Asthma and lower airway disease
Traffic-related air pollution exposure is associated with allergic sensitization, asthma, and poor lung function in middle age

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Background

Traffic-related air pollution (TRAP) exposure is associated with allergic airway diseases and reduced lung function in children, but evidence concerning adults, especially in low-pollution settings, is scarce and inconsistent.

Objectives

We sought to determine whether exposure to TRAP in middle age is associated with allergic sensitization, current asthma, and reduced lung function in adults, and whether these associations are modified by variants in Glutathione S-Transferase genes.

Methods

The study sample comprised the proband 2002 laboratory study of the Tasmanian Longitudinal Health Study. Mean annual residential nitrogen dioxide (NO2) exposure was estimated for current residential addresses using a validated land-use regression model. Associations between TRAP exposure and allergic sensitization, lung function, current wheeze, and asthma (n = 1405) were investigated using regression models.

Results

Increased mean annual NO2 exposure was associated with increased risk of atopy (adjusted odds ratio [aOR], 1.14; 95% CI, 1.02-1.28 per 1 interquartile range increase in NO2 [2.2 ppb]) and current wheeze (aOR, 1.14; 1.02-1.28). Similarly, living less than 200 m from a major road was associated with current wheeze (aOR, 1.38; 95% CI, 1.06-1.80) and atopy (aOR, 1.26; 95% CI, 0.99-1.62), and was also associated with having significantly lower prebronchodilator and postbronchodilator FEV1 and prebronchodilator forced expiratory flow at 25% to 75% of forced vital capacity. We found evidence of interactions between living less than 200 m from a major road and GSTT1 polymorphism for atopy, asthma, and atopic asthma. Overall, carriers of the GSTT1 null genotype had an increased risk of asthma and allergic outcomes if exposed to TRAP.

Conclusions

Even relatively low TRAP exposures confer an increased risk of adverse respiratory and allergic outcomes in genetically susceptible individuals.

Section snippets

Study population

The study sample consisted of participants in TAHS. The design of this study has been previously described.12 Subjects included in this analysis were adults who participated in the TAHS proband 2002 laboratory study. Briefly, TAHS started in 1968 by recruiting 8583 Tasmanian children aged 7 years. Participants of the baseline survey were known as “probands.” At the baseline survey, parents of the children completed a respiratory health questionnaire and probands underwent clinical examination

Results

The mean age of the cohort at participation was 44.8 ± 1 years and 49% were men (Table I). More than half (55.8%) of the cohort was sensitized to at least 1 of the aeroallergens tested. Sensitization to house dust mite (HDM) was the most prevalent type of allergic sensitization (41.3%), followed by perennial rye grass (32.0%) and mixed grasses (30.7%). The prevalence of current asthma and wheeze was 23.6% and 28.5%, respectively. Study characteristics of the participants without a geocoded

Discussion

Our study provides evidence that current TRAP exposure is associated with an increased risk of allergic sensitization, asthma, and wheeze, and some measures of lung function in adults. The majority of our findings are consistent for both the measures related to TRAP exposure we assessed: annual mean NO2 estimated by a satellite-based LUR model and living less than 200 m from a major road. The mean annual NO2 exposure in our study is very low compared with that in other TRAP exposure studies,

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    • Cited by (0)

    This study was supported by the Centre for Air Quality and Health Research and Evaluation (CAR), a National Health & Medical Research Council Centre of Research Excellence, Australia.

    Disclosure of potential conflict of interest: L. D. Knibbs has received research support from the National Health and Medical Research Council (NHMRC; grant no. APP1036620). A. J. Lowe has received research support from the NHMRC and other philanthropic organizations. G. B. Marks has received research support from the NHMRC of Australia, AstraZeneca, and GlaxoSmithKline and was on the Novartis Pharmaceutical COPD Advisory Board. M. J. Abramson has received research support from the NHMRC, Pfizer, and Boehringer Ingelheim; has received consultancy fees from AstraZeneca; and has received travel support from Boehringer Ingelheim and Sanofi. The rest of the authors declare that they have no relevant conflicts of interest.

    ∗

    These authors contributed equally as senior authors.

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