In a study of the effect of exposure to air pollution on children with asthma in 12 Southern California communities, researchers concluded that organic carbon and nitrogen dioxide deserve greater attention as potential causes of chronic bronchitis in children with asthma. They also assert that previous cross-sectional studies may have underestimated the risks associated with air pollution. The researchers examined 475 children with asthma. Under investigation were different size fractions of particulate matter, particulate organic compound, elemental carbon, nitrogen dioxide, and other-traffic related pollutants. Among the 475 children with asthma in the Children's Health Study, 184 (38.7 percent) had symptoms of bronchitis during the first year they were involved in the analysis. Children with a history of wheeze during the first year before study entry or allergies in the past were significantly more likely to report symptoms. The researchers noted that team sports modified the yearly variability of nitrogen dioxide, which affected only children playing team sports. As assessed by the researchers from 1996 through 1999, the children's symptoms were associated with the yearly variability in the amount of particulate matter. The authors said that organic carbon accounts for almost half of the "fine" particulate matter mass in the Los Angeles air basis. They point out that organic carbon is largely due to emissions from gasoline and diesel vehicle exhaust in Southern California. The study appears in the first issue for October 2003 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.
AIRWAY INFLAMMATION IN CHILDREN WITH ASTHMA SHOWS PATHOLOGIC FEATURES OF ADULT DISEASE
Italian researchers have shown that pathologic features characteristic of adult asthma are already present in children with mild to moderate disease. The elements revealed by the investigators are comprised of basement membrane thickening, plus an increase in eosinophils, which have already appeared in the children with asthma. The authors' results were based on an analysis of bronchial biopsies from 23 children undergoing bronchoscopy for clinical problems other than asthma. In the study group, seven of nine children had mild asthma, with two having moderate disease; six had atopy (inherited tendency toward an allergy) without asthma; eight were normal controls without either atopy or asthma. The authors said that their observation about the presence of both thickening of the basement membrane and airway eosinophilia in children with mild asthma suggest that airway remodeling processes begin early in the course of the disease and most likely occur in parallel with the establishment of chronic inflammation and not sequential to it. (Eosinophilia is an increase in the number of eosinophils, a type of white blood cell, which commonly occurs in allergic reactions.) They said that as far as they knew no study had addressed the issue of quantifying airway inflammatory and structural changes in children with mild to moderate asthma and comparing them with appropriate pediatric control subjects. The study appears in the first issue for October 2003 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.
NEW ALPHA-1 ANTITRYPSIN DEFICIENCY STANDARDS
FOR DISEASE DIAGNOSIS AND MANAGEMENT
Alpha-1 antitrypsin (AAT) deficiency, a hereditary disorder that can cause liver and lung disease, is frequently under recognized and misdiagnosed by clinicians, according to the latest "Standards for the Diagnosis and Management of Individuals with Alpha-1 Antitrypsin Deficiency." The new guidelines are published in the first issue for October 2003 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine. Under sponsorship of the American Thoracic Society, the European Respiratory Society, and the Alpha-1 Foundation, the report by a large group of international experts urges physicians to look for certain features that should raise their index of suspicion about the presence of this problem. These characteristics include: early onset of emphysema (age 45 or less); emphysema without the presence of other recognized risk factors such as smoking, occupational dust exposure, etc.; and a family history of emphysema, together with several other lung diseases. For related liver disease, relatives with liver disease offer a significant risk. The prevalence, estimated from several large population studies, seems to vary from 1 in 1,600 newborns to 1 in over 5,000 newborns, depending on study and location. From a clinical standpoint, pulmonary emphysema appears to be related most prominently to the deficiency and is a major cause of disability and death. Cirrhosis and carcinoma of the liver affect about 30 to 40 percent of those with AAT deficiency over the age of 50. The obstructive lung disease associated the deficiency is treatable with general medical management. No specific therapy for advanced liver disease is available, other than transplantation.
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Journal
American Journal of Respiratory and Critical Care Medicine