Abstract
BackgroundA symposium on the mechanisms of action of inhaled airborne particulate matter (PM), pathogenic particles and fibers such as silica and asbestos, and nanomaterials, defined as synthetic particles or fibers less than 100 nm in diameter, was held on October 27 and 28, 2005, at the Environmental Protection Agency (EPA) Conference Center in Research Triangle Park, North Carolina. The meeting was the eighth in a series of transatlantic conferences first held in Penarth, Wales, at the Medical Research Council Pneumoconiosis Unit (1979), that have fostered long-standing collaborations between researchers in the fields of mineralogy, cell and molecular biology, pathology, toxicology, and environmental/occupational health.ResultsThe goal of this meeting, which was largely supported by a conference grant from the NHLBI, was to assemble a group of clinical and basic research scientists who presented and discussed new data on the mechanistic effects of inhaled particulates on the onset and development of morbidity and mortality in the lung and cardiovascular system. Another outcome of the meeting was the elucidation of a number of host susceptibility factors implicated in adverse health effects associated with inhaled pathogenic particulates.ConclusionNew models and data presented supported the paradigm that both genetic and environmental (and occupational) factors affect disease outcomes from inhaled particulates as well as cardiopulmonary responses. These future studies are encouraged to allow the design of appropriate strategies for prevention and treatment of particulate-associated morbidity and mortality, especially in susceptible populations.
Highlights
A symposium on the mechanisms of action of inhaled airborne particulate matter (PM), pathogenic particles and fibers such as silica and asbestos, and nanomaterials, defined as synthetic particles or fibers less than 100 nm in diameter, was held on October 27 and 28, 2005, at the Environmental Protection Agency (EPA) Conference Center in Research Triangle Park, North Carolina
PM can occur as coarse particles with a diameter of more than 2.5 μm that generally are derived from natural sources such as soil and sea salts, whereas fine (0.1 to 2.5 μm in diameter) and ultrafine (< .1 μm in diameter) PM occurs as by-products of combustion of fossil fuels
The complexity and seasonal variations of the many components of PM which include metals, nitrates, sulfates, and organic hydrocarbons, make it difficult to identify the precise toxic species that contribute to inflammation, lung disease and cardiovascular effects
Summary
Airborne particulate matter – cardiopulmonary effects and host susceptibility factors Airborne particulate matter (PM) from vehicle exhaust, combustion, road dust and windblown soil, has been associated with increases in respiratory and cardiac morbidity and mortality. Increased cyclin D1 and Ki-67expression, an indication of cell cycle progression, are observed in mice after inhalation of chrysotile asbestos, and these markers of proliferation are increased in asbestos-exposed MPO null mice in comparison to MPO sufficient, wild type mice that exhibited more lung inflammation [31] These results suggest that MPO as an oxidant generating enzyme primarily found in neutrophils that may regulate epithelial responses to asbestos. A complex mixture of chemicals and particulates, is a co-factor in the development of asbestos and silica-induced pulmonary fibrosis and lung cancers, and rodent and human bronchial epithelial cells (1HAEo and HBE1) in vitro exhibit alterations in differentiation including induction of SPRR1B, a marker of squamous metaplasia that is an early lesion in the pathway to carcinoma. These approaches and studies summarized above using nanomaterials are strengthened by collaborations between chemists, biologists, toxicologists, and clinicians
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