Your SlideShare is downloading. ×
WHAT YOU SHOULD HAVE READ BUT….2012                 atopy risk &                protective factorsAttilio BonerUniversity...
• Prevalence and time         trends
Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy.           ...
Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy.           ...
Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy.           ...
Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy.           ...
Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy.           ...
Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy.           ...
Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy.           ...
Resilience in low-socioeconomic-status children            with asthma: adaptations to stress.                      Chen, ...
Resilience in low-socioeconomic-status children             with asthma: adaptations to stress.                           ...
Resilience in low-socioeconomic-status children             with asthma: adaptations to stress.                           ...
Resilience in low-socioeconomic-status children             with asthma: adaptations to stress.                           ...
Allergy is associated with suicide completion with apossible mediating role of mood disorder-a population-          based ...
Allergy is associated with suicide completion with apossible mediating role of mood disorder-a population-          based ...
Allergy is associated with suicide completion with apossible mediating role of mood disorder-a population-          based ...
Allergy is associated with suicide completion with apossible mediating role of mood disorder-a population-          based ...
Impaired type I and III interferon response to    rhinovirus infection during pregnancy and asthma                    Forb...
Impaired type I and III interferon response to     rhinovirus infection during pregnancy and asthma                      F...
Impaired type I and III interferon response to  rhinovirus infection during pregnancy and asthma                   Forbes,...
Impaired type I and III interferon response to   rhinovirus infection during pregnancy and asthma                     Forb...
Impaired type I and III interferon response to   rhinovirus infection during pregnancy and asthma                     Forb...
Febrile respiratory illnesses in infancy and atopy are    risk factors for persistent asthma and wheeze                   ...
Febrile respiratory illnesses in infancy and atopy are    risk factors for persistent asthma and wheeze                   ...
Febrile respiratory illnesses in infancy and atopy are    risk factors for persistent asthma and wheeze                   ...
Febrile respiratory illnesses in infancy and atopy are   risk factors for persistent asthma and wheeze                 Kus...
Staphylococcal-derived superantigen enhances peanut          induced Th2 responses in the skin.            Forbes-Blom, Cl...
Staphylococcal-derived superantigen enhances peanut          induced Th2 responses in the skin.            Forbes-Blom, Cl...
Staphylococcal-derived superantigen enhances peanut         induced Th2 responses in the skin.             Forbes-Blom, Cl...
Staphylococcal enterotoxin B compromises   the immune tolerant status in the airway mucosa.                 Liu T, Clin Ex...
Staphylococcal enterotoxin B compromises   the immune tolerant status in the airway mucosa.                 Liu T, Clin Ex...
Staphylococcal enterotoxin B compromises    the immune tolerant status in the airway mucosa.                 Liu T, Clin E...
Staphylococcal enterotoxin B compromises    the immune tolerant status in the airway mucosa.                 Liu T, Clin E...
Gram+ bacteria on grass pollen exhibit adjuvant activity       inducing inflammatory T cell responses           Heydenreic...
Gram+ bacteria on grass pollen exhibit adjuvant activity       inducing inflammatory T cell responses             Heydenre...
Gram+ bacteria on grass pollen exhibit adjuvant activity       inducing inflammatory T cell responses             Heydenre...
Gram+ bacteria on grass pollen exhibit adjuvant activity       inducing inflammatory T cell responses             Heydenre...
Gram+ bacteria on grass pollen exhibit adjuvant activity       inducing inflammatory T cell responses             Heydenre...
Gram+ bacteria on grass pollen exhibit adjuvant activity       inducing inflammatory T cell responses          Heydenreich...
Innate lymphoid cells responding to IL-33 mediate    airway hyperreactivity independently of adaptive             immunity...
Innate lymphoid cells responding to IL-33 mediate  airway hyperreactivity independently of adaptive           immunity Kim...
Innate lymphoid cells responding to IL-33 mediate  airway hyperreactivity independently of adaptive           immunity Kim...
Innate lymphoid cells responding to IL-33 mediate   airway hyperreactivity independently of adaptive            immunity K...
Gestational age at birth and risk of allergic rhinitis  in young adulthood. Crump JACI 2011;127:1173                      ...
Gestational age at birth and risk of allergic rhinitis  in young adulthood. Crump JACI 2011;127:1173     These findings su...
Infant antibiotic use and wheeze and asthma risk: a         systematic review and meta-analysis                     Pender...
Infant antibiotic use and wheeze and asthma risk: a        systematic review and meta-analysis                Penders ERJ ...
Prenatal or Early-Life Exposure to Antibiotics and Risk      of Childhood Asthma: A Systematic Review                Murk ...
Prenatal or Early-Life Exposure to Antibiotics and Risk      of Childhood Asthma: A Systematic Review                Murk ...
Prenatal or Early-Life Exposure to Antibiotics and Risk      of Childhood Asthma: A Systematic Review                Murk ...
•paracetamol
The Association of Acetaminophen and Asthma Prevalence and Severity McBride Pediatrics 2011;128:1181• The epidemiologic as...
The Association of Acetaminophen and Asthma Prevalence and Severity McBride Pediatrics 2011;128:1181• The epidemiologic as...
The Association of Acetaminophen and Asthma Prevalence and Severity McBride Pediatrics 2011;128:1181• The epidemiologic as...
•Allergens
Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city            p...
Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city            p...
Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city            p...
Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city            p...
•Allergens  •acari
Inhibition of house dust mite–induced allergic airwaysdisease by antagonism of microRNA-145 is comparable  to glucocortico...
Inhibition of house dust mite–induced allergic airwaysdisease by antagonism of microRNA-145 is comparable  to glucocortico...
Inhibition of house dust mite–induced allergic airwaysdisease by antagonism of microRNA-145 is comparable  to glucocortico...
Invariant NKT cells are required for airway inflammation           induced by environmental antigens                  Wing...
Invariant NKT cells are required for airway inflammation           induced by environmental antigens                Wingen...
Invariant NKT cells are required for airway inflammation           induced by environmental antigens               Wingend...
House dust mite extract downregulates C/EBPα* in         asthmatic bronchial smooth muscle cells                          ...
House dust mite extract downregulates C/EBPα* in         asthmatic bronchial smooth muscle cells                          ...
Playing a dirty trick on airway smooth muscle: house dust       mite does it again    Zuyderduyn ERJ 2011;38:4   Airway s...
Playing a dirty trick on airway smooth muscle: house dust       mite does it again    Zuyderduyn ERJ 2011;38:4   In addit...
Playing a dirty trick on airway smooth muscle: house dust       mite does it again    Zuyderduyn ERJ 2011;38:4   Exposure...
Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and     non-sensit...
Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and     non-sensit...
Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and     non-sensit...
Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and     non-sensit...
Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and     non-sensit...
Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and     non-sensit...
Protease-activated receptor 2-dependent fluid secretion   from airway submucosal glands by house dust mite              ex...
Protease-activated receptor 2-dependent fluid secretion   from airway submucosal glands by house dust mite              ex...
Protease-activated receptor 2-dependent fluid secretion   from airway submucosal glands by house dust mite              ex...
Protease-activated receptor 2-dependent fluid secretion   from airway submucosal glands by house dust mite              ex...
Protease-activated receptor 2-dependent fluid secretion   from airway submucosal glands by house dust mite              ex...
Protease-activated receptor 2-dependent fluid secretion   from airway submucosal glands by house dust mite              ex...
Gene-by-environment effect of house dust mite on  purinergic receptor P2Y12 (P2RY12) & lung function in                  c...
Gene-by-environment effect of house dust mite on  purinergic receptor P2Y12 (P2RY12) & lung function in                  c...
Gene-by-environment effect of house dust mite on  purinergic receptor P2Y12 (P2RY12) & lung function in                  c...
Gene-by-environment effect of house dust mite onpurinergic receptor P2Y12 (P2RY12) & lung function in                child...
•Allergens•Cane e gatto
The long-term protective effects of domestic animals         in the home. Erwin CEA 2011;41:920 There is a critical age a...
The long-term protective effects of domestic animals         in the home. Erwin CEA 2011;41:920 Children living in a hous...
Lifetime dog and cat exposure and dog- and cat-        specific sensitization at age 18 years                  Wegienka CE...
Lifetime dog and cat exposure and dog- and cat-        specific sensitization at age 18 years                  Wegienka CE...
Lifetime dog and cat exposure and dog- and cat-        specific sensitization at age 18 years                  Wegienka CE...
Risk factors for new-onset cat sensitization amongadults: A population-based international cohort study                  O...
Risk factors for new-onset cat sensitization among adults: A population-based international cohort study                  ...
Risk factors for new-onset cat sensitization among adults: A population-based international cohort study                  ...
Risk factors for new-onset cat sensitization amongadults: A population-based international cohort study                   ...
Effect of prenatal indoor pet exposure on the trajectory          of total IgE levels in early childhood                  ...
Effect of prenatal indoor pet exposure on the trajectory          of total IgE levels in early childhood                  ...
Effect of prenatal indoor pet exposure on the trajectory          of total IgE levels in early childhood                  ...
Effect of prenatal indoor pet exposure on the trajectory          of total IgE levels in early childhood                  ...
Effect of prenatal indoor pet exposure on the trajectory          of total IgE levels in early childhood                  ...
Effect of prenatal indoor pet exposure on the trajectory          of total IgE levels in early childhood                  ...
Effect of prenatal indoor pet exposure on the trajectory          of total IgE levels in early childhood                  ...
High environmental relative moldiness index during  infancy as a predictor of asthma at 7 years of age       Reponen Ann A...
High environmental relative moldiness index during infancy as a predictor of asthma at 7 years of age          Reponen Ann...
Asthma related to Alternaria sensitization:    an analysis of skin-test and serum-specific IgE   efficiency based on the b...
Asthma related to Alternaria sensitization:    an analysis of skin-test and serum-specific IgE   efficiency based on the b...
Asthma related to Alternaria sensitization:    an analysis of skin-test and serum-specific IgE   efficiency based on the b...
Meta-analysis of mould and dampness exposure on  asthma and allergy in eight European birth cohorts:    an ENRIECO initiat...
Meta-analysis of mould and dampness exposure on  asthma and allergy in eight European birth cohorts:    an ENRIECO initiat...
Lung function decline in relation to mould and      dampness in the home: the longitudinal European      Community Respira...
Lung function decline in relation to mould and      dampness in the home: the longitudinal European      Community Respira...
Lung function decline in relation to mould and     dampness in the home: the longitudinal European     Community Respirato...
Lung function decline in relation to mould and   dampness in the home: the longitudinal European   Community Respiratory H...
•Smokingpassive-active
School absenteeism among children living with smokers                  Levy Pediatrics 2011;128:650                       ...
School absenteeism among children living with smokers                  Levy Pediatrics 2011;128:650                       ...
School absenteeism among children living with smokers                 Levy Pediatrics 2011;128:650                        ...
Secondhand Smoke Exposure and Neurobehavioral     Disorders Among Children in the United States                     Kabir,...
Secondhand Smoke Exposure and Neurobehavioral  Disorders Among Children in the United States                 Kabir, Pediat...
Secondhand Smoke Exposure and Neurobehavioral  Disorders Among Children in the United States         Children exposed to S...
Parental Smoking and Vascular Damage             in Their 5-year-old Children                Geerts, Pediatrics 2012;129;4...
Parental Smoking and Vascular Damage             in Their 5-year-old Children                Geerts, Pediatrics 2012;129;4...
Parental Smoking and Vascular Damage             in Their 5-year-old Children                Geerts, Pediatrics 2012;129;4...
Parental Smoking and Vascular Damage             in Their 5-year-old Children                Geerts, Pediatrics 2012;129;4...
Parental Smoking and Vascular Damage             in Their 5-year-old Children                Geerts, Pediatrics 2012;129;4...
Parental Smoking and Vascular Damage           in Their 5-year-old Children              Geerts, Pediatrics 2012;129;45Dif...
Parental Smoking and Vascular Damage            in Their 5-year-old Children               Geerts, Pediatrics 2012;129;45D...
Parental Smoking and Vascular Damage      in Their 5-year-old Children        Geerts, Pediatrics 2012;129;45Paternal and m...
Parental Smoking and the Risk of Middle Ear Disease           in Children. Jones L, APAM 2012;166:18                      ...
Parental Smoking and the Risk of Middle Ear Disease           in Children. Jones L, APAM 2012;166:18                      ...
Parental Smoking and the Risk of Middle Ear Disease           in Children. Jones L, APAM 2012;166:18                      ...
Secondhand Smoke Exposure in Cars Among Middle and High School Students—United States, 2000–2009              King, Pediat...
Secondhand Smoke Exposure in Cars Among Middle and High School Students—United States, 2000–2009                King, Pedi...
Exposure to parental and sibling smoking and the risk   of smoking uptake in childhood and adolescence:        a systemati...
Exposure to parental and sibling smoking and the risk   of smoking uptake in childhood and adolescence:        a systemati...
Exposure to parental and sibling smoking and the risk   of smoking uptake in childhood and adolescence:        a systemati...
Smoking    inpregnancy
Promoting Tobacco to Women of Reproductive Age       Harms Fetuses. Farber H, Chest 2012;141:839 In utero tobacco smoke e...
Promoting Tobacco to Women of Reproductive Age       Harms Fetuses. Farber H, Chest 2012;141:839 Smoking cessation either...
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
What 2012 atopy risk protective factor
Upcoming SlideShare
Loading in...5
×

What 2012 atopy risk protective factor

5,181

Published on

Published in: Health & Medicine, Technology
0 Comments
3 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total Views
5,181
On Slideshare
0
From Embeds
0
Number of Embeds
3
Actions
Shares
0
Downloads
0
Comments
0
Likes
3
Embeds 0
No embeds

No notes for slide

Transcript of "What 2012 atopy risk protective factor"

  1. 1. WHAT YOU SHOULD HAVE READ BUT….2012  atopy risk & protective factorsAttilio BonerUniversity ofVerona, Italy
  2. 2. • Prevalence and time trends
  3. 3. Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:545Background: Prenatal exposure to both stress & aeroallergens(dust mite) may modulate the fetal immune system. These exposuresmay interact to affect the newborn immune response. We examinedassociations between prenatal maternal stress & cord blood total IgEin 403 predominately low-income minority infants enrolledin the Asthma Coalition on Community, Environment and Social Stress(ACCESS) project. We also examined potential modifying effectsof maternal atopy and maternal dust mite exposure.
  4. 4. Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:545 1) Overall the negative domains score was The Crisis in Family positively associated Systems survey with increased was administered cord blood IgE. to mothers prenatally. 2) Cord blood IgE levels Negative life event increased 0.10 IU/ml domain score was derived. for each unit increase Dust mite allergen in dust in the number of negative from pregnant mothers„ domains reported bedrooms. by the mother.
  5. 5. Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:545 Relationship for atopic mothers between log cord blood IgE & n°of domains with negative life events by high vs low dust mite allergen. The Crisis in Family Systems survey was administered to mothers prenatally. Negative life event domain score was derived. Dust mite allergen in dust from pregnant mothers„ bedrooms.
  6. 6. Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:545 Relationship for atopic mothers between log cord blood IgE & n°of domains with negative life events by high vs low dust mite allergen. Among children The Crisis in Family of atopic Systems survey mothers, the positive was administered association between to mothers prenatally. stress & IgE Negative stronger was life event domain high dust mite in the score was derived. group. Dust mite allergen in dust from pregnant mothers„ bedrooms.
  7. 7. Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:545 Relationship for nonatopic mothers between log cord blood IgE & n°of domains with negative life events by high vs low dust mite allergen. The Crisis in Family Systems survey was administered to mothers prenatally. Negative life event domain score was derived. Dust mite allergen in dust from pregnant mothers„ bedrooms.
  8. 8. Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:545 Relationship for nonatopic mothers between log cord blood IgE & n°of domains with negative life events by high vs low dust mite allergen. In children Themothers without of Crisis in Family Systems survey a history of atopy, was administered the positive to mothers prenatally. association between Negative & IgE was stress life event most evident domain score was derived. in the low allergen Dust mite allergen in dust group. from pregnant mothers„ bedrooms.
  9. 9. Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:5451) These data suggest that prenatal maternal stress may influence fetal immune system development in children born to mothers both with and without a history of atopy.2) Moreover, the demonstration of synergistic effects of stress & aeroallergen exposure points to the need for a multi pronged intervention approach to reducing disease risk.
  10. 10. Resilience in low-socioeconomic-status children with asthma: adaptations to stress. Chen, JACI 2011;128:970Background:Low socioeconomic status (SES) is a strong predictor of manyhealth problems, including asthma impairment;however, little is understood about why some patients defy this trendby exhibiting good asthma control despite living in adverseenvironments.Objective:This study sought to test whether a psychological characteristic,the shift-and-persist strategy (dealing with stressors by reframingthem more positively while at the same time persisting in optimisticthoughts about the future), protects low-SES children with asthma.
  11. 11. Resilience in low-socioeconomic-status children with asthma: adaptations to stress. Chen, JACI 2011;128:970 121 children aged 9 to 18 yrs with asthma. 1) „„I thought about the Shift-and-persist scores. things I was learning The tendency to shift oneself from the situation or in response to stressors about something good was measured by using the that would come from it‟‟. Cognitive Restructuring scale of the Responses to Stress questionnaire. 2) „„I always feel good about Smith, J Consult Clin Psychol 2000;68:976. my future‟‟. Higher scores indicated a higher tendency to positively reappraise stressful situations.
  12. 12. Resilience in low-socioeconomic-status children with asthma: adaptations to stress. Chen, JACI 2011;128:970 121 children aged 9 to 18 yrs with asthma. Children who came from Shift-and-persist scores. low-SES backgrounds The tendency to shift oneself but who engaged in in response to stressors shift-and-persist strategies was measured by using the displayed less asthma Cognitive Restructuring scale inflammation at baseline of the Responses to Stress questionnaire. (p <0.05) Smith, J Consult Clin Psychol 2000;68:976. as well as less asthma impairment Higher scores indicated a higher (p <0.01) tendency to positively reappraise stressful situations. at the 6-mo period.
  13. 13. Resilience in low-socioeconomic-status children with asthma: adaptations to stress. Chen, JACI 2011;128:970 121 children aged 9 to 18 yrs with asthma. Children In contrast, Shift-and-persist scores. who came from shift-and-persist low-SES backgrounds The tendency to shift oneself but who engaged in strategies in response to stressors shift-and-persist strategies were not beneficial was measured by using the displayed less asthma Cognitive Restructuring scale among high-SES of the Responses to Stress inflammation at baseline children with questionnaire. (p <0.05) as well as asthma. Smith, J Consult Clin Psychol 2000;68:976. less asthma impairment Higher scores indicated a higher (p <0.01) tendency to positively reappraise stressful situations. at the 6-mo period.
  14. 14. Allergy is associated with suicide completion with apossible mediating role of mood disorder-a population- based study Qin, Allergy 2011;66:658 % subjects with a history of hospital contact for allergy 2 – 27 096 completedsuicides.467 571 live controls. 1 – 1.17 % 0.79 % 0 Suicide Controls
  15. 15. Allergy is associated with suicide completion with apossible mediating role of mood disorder-a population- based study Qin, Allergy 2011;66:658 % subjects with a history of hospital contact for allergy 2 – We observed a 27nonsignificantly 096 completed stronger effectsuicides. in women than in men and a467 571 live controls. 1 – 1.17 % stronger effect 0.79 % for individuals at high ages 0 Suicide Controls
  16. 16. Allergy is associated with suicide completion with apossible mediating role of mood disorder-a population- based study Qin, Allergy 2011;66:658 OR for suicide 2 – 27 096 completedsuicides. 1.59467 571 live controls. 1 – 0 Allergy that led to inpatient treatment
  17. 17. Allergy is associated with suicide completion with apossible mediating role of mood disorder-a population- based study Qin, Allergy 2011;66:658 OR for suicide Allergy increased 2 – suicide risk only in 27 persons with no 096 completedsuicides. history of mood 1.59 disorder, whereas467 571eliminated it live controls. 1 – suicide risk in those with a history of mood disorder. 0 Allergy that led to inpatient treatment
  18. 18. Impaired type I and III interferon response to rhinovirus infection during pregnancy and asthma Forbes, Thorax 2012;67:209Background:• Acute respiratory tract infections are common ailments to all individuals and the human rhinoviruses (HRVs) cause most of these infections.• Pregnant women have increased susceptibility and disease severity to viral infections like influenza and HRVs, as do asthmatics.• Successful pregnancy requires immunological modulation to permit fetal tolerance.
  19. 19. Impaired type I and III interferon response to rhinovirus infection during pregnancy and asthma Forbes, Thorax 2012;67:209 A) Pregnant women had significantly reduced 1) 10 stable pregnant asthmatics; innate IFN responses 2) 10 stable not pregnant asthmatics; to HRV infection 3) 10 pregnant non-asthmatic women; (p<0.02), persistin 4) 10 who were ≥6 mo post partum; g ≥6 mo 5) 10 who were not pregnant. post partum (p≤0.02). Peripheral blood mononuclear cells (PBMCs) cultured with B) Pregnant asthmatics HRV43 and HRV1B. had significantly reduced IFNλ responses IFNα and IFNλ (lambda) compared with from culture supernatants. healthy non-pregnant women (p≤0.034).
  20. 20. Impaired type I and III interferon response to rhinovirus infection during pregnancy and asthma Forbes, Thorax 2012;67:209 Interferon-α (IFNα) and IFNλ responsesof peripheral blood mononuclear cells (PBMCs) from pregnant women to in vitro human rhinovirus (HRV) stimulation. Isolated PBMCs from pregnant (P), postpartum (PP) and non-pregnant healthy control (HC) women were stimulated with HRV43 or HRV1B. = IFNα = IFNλ
  21. 21. Impaired type I and III interferon response to rhinovirus infection during pregnancy and asthma Forbes, Thorax 2012;67:209 Interferon-α (IFNα) and IFNλ responsesof peripheral blood mononuclear cells (PBMCs) from asthmatic women to in vitro human rhinovirus (HRV) stimulation. Isolated PBMCs from non-pregnant healthy control (HC) women and asthmatics who were pregnant (PA) and not pregnant (A) were stimulated = IFNα = IFNλ with HRV43 or HRV1B.
  22. 22. Impaired type I and III interferon response to rhinovirus infection during pregnancy and asthma Forbes, Thorax 2012;67:209 Interferon-α (IFNα) and IFNλ responses Reduced antiviral IFNsof peripheral blood mononuclear asthma provide an asthmatic women during pregnancy and cells (PBMCs) from important to in vitro human rhinovirus (HRV) stimulation. mechanism for increased susceptibility, morbidity and mortality in pregnant women with respiratory viral infection. Isolated PBMCs from non-pregnant healthy control (HC) women and asthmatics who were pregnant (PA) and not pregnant (A) were stimulated = IFNα = IFNλ with HRV43 or HRV1B.
  23. 23. Febrile respiratory illnesses in infancy and atopy are risk factors for persistent asthma and wheeze Kusel, Eur Respir J 2012;39:876 At age of 10 years % of children 60 - 147 children at 60% 50 – high atopic risk. 40 – Followed from birth to age 10 yrs. 30 – Respiratory infections 20 – 26% collected prospectively 20.4% and viral aetiology 18% 10 – ascertained. 000 Current Current Persistent Atopy wheeze and Atopic doctor-diagnosed eczema asthma wheeze eczema and asthma.
  24. 24. Febrile respiratory illnesses in infancy and atopy are risk factors for persistent asthma and wheeze Kusel, Eur Respir J 2012;39:876 At age of 10 years % of children 60 - 147 children at 60% 50 – high atopic risk. 35.8% experienced 40 – Followed from lower at least one birth to age 10 yrs.respiratory infection 30 – (LRI) associated Respiratory infections with fever and/or 20 – 26% collected prospectively 20.4% wheeze in first and viral aetiology 18% 10 – ascertained. life. year of 000 Current Current Persistent Atopy wheeze and Atopic doctor-diagnosed eczema asthma wheeze eczema and asthma.
  25. 25. Febrile respiratory illnesses in infancy and atopy are risk factors for persistent asthma and wheeze Kusel, Eur Respir J 2012;39:876 In children who had wheezy or febrile LRI in infancy and were atopic by 2 yrs 147 children at RR at age 10yrs for high atopic risk. 5 - 4.92 Followed from birth 4 - p<0.001 to age 10 yrs. 3 – 3.51 Respiratory infections p<0.001 collected prospectively and viral aetiology 2 – ascertained. 1 – Atopy wheeze and doctor-diagnosed eczema and asthma. 0 persistent current wheeze asthma
  26. 26. Febrile respiratory illnesses in infancy and atopy are risk factors for persistent asthma and wheeze Kusel, Eur Respir J 2012;39:8761. Severe viral respiratory infections in infancy and early atopy are risk factors for persistent wheeze and asthma.2. The strongest marker of the asthmatogenic potential of early life infections was concurrent fever.3. The occurrence of fever during respiratory illnesses is an important marker of risk for wheeze and asthma later in childhood, suggesting it should be measured in prospective studies of asthma aetiology.
  27. 27. Staphylococcal-derived superantigen enhances peanut induced Th2 responses in the skin. Forbes-Blom, Clin Exp Allergy 2012;42:305 Concomitant exposure to Peanut extract (PE) staphylococcal-derived superantigenTh2 model Th2 response in the skin draining lymph nodes
  28. 28. Staphylococcal-derived superantigen enhances peanut induced Th2 responses in the skin. Forbes-Blom, Clin Exp Allergy 2012;42:305 Concomitant exposure to Peanut extract (PE) staphylococcal-derived superantigen Significantly enhanced specific Th2 responses.Th2 model (+) Th2 response in the skin draining lymph nodes
  29. 29. Staphylococcal-derived superantigen enhances peanut induced Th2 responses in the skin. Forbes-Blom, Clin Exp Allergy 2012;42:305Exposure of staphylococcal enterotoxin B (SEB) when being primed to peanut extract (PE) leads to an enhanced PE-dependent CD4 Th2 response.c (a) (b) Absolute n° (a) and proportion (b) of CD4+ GFP+ T cells present in the draining auricular lymph node 24h after final intradermal boost.
  30. 30. Staphylococcal enterotoxin B compromises the immune tolerant status in the airway mucosa. Liu T, Clin Exp Allergy 2012;42:3751) Staphylococcal enterotoxin B (SEB) is an enterotoxin produced by the bacterium Staphylococcus aureus. SEB may contaminate ingested food and induce gastrointestinal dysfunction. SEB interferes with the function of the immune system in the airway mucosa, such as to be involved in the pathogenesis of airway allergy.2) Integrin alphavbeta6 (avb6) is produced by epithelial cells in response to external stimuli, such as wound and inflammation. Our recent study data also show that intestinal epithelial cells express detectable avb6 that has protelytic activity and can convert the precursor of transforming growth factor (TGF)β into the active form of TGFβ. TGFβ plays a critical role in the Treg development. Tolergenic DCs (TolDC) express TGFβ and aldehyde dehydrogenase (ALDH) that can induce CD4+ CD25- T cells to Foxp3+ Tregs.
  31. 31. Staphylococcal enterotoxin B compromises the immune tolerant status in the airway mucosa. Liu T, Clin Exp Allergy 2012;42:3751) Staphylococcal enterotoxin B (SEB) is an enterotoxin produced by the bacterium Staphylococcus aureus. SEB may contaminate ingested food and induce gastrointestinal dysfunction. in avb6 The increases in SEB and decreases SEB interferes with the function of the immune system in the airway mucosa, such as to be involvedassociated in nasal epithelium are in the pathogenesis of airway allergy. compromises of immune tolerance with the in the nasal mucosa.2) Integrin alphavbeta6 (avb6) is produced by epithelial cells in response SEB has stimuli,ability wound and inflammation. to external the such as to suppress Our recent study data also show that intestinal epithelial cells express detectable avb6 that has protelyticavb6 and can convert the expression of activity in nasal epithelial cells. the precursor of transforming growth factor (TGF)β into the active form of TGFβ. TGFβ plays a critical role in the Treg development. Tolergenic DCs (TolDC) express TGFβ and aldehyde dehydrogenase (ALDH) that can induce CD4+ CD25- T cells to Foxp3+ Tregs.
  32. 32. Staphylococcal enterotoxin B compromises the immune tolerant status in the airway mucosa. Liu T, Clin Exp Allergy 2012;42:375 Avb6 expression is suppressed in the allergic rhinitis (AR) nasal epithelium• The immune tolerant components, tolerogenic dendritic cells (TolDC) P<0.01 & regulatory T cells (Treg), were assessed in the surgically removed nasal mucosa from patients with allergic rhinitis (AR) Staphylococcal enterotoxin B (SEB) or non-AR chronic rhinitis. levels are increased in the allergic rhinitis nasal epithelium.• Contents of Staphylococcal enterotoxin B & integrin alphavbeta6 P<0.01 (avb6) in the nasal epithelium assessed using enzyme-linked immunoassay.
  33. 33. Staphylococcal enterotoxin B compromises the immune tolerant status in the airway mucosa. Liu T, Clin Exp Allergy 2012;42:375 Avb6 expression is suppressed in the allergic rhinitis (AR) nasal epithelium• The immune tolerant components, tolerogenic dendritic cells (TolDC) The components P<0.01 & regulatory T cells (Treg), were of immune tolerance assessed in the surgically removed machinery, nasal mucosa from patients with allergic rhinitisTregs TolDCs & (AR) Staphylococcal enterotoxin B (SEB) or non-AR chronic rhinitis. were suppressed levels are increased in the allergic rhinitis nasal epithelium. in the AR• Contents of Staphylococcal enterotoxin B &mucosa. nasal integrin alphavbeta6 P<0.01 (avb6) in the nasal epithelium assessed using enzyme-linked immunoassay.
  34. 34. Gram+ bacteria on grass pollen exhibit adjuvant activity inducing inflammatory T cell responses Heydenreich, Clin Exp Allergy 2012;42:76 Background Recently, it has been established that pollen grains contain Th2-enhancing activities besides allergens. Objective The aim of this study was to analyse whether pollen carry additional adjuvant factors like microbes and what immunological effects they may exert.
  35. 35. Gram+ bacteria on grass pollen exhibit adjuvant activity inducing inflammatory T cell responses Heydenreich, Clin Exp Allergy 2012;42:76 A complex mixture of bacteria and moulds was detected on grass pollen: Timothy pollen grains collected and disseminated - Gram-negative that are known on agar plates. to favour Th1-directed immune responses. Immunologic effects of microbial products - Gram positive bacteria e.g on DC & T cell responses. Bacillus cereus & Bacillus subtilis. - Moulds.
  36. 36. Gram+ bacteria on grass pollen exhibit adjuvant activity inducing inflammatory T cell responses Heydenreich, Clin Exp Allergy 2012;42:76 Supernatants of homogenized Gram+ bacteria induce CD80, CD83 expression in immature dendritic cells. Timothy pollen grains collected and disseminated on agar plates. Immunologic effects of microbial products on DC & T cell responses.
  37. 37. Gram+ bacteria on grass pollen exhibit adjuvant activity inducing inflammatory T cell responses Heydenreich, Clin Exp Allergy 2012;42:76 Supernatants of homogenized Gram+ Contact of immature bacteria induce CD80, CD83 expression in dendritic cells (DC) immature dendritic cells. from grass pollen allergic Timothy pollensupernatants donors with grains collected homogenized of and disseminated on Gram-positive bacteria agar plates. induced maturation of DC Immunologic effects as measured of microbial products by up-regulation of CD80 on DC & T cell responses. and CD83.
  38. 38. Gram+ bacteria on grass pollen exhibit adjuvant activity inducing inflammatory T cell responses Heydenreich, Clin Exp Allergy 2012;42:76 Induction of proinflammatory cytokines in immature dendritic cells. Timothy pollen grains collected and disseminated on agar plates. Immunologic effects of microbial products on DC & T cell responses.
  39. 39. Gram+ bacteria on grass pollen exhibit adjuvant activity inducing inflammatory T cell responses Heydenreich, Clin Exp Allergy 2012;42:76Conclusions and Clinical Relevance These data indicatethat grass pollen is colonized by several microorganismsthat influence the immune response differently.Similar to LPS, supernatants of homogenizedGram-positive bacteria may serve as adjuvantsby augmenting DC maturation and inflammatory Th1, Th2and Th17 responses helping to initiate allergicimmune responses.
  40. 40. Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity Kim JACI 2012;129:216BackgroundAsthma has been considered an immunologic diseasemediated by TH2 cells and adaptive immunity.However, clinical and experimental observationssuggest that additional pathways might regulateasthma, particularly in its nonallergic forms,such as asthma associated with air pollution,stress, obesity, and infection.ObjectivesOur goal was to understand TH2 cell–independent conditions that mightlead to airway hyperreactivity (AHR), a cardinal feature of asthma.
  41. 41. Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity Kim JACI 2012;129:216 Glycolipid antigens directly induced alveolar macrophages1) Activate natural killer T (NKT) cells. to produce IL-33, as well as IL-13.2) Airway hyperreactivity developed rapidly
  42. 42. Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity Kim JACI 2012;129:216 Glycolipid antigens directly induced Because plant pollens, house dust, andalveolar macrophages some bacteria1) Activate natural killer T (NKT) cells. activate NKT cells, contain glycolipids that can directly to produce IL-33, these studies suggest that as well as IL-13. AHR and asthma can fully develop or be greatly enhanced2) Airway hyperreactivity developed rapidly through innate immune mechanisms.
  43. 43. Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity Kim JACI 2012;129:216 Schematic of the IL-33–ST2 axis in the development of AHR. On activation by glycolipid antigens, NKT cells induce macrophages, DCs, and type II pneumocytes toproduce IL-33, which in turnactivates natural helper andNKT cells to produce IL-13,resulting in the development of AHR.IL-33 can also activate mast cells, eosinophils, and basophils. ST2 = IL-33R = IL-33 Receptor
  44. 44. Gestational age at birth and risk of allergic rhinitis in young adulthood. Crump JACI 2011;127:1173 For subjects born extremely preterm (23-28 weeks) OR for 630,090 infants born in Sweden including 27,953 1.0 – born preterm (<37 wks). Prescription of nasal 0.5 – 0.70 corticosteroids and oral 0.45 antihistamines 0.0 Nasal corticosteroid Both nasal age, 25.5-37.0 yrs. prescription corticosteroid and oral antihistamine prescription
  45. 45. Gestational age at birth and risk of allergic rhinitis in young adulthood. Crump JACI 2011;127:1173 These findings suggest that low gestational age For subjects born extremely at birth independent preterm (23-28 weeks) OR for 630,090 infants born in of fetal growth is Sweden including 27,953 1.0 – associated with a born preterm (<37 wks). decreased risk of Prescription of nasal young allergic rhinitis in 0.5 – 0.70 corticosteroids and oral adulthood, possibly 0.45 antihistaminesa protective because of 0.0 Nasal corticosteroid Both nasal effect of earlier age, 25.5-37.0 yrs. prescription corticosteroid and exposure to pathogens. oral antihistamine prescription
  46. 46. Infant antibiotic use and wheeze and asthma risk: a systematic review and meta-analysis Penders ERJ 2011;38:295 OR for 2 – wheeze/asthma 18 longitudinal studies. Effect of antibiotic use on wheeze/ asthma. 1 – 1.27 Early antibiotic use
  47. 47. Infant antibiotic use and wheeze and asthma risk: a systematic review and meta-analysis Penders ERJ 2011;38:295 When we eliminated OR for studies with possible 2 – wheeze/asthma reverse causation 18 longitudinal studies. and respiratory tract infections leading Effect of antibiotic use to antibiotic use, on wheeze/ asthma. the pooled risk estimate 1 – 1.27 was attenuated to OR 1.12. Early antibiotic use
  48. 48. Prenatal or Early-Life Exposure to Antibiotics and Risk of Childhood Asthma: A Systematic Review Murk Pediatrics 2011;127:1125 OR for asthma if exposed to Studies published 3 – antibiotic in the first yr of life between 1950 and July 1, 2010, that assessed associations 2 – between antibiotic 2.04 exposure during 1.52 1.25 pregnancy or in the 1 – first year of life and asthma at ages 0 to 18 yrs. 0 all studies retrospective prospective studies studies
  49. 49. Prenatal or Early-Life Exposure to Antibiotics and Risk of Childhood Asthma: A Systematic Review Murk Pediatrics 2011;127:1125 OR for asthma if exposed to Studies published 3 – antibiotic in the first yr of life between 1950 and Risk estimate July 1, 2010, that assessed studies for associations 2 – between adjusted that antibiotic 2.04 for respiratory exposure during 1.52 1.25 pregnancy or in the infections is 1 – first year 1.16 OR of life and asthma at ages 0 to 18 yrs. 0 all studies retrospective prospective studies studies
  50. 50. Prenatal or Early-Life Exposure to Antibiotics and Risk of Childhood Asthma: A Systematic Review Murk Pediatrics 2011;127:1125 OR for asthma if exposed to Studies published to Antibiotics seem 3 – antibiotic in the first yr of life between 1950 and slightly increase July 1, 2010, that the risk of assessed associations childhood asthma. 2 – between antibiotic Reverse causality and 2.04 exposure during protopathic bias seem 1.52 1.25 pregnancy possible to be or in the 1 – first year of life confounders for and asthma at this relationship. ages 0 to 18 yrs. 0 all studies retrospective prospective studies studies
  51. 51. •paracetamol
  52. 52. The Association of Acetaminophen and Asthma Prevalence and Severity McBride Pediatrics 2011;128:1181• The epidemiologic association between acetaminophen use and asthma prevalence and severity in children and adults is well established.• A variety of observations suggest that acetaminophen use has contributed to the recent increase in asthma prevalence in children: 1) the strength of the association; 2) the consistency of the association across age, geography, and culture; 3) the dose-response relationship; 4) the timing of increased acetaminophen use and the asthma epidemic;
  53. 53. The Association of Acetaminophen and Asthma Prevalence and Severity McBride Pediatrics 2011;128:1181• The epidemiologic association between acetaminophen use and asthma prevalence and severity in children and adults is well established.• A variety of observations suggest that acetaminophen use has contributed to the recent increase in asthma prevalence in children: 5) the relationship between per-capita sales of acetaminophen and asthma prevalence across countries; 6) the results of a double-blind trial of ibuprofen and acetaminophen for treatment of fever in asthmatic children; 7) the biologically plausible mechanism of glutathione depletion in airway mucosa.
  54. 54. The Association of Acetaminophen and Asthma Prevalence and Severity McBride Pediatrics 2011;128:1181• The epidemiologic association between acetaminophen use and Until future studies document the safety asthma prevalence and severity in children and adults is well of this drug, children with asthma or at established. risk for asthma should avoid the use of• A variety of observations suggest that acetaminophen use has acetaminophen. contributed to the recent increase in asthma prevalence in children: 5) the relationship between per-capita sales of acetaminophen and asthma prevalence across countries; 6) the results of a double-blind trial of ibuprofen and acetaminophen for treatment of fever in asthmatic children; 7) the biologically plausible mechanism of glutathione depletion in airway mucosa.
  55. 55. •Allergens
  56. 56. Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city population Wang JACI 2011;128:834 Shrimp specific IgE levels were correlated with exposure to cockroach but only among children with positive IgE levels to cockroach. 504 serum samples. sIgE to shrimp, cockroach (Blattella germanica) and Dermatophagoides farinae.
  57. 57. Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city population Wang JACI 2011;128:834 Shrimp specific IgE levels were correlated with exposure to cockroach but only among children with positive IgE levels to cockroach. High exposure to 504 serum samples. B. Germanica in sIgEtheshrimp, was to home cockroach significantly (Blattella germanica) andcorrelated with Dermatophagoides IgE higher shrimp farinae. levels.
  58. 58. Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city population Wang JACI 2011;128:834 Shrimp specific IgE levels were correlated with exposure to cockroach but only among children with positive IgE levels to cockroach. In contrast, 504 high exposure serum samples. sIgE to shrimpmite to dust , cockroach in the home (Blattella germanica) and was not correlated with Dermatophagoides farinae. IgE levels. shrimp
  59. 59. Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city population Wang JACI 2011;128:834Conclusions•For children with evidence of IgE-mediated sensitization tocockroach and shrimp, having high exposure to cockroach in thehome can contribute to higher shrimp IgE levels, which might notcorrelate with clinical reactivity.•Further patient evaluations with clinical historiesof shrimp exposure and reactions, as well as oral food challenges,would have to be performed to confirm these findings.
  60. 60. •Allergens •acari
  61. 61. Inhibition of house dust mite–induced allergic airwaysdisease by antagonism of microRNA-145 is comparable to glucocorticoid treatment. Collison JACI 2011;128:160  MicroRNAs (miRNAs) are important regulators of the immune system by promoting the catabolism of their target transcripts as well as attenuating their translation.  Blocking miRNA function may provide a new nonsteroidal anti-inflammatory approach to treatment.
  62. 62. Inhibition of house dust mite–induced allergic airwaysdisease by antagonism of microRNA-145 is comparable to glucocorticoid treatment. Collison JACI 2011;128:160 Sensitized and then aeroallergen- challenged with house dust mite Allergic airways disease, and alterations in the expression ofmiRNAs: miR-145, miR-21, and let-7b
  63. 63. Inhibition of house dust mite–induced allergic airwaysdisease by antagonism of microRNA-145 is comparable to glucocorticoid treatment. Collison JACI 2011;128:160 Sensitized and then aeroallergen- challenged with house dust mite Inhibition of miR-145, but not miR-21 or lethal-7b, inhibited eosinophilic inflammation, mucus hypersecretion, TH2 cytokine production, and airway hyperresponsiveness. Allergic airways disease, and alterations in the expression ofmiRNAs: miR-145, miR-21, and let-7b
  64. 64. Invariant NKT cells are required for airway inflammation induced by environmental antigens Wingender J Exp Med 2011;208:1151• Recent increases in the prevalence of asthma and other allergic diseases have prompted investigators to consider the role of the environment in the genesis of atopy.• We have previously reported that house dust extracts (HDEs) contain ligands that activate DCs by toll-like receptor 2 (TLR-2)-, TLR4-, and TRL9- dependent pathways. Boasen J JACI 2005;116:185-191. Batzer G Immunobiology 2007;212:491-498.• We have further established that HDEs have the potential to function as Th2 adjuvants in mice receiving intranasal (i.n.) OVA vaccinations. Ng N. JACI 2006;117:1074-1081. Lee S.M. AJRCMB 2011;44:341-349.
  65. 65. Invariant NKT cells are required for airway inflammation induced by environmental antigens Wingender J Exp Med 2011;208:1151• Novel invariant natural killer T cell-activating antigens found in house dust extracts.• Invariant natural killer T (iNKT) cells are effector cells activated by CD1d presentation of glycolipid antigens.• Until now, iNKT antigens have been found in 2 bacteria, one of which is the causative agent in Lyme disease.• We report the discovery of iNKT antigens in house dust extracts.
  66. 66. Invariant NKT cells are required for airway inflammation induced by environmental antigens Wingender J Exp Med 2011;208:1151• These experimental findings highlights the complexity of house dust as an immunostimulant.• More specifically, we provide direct evidence that living environments have the potential to activate iNKT cells through their T-cell receptor and potentially by other pathways, adding support to the view that iNKT cells have clinical relevance in human asthma and other diseases.
  67. 67. House dust mite extract downregulates C/EBPα* in asthmatic bronchial smooth muscle cells Miglino ERJ 2011;38:50 1. Increased IL-6 protein House dust mite and proliferation of BSM (HDM) extracts cells of asthma patients only. 2. HDM extract reduced the C/EBPα expression in BSM cells of asthma patients. 3. HDM extract elicited both protease-dependent Bronchial smooth muscle cells and –independent (BSM) responses.* enhancer-binding protein
  68. 68. House dust mite extract downregulates C/EBPα* in asthmatic bronchial smooth muscle cells Miglino ERJ 2011;38:50 1. Increased IL-6 protein House dust mite and proliferation of BSM HDM exposure (HDM) extracts cells of asthma patients contributes only. to inflammation and remodelling 2. HDM extract reduced the C/EBPα expression in BSM by a nonimmune cells of asthma patients. cell-mediated mechanism via a direct interaction 3. HDM extract elicited both protease-dependent with BSM cells. and –independent Bronchial smooth muscle cells (BSM) responses.* enhancer-binding protein
  69. 69. Playing a dirty trick on airway smooth muscle: house dust mite does it again Zuyderduyn ERJ 2011;38:4  Airway smooth muscle cells isolated from asthmatic proliferate faster in culture and produce more chemokines and an altered array of extracellular matrix proteins compared with those of healthy individuals.  The increase in ASM proliferation in asthma is thought to be associated with decreased levels of CCAAT enhancer protein (c/EBP)α (encoded by the CEBPA gene), a crucial controller of cell cycle progression, differentiation and inflammation.
  70. 70. Playing a dirty trick on airway smooth muscle: house dust mite does it again Zuyderduyn ERJ 2011;38:4  In addition to increased proliferation, interleukin (IL)-6 release (induced by growth factors) is increased in ASM from asthmatics.  House dust mite (HDM) exerts direct effects on various cell types, including protease-dependent cell detachment in epithelial cells and IgE-independent activation of mast cells.
  71. 71. Playing a dirty trick on airway smooth muscle: house dust mite does it again Zuyderduyn ERJ 2011;38:4  Exposure of rabbit ASM strips to the purified Der p 1 allergen increased airway hyperresponsiveness to acetylcholine and reduced relaxation responses to isoproterenol, and this effect was attributed to the protease activity of Der p 1.  These data suggest that the effects of HDM can be IgE-dependent and –independent, as well as protease-dependent and –independent.
  72. 72. Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and non-sensitised children. Hales, Thorax 2012;67:321Background:Infants who develop house dust mite (HDM) allergyand HDM sensitised children with severe persistent asthma havelow antibody responses to the P6 antigen of Haemophilus influenzae.Objective:1) To measure the development of antibody to 2 ubiquitous bacteria of the respiratory mucosa in a prospective birth cohort at high risk of allergic disease.2) To assess which responses are associated with asthma and atopy.
  73. 73. Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and non-sensitised children. Hales, Thorax 2012;67:321 Development of IgG1 antibody (ng/ml) IgG1 and IgG4 antibody to: - H. influenzae (P4, P6) - S. pneumoniae (PspA, PspC) surface antigens. Yearly blood samples * * ** * *** * * of children aged 1-5 yrs. Children were stratified based on: - HDM sensitisation - Asthma * ** at 5 yrs of age. *p<0.05, **p<0.01, ***p<0.001
  74. 74. Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and non-sensitised children. Hales, Thorax 2012;67:321 Development of IgG1 antibody (ng/ml) IgG1 and IgG4 antibody to: - H. influenzae (P4, P6) HDM-sensitised children - S. pneumoniae (PspA, PspC) surface had lower antigens. IgG1 antibody titres to the blood samples Yearly bacterial antigens, * * ** * *** * * of and early responses children aged 1-5 yrs. (<3yrs and before Children were stratified based on:development the of HDM sensitisation - HDM sensitisation - Asthma asthma). and * ** at 5 yrs of age. *p<0.05, **p<0.01, ***p<0.001
  75. 75. Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and non-sensitised children. Hales, Thorax 2012;67:321 Development of IgG1 antibody (ng/ml) IgG1 and IgG4 antibody to: - H. influenzae (P4, P6) - S. HDM-sensitisedPspC) pneumoniae (PspA, surface antigens. children have early defective Yearly blood samples * * ** * *** * * ofantibody responses children aged 1-5 yrs. to bacteria Children were stratified that are associated based on: - HDM sensitisation with asthma. - Asthma * ** at 5 yrs of age. *p<0.05, **p<0.01, ***p<0.001
  76. 76. Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and non-sensitised children. Hales, Thorax 2012;67:321Possible explanations1. The low IgG antibody response could enhance atopy and asthma by increasing the susceptibility to bacterial infection and the exposure to pharmacologically active bacterial products.2. Underlying immune responses to the bacteria and allergens influence immune responses to each other when they are copresented at the mucosa to increase the degree of sensitisation.3. Altered antibody responses are just markers that show people with atopy and asthma have alterations in an aspect of their mucosal immune system that extends beyond the response to allergens.
  77. 77. Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and non-sensitised children. Hales, Thorax 2012;67:321Possible explanations1. The low IgG antibody response could enhance atopy and asthma by increasing the susceptibility to bacterial infection Increased bacterial colonisation, and the exposure to pharmacologically active bacterial products. including both H influenzae and S pneumoniae,2. Underlying immune responses to the bacteria and allergens has been associated with susceptibility influence immune responses to each other when they are copresented at the mucosaasthma and degree of sensitisation. to to increase the wheezing attacks.3. Altered antibody responses are just markers that show people with atopy and asthma have alterations in an aspect of their mucosal immune system that extends beyond the response to allergens.
  78. 78. Protease-activated receptor 2-dependent fluid secretion from airway submucosal glands by house dust mite extract Cho JACI 2012;129:529BackgroundThe submucosal gland (SMG) is important in the control of airwaysurface fluid.Protease-activated receptor (PAR) 2 contributes to the pathophysiologyof allergies in response to nonspecific allergens bearing proteases andanion secretion.House dust mites (HDMs) have abundant proteases that can activatePAR2, but little is known about the direct effect of HDM on SMGsecretion.ObjectiveTo investigate the effect of HDMs on glandular secretion and itsmechanism in allergic patients, patients with chronic rhinosinusitis(CRS), or both.
  79. 79. Protease-activated receptor 2-dependent fluid secretion from airway submucosal glands by house dust mite extract Cho JACI 2012;129:529Inferior nasal 1) HDM induced a turbinates. significantly higher55 patients classified secretion rate into four groups: and number of 1. the control, 2. allergic rhinitis (AR), responding glands 3. chronic rhinosinusitis (CRS), in the AR and 4. AR + CRS. AR+CRS groupsMucus bubbles from than in the individual submucosal control group. gland (SMGs).
  80. 80. Protease-activated receptor 2-dependent fluid secretion from airway submucosal glands by house dust mite extract Cho JACI 2012;129:529Inferior nasal 2) Patients in the turbinates. CRS group, who had no55 patients classified HDM-specific IgE, into four groups: showed a 1. the control, higher response 2. allergic rhinitis (AR), than the control group, 3. chronic rhinosinusitis (CRS), and its response 4. AR + CRS. was suppressed byMucus bubbles from a PAR2-selective individual submucosal antagonist. gland (SMGs).
  81. 81. Protease-activated receptor 2-dependent fluid secretion from airway submucosal glands by house dust mite extract Cho JACI 2012;129:529 Quantitative measurement of glandular secretion.A. Harvest of nasal mucosa from the inferior nasal turbinate.B. Experimental setup.C. Mucus bubbles from glands under oil are visualized by using bright-field microscopy and side-light illumination.D. Example of mucus bubbles formed on the surface of nasal turbinates 30 minutes after stimulation.
  82. 82. Protease-activated receptor 2-dependent fluid secretion from airway submucosal glands by house dust mite extract Cho JACI 2012;129:529 Responses to HDM. Plots of averaged secretion rates versus time for each group.Inferior nasal *p < 0.05 turbinates.55 patients classified into four groups: 1. the control, 2. allergic rhinitis (AR), 3. chronic rhinosinusitis (CRS), 4. AR + CRS.Mucus bubbles from individual submucosal gland (SMGs).
  83. 83. Protease-activated receptor 2-dependent fluid secretion from airway submucosal glands by house dust mite extract Cho JACI 2012;129:529 Conclusions HDM allergens can induce glandular secretion in patients with AR, CRS, or both, and PAR2 represents a possible mechanism for nonspecific hyperreactivity in inflammatory airway diseases.
  84. 84. Gene-by-environment effect of house dust mite on purinergic receptor P2Y12 (P2RY12) & lung function in children with asthma. Bunyavanich, Clin Exp Allergy 2012;42:229Background Distinct receptors likely exist for leukotriene (LT)E4,a potent mediator of airway inflammation.Purinergic receptor P2Y12 is needed for LTE4-induced airwaysinflammation, and P2Y12 antagonism attenuates house dust miteinduced pulmonary eosinophilia in mice. Although experimental datasupport a role for P2Y12 in airway inflammation, its role in humanasthma has never been studied.Objective To test for association between variants in the P2Y12 gene(P2RY12) and lung function in human subjects with asthma,and to examine for gene-by-environment interaction with housedust mite exposure.
  85. 85. Gene-by-environment effect of house dust mite on purinergic receptor P2Y12 (P2RY12) & lung function in children with asthma. Bunyavanich, Clin Exp Allergy 2012;42:229Background Distinct receptors likely exist for leukotriene (LT)E4,a potent mediator of airway inflammation. House dust mitePurinergic receptor P2Y12 is needed for LTE4-induced airwaysinflammation, and P2Y12 antagonism attenuates house dust mite exposure causedinduced pulmonary eosinophilia in mice. Although experimental data significantsupport a role for P2Y12 in airway inflammation, its role in humanasthma has never been studied. gene-by-environmentObjective To test for association between variants in the P2Y12 gene(P2RY12) and lung functioneffects. in human subjects with asthma,and to examine for gene-by-environment interaction with housedust mite exposure.
  86. 86. Gene-by-environment effect of house dust mite on purinergic receptor P2Y12 (P2RY12) & lung function in children with asthma. Bunyavanich, Clin Exp Allergy 2012;42:229 •5 SNPs in P2RY12 were associated with multiple lung function measures 19 single nucleotide (P-values 0.006–0.025). polimorphisms (SNPs) •Haplotypes in P2RY12 were also associated with lung function in P2RY12. (P-values 0.0055–0.046). Children with asthma (n=422) •House dust mite exposure modulated associations between & their parents (n=1266) . P2RY12 and lung function, with minor allele homozygotes exposed to Associations between house dust mite demonstrating these SNPs & lung function. worse lung function than those unexposed (significant interaction P- House dust mite exposure. values 0.0028–0.040).
  87. 87. Gene-by-environment effect of house dust mite onpurinergic receptor P2Y12 (P2RY12) & lung function in children with asthma. Bunyavanich, Clin Exp Allergy 2012;42:229 Relationship between P2RY12 single nucleotide polymorphisms & airways responsiveness stratified by house dust mite exposure. (a) House dust mite exposure
  88. 88. •Allergens•Cane e gatto
  89. 89. The long-term protective effects of domestic animals in the home. Erwin CEA 2011;41:920 There is a critical age at which exposure to animals can have a protective effect. Specifically, animal exposure needs to occur in the first year of life. When tolerance to cats was first described, many authors assumed that it would be comparable with the effect of farm animals, which appears to be dependant on an early exposure to endotoxin or environmental microorganisms. But in many studies, measurements of endotoxin have not been higher in homes with domestic animals and the effect of cat ownership appears to be cat specific.
  90. 90. The long-term protective effects of domestic animals in the home. Erwin CEA 2011;41:920 Children living in a house with a cat can produce high levels of IgE to mite while remaining „tolerant‟ to the cat. Current estimates of high exposure to cat suggest that 20–50 times more allergen is inhaled as compared with mite allergen. A large part of the estimated 1 μg of cat allergen inhaled per day is swallowed. On this basis, daily exposure to cat, or dog, allergens is not far different from the doses used for sublingual „desensitization‟.
  91. 91. Lifetime dog and cat exposure and dog- and cat- specific sensitization at age 18 years Wegienka CEA 2011;41:979 Detroit Childhood OR for sensibilization Allergy Study birth to dog at age 18 yrs cohort contacted at 1.0 – the age 18 years. Sensitization to dog 0.5 – or cat defined as animal-specific 0.50 0.0 IgE ≥ 0.35 kU/L. Those with an indoor dog during the first year of life
  92. 92. Lifetime dog and cat exposure and dog- and cat- specific sensitization at age 18 years Wegienka CEA 2011;41:979 Detroit Childhood OR for sensibilization Allergy Study birth to cat at age 18 yrs cohort contacted at 1.0 – the age 18 years. Sensitization to dog 0.5 – or cat defined as animal-specific 0.52 0.0 IgE ≥ 0.35 kU/L. With an indoor cat in the first year of life
  93. 93. Lifetime dog and cat exposure and dog- and cat- specific sensitization at age 18 years Wegienka CEA 2011;41:979 Detroit Childhood life The first year of OR for sensibilization Allergy Study birth is the critical period to cat at age 18 yrs cohort contacted at during childhood when 1.0 – the age 18 years. to indoor exposure dogs or cats 0.5 – Sensitization to dog 0.52 influences or cat defined as to sensitization animal-specific these animals. 0.0 IgE0.35 kU/L. With an indoor cat in the first year of life
  94. 94. Risk factors for new-onset cat sensitization amongadults: A population-based international cohort study Olivieri JACI 2012;129:420BackgroundCat exposure during childhoodhas been shown to increase the risk ofdeveloping cat sensitization, while the effectofcat exposure in adulthood has not yet been established.ObjectiveTo evaluate new-onset sensitization to cat in adulthoodin relation to changes in cat keeping.
  95. 95. Risk factors for new-onset cat sensitization among adults: A population-based international cohort study Olivieri JACI 2012;129:420 % adults who became6292 European sensitized to cat 4.0 – Community Respiratory Health Survey I (ECRHS I) 3.5 – 3.0 – 3.7% participants 2.5 – (20 to 44 years). 2.0 –Reevaluated 1.5 – 9 years later. 1.0 –Serum IgE level 0.5 - ≥0.35 kU/L. 0.0
  96. 96. Risk factors for new-onset cat sensitization among adults: A population-based international cohort study Olivieri JACI 2012;129:4206292 European RR for new onset Community Respiratory cat sensitization Health Survey I 2.0 – (ECRHS I) participants 1.5 – 1.85 (20 to 44 years). 1.0 –Reevaluated 9 years later. 0.5 -Serum IgE level 0.0 Cat acquisition during follow-up when ≥0.35 kU/L. compared with those without a cat at both surveys.
  97. 97. Risk factors for new-onset cat sensitization amongadults: A population-based international cohort study Olivieri JACI 2012;129:420ConclusionAcquiring a cat in adulthood nearly doubles the riskof developing cat sensitization.Hence, cat avoidance should be considered in adults, especiallyin those sensitized to other allergens and reporting a historyof allergic diseases.
  98. 98. Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 Background The presence of pets in a home during the prenatal period and during early infancy has been associated with a lower prevalence of allergic sensitization and total IgE levels in middle childhood. No studies have examined the effect of pet exposure in a population-based cohort by using multiple early-life measures of serum total IgE. Objectives We sought to examine within-individual longitudinal trends in total IgE levels during early childhood and assess the effect of indoor prenatal pet exposure on those trends.
  99. 99. Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 Log-transformed IgE values by age. Birth cohort. 1187 infants. 1 to 4 measurements of total IgE collected from birth to 2 yrs of age.
  100. 100. Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 Log-transformed IgE values by age. The trajectory Birth cohort. of IgE levels was 1187 infants. nonlinear, with an 1 to 4 measurements of total accelerated IgE collected from birth to 2 yrs increase before of age. 6 months.
  101. 101. Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 Birth cohort. 1187 infants. 1 to 4 measurements of total IgE collected from birth to 2 yrs of age.
  102. 102. Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 Total IgE levels were lower across Birth entire early-life period the cohort. 1187 infants. there was when prenatal indoor 1 to 4 measurements of total pet exposure IgE collected from birth to 2 yrs of age. 0.001). (p<
  103. 103. Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 % reduction in total IgE due to pet exposure and type of delivery. 0 – Birth cohort. vaginal Cesarean 1187 infants. -10 – -16% section 1 to 4 measurements of total -20 – p<0.06 IgE collected from birth to 2 yrs of age. -30 – -40 - -43% p<0.001 -50 –
  104. 104. Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 % reduction in total IgE due to pet exposure and type of delivery. 0 – Birth cohort. vaginal Cesarean Pet exposure and 1187 infants. delivery mode -10 – -16% section 1 to 4 measurements of total -20 – p<0.06 might be markers IgE collected from birth to 2 yrs infant exposure of of age. -30 – to distinct microbes. -40 - -43% p<0.001 -50 –
  105. 105. High environmental relative moldiness index during infancy as a predictor of asthma at 7 years of age Reponen Ann Allergy Asthma Immunol 2011;107:120 % children asthmatic at the age 7 yrs 20 – A high-risk birth cohort from infancy to 7 years of age. 15 – 18% 10 – Mold assessed by a DNA-based analysis for 05 – the 36 molds. 00
  106. 106. High environmental relative moldiness index during infancy as a predictor of asthma at 7 years of age Reponen Ann Allergy Asthma Immunol 2011;107:120 aORs (95% CIs) for Asthma Diagnosis at 7 Years of Age by Predictor Variables of the 176 Study ChildrenAbbreviations: aOR, adjusted odds ratio; CI, confidence interval;ERMI, Environmental Relative Moldiness Index.These variables remained statistically significant (P <0.05) in a full multivariate model.
  107. 107. Asthma related to Alternaria sensitization: an analysis of skin-test and serum-specific IgE efficiency based on the bronchial provocation test Fernández CEA 2011;41:649 % pts with a (+) specific challenge 70 – 74 asthmatic 60 – patients sensitized to Alternaria . 50 – 61% 40 – Specific bronchial 30 – challenge with this 20 – mould. 10 – .0
  108. 108. Asthma related to Alternaria sensitization: an analysis of skin-test and serum-specific IgE efficiency based on the bronchial provocation test Fernández CEA 2011;41:649 % pts with a (+) specific Skin prick testing challenge almost perfectly 70 – 74 asthmatic outcome predicted the 60 – of bronchoprovocation patients sensitized to Alternaria . tests. 50 – 61% 40 – Weals around 5.5 mm Specific bronchial 90% in diameter had 30 – challenge with this a probability of 20 – mould. positive challenge. 10 – .0
  109. 109. Asthma related to Alternaria sensitization: an analysis of skin-test and serum-specific IgE efficiency based on the bronchial provocation test Fernández CEA 2011;41:649 % pts with a (+) specific A CAP value 70 – challenge 74 asthmatickUA/L ≥ 16 60 – predicted a positive patients sensitized tobronchial challenge Alternaria . 50 – 61% 40 – result with 99% Specific bronchial accuracy, 30 – challenge with this 20 – mould. 10 – .0
  110. 110. Meta-analysis of mould and dampness exposure on asthma and allergy in eight European birth cohorts: an ENRIECO initiative Tischer, Allergy 2011;66:1570 OR for early asthma symptoms 0,3 – 31 742 children from 8 ongoing European birth 0.2 – cohorts. Reported mould or 1.39 dampness exposure in 0.1 – early life. Development of allergic 0.0 – disorders in children. Exposure to visible mould and/or dampness during first 2 yrs of life
  111. 111. Meta-analysis of mould and dampness exposure on asthma and allergy in eight European birth cohorts: an ENRIECO initiative Tischer, Allergy 2011;66:1570 A moudly home OR for early asthma symptoms enviroment in early life 0,3 – is associated with an 31 742 children from 8 increased risk of ongoing European birth 0.2 – asthma particulary in cohorts. young children and Reported mould or allergic rhinitis 1.39 dampness exposure in symptoms in 0.1 – early life. school-age children Development of allergic 0.0 – disorders in children. Exposure to visible mould and/or dampness during first 2 yrs of life
  112. 112. Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:396 % of houses with Participants in the 50 – European Respiratory 50.1% Health Survey initially examined aged 20-45 yrs 40 – 41.3% and 9 yrs later (n=6443). 30 – Dampness (water damage 20 – or damp spots) and indoor mould, ever and in 10 – the last 12 months. 0 Any dampness Indoor mould
  113. 113. Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:396 Additional decline in FEV1 ml/year 0 Participants in the European Respiratory -2.25 Health Survey initially examined aged 20-45 yrs and 9 yrs later (n=6443). -5 Dampness (water damage -7.43 or damp spots) and indoor mould, ever and in the last 12 months. -10 Women with In women with dampness observed damp spots at home in the bedroom
  114. 114. Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:396 Additional decline in FEV1 ml/year 0 Participants in the Dampness and Europeanmould growth indoor Respiratory -2.25 Health Survey initially is common in examined aged 20-45 yrs dwellings, and the andpresence of(n=6443). 9 yrs later damp -5 is a risk factor for Dampness (water damage lung function decline, -7.43 orespecially in women. damp spots) and indoor mould, ever and in the last 12 months. -10 Women with In women with dampness observed damp spots at home in the bedroom
  115. 115. Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:3961) The additional mean lung function decline, -2.25 ml/year for self- reported dampness and -7.43 ml/year for observed dampness in the bedroom, is of the same order of magnitude as estimated for moderate tobacco smoking in the same ECRHS cohort.2) The reason for the sex difference in effect remains unclear, but could be due to either higher susceptibility or a longer exposure time in the dwelling for women.
  116. 116. •Smokingpassive-active
  117. 117. School absenteeism among children living with smokers Levy Pediatrics 2011;128:650 More days absent from school per years than children living with 0 smokers in the home. 2 – Health and absenteeism among school children aged 1 – 1.54 6 to 11 yrs. 1.06 0 1 ≥2 Adults who smoked in the home
  118. 118. School absenteeism among children living with smokers Levy Pediatrics 2011;128:650 Living with ≥2 adults who smoked in the home OR for 3 – Health and absenteeism among 2 – 2.65 school children aged 6 to 11 yrs. 1 – 1.77 00 ≥3 ear infections Having a chest in the previous 12 cold in the 2 months weeks before interview
  119. 119. School absenteeism among children living with smokers Levy Pediatrics 2011;128:650 Living with ≥2 adults who smoked in the home OR for 3 – Tobacco smoke Health and exposure has absenteeism among significant 2 – 2.65 school children aged consequences for 6children and families to 11 yrs. 1 – 1.77 above and beyond child morbidity, including academic disadvantage 00 and financial burden. ≥3 ear infections Having a chest in the previous 12 cold in the 2 months weeks before interview
  120. 120. Secondhand Smoke Exposure and Neurobehavioral Disorders Among Children in the United States Kabir, Pediatrics 2011;128:263 % children exposed to SHS in the home Children ≤12 yrs 7 – in the United States. 6 – Excess neurobehavioral 5 – 6% disorders attributable to 4 – secondhand smoke (SHS) exposure in the home. 3 – 2 – 1 – 0
  121. 121. Secondhand Smoke Exposure and Neurobehavioral Disorders Among Children in the United States Kabir, Pediatrics 2011;128:263 PREVALENCE OF (exposed vs nonexposed)20 –18 –16 –14 – 15.1%12 – 13.0%10 –08 – 8.7%06 – 7.2%04 – 5.5% 2.8%02 – 0 LEARNING ATTENTION- BEHAVIORAL AND DISABILITIES DEFICIT/HYPERACTIVITY CONDUCT DISORDER DISORDERS
  122. 122. Secondhand Smoke Exposure and Neurobehavioral Disorders Among Children in the United States Children exposed to SHS at home had a 50% increased odds of2011;128:263 Kabir, Pediatrics having ≥2 childhood neurobehavioral disorders PREVALENCE OF (exposed vs nonexposed)20 – compared with children who were18 – not exposed to SHS.16 –14 – 15.1%12 – 13.0%10 –08 – 8.7%06 – 7.2%04 – 5.5% 2.8%02 – 0 LEARNING ATTENTION- BEHAVIORAL AND DISABILITIES DEFICIT/HYPERACTIVITY CONDUCT DISORDER DISORDERS
  123. 123. Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45 Video still from the carotid artery intima-media thickness Birth cohort. (CIMT) measurement. Smoking of parents during pregnancy. 259 participating children 5 years of age. Children‟s carotid artery intima-media thickness (CIMT) and arterial wall distensibility were measured by using ultrasonography.
  124. 124. Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45 Video still from the carotid artery intima-media thickness Birth cohort. (CIMT) measurement. Smoking of parents during pregnancy. 259 participating children 5 years of age. Children‟s carotid artery Diameter and intima- intima-media thickness media thickness on the (CIMT) and arterial wall far wall is automatically distensibility were measured detected by using ultrasonography. and measured.
  125. 125. Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45 Children of mothers who had Birth cohort. smoked throughout pregnancy had 18.8 µm thicker CIMT Smoking of parents during (P=0.04) and 15% lower pregnancy. distensibility (P =0.02) after 259 participating children adjustment for child‟s age, 5 years of age. maternal age, gender, and breastfeeding. Children‟s carotid artery intima-media thickness (CIMT) and arterial wall distensibility were measured by using ultrasonography.
  126. 126. Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45 Children of mothers who had Birth cohort. smoked throughout pregnancy The associations had 18.8 µm thicker CIMT Smoking of parents during were not found (P=0.04) and 15% lower pregnancy. in children of distensibility (P =0.02) after mothers who had not 259 participating children adjustment for child‟s age, smoked of age. 5 years in pregnancy maternal age, gender, and breastfeeding. but had smoked Children‟s carotid artery thereafter. intima-media thickness (CIMT) and arterial wall distensibility were measured by using ultrasonography.
  127. 127. Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45 If both parents had smoked Birth cohort. during pregnancy, with 27.7 mm thicker Smoking of parents during CIMT (95%) and pregnancy. 21% lower distensibility. 259 participating children 5 years of age. Children‟s carotid artery intima-media thickness (CIMT) and arterial wall distensibility were measured by using ultrasonography.
  128. 128. Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45Difference in CIMT (A) and distensibility (B) in children bysmoking habits of mother in pregnancy and current smoking
  129. 129. Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45Dose of tobacco smoke exposure in pregnancy and difference in CIMT (A) and distensibility (B) in the children
  130. 130. Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45Paternal and maternal smoking during pregnancy and vascular outcome in their children.
  131. 131. Parental Smoking and the Risk of Middle Ear Disease in Children. Jones L, APAM 2012;166:18 OR for middle ear disease in children 2 – Systematic review 1.62 and meta-analysis. 1 – 1.37 Association between secondhand tobacco smoke and middle ear disease 0 in children. maternal any household member smoking living with a smoker
  132. 132. Parental Smoking and the Risk of Middle Ear Disease in Children. Jones L, APAM 2012;166:18 Risk for surgery 2 – 1.86 1.83 Systematic review and meta-analysis. 1 – Association between secondhand tobacco smoke and middle ear disease 0 in children. maternal paternal living with a smoker
  133. 133. Parental Smoking and the Risk of Middle Ear Disease in Children. Jones L, APAM 2012;166:18 Risk for surgery Exposure to 2 – SHTS, particularly to smoking by the 1.86 1.83 Systematic review mother, significantly and meta-analysis. of increases the risk 1 – Middle Ear Disease Association between in childhood; this risk secondhand tobacco is particularly strong smoke and requiring for MED middle ear disease surgery 0 in children. maternal paternal living with a smoker
  134. 134. Secondhand Smoke Exposure in Cars Among Middle and High School Students—United States, 2000–2009 King, Pediatrics 2012;129;446 % children exposed to secondhand smoke in car 100 –Students in grades 90 – p<0.001 6 to 12. 80 – 82.3% 70 – 75.3% 60 –Trends in 50 – secondhand smoke 40 – (SHS) exposure in 30 – a car. 20 – 10 – 0 2000 2009
  135. 135. Secondhand Smoke Exposure in Cars Among Middle and High School Students—United States, 2000–2009 King, Pediatrics 2012;129;446 % children exposed to SHS exposure in cars secondhand smoke in car 100 – decreased significantlyStudents in grades among US middle and 90 – p<0.001 6 to 12. high school students 80 – 82.3% from 2000 to 2009. 70 – 75.3% 60 –Nevertheless, in 2009, Trends in 50 – over 1/5 of secondhand smoke 40 – nonsmoking students (SHS) exposure in 30 – a car. exposed to were 20 – SHS in cars. 10 – 0 2000 2009
  136. 136. Exposure to parental and sibling smoking and the risk of smoking uptake in childhood and adolescence: a systematic review and meta-analysis Leonardi-Bee Thorax 2011;66:847 OR of uptake of smoking in children 3 – 2.19 2 –Meta-analyses 1.72 of 58 studies. 1.66 1 – At least one Smoking Smoking
  137. 137. Exposure to parental and sibling smoking and the risk of smoking uptake in childhood and adolescence: a systematic review and meta-analysis Leonardi-Bee Thorax 2011;66:847 OR of uptake of smoking in children 3 – 2.73 2.3 2 –Meta-analyses of 58 studies. 1 – Both parents Smoking by
  138. 138. Exposure to parental and sibling smoking and the risk of smoking uptake in childhood and adolescence: a systematic review and meta-analysis Leonardi-Bee Thorax 2011;66:847 OR of uptake of smoking in children It is estimated that, 3 – in England and Wales, 2.73 around 17000 young people take up smoking 2.3 by the age of 15 each 2 –Meta-analyses year as a consequence of 58of exposure studies. to household smoking. 1 – Both parents Smoking by
  139. 139. Smoking inpregnancy
  140. 140. Promoting Tobacco to Women of Reproductive Age Harms Fetuses. Farber H, Chest 2012;141:839 In utero tobacco smoke exposure has been repeatedly found to be associated with increased risk for premature birth, low birth weight, and sudden infant death syndrome. In utero tobacco smoke exposure only, in utero and postnatal smoke exposure, and postnatal smoke exposure all associated with increased risk of wheezing in the offspring compared with those of nonsmoking mothers.
  141. 141. Promoting Tobacco to Women of Reproductive Age Harms Fetuses. Farber H, Chest 2012;141:839 Smoking cessation either before pregnancy or early in gestation among women who are tobacco dependent can minimize the harm to their offspring. Tobacco-dependence treatment medications are preferable to continued in utero smoke exposure, which has well-defined harms to the fetus.

×