Perfluorinated alkyl acids in the serum and follicular fluid of UK women with and without polycystic ovarian syndrome undergoing fertility treatment and associations with hormonal and metabolic parameters.

Women with polycystic ovarian syndrome (PCOS) undergoing treatment for infertility could be a sensitive subpopulation for endocrine effects of exposure to perfluorinated alkyl acids (PFAAs), persistent organic pollutants with potential endocrine activity. Women with, PCOS (n = 30) and age- and BMI-matched controls (n = 29) were recruited from a UK fertility clinic in 2015. Paired serum and follicular fluid samples were collected and analysed for 13 PFAAs. Sex steroid and thyroid hormones, and metabolic markers were measured and assessed for associations with serum PFAAs. Four PFAAs were detected in all serum and follicular fluid samples and concentrations in the two matrices were highly correlated (R2 > 0.95): perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), perfluorohexane sulfonate (PFHxS), and perfluorononanoic acid (PFNA). Serum PFOS was positively associated with age (1 ng/mL per yr, p < 0.05) and was higher in PCOS cases than controls (geometric mean [GM] 3.9 vs. 3.1 ng/mL, p < 0.05) and in women with irregular vs. regular menstrual cycles (GM 3.9 vs. 3.0 ng/mL, p = 0.01). After adjustment for confounders, serum testosterone was significantly associated with PFOA, PFHxS, PFNA, and the molar sum of the four frequently detected serum PFAAs (approximately 50 percent increase per ln-unit) among controls but not PCOS cases. HbA1c in PCOS cases was inversely associated with serum PFOA, PFHxs, and sum of PFAAs (2-3 mmol/mol per ln-unit). In controls, fasting glucose was positively associated with serum PFOA and sum of PFAAs (0.25 nmol/L per ln-unit increase in PFAAs). Few other associations were observed. The analyses and findings here should be considered exploratory in light of the relatively small sample sizes and large number of statistical comparisons conducted. However, the data do not suggest increased sensitivity to potential endocrine effects of PFAAs in PCOS patients.

Emerging contaminants (pharmaceuticals, personal care products, a food additive and pesticides) in waters of Sydney estuary, Australia.

The current investigation of marine water from 30 sites adjacent to stormwater outlets across the entire Sydney estuary is the first such research in Australia. The number of analytes detected were: 8/59 pharmaceutical compounds (codeine, paracetamol, tramadol, venlafaxine, propranolol, fluoxetine, iopromide and carbamazepine), 7/38 of the pesticides (2,4-dichlorophenoxyacetic acid (2,4-D), 3,4-dichloroaniline, carbaryl, diuron, 2-methyl-4-chlorophenoxyacetic acid (MCPA), mecoprop and simazine) and 0/3 of the personal care products (PCPs) analysed. An artificial sweetener (acesulfame) was detected, however none of the nine antibiotics analysed were identified. Sewage water is not discharged to this estuary, except infrequently as overflow during high-precipitation events. The presence of acesulfame (a recognised marker of domestic wastewater) and pharmaceuticals in water from all parts of the estuary after a dry period, suggests sewage water is leaking into the stormwater system in this catchment. The pesticides are applied to the environment and were discharged via stormwater to the estuary.

Studies into the formation of PBDEs and PBDD/Fs in the iron ore sintering process.

Polybrominated diphenyl ethers (PBDEs) and polybrominated dibenzo-p-dioxins and furans (PBDD/Fs) were detected in stack emissions from UK sinter plants. The sum of 36 PBDE congeners was measured at a mean concentration of 295 ng/N m(3) with a standard deviation of 96 ng/N m(3). The mean PBDD/F concentrations were 0.14 ng WHO-TEQ/m(3) (range=0.03-0.39). PBDD/F emission concentrations were approximately ten times lower than their PCDD/F homologues. To understand the possible formation mechanisms of brominated organic species in iron ore sintering, both full-scale and laboratory experiments using an experimental sintering process were carried out. A complete PBDE mass balance was undertaken for a full scale sinter plant showing that PBDEs were already present in the raw materials such as iron ores and coke breeze and that a significant proportion of the PBDE inputs were actually destroyed during the process. A number of controlled experiments were conducted using a laboratory-scale sintering apparatus (sinter pot). These were designed to investigate: (a) mass balance of PBDEs during sintering, (b) the relationship between the availability of bromide (as KBr) and PBDE emissions, and (c) the influence of the availability of both bromide and PBDEs on PBDD/F formation. As observed in the full scale plant, the PBDEs already present in the raw materials were mostly destroyed during the process (79-96%) for all sinter pot experiments. Increasing amounts of KBr in the raw sinter mix did not result in a significant increase in PBDE formation suggesting that there was no PBDE formation in sintering via de novo synthesis. No relationship was observed between PBDE inputs and PBDD/F emissions indicating that PBDEs did not act as precursors for PBDD/Fs formation. Finally, PBDD/F formation was enhanced substantially with increasing amounts of KBr suggesting that their formation mechanism was similar to that of PCDD/Fs via de novo synthesis.