Cigarette smoke particles, exposure

Cells are typically exposed to ambient PM (PMio, PM2.5, UF), diesel exhaust particles (DEP), or cigarette smoke using these exposure systems (MazzareUa et al. 2007 Fukano et al. 2006 Hetland et al. 2004 Li et al. 2002). Some smdies have used well-characterized standard reference materials (SRMs) from the National Institutes of Standards and Technology (NIST 2009) and engineered nanoparticles, such as zinc oxide, titanium dioxide, in liquid medium (Li et al. 2003 Oberdorster 2001 Boland et al. 1999). Although standard or engineered materials are not true ambient PM, the materials are representative of ambient PM. These materials also elicit similar responses in cells to the ambient PM. The majority of the in vitro studies use doses in the range of 10-1000 pg/mL (PM mass/volume of the suspension solutions) with exposure durations of 2-72 h (Mitschik et al. 2008). 

Human exposure mainly arises from combustion of fuels, plants, and waste, and consumption of adventitious cadmium present in food and water [83]. Humans and animals breathe cadmium-containing particles (mainly the oxide) and ingest cadmium complexes with their food and drinks. Cigarette smoking is a major route of uptake, whereas skin contact is not widespread owing to the natural dilution of cadmium, except for occupational settings. Dietary cadmium is more concentrated in some food items such as shellfish, offal, grains, and seeds. Some crops, such as rice, soybeans, or wheat, are more likely to accumulate cadmium firom polluted soils than others. 

After inhalation exposure, the absorption of Cd compotmds varies greatly depending on the physico-chemical properties of the Cd compounds involved, site of deposition in the lungs and particle size [22]. In the Itmgs, deposition, mucociliary clearance, and alveolar clearance determine the absorption of inhaled particles. Large particles, dusts (>10 pm in diameter) tend to be deposited in the upper airways, while small particles, fumes, cigarette smoke (approximately 0.1 pm in diameter) penetrate into the alveoli, which are the major site of absorption. Between 50-100% of Cd in the alveoli are transferred to the blood. In the average... 

Uptake ean similarly be increased by exogenous sources of AOS. Brief exposure to whole cigarette smoke, which is a highly concentrated source of AOS and other radicals, and then to a mineral dust suspension produces considerably greater uptake of asbestos, titanium dioxide, fibrous silicon carbide, and talc (51 -53 Fig. 2). The increase in uptake is proportional to the dose of cigarette smoke, and the smoke effect can be inhibited by catalase, superoxide dismutase (which destroys superoxide anion), or deferoxamine (see Fig. 2). The effects of low levels of ozone are similar (Fig. 3), but differ from cigarette smoke in that superoxide dismutase is not protective (126). Smoke also fails to enhance the uptake of nonfibrous silicon carbide or iron oxide (hematite 53) the latter observation is particnlarly interesting because it was recently shown (127) that hematite does not catalyze the formation of AOS. This observation emphasizes the idea that redox-active surface iron, as opposed to compositional iron, is cracial to AOS formation and particle nptake. 

E-cadherin expression. Smoke extract, on pig airway epithelial cells and mouse trachea, produced a decrease of E-cadherin expression on membrane and an increase of cytoplasmic expression at 12 and 24 hours after exposure. The expression at 24 hours was higher than at 12 hours k Electron transport inhibition. Acetonitrile extracts of cigarette tar inhibited stage three and four respiration of intact mitochondria. Exposure of respiring submito-chondrial particles to the acetonitrile extracts of cigarette tar results in a dose-dependent inhibition of oxygen consumption... 

Ultimately, the question is not how many deaths are attributable to particulate air pollution, but whether these associations represent substantial loss of life expectancy. In the Six-Cities Study, the estimated effect of air pollution across the range of exposures for never-smokers was 1.19 (95% Cl 0.90-1.57). Applying this increased probability of death at each age between 25 and 85 years for the U.S. population (86) gives a decrease in life expectancy of 2.0 years (95% Cl 1.2-5.1 years). The American Cancer Society estimates for effect of fine particles on never-smokers [relative risk of 1.22 (95% Cl 1.07-1.39)] would similarly estimate decreased life expectancy of 2.3 years (95% Cl 0.8-3.7 years). For comparison, based on the Six-Cities Study results, smoking one pack of cigarettes per day starting at age 25 would lead to a decreased life expeetancy of 8.5 years. 

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