A study of the relationship between mite IgE in serum of school children and smoking habits in mothers.

Osaka, Fumio; Kasuga, Hitoshi; Sugita, Minoru; Matsuki, Hideaki; Miyake, Teruki

doi:10.1265/jjh.40.789

Cited by 8 publications

(4 citation statements)

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“…Ownby and McCullough (36) found no increase in either total or allergen-specific IgE in children aged 1-19 years exposed to parental smoking. Although Osaka et al (8) reported an increase in mite-specific IgE levels in Japanese children of smoking parents, Ozasa et al (9) found a negative association between Japanese cedar pollen-specific IgE and passive smoking in the same population.…”

Section: Discussionmentioning

confidence: 97%

“…Maternal smoking is often associated with allergic disease and increased skin test reactivity, serum IgE, and prevalence of eosinophilia in children. (5)(6)(7)(8)(9) However, other studies have failed to see such an association (10) and experimental data supporting these claims is scant. Although the role of pollutants in allergic inflammation has been extensively studied in many animal models, few studies have used these models to study the association between environmental tobacco smoke (ETS) 3 (3) (commonly referred to as "secondhand smoke") and allergy/ asthma.…”

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confidence: 99%

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Secondhand Smoke Induces Allergic Sensitization in Mice

Rumold

Jyrala²,

Díaz-Sánchez

2001

The Journal of Immunology

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Epidemiological studies have suggested increased prevalence of atopy in children of maternal smokers. Although secondhand smoke or environmental tobacco smoke (ETS) has been shown to augment allergic responses, its role in atopic sensitization is still controversial. We studied whether ETS could initiate a Th2 response and thus induce primary allergic sensitization. Mice were exposed for 10 consecutive days to either 1% aerosolized OVA, ETS (5 cigarettes), or both ETS and OVA. C57BL/6 mice receiving both ETS and OVA developed OVA-specific IgE and IgG1, 12, 14, and 25 days after the initial exposure, whereas those receiving OVA alone did not. Thirty days after the initial challenge (20 days after its completion), mice were re-exposed to OVA. Bronchoalveolar lavage performed 24 h later revealed an influx of eosinophils in the group initially challenged with both ETS and OVA, but not in those exposed to ETS alone or OVA alone. Increases in IL-5, GM-CSF, and IL-2 were observed in bronchoalveolar lavage from this OVA/ETS-exposed group, whereas IFN-γ levels were significantly inhibited. These results suggest that ETS can induce allergic sensitization to a normally harmless Ag, and they may explain why secondhand smoke is a major risk factor for the development of allergy in children.

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Section: Discussionmentioning

confidence: 97%

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confidence: 99%

Secondhand Smoke Induces Allergic Sensitization in Mice

Rumold

Jyrala²,

Díaz-Sánchez

2001

The Journal of Immunology

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“…Although, a genetic predisposition to the development of allergic asthma is recognized (Daniels et al, 1996;Gern et al, 1999) evidence strongly suggests that environmental agents such as ETS increase its phenotypic expression (el-Nawawy et al, 1996;Gilliland et al, 2001). Some studies have shown that males are more likely to be allergic from exposure to ETS or mainstream smoke than females (Ronchetti et al, 1992;Omenaas et al, 1994;Jarvis et al, 1995), while others have reported no sex differences in the prevalence of allergy (Osaka et al, 1985). These studies, while intriguing, are also controversial due to the multiple environmental factors that affect human beings, making it difficult to evaluate the true impact of ETS on the prevalence and severity of allergy.…”

Section: Introductionmentioning

confidence: 99%

Gender Differences in the Allergic Response of Mice Neonatally Exposed to Environmental Tobacco Smoke

Seymour

Friebertshauser

Peake

et al. 2002

Journal of Immunology Research

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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.

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“…[9][10][11][12][13][14][15] These studies have shown associations between environmental tobacco smoke (ETS; commonly referred to as second-hand smoke or passive smoking) and increased skin test reactivity, serum IgE, and prevalence of eosinophilia in children. Yet despite claims that with regards to allergy, ''tobacco smoke is by far the most important single environmental factor,'' 16 this is still a matter of contention, and very few studies have tested this supposition by direct experimentation.…”

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confidence: 99%