Table 1.
List of articles from PubMed where PM exposure was performed in mice and rats and the objectives of each study as related by the authors. The dataset includes 30 articles published in 2017 and 45 articles published in previous years.
| Exposure protocols | Objectives | Authors |
|---|---|---|
| CAP inhalation | The objective of this study was to determine whether short-term exposures to concentrated ambient particles alter the morphology of small pulmonary arteries in normal rats and rats with chronic bronchitis (CB). | [15] |
| CAP inhalation | Our objective was to provide experimental plausibility for epidemiological observations by testing the hypothesis that exposure to particulate matter with nominal mean aerodynamic diameters of 2.5 μm or less (PM2.5) during discrete periods of pregnancy results in preterm birth (PTB) and low birth weight (LBW). | [16] |
| CAP inhalation | The objectives of the present study were: 1) to determine whether acute exposure to low levels of particles promotes measurable acute systemic and cardiopulmonary effects; and 2) to assess if the magnitude of the observed alterations is influenced by season. | [17] |
| CAP inhalation | This study investigates the effects of inhaled ammonium sulphate, which is a major compound of inorganic air pollutants in PM2.5, on adult neurogenesis in aged Sprague-Dawley rats. | [18] |
| CAP inhalation | The hypothesis tested was that older animals would exhibit more severe pulmonary inflammation and haematological changes following the CAP exposure when compared to young, normal animals. | [19] |
| CAP inhalation | We evaluated the effects of air pollution on the adrenal cortex using female mice. One group was conditioned daily in a chamber with exposure to particulate matter. | [20] |
| CAP inhalation | Mice were used to investigate the effects of iRhom2 on PM2.5-induced hepatic dyslipidaemia. | [21] |
| CAP inhalation | The present work was designed to: (i) determine whether short-term exposure to concentrated air particles causes pulmonary inflammation in normal rats; (ii) characterize the component(s) of CAP that are significantly associated with the development of the inflammatory reaction; and (iii) define the induction of mediators and other pathophysiological response elements of the lung with CAP exposure. | [22] |
| CAP inhalation | The aim of this study was to investigate the mechanism by which PM2.5 influences the Notch signalling pathway leading to worsening immune disorder and accelerating chronic obstructive pulmonary disease (COPD) development. | [23] |
| CAP inhalation | We investigated the roles of T-helper (Th)1–Th2 cytokines and nasal remodelling after ambient PM2.5 exposure in a rat model of allergic rhinitis. | [13] |
| CAP inhalation | We investigated the in vivo effects of PM2.5 exposure on the inflammatory response, oxidative stress, the enzyme activities of Na + K + -ATPase and Ca2+-ATPase, and the morphology and function of mitochondria in the nasal mucosa of rats. | [24] |
| CAP inhalation | To evaluate the ability of particulate air pollution to promote oxidative stress and tissue damage in vivo, we studied a rat model of short-term exposure to concentrated ambient particles. | [25] |
| CAP inhalation | We conducted a study to compare the inflammatory response of the lung to instilled versus inhaled particles. | [26] |
| CAP inhalation | We have investigated whether long-term inhalation exposure to diesel engine exhaust, a dominant contributor to particulate air pollution in urban environments, can aggravate Alzheimer's Disease (AD)-like effects in female 5X Familial AD (5XFAD) mice and their wild-type female littermates. | [27] |
| CAP inhalation | The aim of this study was to identify the impact of titanium dioxide (TiO2) nanoparticles on inflammasome in a mouse model of allergic asthma. | [28] |
| CAP inhalation | To test the impact of chronic airborne particulate matter exposure on the upper respiratory system in vivo. | [12] |
| CAP inhalation | To determine whether oxidants are implicated in PM-dependent lung inflammation, we tested the ability of N-acetylcysteine (NAC) to prevent lung inflammation in a rat model of short-term exposure to concentrated ambient particles. | [29] |
| CAP inhalation | The objectives of this study were (1) to determine whether short-term exposures to concentrated air particles cause pulmonary inflammation in normal rats and rats with chronic bronchitis (CB); (2) to identify the site within the lung parenchyma where CAP-induced inflammation occurs; and (3) to characterize the component(s) of CAP that is significantly associated with the development of the inflammatory reaction. | [30] |
| CAP inhalation | The objective was to identify and quantify estrogenic receptor-b (ERb), aryl hydrocarbon receptor (AhR), the cytochrome P450 enzymes CYP1A1, 1A2, 1B1, and mucus profile in the nasal epithelium of mice | [31] |
| CAP inhalation | This study evaluated the inflammatory differences in BALB/c mouse males and females in three phases of the estrous cycle that were exposed to ambient air or concentrated ambient particles. | [32] |
| CAP inhalation | The purpose of this study was to determine the respiratory effects of inhaled ultrafine iron particles in rats. | [33] |
| CAP inhalation and intranasal instillation | We compared the physiological consequences of short-term exposure to diesel exhaust via inhalation to those due to exposure to the same diesel exhaust particles suspended in solution and delivered intranasally. | [34] |
| CAP inhalation and intratracheal instillation | The present study was designed to compare intratracheal instillation to inhalation exposure derived health endpoints of acute lung toxicity in the rat that relate to homologous clinical outcomes that have been reported with ambient PM using a well characterized model emission PM, which would have demonstrable and relevant effects at low lung doses by both methods. | [35] |
| CAP inhalation and intratracheal instillation | We used pharmacological strategies to determine whether oxidants are implicated in PM-dependent cardiac dysfunction and whether PM-induced increase in autonomic stimulation on the heart mediates cardiac oxidative stress and toxicity. | [36] |
| EAP inhalation | The aim of this study was to verify the effects of ambient air pollution of São Paulo City on coronary of healthy non-isogenic Swiss mice, chronically exposed since birth until adulthood. | [37] |
| EAP inhalation | We investigated effects of chronic exposure (2 months) to ambient levels of particulate matter on development of protease-induced emphysema and pulmonary remodelling in mice. | [38] |
| EAP inhalation | The aim of the present study was to analyse the effects of air pollution in the city of São Paulo on mouse female fertility. | [39] |
| EAP inhalation | The present study was conducted to a) determine whether short-term exposure to ambient levels of particulate air pollution from vehicles elicits inflammatory responses and lipid peroxidation in rat lungs, and b) determine if intermittent short-term exposures induce some degree of tolerance. | [40] |
| Intranasal instillation | To investigate how the combination of soybean allergens and diesel exhaust particles (DEP) can affect the induction or exacerbation of asthma in a murine model. | [41] |
| Intranasal instillation | We hypothesized that sub-chronic exposure to PM2.5 in HFD-treated mice, susceptible to type 2 diabetes mellitus (T2DM), would also be able to change nutrient metabolism-related tissues (NMRT) cellular antioxidant defense, and the balance between intracellular 70-kDa heat shock proteins (iHSP70) and extracellular 72-kDa heat shock proteins (eHSP72) contents expressed as [eHSP72]/[iHSP70] ratio, predisposing for a major risk of cellular damage and development T2DM. | [42] |
| Intranasal instillation | We assessed the effects of Bufei Huoxue (BFHX) capsules on PM2.5-induced pulmonary inflammation and the underlying mechanisms of action. | [43] |
| Intranasal instillation | This study aimed to investigate the effects of winter and spring particulate matter on airway inflammation and allergies in a mouse asthma model. | [44] |
| Intranasal instillation | This study aimed to investigate the effects of AD on the early stage of antigen sensitization using a mouse model of asthma, as well as the role of leukotrienes (LTs) in antigen-induced airway inflammation potentiated by AD particles. | [45] |
| Intranasal instillation | In order to assess the relationship between PM2.5 exposure and autism spectrum disorder, neonatal male Sprague–Dawley rats were chosen and exposed to PM2.5 by intranasal instillation. | [46] |
| Intranasal instillation | The aim of this work was to evaluate the time changes of systemic markers of oxidative stress and inflammation, after an acute exposure to Residual Oil Fly Ash (ROFA). | [47] |
| Intranasal instillation | Our objective was to analyse air PM from downtown Buenos Aires (UAP-BA) and evaluate its biological impact on normal airways. We studied the inflammatory response to intranasal instillation of UAP-BA in a short-term-exposure mouse model. | [48] |
| Intranasal instillation | We studied lung responses to low doses of urban air particulate matter from Buenos Aires (UAP-BA), with special emphasis on oxidative balance. | [49] |
| Intranasal instillation | The objective was to verify how these organic compartments respond to increasing concentrations of particles of known elemental composition. | [50] |
| Intranasal instillation | The aim of this study was to analyse in vivo the acute biological impact of two environmental particles, urban air particles from Buenos Aires and Residual Oil Fly Ash, on the cardiorespiratory system of middle-aged mice, evaluating oxidative metabolism and inflammation. | [51] |
| Intranasal instillation | We tested the hypothesis that a single acute exposure to low doses of fine particulate matter (PM2.5) may induce functional and histological lung changes and unchain inflammatory and oxidative stress processes. PM2.5 was collected from the urban area of São Paulo city during 24 h and underwent analysis for elements and polycyclic aromatic hydrocarbon contents. | [52] |
| Intranasal instillation | The aim of this study was to evaluate the effects of subchronic exposure to low doses of diesel exhaust particles (DEP) instilled in the respiratory tract of mice. | [53] |
| Intranasal instillation | The therapeutic effects of stemonine on mice with PM2.5-induced COPD were investigated in the present study. | [54] |
| Intranasal instillation | To test our hypothesis that cardiovascular diseases associated with sulphur dioxide (SO2), nitrogen dioxide (NO2), or PM2.5 exposure are the result of increased heart rate (HR), decreased blood pressure (BP) and enhanced systemic inflammation. | [55] |
| Intratracheal instillation | The aim of the present study was to evaluate the effects of PM10 on electrocardiogram (ECG) parameters, blood pressure, lipid peroxidation (MDA), xanthine oxidase, and antioxidant enzyme in healthy rats and also to examine the protective effects of vanillic acid (VA) in this respect. | [56] |
| Intratracheal instillation | This study aims to observe whether the combined treatment with vitamin E (vit E) and omega-3 polyunsaturated fatty acids (U-3 FA) could prevent the fine particulate matter (PM2.5)-induced cardiovascular injury through alleviating inflammation and oxidative stress. | [57] |
| Intratracheal instillation | The purpose of our study is to investigate PM10 sum effects on lungs and extra pulmonary tissues. The aim of this study is to disclose the pulmonary short-term effects and extra-pulmonary translocation of PM10 sum collected in Milano urban centre. | [58] |
| Intratracheal instillation | To assess susceptibility to lung infection following coexposure to particulate matter. | [59] |
| Intratracheal instillation | In this study, we evaluated the primary oxidative stress produced in the lung by crystalline silica (SiO2) in the early phase after SiO2 exposure. The aim of this study is to understand the crystalline SiO2-induced pulmonary oxidative stress in the early phase. | [60] |
| Intratracheal instillation | This study was conducted to investigate the possible protective effects and mechanisms of aspirin, Vitamin C, Vitamin E, or ozone on fertility in female mice treated with PM2.5. | [61] |
| Intratracheal instillation | We investigated the association of the chemical composition and sources of urban air fine (PM2.5−0.2) and coarse (PM10−2.5) particulate samples with the inflammatory activity in the mouse lung. | [62] |
| Intratracheal instillation | This study was undertaken to clarify the effects of Asian sand dust on lung eosinophilia in mice immunized beforehand by ovalbumin (OVA). | [63] |
| Intratracheal instillation | In the present study, urban PM2.5 and coarse particulate matter (CPM) collected during haze events of Northeast China in the winter season were used. The exacerbating effects of PM2.5 and CPM on OVA-induced allergic inflammation in murine lungs were compared to clarify the role of the chemicals and microbial materials in the two types of PM. | [64] |
| Intratracheal instillation | In order to further understand the roles of microRNAs in regulating the imbalance of T-helper 1 (Th1)/T-helper 2 (Th2) differentiation triggered by PM2.5. | [65] |
| Intratracheal instillation | The current study aimed to evaluate the effects of size-fractioned PM on lung immune responses in healthy BALB/c mice. | [66] |
| Intratracheal instillation | we investigated whether exposure to PM2.5, a PM with an aerodynamic diameter of less than 2.5 mm, enhances inflammation-related toxicity in the human respiratory system through activation of the epidermal growth factor receptor (EGFR) signalling pathway. | [67] |
| Intratracheal instillation | This study investigated the effect of acute respiratory exposure to PM on eyes, as induction of retinal thickening. | [68] |
| Intratracheal instillation | We investigated whether PM instillation in the airway could alter the course of acute lung injury, using a murine model with experimental lung injury induced by intratracheal lipopolysaccharide (LPS) challenge. | [69] |
| Intratracheal instillation | The objective is to investigate the influence of PM2.5 exposure on peripheral blood lymphocyte subsets in pregnant mice and the antagonism of quercetin on adverse effects induced by PM2.5 exposure. | [70] |
| Intratracheal instillation | We intend to investigate the toxic effects of PM2.5 during summer and winter on reproductive cells and tissues and focus on endoplasmic reticulum stress (ERS) to illustrate the possible molecular mechanisms. | [71] |
| Intratracheal instillation | We wished to investigate the impact of PM2.5 on placenta and prenatal outcomes and its related mechanisms in a rat model. | [72] |
| Intratracheal instillation | We assessed the effect of prolonged exposure to diesel exhaust particles (DEP) on chronic renal failure induced by adenine, which is known to involve inflammation and oxidative stress. | [73] |
| Intratracheal instillation | To evaluate the effect of airborne particulate matter 2.5 (PM2.5) in winter on airway inflammation, water-soluble supernatant (Sup) and water-insoluble precipitate (Pre) in PM2.5 were inoculated in NC/Nga mice with high sensitivity to mite allergens. | [74] |
| Intratracheal instillation | To evaluate the allergic effect of airborne particulate matter (PM) on the airway, separated soluble supernatant (Sup) and insoluble precipitate (Pre) in suspended PM were inoculated into NC/Nga mice with a high sensitivity for mite allergens. | [75] |
| Intratracheal instillation | The allergic inflammatory effects of particulate matter PM2.5, collected with the cyclone system in Yokohama city in Japan, were investigated in NC/Nga mice. | [2] |
| Intratracheal instillation | We aimed to explore the toxic mechanisms of cardiovascular injuries induced by ambient fine particulate matter (PM2.5) in atherosclerotic-susceptible ApoE−/− mice. | [76] |
| Intratracheal instillation | We investigated by the optical microscopy some cytological characteristics of the bronchoalveolar lavage fluid cell population 24 h after intratracheal instillation of microscale manganese dioxide (MnO2) and barium chromate (BaCrO4) particles (separately or together at two different doses) into the lungs of Wistar rats. | [77] |
| Intratracheal instillation | The aim of this study is to disclose short-term adverse effects on respiratory and cardiovascular systems induced by winter fine particles exposure. | [78] |
| Intratracheal instillation | The immune cells, including pulmonary macrophages of Sprague–Dawley (SD) rats and Raw 264.7 cells, were applied to further investigate the effect of PM2.5 on cell autophagy of macrophages, thus clarified the possible molecular mechanism of immunotoxicity caused by PM2.5. | [79] |
| Intratracheal instillation | We hypothesized that mechanisms independent of inflammation contribute to accelerated thrombus formation following exposure to diesel exhaust particles (DEP). | [80] |
| Intratracheal instillation | The primary objective of this study was to provide insights on the factors affecting the toxicological potency of exhaust PM emitted from different light-duty vehicles. This study presents different research techniques linked together to improve our understanding of the particulate matter (PM) impacts on health. The study develops conceptual dose–response functions for the different vehicle configurations. | [81] |
| Intratracheal instillation | In order to understand the comprehensive pulmonary response to PM2.5 stress, a non-targeted high-throughput metabolomics strategy was adopted to characterize the overall metabolic changes and relevant toxicological pathways. | [82] |
| Intratracheal instillation | We constructed a rat model to investigate the roles of autophagy in blood-testis barrier (BTB) toxicity induced by PM2.5. Sprague–Dawley rats were developmentally exposed to normal saline (NS) or PM2.5 with the doses via intratracheal instillation. | [83] |
| Intratracheal instillation | Short- and long-term exposure to particulate matter (PM) 2.5 instigates adverse health effect upon the cardiovascular system. We demonstrated that Wuhan PM2.5 exposure induced elevation of systemic Angiotensin II (ANGII) and local angiotensin-converting enzyme (ACE)/ANGII/ANGII type 1 receptor (AT1R) axis activation and the subsequent oxidative stress and proinflammatory responses in the vascular endothelium. | [84] |
| Intratracheal instillation | In order to investigate the mechanisms in PM2.5 toxicity, we explored the endogenous metabolic changes and possible influenced metabolic pathways in rats after intratracheal instillation of PM2.5. | [85] |
| Intratracheal instillation | The aim of this study was to evaluate the inflammatory response to SiO2 nanoparticles using in vivo test systems. | [86] |
EAP: environmental air PM, CAP: concentrated air PM.