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ABSTRACT: In order to explore the potential mechanism that animals with cardiopulmonary diseases were more susceptible than healthy animals, the spontaneously hypertensive rats (SHR) as a model of human cardiovascular disease were used. SHR and wistar kyoto rats (WKY) were exposed by intratracheal instillation to fine particles with the doses of 0.0 (saline), 1.6, 8.0 and 40.0mg/kg body weight, respectively. The exposure was done once a day, for three continuous days. The rats were killed after 24h following the last exposure, followed by analysis of bronchoalveolar lavage fluid (BALF) to estimate the lung injury. Meantime, parameters of oxidative stress, cytokines and cell surface receptors related to inflammation and anti-inflammation were also measured. The results showed that lactate dehydrogenase (LDH) activity, percentages of neutrophils and lymphocytes, and expression of TBA-reactive substances and cytokines (IL-1beta, TNF-alpha, MIP-2, OPN, NF-kappaB, CC16 and HO-1) and cell surface receptors (CD44 and TLR-4) were increased in rats, but percentage of macrophages decreased. Meanwhile, at the same dose exposed, the levels of those parameters were higher in SHR than that in WKY rats. The results indicated that inflammation might be one of the mechanisms of lung injury induced by fine particles. Results of comparisons of different response to fine particles between SHR and WKY rats suggested that lung injury induced by fine particles was greater in SHR than that in WKY rats.
Toxicology Letters 08/2007; 171(3):126-37. · 3.23 Impact Factor
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ABSTRACT: Study adverse effects of volatile organic compounds volatile organic compounds (VOCs) on brain amino acid neurotransmitter in mice.
Four groups of mouse were respectively exposed to 0, low, middle and high concentration of VOCs for two hours every day for 30 days. The content of brain amino acid neurotransmitter was determined.
The result showed that the content of Glu and ASP in brain of VOCs -exposed mouse decreased and GABA and Gly increased compared with that of control.
The memory impair in mice induced by exposing VOCs may relate to the chang of content of amino acid neurotransmitter.
Wei sheng yan jiu = Journal of hygiene research 06/2007; 36(3):269-72.
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ABSTRACT: Explore the adverse impact of ambient particulate matter pollution on human health.
Generalized additive model (GAM) extended poisson regression was used to examined the exposure--response relationship between ambient PM10, PM2.5 pollution and daily mortality in a district in Shanghai. Regression analyses was used for analysis with adjustment for controlling time trends, weather, season, the day of the week.
A 10 micrograms/m3 increase in PM10, and PM2.5 were associated with 0.53% (0.22%-0.85%), 0.85% (0.32%-1.39%) increase in total daily mortality respectively.
Ambient particulate pollution has potential acute adverse health effects on human.
Wei sheng yan jiu = Journal of hygiene research 06/2004; 33(3):293-7.
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ABSTRACT: In order to study the acute toxicity of PM2.5 and to explore the role of immunoreaction and oxidative stress in mouse pulmonary acute injury induced by PM2.5.
Kunming mice were randomly divided into five groups including blank control group, saline control group, three level PM2.5 (low, middle and high) groups. Three level PM2.5 groups were inoculated with suspensions of PM2.5 via trachea for 24 hours and saline control group were inoculated saline, Pulmonary pathological injury and bronchoalveolar lavage fluid (BALF) of all mice were later examined, including the level of LDH, AKP, ACP, ALB, NO, NOS, MDA, SOD, activities of TNF-alpha, IL-1 and phagocytosis of Alveolar macrophages (AM).
The amount of LDH, AKP, ACP, ALB, NO, NOS, MDA and activities of TNF-alpha, IL-1 in exposed groups were significantly higher than those in control(P < 0.05), and at the same time the amount of SOD and phagocytosis of AM decreased significantly (P < 0.05). Dose-response relationships were observed in all indexes.
Air-borne PM2.5 could have acute toxic effects on mouse pulmonary cells and membrane tissues via immunotoxicity and oxidative stress injury.
Wei sheng yan jiu = Journal of hygiene research 05/2004; 33(3):264-6.
