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2. : , SENSITIZATION -- : - , , outdoor indoor ? - , ? - , ( )- , ? - , 0lag- - , , . - , - - , - 3. : RESIRATORY ALLERGIC DISEASES - , : -, 4. Bibliographic search: articles published 2005-2011 : PubMed (NLM and NIH), Embase.com (Elsevier). ScienceDirect, Informaworld, SpringerLink, Science, Scholar Google. Key words: short term/acute exposure; traffic-related airpollution; schoolchildren; health ; health-outcome Inclusion: 9 studies on Exposure to outdoor and indoor air pollution School children between ages 6-20 years old. Study design: cross-sectional / cohort studies. Geographical ascription: (world-wide) Europe; Canada; USA; 5. Airborne particulates: PM10, PM2.5, PM1.0 (ultra-fine) Nitrogen oxides (NOX): NO, NO2 Sulfur dioxide (SO2) Carbon monoxide (CO) Ozone (O3) EC (elemental carbon), BC (black carbon) andOC (optical carbon) fractions (soot) Benzene 6. Asthma, respiratory outcomes, allergy (Nicolai et al 2003) symptoms of asthma and allergic sensitisation(Annesi-Maesano et al 2007, Brunekreef et al2009). Lung function decrements (Dales et al 2009) Lung function (Delfino et al 2008) Respiratory outcomes (Oconnor et al 2008, Graveland et al 2010, Patel et al 2010, Spira-Cohen et al 2011) Lung function and atopy (Romieu et al 2008), 7. Large studies - the ISAAC (International Study of Asthma and Allergies inChildhood) protocol: Munich, Germany (Phase II): 7,509.childrenSchool beginners (57 yrs), Fourth grade (911 yrs) The French six study (6C): 5,338 elementary children (10.40.7 yrs). World-wide study (Phase III): 45 developing, 30 developed countries: 315,572 children 1314 yrs, 110 centers (46 countries) 197,515 children 67 yrs, 70 centers (29 countries) Netherlands, 9 Dutch schools 30000vehiclesday-1 in street segment 30000 vTable 5: Respiratory and atopic outcomes in relation to traffic counts (high exposure tertile) ehiclesday-1 in street segment 8 years). In Dutch children: Short-term (not long-term) changes in ambient PM10largely attributable to biomass burning are associated with increased levelsof exhaled NO (marker of airway inflammation) 36. In Canadian children with asthma: Relatively low concentrations of urban air pollution worsenlung function over a short period of time, even within a day. (PM2.5 appears to be the mostimportant pollutant). In US inner-city children with asthma: short-term increases in air pollutant concentrationsbelow the National Ambient Air Quality Standards were associated with adverse respiratoryhealth effects (reflected in pulmonary function) / absence from school . (The associations withNO2 suggest that motor vehicle emissions may be causing excess morbidity in thispopulation). In US adolescents: Acute exposures to traffic-related pollutants- DEPs (diesel exhaustparticles- a local driver of urban PM2.5); and/or NO2 may contribute to increased respiratorymorbidity ; urban residents (compared with suburban) and asthmatics may be at increasedrisk. In NY-Bronx: Significantly elevated same-day relative risks of cough , wheeze ,shortness ofbreath and total symptoms were found with an increase in personal EC, but not with personalPM2.5 mass.Increased risk of cough and total symptoms was found with increased one-day lag and two-day average school-site.Adverse health associations were strongest with personal measures of EC exposure,suggesting that the diesel soot fraction of PM2.5 is most responsible for pollution-relatedasthma exacerbations among children living proximal to roadways. Studies that rely onexposure to particulate mass may underestimate PM health impacts.