161277
Passive Smoking, Inflammatory Markers and Childhood Asthma
Monday, November 5, 2007: 5:30 PM
Arnold Platzker, MD
,
Pediatrics, Children's Hospital, Los Angeles, Los Angeles, CA
Children from 0 to 4 years have the highest hospitalization and prevalence rates in the U.S. Smoking during pregnancy has been implicated as a risk factor for childhood asthma and may affect severity. One of the great challenges in pediatric respiratory medicine is to identify early stages of asthma during the first years of life. Serum eosinophilic cationic protein (ECP) and urinary eosinophilic protein X (EPX) have the potential for a medical breakthrough in the diagnosis of asthma in children. Serum ECP is associated with asthma activity, anti-inflammatory treatment, atopy, and environmental tobacco smoke (ETS), whereas uEPX increases with wheeze/asthma, decreasing age, and eczema. Remarkably, sECP and uEPX and the role of ETS have never been investigated in young children. We hypothesize that sECP and/or uEPX may be valuable measures of eosinophil activation in young asthmatics, particularly those exposed to ETS during pregnancy and postnatally (via breast-feeding). A prospective study is being conducted to recruit approximately 140 Caucasian, African-American, Hispanic, and Asian children (0-4 years), newly diagnosed with asthma at hospitals in Southern California. A comparison group of 140 controls, matched on age, race, sex, and hospital are also being recruited from pediatrics clinics. All parents complete a detailed telephone interview, 2 follow-up questionnaires, and a diary on asthma symptoms. Infants also provide urine and serum at baseline, and every 4 months, for one year. SECP and uEPX may be predictors of future asthma development and severity, and permit differentiation of susceptible infants exposed to ETS in utero/postnatally.
Learning Objectives: 1. To gain an appreciation of the high prevalence of childhood asthma in infants and young children, and to recognize the importance of this understudied and undertreated population in research.
2. To understand the joint role of environmental tobacco smoke in utero/ postnatally and genetic predisposition in pediatric asthma.
3. To become familiar with two novel inflammatory markers in the blood and urine that may identify future childhood asthmatics earlier in life, before they develop permanent lung damage.
Presenting author's disclosure statement:Any relevant financial relationships? No Any institutionally-contracted trials related to this submission?
I agree to comply with the American Public Health Association Conflict of Interest and Commercial Support Guidelines,
and to disclose to the participants any off-label or experimental uses of a commercial product or service discussed
in my presentation.
|