Purpose: This study aimed to explore the relationship between serum inflammatory biomarkers and the carotid atherosclerotic plaque characteristics, given prior evidence suggesting a key role of inflammation in the development of atherosclerosis. Methods: In this prospective study, patients with carotid atherosclerotic plaque were recruited. Serum high-sensitivity CRP (Hs-CRP), homocysteine (Hcy) concentrations, and neutrophil-to-lymphocyte ratio (NLR) were obtained for all enrolled patients. Carotid atherosclerosis characteristics (such as intraplaque hemorrhage [IPH] and lipid-rich necrotic core [LRNC]) were determined by three-dimensional high-resolution vessel wall imaging. The associations between Hs-CRP, Hcy, NLR, and plaque characteristics were assessed. Results: In total, 128 patients (84.4% men; mean age, 58.0 ± 8.7 years) were included. Multivariate logistic regression indicated that increased Hs-CRP levels were associated with the presence of LRNC (OR = 1.23, 95% CI: 1.07–1.40, p = 0.003) and IPH (OR = 1.26, 95% CI: 1.10–1.45, p = 0.001). Multivariate linear regression confirmed a significant correlation between Hs-CRP level (β = 3.24, 95% CI: 0.66–5.81, p = 0.014) and the IPH volume. For plaque burden, higher Hs-CRP levels were associated with larger max normalized wall index (NWI) (β = 0.01, 95% CI: 0.00–0.02, p = 0.005) and larger Max wall thickness (β = 0.08, 95% CI: 0.02–0.14, p = 0.006). NLR and Hcy levels did not show significant associations with the carotid plaque characteristics. Conclusions: Elevated Hs-CRP levels were found to be closely associated with plaque burden and vulnerable plaque characteristics. The relationship between the elevated Hs-CRP and plaque vulnerability highlights its potential role in risk stratification and early intervention strategies. Further validation in larger, multicenter population studies is required to confirm these associations.

Bronchopulmonary dysplasia (BPD) is a prevalent chronic lung disease in extremely preterm infants, characterized by arrested alveolarization and pulmonary vascular impairment. In neonatal mice and A549 cells, hyperoxia exposure significantly downregulated SIRT3 expression and PDH activity, resulting in severe mitochondrial structural and functional damage. Quantitative acetylome analysis revealed this deficiency leads to the hyperacetylation of PDHA1 at lysine 83. This modification inhibits PDH activity, forcing a pathogenic metabolic shift toward lactate accumulation and mitochondrial dysfunction. In vitro, a deacetylation-mimetic PDHA1-K83R mutant restored PDH activity and mitigated hyperoxia-induced mitochondrial injury. In vivo, pharmacological activation of SIRT3 with Honokiol prevented PDHA1 hyperacetylation, preserved mitochondrial function, and alleviated alveolar simplification. PDHA1 hyperacetylation at K83 is an important downstream event associated with SIRT3 deficiency and contributes to mitochondrial and metabolic dysfunction in hyperoxia-induced BPD. Targeting the SIRT3/PDHA1 axis provides a promising metabolic intervention strategy for BPD treatment.

Background: As a well-known environmental hazard, ambient fine particulate matter (PM2.5, aerodynamic diameter ≤ 2.5 µm) has been positively correlated with an increased risk of digestive system diseases, including appendicitis, inflammatory bowel disease, and gastrointestinal cancer. Additionally, PM2.5 exposure has been shown to alter microbiota composition and diversity in human and animal models. However, its impact on goblet cells and gut mucus barrier integrity remains unclear. Methods: To address this, 8-week-old male and female interleukin-10 knockout (IL10−/−) mice, serving as a spontaneous colitis model, were exposed to concentrated ambient PM2.5 or filtered air (FA) in a whole-body exposure system for 17 weeks. Colon tissues from the PM2.5-exposed mice and LS174T goblet cells were analyzed using H&E staining, transmission electron microscopy (TEM), and transcriptomic profiling. Results: The average PM2.5 concentration in the exposure chamber was 100.20 ± 13.79 µg/m3. PM2.5 exposure in the IL10−/− mice led to pronounced colon shortening, increased inflammatory infiltration, ragged villi brush borders, dense goblet cells with sparse enterocytes, and lipid droplet accumulation in mitochondria. Similar ultrastructure changes were exhibited in the LS174T goblet cells after PM2.5 exposure. Transcriptomic analysis revealed a predominantly upregulated gene expression spectrum, indicating an overall enhancement rather than suppression of metabolic activity after PM2.5 exposure. Integrated enrichment analyses, including GO, KEGG, and GSEA, showed enrichment in pathways related to oxidative stress, xenobiotic (exogenous compound) metabolism, and energy metabolism. METAFlux, a metabolic activity analysis, further substantiated that PM2.5 exposure induces a shift in cellular energy metabolism preference and disrupts redox homeostasis. Conclusions: The findings of exacerbated gut barrier impairment and goblet cell dysfunction following PM2.5 exposure provide new evidence of environmental factors contributing to colitis, highlighting new perspectives on its role in the pathogenesis of colitis.

Social isolation, loneliness, and fine particulate matter (PM2.5) exposure are significant social and environmental factors that frequently cooccur in vulnerable populations. The joint effects of these factors on the risk of cardiovascular disease (CVD), however, are not well supported by data. This study aimed to evaluate the independent and combined effects of social isolation, loneliness, and long-term PM2.5 exposure on CVD risk and to assess the interactions between social isolation or loneliness and PM2.5 exposure on CVD risk. We used Cox proportional hazards models to estimate the independent and combined effects of loneliness, social isolation, and long-term PM2.5 exposure on CVD incidence. We also conducted interaction analyses to investigate whether the effects of social factors on CVD are modified by the level of PM2.5 exposure. This study included 12,544 participants, with mean age of 58.7 ± 9.4 years. The median follow-up was 7 years, with 1761 CVD events occurred. Individuals with loneliness presented a 29

This prospective study aimed to investigate the associations of untreated cholesterol levels and their longitudinal changes, especially low levels, with all-cause and cause-specific mortality in different populations. Participants were drawn from two Chinese cohorts and the UK Biobank, excluding those with lipid-lowering medications, coronary heart disease (CHD), stroke, cancer, clinically diagnosed chronic obstructive pulmonary disease, low body mass index (< 18.5 kg∙m–2) at baseline, and deaths within the first two years to minimize reverse causality. Individual cholesterol changes were assessed in a subset who attended the resurvey after over four years. Mortality data were linked to registries, and risks were estimated using Cox proportional hazards models. A total of 163 115 Chinese and 317 305 UK adults were included (mean age, 49–61 years), with 43%, 81%, and 44% males in Dongfeng–Tongji, Kailuan, and UK Biobank cohorts, respectively. During a median follow-up of 9.7–12.9 years, 9 553 and 15 760 deaths were documented in the Chinese cohorts and UK Biobank, respectively. After multivariate adjustments, nonlinear relationships were observed between total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and non-high-density lipoprotein cholesterol (non-HDL-C) levels and mortality. In both populations, high cholesterol was primarily associated with CHD mortality, while low cholesterol associated with all-cause and cancer mortality (Pnonlinear ≤ 0.0161). The optimal levels for all-cause mortality risk in Chinese adults (TC: 200 mg∙dL–1; LDL-C: 130 mg∙dL–1; non-HDL-C: 155 mg∙dL–1) were lower than those in the UK Biobank but consistent with guideline recommendation. Additionally, decreasing cholesterol levels over four years were associated with higher all-cause and cancer mortality in the Chinese cohorts (Pnonlinear ≤ 0.0100). Participants with low TC, LDL-C, or non-HDL-C levels at both baseline and resurvey experienced elevated all-cause mortality risks in both populations, as did those with low/medium baseline levels and > 20% reductions over time in Chinese adults. In conclusion, higher TC, LDL-C, and non-HDL-C levels are associated with elevated CHD mortality. Importantly, low and/or longitudinally decreasing cholesterol levels are robustly associated with increased all-cause and cancer mortality, potentially serving as markers of premature death. Regular cholesterol monitoring, with attention to both high and low levels, is recommended to inform guideline updates and clinical strategies.

Phthalates, the most widely used plasticizers, have been reported to be correlated with metabolic disorders. Recent experimental studies found that phthalates may be correlated to cardiovascular diseases; however, the epidemiological evidence, particularly regarding hypertension, remains limited. Therefore, this study aimed to investigate the associations between phthalate exposure and hypertension risk and blood pressure levels, and to determine the mediating role of oxidative stress (OS). Urinary concentrations of 6 phthalate metabolites and 2 OS biomarkers were measured in 1199 general adults in Wuhan, China. The results showed that multiple phthalate metabolites (MEP, MBP, MiBP and MBzP) and the sum of 6 phthalate metabolites (ΣPAEs) were positively associated with hypertension risk and elevated blood pressure levels. In the weighted quantile sum (WQS) models, MEP was identified as the dominant contributor of phthalate mixture-induced hypertension risk. Meanwhile, all urinary phthalate metabolite concentrations were associated with elevated levels of 8-hydroxy-2-deoxyguanosine (8-OHdG) and malondialdehyde (MDA), which in turn were positively related to hypertension and blood pressure. Furthermore, the mediation analysis revealed that 8-OHdG and MDA partially mediated the effects of phthalate exposure on the increase in hypertension risk and blood pressure levels, with mediated proportions ranging from 14.0 % to 59.7 %. These results indicate that phthalate exposure may increase the risk of hypertension, and OS-related oxidative DNA damage and lipid peroxidation damage may be potential mediating mechanisms.

Dual carbon target is the definition of carbon peak and carbon neutrality, on the one hand reducing fossil consumption in order to reduce carbon emissions, and on the other hand using afforestation to increase carbon absorption.In recent years, Sichuan ethnic areas actively implemented the "double carbon" strategy, committed to promoting the low-carbon development of agriculture.In this paper, the agricultural carbon emissions of Sichuan ethnic areas from 2006 to 2021 were measured, and then the efficiency was calculated by the super-efficiency SBM model and the influencing factors were calculated by the Tobit model.The results show that the agricultural carbon emissions in ethnic areas of Sichuan show an increasing trend, with the carbon emissions in Liangshan Prefecture being the largest, and its increase is also the largest.Agricultural carbon emission efficiency showed a fluctuating trend and gradually changed to the effective state, but the efficiency in Ganzi Prefecture was the lowest in 2021.Agricultural mechanization level, agricultural economic development level, and farmland irrigation rate can promote agricultural carbon emission efficiency, while fertilizer application rate has a negative effect on it.Based on this, the paper puts forward some suggestions on the scientific use of chemical fertilizers, the vigorous implementation of water-saving actions, the emphasis on improving farmers' environmental awareness, the transformation and upgrading of agriculture, and the optimization of agricultural industrial structures and agricultural products.

Exposure to metal mixtures compromises the immune system, with the complement system connecting innate and adaptive immunity. Herein, we sought to explore the relationships between blood cell metal mixtures and the third and fourth components of serum complement (C3, C4). A total of 538 participants were recruited in November 2017, and 289 participants were followed up in November 2021. We conducted a cross-sectional analysis at baseline and a longitudinal analysis over 4 years. Least Absolute Shrinkage and Selection Operator (LASSO) was employed to identify the primary metals related to serum C3, C4; generalized linear model (GLM) was further used to evaluate the cross-sectional associations of the selected metals and serum C3, C4. Furthermore, participants were categorized into three groups according to the percentage change in metal concentrations over 4 years. GLM was performed to assess the associations between changes in metal concentrations and changes in serum C3, C4 levels. At baseline, each 1-unit increase in log10-transformed in magnesium, manganese, copper, rubidium, and lead was significantly associated with a change in serum C3 of 0.226 (95

Background: Higher greenness was associated with a lower risk of adult mortality. However, the effects of greenness on the mortality of infant and child under-5 have not been fully examined. Objectives: The association of greenness on the infant mortality rate (IMR) and child under-5 mortality rate (U5MR) in 147 Chinese cities from 2009 to 2020 was evaluated. Methods: Average and maximum annual population-weighted greenness, IMR (per 1000 live births), and U5MR (per 1000 live births) in 147 cities from 2009 to 2020 were collected, and a longitudinal panel study was conducted. Greenness exposure was evaluated using satellite-derived data at a spatial resolution of 250 m x250 m in urban regions, and linear mixed-effect models were applied to assess the associations between greenness and IMR or U5MR in China. Results: This national study showed that long-term exposure to greenness was associated with lower IMR and U5MR, respectively. Specifically, a 0.1 increase of Normalized Difference Vegetation Index (NDVI) in greenness was statistically significant with a decrease in IMR (-1.05 %o , 95 % CI:-1.48,-0.63 %o ) and U5MR (-1.82 %o , 95 % CI:-2.39,-1.25 %o ) in fully-adjusted model, respectively. In the stratified analyses, greenness effects on U5MR in the western (-2.33 %o , 95 % CI:-3.43,-1.23 %o ) and central regions (-2.06 %o , 95 % CI:-3.01,-1.10 %o ) were stronger than that in the eastern region (-0.86 %o , 95 % CI:-1.66,-0.07 %o ) . Conclusions: This nationwide study indicated that exposure to higher greenness was associated with lower mortality rates in infant and child under-5 in China.

Parabens (PBs) are the most widely used preservatives. Recent epidemiological studies have indicated that environmental exposure to parabens has adverse health effects, such as increased metabolic diseases risk. However, limited information is available on the cardiovascular effect of paraben exposure. Hence, we conducted a cross-sectional study investigating the associations between exposure to parabens with high blood pressure risk and blood pressure levels among the general Chinese population. In this study, we enrolled 1405 individuals from a medical center in Wuhan, China. Urinary methylparaben (MeP), ethylparaben (EtP), propylparaben (PrP) and butylparaben (BuP) concentrations were determined. Multivariable logistic and linear regression models were applied to analyze the associations between urinary parabens and high blood pressure risk and blood pressure level changes. Bayesian kernel machine regression (BKMR) models were applied to estimate the combined effect of the four parabens. Compared with the first quartile group, participants with the fourth quartile of EtP, PrP, and ∑parabens (∑PBs) concentrations had a 2.10-fold (95% CI: 1.40, 3.00), 1.83-fold (95% CI: 1.27, 2.62) and 1.84-fold (95% CI: 1.27, 2.65) increased the risk of hypertension, respectively. High urinary EtP, PrP, and ∑PBs levels were found to increase the levels of systolic and diastolic blood pressure (SBP and DBP), mean arterial pressure (MAP), and mid-blood pressure (MBP). BKMR models indicated the overall effects of the paraben mixture were significantly associated with high blood pressure risk and blood pressure level changes. Furthermore, after stratification by sex, the associations of EtP exposure and blood pressure levels were more pronounced in males. Our results suggest that environmental exposure to parabens might elevate blood pressure levels and increase the risk of high blood pressure.

Few studies are available on associations between metal mixture exposures and disrupted thyroid hormone homeostasis; particularly, the role of iodine status was ignored. Here, we aimed to explore the cross-sectional relationship of blood cell metals with thyroid homeostasis and explore the potential modifying effect of iodine status. Among 328 workers from the manganese-exposed workers healthy cohort (MEWHC), we detected thyroid function parameters: thyroid stimulating hormone (TSH), total triiodothyronine (TT3), free triiodothyronine (FT3), total tetraiodothyronine (TT4), free tetraiodothyronine (FT4) as well as calculated sum activity of peripheral deiodinases (G D ) and thyroid’s secretory capacity (G T ). Inductively coupled plasma mass spectrometry (ICP-MS) was used to measure 22 metal concentrations in blood cells. Based on the consistent results of least absolute shrinkage and selection operator (LASSO) and Bayesian kernel machine regression (BKMR) analyses, there were significant positive associations between copper and TSH (β = 2.016), iron and FT4 (β = 0.403), titanium and G D (β = 0.142), nickel and G D (β = 0.057), and negative associations between copper and FT4 (β = − 0.226), selenium and G D (β = − 0.332), among the participants. Interestingly, we observed an inverted-U shape relationship between magnesium and FT4. Furthermore, we found a synergistic effect between arsenic and copper on the TSH level, while antagonistic effects between nickel and copper as well as nickel and selenium on the TSH level. We observed a modified effect of iodine status on association between strontium and G D ( P interaction = 0.026). It suggests metal mixture exposures can alter thyroid homeostasis among the occupational population, and deiodinase activity had a modified effect on association between strontium and G D . Validation of these associations and elucidation of underlying mechanisms require further researches in the future.

The widely used paraben preservatives have been frequently detected in human urine, and shown to disrupt the endocrine system. Recently, several epidemiologic studies have investigated the associations between paraben exposures and hypertension risk, but findings are inconsistent. Genetic susceptibility variation may contribute to the conflicting results. This study aimed to explore the associations of paraben exposures and their interactions with estrogen receptor genes 1 and 2 (ESR1 and ESR2) polymorphisms with hypertension. We conducted a hospital-based case-control study involving 396 hypertension cases and 396 controls in Wuhan, China. The urinary paraben concentrations were determined using a liquid chromatography-quadrupole time of flight mass spectrometer. The genotyping of ESR1 and ESR2 was performed using the Applied Biosystems 3730 XL sequencer. Multivariable logistic regression models were applied to examine the associations between urinary paraben concentrations and hypertension risk. Gene-environment interactions were estimated on both multiplicative and additive scales. The results showed that urinary ethylparaben (EtP), propylparaben (PrP), and ∑parabens (∑PBs) levels were positively associated with the risk of hypertension (Ptrend<0.05). Compared with their reference groups, subjects in the highest tertile of EtP, PrP, and ∑PBs had a 4.05-fold (95% CI: 2.56, 6.41), 2.72-fold (95% CI: 1.76, 4.20), and 1.60-fold (95% CI: 1.08, 2.36) increased risk of hypertension, respectively. When stratified by sex, the hypertensive effect of EtP was more pronounced in males (Pinteraction = 0.012). Furthermore, interaction analysis showed that PrP exposure interacted with ESR1 rs2234693 polymorphism on hypertension risk, with the significance of multiplicative (Pinteraction = 0.043) and additive (RERI = 1.27, AP = 0.52). Our results suggested that paraben exposure was positively related to hypertension risk, and that ESR1 rs2234693 polymorphism might modify the parabens exposure-related hypertensive effect.

目的 探讨尿液中23种金属浓度与精液质量参数的关联性.方法 招募394名育龄男性,收集精液和尿液样本,使用电感耦合等离子体质谱联用仪(inductively coupled plasma-mass spectrometry,ICP-MS)检测尿液中23种金属浓度,对每种尿液金属浓度四分位数分组(0.05).结论 尿液中锌和铅浓度与精子前向运动活力、精子总活力和精子存活率呈负相关,尿液中锑浓度与精子正常形态率呈负相关.

目的 基于生物信息学对骨关节炎(OA)合并高血压患者相关基因的特征进行鉴定.方法 从GEO数据库与GeneCard数据库分别筛选出OA相关基因和高血压相关基因,交集后获得两者共同疾病基因,并进行基因本体论(GO)及京都基因与基因组百科全书(KEGG)富集分析,构建蛋白质互作网络(PPI),通过网络拓扑分析,利用Cytoscape软件的五种计算方法分别筛选出排名前20位基因再次交集后得到关键(Hub)基因,最后通过miRNet数据库预测Hub基因上游miRNA.结果 共筛选出131个共同疾病基因,其主要在受体配体活性、细胞因子活性等生物功能和磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(Akt)、肿瘤坏死因子(TNF)、白细胞介素-17(IL-17)等信号通路方面显著富集;最后通过分析获得白细胞介素-6(IL6)、血管内皮生长因子A(VEGFA)、基质金属蛋白酶-9(MMP-9)等11个Hub基因和has-mir-155-5P、has-mir-16-5p、has-mir-124-3p等5个关键miRNA.结论 OA与高血压共同发病基因在多种生物活性及信号通路上发挥重要调控作用;IL-6、VEGFA、MMP-9等11个关键基因及has-mir-155-5P、has-mir-16-5p、has-mir-124-3p等5个关键miRNA是OA合并高血压患者的重要调控分子.

Organoids are playing a significant role in developmental biology, disease modeling and drug screening. However, conventional organoid technologies are complex in manipulations and meet challenges for standardization, which greatly limit their applications. Furthermore, these methods can not precisely recapitulate the real physiological/pathological microenvironment in vivo, resulting in organoids with poor homogeneity and low maturity. All the facts make the current organoid technology insufficient to meet the increasing demand of clinical research. Microfluidics is an emerging technology that enables precise fluid manipulation at micro-scale. It has the ability to accurately control the microenvironment factors (such as biochemical factor gradients, shear force, nutrient supply and so on) during organoid culture. In addition, the construction of microfluidic chips is highly flexible and can integrate with microsystems such as biosensors to simulate different kinds of organs or enable continuous monitoring. Therefore, microfluidics has the potential to replace traditional methods and endow organoids with great significance in fundamental research and biomedical applications. This review systematically introduces the role of microfluidics in different kinds of organoid technologies as well as discusses its limitations and prospects.

Personal exposure to fine particulate matter (PM2.5)-bound polycyclic aromatic hydrocarbons (PAHs) can cause serious adverse health effects. However, limited information is available on the impact of a mixture of PAHs in air-borne PM2.5 on lung function. We conducted a repeated-measures pilot study for four seasons during the period of 2014-2015, monitored the concentrations of 13 PAHs in PM2.5 samples from the outdoor and indoor microenvironments using a gas chromatograph-mass spectrometry, estimated inhaled dose of PM2.5-bound PAHs based on the outdoor and indoor PM2.5-bound PAHs concentrations as well as individual time-activity diary, and analyzed independent and joint effects of PM2.5-bound 13 PAHs on lung function by linear mixed effect (LME) and Bayesian kernel machine regression (BKMR) models, respectively. LME models indicated the negative association of phenanthrene or benzo [a] pyrene with forced expiratory volume in 1 s (FEV1) or forced vital capacity (FVC) in warm season. BKMR models revealed that an overall negative association of the mixture of 13 PAHs in PM2.5 with FVC, FEV1, PEF or MW values in warm season but only overall negative association of the mixture of 13 PAHs in PM2.5 with MW values in cold season. In warm season, young adults with higher exposure to certain PAHs or the mixture of 13 PAHs in PM2.5 showed significant impairment in lung function, implying that health risk assessment of the mixture of PAHs in PM2.5 attributed to PM2.5 from traffic emission.

In this study, 123 PM2.5 filter samples were collected in Wuhan, Hubei province from December 2014 to November 2015. Water- soluble inorganic ions (WSIIs), elemental carbon (EC), organic carbon (OC) and inorganic elements were measured. Source apportionment and back trajectory was investigated by the positive matrix factorization (PMF) model and the hybrid single particle lagrangian integrated trajectory (HYSPLIT) model, respectively. The annual PM2.5 concentration was 80.5 ± 38.2 μg/m3, with higher PM2.5 in winter and lower in summer. WSIIs, OC, EC, as well as elements contributed 46.8%, 14.8%, 6.7% and 8% to PM2.5 mass concentration, respectively. SO42−, NO3− and NH4+ were the dominant components, accounting for 40.2% of PM2.5 concentrations. S, K, Cl, Ba, Fe, Ca and I were the main inorganic elements, and accounted for 65.2% of the elemental composition. The ratio of NO3−/SO42− was 0.86 ± 0.72, indicating that stationary sources play dominant role on PM2.5 concentration. The ratio of OC/EC was 2.9 ± 1.4, suggesting the existence of secondary organic carbon (SOC). Five sources were identified using PMF model, which included secondary inorganic aerosols (SIA), coal combustion, industry, vehicle emission, fugitive dust. SIA, coal combustion, as well as industry were the dominant contributors to PM2.5 pollution, accounting for 34.7%, 20.5%, 19.6%, respectively.

目的 探讨多学科护理团队协作模式在老年围手术期患者中的应用效果.方法 选取笔者所在科室2018年1—12月就诊并行手术治疗的65岁以上老年患者50例为对照组,选取2019年1—12月就诊行手术治疗的65岁以上老年患者50例为观察组.对照组给予老年科常规围手术期护理,观察组在对照组基础上给予多学科护理团队协作模式进行干预,比较2组患者术后并发症、护理不良事件发生率及平均住院天数.结果 观察组术后并发症及护理不良事件发生率均低于对照组(χ2=5.086,P=0.024;χ2=4.396,P=0.036);平均住院天数短于对照组(t=5.913,P=0.016).结论 多学科护理团队协作模式可以降低老年患者术后并发症的发生率,缩短平均住院时间.

Exposure to phthalates poses potential to damage multiple organs and system in the body. However, limited data are available regarding effects of seasonal exposure levels of phthalates and indicators reflecting inflammatory response. We designed a pilot study with repeated measures. We recruited 106 eligible habitants from Wuhan city, China. They completed questionnaires, physical examinations and provided urine specimens in winter and summer seasons. We found that urinary levels of low-molecular-weight phthalate metabolites were higher in summer than in winter (all P < 0.01). In winter, an interquartile range increase (1.264 μg/L) in 3-day moving average of high-molecular-weight phthalate metabolites corresponded to a 13.634% (95% CI: −22.331, −3.941) decrease in mean platelet volume, 25.879% (95% CI: −37.424, −12.204) for lymphocyte count or 10.862% (95% CI: −18.716, −2.125) for platelet count (P < 0.05 or P < 0.01). However, in summer, an interquartile range increase (1.215 μg/L) in urinary levels of high-molecular-weight phthalate metabolites corresponded to an 8.743% (95% CI: 4.217, 13.467) increase in platelet distribution width value or a 4.597% (95% CI: 2.335, 6.780) for mean platelet volume value at 3-day lag (both P < 0.01). In conclusion, phthalate exposure exhibited the potential for the activation of platelet function, particularly in winter. Seasonal variations of phthalate exposure should be considered when assessing health risk.