Due to new European legislation, products entering the waste stream containing some perfluoro alkyl substances (PFAS) are subject to “low persistent organic pollutant concentration limits”. Concentrations of restricted PFAS must be below this limit for them to be legally recycled or disposed of. A rapid extraction and clean-up method was developed for the determination of 21 PFAS in various polymers used in soft furnishings and upholstery. The optimised method used vortexing and ultrasonication in methanol (0.1% NH₄OH), followed by a dilution and syringe filter clean-up step. PFAS were subsequently determined via UPLC-TripleTOF/MS. Good recoveries (80–120%) of target analytes were obtained with tall and narrow chromatogram peaks. The method was validated using control matrix samples spiked with target analytes. Repeated measurements of concentrations of target compounds showed good agreement with the spiked concentrations demonstrating good accuracy and precision. The resultant extracts provided low noise levels resulting in low limits of quantification ranging from 0.1 to 0.4 mg/kg. The developed method was applied successfully to real consumer products and it provided various advantages over traditional methods, including a substantially reduced analysis time, consumables and solvent consumption, and a high sample throughput which is critical to comply with implemented and proposed legislation.

Polybrominated diphenyl ethers (PBDEs) and hexabromocyclododecane (HBCDD) were used intensively as flame retardants, worldwide. They have been detected in human serum samples and PBDEs have been found to be elevated in young children. Commercial Penta- and Octa-PBDE mixtures were banned in Australia in 2005, while HBCDD was banned worldwide in 2013. We investigated PBDE and HBCDD concentrations in serum collected from young children. We also investigated temporal trends in PBDE concentration 10 years after their Australian ban. Surplus human blood serum samples were collected through a pathology clinic (n = 800), in 2014/15, stratified by age (0-6, 6-12, 12-18, 18-24, 24-30, 30-36, 36-42, 42-48, 48-54 and 54-60 months) and sex and pooled for analysis of PBDEs (BDEs -28, -47, -99, -100, -153, -154, -183) and HBCDD. In 2014/15, the geometric mean concentration of the sum of all PBDEs measured (ΣPBDEs) was 4.5 ng/g lipid (median: 4.6 ng/g lipid, range: 0.88-26 ng/g lipid). A positive association between BDE-47 concentration and age was observed (R = 0.41, p = 0.008), however there were no trends between other PBDE congeners or HBCDD and age. There were no significant differences between genders for PBDEs (t-test, p = 0.802) or HBCDD (t-test, p = 0.740).The highest concentrations observed were in pools from the females 30-36 month (26 ng/g lipid) and Males 6-12 month (21 ng/g lipid) categories. BDEs -47 and -99 were the predominant congeners with a combined average contribution of 75% of ΣPBDEs. PBDEs showed a significant reduction in children aged 0-4 years over an eight year period. In 2014/15, the mean (range) concentration of BDE-47 is 2.8 (0.23 to 11) ng/g lipid compared to pools in 2006/07 at 19 (3-55) ng/g lipid (p < 0.0001) and for BDE-153 is 0.73 (<0.1 = -2.9) ng/g lipid compared to pools in 2006/07 at 4.7 (2-10) ng/g lipid (p < 0.0001). HBCDD concentrations were lower than PBDEs with a mean concentration of 0.45 ng/g lipid. There were no temporal trends observed for HBCDD when compared to samples collected in 2012. The dominant stereoisomer was α-HBCDD (mean = 0.38 ng/g lipid) with an average contribution of 65% towards ΣHBCDD. Levels of PBDEs in young Australian children have significantly decreased since the bans of commercial Penta- and Octa-BDE in 2005. There has been no observed decrease in HBCDD levels in Australian children since its ban in 2012.

In human population studies, organochlorine pesticides (OCPs) have been linked to vitamin D deficiency. Therefore, this study examined the association between OCPs, vitamin D₃ (cholecalciferol, 25(OH)D₃), and the active metabolite 1,25-dihydrovitamin D₃ (1,25(OH)₂D₃) in a cohort of non-obese women. The serum samples of 58 female participants (age—31.9 ± 4.6 years; body mass index (BMI)—25.7 ± 3.7 kg/m²) were screened for 10 indicator OCPs. 25(OH)D₃ and 1,25(OH)₂D₃ levels were determined via isotope dilution liquid chromatography tandem mass spectrometry. In this cohort, the 25(OH)D₃ and 1,25(OH)₂D₃ levels were 22.9 ± 11.2 ng/mL and 0.05 ± 0.02 ng/mL, respectively, with 28 participants classified as 25(OH)D₃-deficient (<50 nmol/L). In the study cohort, no correlations were found between individual or total OCPs (ƩOCPs) and 25(OH)D₃. p,p′-dichlorodiphenyldichloroethylene (DDE) and ƩOCPs correlated positively with 1,25(OH)₂D₃, with the latter being negatively correlated with estimated glomerular filtration rate (eGFR). In women with sufficient 25(OH)D₃ levels, p,p′-dichlorodiphenyltrichloroethan (DDT) was positively correlated with 1,25(OH)₂D₃, whilst in the deficient group, hexachlorobenzene (HCB) and p,p′-(DDE) were positively correlated with 1,25(OH)₂D₃, β-Hexachlorocyclohexane (HCH) was positively correlated with 25(OH)D₃, and none of the OCPs were associated with measures of renal function. Overall, OCPs and ƩOCPs were not associated with 25(OH)D₃, suggesting that they are unrelated to vitamin D deficiency, but p,p′-DDE and ƩOCPs correlated positively with active 1,25(OH)₂D₃, while ƩOCPs correlated negatively with eGFR, suggesting a possible renal effect. Analysis of vitamin D deficiency revealed an association between β-HCH and 25(OH)D₃, and between HCB and p,p′-DDE and 1,25(OH)₂D₃, suggesting that OCP effects may be enhanced in cases of vitamin D deficiency.