Per- and polyfluoroalkyl substances (PFASs) and toxic metals co-occur in the same people and have each been linked to cardiovascular and all-cause mortality, yet their joint contribution is poorly characterized. We examined PFOA, PFOS, lead, cadmium, and mercury jointly in NHANES 2011–2018 linked to 2019 mortality files, 3982 adults, 19,090 person-years, 236 all-cause, and 60 heart-disease deaths, using Cox models and Bayesian kernel machine regression. Heart disease was the primary cause-specific endpoint, the only category defined consistently across all four cycles. For a one-interquartile-range increase in all five exposures together, the joint hazard ratio was 0.89 (0.75, 1.06) for all-cause mortality, 1.00 (0.73, 1.37) for heart disease, and 0.94 (0.70, 1.28) for cardiovascular mortality including stroke; full socioeconomic adjustment gave 0.86 (0.69, 1.06). Individually, cadmium was the one component consistently associated with higher all-cause mortality, 1.12 (1.05, 1.20), retained across every specification examined. Mercury ran in the opposite direction, 0.91 (0.82, 1.00), consistent with blood mercury marking fish consumption and the dietary patterns accompanying it rather than toxicity; estimates below one are therefore not read as evidence of protection. PFOA, PFOS, and lead were null. The mixture model agreed with the regressions, the contrast between the joint 75th and 25th percentile profiles being −0.028 (−0.132, +0.047). How time at risk was handled mattered more than any modeling choice: with covariates and exposure contrast held fixed, a binary mortality indicator gave an odds ratio of 1.10 (0.93, 1.31), whereas a Poisson model with a log person-time offset gave 0.90 (0.75, 1.07), Cox regression 0.89 (0.75, 1.06), and restriction to a common 60-month window 0.74 (0.58, 0.95). Longer-observed participants were also more exposed, with the binary estimate potentially confounded by time at risk. Cadmium is therefore the component warranting priority in mixture surveillance, and pooled-cycle NHANES analyses should model time at risk directly.
Organophosphate flame retardants (OPFRs) are widely detected in terrestrial ecosystems. Evaluating their soil–water transfer remains challenging because initial sorption loading does not necessarily dictate long-term retention. Here, the compound-specific sorption and desorption behaviors of 10 structurally diverse OPFRs were systematically investigated in a surface soil using batch kinetic and isotherm experiments. Adsorption proceeded rapidly within the first 4 h and approached equilibrium by 24 h. Single-solute kinetic desorption revealed strong compound-specific divergence: aromatic OPFRs exhibited near-complete solid-phase immobilization (>99.5% operational retention), whereas chlorinated and ether-linked OPFRs displayed substantial secondary release, desorbing 57.3–79.5% of their pre-sorbed mass. Equilibrium isotherms indicated stronger soil affinity for aromatic OPFRs than for more hydrophilic analogues. This contrast highlights a competitive site-blocking and matrix occlusion mechanism, wherein hydrophobic aromatic species occupy high-energy sites and pore throats, physically restricting the outward diffusion of co-sorbed compounds. Freundlich hysteresis indices (0.830–0.905) reflected progressive occupation of high-energy sorption sites. The results indicate that initial solid-phase loading and short-term release potential should be evaluated separately when comparing OPFRs behavior in soil. These insights provide a crucial foundation for accurately modeling the environmental fate and ecological risks of emerging OPFRs in soil–water systems.
Nanoplastics are emerging aquatic contaminants whose cellular effects induced in freshwater fish remain incompletely understood. In this study, RTgill-W1 epithelial cells of rainbow trout (Oncorhynchus mykiss) gills were incubated with polystyrene nanoplastics (PS-NPLs) at concentrations of 1–500 µg/mL for 24 and 72 h. Cytotoxicity was evaluated by Live/Dead staining and lactate dehydrogenase (LDH) release, while cytoskeletal alterations were assessed by F-actin staining. Oxidative stress-associated responses were investigated by measuring reduced glutathione (GSH), malondialdehyde (MDA), and the expressions of Hsp60 and Hsp70 proteins. PS-NPLs induced cellular responses that varied with concentration and exposure duration, with the most pronounced cytotoxic effects observed at 500 µg/mL. At this concentration, reduced cell density, altered cellular morphology, changes in F-actin organization, and increased LDH release were observed, particularly after 72 h. GSH and MDA levels increased relative to controls, with the strongest responses occurring after 24 h at 500 µg/mL and attenuating after prolonged exposure. Hsp60 and Hsp70 protein expression was elevated after 24 h, whereas after 72 h, Hsp70 expression was no longer significantly different from the control at either concentration, and Hsp60 expression remained elevated at 50 µg/mL but was not significantly different from the control at 500 µg/mL. These findings indicate that PS-NPLs exhibit dynamic responses in fish gill epithelial cells, involving membrane damage, cytoskeletal remodelling, lipid peroxidation, antioxidant responses, and modulation of stress-related proteins. The results support the use of RTgill-W1 cells as a mechanistically informative in vitro model for investigating cellular responses to nanoplastic exposure in fish.
Weathered petroleum contamination in desert soils resists conventional remediation because aged hydrocarbons are strongly sorbed under arid conditions. A hybrid ultrasonic–mechanical soil-washing system with a biodegradable saponin biosurfactant was evaluated on crude oil-contaminated sand from the Kuwaiti desert. Operating conditions were screened one factor at a time, and mechanical, ultrasonic and combined washing compared over cycles (n = 6). Total petroleum hydrocarbons (TPH) were determined gravimetrically, as an operationally defined measure of solvent-extractable material. Under the selected conditions (50 °C, 1000 rpm, 20 min), combined washing removed 89.9 ± 0.9% of TPH after three cycles, against 75.5 ± 1.5% and 72.3 ± 1.8% for mechanical and ultrasonic washing alone. A fourth cycle raised cumulative removal to 97.0 ± 0.1%, leaving 9985 ± 325 mg/kg. This places the soil at the Kuwaiti action level of 10,000 mg/kg rather than reliably below it: three of six replicates exceeded that value, and all six fell below only after a fifth cycle. Electron microscopy and turbidity indicated rougher surfaces, less hydrocarbon coating and greater disaggregation. The proposed cavitation-based mechanisms are inferred rather than demonstrated; the process transfers hydrocarbons into the wash effluent rather than degrading them, so effluent management is integral to field application.
This cross-sectional, hypothesis-generating analysis examined six blood metal and volatile organic compound (VOC) biomarkers in relation to self-reported lifetime cancer history among 136 adults whose longest-held job was in construction in the 2009–2010 National Health and Nutrition Examination Survey (NHANES). The 16 participants reporting cancer contributed 17 cancer reports spanning 10 reported categories; among the 10 cases with an examination age below 80 years and a valid reported diagnosis age, the age-based interval from first reported diagnosis to biomarker measurement had a median of 17 years (range 2–25). Thus, recent blood measurements cannot represent exposure at diagnosis. Hierarchical Bayesian kernel machine regression (BKMR) was fitted to 20 multiply imputed data sets. VOC and metal group posterior inclusion probabilities (PIPs) were 0.586 and 0.474; these are model-dependent selection summaries, not effects or evidence of an occupational source. All primary overall-mixture, single-biomarker, and interaction contrasts had 95% credible intervals spanning zero. The existing model sensitivities included reduced covariates and a joint recode of structurally skipped smoking responses and unobserved alcohol values; in that joint recode, two overall contrasts excluded zero in the inverse direction by a narrow margin. Public NHANES smoking and cotinine files were linked for additional unweighted descriptive checks. Serum cotinine correlated with benzene (Spearman ρ = 0.75), consistent with a substantial recent tobacco-related component but not source attribution. With 16 heterogeneous cases, a time mismatch, unweighted analyses, and an originally imputed smoking skip pattern, the models cannot establish cancer associations or rank causal agents. The results describe this sampled group and remain exploratory.
