Study may direct solutions for air pollution disease affecting agricultural, industrial workers

(December 17, 2002) Bethesda, MD Infiltration of airway mucus with inflammatory cells is thought to be a key factor in the cause of airway disorders, including asthma and chronic bronchitis. At the same time, neutrophils ["polymorphonuclear leukocytes" or (PMNs)] contribute to the immune response of the airway to infectious and noninfectious irritants. Although it is usually protective and beneficial, this response to the threat of inflammation has the potential to cause tissue injury.


Neutrophils that respond to airway inflammation cause tissue damage via the production and release of oxygen radicals, proteases, and soluble mediators of inflammation. Inhaled irritants such as cigarette smoke, ozone, and bacterial endotoxin can produce inflammation through nonallergic mechanisms. Endotoxin [or lipopolysaccharide (LPS)], a component of the cell wall of gram-negative bacteria, is ever-present in the environment, with high concentrations in organic dusts, such as dust from grain, and air-pollution particles.

Several studies have demonstrated that inhalation of air that is contaminated with endotoxin is associated with the classic features of asthma, including reversible airflow obstruction and inflammation and persistent airway hyperreactivity and remodeling. Epidemiological studies have shown that the concentration of inhaled endotoxin in the air is strongly and consistently associated with reversible airflow obstruction among cotton workers, agricultural workers, and fiberglass workers.

Previous studies have shown that the concentration of endotoxin in the air is the most important occupational exposure associated with airway disease found in agricultural workers. Experimentally, inhalation of endotoxin can cause reversible airflow obstruction and airway inflammation in previously unexposed healthy study subjects. In fact, healthy study subjects challenged with dust from animal-confinement buildings develop airflow

Contact: Donna Krupa
American Physiological Society

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