wood smoke PM2.5 / inflammation and DNA damage

Research studies on wood smoke and other air pollution.

wood smoke PM2.5 / inflammation and DNA damage

Postby Wilberforce » Mon May 13, 2013 10:49 pm

Comparison of wood smoke PM2.5 obtained from the combustion of FIR and beech pellets on inflammation and DNA damage in A549 and THP-1 human cell lines
Corsini et al
http://umu.diva-portal.org/smash/get/di ... TEXT01.pdf
The aim of this study was to investigate the effect on the induction of interleukin-8 of particulate matter (PM) from fir and beech pellets burnt in domestic appliances on two human cells lines, namely the lung epithelial cell line A549 and the promyelocytic cell line THP-1. The effects of PM2.5 obtained from combustion of beech and fir pellets were compared to reference diesel exhaust particulates (DEP). In parallel, wood smoke PM-induced genotoxicity and oxidative stress were also investigated in A549 cells. Cells were treated for different times (3–72 h) with increasing concentrations of PM2.5 obtained from sequential combustions of fir and beech pellets or reference DEP. Cell viability was assessed by lactate dehydrogenase leakage, and the release of interleukin-8 or CXCL8 (IL-8) was measured to evaluate the pro-inflammatory effect. Oxidative stress was evaluated by the 5(6)-carboxy-2′,7′dichlorofluorescein diacetate (DCFH-DA) assay and DNA damage by the alkaline comet assay and micronucleus frequency by flow cytometry. Both A549 and THP-1 cells responded in a dose- and time-related manner to wood smoke PM2.5 with IL-8 release, particles obtained from late combustions being the most active. THP-1 cells were more sensitive than A549 cells. On a mass base, similar effects were observed for both fir and beech PM2.5. However, the combustion of beech pellets generated approximately three times more PM2.5 than fir pellets. Regarding the mechanism of PM2.5 uptake, in both THP-1 and A549 cells, cytochalasin D prevented PM2.5-induced IL-8 mRNA expression and cytokine release, indicating a key role for actin polymerization in particles uptake and that the production of IL-8 correlated with particle phagocytosis. As signal transduction pathway involvement, in both THP-1 and A549 cells, PM2.5-induced IL-8 release could be completely blocked by the selective inhibitor SB203580, indicating a role of p38 MAPK activation. PM2.5 from both fir and beech pellets also induced modest DNA lesions dose related, measured as strand breaks, whereas no increase in the number of micronucleus was observed. Similar effects were observed with DEP, arguing against less dangerous effects of wood smoke particles than other categories of combustion-derived particles in the same size range. Overall, results suggest that combustion conditions can significantly affect the characteristics of particles and the consequent toxicity, and that different woods can generate different amounts of PM2.5.
• The Surgeon General has determined that there is no safe level of exposure to ambient smoke!

• If you smell even a subtle odor of smoke, you are being exposed to poisonous and carcinogenic chemical compounds!

• Even a brief exposure to smoke raises blood pressure, (no matter what your state of health) and can cause blood clotting, stroke, or heart attack in vulnerable people. Even children experience elevated blood pressure when exposed to smoke!

• Since smoke drastically weakens the lungs' immune system, avoiding smoke is one of the best ways to prevent colds, flu, bronchitis, or risk of an even more serious respiratory illness, such as pneumonia or tuberculosis! Does your child have the flu? Chances are they have been exposed to ambient smoke!
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