Telomere length (TL) is an index of cellular aging and can predict the incidences of many age-related diseases. Change of TL might be affected by environmental pollution and individual's genetic background. In this cohort study, we aimed to evaluate the associations between polycyclic aromatic hydrocarbons (PAHs) exposure and longitudinal TL shortening, and investigate whether genetic variations in TERT-CLPTM1L can modify these associations. We measured the baseline concentrations of twelve urinary PAH metabolites and genotyped six variants at TERT-CLPTM1L among 1243 coke-oven workers. The relative leukocyte TL was detected in both baseline and follow-up (4 years later) visits. The TL shortening were estimated by TL decline and TL ratio. We found that the urinary level of 1-hydroxypyrene (1-OHP) had significant dose-response relationships with increased TL decline [β(95%CI) = 0.078(0.023, 0.133), P = 0.005] and TL ratio [β(95%CI) = 0.096(0.037, 0.155), P = 0.002]. Besides, urinary 1-hydroxynaphthalene (1-OHNa) was marginally dose-related with elevated TL decline [β(95%CI) = 0.053(-0.001, 0.107), P = 0.055] and TL ratio [β(95%CI) = 0.057(-0.002, 0.116), P = 0.058]. Analyses of TERT-CLPTM1L variants showed that the rs401681 and rs465498 could modify the effect of 1-OHP on increasing TL decline (Pᵢₙₜₑᵣₐcₜᵢₒₙ = 0.012 and 0.035, respectively) and TL ratio (Pᵢₙₜₑᵣₐcₜᵢₒₙ = 0.014 and 0.067, respectively), which were pronounced among rs401681TT and rs465498CC carriers, but not seen among rs401681TC + CC and rs465498CT + TT carriers. In conclusion, elevated exposure to PAHs can accelerate the TL shortening and this effect can be modified by TERT-CLPTM1L variants. These results may add potential evidence for gene-environment interactions on dynamic changes of telomere length. Further studies are warranted to validate these findings and uncover the underlying mechanisms.

Perfluoroalkyl substances (PFAS) are a diverse class of manufactured compounds used in a wide range of industrial processes and consumer products and have been detected in human serum worldwide. Previous cross-sectional and cohort studies in humans have suggested exposure to PFAS is associated with a wide array of chronic diseases, including endocrine disruption, developmental health effects, cancer and metabolic changes. We examined the associations between a panel of eight PFAS and indicators of thyroid disruption, kidney function, and body mass index (BMI), all of which were measured at repeated time points (1990–2008) over the course of the study. Participants (N = 210) were selected from the Fernald Community Cohort based on household water supply from a PFAS-contaminated aquifer. In adjusted repeated measures models, we observed several notable associations between serum PFAS and thyroid hormones as well as kidney function as measured by estimated glomerular filtration rate (eGFR). An interquartile (IQR) increase in serum PFOS was associated with a 9.75% (95% CI = 1.72, 18.4) increase in thyroid stimulating hormone. An IQR increase in serum PFNA, PFHxS, and PFDeA was associated with a −1.61% (95% CI = −3.53, −0.59), −2.06% (95% CI = −3.53, −0.59), and −2.20% (95% CI = −4.25, −0.14) change in eGFR, respectively. On the other hand, an IQR increase in serum Me-PFOSA was associated with a 1.53% (95% CI = 0.34, 2.73) increase in eGFR. No significant associations with BMI and serum PFAS were noted. Our findings are in agreement with previous reports that serum PFAS are associated with altered kidney and thyroid function.

Multiple cross-sectional studies indicated an association between hypertension and road traffic noise and they were recently synthetized in a WHO systematic evidence review. However, recent years have seen a growing body of high-quality, large-scale research, which is missing from the WHO review. Therefore, we aimed to close that gap by conducting an updated systematic review and meta-analysis on the exposure-response relationship between residential road traffic noise and the risk of hypertension in adults. Studies were identified by searching MEDLINE, EMBASE, the Internet, conference proceedings, reference lists, and expert archives in English, Russian, and Spanish through August 5, 2017. The risk of bias for each extracted estimate and the overall quality of evidence were evaluated using a list of predefined safeguards against bias related to different study characteristics and the Grading of Recommendations Assessment, Development and Evaluation system, respectively. The inverse variance heterogeneity (IVhet) model was used for meta-analysis. The possibility of publication bias was evaluated by funnel and Doi plots, and asymmetry in these was tested with Egger's test and the Luis Furuya-Kanamori index, respectively. Sensitivity analyses included leave-one-out meta-analysis, subgroup meta-analysis with meta-regressions, and non-linear exposure-response meta-analysis. Based on seven cohort and two case-control studies (n = 5 514 555; 14 estimates; Lden range ≈ 25–90 dB(A)), we found “low” evidence of RR per 10 dB(A) = 1.018 (95% CI: 0.984, 1.053), moderate heterogeneity (I2 = 46%), and no publication bias. In the subgroup of cohort studies, we found “moderate” evidence of RR per 10 dB(A) = 1.018 (95% CI: 0.987, 1.049), I2 = 31%, and no publication bias. In conclusion, residential road traffic noise was associated with higher risk of hypertension in adults, but the risk was lower than previously reported in the systematic review literature.

Maternal arsenic exposure leads to adverse birth outcomes, but the critical window of this susceptibility keeps unclear. To determine whether the associations between maternal arsenic exposure and birth outcomes were trimester-specific, we conducted a birth cohort study of 1390 women from 2014 to 2016 in Wuhan, China. We examined associations between total urinary arsenic concentrations in three trimesters and birth weight, birth length and the risk of small for gestational age (SGA), and the differences of these associations across trimesters using generalized estimating equations. Maternal urinary arsenic concentrations varied across trimesters and were weakly correlated. Arsenic concentrations in the 3rd trimester, but not in the 1st and 2nd trimesters, were associated with birth outcomes. For each doubling of arsenic levels in the 3rd trimester, birth weight was decreased 24.27 g (95% confidence interval (CI): −46.99, −1.55), birth length was decreased 0.13 cm (95% CI: −0.22, −0.04), and the risk for SGA birth was increased 25% (95% CI: 1.03, 1.49). Further, stratified analyses indicated that these associations were only observed in female infants. Our findings indicate maternal arsenic levels in the 3rd trimester seemed to have significant impacts on birth outcomes, and also emphasize the public health interventions relevance to arsenic exposure in late pregnancy.

Inflammation may play an important role in the association between exposure to polycyclic aromatic hydrocarbons (PAHs) and atherosclerotic cardiovascular disease (ASCVD) risk. However, the underlying mechanisms remain unclear.To investigate the association of PAHs exposure with ASCVD risk and effects of mean platelet volume (MPV) or Club cell secretory protein (CC16) on the association.A total of 2022 subjects (689 men and 1333 women) were drawn from the baseline Wuhan residents of the Wuhan-Zhuhai Cohort study. Data on demography and the physical examination were obtained from each participant. Urinary monohydroxy PAH metabolites (OH-PAHs) levels were measured by a gas chromatography-mass spectrometry. We estimated the association between each OH-PAHs and the 10-year ASCVD risk or coronary heart disease (CHD) risk using logistic regression models, and further analyze the mediating effect of MPV or plasma CC16 on the association by using structural equation modeling.The results of multiple logistic regression models showed that some OH-PAHs were positively associated with ASCVD risk but not CHD risk, including 2-hydroxyfluoren (β = 1.761; 95% CI: 1.194–2.597), 9-hydroxyfluoren (β = 1.470; 95% CI: 1.139–1.898), 1-hydroxyphenanthrene (β = 1.480; 95% CI: 1.008–2.175) and ΣOH-PAHs levels (β = 1.699; 95% CI: 1.151–2.507). The analysis of structural equation modeling shows that increased MPV and increased plasma CC16 levels contributed 13.6% and 15.1%, respectively, to the association between PAHs exposure and the 10-year ASCVD risk (p < 0.05).Exposure to PAHs may increase the risk of atherosclerosis, which was partially mediated by MPV or CC16.

Prenatal disinfection by-products (DBPs) exposure is linked with adverse birth outcomes. Genetic susceptibility to DBP metabolism may modify the exposure-outcome associations.To investigate whether CYP2E1 and GSTZ1 genetic polymorphisms modified the associations of prenatal DBP exposures with adverse birth outcomes.Two biomarkers of DBP exposures including trihalomethanes (THMs) in blood and trichloroacetic acid (TCAA) in urine were determined among 426 pregnant women from a Chinese cohort study. CYP2E1 (rs2031920, rs3813867, and rs915906) and GSTZ1 (rs7975) polymorphisms in cord blood were genotyped. Statistical interactions between prenatal DBP exposures and newborns CYP2E1 and GSTZ1 polymorphisms on birth outcomes (birth weight, birth length, and gestational age) were examined by multivariable linear regression with adjustment for potential confounders.We found that newborns CYP2E1 genetic polymorphisms (rs2031920 and rs3813867) modified the associations of maternal blood THMs or urinary TCAA levels with birth outcomes. However, these interactions were nonsignificant after Bonferroni correction for multiple comparisons, except for the interaction between maternal blood BrTHMs [sum of dibromochloromethane (DBCM), bromodichloromethane (BDCM), and bromoform (TBM)] and newborns CYP2E1 gene rs2031920 polymorphisms on birth weight (P for interaction = 0.003).Newborns genetic variations of CYP2E1 rs2031920 may modify the impacts of prenatal BrTHM exposure on birth weight. This finding needs to be further confirmed.

The effect of ambient air pollution exposure on childhood hypertension has emerged as a concern in China, and previous studies suggested pet ownership is associated with lower blood pressure (BP). However, limited information exists on the interactive effects pet ownership and air pollution exposure has on hypertension. We investigated the interactions between exposure to pet ownership and air pollutants on hypertension in Chinese children. 9354 students in twenty-four elementary and middle schools (aged 5–17 years) in Northeastern China were evaluated during 2012–2013. Four-year average concentrations of particulate matter with aerodynamic diameter of ≤10 μm (PM10), SO2, NO2, and O3, were collected in the 24 districts from 2009 to 2012. Hypertension was defined as average diastolic or systolic BP (three time measurements) in the 95th percentile or higher based on height, age, and sex. To examine effects, two-level regression analysis was used, controlling covariates. Consistent interactions between exposure to pet and air pollutants were observed. Compared to children exposed to pet, those not exposed exhibited consistently stronger effects of air pollution. The highest odds ratios (ORs) per 30.6 μg/m3 increase in PM10 were 1.79 (95%confidence interval [95%CI]: 1.29–2.50) in children without current pet exposure compared to 1.24 (95%CI: 0.85–1.82) in children with current pet exposure. As for BP, only O3 had an interaction for all exposure to pet ownership types, and showed lower BP in children exposed to pet. The increases in mean diastolic BP per 46.3 μg/m3 increase in O3 were 0.60 mmHg (95%CI: 0.21, 0.48) in children without pet exposure in utero compared with 0.34 mmHg (95%CI: 0.21, 0.48) in their counterparts. When stratified by age, pet exposure was more protective among younger children. In conclusion, in this large population-based cohort, pet ownership is associated with smaller associations between air pollution and hypertension in children, suggesting pet ownership reduces susceptibility to the health effects of pollutants.

Pregnant women and their fetuses represent susceptible populations to environmental contaminants. Exposure to polycyclic aromatic hydrocarbons (PAHs) among pregnant women may contribute to adverse birth outcomes such as preterm birth. Multiple previous studies have assessed airborne sources of PAHs among pregnant women but few have measured urinary PAH metabolites which can capture total exposure through multiple routes. The aim of this study was to bridge this knowledge gap by assessing longitudinal urinary PAH metabolite concentrations over two time points in pregnancy cohorts in Boston (N = 200) and Puerto Rico (N = 50) to better understand exposure distributions throughout pregnancy and how they relate to demographic factors. Urine samples were analyzed for 1-NAP, 2-NAP, 2-FLU, 1-PHE, 2,3-PHE, 4-PHE, 9-PHE, and 1-PYR. Concentrations of 2-NAP, 1-PYR, and 4-PHE were higher in Puerto Rico, while all other metabolites were present in higher concentrations in Boston. In Puerto Rico, intraclass correlation coefficients (ICC) were weak to moderate, ranging from 0.06 to 0.42. PAH metabolite concentrations were significantly higher among younger, heavier (except 1-NAP and 9-PHE), and less educated individuals in Boston only. Consistent significant associations between PAH concentrations and measured covariates were not found in Puerto Rico. Our results suggest that potentially important differences in PAH exposure exist between these two populations. Additionally, our results indicate that multiple urinary measurements are required to accurately assess PAH exposure throughout pregnancy.

A prospective cohort study of a Chinese population was conducted to investigate the relationship between prenatal phthalates exposure and maternal hemoglobin or anemia. Based on the Ma'anshan Birth Cohort study, 7 phthalate metabolites were quantified in spot pregnancy urine samples (n = 9263) from 3269 pregnant women during each trimester. The maternal hemoglobin concentrations were obtained from electronic medical records at the same three time points for each participant during pregnancy. Anemia was defined as a hemoglobin concentration below 110 g/L in pregnant women. Repeated measures and trimester-specific analyses were used to estimate the effects of phthalates exposure on maternal hemoglobin and anemia. The prevalence of anemia was 3.6%, 27.0%, and 26.5% during the first, second and third trimester, respectively. Repeated measures analysis showed that hemoglobin concentrations decreased by 0.55, 0.19, 0.57, 0.49, and 0.54 g/L with each 1 ln-transformed concentration increase of MBP, MBzP, MEHP, MEOHP, and MEHHP, respectively. Exposure to MMP, MBP, MEHP, MEOHP, and MEHHP increased the risk of anemia by 1.11-fold, 1.21-fold, 1.20-fold, 1.13-fold, and 1.16-fold, respectively. Trimester-specific regression models stratified by the sample collection time during pregnancy generated consistent results. This is the first study focusing on the effect of prenatal phthalate exposures on hemoglobin or anemia in pregnant Chinese women. We found that prenatal phthalates exposure not only decreased the concentrations of hemoglobin but also showed associations with the prevalence of anemia. Associations appeared stronger for the subsample representing women pregnant with a male fetus than those pregnant with a female fetus. Anemia remains a moderate public health problem in China, and effective measures should be implemented.

The impact of ambient air pollution on pregnant women is a concern in China. However, little is known about the association between air pollution and preeclampsia and the potential modifying effects of meteorological conditions have not been assessed. This study aimed to assess the effects of prenatal exposure to air pollution on preeclampsia, and to explore whether temperature and humidity modify the effects. We performed a retrospective cohort study based on 1.21 million singleton births from the birth registration system in Shenzhen, China, between 2005 and 2012. Daily average measurements of particulate matter <10 μm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), air temperature (T), and dew point (Td) were collected. Logistic regression models were performed to estimate associations between air pollution and preeclampsia during the first and second trimesters, and during the entire pregnancy. In each time window, we observed a positive gradient of increasing preeclampsia risk with increasing quartiles of PM10 and SO2 exposure. When stratified by T and Td in three categories (<5th, 5th −95th, and >95th percentile), we found a significant interaction between PM10 and Td on preeclampsia; the adverse effects of PM10 increased with Td. During the entire pregnancy, there was a null association between PM10 and preeclampsia under Td < 5th percentile. Preeclampsia risk increased by 23% (95% CI: 19–26%) when 5th < Td < 95th percentile, and by 34% (16–55%) when Td > 95th percentile. We also found that air pollution effects on preeclampsia in autumn/winter seasons were stronger than those in the spring/summer. This is the first study to address modifying effects of meteorological factors on the association between air pollution and preeclampsia. Findings indicate that prenatal exposure to PM10 and SO2 increase preeclampsia risk in Shenzhen, China, and the effects could be modified by humidity. Pregnant women should limit air pollution exposure, particularly during humid periods.