Approaches to characterising human exposure to hazardous environmental pollutants generally fall into two broad categories: external exposure monitoring vs. internal exposure monitoring (human biomonitoring). Time lags exist between the first use of chemicals, their initial occurrence in the abiotic environment, their emergence in the human diet, and their eventual manifestation in human bodies. We suggest that the optimum time to become aware of potentially problematic chemical exposures is at the earliest possible opportunity. Therefore, we propose an indoor passive monitoring programme as a complementary strategy to existing dietary exposure monitoring and human biomonitoring efforts. Indoor passive monitoring combining targeted analysis and non-target screening of vacuum cleaner dust, silicone wristbands, and passive air samplers, facilitates timely detection of emerging contaminants and assessment of human health risks, which is cost-effective and ethically advantageous. This indoor passive monitoring framework effectively leverages citizen science, enabling proactive interventions and improved public health outcomes.
Traffic-related activity patterns, including transportation mode choices and time spent in transit, critically influence individuals’ exposure to air pollution. This study analyzed data from three cross-sectional surveys conducted in Lanzhou, China (2015-2020), to investigate variations in transportation behavior and their impact on daily cumulative PM2.5 inhalation exposure. Results showed that walking was the most frequently used mode, accounting for over 70% of trips, while car use involved the longest average travel time - exceeding 60 min per day. However, trends in mode share and usage time were not synchronized, and the use of different transportation modes was interrelated. Sociodemographic factors and built environment features near homes and workplaces were dynamically associated with transportation behaviors. Time spent in transit had the strongest influence on cumulative daily exposure, explaining more than 90% of the variation across modes. Open modes of transport were linked to the highest exposure levels due to elevated pollutant concentrations and increased inhalation rates, whereas car transportation resulted in the lowest exposure despite its longer duration. These findings underscore the need to incorporate transportation behavior into air pollution exposure assessments and suggest that transportation policies and infrastructure planning should align mobility objectives with public health priorities.
Air pollution and high low-density lipoprotein cholesterol (LDL-C) levels are both among the top ten global risk factors. This study aims to investigate the impact of long-term exposure to ambient PM2.5 and O3 on LDL-C concentrations in peripheral blood and their effects on hepatic metabolism of LDL-C, based on epidemiological research and animal experiments. Epidemiological research employed a cross-sectional design, enrolling 27,642 male health examinees aged 20-50 in Beijing from March 2021 to February 2023, with an exposure period of one year. Generalized additive models were employed to explore the association between exposure to PM2.5 and O3 and levels of LDL-C. The animal experiment involved rats exposed to an atmosphere containing PM2.5 and O3, alongside a control group breathing air devoid of PM2.5 and O3, with an exposure duration of 15 months. Reverse transcription quantitative polymerase chain reaction and immunohistochemical staining were utilized to detect differences in mRNA expression and protein expression at key loci of LDL-C metabolism between the two groups. In our results, the epidemiological research showed that long-term exposure to PM2.5 was primarily associated with increased levels of LDL-C and elevated risk of LDL-C abnormality. The animal experiments demonstrated that long-term exposure to air pollution suppressed the liver's ability to absorb LDL-C and inhibited the expression of GRP78, which may be one of the mechanisms leading to increased serum LDL-C levels.
Beta-2-microglobulin (β2M) is released into plasma from nucleated cells, filtered by glomeruli, and degraded by proximal tubular cells (PTCs). Normally, < 1% of filtered β2M is excreted in urine. Intoxication of PTCs by cadmium (Cd) reduces degradation and increases excretion of β2M (TDβ2M and Eβ2M). Diabetes may exacerbate these effects or produce them independently. Herein, we normalized fluxes to creatinine clearance (Ccr) to quantify amounts of β2M excreted and degraded per volume of filtrate (Eβ2M/Ccr and TDβ2M/Ccr). We then performed a case-control study of diabetics (DM, n = 65) and non-diabetics (CTRL, n = 72) with modest Cd exposure. β2M influx (Iβ2M, equated with β2M filtration rate), serum β2M ([β2M]s), and TDβ2M/Ccr were higher in DM. Fractional tubular degradation of filtered β2M (FrTDβ2M) emerged as the least confounded descriptor of PT β2M processing, and low values of FrTDβ2M were seen in a subset of diabetics with minimal Cd intoxication. FrTDβ2M varied inversely with ECd/Ccr in DM and directly with estimated GFR (eGFR) in DM and CTRL. In both groups, Eβ2M/Ccr was inversely related to eGFR and
Per- and polyfluoroalkyl substances (PFASs) in urban rivers of rapidly industrializing regions remain understudied, particularly in South Asia. This study assessed the occurrence, sources, and ecological risks of 15 PFASs in water and sediment from three major rivers (Buriganga, Turag, Shitalakkha) in Dhaka, Bangladesh. PFASs were quantified using HPLC-MS/MS, and sources were identified via principal component analysis (PCA). All target compounds were detected, with total concentrations in water ranging from 23.96 to 89.35 ng/L and sediment from 2.18 to 11.67 ng/g dry weight. Perfluorooctanoic acid (PFOA) dominated water samples (34%-59% of ΣPFASs), reflecting its ongoing industrial use and high water solubility, while perfluorooctane sulfonate (PFOS) prevailed in sediments (up to 71% of ΣPFASs) due to historical accumulation. The Buriganga River exhibited the highest contamination, driven by untreated effluents from tanneries, textiles, and chemical industries. Risk quotient (RQ) analysis revealed low-to-moderate ecological risks for most PFASs, but PFOS in sediments posed a high risk (RQ = 1.68) near industrial clusters. Compared with global data, PFAS levels in rivers around Dhaka city exceeded those in less industrialized regions but were lower than those in heavily polluted systems. These findings highlight the urgent need for stricter regulation of industrial discharges, improved wastewater treatment, and long-term monitoring to mitigate PFAS contamination in urban waterways. This study also provides critical baseline data to inform environmental policy and sustainable water management in developing regions.
Urinary phthalate (PAE) metabolites are prevalent environmental pollutants linked to various health risks. Although several promising DNA methylation (DNAm) algorithms have emerged as strong predictors of biological age and adverse health outcomes in older adults, the specific relationship between exposure to these chemical contaminants and DNAm algorithms remains largely unexplored. This study aimed to evaluate this association of urinary PAE metabolites with five widely used DNAm-based aging signatures in a representative sample of U.S. adults. Data from the National Health and Nutrition Examination Survey 1999-2002 were analyzed, focusing on urine samples from 831 participants for seven PAE metabolites. Methylation data were generated using the EPIC array (Illumina, San Diego, CA, USA), and five DNAm-based aging signatures, the HannumAgeacc, SkinBloodAgeacc, PhenoAgeacc, GrimAgeMortacc, and GrimAge2Mortacc, were estimated and employed in linear models to investigate their relationships with urinary PAE metabolite concentrations. Significant associations (P-values: 0.0001-0.0393) were observed between MBzP and all five DNAm aging algorithms, with multivariable adjusted β values ranging from 0.22 (95%CI: 0.07-0.38) for GrimAgeMortacc to 0.68 (95%CI: 0.18-1.18) for PhenoAgeacc. In males, significant associations between MBzP and PhenoAgeacc, GrimAgeMortacc, and GrimAge2Mortacc were noted (P-values: 0.0027-0.0205). Among participants aged 50-64, MBzP exhibited significant associations with all five DNAm aging algorithms (P-values: 0.0012-0.0155), with multivariable adjusted β values ranging from 0.30 (95%CI: 0.10-0.51) for GrimAgeMortacc to 0.93 (95%CI: 0.34-1.52) for PhenoAgeacc. These findings suggest that MBzP may accelerate biological aging in older populations, particularly in males aged 50-64.
Spices and herbs are widely used food ingredients with both cultural and dietary importance, but there is a concern that these products contain heavy metal contaminants. In this study, the levels of heavy metals (aluminium, arsenic, cadmium, chromium, lead, mercury, nickel, strontium) were investigated in dried spice and herb samples
Bisphenol AF (BPAF), a widely used substitute for bisphenol A (BPA), has been widely detected in pregnant women, raising concerns about its potential effects on reproductive health. However, studies on the reproductive toxicity of BPAF in mammals remain limited. This study aimed to investigate the reproductive toxicity and underlying mechanisms of BPAF exposure during gestation and lactation. Pregnant Sprague-Dawley rats were randomly assigned to four groups (n = 10/group) and administered BPAF by oral gavage (0, 2, 10, or 50 mg/kg/d in corn oil) from gestational day (GD) 0 to postnatal day (PND) 21. Female offspring [first filial generation (F1)] were examined at PND21 and PND70 for reproductive outcomes and steroidogenic alterations. Gestational and lactational BPAF exposure significantly reduced anogenital distance (AGD) at PND21, from 12.05 ± 0.59 mm in controls to 11.54 ± 0.50 mm in the 50 mg/kg group (P < 0.001). At PND21, serum estradiol (E2) levels were decreased in the 2 and 10 mg/kg BPAF groups compared with controls (P < 0.05). By PND70, all BPAF-exposed offspring showed reduced E2 and testosterone (T) levels (P < 0.05). In addition, BPAF exposure increased follicular atresia and downregulated the mRNA expression of key steroidogenic genes (StAR, CYP11A1, 17β-HSD, and CYP19A1; P < 0.05) at PND70. Our findings indicate that BPAF exposure during gestation and lactation impairs reproductive function in F1 females and may exert long-term effects through disruption of ovarian steroidogenesis. Further research is warranted to confirm these outcomes.
Kidney and bone destruction in patients with itai-itai disease is caused by consuming rice contaminated with the heavy metal cadmium (Cd). Based on a lifetime intake of 2 g of Cd, and an elevation of β2-microglobulin (β2M) excretion rate, a tolerable Cd intake level was 0.83 µg/kg body weight per day (58 µg/day for a 70 kg person), with a threshold of 5.24 µg/g creatinine. However, current evidence suggests that these guidelines are inadequate to protect public health. Using experimental dosing and human population data, this review highlights the imprecision in determining exposure, internal doses, and adverse effects, leading to erroneous conclusions that Cd exposure did not diminish the estimated glomerular filtration rate (eGFR) nor did it accelerate progressive eGFR decline toward kidney failure among Cd-exposed people. It discusses the principles and application of the benchmark dose (BMD) modeling to human exposure-effect relationships from which the critical Cd exposure levels can be identified reliably, with kidney effect indicators other than the β2M excretion. It offers insights into the utility of multiple mathematical dose-response models to define the benchmark dose limit (BMDL) value for Cd exposure, which carries discernible health risk. From BMD modeling studies, Cd excretion benchmarks for early kidney effects, reflected by excretion of total proteins, N-acetyl-β-D-glucosaminidase, and eGFR decline, were 0.95, 1.34, and 3.24% of the current threshold, respectively. These Cd excretion levels are ideal for the derivation of safe Cd exposure guidelines because they are equivalent to no-observed-adverse-effect levels (NOAELs).
Emerging contaminants (ECs) have garnered growing attention as potential contributors to adverse metabolic outcomes during pregnancy, particularly gestational diabetes mellitus (GDM). Despite increasing recognition of their endocrine-disrupting capabilities, the precise relationship between EC exposure and glucose dysregulation in the gestational context remains inadequately characterized. The scarcity of longitudinal human studies, along with limited mechanistic elucidation, highlights a critical gap in understanding how these ubiquitous environmental pollutants may perturb maternal metabolic homeostasis. This review consolidates current epidemiological evidence linking key classes of ECs, including per- and polyfluoroalkyl substances (PFAS), polychlorinated biphenyls (PCBs), phthalates (PAEs), bisphenols, organochlorine pesticides (OCPs), parabens, and alkylphenols, with GDM risk and impaired glycemic control. Parallel examination of in vivo and in vitro studies reveals plausible biological mechanisms, including oxidative stress, mitochondrial dysfunction, inflammatory signaling, and insulin resistance (IR), through which these compounds may mediate their effects. By integrating data across human and experimental research domains, this review underscores the urgent need for high-resolution exposure assessments, mixture toxicity frameworks, and mechanistic validation. Such insight is essential for advancing etiological understanding, informing regulatory action, and guiding preventive strategies to mitigate the impact of environmental exposures on maternal-fetal metabolic health.
The FAIREHR (Findable, Accessible, Interoperable, Reusable Environmental and Health Registry) platform is a state-of-the-art online registry for prospective harmonization of human biomonitoring (HBM). It was developed by the HBM working group of the Europe Regional Chapter of the International Society of Exposure Science (ISES Europe) and is supported by the HBM Global Network. FAIREHR is designed to harmonize HBM metadata and support the implementation of the FAIR (Findable, Accessible, Interoperable and Reusable) Guiding Principles throughout HBM studies or programs. The registry enables preregistration of HBM by capturing key metadata on study design, metadata management, and planned methods before participant recruitment. This process enhances transparency and reproducibility in environmental and occupational health research. FAIREHR includes both study-level and program-level metadata. Its harmonized metadata template facilitates the storage of results (measurement data) in repositories such as IPCHEM and PEH. Here we outline the unique features of the FAIREHR platform, emphasizing its role in increasing research visibility, improving metadata comparability and harmonization, and strengthening the exchange of information. By supporting the effective use of HBM data, FAIREHR is expected to yield significant benefits for researchers, policymakers, and the broader fields of environmental and occupational health.
Human exposure to bisphenol analogues (BPs) and their health risks have raised increasing concern due to their potential toxicity. However, limited data are available on exposure levels and associated risks in school-aged children. In this study, we quantified 26 BPs in urine samples from 184 school-aged children living in representative rural and urban areas of South China, using a high-throughput, sensitive analytical method. The aim was to assess the co-exposure levels and potential non-carcinogenic risks. The detection frequency (DF) of the total concentration of 26 BPs (∑BPs) was 100.0%. Concentrations of ∑BPs ranged from 0.089 to 45.33 μg/L, with a median of 2.14 μg/L. The predominant compounds were bisphenol A (BPA, median 0.803 μg/L, DF 97.8%), 2,4’-bisphenol S (2,4-BPS, 0.068 μg/L, DF 93.5%), 4,4’-dihydroxytetraphenyl methane (BPBP, 0.041 μg/L, DF 66.3%), and bisphenol F (BPF, 0.033 μg/L, DF 61.4%), accounting for 77.2%, 6.5%, 4.0%, and 3.2% of ∑BPs, respectively. Both the concentration and DF of 2,4-BPS were much higher than those of bisphenol S (BPS, <0.003 μg/L, DF 48.9%), suggesting that 2,4-BPS was the predominant derivative. BPA concentrations were positively associated with family income levels, while 2,4-BPS concentrations were linked to plastic-bottled water consumption. BPF concentrations were associated with both instant noodle consumption frequency and maternal education level. The median estimated daily intakes of BPA, 2,4-BPS, and BPF were 0.035, 0.003, and 0.002 μg/kg-bw/day, respectively. Although non-carcinogenic risk assessments indicated minimal risk, revised tolerable daily intake values suggested potential health concerns for school-aged children. These findings highlight the need for continued monitoring of BPs in susceptible populations, and further research should focus on cumulative risks and exposure sources of BPs.
With the restriction of bisphenol A (BPA) in certain consumer products due to its endocrine-disrupting properties, structurally analogous alternatives such as bisphenol S (BPS) and bisphenol F (BPF) have rapidly entered the market. This shift has led to a wave of “regrettable substitutions” - chemicals that appear more environmentally friendly but may pose comparable or even unforeseen risks. Based on the latest toxicological evidence and population biomonitoring data, this perspective highlights that most mainstream BPA alternatives exhibit estrogenic/anti-androgenic activity, metabolic disruption potential, reproductive toxicity, and neurodevelopmental effects similar to those of BPA. Their widespread presence, environmental persistence, and hidden health hazards expose critical weaknesses in the current “like-for-like substitution” regulatory approach. To address this challenge, it is imperative to establish a safer assessment framework that integrates early endocrine disruption screening with exposome-based evaluation. Shifting from “hazard substitution” to a “functional safe-by-design” strategy is critical to circumvent the pitfalls of structural-analogue substitution, protect public health, and support sustainable development.
The effects of low-level exposure to metal mixtures on oxidative stress (OS) in adolescents are poorly understood. We examined the associations of blood concentrations of arsenic (As), cadmium (Cd), lead (Pb), and mercury (Hg) with urinary levels of F2-isoprostane (F2-IsoP) and 8-hydroxy-2’-deoxyguanosine (8-OHdG). Data for this cross-sectional study were drawn from the Salud Ambiental Montevideo cohort, which originally enrolled children at ages 6-8 years. In 2021-2023, participants - now aged 12.1 2.1 years - provided venous blood and spot urine samples. Metals were quantified in blood via Inductively Coupled Plasma-Tandem Mass Spectrometry (ICP-MS/MS), while urinary OS markers were measured using competitive enzyme immunoassay (F2-IsoP) and LC-MS (8-OHdG). Associations between metals, considered individually and as a mixture, and each OS marker were evaluated using multivariable linear regression and Bayesian Kernel Machine Regression, respectively. Of the 430 adolescents (49.3% male) who attended a study visit, 361 were included in the complete-case sample. Median blood concentrations were As 0.30 µg/L, Cd 0.06 µg/L, Hg 0.22 µg/L, and Pb 1.17 µg/dL. Correlations among metals were generally low. We observed no associations between individual metals and OS biomarkers, and no evidence of interactions among metals when modeled as a mixture. F2-IsoP concentrations decreased slightly with increasing quantiles of the metal mixture, but the effect size was minimal. The metal mixture was unrelated to