MEDICAL WASTE MAY BE A SOURCE OF M TUBERCULOSIS

Contaminated medical waste is a potential source of Mycobacterium tuberculosis infection, according to the results of a recently published environmental study.

Johnson et al studied three employees of a Washington State waste treatment facility who presented with pulmonary tuberculosis. After intensive investigation, the authors concluded that the source of the infections was occupational exposure to infectious medical waste. Among their findings:

• There was no evidence that the infections occurred as a result of exposure to an infected person in the community. DNA fingerprinting also ruled out worker-to-worker transmission.
• Forty-five percent of fellow employees of the three workers had positive tuberculin skin test results.
• Forty-nine percent of Washington State laboratories shipped viable M tuberculosis cultures to medical waste disposal facilities.
• An environmental investigation of the waste disposal facility indicated that workers could have been exposed to contaminated aerosols released by shredded waste in a manner that made them susceptible to infection.
• A DNA fingerprint pattern for an isolate from one of the workers was identical to the pattern for an isolate from a patient whose only exposure had been to the medical waste.

The authors recommended that laboratories review their procedures for disposal of viable M tuberculosis material and that waste treatment facilities not accept contaminated laboratory waste. In addition, people who work with medical waste should undergo extensive and continuous safety training.

Johnson KR, Braden CR, Cairns KL, et al. Transmission of Mycobacterium tuberculosis from medical waste. JAMA. 2000;284:1683-1688.

CLINICAL INDEX PREDICTS ASTHMA RISK IN YOUNG CHILDREN

Simple, easily obtainable clinical criteria can be used in infants and young children to predict their subsequent risk of asthma, data from the Tucson Children's Respiratory Study suggest.

Castro-Rodríguez et al used these data to develop and compare two clinical indexes to assess asthma risk. The criteria in the "stringent" index included frequent wheezing during the first three years of life and either one major risk factor (physician-diagnosed eczema or a parental history of asthma) or two of three minor risk factors (physician-diagnosed allergic rhinitis, wheezing without colds, and eosinophilia of 4% or greater). The criteria in the "loose" index included any wheezing during the first three years of life plus the aforementioned major and minor risk factors. The information needed to apply the loose and stringent indexes was available for 986 and 1,002 children, respectively.

Children who met the criteria for the loose index were 2.6 to 5.5 times more likely to develop asthma at some time during their school years than were those who did not meet these criteria. Children who met the criteria for the stringent index were 4.3 to 9.8 times more likely to subsequently have asthma than were the other children. More than 95% of the children who did not meet the criteria for the stringent index never experienced any symptoms of asthma.

Castro-Rodríguez et al calculated that the loose index had a sensitivity of 41.6%, specificity of 84.7%, positive predictive value of 59.1%, and negative predictive value of 73.2% for subsequent asthma. For the stringent index, the corresponding figures were 15.7%, 97.4%, 76.6%, and 68.3%.

The Tucson Children's Respiratory Study is a longitudinal evaluation of respiratory illnesses in children.

Castro-Rodríguez JA, Holberg CJ, Wright AL, Martinez FD. A clinical index to define risk of asthma in young children with recurrent wheezing. Am J Respir Crit Care Med. 2000;162:1403-1406.

INHALED STEROIDS AND CHILDHOOD GROWTH

Inhaled corticosteroids are a mainstay of therapy for childhood asthma; however, questions have been raised about the effect of these agents on pediatric growth rates. According to two prospective, randomized studies, children who use inhaled budesonide have a reduced growth velocity early in the course of treatment but eventually reach a normal adult height.

In one study, Agertoft and Pedersen reported on 160 adolescents and young adults with persistent asthma. Of these, 142 had been treated with inhaled budesonide (mean daily dose, 412 µg) for an average of 9.2 years; the remaining 18 had never received inhaled corticosteroids and served as controls. The mean ages of the two groups at the time they attained adult height were 18.0 and 18.5, respectively. The authors also examined 51 siblings of the budesonide-treated children (average age, 21.4 years); these siblings were also used as controls. In all three groups, more than 95% of the children reached an adult height within 9 cm of their target adult height. (Normally, 95% of the general population is expected to attain an adult height within that range.) A reduction in annual growth rate was found to have occurred during the early years of budesonide therapy, but it proved to be transient.

In the other study, investigators from the Childhood Asthma Management Program Research Group compared the efficacy of budesonide with that of nedocromil in 1,041 children, ages 5 through 12 years, with mild-to-moderate asthma. Of these, 311 were randomized to budesonide (200 µg twice daily), 312 to nedocromil (8 mg twice daily), and 418 to placebo. Treatment continued for four to six years.

Neither of the active treatments was found to be superior to placebo in its ability to improve lung function (as measured by the change in FEV1 following bronchodilator use). However, budesonide was more effective than nedocromil or placebo in improving airway responsiveness to methacholine challenge and, more significantly, in controlling asthma symptoms.

At the end of the study, the average increase in height among the budesonide-treated children was about 1 cm less than that in the nedocromil-treated patients or controls. The difference in growth rate was most apparent during the first year of treatment. By the study's end, the projected final height was similar in all three groups.

In an accompanying editorial, Wohl and Majzoub agreed that the results of both studies are reassuring. However, they noted that neither study addressed the effect of inhaled corticosteroids on the growth of organs such as the brain and lung. The current lack of understanding about the effect of inhaled corticosteroids on the development of these organs suggests that a cautious approach to their use in young children is advisable. Thus, Wohl and Majzoub maintained that it would be injudicious to use the findings of these two studies as a basis for prescribing inhaled corticosteroids for young children with mild disease.

Agertoft L, Pedersen S. Effect of long-term treatment with inhaled budesonide on adult height in children with asthma. N Engl J Med. 2000;343:1064-1069.
The Childhood Asthma Management Program Research Group. Long-term effects of budesonide or nedocromil in children with asthma. N Engl J Med. 2000;343:1054-1063.
Wohl ME, Majzoub JA. Asthma, steroids, and growth. N Engl J Med. 2000;343:1113-1114.

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