@article {99,
	title = {Coal fly ash impairs airway antimicrobial peptides and increases bacterial growth.},
	journal = {PLoS One},
	volume = {8},
	year = {2013},
	note = {CAPLUS AN 2013:396251(Journal; Online Computer File)},
	pages = {e57673},
	publisher = {Public Library of Science},
	abstract = {Air pollution is a risk factor for respiratory infections, and one of its main components is particulate matter (PM), which is comprised of a no. of particles that contain iron, such as coal fly ash (CFA).  Since free iron concns. are extremely low in airway surface liq. (ASL), we hypothesize that CFA impairs antimicrobial peptides (AMP) function and can be a source of iron to bacteria.  We tested this hypothesis in vivo by instilling mice with Pseudomonas aeruginosa (PA01) and CFA and det. the percentage of bacterial clearance.  In addn., we tested bacterial clearance in cell culture by exposing primary human airway epithelial cells to PA01 and CFA and detg. the AMP activity and bacterial growth in vitro.  We report that CFA is a bioavailable source of iron for bacteria.  We show that CFA interferes with bacterial clearance in vivo and in primary human airway epithelial cultures.  Also, we demonstrate that CFA inhibits AMP activity in vitro, which we propose as a mechanism of our cell culture and in vivo results.  Furthermore, PA01 uses CFA as an iron source with a direct correlation between CFA iron dissoln. and bacterial growth.  CFA concns. used are very relevant to human daily exposures, thus posing a potential public health risk for susceptible subjects.  Although CFA provides a source of bioavailable iron for bacteria, not all CFA particles have the same biol. effects, and their propensity for iron dissoln. is an important factor.  CFA impairs lung innate immune mechanisms of bacterial clearance, specifically AMP activity.  We expect that identifying the PM mechanisms of respiratory infections will translate into public health policies aimed at controlling, not only concn. of PM exposure, but physicochem. characteristics that will potentially cause respiratory infections in susceptible individuals and populations. [on SciFinder(R)]},
	isbn = {1932-6203},
	author = {Borcherding, Jennifer A. and Chen, Haihan and Caraballo, Juan C. and Baltrusaitis, Jonas and Pezzulo, Alejandro A. and Zabner, Joseph and Grassian, Vicki H. and Comellas, Alejandro P.}
}
@article {101,
	title = {Effects of Eyjafjallajokull volcanic ash on innate immune system responses and bacterial growth in vitro},
	journal = {Environmental health perspectives},
	volume = {121},
	year = {2013},
	note = {MEDLINE AN 2013450089(Journal; Article; (JOURNAL ARTICLE); (RESEARCH SUPPORT, N.I.H., EXTRAMURAL); (RESEARCH SUPPORT, U.S. GOV{\textquoteright}T, NON-P.H.S.))},
	pages = {691 - 8},
	abstract = {BACKGROUND:  On 20 March 2010, the Icelandic volcano Eyjafjallajokull erupted for the first time in 190 years.  Despite many epidemiological reports showing effects of volcanic ash on the respiratory system, there are limited data evaluating cellular mechanisms involved in the response to ash.  Epidemiological studies have observed an increase in respiratory infections in subjects and populations exposed to volcanic eruptions.  METHODS:  We physicochemically characterized volcanic ash, finding various sizes of particles, as well as the presence of several transition metals, including iron.  We examined the effect of Eyjafjallajokull ash on primary rat alveolar epithelial cells and human airway epithelial cells (20-100 μg/cm(2)), primary rat and human alveolar macrophages (5-20 μg/cm(2)), and Pseudomonas aeruginosa (PAO1) growth (3 μg/104 bacteria).  RESULTS:  Volcanic ash had minimal effect on alveolar and airway epithelial cell integrity.  In alveolar macrophages, volcanic ash disrupted pathogen-killing and inflammatory responses.  In in vitro bacterial growth models, volcanic ash increased bacterial replication and decreased bacterial killing by antimicrobial peptides.  CONCLUSIONS:  These results provide potential biological plausibility for epidemiological data that show an association between air pollution exposure and the development of respiratory infections.  These data suggest that volcanic ash exposure, while not seriously compromising lung cell function, may be able to impair innate immunity responses in exposed individuals.[on SciFinder (R)]},
	isbn = {1552-9924},
	author = {Monick, Martha M. and Baltrusaitis, Jonas and Powers, Linda S. and Borcherding, Jennifer A. and Caraballo, Juan C. and Mudunkotuwa, Imali and Peate, David W. and Walters, Katherine and Thompson, Jay M. and Grassian, Vicki H. and Gudmundsson, Gunnar and Comellas, Alejandro P.}
}
