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Ambient air particles

Variation of the content of impurities in the different CNT preparations [21] offers additional challenges in the accurate and consistent assessment of CNT toxicity. As-produced CNTs generally contain high amounts of catalytic metal particles, such as iron and nickel, used as precursors in their synthesis. The cytotoxicity of high concentrations of these metals is well known [35, 36], mainly due to oxidative stress and induction of inflammatory processes generated by catalytic reactions at the metal particle surface [37]. Another very important contaminant is amorphous carbon, which exhibits comparable biological effects to carbon black or relevant ambient air particles. [Pg.180]

In the early 1940s, Leiter et al. (1942) demonstrated that a similar phenomenon occurred with organic extracts of ambient air particles—that is, injection of tars extracted from atmospheric dusts collected at locations throughout New York City produced subcutaneous sarcomas in mice. Shortly thereafter, Leiter and Shear (1943) reported that marginal doses of 3,4-benzpyrene (known today as benzol a jpyrene, BaP, I), the powerful carcinogen earlier isolated from coal tar and synthesized by Cook et al. (1933), also produced subcutaneous tumors in mice. [Pg.440]

This modification has been applied in a variety of studies, including the mutagenic activity of fine ambient air particles as a function of particle size (Kado et... [Pg.479]

A number of variables influence the overall levels of mutagenicity to which the general public is exposed through inhalation of ambient air particles. (Note, however, that total exposure also includes gas-phase mutagens see later.) The factors include, for example, (a) the inherent mutagenic potencies (rev /Ag" of extract) of the fine particles emitted by each type of combustion... [Pg.488]

The impact of close proximity to a major source on the mutagenicity levels of ambient air particles (rev m 3) is seen in Fig. 10.17 for a site immediately adjacent to, and generally downwind from, a heavily traveled freeway in west Los Angeles (Pitts et al., 1985a). Peak levels were 120 ( + S9) and 100 ( —S9) rev m-3 during the midmorning rush hour and — 110 ( + S9)... [Pg.489]

An interesting aspect of the long-range transport of mutagenic compounds is a field study by De Pollok and co-workers (1997), who collected and measured ambient air particles at three different levels of a TV tower (surface, <1 m mid, 240 m, and top 433 m) near... [Pg.490]

Polycyclic Aromatic Hydrocarbons (PAHs). The most highly studied class of compounds in combustion effluents 1s the PAHs. However, very little information about the amounts present in the vapor phase and on particles in the effluents from the efficient combustion of coal is available. The data in Table II partially fills this informational gap. The amounts in the vapor phase varied according to the firing conditions and the stack temperature that was 170 C. Even 1f all these PAHs were to condense on the particles, the amounts are well below the multiple ng/g quantities present on ambient air particles. [Pg.123]

Fig. 2a-c Typical urban ambient air particle number size distribution measured in Brisbane... [Pg.127]

Lopez Cancio JA, Vera Castellano A, Santana Martin S, Santana Rodriguez JF (2004) Size distributions of PAHs in ambient air particles of two areas of Las Palmas de Gran Canaria. Water Air Soil Pollut 154 127-138... [Pg.60]

Hetland RB, Cassee FR, Refsnes M et al (2004) Release of inflammatory cytokines, cell toxicity and apoptosis in epithelial lung cells after exposure to ambient air particles of different size fractions. Toxicol In Vitro 18 203-212... [Pg.447]

Rundell KW, Hoffman JR, Caviston R et al (2007) Inhalation of ultrafine and fine particulate matter dismpts systemic vascular function. Inhalation Toxicol, doi 10.1080/08958370601051727 Saldiva PH, Clarke RW, Coull BA et al (2002) Lung inflammation induced by concentrated ambient air particles is related to particle composition. Am J Respir Crit Cate Med 165 1610-1617... [Pg.448]

The oxygen burst of monocytes induced by ambient air particles (with the exception of oil fly ash particles) was less than the response elicited by polymorphonuclear leucocytes (Prahalad etal. 1999). The luminol-enhanced chemiluminescence response of polymorphonuclear leucocytes separated from heparinised human blood was generally increased with all washed particles, with oil fly ash and one urban air particle showing statistically significant (P <0.05) differences between dHjO-washed and unwashed particles. The luminol-enhanced chemiluminescence activity in polymorphonuclear leucocytes induced in post particles... [Pg.11]

A.J. Ohio, C. Kim, R.B. Devlin, Concentrated ambient air particles induce mild pulmonary inflammation in healthy human volunteers. Am. J. Respir. Crit. Care Med. 162 (2000) 981-988. [Pg.485]

The approach of our laboratory to understand mechanisms of mortality and morbidity caused by ambient air particles uses animal models of human diseases associated with inereased sensitivity in the epidemiologieal stndies. Underlying concepts include (1) The effects of ambient particles are best defined nsing real-... [Pg.577]

A central hypothesis derived from this data is as follows Ambient air particles are complex mixtures with intrinsic toxicity. In concert with preexisting inflammation, particulate exposure results in stimulation of lung receptors and immune cells, release of reactive oxygen species (ROS), and induction of pro-inflammatoiy mediators that lead to local and systemic effects, which ultimately account for the epidemiological associations between adverse health effects and particulate air pollution. Hypothetical mechanistic pathways by which inhalation of ambient particles in urban air may lead to morbidity and mortality are outlined in Figure 1. [Pg.578]

Although death may be attributable to many tmderlying conditions, the final common pathway remains the cessation of the heart electrical activity. With hospitalized patients, cardiac arrest is usually manifested by ventrieular fibrillation, from which the patient may or may not be resuscitated. Sudden eardiae death, which claims over 350,000 lives annually in the United States, results from abrupt disruption of heart rhythm, also primarily in the form of ventricular fibrillation. Death in those instances is due not to extensive cardiac injury, but rather, to transient triggers that impinge on the electrically unstable heart (65-67). Identification of individuals at risk for sudden cardiac death remains a major objective in cardiology. Similarly, the specific mechanism linking ambient air particle exposure to death is unknown. [Pg.582]

E. Hypoxia Resulting from Increasing Airway Obstruction or Hypoventilation in Concert with Pulmonary Inflammation Following Inhalation of Ambient Air Particles... [Pg.583]

Godleski JJ, Sioutas C, Katler M, Koutrakis P. Death from inhalation of concentrated ambient air particles in animal models of pulmonary disease. Am J Respir Crit Care Med 1996 153 A15. [Pg.595]


See other pages where Ambient air particles is mentioned: [Pg.411]    [Pg.1130]    [Pg.23]    [Pg.419]    [Pg.440]    [Pg.466]    [Pg.479]    [Pg.487]    [Pg.487]    [Pg.622]    [Pg.626]    [Pg.460]    [Pg.411]    [Pg.233]    [Pg.411]    [Pg.179]    [Pg.456]    [Pg.577]    [Pg.578]    [Pg.579]    [Pg.583]    [Pg.635]   
See also in sourсe #XX -- [ Pg.577 ]




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