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PubMedDate not supplied

Experimental deposition of environmental tobacco smoke submicrometer particulate matter in the human respiratory tract.

Measurements of 15 nonsmokers and 3 smokers breathing environmental tobacco smoke (ETS), were conducted to study particle deposition within the human respiratory tract. The subjects inhaled ETS of count median diameter (CMD) of about 0.2 micron and geometric standard deviation (GSD) of 1.7 The particle size distribution in the submicrometer range in the inhaled and exhaled air from the subjects was measured using a scanning mobility particle sizer (SMPS). A deposition of 56.0 +/- 15.9% was observed for nonsmokers while breathing ETS through the nose and 48.7 +/- 11.6% while breathing ETS through the mouth. One individual tested four times gave an average deposition of 57.4 +/- 11.5%, providing an indication of intraindividual variation. Such a variation is expected since the breathing rate was not controlled in order that an indication of the deposition experienced on a day-to-day basis could be obtained. For nonsmokers the deposition while breathing through the mouth was lower than through the nose and the variability within the measurements was also lower for mouth breathing. The latter could be due to the variation in individual size and shape of the nasal passage. Smokers had, on average, a higher rate of deposition but also a higher interindividual variability making it difficult to draw conclusions with respect to the affect of smoking on ETS particle deposition. The average deposition of the three smokers was 65.3 +/- 24.1% for nasal breathing and 66.1 +/- 17.6% for mouth breathing.

Adult↗
PubMedDate not supplied

Associations of London, England, daily mortality with particulate matter, sulfur dioxide, and acidic aerosol pollution.

During the extreme pollution episodes of 1952 and 1962 in London, England, excesses in daily mortality were clearly evident. In this study, we examined daily British Smoke, sulfur dioxide, acid aerosols, and weather variables for their short-term associations with daily mortality in the more typical (nonepisodic) winters of 1965-1972. Consideration of the acid aerosol data was of special interest because this chemical component has been suspected as a causal agent in past episodes. Temporal lag structures between the variables were examined after removal of long-term components from each series in order to obtain "rational" cross-correlations. Significant associations between same-day and lagged pollution variables and mortality were found. Alternative regression models with pollution and weather variables were also developed. The coefficients obtained were applied to the 1962 pollution episode to examine the continuity of the estimated slopes. The pollution-predicted deaths fit the observed deaths well, which supports the applicability of such deviation-derived coefficients to the absolute scale. These models were also employed to estimate mean excess daily deaths attributed hypothetically to air pollution. On average, mean effect ranged from 2-7% of all deaths during the nonepisodic winters in Greater London, but the 95% confidence intervals of these estimates overlapped for all model specifications examined. This estimated pollutant mixture "effect" cannot be attributed to a particular pollutant because of a lack of quantitative information on the relative downward biases caused by both analytical errors and errors in the spatial representativeness of each respective pollution index.

Acids↗
PubMed2004

Hypertensive rats are susceptible to TLR4-mediated signaling following exposure to combustion source particulate matter.

Toll-like receptor 4 (TLR4) has been shown to play a role in cell signaling that results in neutrophilic inflammation in response to lipopolysaccharide and respiratory syncytial virus infection. TLR4 also interacts with CD14, which upon complex formation triggers TLR4-associated signaling pathways to produce a proinflammatory response. This mechanism results in the activation of NF-kappa B and subsequent inflammatory gene induction. In order to determine the effect of combustion source particle matter (PM), rich in zinc and nickel but with negligible endotoxin, on a possible activation of TLR4-mediated cell signaling and inflammation, we intratracheally (IT) instilled 3.3 mg/kg of PM into 12-w-old healthy male Wistar Kyoto (WKY) and susceptible spontaneously hypertensive (SH) rats. Inflammation, inflammatory-mediator gene expression, bronchoalveolar lavage fluid (BALF) protein and LDH, TLR4 and CD14 protein, and NF-kappa B activation in the lung were determined after 24 h. Dose-response data (0.0, 0.83, 3.33, and 8.3 mg/kg PM) for BALF LDH were obtained as a marker of lung cell injury in SH rats. BALF neutrophils, but not macrophages, were significantly increased in the PM-exposed WKY and SH rats. SH rats showed a greater PMN increase than WKY rats. Similarly, BALF protein and LDH levels were also increased following PM exposure but to a significantly greater extent in SH rats. Plasma fibrinogen was increased only in SH rats exposed to PM. The increased inflammation seen in PM-exposed SH rats was accompanied by a significant increase in TLR4 protein in the lung tissue, which was primarily localized in alveolar macrophages and epithelial cells. CD14 was also increased by PM exposure in both SH and WKY rats but was significantly greater in the SH rats. These increases were associated with greater translocation of NF-kappa B in the lungs of SH rather than WKY rats. This was accompanied by increased macrophage inhibitory protein (MIP)-2 mRNA expression at 24 h of exposure. These data suggest that the increased inflammation in the lungs of PM-exposed SH rats compared to WKY rats is accompanied by an increase in TLR4-mediated cell signaling. Thus, one of the mechanisms for greater susceptibility of SH rats to PM exposure may involve an increased activation of the TLR4 signaling pathway.

Air Pollutants↗
PubMed2004

Adjuvant activity of ambient particulate matter in macrophage activity-suppressed, N-acetylcysteine-treated, iNOS- and IL-4-deficient mice.

In previous studies, we have shown strong adjuvant activity for Ottawa dust (EHC-93) after coexposure of the BALB/c mouse to EHC-93 and ovalbumin. Mice were intranasally sensitized at days 0 and 14 with 200 microg ovalbumin and 150 microg EHC-93, and challenged with ovalbumin at days 35, 38, and 41 with 200 microg ovalbumin. Mice were autopsied at day 42. This adjuvant activity was shown for the antibody response to ovalbumin (immunoglobulins E, G1, and G2a), histopathological lesions in the lung, cytokines, and the numbers of eosinophils in lung lavages. To study the mechanisms of this adjuvant activity, mice (BALB/cC.D2-Vil6) with natural-resistance-associated macrophage protein (Nramp1s), BALB/c mice pretreated with the antioxidant N-acetylcysteine (NAC), mice (B6.129P2-Nos2tmLau) deficient in inducible nitric oxide synthase (iNOS), and mice with interleukin-4 (IL-4) deficiency (BALB/cIl4< tm2Nnt) were coexposed to ovalbumin and EHC-93. Our studies have shown that the adjuvant activity induced after such coexposure does not change if the macrophage activation of the mice is disturbed or if the mice have been pretreated with N-acetylcysteine. In addition, the adjuvant activity does not develop through the pathway in which inducible nitric oxide synthase is involved. Because the histopathological lesions are statistically significant less in the IL-4 knockout strain in comparison with the wild type, we conclude that interleukin-4 might play an important role in the adjuvant activity caused by EHC-93.

Acetylcysteine↗
PubMed2000

Characterization of fine particulate matter produced by combustion of residual fuel oil.

Combustion experiments were carried out on four different residual fuel oils in a 732-kW boiler. PM emission samples were separated aerodynamically by a cyclone into fractions that were nominally less than and greater than 2.5 microns in diameter. However, examination of several of the samples by computer-controlled scanning electron microscopy (CCSEM) revealed that part of the PM2.5 fraction consists of carbonaceous cenospheres and vesicular particles that range up to 10 microns in diameter. X-ray absorption fine structure (XAFS) spectroscopy data were obtained at the S, V, Ni, Fe, Cu, Zn, and As K-edges and at the Pb L-edge. Deconvolution of the X-ray absorption near edge structure (XANES) region of the S spectra established that the dominant molecular forms of S present were sulfate (26-84% of total S) and thiophene (13-39% of total S). Sulfate was greater in the PM2.5 samples than in the PM2.5+ samples. Inorganic sulfides and elemental sulfur were present in lower percentages. The Ni XANES spectra from all of the samples agreed fairly well with that of NiSO4, while most of the V spectra closely resembled that of vanadyl sulfate (VO.SO4.xH2O). The other metals investigated (i.e., Fe, Cu, Zn, and Pb) also were present predominantly as sulfates. Arsenic was present as an arsenate (As+5). X-ray diffraction patterns of the PM2.5 fraction exhibit sharp lines due to sulfate compounds (Zn, V, Ni, Ca, etc.) superimposed on broad peaks due to amorphous carbons. All of the samples contain a significant organic component, with the loss on ignition (LOI) ranging from 64 to 87% for the PM2.5 fraction and from 88 to 97% for the PM2.5+ fraction. Based on 13C nuclear magnetic resonance (NMR) analysis, the carbon is predominantly condensed in graphitic structures. Aliphatic structure was detected in only one of seven samples examined.

Air Pollution↗