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

Abstract

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 (FEV1). 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 PM2.5 and PM10 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 O3, SO2, and NO2 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.

Progress in Understanding Oxidative Stress, Aging, and Aging-Related Diseases

“…Research suggests that OS could be the main potential cause of respiratory system injuries due to air pollution. Numerous studies have investigated the relationships among atmospheric particulates (such as PM 2.5 and PM 10 ), gaseous pollutants (such as O 3 , SO 2 , NO 2 , and CO), and various OS biomarkers [18]. Li et al [19] found that the exposure time of PM 2.5 and SO 2 was positively correlated with the level of OS biomarkers.…”

“…Li et al [19] found that the exposure time of PM 2.5 and SO 2 was positively correlated with the level of OS biomarkers. Zeng et al [18] demonstrated that exposure to PM 10 is associated with elevated levels of inflammation biomarkers, such as interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-α, and 8-epi-pgf2α, which is closely related to OS.…”

Causal associations of particulate matter 2.5 and cardiovascular disease: A two-sample mendelian randomization study

“…Additionally, no research has yet looked at the combined impact of PM2.5 and genetic polymorphisms on the risk of CVD. Prior research indicates that genetic polymorphism should be taken into account when exploring the effects of pollutants on various physiological and immunological processes in humans, especially in cardiovascular diseases and respiratory diseases [11,12]. For instance, a panel study revealed that individuals with the glutathione Stransferase mu 1 genotype are more vulnerable to air pollution [12].…”