Tasmanian Longitudinal Health Study Research Articles

The Interplay between the Effects of Lifetime Asthma, Smoking, and Atopy on Fixed Airflow Obstruction in Middle Age

The contribution by asthma to the development of fixed airflow obstruction (AO) and the nature of its effect combined with active smoking and atopy remain unclear. To investigate the prevalence and relative influence of lifetime asthma, active smoking, and atopy on fixed AO in middle age. The population-based Tasmanian Longitudinal Health Study cohort born in 1961 (n = 8,583) and studied with prebronchodilator spirometry in 1968 was retraced (n = 7,312) and resurveyed (n = 5,729 responses) from 2002 to 2005. A sample enriched for asthma and chronic bronchitis underwent a further questionnaire, pre- and post-bronchodilator spirometry (n = 1,389), skin prick testing, lung volumes, and diffusing capacity measurements. Prevalence estimates were reweighted for sampling fractions. Multiple linear and logistic regression were used to assess the relevant associations. Main effects and interactions between lifetime asthma, active smoking, and atopy as they relate to fixed AO were measured. The prevalence of fixed AO was 6.0% (95% confidence interval [CI], 4.5-7.5%). Its association with early-onset current clinical asthma was equivalent to a 33 pack-year history of smoking (odds ratio, 3.7; 95% CI, 1.5-9.3; P = 0.005), compared with a 24 pack-year history for late-onset current clinical asthma (odds ratio, 2.6; 95% CI, 1.03-6.5; P = 0.042). An interaction (multiplicative effect) was present between asthma and active smoking as it relates to the ratio of post-bronchodilator FEV(1)/FVC, but only among those with atopic sensitization. Active smoking and current clinical asthma both contribute substantially to fixed AO in middle age, especially among those with atopy. The interaction between these factors provides another compelling reason for atopic individuals with current asthma who smoke to quit.

Does eczema in infancy cause hay fever, asthma, or both in childhood? Insights from a novel regression model of sibling data

The atopic march hypothesis proposes that eczema precedes the development of asthma and allergic rhinitis. We sought to assess the evidence for a causal effect of infantile eczema on childhood hay fever, asthma, or both. We used parental reports on infantile eczema and childhood asthma and hay fever for 3778 pairs of 7-year-olds matched to their sibling closest in age within 2 years from the Tasmanian Longitudinal Health Study. We analyzed paired sibling data using a logistic regression model that allowed inference about a causal effect of a familial predictor on a child's outcome by examining the change in association with their cosibling's predictor after adjusting for their own predictor status. Siblings were concordant for infantile eczema (tetrachoric correlation, 0.40). For having both hay fever and asthma by age 7 years, the association with cosibling's eczema was an odds ratio (OR) of 1.98 (95% CI, 1.37-2.86), which reduced after adjusting for own eczema to an OR of 1.65 (95% CI, 1.17-2.34). For having hay fever only, the association with cosibling's eczema was an OR of 1.68 (95% CI, 1.22-2.31) before and an OR of 1.59 (95% CI, 1.19-2.14) after adjusting for own eczema. There was no association between having asthma only and cosibling's eczema (OR, 1.00; 95% CI, 0.77-1.30). Eczema in infancy might have a causal effect on hay fever in children with and perhaps without asthma. The association of infantile eczema on asthma in children without hay fever, which might be early transient wheeze, is unlikely to be causal or familial. These findings have implications for hay fever prevention.

Childhood Infections and the Risk of Asthma: A Longitudinal Study Over 37 Years

Few studies have examined common childhood infections and adult asthma. We examined associations between childhood infectious diseases, childhood pneumonia, and current, persisting, and incident asthma to middle age. We analyzed data from the Tasmanian Longitudinal Health Study (TAHS). A history of pneumonia was ascertained from their parents when the TAHS participants were 7 years old. Measles, rubella, mumps, chickenpox, diphtheria, and pertussis were identified from school medical records. Associations with current, persisting, or incident asthma were examined using regression techniques. Greater infectious diseases load was negatively associated with persisting asthma at all ages. Individually, pertussis (adjusted OR [aOR], 0.53; 95% CI, 0.28-1.00) was negatively associated with asthma persisting to age 13 years, chickenpox (aOR, 0.58; 95% CI, 0.38-0.88) was negatively associated with asthma persisting to age 32 years, and rubella was negatively associated with asthma persisting to ages 32 (aOR, 0.61; 95% CI, 0.31-0.96) and 44 years (aOR 0.53; 95% CI, 0.35-0.82). Pertussis was associated with preadolescent incident asthma (adjusted hazard ratio [aHR], 1.80; 95% CI, 1.10-2.96), whereas measles was associated with adolescent incident asthma (aHR, 1.66; 1.06-2.56). Childhood pneumonia was associated with current asthma at ages 7 (aOR, 3.12; 95% CI, 2.61-3.75) and 13 years (aOR, 1.32; 95% CI, 1.00-1.75), an association stronger in those without than those with eczema (aOR, 3.46; 95% CI, 2.83-4.24 vs aOR, 2.08; 95% CI, 1.38-3.12). Overall, childhood infectious diseases protected against asthma persisting in later life, but pertussis and measles were associated with new-onset asthma after childhood. Measles and pertussis immunization might lead to a reduction in incident asthma in later life.

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Childhood eczema and rhinitis predict atopic but not nonatopic adult asthma: A prospective cohort study over 4 decades

The evidence on whether the atopic march observed in childhood (ie, the progression from eczema to allergic rhinitis and asthma) extends to adulthood is sparse, and there is no evidence on whether the progression leads to a specific phenotype of asthma. We sought to assess whether childhood eczema and rhinitis are risk factors for specific phenotypes of adult asthma. Participants of the Tasmanian Longitudinal Health Study recruited in 1968 (age range, 6.0-7.0 years) were followed up at age 44 years. The risk of current atopic or nonatopic asthma in middle age characterized by sensitization to aeroallergens given childhood eczema, rhinitis, or both was calculated by using multinomial logistic regression. No association was found between childhood eczema or rhinitis and nonatopic adult asthma. In contrast, childhood eczema and rhinitis in combination predicted both new-onset atopic asthma by middle age (adjusted multinomial odds ratio [aMOR], 6.3; 95% CI, 1.7-23.2) and the persistence of childhood asthma to adult atopic asthma (aMOR, 11.7; 95% CI, 3.6-37.9). Participants with childhood eczema alone were at increased risk of new-onset atopic asthma (aMOR, 4.1; 95% CI, 1.9-8.8), whereas rhinitis alone predicted the persistence of childhood asthma to atopic asthma (aMOR, 2.7; 95% CI, 1.3-5.6). Of all asthma, 29.7% of persistent atopic asthma and 18.1% of new-onset atopic asthma could be attributed to having childhood eczema and rhinitis. Childhood eczema and rhinitis are strongly associated with the incidence and persistence of adult atopic asthma.

Factors influencing asthma remission: a longitudinal study from childhood to middle age

ObjectiveTo examine asthma remission from childhood to middle age.MethodsThis was a population-based cohort study. In 1968 the Tasmanian Longitudinal Health Study enrolled 8583 7-year-old Tasmanian schoolchildren who were re-surveyed in...

Ambient wood smoke exposure and respiratory symptoms in Tasmania, Australia

Wood smoke exposure has been associated with adverse respiratory health outcomes, with much of the current research focused on wood smoke from domestic heating and cooking. This study examined the association between respiratory symptoms and outdoor wood smoke in Launceston, Tasmania, where ~ 30% of homes use wood burners for domestic heating. This ecological study examined data from participants of the 2004 Tasmanian Longitudinal Health Study postal survey and compared the prevalence of respiratory symptoms in Launceston ( n = 601) with that in Hobart ( n = 1071), a larger Tasmanian city with much less wood smoke. Multivariate logistic regression models were used to investigate the associations of interest while adjusting for gender, atopy, history of allergic disease and current smoking status. There were no significant differences in symptom prevalence between Launceston and Hobart. Two subgroup analyses, which examined participants with pre-existing chronic respiratory disease, and those who reported actively using a wood burner in their home, also did not find significant differences. Any impact of wood smoke on non-specific respiratory symptoms might have been overshadowed by other important determinants of respiratory health, such as vehicle exhaust and tobacco smoking, or were too small to have been detected. However, the lack of detectable differences in symptom prevalence might also reflect the success of regulatory action by local governments to reduce wood smoke emissions in Launceston. The results of other epidemiological studies support an association between ambient wood smoke exposure and adverse respiratory health. Further investigations of wood smoke exposure in Australian settings are needed to investigate the lack of significant associations found in this study, especially studies of indoor air quality and health impacts in children and elderly populations.

Poor lung function and tonsillectomy in childhood are associated with mortality from age 18 to 44

The aim of this analysis was to examine associations between lung health in childhood and mortality between ages 18 and 44 years in the Tasmanian Longitudinal Health Study (TAHS). The 1961 Tasmanian birth cohort who attended school in 1968 (n=8583) were linked to the Australian National Death Index (NDI) to identify deaths. Additional deaths were notified by families through a 37 year follow-up postal questionnaire. Information on lung health at age 7 years and on potential confounders was obtained from the original 1968 TAHS survey and school medical records. Cox proportional hazards modelling was used to assess determinants of mortality. A total of 264 (3%) deaths were identified. The principal causes of death were external injury (56.1%, n=97) and cancer (17.9%, n=31). Males were more likely than females to have died (p=<0.1). Only two (1.1%) participants had died from respiratory conditions. Having an FEV(1)<80% predicted at 7 years of age was associated with a 2-fold increased incidence of death. Tonsillectomy before age 7 years was associated with a 1.5-fold increase in mortality (p=0.05); being male with a 3.6-fold increase in mortality (p=0.0001); and repeated chest illnesses at age 7 years causing >30 days confinement in the last year, was associated with a 2.2-fold increase in mortality (p=0.03). Childhood lung health appears to be associated with increased mortality in adulthood, perhaps by affecting the ability to survive trauma, major illnesses and other physical stresses.

Childhood immunization and atopic disease into middle-age - a prospective cohort study

The association between childhood immunizations and risk of atopic diseases is unclear. No study has examined possible associations between childhood immunizations and such diseases in middle age. The Tasmanian Longitudinal Health Study (TAHS) is a population based cohort study of respiratory disease. The TAHS participants were followed from 7 to 44 yrs of age. Immunizations during childhood were examined for any association with asthma and atopic disease at age 44 yrs. Multivariable regression models were used to estimate relative risks while adjusting for confounders. Cox regression was used to estimate the association between childhood immunizations and asthma developing after the age of 7 yrs. We found no association between any childhood immunization (Diphtheria, Tetanus, Pertussis, Polio, Smallpox) and asthma (ORs ranged from 0.87 to 1.17 p > 0.05), eczema (ORs ranged from 0.99 to 1.07 p > 0.05), food allergy (ORs ranged from 0.97 to 1.11 p > 0.05), or hay fever (ORs ranged from 1.02 to 1.05 p > 0.05) at age 44. Nor did we find any association between childhood immunizations and an increased risk of incident asthma after the age of 7 yrs (Diphtheria HR = 1.06, 95% CI 0.82, 1.36; Tetanus HR = 1.13, 95% CI 0.88, 1.44; Pertussis HR = 1.03, 95% CI 0.81, 1.30; Polio HR = 1.15, 95% CI 0.86, 1.54; Smallpox HR = 1.21, 95% CI 0.99, 1.48; DTP HR = 1.05, 95% CI 0.85, 1.30). Our analysis does not support any association between common childhood immunizations and risk of asthma and atopic disease in middle-age. Our findings should provide reassurance that in terms of life time risk of asthma and atopic disease, childhood immunization is safe.

Relevance of the Hygiene Hypothesis to Early vs. Late Onset Allergic Rhinitis

Matheson MC, Walters EH, Simpson JA, et al. Clin Exp Allergy. 2009;39(3):370–378PURPOSE OF THE STUDY. To compare the effects of siblings, infections, and rural environment on the development of allergic rhinitis before and after 7 years of age.STUDY POPULATION. The population-based cohort of participants in the Tasmanian Longitudinal Health Study (TAHS) was studied. Initial data were collected on 8583 children 7 years of age, comprising 99% of the schoolchildren in Tasmania born in 1961. The most recent follow-up evaluation occurred in 2004 and captured 5729 of the original participants at the age of 44 years, with the balance either lost to follow-up monitoring or deceased.METHODS. Subjects were categorized according to outcome, as those with early-onset allergic rhinitis (developed before the age of 7 years), those with late-onset allergic rhinitis (developed after the age of 7 years), and a reference group of those who did not report allergic rhinitis. The exposures considered were siblings, infections, tonsillectomy, and farm residence during childhood. Potential confounders considered were gender, maternal and paternal atopy, mother's age at participant's birth, paternal socioeconomic status in 1968, and personal socioeconomic status in 2004. Univariate associations were evaluated by using χ2 tests. Multinomial logistic regression was used to examine independent effects of different exposures on outcome with adjustment for confounders. The main analysis included 3429 subjects.RESULTS. Subjects with sibling exposure before the age of 2 had less early-onset allergic rhinitis than did those with no siblings (<1-year sibling exposure, odds ratio [OR]: 0.6 [95% confidence interval [CI]: 0.3–1.0]; 1- to 3-year sibling exposure, OR: 0.6 [95% CI: 0.4–0.9]; >3-year sibling exposure, OR: 0.4 [95% CI: 0.3–0.8]). This effect was dose dependent, with a P value of .0001 for trend. It was stronger than the effect of sibling exposure before 6 months or before 4 years. The trend for the effect of sibling exposure before the age of 2 was apparent (P = .001), although weaker, in late-onset allergic rhinitis. Early- but not later-onset allergic rhinitis decreased with viral infections during childhood (OR: 0.7 [95% CI: 0.5–0.9]). Tonsillectomy before the age of 7 increased the rate of early- but not later-onset allergic rhinitis (OR: 1.7 [95% CI: 1.2–2.5]).CONCLUSIONS. Exposures related to the hygiene hypothesis are more strongly related to early- than late-onset allergic rhinitis. The immunologic mechanisms for these risk factors are poorly understood. Additional research should focus on early-onset allergic rhinitis when exploring causal relationships for the effects demonstrated in this study.REVIEWERS COMMENTS. This large study is one of the few longitudinal studies to have examined the relationship between sibling exposure and allergic rhinitis; most other studies have been cross-sectional. The method of evaluation of sibling exposure quantifies both timing and dose and helps to pinpoint a potentially fruitful area for further research (before 2 years). One limitation is that the specific viral infections recorded for this study did not include viruses that primarily cause airway damage, such as respiratory syncytial virus and influenza. The mechanism for the effect of tonsillectomy is open to speculation. Possibilities include its significance as a marker of antibiotic use or, alternatively, a marker of severe, repeated, upper respiratory infection resulting in inflammation and, therefore, increased risk of sensitization via increased mucosal permeability.

Adherence to asthma management guidelines by middle-aged adults with current asthma

Background:With the increasing burden of asthma worldwide, much effort has been given to developing and updating management guidelines. Using data from the Tasmanian Longitudinal Health Study (TAHS), the adequacy of...

Relevance of the hygiene hypothesis to early vs. late onset allergic rhinitis

The hygiene hypothesis proposes that reduced exposure to infections in early life increases the risk of developing allergic conditions including allergic rhinitis. We examined the association between markers of the hygiene hypothesis and allergic rhinitis that developed before 7 years of age and allergic rhinitis that developed after 7 years of age. The Tasmanian Longitudinal Health Study (TAHS) is a population-based cohort (n=8583) study of respiratory disease. Participants have been followed from 7 to 44 years of age. Information on potential risk factors, allergies and respiratory symptoms was collected longitudinally. Using multi-nomial logistic regression, exposure to siblings, infections, tonsillectomy and farm residence during childhood were examined as risk factors for allergic rhinitis that developed before or after 7 years of age. All analyses were adjusted for gender, maternal and paternal atopy, mother's age at participant's birth, paternal socio-economic status in 1968 and personal socio-economic status in 2004. Greater cumulative exposure to siblings before the age of 2 years was strongly inversely associated with early onset allergic rhinitis (<1 year sib exposure: OR=0.6, 95% CI 0.3-1.0; 1-3 years sib exposure: OR=0.6, 95% CI 0.4-0.9; >3 years sib exposure: OR=0.4, 95% CI 0.3-0.8) less so with later onset allergic rhinitis. The risk of early onset allergic rhinitis decreased with increasing viral infections (OR=0.7, 95% CI 0.5-0.9) during childhood. Having a tonsillectomy before 7 years of age increased the risk of early onset allergic rhinitis (OR=1.7, 95% CI 1.2-2.5). None of these factors was associated with later onset allergic rhinitis. Exposures relevant to the hygiene hypothesis were important predictors for the development of early onset but less so for later onset allergic rhinitis. The exact mechanisms by which siblings and infections protect against allergic rhinitis are unclear. The stronger findings for earlier onset allergic rhinitis suggest that family structure and infections have most impact on disease risk in early life. Further research should focus on early onset allergic rhinitis when exploring causal explanations for any sibling effect.

Childhood eczema and asthma incidence and persistence: A cohort study from childhood to middle age

The association between eczema and asthma is well documented, but the temporal sequence of this association has not been closely examined. To examine the association between childhood eczema and asthma incidence from preadolescence to middle age, and between childhood eczema and asthma persisting to middle age. A further aim was to examine any effect modification by nonallergic childhood exposures on the association between childhood eczema and both childhood asthma and later life incident asthma. Data were gathered from the 1968, 1974, and 2004 surveys of the Tasmanian Longitudinal Health Study. Multivariable logistic regression examined the association between childhood eczema and childhood asthma. Cox regression examined the association between childhood eczema and asthma incidence in preadolescence, adolescence, and adult life. Binomial regression examined the association between childhood eczema and childhood asthma persisting to age 44 years. Childhood eczema was significantly associated with childhood asthma and with incident asthma in preadolescence (hazard ratio [HR], 1.70; 95% CI, 1.05-2.75), adolescence (HR, 2.14; 95% CI, 1.33-3.46), and adult life (HR, 1.63; 95% CI, 1.28-2.09). Although childhood eczema was significantly associated with asthma persisting from childhood to middle age (relative risk, 1.54; 95% CI, 1.17-2.04), this association was no longer evident when adjusted for allergic rhinitis. Childhood eczema increased the likelihood of childhood asthma, of new-onset asthma in later life and of asthma persisting into middle age.