Impact of GSTM1 Genotype on Airway Response to Inhaled Wood Smoke Particles
Saturday, March 3, 2018
South Hall A2 (Convention Center)
Allison J. Burbank, MD, Michelle L. Hernandez, MD FAAAAI, Katherine H Mills, BA, Neil E Alexis, PhD, David B. Peden, MD MS FAAAAI
RATIONALE: Wood smoke particles (WSP) derived from wildland fires cause abrupt increases in ambient air particulate matter (PM2.5) and can have negative effects on pulmonary health even in healthy people. Glutathione-S-transferase Mu1 (GSTM1) null genotype increases susceptibility to ambient air ozone. The aim of this study is to determine if GSTM1 genotype determines susceptibility to WSP-induced airway inflammation.

METHODS: Healthy volunteers underwent exposure to 500 µg/m3 WSP for 2 hours with alternating 15-minute periods of exercise and rest to achieve minute ventilation of 20 L/min/m2. Induced sputum samples were obtained prior to and 6 hours after exposure for assessment of inflammatory cells and cytokines. Participants were genotyped for GSTM1 status.

RESULTS: Fifteen healthy volunteers provided qualifying sputum. Six participants were GSTM1 null. WSP exposure significantly increased mean sputum percent neutrophils (PMNs) [47% ± 18 (post) vs 31% ±18 (pre), n=15; p=.002] and PMNs/mg of sputum [370 ±152 (post) vs. 212 ±154 (pre), n=15; p=.003]. Sputum IL-8 concentration was significantly increased from baseline at 24 hours post-exposure [8714 pg/mL ± 9663 (post) vs. 3158 pg/mL ± 3151 (pre), n=14; p=.05]. No significant difference was seen in sputum neutrophils or IL-8 concentration between GSTM1 null and sufficient participant samples.

CONCLUSIONS: Exposure to 500 µg/m3 WSP increases airway neutrophilic inflammatory responses, and this effect appears to be independent of GSTM1 genotype. This is an ongoing study, and a larger sample size is needed to draw definitive conclusions about the role of GSTM1 genotype as a modifier of oxidative stress and resultant health effects associated with WSP.