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Free Radic Biol Med. 2016 Jul;96:385-91. doi: 10.1016/j.freeradbiomed.2016.04.202. Epub 2016 May 3.

Effect of GST variants on lung function following diesel exhaust and allergen co-exposure in a controlled human crossover study.

Author information

1
Institute of Environmental Science, Shanxi University, Taiyuan, China; Department of Medicine, Division of Respiratory Medicine, Chan-Yeung Centre for Occupational and Environmental Respiratory Disease, Vancouver Coastal Health Research Institute, University of British Columbia, Vancouver, Canada.
2
Department of Medicine, Division of Respiratory Medicine, Chan-Yeung Centre for Occupational and Environmental Respiratory Disease, Vancouver Coastal Health Research Institute, University of British Columbia, Vancouver, Canada; Institute for Heart and Lung Health, University of British Columbia, Vancouver, Canada.
3
Center for Heart Lung Innovation, University of British Columbia, Vancouver, Canada.
4
Department of Medicine, Division of Respiratory Medicine, Chan-Yeung Centre for Occupational and Environmental Respiratory Disease, Vancouver Coastal Health Research Institute, University of British Columbia, Vancouver, Canada; Institute for Heart and Lung Health, University of British Columbia, Vancouver, Canada. Electronic address: carlsten@mail.ubc.ca.

Abstract

BACKGROUND:

Isolated exposure to diesel exhaust (DE) or allergen can cause decrements in lung function that are impacted by the presence of genetic variants in the glutathione-S-transferase (GST) family but the effect of GST interactions with DE-allergen co-exposure on lung function is unknown. We aimed to assess the impact of DE and allergen co-exposure on lung function and the influence of GSTM1 or GSTT1 variation

METHODS:

We used a blinded crossover study design with 17 atopic subjects exposed to filtered air (FA; the control for DE) or DE for 2h. One hour following each exposure to DE or FA, bronchoscopy was performed to deliver a diluent-controlled segmental allergen challenge (SAC). Methacholine challenge and forced expiratory volume in 1s (FEV1) was performed pre-exposure (baseline airway responsiveness) and 24h post-exposure (effect of co-exposure). Additionally, FEV1 was performed hourly after DE/FA exposure and protein carbonyl content was measured in plasma as an oxidative stress marker.

RESULTS:

Changes in FEV1 from baseline were dependent on time following allergen exposure. DE, as opposed to FA, led to a significant change in FEV1 at 2h post-allergen exposure in GSTT1 variants only (24.5±19.6% reduction in GSTT1 null individuals vs. 9.2±7.3% reduction in GSTT1 present individuals). Moreover, plasma protein carbonyl level 4h after co-exposure was higher in the individuals who have the GSTT1 null genotype.

CONCLUSIONS:

This suggests a gene-environment interaction that endangers susceptible populations co-exposed to DE and allergen.

KEYWORDS:

Air pollution; Airway hyperresponsiveness; Atopy; Diesel exhaust; GSTM1; GSTT1

[Indexed for MEDLINE]

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