Influence of temperature on the risk of gestational diabetes mellitus and hypertension in different pregnancy trimesters.

Previous studies have proved that exposure to extreme temperature in specific windows of pregnancy could cause some complications, such as pregnancy induced hypertension (PIH) and gestational diabetes mellitus (GDM), but differences in the effect of extreme temperature on the 2 complications are rarely studied. We carried a retrospective study on the impact of temperature on GDM/PIH in different trimesters based on data from a maternal and child health center in Beijing, China. Ambient temperatures (°C) were obtained from the China Meteorological Administration from January 1st, 2013 to May 15th, 2018. We use distributed lag non-linear models (DLNMs) combined with logistic regression to calculate the lag exposure-response relationships between the temperature and GDM/PIH from 1st to 24th/20th weeks of pregnancy. In both first and second trimesters, the risk of GDM was increased in summer with high temperatures; in second trimester, the risk of GDM increased in winter with low temperatures. In first half of pregnancy, risk of PIH was decreased in winter with low temperatures. These findings can provide the guideline for preventing the GDM and PIH induced by extreme temperature during pregnancy.

Air pollution exposure and the risk of macrosomia: Identifying specific susceptible months.

Birth weight is an important indicator of future growth and development for newborns. Few studies investigated the potential effects of air pollutants on macrosomia and their susceptible windows. We included 38,971 singleton full-term births from Beijing HaiDian Maternal and Child Health Hospital between 2014 and 2018, and assessed the associations of air pollutants exposure during preconception and pregnancy with macrosomia as well as the corresponding susceptible windows. The concentrations of air pollutants (PM2.5, PM10, SO2, NO2, CO and O3) for participants were calculated by the data from the nearest monitoring stations. Distributed lag models (DLM) incorporating logistic regression models were used to estimate the associations between air pollutants exposure during the 3 months before conception and pregnancy period and the risk of macrosomia, identifying susceptible windows of air pollutants. Weighted quantile sum (WQS) regression was applied to estimate the joint effect of air pollutants. A 10 µg/m3 increase in PM2.5 exposure from 3rd to 8th gestational month was positively associated with the risk of macrosomia, with the strongest effect in the 6th month (OR = 1.010, 95 % CI: 1.002-1.019). For a 10 µg/m3 increase in SO2, the windows of significant exposure were from the 1st preconception month to the 3rd gestational month, with the strongest effect in the 2nd month (OR = 1.030, 95 % CI: 1.010-1.049). We also observed the significant positive associations were in the 5th-8th gestational months for PM10, the 8th-9th gestational months for NO2 and the 3rd-7th gestational months for CO respectively. WQS regression also indicated a positive association between co-exposure to air pollutants and macrosomia. Our results suggest air pollution exposure is associated with increased risk of macrosomia. The windows of exposure for susceptibility to the risk of macrosomia vary between air pollutants. The susceptible exposure windows were middle and late pregnancy for PM, CO and NO2, while for SO2, early pregnancy is the window of vulnerability. Our findings provide the evidence that air pollution exposure is an independent risk factor for macrosomia and a basis for targeted environment policy.

Ozone exposure induced risk of gestational diabetes mellitus.

Numerous studies have shown that air pollution seems to be able to cause many diseases. Considering the possible mechanism of action and the same growth trend, the present study is designed to examine whether and how air pollutants, especially ozone (O3) exposure, are associated with the incidence of gestational diabetes mellitus (GDM). By a retrospective cohort, we analyzed the records of 45439 pregnant women from 2013 to 2018 and matched them to maternal exposure to O3. We found that the increased odds of GDM is associated with increased O3 concentrations from the 1st month before pregnancy to the 3rd month during pregnancy. Specially, the odds ratios (ORs) of these associations were largest in the 1st month before pregnancy, suggesting that the effect of O3 pollution on GDM occurred in pre-pregnancy period. Moreover, the exposure-response plot in the 1st month before pregnancy showed that the odds of GDM increased with the increasing concentration of O3. Our findings provide the evidence that O3 exposure in both pre-pregnancy and pregnancy period elevates the odds of GDM, suggesting that more intensive air pollution controls are needed to improve the health of pregnant women and their offspring.

Role of serum vitamin A and E in pregnancy.

Serum levels of vitamin A and E in early, middle and late pregnancy were analyzed to evaluate vitamin nutritional status in pregnancy, and provide guidance for pregnant women about vitamin supplements in pregnancy. In total, 28,023 serum samples were randomly selected from pregnant women in early, middle and late pregnancy between January 2013 and June 2014 in Beijing. High performance liquid chromatography (HPLC) method was used to determine the concentration of serum vitamin A and E in pregnancy. The concentration of serum vitamin A in early, middle and late pregnancy was 0.33±0.08, 0.37±0.09 and 0.33±0.15 mg/l, respectively, total abnormal rate was 25.31%, and deficiency (24.98%) was the main feature. The rate of deficiency in the early pregnancy (38.22%) was greater than that in late pregnancy (35.13%). The serum vitamin E in early, middle and late pregnancy was 9.10±2.47, 14.24±3.66 and 15.80±5.01 mg/l, respectively, total abnormal rate was 5.60%, and excess (5.37%) was the main feature. The excess rate in early pregnancy was at the lowest level (0.50%), and reached the highest level (15.32%) in late pregnancy. The serum levels of vitamin A and E are different during pregnancy. Generally, vitamin A is deficient and vitamin E is in excess. Therefore, monitoring the vitamin A and E levels, and strengthening perinatal education and providing guidance for pregnant women to supply vitamins rationally play important role in guaranteeing maternal and fetal safety.

Circulating IL-1beta levels, polymorphisms of IL-1B, and risk of cervical cancer in Chinese women.

PURPOSE: Long-term human papillomavirus (HPV) infection is a prerequisite for cervical cancer. IL-1beta and IL-1Ra expression levels play an important role in cervical carcinogenesis. Several functional genetic variants in IL1B and IL-RN have been reported to be associated with IL-1beta expression and cancer susceptibility. In the current study, we hypothesized that plasma IL-1beta levels, IL-1B and IL-RN polymorphisms were candidate biomarkers for cervical cancer. METHODS: We measured plasma IL-1beta levels and genotyped IL-1B and IL-RN polymorphisms in a case-control study of 404 cervical cancer cases and 404 controls in Chinese women. RESULTS: The mean plasma IL-1beta levels in cervical cancer cases (42.19 +/- 31.55 pg/ml) was significantly higher than those in controls (34.86 +/- 22.68 pg/ml, P = 0.0002), and plasma IL-1beta levels above the 75% quartiles in controls (IL-1beta > or = 46.94 pg/ml) were associated with a 1.74-fold significantly increased risk of cervical cancer [95% confidence interval (CI), 1.28-2.36], compared with those of lowest quartile. Multivariate logistic regression analyses revealed that the variant genotypes, IL-1B T-31C TC/CC and C-511T CT/TT, were associated with a significantly increased risk of cervical cancer [adjusted odds ratio (OR), 1.60; 95% CI, 1.16-2.21 for -31TC/CC, and adjusted OR, 1.52; 95% CI, 1.10-2.09 for -511CT/TT, respectively), especially among subjects having higher levels of IL-1beta. However, IL-RN VNTR polymorphism was not associated with cervical cancer risk in the current study. Furthermore, the significant differences of IL-1beta concentration between cervical cancer cases and controls were observed only among subjects carrying T-31C or C-511T variant genotypes. CONCLUSION: Functional IL-1B genotypes may modify plasma IL-1beta concentrations to contribute to the etiology of cervical cancer in Chinese women; however, further perspective studies are warranted to test the causal effects of IL-1beta concentration in cervical carcinogenesis.

Interactions of IL-12A and IL-12B polymorphisms on the risk of cervical cancer in Chinese women.

PURPOSE: Accumulative evidence suggests that interleukin-12 (IL-12) plays a central role in the Th1 responses and thus participates in the carcinogenesis of human papillomavirus-related cervical cancer. We hypothesized that potentially functional polymorphisms in IL12A and IL12B may individually and jointly contribute to cervical cancer risk. EXPERIMENTAL DESIGN: We genotyped IL12A rs568408 [3' untranslated region (UTR) G>A] and rs2243115 (5'UTR T>G) and IL12B rs3212227 (3'UTR A>C) in a hospital-based study of 404 cervical cancer cases and 404 cancer-free controls. RESULTS: The IL12A rs568408 GA/AA and IL12B rs3212227 AC/CC variant genotypes were associated with a significantly increased risk of cervical cancer [adjusted odds ratio, 1.43; 95% confidence interval (CI), 1.06-1.93; and adjusted odds ratio, 1.30; 95% CI, 0.97-1.75, respectively], compared with their corresponding wild-type homozygotes. Moreover, a significant gene-gene interaction of these 2 loci were evident in the risk of cervical cancer, and subjects carrying variant genotypes of both loci had a 1.82-fold (95% CI, 1.28-2.57) increased risk of cervical cancer. In the stratified analyses, the combined genetic effect was more pronounced in patients who had early-stage tumors or more parities. Subjects carrying rs568408 AG/AA and rs3212227 AC/CC genotypes and having >2 parities showed a 6.00-fold (95% CI, 2.86-12.56) elevated cervical cancer risk (P for multiplicative interaction = 0.046). CONCLUSION: These findings suggest that IL12A rs568408 and IL12B rs3212227 may individually and jointly contribute to the risk of cervical cancer and may modify cervical cancer risk associated with parity, but these data need further validation.