Inhalation exposure to fine particulate matter (PM₂.₅) represents a global concern due to the adverse effects in human health. In the last years, scientific community has been adopted the assessment of the PM₂.₅-bound pollutant fraction that could be released (bioaccessible fraction) in simulated lung fluids (SLFs) to achieve a better understanding of PM risk assessment and toxicological studies. Thus, bioaccessibility of 49 organic pollutants, including 18 polycyclic aromatic hydrocarbons (PAHs), 12 phthalate esters (PAEs), 11 organophosphorus flame retardants (OPFRs), 6 synthetic musk compounds (SMCs) and 2 bisphenols in PM₂.₅ samples was evaluated. The proposed method consists of a physiologically based extraction test (PBET) by using artificial lysosomal fluid (ALF) to obtain bioaccessible fractions, followed by a vortex-assisted liquid-liquid microextraction (VALLME) and a final analysis by programmed temperature vaporization-gas chromatography-tandem mass spectrometry (PTV-GC-MS/MS). The highest inhalation bioaccessibility ratio was found for bisphenol A (BPA) with an average of 83%, followed by OPFRs, PAEs and PAHs (with average bioaccessibilities of 68%, 41% and 34%, respectively). Correlations between PM₂.₅ composition (major ions, trace metals, equivalent black carbon (eBC) and UV-absorbing particulate matter (UVPM)) and bioaccessibility ratios were also assessed. Principal Component Analysis (PCA) suggested that PAHs, PAES and OPFRs bioaccessibility ratios could be positively correlated with PM₂.₅ carbonaceous content. Furthermore, both inverse and positive correlations on PAHs, PAEs and OPFRs bioaccessibilites could be accounted for some major ions and metal (oid)s associated to PM₂.₅, whereas no correlations comprising considered PM₂.₅ major ions and metal (oid)s contents and BPA bioaccessibility was observed. In addition, health risk assessment of target PM₂.₅-associated PAHs via inhalation was assessed in the study area considering both total and bioaccessible concentrations, being averaged human health risks within the safe carcinogenic and non-carcinogenic levels.

We aimed to investigate the associations between chemical mixtures and the risk of nonalcoholic fatty liver disease (NAFLD) in this study. A total of 127 exposure analytes within 13 chemical mixture groups were included in the current analysis. Associations between chemical mixture exposure and prevalence of NAFLD were examined using weighted quantile sum (WQS) regressions. NAFLD was diagnosed by hepatic steatosis index (HSI) and US fatty liver index (USFLI). In USFLI-NAFLD cohort, chemical mixtures positively associated with NAFLD development included urinary metals (OR: 1.10, 95% CI: 1.04–1.16), urinary perchlorate, nitrate and thiocyanate (OR: 1.06, 95% CI: 1.02–1.11), urinary pesticides (OR: 1.24, 95% CI: 1.09–1.40), urinary phthalates (OR: 1.18, 95% CI: 1.09–1.28), urinary polyaromatic hydrocarbons (PAHs) (OR: 1.08, 95% CI: 1.03–1.14), and urinary pyrethroids, herbicides, and organophosphate pesticides metabolites (OR: 1.32, 95% CI: 1.15–1.51). All of the above mixtures were also statistically significant in WQS regressions in the HSI-NAFLD cohort. Besides, some chemical mixtures were only significant in HSI-NAFLD cohort including urinary arsenics (OR: 1.07, 95% CI: 1.02–1.12), urinary phenols (OR: 1.10, 95% CI: 1.02–1.19) and blood polychlorinated dibenzo-p-dioxins (OR: 1.10, 95% CI: 1.03–1.17). Three types of chemical mixtures only showed significant associations in the healthy lifestyle score (HLS) of 3–4 subgroup, including urinary perchlorate, nitrate and thiocyanate, urinary PAHs and blood polychlorinated dibenzo-p-dioxins. In conclusion, the exposure of specific types of chemical mixtures were associated with elevated NAFLD risk, and the effects of some chemical mixtures on NAFLD development exhibited differences in participants with different lifestyles.

Many communities around the country are undergoing contentious battles over the installation of artificial turf. Opponents are concerned about exposure to hazardous chemicals leaching from the crumb rubber cushioning fill made of recycled tires, the plastic carpet, and other synthetic components. Numerous studies have shown that chemicals identified in artificial turf, including polycyclic aromatic hydrocarbons (PAHs), phthalates, and per- and polyfluoroalkyl substances (PFAS), are known carcinogens, neurotoxicants, mutagens, and endocrine disruptors. However, few studies have looked directly at health outcomes of exposure to these chemicals in the context of artificial turf. Ecotoxicology studies in invertebrates exposed to crumb rubber have identified risks to organisms whose habitats have been contaminated by artificial turf. Chicken eggs injected with crumb rubber leachate also showed impaired development and endocrine disruption. The only human epidemiology studies conducted related to artificial turf have been highly limited in design, focusing on cancer incidence. In addition, government agencies have begun their own risk assessment studies to aid community decisions. Additional studies in in vitro and in vivo translational models, ecotoxicological systems, and human epidemiology are strongly needed to consider exposure from both field use and runoff, components other than crumb rubber, sensitive windows of development, and additional physiological endpoints. Identification of potential health effects from exposures due to spending time at artificial turf fields and adjacent environments that may be contaminated by runoff will aid in risk assessment and community decision making on the use of artificial turf.

The coexistence of di (2-ethylhexyl) phthalate (DEHP), Cd, and Zn poses a serious challenge to soil ecosystems. This study aimed to evaluate the phytoremediation potential of rice assisted with a plant growth promoting rhizobacteria (PGPR) consortium for the remediation of DEHP, Cd, and Zn co-contaminated soil. The consortium consisted of four bacterial strains, all of which exhibited Cd–Zn resistance and DEHP degradability. The results showed that the rice assisted by the bacterial consortium dissipated 86.1% DEHP while removing 76.0% Cd²⁺ and 92.2% Zn²⁺ from soil within 30 d. The presence of the PGPR consortium promoted plant growth and improved soil enzymatic activity, which may have helped enhance the removal of DEHP and heavy metals from the soil. Moreover, the application of the consortium modified the bacterial community and increased the relative abundance of bacteria related to DEHP degradation (Sphingomonas, Xanthobacteraceae), heavy metal immobilization (Massilia), and soil nutrient cycling (Nitrospira, Vicinamibacterales), which promoted plant growth and the removal of DEHP and heavy metals from soil. Notably, the DEHP and heavy metal contents in rice decreased substantially during the phytoremediation process. Therefore, the PGPR consortium could be beneficial for enhancing the removal of DEHP and heavy metals from the soil, without inducing the accumulation of these pollutants in rice. In general, this study confirmed that the combined use of rice and the PGPR consortium could remedy DEHP and heavy metal co-contaminated soil economically and ecologically without simultaneously posing risks for rice consumption.

The association of co-exposure to polycyclic aromatic hydrocarbons (PAHs) and phthalates (PAEs) with blood cell-based inflammatory biomarkers is largely unknown. We conducted a panel study of 144 children aged 4–12 years, with up to 3 repeated visits across 3 seasons. For each visit, we collected the first-morning urine for 4 consecutive days and fasting blood on the day of physical examination. We developed a gas chromatography/tandem mass spectrometry method to detect the metabolites of 10 PAHs (OH-PAHs) and 10 PAEs (mPAEs) in urine samples. We employed linear mixed-effects models to evaluate the individual associations of each OH-PAH and mPAE with blood cell-based inflammatory biomarkers over different lag times. Bayesian kernel machine regression (BKMR) and quantile g-computation were used to evaluate the overall associations of OH-PAHs and mPAEs mixtures with blood cell-based inflammatory biomarkers. After multiple adjustments, we found positive associations of summed hydroxylphenanthrene (∑OHPHE), summed OH-PAHs, and mono-n-butyl phthalate with inflammatory biomarkers such as neutrophil count, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and the systemic immune-inflammation index (SII) at lag 0 (the day of physical examination). Each 1% increase in ∑OHPHE was related to a 0.18% (95% confidence interval: 0.10%, 0.25%) increase in SII, which was the strongest among the above associations. The results of BKMR and quantile g-computation suggested that co-exposure to PAHs and PAEs mixture was associated with an elevated white blood cell count, neutrophil count, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and SII, to which ∑OHPHE and 1-hydroxypyrene (1-OHPYR) might be the major contributors. In addition, gender and age modified the associations of ∑OHPHE and 1-OHPYR with inflammatory biomarkers, where girls and younger children were more susceptible. In conclusion, co-exposure to PAHs and PAEs was associated with elevated inflammation in children, in which ∑OHPHE and 1-OHPYR might play important roles.

A vast amount of evidence indicates that bisphenol A (BPA) and phthalates are widely distributed in the environment since these compounds are mass-produced for the manufacture of plastics and plasticizers. These compounds belong to a large group of substances termed endocrine-disrupting chemicals (EDC). It is well known that humans and living organisms are unavoidably and unintentionally exposed to BPA and phthalates from food packaging materials and many other everyday products. BPA and phthalates exert their effect by interfering with hormone synthesis, bioavailability, and action, thereby altering cellular proliferation and differentiation, tissue development, and the regulation of several physiological processes. In fact, these EDC can alter fetal programming at an epigenetic level, which can be transgenerational transmitted and may be involved in the development of various chronic pathologies later in the adulthood, including metabolic, reproductive and degenerative diseases, and certain types of cancer.In this review, we describe the most recent proposed mechanisms of action of these EDC and offer a compelling selection of experimental, epidemiological and clinical studies, which show evidence of how exposure to these pollutants affects our health during development, and their association with a wide range of reproductive, metabolic and neurological diseases, as well as hormone-related cancers. We stress the importance of concern in the general population and the urgent need for the medical health care system to closely monitor EDC levels in the population due to unavoidable and involuntary exposure to these pollutants and their impact on human health.

Agricultural plastic greenhouse (PG) production can extend the growing season of crops to satisfy domestic consumption in countries such as China. Workers in PGs have potential higher phthalate exposure risks than the general population as phthalate accumulation has been observed in greenhouse soil, air, and crops. To date, biomonitoring tests of phthalates for the working population have not been carried out. To address this shortage, we conducted a pilot study in Shaanxi Province, China, among 35 healthy PG workers by follow-up recording their seasonal dietary habits and work activities and urine sample collection and measurement between 2018 and 2019. The objectives were to uncover the association between phthalate metabolites and the population characteristics, seasonal and diurnal variations and causes, and to estimate exposure risks and contributions of exposure pathways from PG production systems. A total of 13 phthalate metabolite concentrations (Σ₁₃ phthalate metabolites) ranged from 102 to 781 (5th-95th) ng/mL (median: 300 ng/mL). Mono-n-butyl phthalate (MNBP) made up 51.3% of Σ₁₃ phthalate metabolites, followed by the sum of four di-2-ethylhexyl phthalate (DEHP) metabolites (24.2%), mono-2-isobutyl phthalate (MIBP) (13.4%), and mono-ethyl phthalate (MEP) (9.8%). The concentrations of MNBP and MIBP in summer were significantly higher than the levels in winter (p < 0.0001). A total of 62.3% of the PG worker population was shown to have exposure risks, and the proportion was as high as 79.4% in summer. Phthalate exposure of the workers from PG production systems constituted over 20% of the total creatinine-based daily intake, and consuming vegetables and fruit planted in PGs and inhalation in PGs were the two largest exposure pathways. Our findings demonstrate that it is important to protect workers in PGs from phthalate exposure risks, and phasing out the use of plastic materials containing phthalates in PGs is imperative, to guarantee food safety in PGs.

Because most relevant studies have used small sample sizes, to date, representative atmospheric monitoring of persistent organic pollutants (POPs) on a regional scale has been very limited, which makes it difficult to precisely identify “hotspots” and possible pollution sources. In this study, an ultrahigh resolution monitoring technique was used to measure the atmospheric spatial variations in POP concentrations on a regional scale, throughout Campania, Italy. The occurrence of specific POPs—including polychlorinated biphenyls (PCBs), organochlorine pesticides (OCPs), polycyclic aromatic hydrocarbons (PAHs), polybrominated diphenyl ethers (PBDEs) and phthalate esters (PAEs)—were investigated using polyurethane foam-based passive air samplers (PUF-PAS), which were deployed at 129 sites across the Campania Territory between April and July 2016. The results show that the highest POP levels occurred in the Naples metropolitan area (NMA), although there were other problematic spots throughout the Territory. More specifically, hotspot areas in the NMA that depict serious POP pollution were found in the Bagnoli brownfield site, Sarno River Basin, and parts of the northeastern NMA sector. The atmospheric POP contamination in Campania is jointly controlled by the contributions of local emissions and long-range atmospheric transport. Diffusion model was employed to identify the potential sources of various POPs. The simulation showed that all the POP sources are located in the NMA and are closely related to industrial sites. This study demonstrates the advantage of using large sample sizes to identify POP source locations and achieve geospatial visualization of POP concentration and risk assessment levels.

The potential risks of phthalates affecting human and animal health as well as the environment are emerging as serious concerns worldwide. However, the mechanism by which phthalates induce developmental effects is under debate. Herein, we found that embryonic exposure of zebrafish to di-(2-ethylhexyl) phthalate (DEHP) and di-butyl phthalate (DBP) increased the rate of heart defects including abnormal heart rate and pericardial edema. Changes in the transcriptional profile demonstrated that genes involved in the development of the heart, such as tbx5b, nppa, ctnt, my17, cmlc1, were significantly altered by DEHP and DBP at 50 μg/L, which agreed with the abnormal cardiac outcomes. Methylated DNA immunoprecipitation sequencing (MeDIP-Seq) further showed that significant hypomethylation of nppa and ctnt was identified after DEHP and DBP exposure, which was consistent with the up-regulation of these genes. Notably, hypermethylation on the promoter region (<1 kb) of tbx5b was found after DEHP and DBP exposure, which might be responsible for its decrease in transcription. In conclusion, phthalates have the potential to induce cardiac birth defects, which might be associated with the transcriptional regulation of the involved developmental factors such as tbx5b. These findings would contribute to understand the molecular pathways that mediated the cardiac defects caused by phthalates.

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.