Association of temporal distribution of fine particulate matter with glucose homeostasis during pregnancy in women of Chiayi City, Taiwan
Introduction
Air pollution is a heterogeneous, complex mixture of particulate matter and gaseous pollutants (Brook et al., 2004, Brook et al., 2010) and is a major environmental health risk (Beelen et al., 2014, Rückerl et al., 2011). Recent epidemiological studies have demonstrated that air pollution exposure is associated with impaired glucose homeostasis in susceptible populations (Chuang et al., 2011, Tamayo et al., 2014, Wei et al., 2016, Whitsel et al., 2009). Additionally, recent studies have demonstrated that exposure to air pollution during pregnancy or preconception was associated with impaired glucose homeostasis or gestational diabetes mellitus (GDM) (Fleisch et al., 2014, Hu et al., 2015, Malmqvist et al., 2013, Robledo et al., 2015). Three studies have reported positive associations between GDM and air pollutants including sulfur dioxide (SO2) (Robledo et al., 2015), nitrogen dioxides (NOx=NO2+NO) (Malmqvist et al., 2013, Robledo et al., 2015), ozone (O3), particulate matter <2.5 µm in aero dynamic diameter (PM2.5) (Hu et al., 2015), but a study showed a negative association with O3 and GDM during 3-month preconception (Robledo et al., 2015). For PM2.5, a recent study reported that exposure to PM2.5 and other traffic-related pollutants during pregnancy were associated with IGT but not GDM (Fleisch et al., 2014). Air pollution may contribute to impaired glucose homeostasis and GDM during pregnancy and preconception. However, data on the effect of PM2.5 on indicators of glucose homeostasis during pregnancy – namely, the glucose levels resulting from the oral glucose tolerance test (OGTT) – are lacking.
The 100-g OGTT has been used to detect and diagnose GDM. Glucose levels in response to the 100-g OGTT have been used to evaluate glucose homeostasis during pregnancy. The fasting, 1-h, 2-h and 3-h glucose levels after drinking 100-g glucose water during the OGTT represent different mechanisms of glucose homeostasis (Bartoli et al., 2011). The objective of this study was to investigate the effects of PM2.5 on fasting, 1-h, 2-h and 3-h glucose levels during the OGTT.
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Ethics statement
This study was approved by the Institutional Review Board of Ditmanson Medical Foundation Chia-Yi Christian Hospital (DMF-CYCH) (CYCH IRB No: 100006). Because of the study used a retrospective medical chart review, the committee agreed that the informed consent of each participant was not necessary.
Study participants
This retrospective study enrolled all pregnant women who underwent a two-step approach for GDM diagnosis and who gave birth at the Department of Obstetrics and Gynecology of DMF-CYCH, a tertiary
Results
Among the 3288 women enrolled in the study, 8.9% had repeated conceptions; therefore, 3589 pregnancies were enrolled in the study. The mean maternal age was 31.4 years, and 49.9% of the participants were nulliparous. BMI data at the time of OGTT administration was missing for 0.8%; the mean BMI at the time of the OGTT was 26.3 (±3.9) kg/m2, but pre-pregnancy BMI data were missing for 59.5% of the pregnancies (Table 1). Table 2 shows that PM2.5 had moving averages of 40.3–43.0 μg/m3 1 month to 12
Discussion
In this large sample of 3589 pregnant women who underwent universal screening for GDM according to policy in Taiwan, we were able to obtain the glucose levels of pregnant women and detect their associations with PM2.5 exposure. We found positive associations between PM2.5 and glucose levels in response to OGTT during pregnancy. The findings support previous reports that PM2.5 may contribute to impaired glucose homeostasis and the development of GDM (Fleisch et al., 2014, Hu et al., 2015). The
Conclusion
Long-term exposure to PM2.5 was associated with indicators of glucose homeostasis during pregnancy, especially pronounced for the fasting and 1-h glucose levels. PM2.5 exposure in the second trimester may enhance this effect. Our findings provided evidence linking PM2.5 exposure, glucose homeostasis and GDM.
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