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.

Ambient particles with aerodynamic diameter <0.1 μm (PM₀.₁) have been suggested to have significant health impact. However, studies on the association between long-term PM₀.₁ exposure and human blood lipid metabolism are still limited. This study was aimed to evaluate such association based on multiple lipid biomarkers and dyslipidemia indicators. We matched the 2006–2009 average PM₀.₁ concentration simulated using the neural-network model following the WRF-Chem model with the clinical and questionnaire data of 15,477 adults randomly recruited from 33 communities in Northeast China in 2009. After controlling for social demographic and behavior confounders, we assessed the association of PM₀.₁ concentration with multiple lipid biomarkers and dyslipidemia indicators using generalized linear mixed-effect models. Effect modification by various social demographic and behavior factors was examined. We found that each interquartile range increase in PM₀.₁ concentration was associated with a 5.75 (95% Confidence interval, 3.24–8.25) mg/dl and a 6.05 (2.85–9.25) mg/dl increase in the serum level of total cholesterol and LDL-C, respectively. This increment was also associated with an odds ratio of 1.25 (1.10–1.42) for overall dyslipidemias, 1.41 (1.16, 1.73) for hypercholesterolemia, and 1.90 (1.39, 2.61) for hyperbetalipoproteinemia. Additionally, we found generally greater effect estimates among the younger participants and those with lower income or with certain behaviors such as high-fat diet. The deleterious effect of long-term PM₀.₁ exposure on lipid metabolism may make it an important toxic chemical to be targeted by future preventive strategies.

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.

Evidence is available about the associations of phthalates or their metabolites with blood lipids, however, the mixture effects of multiple phthalate metabolites on blood lipid traits remain largely unknown. In this pilot study, 106 individuals at three age groups of <18, 18- and ≥60 years were recruited from the residents (n = 1240) who were randomly selected from two communities in Wuhan city, China. The participants completed the questionnaire survey and physical examination as well as provided urine samples in the winter of 2014 and the summer of 2015. We measured urinary levels of nine phthalate metabolites using a high-performance liquid chromatography-tandem mass spectrometry. We estimated the associations of individual phthalate metabolite with blood lipid traits by linear mixed effect (LME) models, and assessed the overall association of the mixture of nine phthalate metabolites with blood lipid traits using Bayesian kernel machine regression (BKMR) models. LME models revealed the negative association of urinary mono-2-ethylhexyl phthalate (MEHP) with total cholesterol (TC) as well as of urinary mono-benzyl phthalate or urinary MEHP with low density lipoprotein cholesterol (LDL-C). BKMR models revealed the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C, and DEHP metabolites (especially MEHP) had a greater contribution to TC or LDL-C levels than non-DEHP metabolites. The findings indicated the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C. Among nine phthalate metabolites, MEHP was the most important component for the changes of TC or LDL-C levels, implying that phthalates exposure may disrupt lipid metabolism in the body.

Adverse health effects of exposure to air pollution have been investigated in many previous studies. However, there is no study available on the association between maternal exposure to air pollution during pregnancy and cord blood lipid profile. This study, based on 150 mother-newborn pairs residing in Sabzevar, Iran (2018), evaluated the association of exposure to ambient air pollution as well as traffic indicators (total street length in different buffers around residential address and distance to major roads) during entire pregnancy with lipid levels cord blood lipid profile. Concentrations of PM₁₀, PM₂.₅, and PM₁ at maternal residential address were estimated using land use regression (LUR) models. We measured triglyceride (TAG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC) levels and TC/HDL-C and TAG/HDL-C ratio in the cord blood samples to characterize their lipid profile. Multiple linear regression models were developed to estimate the association of exposure to air pollution and traffic indicators with cord blood lipid profile controlled for relevant covariates. Higher concentrations of PM₂.₅ and PM₁₀ were associated with higher levels of TAG, TC, HDL-C, TC/HDL-C, and TAG/HDL-C in cord blood samples. Moreover, higher concentration of PM₁ was associated with higher levels of TAG, TC and LDL-C. There was also a positive association between total street length in 100 m buffer around home and serum levels of TC, TAG, LDL-C and TC/HDL ratio (β = 3.73, 95% confidence intervals (CI): 1.76, 5.71; β = 2.75, 95% CI: 0.97, 4.53; β = 1.87, 95% CI: 0.64, 3.09; β = 0.06, 95% CI: 0.01, 0.11, respectively). However, the associations for total street length in larger buffers and distance to major roads were not statistically significant. Our findings support a relationship between exposure to air pollution during pregnancy and increase in cord blood lipid levels.

Associations between polycyclic aromatic hydrocarbons (PAHs) and respiratory diseases have been widely studied, but the effects of PAH on liver toxicity in adolescents are unclear. Here, 3194 adolescents with NHANES data from 2003 to 2016 were selected. PAH exposure was assessed by measuring PAH metabolites in urine. The outcome variables were the levels of alanine aminotransferase (ALT), aspartate amino transferase (AST) and gamma-glutamyl transpeptidase (GGT). The association between PAH exposure and liver function was evaluated by the weighted quantile sum (WQS) and logistic regression, and the associations between PAHs and inflammation and blood lipids were evaluated by linear regression. Covariates were adjusted for age, ethnicity, BMI, physical activity, family income, cotinine, and urinary creatinine. The results showed that for females, mixed PAH exposure was related to an increased ALT level (OR = 2.33, 95% CI 1.15, 4.72), and 2-fluorene contributed the most (38.6%). Urinary 2-fluorene was positively associated with an elevated ALT level (OR = 2.19 95% 1.12, 4.27, p for trend = 0.004). Mechanistically, 2-fluorene can cause a 3.56% increase in the white blood cell count, a 6.99% increase in the triglyceride level, and 1.70% increase in the total cholesterol level. PAHs may have toxic effects, possibly mediated by inflammation and blood lipids, on the adolescent female liver. Additional confirmatory studies are needed.

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.

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.

Bisphenol S (BPS) has replaced bisphenol A (BPA), a known non-persistent endocrine disrupting chemical, in several products. Considering that little is known regarding BPS effects, especially during critical windows of ontogenetic development, and that BPA, which is quite similar to BPS, is know to be transferred to the offspring via the placenta and milk, in the present study we investigated the behavioral, biochemical and endocrine profiles of Wistar rats born from dams that were BPS-exposed [groups: BPS10 (10 μg/kg/day), BPS50 (50 μg/kg/day)] during pregnancy and lactation. Due to the non-monotonic dose-response effect of bisphenol, the data of both BPS groups were directly compared with those of the controls, not to each other. Males and females were analyzed separately. At weaning, male BPS50 offspring had hypotriglyceridemia and hyperthyroxinemia, whereas BPS50 females showed higher 25(OH)D levels. At adulthood, BPS offspring of both sexes had lower food intake. BPS males showed lower visceral adiposity. BPS50 females had smaller fat droplets in brown adipocytes. BPS males showed higher anxiety and higher locomotor activity, while BPS10 females showed lower exploration. During a food challenge test at adulthood, BPS males consumed more high-fat diet at 30 min. BPS10 females initially (at 30 min) consumed more high-fat diet but, after 12 h, less of this diet was consumed. BPS50 males had hypertriglyceridemia and lower plasma T3, while BPS females showed lower plasma T4. BPS10 females had lower progesterone, whereas BPS50 females had higher plasma 25(OH)D. Maternal BPS exposure has adverse effects on the triacylglycerol, hormones levels and behavior of the progeny. Furthermore, the increased preference for the fat-enriched diet suggests an increased risk for obesity and its health consequences in the long term.