Per- and polyfluoroalkyl substances (PFASs) are highly persistent synthetic chemicals, some of which have been associated with cancer, developmental toxicity, immunotoxicity, and other health effects. PFASs in grease-resistant food packaging can leach into food and increase dietary exposure. We collected ~400 samples of food contact papers, paperboard containers, and beverage containers from fast food restaurants throughout the United States and measured total fluorine using particle-induced γ-ray emission (PIGE) spectroscopy. PIGE can rapidly and inexpensively measure total fluorine in solid-phase samples. We found that 46% of food contact papers and 20% of paperboard samples contained detectable fluorine (>16 nmol/cm2). Liquid chromatography/high-resolution mass spectrometry analysis of a subset of 20 samples found perfluorocarboxylates, perfluorosulfonates, and other known PFASs and/or unidentified polyfluorinated compounds (based on nontargeted analysis). The total peak area for PFASs was higher in 70% of samples (10 of 14) with a total fluorine level of >200 nmol/cm2 compared to six samples with a total fluorine level of <16 nmol/cm2. Samples with high total fluorine levels but low levels of measured PFASs may contain volatile PFASs, PFAS polymers, newer replacement PFASs, or other fluorinated compounds. The prevalence of fluorinated chemicals in fast food packaging demonstrates their potentially significant contribution to dietary PFAS exposure and environmental contamination during production and disposal.
Landfills are the final stage in the life cycle of many products containing per- and polyfluoroalkyl substances (PFASs) and their presence has been reported in landfill leachate. The concentrations of 70 PFASs in 95 samples of leachate were measured in a survey of U.S. landfills of varying climates and waste ages. National release of PFASs was estimated by coupling measured concentrations for the 19 PFASs where more than 50% of samples had quantifiable concentrations, with climate-specific estimates of annual leachate volumes. For 2013, the total volume of leachate generated in the U.S. was estimated to be 61.1 million m, with 79% of this volume coming from landfills in wet climates (>75 cm/yr precipitation) that contain 47% of U.S. solid waste. The mass of measured PFASs from U.S. landfill leachate to wastewater treatment plants was estimated to be between 563 and 638 kg for 2013. In the majority of landfill leachate samples, 5:3 fluorotelomer carboxylic acid (FTCA) was dominant and variations in concentrations with waste age affected total estimated mass. There were six PFASs that demonstrated significantly higher concentrations in leachate from younger waste compared to older waste and six PFAS demonstrated significant variation with climate.
A wide variety of consumer products that are treated with poly- and perfluoroalkyl substances (PFASs) and related formulations are disposed of in landfills. Landfill leachate has significant concentrations of PFASs and acts as secondary point sources to surface water. This study models how PFASs enter leachate using four laboratory-scale anaerobic bioreactors filled with municipal solid waste (MSW) and operated over 273 days. Duplicate reactors were monitored under live and abiotic conditions to evaluate influences attributable to biological activity. The biologically active reactors simulated the methanogenic conditions that develop in all landfills, producing ∼140 mL CH4/dry g refuse. The average total PFAS leaching measured in live reactors (16.7 nmol/kg dry refuse) was greater than the average for abiotic reactors (2.83 nmol/kg dry refuse), indicating biological processes were primarily responsible for leaching. The low-level leaching in the abiotic reactors was primarily due to PFCAs ≤C8 (2.48 nmol/kg dry refuse). Concentrations of known biodegradation intermediates, including methylperfluorobutane sulfonamide acetic acid and the n:2 and n:3 fluorotelomer carboxylates, increased steadily after the onset of methanogenesis, with the 5:3 fluorotelomer carboxylate becoming the single most concentrated PFAS observed in live reactors (9.53 nmol/kg dry refuse).
The compound BMAA (β-N-methylamino-L-alanine) has been postulated to play a significant role in four serious neurological human diseases: Amyotrophic Lateral Sclerosis/Parkinsonism Dementia Complex (ALS/PDC) found on Guam, and ALS, Parkinsonism, and dementia that occur globally. ALS/PDC with symptoms of all three diseases first came to the attention of the scientific community during and after World War II. It was initially associated with cycad flour used for food because BMAA is a product of symbiotic cycad root-dwelling cyanobacteria. Human consumption of flying foxes that fed on cycad seeds was later suggested as a source of BMAA on Guam and a cause of ALS/PDC. Subsequently, the hypothesis was expanded to include a causative role for BMAA in other neurodegenerative diseases including Alzheimer's disease (AD) through exposures attributed to proximity to freshwaters and/or consumption of seafood due to its purported production by most species of cyanobacteria. The hypothesis that BMAA is the critical factor in the genesis of these neurodegenerative diseases received considerable attention in the medical, scientific, and public arenas. This review examines the history of ALS/PDC and the BMAA-human disease hypotheses; similarities and differences between ALS/PDC and the other diseases with similar symptomologies; the relationship of ALS/PDC to other similar diseases, studies of BMAA-mediated effects in lab animals, inconsistencies and data gaps in the hypothesis; and other compounds and agents that were suggested as the cause of ALS/PDC on Guam. The review concludes that the hypothesis of a causal BMAA neurodegenerative disease relationship is not supported by existing data.
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