Estimating Environmental Hazard and Risks from Perfluorinated and Polyfluorinated Alkyl Substances (PFAS): Outcome of a Focused Topic Meeting
Fluorine Mass Balance in Marine Mammals from the Northern Hemisphere – A combination of targeted, total (organo)fluorine, and non-targeted analysis
There is increasing evidence that the ~20 routinely monitored per- and polyfluoroalkyl substances (PFASs) account for only a fraction of extractable organofluorine (EOF) occurring in the environment. To assess whether PFAS exposure is being underestimated in marine mammals from the Northern Hemisphere, we performed a fluorine mass balance on liver tissues from 11 different species using a combination of targeted PFAS analysis, EOF and total fluorine determination, and suspect screening. Samples were obtained from the east coast United States (US), west and east coast of Greenland, Iceland, and Sweden from 2000-2017. Of the 36 target PFASs, perfluorooctane sulfonate (PFOS) dominated in all but one Icelandic and three US samples, where the 7:3 fluorotelomer carboxylic acid (7:3 FTCA) was prevalent. This is the first report of 7:3 FTCA in polar bears (~1000 ng/g, ww) and cetaceans (<6-190 ng/g, ww). In 18 out of 25 samples, EOF was not significantly greater than fluorine concentrations derived from sum target PFASs. For the remaining 7 samples (mostly from the US east coast), 30-75% of the EOF was unidentified. Suspect screening revealed an additional 33 PFASs (not included in the targeted analysis) bringing the total to 59 detected PFASs from 12 different classes. Overall, these results highlight the importance of a multi-platform approach for accurately characterizing PFAS exposure in marine mammals.
Genotoxicity and DNA damage signaling in response to complex mixtures of PAHs in biomass burning particulate matter from cashew nut roasting
Approximately 3 billion people world-wide are exposed to air pollution from biomass burning. Herein, particulate matter (PM) emitted from artisanal cashew nut roasting, an important economic activity worldwide, was investigated. This study focused on: i) chemical characterization of polycyclic aromatic hydrocarbons (PAHs) and oxygenated (oxy-) PAHs; ii) intracellular levels of reactive oxygen species (ROS); iii) genotoxic effects and time- and dose-dependent activation of DNA damage signaling, and iv) differential expression of genes involved in xenobiotic metabolism, inflammation, cell cycle arrest and DNA repair, using A549 lung cells. Among the PAHs, chrysene, benzo[a]pyrene (B[a]P), benzo[b]fluoranthene, and benz[a]anthracene showed the highest concentrations (7.8–10 ng/m3), while benzanthrone and 9,10-anthraquinone were the most abundant oxy-PAHs. Testing of PM extracts was based on B[a]P equivalent doses (B[a]Peq). IC50 values for viability were 5.7 and 3.0 nM B[a]Peq at 24 h and 48 h, respectively. At these low doses, we observed a time- and dose-dependent increase in intracellular levels of ROS, genotoxicity (DNA strand breaks) and DNA damage signaling (phosphorylation of the protein checkpoint kinase 1 – Chk1). In comparison, effects of B[a]P alone was observed at micromolar range. To our knowledge, no previous study has demonstrated an activation of pChk1, a biomarker used to estimate the carcinogenic potency of PAHs in vitro, in lung cells exposed to cashew nut roasting extracts. Sustained induction of expression of several important stress response mediators of xenobiotic metabolism (CYP1A1, CYP1B1), ROS and pro-inflammatory response (IL-8, TNF-α, IL-2, COX2), and DNA damage response (CDKN1A and DDB2) was also identified. In conclusion, our data show high potency of cashew nut roasting PM to induce cellular stress including genotoxicity, and more potently when compared to B[a]P alone. Our study provides new data that will help elucidate the toxic effects of low-levels of PAH mixtures from air PM generated by cashew nut roasting.
Long-term exposure to particulate air pollution, black carbon and their source components in relation to ischemic heart disease and stroke
Background: Long-term exposure to particulate matter (PM) in ambient air has been associated with cardiovascular mortality but few studies have considered incident disease in relation to PM from different sources.
Objectives: To study associations between long-term exposure to different types of PM and sources, and incident ischemic heart disease (IHD) and stroke in three Swedish cities.
Methods: Based on detailed emission databases, monitoring data and high-resolution dispersion models we calculated source contributions to PM10, PM2.5, black carbon (BC) from road wear, traffic exhaust, residential heating and other sources in Gothenburg, Stockholm, and Umeå. Registry data for participants from four cohorts were used to obtain incidence of IHD and stroke for first hospitalization or death. We constructed time-windows of exposure for same year, 1-5 year and 6-10 year averages preceding
incidence from annual averages at residential addresses. Risk estimates were based on random effects meta-analyses of cohort-specific Cox proportional hazard models. Results: We observed 5166 and 3119 incident IHD and stroke cases respectively in 114,758 participants. Overall, few consistent associations were observed between the different air pollution measures and IHD or stroke incidence. However, same year levels of ambient locally emitted BC (range 0.01-4.6 μg/m3) were associated with a 4.0% higher risk of incident stroke per interquartile range, 0.30 μg/m3 (95% CI: 0.04%, 7.8%). This association was primarily related to BC from traffic exhaust. PM10 (range 4.4-52 μg/m3) and PM2.5 (range 2.9-22 μg/m3) were not associated with stroke. Associations with incident IHD were observed only for PM2.5 exposure from residential heating.
Discussion: Few consistent associations were observed between different particulate components and IHD or stroke. However, long-term residential exposure to locally
emitted BC from traffic exhaust was associated with stroke incidence. The comparatively low exposure levels may have contributed to the paucity of associations.