Effects of inhaled tier-2 diesel engine exhaust on immunotoxicity in a rat model: A hazard identification study. Part II. Immunotoxicology
Diesel exhaust (DE) is an air pollutant containing gaseous compounds and particulate matter. Diesel engines are common on gas extraction and oil sites, leading to complex DE exposure to a broad range of compounds through occupational settings. The US EPA concluded that short-term exposure to DE lead...
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| Format: | Article |
| Language: | English |
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Elsevier
2024-06-01
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| Series: | Toxicology Reports |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2214750024000040 |
| _version_ | 1797350894232141824 |
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| author | Lisa M. Weatherly Hillary L. Shane Rachel Baur Ewa Lukomska Walter McKinney Jenny R. Roberts Jeffrey S. Fedan Stacey E. Anderson |
| author_facet | Lisa M. Weatherly Hillary L. Shane Rachel Baur Ewa Lukomska Walter McKinney Jenny R. Roberts Jeffrey S. Fedan Stacey E. Anderson |
| author_sort | Lisa M. Weatherly |
| collection | DOAJ |
| description | Diesel exhaust (DE) is an air pollutant containing gaseous compounds and particulate matter. Diesel engines are common on gas extraction and oil sites, leading to complex DE exposure to a broad range of compounds through occupational settings. The US EPA concluded that short-term exposure to DE leads to allergic inflammatory disorders of the airways. To further evaluate the immunotoxicity of DE, the effects of whole-body inhalation of 0.2 and 1 mg/m3 DE (total carbon; 6 h/d for 4 days) were investigated 1-, 7-, and 27-days post exposure in Sprague-Dawley rats using an occupationally relevant exposure system. DE exposure of 1 mg/m3 increased total cellularity, number of CD4+ and CD8+ T-cells, and B-cells at 1 d post-exposure in the lung lymph nodes. At 7 d post-exposure to 1 mg/m3, cellularity and the number of CD4+ and CD8+ T-cells decreased in the LLNs. In the bronchoalveolar lavage, B-cell number and frequency increased at 1 d post-exposure, Natural Killer cell number and frequency decreased at 7 d post-exposure, and at 27 d post-exposure CD8+ T-cell and CD11b+ cell number and frequency decreased with 0.2 mg/m3 exposure. In the spleen, 0.2 mg/m3 increased CD4+ T-cell frequency at 1 and 7 d post-exposure and at 27 d post-exposure increased CD4+ and CD8+ T-cell number and CD8+ T-cell frequency. B-cells were the only immune cell subset altered in the three tissues (spleen, LLNs, and BALF), suggesting the induction of the adaptive immune response. The increase in lymphocytes in several different organ types also suggests an induction of a systemic inflammatory response occurring following DE exposure. These results show that DE exposure induced modifications of cellularity of phenotypic subsets that may impair immune function and contribute to airway inflammation induced by DE exposure in rats. |
| first_indexed | 2024-03-08T12:52:36Z |
| format | Article |
| id | doaj.art-a4ede1df3f0d4d928a9d8883e6d96756 |
| institution | Directory Open Access Journal |
| issn | 2214-7500 |
| language | English |
| last_indexed | 2024-03-08T12:52:36Z |
| publishDate | 2024-06-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Toxicology Reports |
| spelling | doaj.art-a4ede1df3f0d4d928a9d8883e6d967562024-01-20T04:45:36ZengElsevierToxicology Reports2214-75002024-06-0112135147Effects of inhaled tier-2 diesel engine exhaust on immunotoxicity in a rat model: A hazard identification study. Part II. ImmunotoxicologyLisa M. Weatherly0Hillary L. Shane1Rachel Baur2Ewa Lukomska3Walter McKinney4Jenny R. Roberts5Jeffrey S. Fedan6Stacey E. Anderson7Correspondence to: Allergy and Clinical Immunology Branch National Institute for Occupational Safety and Health (NIOSH), 1000 Frederick Lane, Morgantown, WV 26508, USA; Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USAHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USAHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USAHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USAHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USAHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USAHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USAHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USADiesel exhaust (DE) is an air pollutant containing gaseous compounds and particulate matter. Diesel engines are common on gas extraction and oil sites, leading to complex DE exposure to a broad range of compounds through occupational settings. The US EPA concluded that short-term exposure to DE leads to allergic inflammatory disorders of the airways. To further evaluate the immunotoxicity of DE, the effects of whole-body inhalation of 0.2 and 1 mg/m3 DE (total carbon; 6 h/d for 4 days) were investigated 1-, 7-, and 27-days post exposure in Sprague-Dawley rats using an occupationally relevant exposure system. DE exposure of 1 mg/m3 increased total cellularity, number of CD4+ and CD8+ T-cells, and B-cells at 1 d post-exposure in the lung lymph nodes. At 7 d post-exposure to 1 mg/m3, cellularity and the number of CD4+ and CD8+ T-cells decreased in the LLNs. In the bronchoalveolar lavage, B-cell number and frequency increased at 1 d post-exposure, Natural Killer cell number and frequency decreased at 7 d post-exposure, and at 27 d post-exposure CD8+ T-cell and CD11b+ cell number and frequency decreased with 0.2 mg/m3 exposure. In the spleen, 0.2 mg/m3 increased CD4+ T-cell frequency at 1 and 7 d post-exposure and at 27 d post-exposure increased CD4+ and CD8+ T-cell number and CD8+ T-cell frequency. B-cells were the only immune cell subset altered in the three tissues (spleen, LLNs, and BALF), suggesting the induction of the adaptive immune response. The increase in lymphocytes in several different organ types also suggests an induction of a systemic inflammatory response occurring following DE exposure. These results show that DE exposure induced modifications of cellularity of phenotypic subsets that may impair immune function and contribute to airway inflammation induced by DE exposure in rats.http://www.sciencedirect.com/science/article/pii/S2214750024000040Diesel exhaustImmunotoxicityImmunomodulationImmune phenotypingWhole-body inhalation |
| spellingShingle | Lisa M. Weatherly Hillary L. Shane Rachel Baur Ewa Lukomska Walter McKinney Jenny R. Roberts Jeffrey S. Fedan Stacey E. Anderson Effects of inhaled tier-2 diesel engine exhaust on immunotoxicity in a rat model: A hazard identification study. Part II. Immunotoxicology Toxicology Reports Diesel exhaust Immunotoxicity Immunomodulation Immune phenotyping Whole-body inhalation |
| title | Effects of inhaled tier-2 diesel engine exhaust on immunotoxicity in a rat model: A hazard identification study. Part II. Immunotoxicology |
| title_full | Effects of inhaled tier-2 diesel engine exhaust on immunotoxicity in a rat model: A hazard identification study. Part II. Immunotoxicology |
| title_fullStr | Effects of inhaled tier-2 diesel engine exhaust on immunotoxicity in a rat model: A hazard identification study. Part II. Immunotoxicology |
| title_full_unstemmed | Effects of inhaled tier-2 diesel engine exhaust on immunotoxicity in a rat model: A hazard identification study. Part II. Immunotoxicology |
| title_short | Effects of inhaled tier-2 diesel engine exhaust on immunotoxicity in a rat model: A hazard identification study. Part II. Immunotoxicology |
| title_sort | effects of inhaled tier 2 diesel engine exhaust on immunotoxicity in a rat model a hazard identification study part ii immunotoxicology |
| topic | Diesel exhaust Immunotoxicity Immunomodulation Immune phenotyping Whole-body inhalation |
| url | http://www.sciencedirect.com/science/article/pii/S2214750024000040 |
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