Lung Injury Induced by Combustion-Generated Particles

Research studies on wood smoke and other air pollution.

Lung Injury Induced by Combustion-Generated Particles

Postby Wilberforce » Tue Jan 29, 2013 9:35 pm

Emerging Mechanistic Targets in Lung Injury Induced by Combustion-Generated Particles
Fariss, et al ... t001.short

The mechanism for biological effect following exposure to combustion-generated particles is incompletely defined. The identification of pathways regulating the acute toxicological effects of these particles provides specific targets for therapeutic manipulation in an attempt to impact disease following exposures. Transient receptor potential (TRP) cation channels were identified as “particle sensors” in that their activation was coupled with the initiation of protective responses limiting airway deposition and inflammatory responses which promote degradation and clearance of the particles. TRPA1, V1, V4, and M8 have a capacity to mediate adverse effects after exposure to combustion-generated particulate matter (PM); relative contributions of each depend upon particle composition, dose, and deposition. Exposure of human bronchial epithelial cells to an organic extract of diesel exhaust particle was followed by TRPV4 mediating Ca++ influx, increased RAS expression, mitogen-activated protein kinase signaling, and matrix metalloproteinase-1 (MMP-1) activation. These novel pathways of biological effect can be targeted by compounds that specifically inhibit critical signaling reactions. In addition to TRPs and calcium biochemistry, humic-like substances (HLS) and cell/tissue iron equilibrium were identified as potential mechanistic targets in lung injury after particle exposure. In respiratory epithelial cells, iron sequestration by HLS in wood smoke particle (WSP) was associated with oxidant generation, cell signaling, transcription factor activation, and release of inflammatory mediators. Similar to WSP, cytotoxic insoluble nano-sized spherical particles composed of HLS were isolated from cigarette smoke condensate. Therapies that promote bio-elimination of HLS and prevent the disruption of iron homeostasis could function to reduce the harmful effects of combustion-generated PM exposure.
• 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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