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exposures. With the exception of effects limited to upper airway irritation (non-productive cough, hoarseness), most of these may be grouped together as obstructive lung diseases, a term that includes several different clinical syndromes: simple chronic bronchitis (mucus hypersecretion); chronic obstructive bronchitis (characterized by mucus hypersecretion and chronic airflow limitation, largely irreversible); emphysema (defined in anatomical terms as an increase in the size of the distal airspaces and destruction of their walls); and a variety of airway reactivity conditions including allergic bronchoconstriction (acute recurrent episodic reversible airflow limitation with specific airway hypersensitivity), inflammatory bronchoconstriction (acquired airway hyperresponsiveness from nonimmunogenic irritant exposures characterized by reversible airflow obstruction and nonspecific airway hypersensitivity), and pharmacologic bronchoconstriction (reversible airflow limitation without evidence of a hypersensitive subgroup of the population of exposed). As with any set of clinical syndromes, there is a degree of overlap, and classification changes as understanding the underlying mechanism improves.

Simple Chronic Bronchitis

Basically there are no good population data on this condition as in and of itself it is not considered to be a disabling (therefore relevant) condition.

Chronic Obstructive Bronchitis and Emphysema

The British hypothesis suggests that chronic bronchitis and chronic airflow limitation (by implication, emphysema) are separate parallel disease processes affecting different parts of the respiratory tract. Both were related at least to cigarette smoking and asthma was unrelated to either. The Dutch hypothesis focuses on individual susceptibility, hyperreactive airways, as key in both conditions and independent of cigarette smoking. Follow-up study suggests both are correct. Smokers who develop chronic airflow limitation (a minority) have been shown to have increased airway reactivity while both air pollutants and cigarettes produced accelerated decline in pulmonary function independent of airway reactivity.

Both chronic obstructive bronchitis and emphysema have been shown to be related independently to the irritant effects of inhaled airborne dust but not to each other. Similar results are seen in response to chronic exposures to irritant gases or vapors. As in the case of cigarettes, although dose-response relationships have generally been demonstrated to both the level and the intensity of exposure, not all

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