Smoking exposure and allergic sensitization in children according to maternal allergies.

BACKGROUND: Although the negative impact of environmental tobacco smoke (ETS) on airway diseases in children is well known, the effect of ETS on allergic sensitization is still debated. OBJECTIVE: To evaluate how maternal allergies modulate the effect of tobacco exposure on allergic sensitization in childhood. METHODS: Of 9000 children in grades 4 and 5 selected in 6 cities in France, 7798 participated in a survey that consisted of an epidemiologic questionnaire, skin prick testing to common allergens, and skin examination for eczema. Tobacco exposure was obtained from parent questionnaires. RESULTS: Twenty-five percent of the children had allergic sensitization, 25.2% had eczema, 11.6% had allergic rhinitis, 9.9% had asthma, and 8.3% had exercise-induced asthma. Twenty percent of the children were exposed to tobacco in utero. Maternal exposure had a greater impact than paternal exposure on children's allergic sensitization. Prenatal exposure was more associated with sensitization than postnatal exposure. Children with maternal allergies and exposure to maternal ETS during pregnancy were at higher risk for sensitization to house dust mite (25.7% vs. 14.0%; odds ratio, 1.95; 95% confidence interval, 1.19-3.18; P = .006). In contrast, sensitization to food allergens was not associated with tobacco exposure. CONCLUSIONS: Children exposed to maternal smoking had a higher risk of sensitization to house dust mite, especially when the mothers were allergic.     

Natural course of sensitization to food and inhalant allergens during the first 6 years of life

BACKGROUND: Specific IgE antibody responses to alimentary and environmental allergens are one of the hallmarks of atopic diseases. The knowledge of the time course of allergic sensitization during early life may facilitate measures for preventive interventions. OBJECTIVE: In a prospective birth cohort study (the Multicenter Allergy Study [MAS]) we investigated annual incidence and prevalence rates of sensitization to food and inhalant allergens during the first 6 years of life. METHODS: For 216 children of a prospective birth cohort (MAS), a complete follow-up of specific IgE measurements to 9 food and inhalant allergens was available at 1, 2, 3, 5, and 6 years of age. On the basis of these measurements, sensitization rates were estimated for the reference population of 4082 children by weighted analysis. RESULTS: Annual incidence rates of sensitization to food allergens decreased from 10% at 1 year of age to 3% at the 6 years of age. Incidences of sensitization to inhalant allergen, however, increased with age (from 1.5% at 1 year to 8% at 6 years). Point prevalences of allergic sensitization to at least 1 of the 9 tested allergens increased from 11% at 1 year up to 30% at 6 years. This increase was due to markedly increasing sensitization rates to inhalant allergens (1.5% to at least 1 inhalant allergen at 1 year and 26% at 6 years of age), whereas sensitization rates to food allergens remained stable during the first 6 years of life (10%). CONCLUSION: The earliest serologic marker for atopic immunoreactivity in infancy is the presence of IgE antibodies to egg, followed by milk. The development of sensitization to inhalant allergens occurs mostly after infancy. Beyond the third birthday annual incidence and prevalence increase markedly with age. Rates for outdoor allergens are twice those for indoor allergens.     

Early endotoxin exposure and atopy development in infants: results of a birth cohort study

BACKGROUND: Exposure to endotoxin in childhood is currently discussed to protect from the development of allergic diseases. OBJECTIVE: To study the effect of early endotoxin exposure on incidence of atopic sensitization, atopic dermatitis and wheezing until the age of 2 years in infants with different risk status in terms of parental atopy. METHODS: Data of 1942 infants of an ongoing birth cohort study were analysed by logistic regression. Endotoxin was measured in settled dust of the mothers' mattresses at infants' age of 3 months. Data on allergic symptoms and physicians' diagnoses were gathered by questionnaire. Sensitization to common food and inhalant allergens was assessed by specific serum IgE. RESULTS: High endotoxin levels increased the risk of repeated wheeze [adjusted odds ratio (OR) for 4th exposure quartile (Q4) 1.52, 95% confidence interval (CI) 1.08-2.14], but were associated with neither sensitization to food allergens nor atopic dermatitis. Stratification by parental atopy showed that there was an association of endotoxin exposure with incidence of repeated wheeze as well as with sensitization to inhalant allergens (P for trend = 0.008 and 0.044, respectively) only in infants with parental atopy, with the highest risk in the 4th exposure quartile (repeated wheeze: ORQ4 1.77, 95% CI 1.14-2.73; sensitization to inhalant allergens: ORQ4 1.69, 95% CI 0.70-4.11). CONCLUSION: Early endotoxin exposure in terms of mattress dust endotoxin levels seemed to increase the risk of atopic reactions to inhalant allergens at the age of 2 years, especially in infants at risk due to parental atopy. Our data disagree with an early protective effect of endotoxin on atopy development until the age of 2 years.     

Dichotomy of food and inhalant allergen sensitization in eosinophilic esophagitis

BACKGROUND: Eosinophilic esophagitis (EE) is an emerging condition where patients commonly present with symptoms of gastroesophageal reflux disease and fail to respond adequately to anti-reflux therapy. Food allergy is currently recognized as the main immunological cause of EE; recent evidence suggests an etiological role for inhalant allergens. The presence of EE appears to be associated with other atopic illnesses. OBJECTIVES: To report the sensitization profile of both food and inhalant allergens in our EE patient cohort in relation to age, and to profile the prevalence of other allergic conditions in patients with EE. METHOD: The study prospectively analyzed allergen sensitization profiles using skin prick tests to common food allergens and inhalant allergens in 45 children with EE. Patch testing to common food allergens was performed on 33 patients in the same cohort. Comorbidity of atopic eczema, asthma, allergic rhinitis and anaphylaxis were obtained from patient history. RESULTS: Younger patients with EE showed more IgE and patch sensitization to foods while older patients showed greater IgE sensitization to inhalant allergens. The prevalence of atopic eczema, allergic rhinitis and asthma was significantly increased in our EE cohort compared with the general Australian population. A total of 24% of our cohort of patients with EE had a history of anaphylaxis. CONCLUSION: In children with EE, the sensitization to inhalant allergens increases with age, particularly after 4 years. Also, specific enquiry about severe food reactions in patients presenting with EE is strongly recommended as it appears this patient group has a high incidence of anaphylaxis.     

Influence of early and current environmental exposure factors on sensitization and outcome of asthma in pre-school children

BACKGROUND: Exposure to furred pets in early life has been considered to increase the risk of allergic sensitization and consequent development of asthma later in children. However, recently, it has been suggested that early exposure to pets prevents sensitization. The aim of this study was to evaluate the importance of early exposure to pets and other environmental risk factors in asthmatic children. METHODS: This is a follow-up study after 2 years of a previously investigated group of 193 asthmatic children, aged 1-4 years. The study was completed by 181 children, who were clinically examined; serum IgE antibodies were also measured and a questionnaire was answered. RESULTS: Children with reported exposure to cats during the first 2 years of life were more likely to have developed sensitization to cat by 4 years of age than unexposed children. High levels of cat allergen (Fel d 1> or =8 microg/g dust) were associated with an increased risk of sensitization to cat and, in combination with tobacco smoke, also with the development of more severe asthma. CONCLUSION: In young asthmatic children, early exposure to cat and tobacco smoke increased the risk of allergic sensitization and further development of more severe asthma later in childhood.     

Immunoglobulin G4-antibodies to rBet v 1 and risk of sensitization and atopic disease in the child

BACKGROUND: In 1993 extremely high levels of birch-pollen were recorded in Stockholm, Sweden. This provided an opportunity to evaluate the effects of aeroallergen exposure (exp.) on the early immune response. OBJECTIVE: To assess the influence of exp. to birch-pollen during pregnancy and infancy on the allergen-specific IgE- and IgG4-antibody (ab) response and the development of atopic disease in children. METHODS: A total of 970 children with atopic heredity and born in Stockholm 1992, 1993 or 1994 were investigated at age 4.5-5 years. They were divided into five groups; high-dose exp. at 1 year of age, high-dose exp. at 0-3 months, low-dose exp. at 0-3 months, high-dose exp. during pregnancy and low-dose exp. during pregnancy. The children were examined and skin prick tested with inhalant and food allergens. IgE abs (against birch-pollen and recombinant Bet v 1(rBet v1)) and IgG4 abs (against rBet v 1) were analysed in serum. All children were assembled in one group to assess the effects of different ab responses (IgE/IgG4) on the development of atopic disease. RESULTS: Children exposed to high doses of birch-pollen during the first 3 months of life more often had detectable levels of IgG4 abs to rBet v 1 than the children in the other groups (P < 0.001), independent of sensitization to birch. Overall, the risk of allergic rhinoconjunctivitis was increased among children sensitized to birch-pollen and appeared more pronounced in children without detectable levels of IgG4 ab to rBet v 1 (Odds ratio 9.4; 95% Confidence interval: 5.5-16.1). IgE sensitization to birch-pollen seemed to have a stronger influence on the development of atopic disease than the IgG4-ab response. CONCLUSION: Exposure to high doses of inhalant allergens during the early postnatal period is associated with detectable levels of allergen-specific IgG4 ab even at 5 years of age. An immune modulating effect by IgG4 on symptoms of allergic rhinoconjunctivitis is suggested in children sensitized to birch.     

Development of allergies and asthma in infants and young children with atopic dermatitis--a prospective follow-up to 7 years of age

BACKGROUND: The prognosis of atopic dermatitis is usually good, but the risk of developing asthma and allergic rhinitis is very high. The aim of this study was to follow children with atopic eczema up to school age to chart the course of sensitization and development of clinical allergy, as well as to study risk factors of sensitization. METHODS: Ninety-four children with atopic dermatitis were followed up to 7 years of age. The children were examined twice a year up to 3 years of age, and thereafter once yearly. At each visit, a clinical examination was performed, and a blood sample was taken. After 3 years of age, skin prick tests (SPTs) with inhalation allergens were performed at each visit. Information was obtained about atopy in the family, feeding patterns during infancy, symptoms of atopic disease, infections, and environmental factors. RESULTS: During the follow-up, the eczema improved in 82 of the 94 children, but 43% developed asthma and 45% allergic rhinitis. The risk of developing asthma was higher in children with a heredity of eczema. Presence of severe eczema at the time of inclusion in the study was associated with an increased tendency to produce food-specific IgE. An early onset of eczema was associated with an increased risk of sensitization to inhalant allergens, and development of urticaria. Early allergic reactions to food were associated with later reactions to food, allergic rhinitis, urticaria, and sensitization to both food and inhalant allergens. Early feeding patterns, time of weaning, and introduction of solid food did not influence the risk of development of allergic symptoms. A large number of periods or days with fever during the follow-up was associated with an increased risk of developing allergic rhinitis and urticaria. CONCLUSIONS: Our results confirm the good prognosis for the dermatitis and the increased risk of developing asthma and allergic rhinitis. Development of other allergic symptoms or sensitization was associated with the following factors: a family history of eczema, age at onset of eczema and its severity, early adverse reactions to foods, and proneness to infections.     

Exposure to high doses of birch pollen during pregnancy,and risk of sensitization and atopic disease in the child

BACKGROUND: The role of maternal allergen exposure during pregnancy in sensitization and development of atopic disease in the child remains controversial. In the spring of 1993, extremely high levels of birch pollen were recorded in Stockholm, Sweden. In 1994, the corresponding pollen levels were low. The aim of this study was to assess the influence of exposure during pregnancy to high/low doses of birch pollen on the risk of sensitization and development of atopic disease in children. In addition, a comparison was made with children exposed to birch pollen in early infancy. METHODS: Three hundred and eighty-seven children with atopic heredity, born in Stockholm in July-October 1993 or 1994 (mothers exposed during pregnancy), were investigated at age 4.5 years. The children were clinically examined and were skin prick tested (SPT) with inhalant and food allergens. IgE antibodies (RAST) against birch pollen and recombinant birch pollen allergen (rBet v 1) were analysed in serum. A comparison was made with a similar group of children exposed during the same incident, but in the first 3 months of life, in 1993. RESULTS: The children of mothers high-dose exposed during pregnancy in 1993 tended to be more sensitized (SPT > or = 3 mm) to birch pollen than the children with low-dose exposure during the corresponding period in 1994 (7.6 and 4.6%, respectively, OR: 1.7; 95% CI: 0.7-4.1). A similar but weak tendency was seen for positive RAST analyses (> or =0.35 kU/l) against birch pollen and rBet v 1. Children of mothers high-dose exposed during pregnancy were significantly less sensitized to birch pollen than the children high-dose exposed in early infancy (17.9%, OR: 0.4; 95% CI: 0.2-0.7). There was an overall trend towards a slightly increased prevalence of bronchial asthma, allergic rhinoconjunctivitis and atopic dermatitis in the group with mothers high-dose exposed during pregnancy, compared to those with low exposure. CONCLUSION: Exposure of the mother during pregnancy to high levels of birch pollen resulted in a tendency towards increased risk of sensitization to the same allergen and symptoms of atopic disease in children with atopic heredity. Furthermore, our data indicate that exposure of the mother during pregnancy to inhalant allergens is less likely to result in sensitization in the child than exposure of the child in early infancy.     

Sensitization to different pollens and allergic disease in 4-year-old Swedish children

BACKGROUND: Although the relationship between sensitization to different inhalant allergens in adolescents and adults has been intensively studied, information concerning sensitization in children is scarce in particular to pollens. OBJECTIVES: In 4-year-old children to elucidate the pollen immunoglobulin (IgE) antibody profile (birch only, timothy only and combinations of three pollens (birch, timothy or mugwort) and to relate the results to other inhalant and food allergens, as well as the presence of allergic diseases. METHODS: A total of 2551 4-year-old children belonging to a prospective birth cohort, which has been followed longitudinally (BAMSE), were investigated with respect to IgE antibodies to pollen and other inhalant and food allergens, and expression of allergic disease, based on questionnaire data. RESULTS: Eleven percent (n=285) of the children were sensitized to pollen. Birch was the dominating cause of pollen sensitization (birch sensitization only, n=133); followed by timothy grass pollen (n=56) and a combination of two (n=64) or three (n=30) pollens. A remarkably high proportion of the children sensitized only to birch was also sensitized to other inhalant allergens. This was not seen for children sensitized only to timothy. The highest frequencies of IgE reactivity to food were found in the group of children sensitized to the combination of birch, timothy and mugwort pollen. Children sensitized to timothy only, exhibited symptoms of allergic disease significantly less frequently compared with children sensitized to birch only. Sensitization to birch pollen was found to be closely associated with rhinitis and eczema compared with asthma. The highest frequency of asthma and/or rhinitis and/or eczema was reported in children sensitized to at least two pollens. CONCLUSION: Our results demonstrate that birch is the dominating source of pollen sensitization at the age of four in Sweden. This might associate with the pattern of sensitization to other inhalant and food allergens as well as influence on the expression of allergic disease in this particular age group.     

Fish consumption during the first year of life and development of allergic diseases during childhood

BACKGROUND: Fish consumption during infancy has been regarded as a risk factor for allergic disease but later evidence suggests a protective role. However, methodological limitations in the studies make conclusions uncertain. The aim of this study was to assess the association between fish consumption during the first year of life and development of allergic diseases by age 4. METHODS: A prospective birth cohort of 4089 new-born infants was followed for 4 years using parental questionnaires at ages 2 months, 1, 2 and 4 years to collect information on exposure and health effects. The response rate at 4 years was 90%. A clinical investigation was performed at age 4 years, which included blood sampling for analysis of specific IgE to common food and airborne allergens. RESULTS: Parental allergic disease and onset of eczema or wheeze during the first year of life delayed introduction of fish in the child's diet. After exclusion of such children to avoid disease-related modification of exposure, regular fish consumption during the first year of life was associated with a reduced risk for allergic disease by age 4, OR(adj) 0.76 (95% CI 0.61-0.94) and sensitization, OR(adj) 0.76 (0.58-1.0). The reduced risk appeared most pronounced for multiple disease, OR(adj) 0.56 (0.35-0.89). IgE-sensitization to fish was only present among 18 of the 2614 children. CONCLUSION: Regular fish consumption before age 1 appears to be associated with a reduced risk of allergic disease and sensitization to food and inhalant allergens during the first 4 years of life.     

Exposure to birch pollen in infancy and development of atopic disease in childhood

BACKGROUND: The relationship between early allergen exposure, sensitization, and development of atopic disease remains controversial. In 1993, extremely high levels of birch pollen were recorded in Stockholm, Sweden, creating the unique opportunity to study children with different exposures during infancy. OBJECTIVE: We sought to assess the influence of early high-dose exposure to an inhalant allergen (birch pollen) on sensitization and development of atopic disease in children. METHODS: A total of 583 children with atopic heredity born in Stockholm in February through April 1992, 1993, or 1994 were investigated at age 4.5 to 5 years. The children were examined and underwent skin prick testing with inhalant and food allergens. IgE antibodies (RAST) against birch pollen and recombinant birch pollen allergen (rBet v 1) were analyzed in serum. RESULTS: The children born in 1993 (high-dose exposure at 0-3 months) were more often sensitized (ie, positive skin prick test response) to birch pollen than the children born in 1994 (low-dose exposure; 17.8% and 8.8%, respectively; odds ratio [OR], 2.4; 95% CI, 1.2-4.6). A tendency in the same direction was seen for children born in 1992 (high-dose exposure at 12-15 months; OR, 1.7; 95% CI, 0.9-3.2). The results were supported by the RAST analyses. The prevalence of bronchial asthma, allergic rhinoconjunctivitis, and atopic dermatitis did not differ between the birth-year groups. However, the prevalence of pollen- and animal dander-induced allergic asthma was increased in the children born in 1993 (OR, 2.6; 95% CI, 1.2-5.6). An interaction between early high-dose exposure to birch pollen and cat in the household was suggested for sensitization to cat (P =.06). CONCLUSION: Exposure to high levels of birch pollen in infancy increases the risk of sensitization to the same allergen, as well as the risk of allergic asthma.     

Risk factors for wheezing in a subtropical environment: role of respiratory viruses and allergen sensitization

BACKGROUND: Risk factors for acute wheezing among children in subtropical areas are largely unknown. OBJECTIVE: To investigate the role of viral infections, allergen sensitization, and exposure to indoor allergens as risk factors for acute wheezing in children 0 to 12 years old. METHODS: One hundred thirty-two children 0 to 12 years of age who sought emergency department care for wheezing and 65 children with no history of wheezing were enrolled in this case-control study. Detection of respiratory syncytial virus antigen, rhinovirus and coronavirus RNA, adenovirus, influenza, and parainfluenza antigens was performed in nasal washes. Total IgE and specific IgE to mites, cockroach, cat, and dog were measured with the CAP system. Major allergens from mites, cockroach, cat, and dog were quantified in dust samples by ELISA. Univariate and multivariate analyses were performed by logistic regression. RESULTS: In children under 2 years of age, infection with respiratory viruses and family history of allergy were independently associated with wheezing (odds ratio, 15.5 and 4.2; P = .0001 and P = .008, respectively). Among children 2 to 12 years old, sensitization to inhalant allergens was the major risk factor for wheezing (odds ratio, 2.7; P = .03). High-level allergen exposure, exposure to tobacco smoke, and lack of breast-feeding showed no association with wheezing. CONCLUSIONS: Some risk factors for wheezing previously identified in temperate climates were present in a subtropical area, including respiratory syncytial virus infection in infants and allergy in children older than 2 years. Rhinovirus was not associated with wheezing and did not appear to be a trigger for asthma exacerbations.     

Atopic sensitization among children in an Arctic environment

BACKGROUND: Asthma has been reported to be rare among Inuits, but so far total and specific IgE levels have never been determined in arctic populations. OBJECTIVE: To determine the prevalence of atopy in children living in an arctic environment, and to examine whether atopy and total IgE levels were associated with parental place of birth, as a measure of ethnicity, and travel history. MATERIAL AND METHODS: All schoolchildren in Sisimiut, a community on the West coast of Greenland, were screened for atopy. Blood samples were analysed for total IgE and for specific IgE against inhalant and food allergens. Information on place of birth of children and their parents was obtained from national registries. Information on travel history was obtained from self-administered questionnaires. RESULTS: A total of 1031 schoolchildren aged 5 to 18 years had a blood sample drawn (85% of available children for the study). Of these, 151 (14.6%) children were sensitized to at least one inhalant allergen and 42 (4.1%) to at least one food allergen. Sensitization to grass was most common, whereas sensitization to mugwort, birch, animal-dander and house-dust mite was infrequent. Children whose parents were both born abroad had a higher risk of sensitization to inhalant allergens compared with children born of Greenlandic parents (OR = 8.6, 95% CI 2.8-27.1). Furthermore, children who had been abroad had a higher risk of sensitization towards pollen (OR = 1.6, 95% CI 1.0-2.5) and animal-dander (OR = 2.1, 95% CI 1.0-4.6) after adjustment for confounders. Both atopic and non-atopic children demonstrated high levels of total IgE (medians of 251 and 58 kU/L). CONCLUSIONS: Compared with European findings Greenlandic children have high levels of total IgE but a low prevalence of allergic sensitization towards inhalant allergens. This may be due to a low genetic susceptibility to atopy and less allergen exposure, as well as to living conditions in an arctic environment.     

Effects of environmental tobacco smoke on the developing immune system of infant monkeys

BACKGROUND: Exposure to environmental tobacco smoke (ETS) is associated with an increased incidence of allergic and infectious diseases among children that is thought to be partly due to the immaturity of the immune system. OBJECTIVE: We sought to investigate the effects of ETS exposure on immune development during the first year of life in the nonhuman primate. METHODS: Fifteen neonatal rhesus monkeys studied to 13 months of postnatal age were randomized into 3 groups: (1) exposure to filtered air, (2) continuous ETS exposure beginning at gestation day 50 (perinatal ETS); and (3) exposure to ETS beginning at 6 months of age (6-month ETS). Complete blood counts, lymphocyte subsets, and mRNA levels of 12 cytokines in PBMCs were measured. RESULTS: Fetal/infant exposure to ETS altered the normal maturation of mRNA levels of IFN-gamma, IL-2, and IL-10, as well as the ratio of CD4 to CD8 lymphocytes, compared with filtered-air control levels. Blood lymphocyte subset distribution also significantly differed based on the onset of exposure to ETS. Subacute exposure to ETS for 2 weeks in 6-month-old infants was found to increase levels of peripheral blood neutrophils and IL-6 mRNA. CONCLUSIONS: Short-term exposure to ETS can induce an acute systemic inflammatory response in the neonatal nonhuman primate, and long-term exposure to ETS beginning in utero or at 6 months of postnatal age can significantly alter immune effectors. CLINICAL IMPLICATIONS: Normal immune system development is compromised by in utero and postnatal exposure to ETS and might contribute to ETS-related childhood diseases.     

Progesterone and environmental tobacco smoke act synergistically to exacerbate the development of allergic asthma in a mouse model

BACKGROUND: Asthma affects males and females differently. Females have a higher incidence than males after the onset of puberty. This suggests a hormonal component to the development of the disease. Progesterone, a female hormone, has previously been shown to illicit a T-helper type 2 (TH2) immune response similar to that seen in allergic asthma. Previous studies performed by our laboratory have shown that exposure to environmental tobacco smoke (ETS) enhances the immune response to allergens. OBJECTIVE: To determine if the combination of exposure to ETS and progesterone would further exacerbate the immune response in a mouse model of allergic asthma. METHODS: Female mice were ovariectomized and then implanted with time-release progesterone pellets. Mice were housed in either filtered air (FA) or ETS chambers and half were exposed to aerosolized house dust mite allergen (HDMA). Bronchoalveolar lavage was performed for cell differentials; lung and spleen cells were harvested to compare IL-4 and IFN-gamma production by ELISPOT. RESULTS: Progesterone pellet implantation resulted in increased serum progesterone levels (28.3+/-8.43 vs. 13.5+/-7.22 ng/mL in placebo-treated mice, P<0.0001). Serum total IgE levels were significantly greater in progesterone vs. non-progesterone treated animals that were also exposed to HDMA. ETS exposure enhanced total IgE levels as well. Lung homogenate cells from HDMA/progesterone-treated animals stimulated with Concavalin A produced significantly more IL-4 compared with HDMA/placebo-treated animals (200+/-17.6 vs. 146+/-17.5 spots/well, P<0.01 in ETS exposed animals and 221+/-28.9 vs. 167+/-23.4 spots/well, P<0.01 in animals housed in FA). HDMA/ETS-treated animals had higher eosinophilia in lavage than all other groups. CONCLUSION: Increased serum progesterone levels exacerbate the allergic asthmatic phenotype in a mouse model. These effects are further exacerbated by the addition of environmental tobacco smoke. Progesterone provides a major contribution to the gender differences seen in the development and elicitation of the asthmatic response.     

Exposure to house dust endotoxin and allergic sensitization in adults

BACKGROUND: It has been suggested that exposure to elevated levels of endotoxin decreases the risk of allergic sensitization. OBJECTIVE: To examine the associations between current exposure to bacterial endotoxin in house dust and allergic sensitization in adults. METHODS: In 1995-1996, we conducted a nested case-control study following a cross-sectional study performed within the European Community Respiratory Health Survey (ECRHS). Data of 350 adults aged 25-50 years was analysed. Allergic sensitization was assessed by measurement of specific immunoglobulin E (IgE) against several inhalant allergens. Living room floor dust samples were taken. The endotoxin content was quantified using a chromogenic kinetic Limulus amoebocyte lysate test. RESULTS: Multiple logistic regression analysis showed a negative association between exposure to house dust endotoxin and severe allergic sensitization. Odds ratios (95% CI) adjusted for place of residence, gender, age, and 'caseness' were 0.80 (0.64-1.00) for sensitization to >/=1 allergen and 0.72 (0.56, 0.92) for sensitization to >/=2 allergens using 3.5 kU/l as a cut-off value for sensitization. With regard to single allergens, the protective effect of endotoxin was strongest for pollen sensitization [aOR (95% CI) = 0.74 (0.58, 0.93)]. CONCLUSION: Our results indicate that current exposure to higher levels of house dust endotoxin might be associated with a decreased odds of allergic sensitization in adults.     

Association between sensitized to food allergens and childhood allergic respiratory diseases in Taiwan

BackgroundSensitization to allergen has long been known to be relate to childhood allergic diseases. Polysensitised children have more severe atopic diseases, whereas allergic rhinitis or asthma children with cosensitized to food and inhalant allergens were under-researched.ObjectiveTo realize the association between sensitization to food allergens and pediatric allergic rhinitis and asthma in Taiwan.MethodsWe included 138 participants with sensitized to allergen as assessed by serum-specific IgE. 87 of 138 participants had allergic rhinitis and 51 participants had asthma. All participants underwent a physical examination and measurement of serum total and specific IgE values. Besides, nasal peak expiratory flow rate (nPEFR) that was performed by the participants with allergic rhinitis and were requested to complete the Pediatric Rhinoconjunctivitis Quality of Life Questionnaires (PRQLQ). Lung function test and asthma control test (ACT)/child asthma control test (C-ACT) were performed by the participants with asthma.Results39 of 87 allergic rhinitis participants with sensitized to food and inhalant allergens (AR food group), 48 of 87 allergic rhinitis participants with sensitized to inhalant allergen alone (AR inhalant group). The AR food group had significantly lower nPEFR values and higher total IgE values (p < 0.05) compared with the AR inhalant group. The AR food group had higher PRQLQ scores than the AR inhalant group. 24 of 51 asthma participants with sensitized to food and inhalant allergens (Asthma food group), 27 of 51 asthma participants with sensitized to inhalant allergen alone (Asthma inhalant group). The Asthma food group had significantly higher total IgE values (p < 0.05) compared with the Asthma inhalant group. The Asthma food group had lower lung function test values and asthma control test (ACT) scores than the other group.ConclusionsChildren with cosensitized to food and inhalant allergens have more severe clinical symptoms and abnormal laboratory findings. Sensitization to food allergen was more related to pediatric allergic rhinitis than asthma. We may need larger, longer and extended studies to confirm these findings.     

Gender differences in the allergic response of mice neonatally exposed to environmental tobacco smoke

Exposure to environmental tobacco smoke (ETS) has been shown to increase allergic sensitization and reactivity and there has been some suggestion that the influence of ETS on the allergic response is dissimilar in males and females. It is to be determined whether gender differences exist in the IgE response to ovalbumin (OVA) sensitization following ETS exposure from the neonatal period through adulthood. To address this thesis, we examined gender differences in OVA sensitization of BALB/c mice housed from birth through adulthood under smoking and nonsmoking conditions. At 6 weeks of age (day 0) all mice were injected i.p. with OVA in aluminum hydroxide adjuvant followed by three 20 min exposures to 1% aerosolized OVA between day 14 and 80. There were significantly (p < 0.05) more total and OVA specific IgE and IgG1 in the serum of females compared to males. Moreover, these sex responses, along with eosinophilia, were further enhanced in mice exposed to ETS. There were also significantly more IgE positive cells in the lungs of female, but not male, mice exposed to ETS compared with ambient air (p < 0.05). There was also an elevation of Th2 cytokines (IL4, IL5, IL10, and IL13) after re-stimulation of lung homogenates following ETS exposure. These data demonstrate that female animals are significantly more susceptible than males to the influence of ETS on the allergic response.     

Second-hand smoke increases bronchial hyperreactivity and eosinophilia in a murine model of allergic aspergillosis

Involuntary inhalation of tobacco smoke has been shown to aggravate the allergic response. Antibodies to fungal antigens such as Aspergillus fumigatus (Af) cause an allergic lung disease in humans. This study was carried out to determine the effect of environmental tobacco smoke (ETS) on a murine model of allergic bronchopulmonary aspergillosis (ABPA). BALB/c mice were exposed to aged and diluted sidestream cigarette smoke to simulate 'second-hand smoke'. The concentration was consistent with that achieved in enclosed public areas or households where multiple people smoke. During exposure, mice were sensitized to Af antigen intranasally. Mice that were sensitized to Af antigen and exposed to ETS developed significantly greater airway hyperreactivity than did mice similarly sensitized to Af but housed in ambient air. The effective concentration of aerosolized acetylcholine needed to double pulmonary flow resistance was significantly lower in Af + ETS mice compared to the Af + AIR mice. Immunological data that supports this exacerbation of airway hyperresponsiveness being mediated by an enhanced type 1 hypersensitivity response include: eosinophilia in peripheral blood and lung sections. All Af sensitized mice produced elevated levels of IL4, IL5 and IL10 but no IFN-gamma indicating a polarized Th2 response. Thus, ETS can cause exacerbation of asthma in ABPA as demonstrated by functional airway hyperresponsiveness and elevated levels of blood eosinophilia.     

Between a cough and a wheeze: dendritic cells at the nexus of tobacco smoke-induced allergic airway sensitization

Exposure to cigarette smoke represents a major risk factor for the development of asthma. Enhanced sensitization toward allergens has been observed in humans and laboratory animals exposed to cigarette smoke. Pulmonary dendritic cells (DCs) are crucially involved in sensitization toward allergens and play an important role in the development of T helper (Th)2-mediated allergic airway inflammation. We propose the concept that aberrant DC activation forms the basis for the deviation of the lung's default tolerogenic response toward allergic inflammation when harmless antigens are concomittantly inhaled with tobacco smoke. This review will summarize evidence suggesting that tobacco smoke can achieve this effect by providing numerous triggers of innate immunity, which can profoundly modulate airway DC biology. Tobacco smoke can affect the airway DC network either directly or indirectly by causing the release of DC-targeted mediators from the pulmonary tissue environment, resulting in the induction of a Th2-oriented pathological immune response. A thorough knowledge of the molecular pathways involved may open the door to novel approaches in the treatment of asthma.