Chronic ethylbenzene exposures and attendant potential health risks for United States children and prospective parents were first evaluated under the United States Environmental Protection Agency’s Voluntary Children’s Chemical Evaluation Program. Using updated data and methods, a 2015 reevaluation observed declines in ethylbenzene releases and concentrations in ambient and indoor air. Both assessments identified inhalation as the dominant exposure route and smoking as the greatest contributor, with dietary intake much lower. Children’s exposure concentrations were similar to that of adults, but their intakes were higher. Neither breastfeeding nor toy mouthing was a significant source. This report updates the previous assessments, summarizing current ethylbenzene concentrations in air and foods, exposures during the use of household and consumer products, nationally representative biomonitoring data, including expanded demographic groups, and a new survey of worker exposures in styrene production facilities. General population ethylbenzene exposures appear to have declined for all age groups. The ethylbenzene/styrene chain of commerce contributes an estimated 0.1% to total air emissions and 7%-12% to dietary concentrations. Total estimated ethylbenzene intakes are consistent with biomonitoring data. Lactational transfer is not a significant exposure pathway for breastfed infants. Production workers’ exposure is well below occupational guidelines. Updated exposure estimates for each pathway suitable for potential health risk assessment are proposed.

The global push towards a circular economy (CE) has led to increasing efforts to improve resource utilization efficiency, including plastics recycling. However, the presence of additives, especially those that are toxic, complicates plastics recycling in several ways. Without sufficient controls, the spread of hazardous additives via recycling activities represents a significant public health challenge, particularly among developing nations. This study demonstrates evidence of such uncontrolled recycling, based on an investigation of four household flexible PVC product groups available in Thailand. A versatile pyrolysis/thermal desorption gas chromatography-mass spectrometry (Py/TD-GC-MS) method was employed to simultaneously screen 18 target plasticizers in these products. Di-(2-ethylhexyl) phthalate (DEHP) and diisononyl phthalate (DINP) are the most frequently detected primary plasticizers. DEHP is dominant in vinyl boots, flooring sheets, and hoses, while DINP is dominant in cable sheaths, likely due to a spill-over effect from the EU Restriction of Hazardous Substances (RoHS) directive. Chlorinated paraffins (CPs) are secondary plasticizers that are also detected in most samples, except for boots. The other plasticizers detected include other ortho-phthalates and non-phthalates. These results provide insight into combinatory patterns of plasticizer ‘cocktails’, that comprise restricted, as-yet-unrestricted, and non-restricted plasticizers, embedded in the same individual samples, with a maximum of seven plasticizers found in a single cable sheath. These findings indicate the existence of potentially risky recycling practices that target embedded plasticizers to save cost, without due consideration of their inherent toxicity. Proper interventions are necessary to ensure that CE and chemical safety can be synergized.

Polycyclic aromatic hydrocarbons (PAHs) in sediment cores from Phayao Lake were investigated in terms of their concentration, distribution, and potential effects on the environment and human health. The concentration of Σ16PAHs ranged from 77.6 to 1251.1 ng g^-1. Additionally, low molecular weight PAHs (two or three fused aromatic rings) were dominant, indicating that the main source of PAHs is the incomplete combustion of organic sources. The toxic equivalent quantities (TEQs) of 16 PAHs varied from 2.67 to 155.09 ng g^-1, with an average of 38.29 ± 46.69 ng g^-1. Furthermore, the TEQs of 9 known carcinogenic PAHs averaged 20.77 ± 30.63 ng g^-1. B[a]P had the highest TEQ, followed by D[a,h]A and B[k]F, with values of 16.93 ± 25.49, 13.89 ± 15.37 and 2.12 ± 3.64, respectively. The RQ_(NCs) of ΣPAHs (RQ_ΣPAHs(NCs)) ranged from 1.65 × 10^-4 to 6.27 × 10^-1 with an average value of 1.18 × 10⁰ ± 1.52 × 10⁰. Moreover, RQ_(NCs) was less than 1 for individual PAHs, indicating a minor risk. However, RQ_(MPCs) was less than 1 for individual PAHs, indicating a moderate risk. The results showed a significant incremental lifetime cancer risk (ILCR) from sediment-bound PAHs with dermal absorption, followed by ingestion and inhalation, as the prevalent route of exposure. The measured ILCR values of all PAHs were less than 10^-6 for both adults and children, which were lower than the baseline value, indicating that each PAH poses a low risk of cancer to humans. This study provides information for control and preventive actions to limit future PAH pollution in Phayao Lake.

The health risks posed by atmospheric brominated flame retardants (BFRs) have been widely studied, but there remains a lack of clarity about exposure differences between clear days and haze days. We sampled the total suspended particle (TSP) and gaseous BFRs on clear days in summer, clear days in winter, and haze days in winter in Harbin, China, to investigate the variations in the concentrations and intakes (dermal and inhalation) in the different weather conditions. The concentrations of atmospheric BFRs were highest on haze days in winter (185 pg/m³), followed by clear days in summer (158 pg/m³), and clear days in winter (79.2 pg/m³), and these concentrations were significantly correlated with the concentrations of TSP. The human intake in the different weather conditions followed the pattern of the BFR concentrations, and the human intake of atmospheric BFRs was dominated by inhalation. A comparison of the BFR levels showed that the human intake of gaseous and particulate BFRs varied in the three weather conditions and that the inhalation intake, but not the dermal intake, was influenced under high concentrations of gaseous BFRs with low molecular weight.

The Minamata disease, first identified in Japan in the 1950s, is caused by severe methylmercury (MeHg) poisoning. To prevent the development of this disease, routine evaluation of MeHg levels in blood samples is crucial. The purpose of this research was to explore the use of derivatization and capillary gas chromatography-negative chemical ionization-mass spectrometry (GC-NCI-MS) for the quantitative detection of both organic and inorganic mercury in blood samples. Alkyl mercury in standard solutions was extracted as halide salts in toluene with hydrohalic acid. Fat contents in whole blood samples were removed by methyl isobutyl ketone and hexane using a cysteine/alkaline solution and then organic mercury was extracted as a bromide complex using toluene and cupper chloride solution. The linearity of the response ratio vs. concentration curves (R²) was 0.987 for methylmercury bromide and 0.990 for ethylmercury (EtHg) bromide, over the calibration range of 0.02 ng/mL to 20 ng/mL. The recovery of MeHg and EtHg was 67.1% and 49.3%, respectively. The concentrations of MeHg in whole blood samples determined using GC with an electron capture detector agreed with those determined using GC-NCI-MS, with a correlation coefficient of 0.923. The mean concentration of MeHg in a certified reference material (NMIJ CRM 7402-a) determined using GC-NCI-MS was 0.64 μg/g, comparable with the certified value of 0.58 μg/g. Our study demonstrates a simple and low-cost approach for analyzing mercury in biological samples, although further optimization is required given the relatively low recovery and the concern about the toxicity of methyl isobutyl ketone.