Air pollution associated acute respiratory inflammation and modification by GSTM1 and GSTT1 gene polymorphisms: a panel study of healthy undergraduates

• Published in: Environmental health Vol. 22; no. 1; pp. 14 - 12
• Main Authors: Zeng, Xiang, Tian, Ge, Zhu, Jingfang, Yang, Fuyun, Zhang, Rui, Li, Huijun, An, Zhen, Li, Juan, Song, Jie, Jiang, Jing, Liu, Dongling, Wu, Weidong
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 27.01.2023; BioMed Central; BMC
• Subjects: Adolescent; Air pollutants; Air Pollutants - adverse effects; Air pollution; Air Pollution - adverse effects; Asthma; Atmospheric models; Biomarkers; Chronic obstructive pulmonary disease; College students; Cytokines; Demographic aspects; Environmental health; Epidemiology; Exposure; Gene polymorphism; Genetic polymorphisms; Genotype; Genotypes; Glutathione; Glutathione S-Transferase; Glutathione transferase; Glutathione Transferase - genetics; GSTM1 protein; GSTT1 gene; GSTT1 protein; Health aspects; Humans; Inflammation; Inflammation - chemically induced; Interleukin 6; Interleukin 8; Interleukins; Longitudinal studies; Lung function; Lungs; Nitrogen dioxide; Outdoor air quality; Oxidative stress; Particulate matter; Particulates; Pollutants; Pollution control; Polymorphism; Polymorphism, Genetic; Prostaglandin F2a; Prostaglandins; Respiratory function; Respiratory tract diseases; Risk factors; Sulfur dioxide; Tumor necrosis factor-α; Young Adult; China; United States > US; Japan; Oxidative stress; Air pollution; Inflammation; Lung function; Air pollutants; Glutathione S-Transferase
• ISSN: 1476-069X; 1476-069X
• DOI: 10.1186/s12940-022-00954-9

Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution remain unclear. This study aimed to investigate the role of glutathione S-transferase (GST) polymorphism in the association between air pollution and lung function levels. A total of 75 healthy young volunteers aged 18–20 years old were recruited for six follow-up visits and examinations. Spirometry was conducted to obtain lung function parameters such as forced vital capacity (FVC), and forced expiratory volume in 1 s (FEV 1 ). Nasal fluid concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and 8-epi-prostaglandin F2α (8-epi-PGF2a) were measured using ELISA kits. Linear mixed-effect models were used to evaluate the association of air pollutants with respiratory outcomes. Additionally, polymorphisms of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) were estimated to explore its role in the association between air pollutants and lung function. We found that short-term exposure to atmospheric particulates such as PM 2.5 and PM 10 can cause an increase in nasal biomarkers of inflammation, oxidative stress, and lung function, while air gaseous pollutant exposure is linked with decreased lung function, except for CO. Stratification analyses showed that an increase in nasal inflammatory cytokines caused by exposure to atmospheric particulates is more obvious in subjects with GSTM1 -sufficient ( GSTM1 + ) than GSTM1 -null ( GSTM1 − ), while elevated lung function levels due to air particles are more significant in subjects with the genotype of GSTM1 − when compared to GSTM1 + . As for air gaseous pollutants, decreased lung function levels caused by O 3 , SO 2 , and NO 2 exposure is more manifest in subjects with the genotype of GSTM1 − compared to GSTM1 + . Taken together, short-term exposure to air pollutants is associated with alterations in nasal biomarkers and lung function levels in young healthy adults, and susceptible genotypes play an important mediation role in the association between exposure to air pollutants and inflammation, oxidative stress, and lung function levels.