PFASs are linked to serious health and environmental concerns. Among their widespread applications, PFASs are known to be used in food packaging and directly contribute to human exposure. However, information about PFASs in food packaging is scattered. Therefore, we systematically map the evidence on PFASs detected in migrates and extracts of food contact materials and provide an overview of available hazard and biomonitoring data. Based on the FCCmigex database, 68 PFASs have been identified in various food contact materials, including paper, plastic, and coated metal, by targeted and untargeted analyses. 87% of these PFASs belong to the perfluorocarboxylic acids and fluorotelomer-based compounds. Trends in chain length demonstrate that long-chain perfluoroalkyl acids continue to be found, despite years of global efforts to reduce the use of these substances. We utilized ToxPi to illustrate that hazard data are available for only 57% of the PFASs that have been detected in food packaging. For those PFASs for which toxicity testing has been performed, many adverse outcomes have been reported. The data and knowledge gaps presented here support international proposals to restrict PFASs as a group, including their use in food contact materials, to protect human and environmental health.

Changes in resident microbiota may have wide-ranging effects on human health. We investigated whether early life microbial disruption alters neurodevelopment and behavior in larval zebrafish. Conventionally colonized, axenic, and axenic larvae colonized at 1 day post fertilization (dpf) were evaluated using a standard locomotor assay. At 10 dpf, axenic zebrafish exhibited hyperactivity compared to conventionalized and conventionally colonized controls. Impairment of host colonization using antibiotics also caused hyperactivity in conventionally colonized larvae. To determine whether there is a developmental requirement for microbial colonization, axenic embryos were serially colonized on 1, 3, 6, or 9 dpf and evaluated on 10 dpf. Normal activity levels were observed in axenic larvae colonized on 1–6 dpf, but not on 9 dpf. Colonization of axenic embryos at 1 dpf with individual bacterial species Aeromonas veronii or Vibrio cholerae was sufficient to block locomotor hyperactivity at 10 dpf. Exposure to heat-killed bacteria or microbe-associated molecular patterns pam3CSK4 or Poly(I:C) was not sufficient to block hyperactivity in axenic larvae. These data show that microbial colonization during early life is required for normal neurobehavioral development and support the concept that antibiotics and other environmental chemicals may exert neurobehavioral effects via disruption of host-associated microbial communities.

Host-associated microbiota can biotransform xenobiotics, mediate health effects of chemical exposure, and play important roles in early development. Bisphenol A (BPA) is a widespread environmental chemical that has been associated with adverse endocrine and neurodevelopmental effects, some of which may be mediated by microbiota. Growing public concern over the safety of BPA has resulted in its replacement with structurally similar alternatives. In this study, we evaluated whether BPA and BPA alternatives alter microbiota and modulate secondary adverse behavioral effects in zebrafish. Zebrafish were developmentally exposed to BPA, Bisphenol AF (BPAF), Bisphenol B (BPB), Bisphenol F (BPF), or Bisphenol S (BPS). At 10 days post fertilization (dpf), toxicity assessments were completed and 16S rRNA gene sequencing was performed to evaluate potential chemical-dependent shifts in microbial community structure and predicted function. A standard light/dark behavioral assay was used to assess locomotor activity. Based on developmental toxicity assessments at 10 dpf, a range of potencies was observed: BPAF > BPB > BPF ∼ BPA > BPS. Analysis of 16S rRNA gene sequencing data showed significant concentration-dependent disruption of microbial community structure and enrichment of putative microbial functions with exposure to BPS, BPA, or BPF, but not BPB or BPAF. Interestingly, microbial disruption was inversely related to host developmental toxicity and estrogenicity. Exposure to BP analogs did not cause behavioral effects at 10 dpf. Our findings indicate that some BP analogs disrupt host microbiota early in life and demonstrate novel chemical-microbiota interactions that may add important context to current hazard identification strategies.

In the battle against plastic pollution, many efforts are being undertaken to reduce, reuse and recycle plastics. If tackled in the right way, these efforts have the potential to contribute to reducing plastic waste and plastic's spread in the environment. However, reusing and recycling plastics can also lead to unintended negative impacts because hazardous chemicals, like endocrine disrupters and carcinogens, can be released during reuse and accumulate during recycling. In this way, plastic reuse and recycling become vectors for spreading chemicals of concern. This is especially concerning when plastics are reused for food packaging, or when food packaging is made with recycled plastics. Therefore, it is of utmost importance that care is taken to avoid hazardous chemicals in plastic food contact materials (FCMs) and to ensure that plastic packaging that is reused or made with recycled content is safe for human health and the environment. The data presented in this review are obtained from the Database on Migrating and Extractable Food Contact Chemicals (FCCmigex), which is based on over 800 scientific publications on plastic FCMs. We provide systematic evidence for migrating and extractable food contact chemicals (FCCs) in plastic polymers that are typically reused, such as polyamide (PA), melamine resin, polycarbonate and polypropylene, or that contain recycled content, such as polyethylene terephthalate (PET). A total of 1332 entries in the FCCmigex database refer to the detection of 509 FCCs in repeat-use FCMs made of plastic, and 853 FCCs are found in recycled PET, of which 57.6% have been detected only once. Here, we compile information on the origin, function and hazards of FCCs that have been frequently detected, such as melamine, 2,4-di-tert-butylphenol, 2,6-di-tert-butylbenzoquinone, caprolactam and PA oligomers and highlight key knowledge gaps that are relevant for the assessment of chemical safety. Impact statement Society has benefited from plastic food packaging: many foodstuffs have become widely available to humanity throughout the year. However, a downside of plastic food packaging is its environmental persistence when local waste management fails or is not available at all. The increasing plastic pollution is being tackled by different means, one of them being a shift to using more recycled content in plastic articles. Another approach is to ramp up reusable packaging by introducing refillable containers. But both approachesreusing and recycling plastic food packagingmust address the issue of chemicals that transfer from packaging into food and that may lead to food safety issues due to the presence of hazardous chemicals that accumulate in plastics throughout their life cycle. In this review article, we zoom in on this issue of chemicals in reusable and/or recyclable plastic food containers, such as packaging and other plastic items that come into contact with food, like kitchen utensils and tableware. We highlight the scientific evidence and key knowledge gaps on chemicals in plastics and how some chemicals of concern found in plastics affect human health.

Per- and polyfluoroalkyl substances (PFASs) are used in a multitude of processes and products, including nonstick coatings, food wrappers, and fire-fighting foams. These chemicals are environmentally-persistent, ubiquitous, and can be detected in the serum of 98% of Americans. Despite evidence that PFASs alter adaptive immunity, few studies have investigated their effects on innate immunity. The report here presents results of studies that investigated the impact of nine environmentally-relevant PFASs [e.g. perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid potassium salt (PFOS-K), perfluorononanoic acid (PFNA), perfluorohexanoic acid (PFHxA), perfluorohexane sulfonic acid (PFHxS), perfluorobutane sulfonic acid (PFBS), ammonium perfluoro(2-methyl-3-oxahexanoate) (GenX), 7H-perfluoro-4-methyl-3,6-dioxa-octane sulfonic acid (Nafion byproduct 2), and perfluoromethoxyacetic acid sodium salt (PFMOAA-Na)] on one component of the innate immune response, the neutrophil respiratory burst. The respiratory burst is a key innate immune process by which microbicidal reactive oxygen species (ROS) are rapidly induced by neutrophils in response to pathogens; defects in the respiratory burst can increase susceptibility to infection. The study here utilized larval zebrafish, a human neutrophil-like cell line, and primary human neutrophils to ascertain whether PFAS exposure inhibits ROS production in the respiratory burst. It was observed that exposure to PFHxA and GenX suppresses the respiratory burst in zebrafish larvae and a human neutrophil-like cell line. GenX also suppressed the respiratory burst in primary human neutrophils. This report is the first to demonstrate that these PFASs suppress neutrophil function and support the utility of employing zebrafish larvae and a human cell line as screening tools to identify chemicals that may suppress human immune function.

Microbiota regulate important physiologic processes during early host development. They also biotransform xenobiotics and serve as key intermediaries for chemical exposure. Antimicrobial agents in the environment may disrupt these complex interactions and alter key metabolic functions provided by host-associated microbiota. To examine the role of microbiota in xenobiotic metabolism, we exposed zebrafish larvae to the antimicrobial agent triclosan. Conventionally colonized (CC), microbe-free axenic (AX), or axenic colonized on day 1 (AC1) zebrafish were exposed to 0.16–0.30 µM triclosan or vehicle on days 1, 6, 7, 8, and 9 days post fertilization (dpf). After 6 and 10 dpf, host-associated microbial community structure and putative function were assessed by 16S rRNA gene sequencing. At 10 dpf, triclosan exposure selected for bacterial taxa, including Rheinheimera. Triclosan-selected microbes were predicted to be enriched in pathways related to mechanisms of antibiotic resistance, sulfonation, oxidative stress, and drug metabolism. Furthermore, at 10 dpf, colonized zebrafish contained 2.5–3 times more triclosan relative to AX larvae. Nontargeted chemical analysis revealed that, relative to AX larvae, both cohorts of colonized larvae showed elevations in 23 chemical features, including parent triclosan and putative triclosan sulfate. Taken together, these data suggest that triclosan exposure selects for microbes that harbor the capacity to biotransform triclosan into chemical metabolites with unknown toxicity profiles. More broadly, these data support the concept that microbiota modify the toxicokinetics of xenobiotic exposure.