Skip to main content

Table 3 Summary of respiratory and immune effects from in vivo models (17 studies)

From: Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter

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
  1. BALF bronchoalveolar lavage fluid, DE diesel exhaust, HDM house dust mite, UFPs ultrafine particles, GD gestational day, CDPM combustion-derived PM, EPFR environmentally persistent free radicals