (30 min/day) neonatal exposure only | CDPM+HDM challenged mice exhibited no noticeable asthma phenotype, AHR, Th2 inflammation, eosinophilia, HDM Ig-specific; CDPM induce immunosuppressive environment; CDPM suppression of Th2 response |
Lee et al. [74] | C57BL/6J mice (neonates < 7-day age) | CDPM (0.2 μm); EPFR (DCB-50 and DCB-230) | 200 μg/m3 | Inhalation | 5 days (30 min/day) | Enhanced morbidity and decreased survival; increased oxidative stress; increased pulmonary Tregs during influenza |
El Sayed et al. [105] | ICR mice | CB-NP (14 nm diameter) | 95 μg/kg BW | Intranasal | GD9 and GD15 (once/day) | Increased total thymocytes and immunophenotypes; increase total lymphocytes in male offspring at PND5 exposed to CBNP; upregulation of mRNA expression of genes involved with induction of peripheral tolerance |
Paul et al. [106] | C57BL/6J mice | TiO2, CeO2, Ag nanoparticles (10 nm diameter) | 10 μL of NPs at 10 mg/mL | Intratracheal | GD2.5, GD9.5, and GD16.5 | Offspring lung development was stunted regardless of nanoparticle exposure |
Jaligama et al. [76] | C57BL/6J mice | CDPM (0.2 μm); EPFR (DCB-230) | 200 μg/m3 | Inhalation | 7 days (30 min/day) neonatal exposure only | Increase in Tregs and IL-10; EPFR+ IL-10−/− neonates exhibited reduced morbidity, viral load, and adaptive T cell response after influenza infection |
de Barros et al. [107] | Balb/c mice | PM2.5 | 600 μg/m3 | Inhalation | GD5.5-GD18.5 (1 h/day) | Increased lung elastance and decreased alveolar number in PND40 offspring; lung volume and BALF were not affected; transcriptomic analysis indicated DNA damage, inflammation, and cell proliferation regulation in PND40 exposed offspring |
Tang et al. [94] | Sprague Dawley rats | PM2.5 | 0.1, 0.5, 2.5, 7.5 mg/kg | Intraperitoneal | GD0-GD18 (once every 3 days) | Ground glass opacity and high-density volumes in lungs of exposed neonates; increased pulmonary inflammation in lungs |
Rychlik et al. [68] | C57BL/6J and Balb/c mice | Ultrafine PM | 100 μg/m3 | Inhalation | GD0-GD18 (6 h/day) | Reduced inflammatory response to HDM; lower WBC counts; less peribronchiolar inflammation; C57Bl/6J offspring exposed to UFPs had increased Treg response and decreased Th2/Th17 response |