Factors in childhood as predictors of asthma in adult life

Jenkins, Mark A.; Hopper, John L.; Bowes, Glenn; Carlin, John B.; Flander, Louisa; Giles, Graham G.

doi:10.1136/bmj.309.6947.90

Cited by 234 publications

(159 citation statements)

References 14 publications

Supporting

Mentioning

133

Contrasting

Unclassified

Order By: Relevance

“…Prenatal exposure to environmental tobacco smoke has been consistently associated with wheezing and the subsequent diagnosis of asthma (8,12,27). In addition, prenatal tobacco smoke exposure has been associated with decreased airflow in infants and children (5,7).…”

Section: Discussionmentioning

confidence: 99%

“…Altogether, these studies suggest that nicotine stimulates lung branching morphogenesis through ␣7 nicotinic acetylcholine receptors and may contribute to dysanaptic lung growth, which in turn may predispose the host to airway disease in the postnatal period. lung growth; nicotinic receptors A RELATIONSHIP BETWEEN environmental tobacco smoke and the subsequent development of wheezing and asthma has been identified in a number of epidemiological studies (8,12,27). In particular, maternal smoking has been independently associated with an increased risk for the development of asthma, diminished lower airway function, and the development of wheezing in infants, which can persist into the first few years of life (5,10).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Nicotine alters lung branching morphogenesis through the α₇ nicotinic acetylcholine receptor

Wongtrakool

Roser‐Page²,

Rivera³

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

There is abundant epidemiological data linking prenatal environmental tobacco smoke with childhood asthma and wheezing, but the underlying molecular and physiological mechanisms that occur in utero to explain this link remain unelucidated. Several studies suggest that nicotine, which traverses the placenta, is a causative agent. Therefore, we studied the effects of nicotine on lung branching morphogenesis using embryonic murine lung explants. We found that the expression of α7 nicotinic acetylcholine receptors, which mediate many of the biological effects of nicotine, is highest in pseudoglandular stage lungs compared with lungs at later stages. We then studied the effects of nicotine in the explant model and found that nicotine stimulated lung branching in a dose-dependent fashion. α-Bungarotoxin, an antagonist of α7 nicotinic acetylcholine receptors, blocked the stimulatory effect of nicotine, whereas GTS-21, a specific agonist, stimulated branching, thereby mimicking the effects of nicotine. Explants deficient in α7 nicotinic acetylcholine receptors did not respond to nicotine. Nicotine also stimulated the growth of the explant. Altogether, these studies suggest that nicotine stimulates lung branching morphogenesis through α7 nicotinic acetylcholine receptors and may contribute to dysanaptic lung growth, which in turn may predispose the host to airway disease in the postnatal period.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Nicotine alters lung branching morphogenesis through the α₇ nicotinic acetylcholine receptor

Wongtrakool

Roser‐Page²,

Rivera³

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

show abstract

“…The methodology and some results of previous surveys have been reported elsewhere. [16][17][18][19] The 36-year follow-up of the Tasmanian Asthma Study involved a postal survey of all traced 1968 probands (n 5 7312; 85.2%). The methodology of tracing participants has been reported previously.…”

Section: Tasmanian Asthma Studymentioning

confidence: 99%

Breast-feeding and atopic disease: A cohort study from childhood to middle age

Matheson

Erbas

Balasuriya

et al. 2007

Journal of Allergy and Clinical Immunology

118

View full text Add to dashboard Cite

“…The asthma affair is a little more intricate: the onset within the first year is certain in 34,5% [23][24][25][26]-56,2% [24,27], of babies, but a higher level (82.4%) is evident between the 4th and the 7th year [24,[27][28][29]. That within the 8th year the asthma onset is manifest in 90% of children [28], is confirmed by the 92% proportion reached in patients less than 20 years of age [31]. As regards AR, the onset may be in the first year in 35% of children and in 59% of those aged 2-5 years [24], who in other studies are affected in 13-19% of cases [23,30].…”

Section: Discussionmentioning

confidence: 98%

In 250 Children we Demonstrate that the Transmission of Allergy and Asthma is Chiefly Genetic, Mainly when these Children are Asthmatic

Cantani¹

2015

Glob J Allergy

View full text Add to dashboard Cite

There seems to be no unanimity of opinion as to the mode of transmission of allergic disease. According to some, allergy is transmitted as a simple Mendelian dominant. In direct contrast, others maintain that the findings favor a recessive mechanism. Further-more, others suggest that the condition is inherited as a "partial dominant" disorder. An additional analysis of family studies as well as data already published, failed to support either the simple dominant or recessive theory. The dominant theory does not explain why in more than half of the pedigrees both parents are normal. The recessive theory is refuted by the existence of pedigrees in which both parents are affected, yet some of the children are normal. To put more order in this complex mess, we have decided to study the genetic risk of children with a family history (FH) of allergy, We have therefore formed this prospective study in 250 children that included: family (FH) and personal history, skin prick tests (SPTs) and specific IgE (RAST), who were admitted to the Pediatric Allergy and Immunology Division of Rome University since they were affected with respiratory allergy. We have prepared a sheet with questions and possible answers. Consequently, we have studied the FH of these children asking whether their parents and brothers/sisters had atopic diseases, and specifying whether such disorders were respiratory or food allergies (FA). The parents of all children gave their informed consent. We analyzed data using the X2 method. 42.3% of their parents were atopic, as well as their 20 brothers/sisters. In total, 90.2% of fathers, 84% of mothers and 65% of brothers/sisters had asthma or allergic rhinitis (AR). We add that some parents had urticarial, further there were mothers and brothers/sisters experiencing atopic dermatitis (AD), and some mothers with food allergy (FA). In 23 children from these parents most had AD and respiratory allergy. In 250 children comparable for age and sex with no respiratory disorder supplied from our out patient clinic 40 parents, 14 mothers and 26 fathers and 9 brothers/sisters had asthma or AR (p = 0.0001), some fathers had also urticaria and two brothers AD. A major part of respiratory allergy is not transmitted by mothers: we stress that 42.3% of parents are atopic, and FH of their children was positive for respiratory allergy in 82-92% of cases. Thus respiratory allergy can have an autosomal dominant mode of inheritance, but considering the other atopic diseases, the transmission can be polygenic. The impact of genetic factors in these children is stressed by the relevant quote of asthmatic brothers/sisters. actual accordance between MZ and DZ twins [5]. Twin studies have also revealed a positive evidence for environmental influences, where unshared environmental influences appeared to be important [6]. Most printed studies in this domain have ascertained that everywhere between 40% and 70% of asthma heredity is preferable to hereditary factors [7]. We stress that several studies on asthma genetics have be...

show abstract

Factors in childhood as predictors of asthma in adult life

Abstract: Objective-To determine which factors measured in childhood predict asthma in adult life.Design-Prospective study over 25 years of a birth cohort initially studied at the age of7.Setting-Tasmania, Australia.

Cited by 234 publications

References 14 publications

Nicotine alters lung branching morphogenesis through the α₇ nicotinic acetylcholine receptor

Nicotine alters lung branching morphogenesis through the α₇ nicotinic acetylcholine receptor

Breast-feeding and atopic disease: A cohort study from childhood to middle age

In 250 Children we Demonstrate that the Transmission of Allergy and Asthma is Chiefly Genetic, Mainly when these Children are Asthmatic

Contact Info

Product

Resources

About

Factors in childhood as predictors of asthma in adult life

Abstract: Objective-To determine which factors measured in childhood predict asthma in adult life.Design-Prospective study over 25 years of a birth cohort initially studied at the age of7.Setting-Tasmania, Australia.

Cited by 234 publications

References 14 publications

Nicotine alters lung branching morphogenesis through the α7 nicotinic acetylcholine receptor

Nicotine alters lung branching morphogenesis through the α7 nicotinic acetylcholine receptor

Breast-feeding and atopic disease: A cohort study from childhood to middle age

In 250 Children we Demonstrate that the Transmission of Allergy and Asthma is Chiefly Genetic, Mainly when these Children are Asthmatic

Contact Info

Product

Resources

About

Nicotine alters lung branching morphogenesis through the α₇ nicotinic acetylcholine receptor

Nicotine alters lung branching morphogenesis through the α₇ nicotinic acetylcholine receptor