Uptake of 19 per- and polyfluoroalkyl substances (PFAS), including C3–C14 perfluoroalkyl carboxylic acids (PFCAs), C4, C6, and C8 perfluoroalkyl sulfonates (PFSAs), and four emerging PFAS, was investigated in two mushroom species (Agaricus bisporus and Agaricus subrufescens) cultivated in a biogas digestate-based substrate. Accumulation of PFAS in mushrooms was low and strongly chain-length dependent. Among the different PFCAs, bioaccumulation factors (log BAFs) decreased from a maximum of −0.3 for perfluoropropanoic acid (PFPrA; C3) to a minimum of −3.1 for perfluoroheptanoate (PFHpA; C7), with only minor changes from PFHpA to perfluorotridecanoate (PFTriDA; C13). For PFSAs, log BAFs decreased from perfluorobutane sulfonate (PFBS; −2.2) to perfluorooctane sulfonate (PFOS; −3.1) while mushroom uptake was not observed for the alternatives 3H-perfluoro-3-[(3-methoxy-propoxy)propanoic acid] (ADONA) and two chlorinated polyfluoro ether sulfonates. To the best of our knowledge, this is the first investigation of the uptake of emerging and ultra-short chain PFAS in mushrooms, and generally the results indicate very low accumulation of PFAS.

Per: and polyfluoroalkyl substances (PFAS) may affect adolescent health, yet factors related to PFAS concentrations in serum are poorly understood. We studied demographic, life-style and physiological determinants of serum PFAS concentrations in Swedish adolescents from a nation-wide survey, Riksmaten Adolescents 2016–17 (RMA, age 10–21 years, n = 1098). Serum samples were analyzed for 42 PFAS, using liquid chromatography-tandem mass spectrometry. The cumulative probability model was used to estimate associations between serum PFAS and determinants, using ordinal logistic regression. Legacy linear (lin-) perfluorooctanoic acid (PFOA), perfluorononaoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnDA), lin-perfluorohexanesulfonic acid (PFHxS) and lin-/branched (br-) perfluorooctanesulfonic acid (PFOS) were quantifiable in ≥70% of the samples. The emerging PFAS 9-chlorohexanedecafluoro-3-oxanone-1-sulfonic acid (9Cl-PF3ONS) was quantified in 5.4% of the samples, suggesting initiation of long-range transport far from production sites. Median concentrations of all legacy PFAS were <2 ng/g serum, with a few participants having very high (>100 ng/g serum) lin-PFHxS and lin-/br-PFOS concentrations due to previous high exposure from PFAS-contaminated drinking water. Legacy PFAS exposure was strongly associated with birth country of the participants and their mothers. 2-fold higher estimated adjusted mean (EAM) concentrations were seen among high income country participants with mothers from high income countries than among low/lower-middle income country participants with mothers from the same category. Menstruating females had lower br-PFOS EAM concentrations than those who were not. Iron status (plasma ferritin) among females may be a marker of intensity of menstrual bleeding, but it was not significantly associated with legacy PFAS concentrations among females. Further studies are needed to determine how physiological changes occurring around menstruation affect the toxicokinetics of PFAS in females. In conclusion, PFAS are pollutants of the industrialized world and some of the identified determinants may be overlooked confounders/effect modifiers that should be included in future PFAS/health studies among adolescents.

Food is an important source of perfluoroalkyl acid (PFAA) exposure for the general adult population, but few data exist for adolescents. Healthy food habits established during adolescence may positively influence health later in life. Associations between serum PFAA concentrations and a healthy eating index (SHEIA15), as well as a diet diversity score (RADDS), were determined in a nationally representative adolescent population from Sweden (Riksmaten Adolescents 2016–2017, RMA). Using consumption data from food registrations and frequency questionnaires, we additionally analyzed associations with commonly consumed food groups. Associations were analyzed by fitting a cumulative probability model using ordinal regression. Among the seven PFAAs detected in ≥70% of the 1098 participants (age 10–21 years), median concentrations ranged from <1 ng/g serum of perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perflurorundecanoic acid (PFUnDA), linear (lin-) perfluorohexanesulfonic acid (PFHxS) and branched (br-) perfluorooctanesulfonic acid (PFOS) to 1–2 ng/g serum of lin-perfluorooctanoic acid (PFOA) and lin-PFOS. PFNA, PFDA, PFUnDA and lin-PFOS concentrations were positively associated with both SHEIA15 and RADDS, a finding most likely driven by higher consumption of seafood. PFDA, PFUnDA and lin-PFOS concentrations were positively related to commonly consumed fish/shellfish groups, such as lean marine fish and shellfish. Inverse associations between PFAA concentrations and dairy consumption suggest an underlying factor behind dairy consumption that similarly affects adolescent exposure to the different PFAAs. Isomeric differences in dietary exposure between lin-PFOS and br-PFOS were suggested, as br-PFOS concentrations, in contrast to lin-PFOS, were not associated with SHEIA15, RADDS and consumption of different food groups. We conclude that Swedish adolescents, adhering to a diverse and healthy diet, appears to be more highly exposed to legacy PFAAs than those eating less healthy. Additional research is necessary for a better understanding of the health implications of healthy eating from a PFAA exposure perspective.

Temporal trends from 1981 to 2013 of 28 per- and polyfluoroalkyl substances (PFASs) were investigated in liver tissue of cod (Gadus morhua) sampled near southeast Gotland, in the Baltic Sea. A total of 10 PFASs were detected, with n-ary sumation (28)PFAS geometric mean concentrations ranging from 6.03 to 23.9 ng/g ww. Perfluorooctane sulfonate (PFOS) was the predominant PFAS, which increased at a rate of 3.4% per year. Most long-chain perfluoroalkyl carboxylic acids increased at rates of 3.9 to 7.3% per year except for perfluorooctanoate (PFOA), which did not change significantly over time. The perfluoroalkyl acid precursors perfluorooctane sulfonamide (FOSA) and 6:2 fluorotelomer sulfonic acid were detected, of which the former (FOSA) declined at a rate of -4.4% per year, possibly reflecting its phase-out starting in 2000. An alternate time trend analysis from 2000 to 2013 produced slightly different results, with most compounds increasing at slower rates compared to the entire study period. An exception was perfluorohexane sulfonate (PFHxS), increasing at a faster rate of 3.7% measured from 2000 on, compared to the 3.0% per year measured starting from 1981. Analysis of the total fluorine content of the samples revealed large amounts of unidentified fluorine; however, its composition (organic or inorganic) remains unclear. Significant negative correlations were found between concentrations of individual PFASs (with the exception of PFOS) and liver somatic index. In addition, body length was negatively correlated with PFOA and perfluorononanoate, but positively correlated with perfluorododecanoate (PFDoDA) and FOSA. Additional studies on endocrine, immunological, and metabolic effects of PFAS in marine fish are essential to assess the environmental risk of these substances. Environ Toxicol Chem 2020;39:300-309. 

A combined method for quantitative analysis, along with suspect and non-target screening of per- and polyfluoroalkyl substances (PFAS) was developed using ultra-high pressure liquid chromatography-ultra-high resolution (Orbitrap) mass spectrometry. The method was applied together with measurements of total- and extractable organofluorine (TF and EOF, respectively), to pooled serum samples from 1996–2017 from first-time mothers living in the county of Uppsala, Sweden, some of which (i.e. 148 of 472 women sampled 1996–2012) were exposed to drinking water contaminated with perfluorohexane sulfonate (PFHxS) and other PFAS until mid-2012. Declining trends were observed for all target PFAS as well as TF, with homologue-dependent differences in year of onset of decline. Only 33% of samples displayed detectable EOF, and amongst these samples the percentage of EOF explained by target PFAS declined significantly (−3.5% per year) over the entire study period. This finding corroborates prior observations in Germany after the year 2000, and may reflect increasing exposure to novel PFAS which have not yet been identified. Suspect screening revealed the presence of perfluoro-4-ethylcyclohexanesulfonate (PFECHS), which displayed declining trends since the year 2000. Non-target time trend screening revealed 3 unidentified features with time trends matching PFHxS. These features require further investigation, but may represent contaminants which co-occurred with PFHxS in the contaminated drinking water.

Standard ecotoxicological testing of microplastic does not provide insight into the influence that environmental weathering by, e.g., UV light has on related effects. In this study, we leached chemicals from plastic into artificial seawater during simulated UV-induced weathering. We tested largely additive-free preproduction polyethylene, polyethylene terephthalate, polypropylene, and polystyrene and two types of plastic obtained from electronic equipment as positive controls. Leachates were concentrated by solid-phase extraction and dosed into cell-based bioassays that cover (i) cytotoxicity; (ii) activation of metabolic enzymes via binding to the arylhydrocarbon receptor (AhR) and the peroxisome proliferator-activated receptor (PPAR gamma); (iii) specific, receptor-mediated effects (estrogenicity, ER alpha); and (iv) adaptive response to oxidative stress (AREc32). LC-HRMS analysis was used to identify possible chain-scission products of polymer degradation, which were then tested in AREc32 and PPAR gamma. Explicit activation of all assays by the positive controls provided proof-of-concept of the experimental setup to demonstrate effects of chemicals liberated during weathering. All plastic leachates activated the oxidative stress response, in most cases with increased induction by UV-treated samples compared to dark controls. For PPAR gamma, polyethylene-specific effects were partially explained by the detected dicarboxylic acids. Since the preproduction plastic showed low effects often in the range of the blanks future studies should investigate implications of weathering on end consumer products containing additives.

We investigated associations between serum perfluoroalkyl acid (PFAA) concentrations in children aged 4, 8, and 12 years (sampled in 2008-2015; n = 57, 55, and 119, respectively) and exposure via placental transfer, breastfeeding, and ingestion of PFAA-contaminated drinking water. Sampling took place in Uppsala County, Sweden, where the drinking water has been historically contaminated with perfluorobutanesulfonate (PFBS), perfluorohexanesulfonate (PFHxS), perfluorooctanesulfonate (PFOS), perfluoroheptanoate (PFHpA), and perfluorooctanoate (PFOA). PFOS showed the highest median concentrations in serum (3.8-5.3 ng g(-1) serum), followed by PFHxS (1.6-5.0 ng g(-1) serum), PFOA (2.0-2.5 ng g(-1) serum), and perfluorononanoate (PFNA) (0.59-0.69 ng g(-1) serum) in children. Including all children, serum PFOA, PFHxS, and PFOS concentrations (adjusted mean), respectively, per unit (ng g(-1) serum) of increase in the maternal serum level (at delivery), the associations being strongest for 4 year-old children. PFHxS and PFOS significantly increased 3.9 and 3.8%, respectively, per month of nursing, with the highest increase for 4 year-olds. PFOA, PFBS, PFHxS, and PFOS increased 1.2, 207, 7.4, and 0.93%, respectively, per month of cumulative drinking water exposure. Early life exposure to PFOA, PFHxS, and PFOS is an important determinant of serum concentrations in children, with the strongest influence on younger ages. Drinking water with low to moderate PFBS, PFHxS, PFOS, and PFOA contamination is an important source of exposure for children with background exposure from other sources.

Per- and polyfluoroalkyl substances (PFASs) represent a class of more than 4000 compounds. Their large number and structural diversity pose a considerable challenge to analytical chemists. Measurement of total fluorine in environmental samples and consumer products is therefore critical for rapidly screening for PFASs and for assessing the fraction of unexplained fluorine(i.e., fluorine mass balance). Here we compare three emerging analytical techniques for total fluorine determination: combustion ion chromatography (CIC), particle-induced gamma-ray emission spectroscopy (PIGE), and instrumental neutron activation analysis (INAA). Application of each method to a certified reference material (CRM), spiked filters, and representative food packaging samples revealed good accuracy and precision. INAA and PIGE had the advantage of being nondestructive, while CIC displayed the lowest detection limits. Inconsistencies between the methods arose due to the high aluminum content in the CRM, which precluded its analysis by INAA, and sample heterogeneity (i.e., coating on the surface of the material), which resulted in higher values from the surface measurement technique PIGE compared to the values from the bulk volume techniques INAA and CIC. Comparing CIC-based extractable organic fluorine to target PFAS measurements of food packaging samples by liquid chromatography-tandem mass spectrometry revealed large amounts of unidentified organic fluorine not captured by compound-specific analysis.

Buoyant plastic in the marine environment is exposed to sunlight, oxidants, and physical stress, which may lead to degradation of the plastic polymer and the release of compounds that are potentially hazardous. We report the development of a laboratory protocol that simulates the exposure of plastic floating in the marine environment to ultraviolet light (UV) and nontarget analysis to identify degradation products of plastic polymers in water. Plastic pellets [polyethylene, polypropylene, polystyrene, and poly(ethylene terephthalate)] suspended in water were exposed to a UV light source for 5 days. Organic chemicals in the water were concentrated by solid phase extraction and then analyzed by ultra-high-performance liquid chromatography coupled to high-resolution mass spectrometry using a nontarget approach with a C18 LC column coupled to a Q Exactive Orbitrap HF mass spectrometer. We designed a data analysis scheme to identify chemicals that are likely chain scission products from degradation of the plastic polymers. For all four polymers, we found homologous series of low-molecular weight polymer fragments with oxidized end groups. In total, we tentatively identified 22 degradation products, which are mainly dicarboxylic acids.

Little is known about factors influencing infant perfluorinated alkyl acid (PFAA) concentrations. Associations between serum PFAA concentrations in 2-4-month-old infants (n = 101) and determinants were investigated by multiple linear regression and general linear model analysis. In exclusively breastfed infants, maternal serum PFAA concentrations 3 weeks after delivery explained 13% (perfluoroundecanoic acid, PFUnDA) to 73% (perfluorohexanesulfonate, PFHxS) of infant PFAA concentration variation. Median infant/maternal ratios decreased with increasing PFAA carbon chain length from 2.8 for perfluoroheptanoic acid and perfluorooctanoic acid (PFOA) to 0.53 for PFUnDA and from 1.2 to 0.69 for PFHxS and perfluorooctanesulfonate (PFOS). Infant PFOA, perfluorononanoic acid (PFNA), and PFOS levels increased 0.7-1.2% per day of gestational age. Bottle-fed infants had mean concentrations of PFAAs 2 times lower than and a mean percentage of branched (%br) PFOS isomers 1.3 times higher than those of exclusively breast-fed infants. PFOA, PFNA, and PFHxS levels increased 8-11% per week of exclusive breast-feeding. Infants living in an area receiving PFAA-contaminated drinking water had 3-fold higher mean perfluorobutanesulfonate (PFBS) and PFHxS concentrations and higher mean %br PFHxS. Prenatal PFAA exposure and postnatal PFAA exposure significantly contribute to infant PFAA serum concentrations, depending on PFAA carbon chain length. Moderately PFBS- and PFHxS-contaminated drinking water is an important indirect exposure source.