Few investigations have assessed the impact of short-term ambient temperature change on pneumonia risk. We aimed to study the relation of temperature variability (TV) with daily hospitalizations for pneumonia in China. We conducted a time-series study in 184 major cities by extracting daily hospital data between 2014 and 2017 from a medical insurance claims database of 0.28 billion beneficiaries. TV was calculated as standard deviation of daily minimum and maximum temperatures over exposure days. We estimated associations of pneumonia admissions with TV for each city using over-dispersed generalized linear models controlling for weather conditions and ambient air pollution, and pooled city-specific estimates using random effects meta-analyses. We also investigated exposure-response relationship curve and potential effect modifiers. We identified 4.2 million pneumonia hospitalizations during the study period. TV was positively related to daily pneumonia admissions. At the national-average level, each 1-°C increase in TV at 0-6 days' exposure corresponded to a 0.65 % (95 % CI: 0.34 %-0.96 %) increase in pneumonia admissions. An approximately linear exposure-response curve for the relation of TV with pneumonia admission was noted. The relations were more evident in cities with larger average age (P = 0.038). As the first study in China to assess the impact of temperature change on pneumonia on a national scale, our results indicated that acute TV exposure was related to higher admissions for pneumonia. Our findings should provide new insight into the health impacts associated with climate change.

ObjectiveTo investigate associations of interpregnancy weight change with preterm birth, low birth weight, macrosomia, small for gestational age (SGA), and large for gestational age (LGA). MethodsThe data on 6 589 pregnant women having two or more singleton live births during 2015 – 2020 and their newborns were extracted from the Maternal and Child Health Information System of Guangdong province. The pregnant women were assigned into four groups according to the changes in their interpregnancy body mass index (BMI) of ＜−1, −1 – ＜1 , 1 – ＜3, and ≥ 3 kg/m2. Logistic regression model was used to assess the associations of interpregnancy BMI change with adverse birth outcomes. ResultsIn all the newborns, the proportion was 5.5% for preterm birth, 4.7% for low birth weight, 2.4% for macrosomia, 11.4% for SGA, and 5.4% for LGA, respectively. The results of logistic regression analysis showed that compared to those with the interpregnancy BMI change of −1 – < 1, the pregnant women having the change of 1 – < 3 have an increased risk of giving a birth to a macrosomia (odds ratio [OR] = 1.66, 95% confidence interval [95% CI]: 1.13 – 2.24); the women with the interpregnancy BMI change of 3 and more have an increased risk of giving a birth to a macrosomia (OR = 2.31, 95% CI: 1.42 – 3.70) and to a LGA infant (OR = 1.87, 95% CI: 1.33 – 2.60); while, each increase of 1 kg/m2 in interpregnancy BMI is associated with a 7% decreased risk of SGA (OR = 0.93, 95% CI: 0.89 – 0.97). No significant association of interpregnancy BMI change with preterm birth or low birth weight was observed (P > 0.05). ConclusionPregnant women′s interpregnancy weight gain is associated with increased risks of macrosomia and LGA of their newborns. The results suggest that body weight control during pregnancy and after delivery need to be promoted among pregnant women.

Abstract Background Evidence linking air pollution to major depressive disorder (MDD) remains sparse and results are heterogeneous. In addition, the evidence about the interaction and joint associations of genetic risk and lifestyle with air pollution on incident MDD risk remains unclear. We aimed to examine the association of various air pollutants with the risk of incident MDD and assessed whether genetic susceptibility and lifestyle influence the associations. Methods This population-based prospective cohort study analyzed data collected between March 2006 and October 2010 from 354,897 participants aged 37 to 73 years from the UK Biobank. Annual average concentrations of PM2.5, PM10, NO2, and NOx were estimated using a Land Use Regression model. A lifestyle score was determined based on a combination of smoking, alcohol drinking, physical activity, television viewing time, sleep duration, and diet. A polygenic risk score (PRS) was defined using 17 MDD-associated genetic loci. Results During a median follow-up of 9.7 years (3,427,084 person-years), 14,710 incident MDD events were ascertained. PM2.5 (HR: 1.16, 95% CI: 1.07–1.26; per 5 μg/m3) and NOx (HR: 1.02, 95% CI: 1.01–1.05; per 20 μg/m3) were associated with increased risk of MDD. There was a significant interaction between the genetic susceptibility and air pollution for MDD (P-interaction < 0.05). Compared with participants with low genetic risk and low air pollution, those with high genetic risk and high PM2.5 exposure had the highest risk of incident MDD (PM2.5: HR: 1.34, 95% CI: 1.23–1.46). We also observed an interaction between PM2.5 exposure and unhealthy lifestyle (P-interaction < 0.05). Participants with the least healthy lifestyle and high air pollution exposures had the highest MDD risk when compared to those with the most healthy lifestyle and low air pollution (PM2.5: HR: 2.22, 95% CI: 1.92–2.58; PM10: HR: 2.09, 95% CI: 1.78–2.45; NO2: HR: 2.11, 95% CI: 1.82–2.46; NOx: HR: 2.28, 95% CI: 1.97–2.64). Conclusions Long-term exposure to air pollution is associated with MDD risk. Identifying individuals with high genetic risk and developing healthy lifestyle for reducing the harm of air pollution to public mental health.

Objective: The present study aims to investigate the association between PM2.5 exposure and major depressive disorder, and to examine whether vitamin D and physical activity could attenuate the impact of PM2.5 on major depressive disorder. Methods: 39168 elderly adults (age >= 60 years) who had valid estimates on exposure of PM2.5 in 2010 and data on major depressive disorder were extracted from the UK Biobank. Major depressive disorder was assessed by lifetime experience of mild, moderate, and severe major depression with validated instruments. Logistic regression models were used to estimate the association between PM2.5 exposure and major depressive disorder. Results: A total of 9079 participants had major depressive disorder, with a prevalence of 23.2%. The odds ratio (OR) of major depressive disorder was 1.096 (1.023, 1.175) for participants in the highest quartile compared with the lowest quartile of PM2.5. The correlation of PM2.5 with major depressive disorder generally increased with the decreasing levels of vitamin D. For instance, in participants with the highest quartile of PM2.5, the corresponding ORs were 1.141 (0.951, 1.369), 1.232 (1.027, 1.478), 1.286 (1.072, 1.543), and 1.390 (1.159, 1.667) for those who had adequate, desirable, insufficient, and deficient levels of vitamin D, respectively. Additionally, significant modification effects of physical activity on the relationship between PM2.5 and major depressive disorder were also observed. Conclusions: Our study suggests that high levels of vitamin D and physical activity may attenuate the relationship between PM2.5 and major depressive disorder among elderly adults.

Background: Evidences on the association between exposure to air pollution and liver enzymes was scarce in low pollution area. We aimed to investigate the association between air pollution and liver enzyme levels and further explore whether alcohol intake influence this association.Methods: This population-based cross-sectional study included 425,773 participants aged 37 to 73 years from the UK Biobank. Land Use Regression was applied to assess individual exposures to ambient air pollutants. Levels of liver enzymes including AST, ALT, GGT and ALP were determined using the enzyme rate method. Multiple linear regression models were performed to explore the associations between air pollutants and liver enzymes.Results: Long-term low-level exposure to PM2.5 (per 5-μg/m3 increase) was significantly associated with AST (0.59% increase, 95% CI, 0.41 to 0.77%), ALT (0.31% increase, 0.03 to 0.59%), and GGT (1.55% increase, 1.18 to 1.93%); PM10 (per 10-μg/m3 increase) with AST (0.45% increase, 0.25 to 0.65%), ALT (0.52% increase, 0.21 to 0.83%), and GGT (0.69% increase, 0.28 to 1.11%) levels; NOX (per 20-μg/m3 increase) with AST (0.17% increase, 0.13 to 0.22%) and GGT (0.37% increase, 0.27 to 0.47%) levels; and NO2 (per 10-μg/m3 increase) with AST (0.22% increase, 0.17 to 0.27%) and GGT (0.30% increase, 0.19 to 0.41%) levels. Significant modification effects by alcohol consumption were found (p-interaction<0.05). The effects of pollutants on AST, ALT and GGT levels gradually increased along with the weekly alcohol drinking frequency.Conclusions: Long-term low-level air pollutants exposure was associated with elevated liver enzyme levels. In addition, alcohol intake may exacerbate the effect of air pollution on liver enzymes.

Objectives: Evidence on the association between long-term exposure to ambient air pollution and serum gly-cosylated hemoglobin A1c (HbA1c) is limited and inconclusive. In addition, whether vitamin D can modify the association between air pollution exposure and glucose metabolism has not been previously investigated. We aimed to evaluate the effects of various air pollutants on serum HbA1c levels in patients with hyperten-sion and, further, to explore the modification effect of individual serum vitamin D levels.Methods: This study was derived from UK Biobank study, and 246 027 participants with hypertension were included in our analysis. Individual exposures to particulate matters (PMs) and nitrogen oxides were esti-mated using the land use regression model. The associations between air pollutants and HbA1c were assessed using the multivariable linear regression model. Among the 222 845 participants with a measurement of serum vitamin D, we explored the associations in subgroups stratified by vitamin D levels.Results: Long-term air pollutant exposures were significantly associated with higher HbA1c levels. After adjusting for potential confounders, 10-mu g/m3 (or 1-m-1) increases in concentrations of PM with diameters <2.5 mu m (PM2.5), PM with diameters <10 mu m, PM with diameters from 2.5 mu m to 10 mu m, PM2.5 absorbance, nitrogen oxides, and nitrogen dioxide were significantly associated with 0.59 (95% confidence interval, 0.28-0.89), 0.49 (0.33-0.65), 0.81 (0.48-1.14), 0.56 (0.44-0.69), 0.06 (0.04-0.09), and 0.16 (0.12-0.21) mmol/mol increase in serum HbA1c levels, respectively. The associations were weakened but remained sig-nificant after additional adjustment of vitamin D. In addition, the associations of air pollutants with HbA1c were more evident in participants with low serum vitamin D levels (all P values for interaction <0.001).Conclusions: Long-term exposures to ambient air pollutants were associated with higher levels of HbA1c in a dos-e-response fashion in a large UK cohort. Serum vitamin D status significantly modified these associations, and high serum vitamin D levels may attenuate the relationships between air pollution exposures and HbA1c levels. (c) 2022 Elsevier Inc. All rights reserved.

Background and aims: The longitudinal trajectories of body mass index (BMI) can reflect the pattern of BMI changes. Lifetime risk quantifies the cumulative risk of developing a disease over the remaining life of a person. We aimed to identify the trajectory of BMI and explore its association with cardiovascular disease (CVD) in the Chinese population.Methods and results: A total of 68,603 participants with a mean age of 55.46 years were included from the Kailuan cohort in Tangshan, China, who were free of CVD and cancer and with repeated measurements of BMI from 2006 to 2010. A latent mixture model was used to identify BMI tra-jectories. An improved Kaplan-Meier estimator was used to predict the lifetime risk of CVD ac-cording to BMI trajectories. During a median follow-up of 7.0 years, 3325 participants developed CVD. Five BMI trajectories were identified at three index ages (35, 45, and 55) respectively. For index age 35 years, compared with the stable low-normal weight group (22.7% [95% CI, 20.0%-25.4%]), the stable high-normal weight (27.6% [25.6%-29.5%]), stable overweight (29.4% [27.4%-31.4%]), stable-low obesity (32.8% [30.0%-35.5%]), and stable-high obesity (38.9% [33.3%-44.5%]) groups had a higher lifetime risk of CVD (P < 0.05). We observed similar patterns for stroke and myocardial infarction. Similarly, the lifetime risk of CVD was higher in the long-term overweight and obese groups at 45 and 55 index ages.Conclusions: Long-term overweight and obesity were associated with an increased lifetime risk of CVD. Our findings could assist in predicting the population burden of CVD.(c) 2022 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Ital-ian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.

ObjectiveTo identify common length, weight and body mass index (BMI) growth trajectories of term infants during infancy, and to determine their association with early-term infants.DesignProspective longitudinal study.SettingWuhan, China.PatientsA total of 4308 term infants (born at 37–41 weeks of gestation) were included. All term infants were single live birth with no defects and birth weight ≥2500 g, and their mothers were permanent residents of Wuhan for more than 2 years. After excluding 887 infants, a total of 3421 term infants (1028 early-term infants born at 37–38 weeks of gestation and 2393 full-term infants born at 39–41 weeks of gestation) entered the statistical analysis stage.Main outcome measuresPatterns of length, weight and BMI growth trajectories by using group-based trajectory modelling.ResultsThree distinct physical growth trajectories were identified as follows: length: low stable (1056, 30.9%), moderate stable (1887, 55.2%) and high increasing (477, 13.9%); weight: low stable (1031, 30.1%), moderate stable (1884, 55.1%) and high increasing (505, 14.8%); BMI: low stable (689, 20.1%), moderate stable (2167, 63.4%) and high increasing (564, 16.5%). Compared with the full-term infants, early-term infants were more likely to remain at low-stable trajectory in length (OR: 1.40; 95% CI: 1.19 to 1.66) and weight (OR:1.29; 95% CI: 1.09 to 1.53). These associations were still statistically significant after adjusting potential confounders and were more evident among girls in the stratified analysis. There was no statistical association between BMI trajectory patterns and gestational age categories.ConclusionOur results suggested the heterogeneity of term infants existed in length, weight and BMI growth trajectories of early childhood. Compared with full-term birth, early-term birth was related to low length and weight trajectories rather than BMI trajectory. Further research is needed to evaluate the duration of these low trajectories and their possible long-term health effects.

Telomere length (TL) is considered a marker of biological aging and lifetime health, and some epidemiological studies report that the environmental exposures may influence TL at birth. We aimed to investigate the associations between prenatal rare earth elements (REE) exposure and newborn TL. A total of 587 mother-newborn pairs were recruited during 2013 to 2015 in Wuhan, China. Maternal urinary concentrations of REE collected during three trimesters were measured by inductively coupled plasma mass spectrometry. Quantitative real-time polymerase chain reaction was used to measure relative cord blood TL. The trimester-specific associations between prenatal REE exposure and cord blood TL were evaluated using multiple informant models. Weighted quantile sum regression was used to estimate the mixture effect of urinary REE on cord blood TL. After adjustment for potential confounders, per doubling of urinary REE (Dy, Yb, Pr, Nd, and Tm) concentrations (μg/g creatinine) during the second trimester was respectively associated with 1.94% (95% CI 0.19%, 3.72%), 2.10% (95% CI 0.31%, 3.92%), 2.11% (95% CI 0.35%, 3.89%), 2.08% (95% CI 0.01%, 4.20%), and 1.38% (95% CI 0.09%, 2.70%) increase in cord blood TL. Furthermore, exposure to the mixture of REE during the second trimester was also significantly associated with increased cord blood TL (percent change 1.20%, 95% CI 0.30%, 2.11%). However, these associations were not statistically significant in the first and third trimesters. This study provides new evidence on the potential effect of prenatal REE exposure on the initial (newborn) setting of offspring’s telomere biology. Further epidemiological studies are warranted to confirm our findings.

BACKGROUND:The effect of long-term exposure to air pollution on the development of chronic obstructive pulmonary disease (COPD) is still controversial, and the role of the interactions of air pollution with genetic risk and lifestyle in COPD risk is unclear.METHODS:We included 452762 participants derived from the UK Biobank. Annual concentrations of air pollutions, including particle matter (PM2.5, PM10), nitrogen oxides (NOx), and nitrogen dioxide (NO2), were assessed using land-use regression model. We applied Cox proportional hazard model to evaluate the associations between air pollution and COPD risk. In addition, we constructed a polygenic risk score and a lifestyle score, and assessed whether genetic susceptibility and lifestyle modified the effect of air pollution on the COPD risk.FINDINGS:Each interquartile range (IQR) increase in annual concentrations of PM2.5, PM10, NOx, and NO2 was associated with 1.17 (95% CI: 1.15,1.19), 1.05 (95% CI: 1.03,1.06), 1.13 (95% CI: 1.11,1.14), and 1.19 (95% CI: 1.16,1.21) times the risk of COPD, respectively. We observed an additive interaction between PM2.5 and genetic risk (P-interact=0.095), and a negative interaction between PM2.5 and lifestyle (P-interact=0.062). The HRs for each IQR increase in PM2.5 were 1.21, (95% CI: 1.16-1.25) and 1.24, (95% CI: 1.21-1.26) in individuals with healthy and unfavourable lifestyle, respectively; and 1.16, (95% CI: 1.13-1.19) and 1.19, (95% CI: 1.16-1.22) in those with low genetic risk and high genetic risk, respectively. Participants with high air pollution exposure, high genetic risk and unfavourable lifestyle showed the highest risk of COPD.INTERPRETATION:Long-term exposure to air pollution was associated with increased risk of COPD, especially in those with high genetic risk and unfavourable lifestyle.FUNDING:None.

Background: Evidence about associations of pollutants with sleep is limited, and most of studies focused on individual sleep behaviors, neglecting their interrelation. We aimed to assess the relationship between ambient air pollution and road traffic noise with overall sleep health. Methods: The study included 378,223 participants from the UK Biobank. Including five sleep behaviors (chronotype, sleep duration, insomnia, snoring, and daytime sleepiness) to construct overall sleep pattern. Ambient air pollution exposure was estimated using Land Use Regression model. Road traffic noise exposure was estimated using a simplified version of the Common Noise Assessment Methods model. Using multinomial and binary logistic regression models to identify the associations between pollutants with overall and individual sleep behaviors, respectively. Results: Participants were derived in three sleep patterns: healthy (n = 140,490), intermediate (n = 220,627), and poor (n = 17,106). After adjustment for potential confounders, compared with the lowest quartile of PM2.5, the highest quartile had higher odds of intermediate and poor compared to healthy sleep pattern [OR (95% CI) for poor: 1.28 (1.21-1.36); for intermediate: 1.11 (1.09-1.14)]. We observed similar relationships for PM10, PM2.5 absorbance, PMcoarse, NOx, and NO2. In unadjusted model, compared with low exposure of Lnight, high Lnight exposure had higher odds of intermediate and poor compared to healthy sleep pattern [OR (95% CI) for poor: 1.13 (1.06-1.20); for intermediate: 1.03 (1.00-1.06)]. However, such associations disappeared after further adjustment for potential confounders. Conclusions: Long-term ambient air pollution is associated with overall sleep health. Road traffic noise itself is weakly associated with overall sleep health.

Background and aims: The relationship between dynamic changes in metabolic syndrome (MetS) status and lifetime risk of cardiovascular disease (CVD) has not been reliably quantified. This study aimed to estimate lifetime risk of CVD and life expectancy with and without CVD according to dynamic MetS status. Methods and Results: Dynamic changes in MetS status were assessed: MetS-free, MetS-chronic, MetS-developed, and MetS-recovery groups. We used Modified Kaplan-Meier method to estimate lifetime risk and used multistate life table method to calculate life expectancy. Participants free of CVD at index ages 35 (n = 40 168), 45 (n = 33 569), and 55 (n = 18 546) years. At index age 35 years, we recorded 1341 CVD events during a median follow-up of 6.1 years. Lifetime risk of 33.9% (95% CI: 26.9%-41.0%) in MetS-recovery group was lower than that of 39.4% (95% CI: 36.1%-42.8%) in MetS-chronic group. Lifetime risk of 37.8% (95% CI: 30.6%-45.1%) in MetSdeveloped group was higher than that of 26.4% (95% CI: 22.7%-30.0%) in MetS-free group. At index age 35 years, life expectancy free of CVD for MetS-recovery group (44.1 years) was higher than that for MetS-chronic group (38.8 years). Life expectancy free of CVD for MetS-developed group (41.9 years) was lower than that for MetS-free group (46.7 years). Conclusions: Recovery from MetS was associated with decreased lifetime risk of CVD and a longer life expectancy free of CVD, whereas development of MetS was associated with increased lifetime risk of CVD and a shorter life expectancy free of CVD. (c) 2021 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.

Aims: -Evidence for the effects of metabolically healthy obese (MHO) status on heart failure (HF) is limited and ignores the dynamic change of metabolic health and obesity phenotypes. We aimed to investigate the associations of metabolic health and its transition with HF across body mass index (BMI) and waist circumference (WC) categories. Methods: -This prospective cohort study was conducted with 93,288 Chinese adults who were free of cardiovascular disease, cancer or HF at baseline (2006-2007). Metabolic health was defined as having no or only one abnormality in blood pressure, glucose, high-density lipoprotein cholesterol, or triglyceride levels. Participants were cross-classified at baseline by metabolic health and obesity (defined by BMI and WC criteria). Transitions in metabolic health status from 2006 to 2007 to 2010 to 2011 were considered. The hazard ratios (HRs) and 95% confidence intervals (CIs) for HF were assessed by Cox proportional hazards regression. Results: -During a mean +/- standard deviation follow-up of 9.7 +/- 1.5 years, 1,628 participants developed HF. Individuals with MHO (HR: 1.78, 95% CI: 1.45, 2.19 for BMI criteria; HR: 1.51, 95% CI: 1.30, 1.76 for WC criteria) had higher risk of HF than those with metabolically healthy normal weight (MH == NW). Individuals with initial MHO who shifted to metabolically unhealthy phenotype during follow-up had higher risk of HF compared with stable MH == NW individuals (HR 3.12; 95% CI: 2.01, 4.85 for BMI categories; HR 1.98; 95% CI: 1.42, 2.77 for WC categories). Even stable MHO individuals were at an increased risk of HF compared with stable MH == NW individuals (HR: 2.17; 95% CI: 1.39, 3.39 for BMI categories; HR: 1.33; 95% CI: 0.96, 1.85 for WC categories). Conclusions: -MHO phenotype is dynamic and its transition to metabolically unhealthy phenotype or even stable MHO is associated with increased risk of HF. Maintaining metabolic health may provide a clue for preventing HF. (c) 2021 Elsevier Masson SAS. All rights reserved.

Background Few studies have used multiple measurements of fasting plasma glucose (FPG) to examine the impact of long-term FPG trajectory patterns on lifetime risk of cardiovascular disease (CVD). We aimed to identify the long-term patterns in FPG trajectories and to estimate the lifetime risk of CVD according to FPG trajectories. Methods Individuals free of CVD at index ages 35 ( n = 72,324), 45 ( n = 62,049), and 55 ( n = 38,113) years were included. FPG concentrations were measured in 2006, 2008, and 2010. The FPG trajectories were identified by latent mixture modeling. The modified Kaplan-Meier method was used to calculate lifetime risk of CVD. Results We identified five distinct FPG trajectories and named them according to FPG range and changing pattern over time: low-stable, moderate-stable, moderate-increasing, elevated-decreasing, and elevated-stable. At index age 35 years, we documented 3110 CVD events in men during 371,219 person-years of follow-up and 357 CVD events in women during 107,447 person-years of follow-up. Among all participants, the elevated-stable FPG pattern experienced the highest lifetime risk of CVD (44.8%, 95% CI: 37.8–51.9%), low-stable pattern was lowest (24.3%, 95% CI: 23.3–25.2%). At index age 55 years, although the elevated-stable and elevated-decreasing FPG patterns had similar original FPG concentrations, individuals with elevated-decreasing pattern (30.0%, 95% CI: 23.9–36.1%) had approximately one-third less lifetime risk of CVD than those with elevated-stable pattern (43.6%, 95% CI: 31.8–55.3%). Conclusions FPG trajectories were significantly associated with the lifetime risk of CVD. Both decrease in FPG over time and consistently lower FPG over 4 years were associated with lower lifetime risk of CVD.

目的 探讨妊娠间隔与小于胎龄儿、大于胎龄儿的关系,为再生育妇女提供孕前咨询及公共卫生政策制定提供依据.方法 选取2015-2020年广东省妇幼保健院有连续2次分娩史的7 752名产妇及胎儿数据,根据妊娠间隔将研究对象分为5组(＜6、6～11、12～17、18～23、≥24个月),采用logistic回归模型对妊娠间隔与小于胎龄儿、大于胎龄儿的关系进行分析.结果 研究对象中小于胎龄儿发生率为12.40％,大于胎龄儿发生率为4.72％.控制可能的混杂因素后,logistic回归分析结果显示,与妊娠间隔12～17个月相比,妊娠间隔＜6个月者,小于胎龄儿的危险性增加(OR=1.42,95％CI=1.14～1.79),妊娠间隔6～11个月发生小于胎龄儿的风险增加(OR=1.36,95％CI=1.13～1.64).妊娠间隔与大于胎龄儿的关联无统计学意义.结论 妊娠间隔＜12个月是小于胎龄儿的独立危险因素,应在产前咨询和健康教育等方面普及适宜的妊娠间隔重要性,以减少短妊娠间隔妊娠;对短时间间隔内再次怀孕的妇女,应该加强监测,减少小于胎龄儿的发生.

BACKGROUND AND AIMS:Elevated lipid levels during pregnancy have been shown to be related to the risk of preterm birth. Despite the importance of apolipoprotein (Apo) in lipid metabolism and transportation, evidence regarding apolipoprotein levels during pregnancy and preterm birth is still limited. Therefore, we aim to investigate the associations between maternal ApoA-1, ApoB, ApoB/ApoA-1 ratio and preterm birth. MATERIALS AND METH:Data were extracted from the information system of Guangdong Women and Children Hospital. Lipoprotein levels were tested using Beckman Coulter AU5800 in mid-pregnancy at a median gestational age of 18 w. Maternal serum ApoB, ApoA-1 and ApoB/ApoA-1 ratio were categorized into tertiles. Logistic regression models were performed to evaluate the odds ratios and 95% confidence intervals for preterm birth. RESULTS:A total of 5,986 maternal-newborn pairs were included in this study. The rate of preterm birth was 5.7% (n = 344). The multivariate-adjusted ORs (95% CI) of preterm birth were 1.51 (1.06, 2.10) for individuals with high ApoB (>90th), 0.63 (0.38, 0.99) for those with low ApoB (<10th), and 1.64 (1.18, 2.24) for those with high ApoB/ApoA-1 (>90th). Subgroup analyses showed that the association of ApoB and preterm birth was only significant among women with pre-pregnancy BMI 18.5-24 kg/m2 (OR = 1.36, 95% CI: 1.12-1.65), age at delivery ≥ 35 years (OR = 1.43, 95% CI: 1.12-1.83). CONCLUSION:Elevated maternal ApoB level and ApoB/ApoA-1 ratio during mid-pregnancy were related to increased risk of preterm birth. Monitoring maternal serum apolipoprotein levels may help to identify the high-risk population of preterm birth.

Recent studies suggest that environmental exposures, including air pollution, may influence initial (newborn) telomere length (TL), which has important implications for lifetime health. However, the effect of prenatal ozone exposure on newborn TL is unclear. This study aimed to examine the association of ozone exposure during pregnancy with newborn TL. We used data from a birth cohort study of 762 mother-newborn pairs performed in Wuhan, China, during 2013–2015. Land-use regression models were used to assess prenatal ozone exposure. Newborn TL was quantified in cord blood by qPCR assay. We applied multiple informant model to explore the relationship of prenatal ozone exposure with newborn TL. After adjustment for potential confounders, an interquartile range (IQR) increase in ozone exposure during the 2nd trimester, 3rd trimester, and whole pregnancy were associated with 6.00% (95% confidence interval [CI]: 1.59%, 10.62%), 12.64% (95% CI: 7.52%, 18.00%), and 7.10% (95% CI: 4.09%, 10.20%) longer cord blood TL, respectively. In contrast, an IQR increase in ozone exposure during the 1st trimester was associated with a 8.39% (95% CI: − 12.90%, − 3.65%) shorter cord blood TL. In multipollutant models, consistent associations were observed between ozone exposures during the 2nd trimester and whole pregnancy and cord blood TL, but not significant for the 1st and 3rd trimesters. In conclusion, our findings suggest positive associations of ozone exposure during the 2nd trimester, 3rd trimester, and whole pregnancy with newborn TL and a negative association during the 1st trimester. This study provides new evidence in humans for a potential “programming” mechanism linking maternal ozone exposure to the initial (newborn) setting of offspring’s telomere biology.

Background and aims: Cardiometabolic multimorbidity has become increasingly com-mon over the past few decades. Little is known about how risk factors affect temporal progres-sion of cardiometabolic multimorbidity. We aim to explore the role of socioeconomic, lifestyle, and clinical risk factors in the progression of cardiometabolic multimorbidity.Methods and results: This prospective cohort study included 56,587 participants aged >= 45 years who were free of diabetes, stroke, and heart disease. Three clusters of risk factors were assessed and each on a 5-point scale: socioeconomic, lifestyle, and clinical factors. We used multi-state models (MSMs) to examine the roles of risk factors in five transitions of multimorbidity trajec-tory: from healthy to first cardiometabolic disease, first cardiometabolic disease to cardiometa-bolic multimorbidity, health to mortality, first cardiometabolic disease to mortality, and cardiometabolic multimorbidity to mortality. In MSMs, socioeconomic (HR: 1.21; 95% CI: 1.19-1.25) and clinical (HR: 1.53; 95% CI: 1.51-1.56) scales were associated with the transition from health to first cardiometabolic. Socioeconomic (HR: 2.39; 95% CI: 2.24-2.54) and lifestyle (HR: 1.22; 95% CI: 1.18-1.26) scales were associated with the transitions from first disease to cardio-metabolic multimorbidity. In addition, socioeconomic and lifestyle scales were associated with increased risk of mortality in people without cardiometabolic disease, with first cardiometabolic disease, and with cardiometabolic multimorbidity. Conclusions: Socioeconomic and lifestyle factors were not only important predictors of multimor-bidity in those with existing cardiometabolic disease, but also important in shaping risk of mor-tality. However, clinical factors were the only key determinants of incidence of a first cardiometabolic disease.(c) 2022 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Ital-ian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.

OBJECTIVE:Telomere length (TL) is a biomarker for biological aging, and the initial setting of TL at birth is a determinant factor of TL in later life. Newborn TL is sensitive to maternal metals concentrations, while study about the association between maternal manganese (Mn) concentrations and newborn TL was not found. Our study aimed to investigate whether newborn TL is related to maternal Mn concentrations. METHODS:Data were collected from a birth cohort study of 762 mother-newborn pairs conducted from November 2013 to March 2015 in Wuhan, China. We measured the Mn concentrations in spot urine samples collected during three trimesters by inductively coupled plasma mass spectrometry (ICP-MS) and relative cord blood TL by quantitative real-time polymerase chain reaction (qPCR). We applied multiple informant models to investigate the associations between maternal Mn concentrations and cord blood TL. RESULTS:The geometric mean of creatinine-corrected urinary Mn concentrations were 1.58 μg/g creatinine, 2.53 μg/g creatinine, and 2.62 μg/g creatinine in the first, second, and third trimester, respectively. After adjusting for potential confounders, a doubling of maternal urinary Mn concentration during the second trimester was related to a 2.10% (95% CI: 0.25%, 3.99%) increase in cord blood TL. Mothers with the highest tertile of urinary Mn concentrations during the second trimester had a 9.67% (95% CI: 2.13%, 17.78%) longer cord blood TL than those with the lowest tertile. This association was more evident in male infants. No relationship was found between maternal urinary Mn concentrations and cord blood TL during the first and third trimesters in our study. CONCLUSIONS:Our findings suggested that maternal Mn concentration during the second trimester was positively associated with newborn TL. These results might provide an epidemiology evidence on the protective role of maternal Mn for newborn TL and offer clues for the early prevention of telomere shortening related diseases.

Background and aims: The risk of adverse health conditions varied according to the number of metabolic syndrome components. We aimed to evaluate the risk of mortality and incident cardiovascular events according to the number of components with high variability. Methods and results: A total of 43,737 Kailuan Study participants with >3 examinations of waist circumference, fasting blood glucose, systolic blood pressure, triglyceride, and high-density lipoprotein during 2006-2013 were included in the present study. Visit-to-visit variability in each parameter was defined by the intraindividual standard deviation across visits. High variability was defined as the highest quartile of variability. Participants were classified numerically according to the number of high-variability components (e.g., a score of 0 indicated no high-variability component). There were 1551 deaths during a median follow-up of 5.9 years, and 950 incident cardiovascular disease (CVD) cases during a median follow-up of 4.9 years. In the multivariable adjusted model, compared with participants with low variability for all components, participants with >3 high-variability components had significantly higher risks for all-cause mortality (hazards ratio [HR], 1.61; 95 % confidence interval [CI], 1.35-1.91) and incident CVD event (HR, 1.45; 95 % CI, 1.16-1.82). Additionally, participants with >3 high-variability components had increased odds of arterial stiffness, as measured by brachia-ankle pulse wave velocity (odds ratio [OR], 1.39; 95 % CI, 1.19-1.63). Conclusions: Our findings suggest that participants with at least three metabolic parameters with high variability experienced increased risk of CVD and all-cause mortality. (c) 2021 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.