Damage effects of dust storm PM2.5 on DNA in alveolar macrophages and lung cells of rats
Introduction
Atmospheric particulate matter constitutes an important component of air pollution. Epidemiological studies have reported a positive correlation between particulate matter (PM) concentrations and the increased incidence of human morbidity and mortality (Dockery et al., 1992, Gouveia and Fletcher, 2000, Klemm et al., 2000, Moolgavkar, 2000, Pope, 2000). Of particular concern is fine PM (PM with aerodynamic diameter less than 2.5 μm, PM2.5), which is comprised of particles that readily penetrate to the lower respiratory tract and cause damage to cells (Wilson and Suh, 1997). Although toxicity may be due to a direct action of PM2.5 on the respiratory tissue, particle composition varies extensively and toxicological effects may also be mediated by compounds present in or associated with PM2.5, such as polycyclic aromatic hydrocarbons (PAHs), nitro-polycyclic aromatic compounds, metals, fungi and water-soluble ions.
Dust storms are common in parts of the world with dry land areas. They are caused by great wind velocity, which deteriorate the visibility due to high concentration of dust and sand in the air. Researchers become increasingly concerned about dust storms, not only due to their effects on both regional and global environment, but also due to detrimental effects on human health made by dust particles (Park et al., 2003). Epidemiological studies have found that respiratory diseases and mortality, cardiovascular diseases in the elderly and even Al Eskan disease (or Desert Storm pneumonitis) were associated with dust storms (Chen et al., 2004, Hefflin et al., 1991, Kwon et al., 2002, Korenyi-Both et al., 1992). It is speculated that these diseases or deaths might be caused mainly by dust storm PM2.5 or ultrafine particles (PM0.1) since the coarse particles (commonly referred to as particles between 10 and 2.5 μm in aerodynamic diameter) are typically filtered by the nose or coughed out of the throat and upper lungs despite that PM10 can in some individuals yield breathing problems or aggravate pre-existing breathing problems, such as asthma (Englert, 2004).
PM2.5 passes into the deepest regions of the lungs and the alveoli (or alveolar sacs). Experiments in vivo and in vitro reveal that fine or ultrafine particulate matters can result in pulmonary inflammation, airway hyperreactivity, alveolar macrophage impairment, epithelial cell damage, and epithelial permeability increase (Okeson et al., 2003, Renwick et al., 2001, Kwon et al., 2002, Korenyi-Both et al., 1992). Although the respiratory toxicities of fine particles deriving from urban atmosphere, coal, oil, fly ash etc. have been evaluated, the data concerning the adverse impact of dust storm PM2.5 have been sparsely investigated.
The present study was aimed at analyzing damage effects of PM2.5 suspensions, their water-soluble fraction and solvent-extractable organics from both dust storm and normal weather on DNA in rat alveolar macrophages in vitro and the damage effects of PM2.5 suspensions on DNA of lung cells of rats in vivo. In addition, the composition and the different toxicity of particulates were investigated between a heavily industrial area and an agricultural area. For this study, PM2.5 samples from dust storm and normal weather were collected in Baotou city, Inner Mongolia Province, and Wuwei city, Gansu Province, China, in March 2004 and the single cell gel electrophoresis technique was used to measure DNA damage in single cells.
Section snippets
Chemicals and animals
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), dimethyl sulfoxide (DMSO), normal melting agarose (NMA), low melting agarose (LMA), sodium sarcosinate, Triton X-100, ethidium bromide (EB) and trypan blue were purchased from Sigma Chemicals Company (St. Louis, USA). RPMI 1640 medium with l-glutamine, penicillin-streptomycin and fetal bovine serum (FBS) were obtained from Gibco BRL (Gaithersburg, MD, USA). All other reagents and solvents used were of the analytical grade. All
Chemical composition of particulates
Table 1 shows that the concentration of OC in PM2.5 from normal weather was higher than that from dust storm in both Baotou city and Wuwei city. And the concentration of OC in PM2.5 from normal weather in Baotou city was higher than that in Wuwei city. There were no significant difference of the concentration of EC in PM2.5 between normal weather and dust storm or between Baotou city and Wuwei city.
The concentrations of and Ca2+ in PM2.5 from dust storm were higher than those from normal
Discussion
The alveolar macrophages, which are commonly located in alveolus and surface of bronchi, act as part of the first defense of lung tissue against microorganism, respirable xenobiotics or particles via phagocytosis (Lukacs et al., 1995). In addition, they play important roles in the defence against tumour development by excretion of cytokines that elicit or alter the immune function. Lei et al. (2004) found dust storm particles could give rise to lung inflammation and injury involving impairment
Acknowledgements
This research was supported by grant 30230310 and 20477023 from the National Natural Science Foundation of China and by grant 20031092 from the Natural Science Foundation of Shanxi Province.
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2022, Journal of Hazardous MaterialsCitation Excerpt :Indeed, PM2.5 exposure was reported to highly inhibit nucleotide excision repair (NER) in human lung cells, resulting in the suppressed DNA repair and promotion of DNA replication errors (Mehta et al., 2008). Meng et al. revealed the potency of DNA damage by PM2.5 from both sand storm and normal weather, and the organic compounds and insoluble particle-core acting as the main contributors (Meng and Zhang, 2007). 8-OHdG, an oxidatively modified guanine derivative, is extensively applied to indicate oxidative stress-mediated DNA damage upon environmental stress like PM2.5 (Zanolin et al., 2015).