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Asthma, which affects 3% of the population, is also a cause of sudden and unexpected death in the medical examiner's population.65 Deaths from it, while uncommon, do occur, with death rates of from 1.1 to 7% reported. Since 1960, there has been an increase in the incidence of deaths from asthma, either because of increased prevalence of the disease or an increase in severity. Deaths in blacks are twice that of whites. Sudden, unexpected death can occur in asthmatics without long-term deterioration or a prolonged attack. The frequency of death from asthma is increased at night or in the early morning, possibly due to a pronounced diurnal variation in airflow limitation. Up to one fourth of deaths from asthma occur within 30 min of onset of the attack.

In acute asthmatic attacks, there is a reduced airflow rate, air trapping, and a ventilation-perfusion imbalance that leads to decreased oxygenation of the blood, elevated carbon dioxide, increased pulmonary vascular resistance, a right ventricular systolic overload, and an increase in the effort needed to breathe. The reduction in airflow is due to a combination of smooth muscle contraction, tenacious mucoid secretions in the bronchi, and an inflammatory infiltrate in the walls of the bronchi. These may develop either gradually or in a very short order. If airflow obstruction is not relieved, there will be steady progression to elevated carbon dioxide, metabolic aci-dosis, exhaustion, and death.

At autopsy, the lungs usually appear overexpanded, completely, occupying their respective chest cavity. This hyperexpanded state may not be present if extensive cardiopulmonary resuscitation has been carried out. In addition to the hyperexpansion of the lungs, a sticky tenacious white mucus deposit will fill the bronchi. Microscopic sections of the lung show a chronic inflammatory infiltrate with numerous eosinophils around the bronchi. The basement membrane of the bronchi is thickened and has a wavy appearance.

A large increase in deaths in the 1960s in Great Britain was originally attributed to abuse of aerosol bronchodilators. It is now generally accepted that such use is not a cause of death from asthma. Rather, the excessive use of bronchodilators is a reflection of the need for more effective therapy for these individuals. The increasingly accepted view is that many deaths from asthma are due to inadequate or delayed treatment.

In the workplace, two types of asthma are encountered: work-aggravated and occupational.66 The former is preexisting asthma that is aggravated by irritants in the workplace. Occupational asthma is caused by exposure to irritants in the workplace. Occupational asthma without a latency period follows exposure to high concentrations of irritant gases, fumes, or chemicals on one or several occasions. The most common examples of such agents are chlorine and ammonia. Occupational asthma with a latency period is the most common type and is caused by exposure to irritants over a period of time that can vary from a few weeks to several years. The majority of individuals developing occupational asthma with latency do not recover.

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