Both air pollution and dyslipidemias contributed to large number of deaths and disability-adjusted life lost years. Long-term air pollution exposure was related to changed blood lipids and risk of dyslipidemias. This study was designed to evaluate relationships between air pollutants, blood lipids and prevalence of dyslipidemias in a Chinese rural population exposed to high-level air pollution based on baseline data of The Henan Rural Cohort study. An amount of 39,057 participants from rural areas in China were included. The 3-year average exposure of air pollutants (PM2.5, PM10, NO2) was estimated by a spatiotemporal model. Logistic and linear regression models were employed to explore relationships between air pollutants, blood lipids (TC, TG, HDL-C and LDL-C) and prevalence of dyslipidemias. The three-year concentration of PM2.5, PM10 and NO2 was 72.8 ± 2.3 μg/m3, 131.5 ± 5.7 μg/m3and 39.1 ± 3.1 μg/m3, respectively. Overall, increased air pollution exposure was related to increased TC and LDL-C, while decreased TG and HDL-C. Each 1-μg/m3 increment of PM2.5 was related to 0.10% (0.07%–0.19%) increase in TC, 0.63% (0.50%–0.77%) increase in LDL-C, 2.93% (2.70%–3.16%) decrease in TG, 0.49% (0.38%–0.60%) decrease in HDL-C; and 5.7% (95%CI: 3.7%–7.6%), 4.0% (95%CI: 2.1%–6.0%) and 3.8% (95%CI: 2.5%–5.1%) increase in odds for hypercholesterolemia, hyperbetalipoproteinemia and hypoalphalipoproteinemia, respectively. Stronger associations were found in male and older participants. Findings suggest that air pollutants were associated with changed blood lipid levels and higher risk of dyslipidemias among rural population. Male and elder people should pay more attention to personal safety protection.

Perfluoroalkyl and polyfluoroalkyl substances (PFASs) are synthetically manufactured chemicals recognized to be toxic, bioaccumulative, and persistent. Previous studies on PFAS exposure and serum lipid levels have mainly focused on individual PFASs; however, the influence of multiple-PFAS exposure on the serum lipid profile remains unclear. This study was performed to evaluate the combined effects of multiple PFASs on serum lipid levels. Based on the National Health and Nutrition Examination Survey (NHANES) data (2011–2014), we first established a linear regression model to estimate the association between single-PFAS exposure and the serum lipid profile. Then, a weighted quantile sum (WQS) regression model and a Bayesian kernel machine regression (BKMR) model were used to evaluate the effects of multiple-PFAS exposure on the serum lipid profile. A mediating effect model was used to assess how albumin mediates these effects. We found that PFASs were significantly associated with the levels of serum lipids, including high-density lipoprotein (HDL), low-density lipoprotein (LDL) and total cholesterol (TC). The WQS index was significantly correlated with the levels of HDL (β: 2.03, 95% CI: 0.74–3.32, P-value = 0.002), LDL (β: 4.16, 95% CI: 1.07–7.24, P-value = 0.008) and TC (β: 6.54, 95% CI: 3.00–10.1, P-value < 0.001). In the BKMR analysis, our results demonstrated that the effect of PFASs on serum lipids increased significantly when the concentrations of the PFASs were at their 60th percentiles or above compared to those at their 50th percentile. Mediation analysis showed that albumin mediated the effects of selected PFASs on the levels of serum lipids except for triglycerides (TG). PFAS exposure was correlated with the levels of serum lipids, and this correlation was mediated by albumin. Our results suggest that a comprehensive evaluation of multi-PFAS exposure could better characterize real-life exposure compared with single-PFAS exposure.

Dyslipidemia may be a potential mechanism linking air pollution to adverse cardiovascular outcomes and this may differ among obese and normal-weight populations. However, the joint effect of multiple air pollutants on lipid profiles and the role of each pollutant are still unclear. This panel study aims to investigate and compare the overall associations of major air pollutants with lipid parameters in obese and normal-weight adults, and assess the relative importance of each pollutant for lipid parameters. Forty-four obese and 53 normal-weight young adults were recruited from December 2017 to June 2018 in Beijing, China. Their fasting blood was collected and serum lipid levels were measured in three visits. Six major air pollutants were included in this study, which were PM₂.₅, PM₁₀, NO₂, SO₂, O₃ and CO. Bayesian kernel machine regression (BKMR) was implemented to estimate the joint effect of the six air pollutants on various lipid parameters. We found that decreased high-density lipoprotein cholesterol (HDL-C) in the obese group and increased low-density lipoprotein cholesterol (LDL-C) and non-HDL-C in the normal-weight group were associated with the exposure to the mixture of six air pollutants above. Significant increases in total cholesterol (TC)/HDL-C and non-HDL-C/HDL-C were observed in both groups, and the effect was stronger in obese group. Of the six air pollutants above, O₃ had the largest posterior inclusion probability in above lipid indices, ranging from 0.75 to 1.00. In the obese group, approximately linear exposure-response relationships were observed over the whole range of logarithmic O₃-8 h max concentration, while in the normal-weight group, these relationships existed when the logarithmic concentration exceeded about 2.8. Therefore, lipid profiles of obese adults may be more sensitive to air pollution and this study highlights the importance of strengthening emissions control efforts for O₃ in the future.

Polybrominated diphenyl ethers (PBDEs) have been used as flame retardants (FRs) in China for decades, even after they were identified as persistent organic pollutants. In this study, serum samples were collected from 172 adults without occupational exposure who were residents of a well-known FR production region (Laizhou Bay, north China), and PBDE congeners were measured to assess their occurrence, congener profile and influencing factors in serum. Moreover, the relationships between serum concentrations of PBDEs and thyroid/liver function indicators were analyzed to evaluate whether human exposure to PBDEs would lead to thyroid/liver injury. All 8 PBDE congeners were detected at higher frequencies and serum concentrations than those found in general populations. The median levels of ∑PBDEs, BDE-209 and ∑₃₋₇PBDEs (sum of tri-to hepta-BDEs) were 64.5, 56.9 and 7.2 ng/g lw (lipid weight), respectively, which indicated that deca-BDE was the primarily produced PBDE in Laizhou Bay and that the lower brominated BDEs were still ubiquitous in the environment. Gender was a primary influencing factor for some BDE congeners in serum; their levels in female serum samples were significantly lower than those in male serum samples. Serum PBDE levels showed a downward trend with increased body mass index (BMI), which might reflect the increasing serum lipid contents. Serum levels of some BDE congeners were significantly positively correlated with certain thyroid hormones and antibodies, including free triiodothyronine (fT3), total triiodothyronine (tT3), total thyroxine (tT4) and thyroid peroxidase antibody (TPO-Ab). Levels of some congeners were significantly negatively correlated with some types of serum lipid, including cholesterol (CHOL), low density lipoprotein (LDL) and total triglyceride (TG). Other than serum lipids, only two liver function indicators, total protein (TP) and direct bilirubin (DBIL), were significantly correlated with certain BDE congeners (BDE-100 and BDE-154). Our results provide new evidence on the thyroid-disrupting and hepatotoxic effects of PBDEs.

Copper have been reported to be associated with metabolic diseases. However, results on copper exposure with blood lipid profiles are inconsistent, and the underlying mechanisms of this association remain unclear. This study focused on investigating associations between urinary copper and blood lipid profiles; and exploring the potential role of systemic inflammation in such relationships. Concentrations of urinary copper, plasma C-reactive protein (CRP), and four blood lipid parameters (e.g., Total cholesterol [TC], triglycerides [TG], low-density lipoprotein cholesterol [LDL-C], and high-density lipoprotein cholesterol [HDL-C]) were measured in the adult participants from Wuhan-Zhuhai cohort. The associations between copper, CRP, and four blood lipids were assessed by the multivariable linear regression models, and the 3D mesh graphs was used to examine the joint effects of copper exposure and CRP on four blood lipid parameters. In addition, we used mediation analysis to investigate the mediated effects of CRP in the relationships between copper exposure and blood lipid profiles. Each 1% increase in urinary copper was statistically significantly associated with a 5.32% (95% CI: 2.48%, 8.24%) increase in TG after adjusting for the confounders (P < 0.05). No significant associations were observed between urinary copper and the other three blood lipid parameters (all P > 0.05). In addition, urinary copper increased monotonically with plasma CRP elevation, which in turn, was positively associated with TC, TG, and LDL-C and negatively related to HDL-C (all P < 0.05). Results from 3D mesh graphs demonstrated that increased levels of plasma CRP with higher urinary copper corresponded to higher TC, TG, LDL-C, and lower HDL-C concentrations. Mediation analysis observed that CRP mediated 6.27% in the relationships of urinary copper and TG. These findings suggest that systemic inflammation partly mediated the association between copper exposure and abnormal blood lipid, and may contribute to the development of dyslipidemias.

Few studies have explored the links of air pollution and childhood lipid profiles and dyslipidemias. We aimed to explore this topic in Chinese children and adolescents. This study included 12,814 children aged 7–18 years who participated in a national survey in 2013. Satellite-based spatial-temporal model was used to predict 3-y (2011–2013) average particles with diameters ≤ 1.0 μm (PM₁), ≤2.5 μm (PM₂.₅), ≤10 μm (PM₁₀), and nitrogen dioxide (NO₂) concentrations. Generalized linear mixed models were employed to evaluate the relationships of air pollution and total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and dyslipidemias. Every 10 μg/m³ increase in PM₁, PM₂.₅, PM₁₀, and NO₂ was related to increases of 6.20% [95% confidence interval (CI): 2.44, 10.10], 5.31% (95%CI: 0.41, 10.44), 3.49% (95%CI: 0.97, 6.08), and 5.25% (95%CI: 1.56, 9.07) in TC, respectively. The odds ratio of hypercholesterolemia associated with a 10 μg/m³ increase in PM₁, PM₂.₅, and NO₂ was 2.15 (95%CI: 1.27, 3.65), 1.70 (95%CI: 1.12, 2.60), and 1.43 (95%CI: 1.05, 1.93), respectively. No associations were found for air pollution and other blood lipids. Long-term PM₁, PM₂.₅, PM₁₀, and NO₂ exposures were positively associated with TC levels and risk of hypercholesterolemia in children and adolescents.

The metabolic syndrome (MetS) is a group of diseases that tend to occur together, including diabetes, hypertension, central obesity, cardiovascular disease and hyperlipidemia. Exposure to persistent organic pollutants (POPs) such as polychlorinated biphenyls (PCBs) and organochlorine pesticides (OCPs) has been associated with increased risk of development of several of the components of the MetS. The goal of this study is to determine whether the associations with POPs are identical for each of the components and for the MetS. The subject population was 601 Native Americans (Akwesasne Mohawks) ages 18 to 84 who answered a questionnaire, were measured for height and weight and provided blood samples for clinical chemistries (serum lipids and fasting glucose) and analysis of 101 PCB congeners and three OCPs [dichlorodiphenyldichloroethylene (DDE), hexachlorobenzene (HCB) and mirex]. Associations between concentrations of total PCBs and pesticides, as well as various PCB congener groups with each of the different components of the MetS were determine so as to ask whether there were similar risk factors for all components of the MetS. After adjustment for other contaminants, diabetes and hypertension were strongly associated with lower chlorinated and mono-ortho PCBs, but not other PCB groups or pesticides. Obesity was most closely associated with highly chlorinated PCBs and was negatively associated with mirex. High serum lipids were most strongly associated with higher chlorinated PCBs and PCBs with multiple ortho-substituted chlorines, as well as total pesticides, DDE and HCB. Cardiovascular disease was not closely associated with levels of any of the measured POPs. While exposure to POPs is associated with increased risk of most of the various diseases comprising the MetS, the specific contaminants associated with risk of the component diseases are not the same.

In epidemiological studies on the toxic effects of prenatal exposure to hexachlorobenzene (HCB), researchers report HCB concentrations, either as wet-weight or per lipid weight basis, in matrices like breast milk, and maternal and cord blood. Conversion of exposures across matrices is needed for comparisons of concentrations and dose effect across cohorts. Using data from a birth cohort study in eastern Slovakia, we derived the maternal blood to cord blood HCB concentration ratio utilizing measured concentrations in 1027 paired maternal and cord blood samples, on a per-lipid basis. In addition to data from the Slovak study, the maternal milk to maternal serum ratio was summarized from 23 published studies on partitioning of HCB between human milk lipid and blood lipid. We identified two distinct groups of milk:blood ratios, those ≤0.45 and those ≥0.85. We assumed that using partition ratios ≤0.45 will underestimate HCB exposure estimates. Taking into account this precautionary measure, we suggest a conversion ratio of 1.21, which is the median of the 16 ratios identified in our literature review. We consider our estimate as conservative and providing appropriate safety in risk analysis.

With the development of society and the economy, many Chinese cities are shrouded in pollution haze for much of the year. Scientific studies have identified various adverse effects of air pollutants on human beings. However, the relationships between air pollution and blood lipid levels are still unclear. The objective of this study is to explore the short and long-term effects of air pollution on eight blood lipid markers among elderly hypertension inpatients complicated with or without type 2 diabetes (T2D). Blood lipid markers which met the pre-established inclusion criteria were exported from the medical record system. Air pollution data were acquired from the official environmental protection website. Associations between the air quality index and the blood lipid indexes were analyzed by one-way ANOVA and further Bonferroni correction. In an exposure time of 7 days or longer, blood lipid markers were somewhat affected by poor air quality. However, the results could not predict whether atherosclerosis would be promoted or inhibited by poorer air condition. Changes of blood lipid markers of hypertension inpatients with or without T2D were not completely the same, but no blood lipid markers had an opposite trend between the two populations. The air quality index was associated with changes to blood lipid markers to some extent in a population of hypertension inpatients with or without T2D. Further studies are needed to investigate the potential mechanism by which air pollutants induce blood lipids changes.

The aim of this research was to study the association of the accumulated human exposure to persistent organic pollutants with serum lipid levels and obesity, in a cohort of 298 adults.In the multivariable analyses, HCB concentrations evidenced a significant quadratic association with levels of total cholesterol, HDL, LDL, and total serum lipids. Likewise, PCBs 138 and 180 were associated with triglycerides and total serum lipids, and PCB 153 with LDL. HCB, p,p′-DDE, and β-HCH showed quadratic associations with BMI. All quadratic models showed a positive trend at low exposure levels, while the slope decreased or even became negative at higher exposure levels. Additionally, PCB 138 was positively associated with BMI but in a linear manner. Our results suggest a potential relationship between historical POP exposure and serum lipids/obesity, which followed a non-linear pattern in most cases.