Histo-Compartmental Analysis of Retained Fine Particles in the Lungs of London Residents Who Expired at the Time of the Great Smog of 1952 (original) (raw)
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Air Pollution and Retained Particles in the Lung
Environmental Health Perspectives, 2001
Epidemiologic evidence associates particulate air pollution with cardiopulmonary morbidity and mortality. The biological mechanisms underlying these associations and the relationship between ambient levels and retained particles in the lung remain uncertain. We examined the parenchymal particle content of 11 autopsy lungs from never-smoking female residents of Mexico City, a region with high ambient particle levels [3-year mean PM 10 (particulate matter ≤ 10 µm in aerodynamic diameter)= 66 µg/m 3 ], and 11 control residents of Vancouver, British Columbia, Canada, a region with relatively low levels (3-year mean PM 10 = 14 µg/m 3 ). Autopsy lungs were dissolved in bleach and particles were identified and counted by analytical electron microscopy. Total particle concentrations in the Mexico City lungs were significantly higher [geometric mean = 2,055 (geometric SD = 3.9) × 10 6 particles/g dry lung vs. 279 (1.8) × 10 6 particles/g dry lung] than in lungs from Vancouver residents. Lungs from Mexico City contained numerous chainaggregated masses of ultrafine carbonaceous spheres, some of which contained sulfur, and aggregates of ultrafine aluminum silicate. These aggregates made up an average of 25% of the total particles by count in the lungs from Mexico City, but were only rarely seen in lungs from Vancouver. These observations indicate for the first time that residence in a region with high levels of ambient particles results in pulmonary retention of large quantities of fine and ultrafine particle aggregates, some of which appear to be combustion products.
Ambient mineral particles in the small airways of the normal human lung
Journal of Environmental Medicine, 1999
Recent epidemiological data have indicated that the ambient concentration of small airways the inhalable fraction of atmospheric particles (PM 10 ) is associated with respirmembranous bronchioles atory and cardiovascular morbidity and mortality. These effects may be related respiratory bronchioles to particle induced inflammatory reactions in the airways, but little actual inforultrafine particles mation is available about the deposition and retention of ambient particles in PM 10 human airways, particularly in the very small airways. To examine this question, PM 2.5 we isolated portions of large airways, large airway carinas, and small airways between the mainstem bronchus and the respiratory bronchioles (RB) from the autopsy lungs of seven never-smokers from the general population, and determined mineral content by analytical electron microscopy. Overall, RB at generations 11,12, and 13 showed consistently high particle concentrations, averaging 25 to 100 times the particle concentration in the mainstem bronchus, but roughly similar elevated concentrations were also seen in the carinas of airway generations 4 and 5. Mean aerodynamic particle sizes by site ranged between 0.30 and 0.60 m, with slightly larger particles in the RB. Crystalline silica was the predominant mineral species in all sites. Ultrafine particles were present in all sites but constituted less than 15% of the total number of particles in any location. Ultrafine particles were largely individual particles of metals and crystalline silica, and no aggregated carbonaceous or noncarbonaceous ultrafine particles were identified. More than 90% of the particles in every site had aerodynamic diameters less than 2.5 m. We conclude that the RB and the carinas of generations 4 and 5 in the normal human lung show very high and roughly equal concentrations of inhaled ambient particles, suggesting that these two anatomic compartments are potential sites of particle toxicity. All portions of the airways effectively retain PM 2.5 . Ultrafine particles are retained throughout the airways and also show concentration peaks in the large airway carinas and RB.
There is substantial evidence that indicates that the exposure to air pollution is associated with a wide spectrum of lung pathologies. Some of the most studied pollutants are gases and aerosols, such as NO2, SO2, CO, and O3. Also particulate matter is part of the air pollution and the size of the particles has health implications. Those larger than 10µm remains in the nose, particles about 5µm diameter arrive to trachea and bronchi, and about 2.5µm reach the bronchioli and alveoli (Spengler and Wilson, 1996). The changes in size of the tubes and in the direction of the airflow in the respiratory ducts will allow a different pattern of particle deposition
Toxicology and Applied Pharmacology, 1997
there is no clear agreement as to a biologically plausible Cytokine Production by Human Airway Epithelial Cells after mechanism which can explain the acute mortality/morbidity Exposure to an Air Pollution Particle Is Metal-Dependent. Carter, associated with PM 10 exposure. In addition there is no con-J. D., Ghio, A. J., Samet, J. M., and Devlin, R. B. (1997). Toxicol. sensus as to which components of PM 10 are responsible for Appl. Pharmacol. 146, 180-188.
Atmospheric Environment, 2015
Deposition fractions of inhaled particles in the human respiratory tract are ca. 56%. Deposition rates in the lung (up to 10 9 particles min -1 ) are larger than in the extra-thoracic region. Deposition rate in the acinar region increases by physical activity. The extra-thoracic region receives the largest surface density deposition rates (up to 10 6 particle cm -2 min -1 ). In the lung, the first few airway generations obtain the highest surface loading (up to 10 5 particle cm -2 min -1 ). a b s t r a c t Realistic median particle number size distributions were derived by a differential mobility particle sizer in a diameter range of 6e1000 nm for near-city background, city centre, street canyon and road tunnel environments in Budapest. Deposition of inhaled particles within airway generations of an adult woman was determined by a stochastic lung deposition model for sleeping, sitting, light and heavy exercise breathing conditions. Deposition fractions in the respiratory tract were considerable and constant for all physical activities with a mean of 56%. Mean deposition fraction in the extra-thoracic region averaged for the urban environments was decreasing monotonically from 26% for sleeping to 9.4% for heavy exercise. The mean deposition fractions in the tracheobronchial region were constant for the physical activities and urban environments with an overall mean of 12.5%, while the mean deposition fraction in the acinar region averaged for the urban locations increased monotonically with physical activity from 14.7% for sleeping to 34% for heavy exercise. The largest contribution of the acinar deposition to the lung deposition was 75%. The deposition rates in the lung were larger than in the extra-thoracic region, and the deposition rate in the lung was increasingly realised in the AC region by physical activity. It was the extra-thoracic region that received the largest surface density deposition rates; its loading was higher by 3 orders of magnitude than for the lung. Deposition fractions in the airway generations exhibited a distinct peak in the acinar region. The maximum of the curves was shifted to peripheral airway generations with physical activity. The shapes of the surface density deposition rate curves were completely different from those for the deposition rates, indicating that the first few airway generations received the highest surface loading in the lung.
Environmental Health Perspectives, 2005
Carolina, USA) performed inductively coupled plasma-mass spectroscopy and ion chromatography analysis of particulate extracts. J. Hovel (Computer Sciences Corporation, Sterling, Virginia) is acknowledged for preparing the superimposed map of weather trajectories. We also thank L. Birnbaum, J. Samet, and W. Russo (U.S. EPA) for their critical review of the manuscript. The research described in this article has been reviewed by the National Health and Environmental Effects Research Laboratory, U.S. EPA, and approved for publication. Approval does not signify that the contents necessarily reflect the views and the policies of the agency, nor does mention of trade names or commercial products constitute endorsement or recommendation for use. The authors declare they have no competing financial interests.
Mankind has been exposed to airborne nanosized particles (<100 nm) for eons, yet mechanization and industrialization of societies has increased the overall load to which humans are exposed to. Ultrafine-particles (below 1 μm in diameter) can thus be incorporated via any organic surface structure and in particular when the area available is large enough – as is the case with the skin (approx. 1.5-2 m2), the digestive tract (intestinal villi, approx. 200 m2) or the lungs (approx. 140 m2). Since aerosolised particles are readily inhaled rather than ingested, the lungs represent an ideal gateway with high penetration efficiency rates. If seen from a toxicological rather than from a therapeutic point of view, deposited xenobiotic particles that interact with biological tissues do so first on a cellular level where they are readily translocated into the cell to interfere with metabolic pathways and eventually induce inflammatory cellular responses. At an organismic level and in response to long-term exposure, these particles become redistributed via the lymphatic or the blood circulatory system to reach sensitive organs or tissues such as the central nervous system, bone marrow, lymph nodes, spleen, and heart. At this organismic level, the persistent particle exposure may trigger or even modulate the severity of chronic diseases.