Biological effects of diesel exhaust particles (DEP). II. Acute toxicity of DEP introduced into lung by intratracheal instillation

Aggravating Impact of Nanoparticles on Immune-Mediated Pulmonary Inflammation

“…In addition, one intriguing aspect of the epidemiologic data is that health effects of PM 2.5 are primarily seen in subjects with predisposing factors, including pneumonia, asthma, chronic obstructive pulmonary disease, compromised immune systems, atherosclerosis, age over 65 years, and possible depressive state [3,4,5,6]. Partially consistent with the epidemiological studies, we and others have experimentally demonstrated that diesel exhaust particles (DEP), major contributors to environmental PM 2.5 in urban areas, exhibit respiratory toxicity with or without predisposing pathologies, including allergic asthma, pulmonary emphysema, and acute renal failure (although we did not provide evidence that DEP significantly exacerbated a murine model of pulmonary emphysema in our system [7]) in vivo [8,9,10,11,12,13,14,15,16].…”

Aggravating Impact of Nanoparticles on Immune-Mediated Pulmonary Inflammation

“…In addition, one intriguing aspect of the epidemiologic data is that health effects of PM 2.5 are primarily seen in subjects with predisposing factors, including pneumonia, asthma, chronic obstructive pulmonary disease, compromised immune systems, atherosclerosis, age over 65 years, and possible depressive state [3,4,5,6]. Partially consistent with the epidemiological studies, we and others have experimentally demonstrated that diesel exhaust particles (DEP), major contributors to environmental PM 2.5 in urban areas, exhibit respiratory toxicity with or without predisposing pathologies, including allergic asthma, pulmonary emphysema, and acute renal failure (although we did not provide evidence that DEP significantly exacerbated a murine model of pulmonary emphysema in our system [7]) in vivo [8,9,10,11,12,13,14,15,16].…”

Facilitating Effects of Nanoparticles/Materials on Sensitive Immune-Related Lung Disorders

“…In addition, one intriguing aspect of the epidemiologic data is that health effects of PM 2.5 are primarily seen in subjects with predisposing factors, including pneumonia, asthma, chronic obstructive pulmonary disease, compromised immune systems, atherosclerosis, age over 65 years old, and maybe depressive states [3][4][5][6]. Partially consistent with the epidemiological studies, we and others have experimentally demonstrated that diesel exhaust particles (DEP), major contributors to environmental PM 2.5 in urban areas, exhibit respiratory toxicity with or without predisposing pathologies including allergic asthma, pulmonary emphysema, and acute renal failure in vivo [7][8][9][10][11][12][13][14][15].…”

In Vivo Hypersensitive Pulmonary Disease Models for Nanotoxicity

“…Moreover, one intriguing aspect of the epidemiological data is that health effects of PM 2.5 are primarily seen in subjects with predisposing factors, including pneumonia, asthma, chronic obstructive pulmonary disease, compromised immune systems, or aged over 65 years old (Dockery et al, 1993). Consistent with the epidemiological studies, we have experimentally demonstrated that diesel exhaust particles (DEPs), major contributors to environmental PM 2.5 in urban areas, exhibit respiratory toxicity with or without predisposing factors in vivo (Ichinose et al, 1995Takano et al, 1997Takano et al, , 2002.…”

Aggravating Impact of Nanoparticles on Immune-Mediated Pulmonary Inflammation

“…In addition, one intriguing aspect of the epidemiologic data is that health effects of PM 2.5 are primarily seen in subjects with predisposing factors, including pneumonia, asthma, chronic obstructive pulmonary disease, compromised immune systems, atherosclerosis, age over 65 years, and possible depressive state [3,4,5,6]. Partially consistent with the epidemiological studies, we and others have experimentally demonstrated that diesel exhaust particles (DEP), major contributors to environmental PM 2.5 in urban areas, exhibit respiratory toxicity with or without predisposing pathologies, including allergic asthma, pulmonary emphysema, and acute renal failure (although we did not provide evidence that DEP significantly exacerbated a murine model of pulmonary emphysema in our system [7]) in vivo [8,9,10,11,12,13,14,15,16].…”

Facilitating Effects of Nanoparticles/Materials on Sensitive Immune-Related Lung Disorders

“…In addition, one intriguing aspect of the epidemiologic data is that health effects of PM 2.5 are primarily seen in subjects with predisposing factors, including pneumonia, asthma, chronic obstructive pulmonary disease, compromised immune systems, atherosclerosis, age over 65 years old, and maybe depressive states [3][4][5][6]. Partially consistent with the epidemiological studies, we and others have experimentally demonstrated that diesel exhaust particles (DEP), major contributors to environmental PM 2.5 in urban areas, exhibit respiratory toxicity with or without predisposing pathologies including allergic asthma, pulmonary emphysema, and acute renal failure in vivo [7][8][9][10][11][12][13][14][15].…”

In Vivo Hypersensitive Pulmonary Disease Models for Nanotoxicity

“…Moreover, one intriguing aspect of the epidemiological data is that health effects of PM 2.5 are primarily seen in subjects with predisposing factors, including pneumonia, asthma, chronic obstructive pulmonary disease, compromised immune systems, or aged over 65 years old (Dockery et al, 1993). Consistent with the epidemiological studies, we have experimentally demonstrated that diesel exhaust particles (DEPs), major contributors to environmental PM 2.5 in urban areas, exhibit respiratory toxicity with or without predisposing factors in vivo (Ichinose et al, 1995Takano et al, 1997Takano et al, , 2002.…”

Aggravating Impact of Nanoparticles on Immune-Mediated Pulmonary Inflammation

“…In addition, one intriguing aspect of the epidemiologic data is that health effects of PM 2.5 are primarily seen in subjects with predisposing factors, including pneumonia, asthma, chronic obstructive pulmonary disease, compromised immune systems, atherosclerosis, age over 65 years, and possible depressive state [3,4,5,6]. Partially consistent with the epidemiological studies, we and others have experimentally demonstrated that diesel exhaust particles (DEP), major contributors to environmental PM 2.5 in urban areas, exhibit respiratory toxicity with or without predisposing pathologies, including allergic asthma, pulmonary emphysema, and acute renal failure (although we did not provide evidence that DEP significantly exacerbated a murine model of pulmonary emphysema in our system [7]) in vivo [8,9,10,11,12,13,14,15,16].…”

Facilitating Effects of Nanoparticles/Materials on Sensitive Immune-Related Lung Disorders

“…In addition, one intriguing aspect of the epidemiologic data is that health effects of PM 2.5 are primarily seen in subjects with predisposing factors, including pneumonia, asthma, chronic obstructive pulmonary disease, compromised immune systems, atherosclerosis, age over 65 years old, and maybe depressive states [3][4][5][6]. Partially consistent with the epidemiological studies, we and others have experimentally demonstrated that diesel exhaust particles (DEP), major contributors to environmental PM 2.5 in urban areas, exhibit respiratory toxicity with or without predisposing pathologies including allergic asthma, pulmonary emphysema, and acute renal failure in vivo [7][8][9][10][11][12][13][14][15].…”

In Vivo Hypersensitive Pulmonary Disease Models for Nanotoxicity

“…Moreover, one intriguing aspect of the epidemiological data is that health effects of PM 2.5 are primarily seen in subjects with predisposing factors, including pneumonia, asthma, chronic obstructive pulmonary disease, compromised immune systems, or aged over 65 years old (Dockery et al, 1993). Consistent with the epidemiological studies, we have experimentally demonstrated that diesel exhaust particles (DEPs), major contributors to environmental PM 2.5 in urban areas, exhibit respiratory toxicity with or without predisposing factors in vivo (Ichinose et al, 1995Takano et al, 1997Takano et al, , 2002.…”