Observations on asthma.
A review of the present understanding of asthma leads to the following conclusions: an elevated IgE is the principal risk factor in the development of childhood asthma; secondary exposure to a wide range of environmental agents (including indoor bioallergens) accounts for the variations in prevalence; prevalence (defined by a positive answer to the question "Have you ever had doctor-diagnosed asthma?") ranges between 4 and 8% in children. Black children have a slightly higher prevalence than white children in the United States, and in both races boys have a higher prevalence than girls. A high prevalence is found in Puerto Rican children in the United States. Patterns of utilization of health care resources (hospital emergency departments, individual physicians, etc.) are dependent on economic circumstances. Low-income children have higher annual morbidity (days in hospital, days off school, etc.) than higher income children and are more dependent on hospital emergency departments for primary care. Relatively little is known about nonatopic asthma in adults, although virus infections and occupational exposures play some part in its induction. There are some striking examples of asthma attack periodicity, and much may be learned from these. Hospital admissions for asthma have increased in many regions over the past 15 years; it is unlikely that this represents the increased admission of milder cases and hence would indicate that asthma has become more severe. This is likely to be a more sensitive indicator of change than mortality. Associations between indices of health effects and air pollutants indicate that these are probably playing a role in the worsening of asthma. Adverse effects related to SO2 and NO2 exposures have been documented, and fine particulate pollution (PM10) is also associated with worsening of asthma. Ozone is an intense respiratory irritant, and, together with acid aerosols, may well be playing a role in the worsening of asthma. It is not known whether any of these agents are affecting prevalence.
Bates
D V
DV
Department of Health Care and Epidemiology, University of British Columbia, Vancouver, Canada.
D000328:Adult; D000393:Air Pollutants / Q000633:toxicity*; D001249:Asthma / Q000453:epidemiology / Q000209:etiology*; D016535:Bronchial Hyperreactivity / Q000209:etiology; D002648:Child; D005260:Female; D006801:Humans; D008297:Male; D009585:Nitrogen Dioxide / Q000633:toxicity; D010083:Oxidants, Photochemical / Q000633:toxicity; D013458:Sulfur Dioxide / Q000633:toxicity; D014481:United States / Q000453:epidemiology
D000393:Air Pollutants; D010083:Oxidants, Photochemical; D013458:Sulfur Dioxide; D009585:Nitrogen Dioxide