Oil droplet fouling on lesser sandeel (Ammodytes marinus) eggshells does not enhance the crude oil induced developmental toxicity.

The oil industry's expansion and increased operational activity at older installations, along with their demolition, contribute to rising cumulative pollution and a heightened risk of accidental oil spills. The lesser sandeel (Ammodytes marinus) is a keystone prey species in the North Sea and coastal systems. Their eggs adhere to the seabed substrate making them particularly vulnerable to oil exposure during embryonic development. We evaluated the sensitivity of sandeel embryos to crude oil in a laboratory by exposing them to dispersed oil at concentrations of 0, 15, 50, and 150 µg/L oil between 2 and 16 days post-fertilization. We assessed water and tissue concentrations of THC and tPAH, cyp1a expression, lipid distribution in the eyes, head and trunk, and morphological and functional deformities. Oil droplets accumulated on the eggshell in all oil treatment groups, to which the embryo responded by a dose-dependent rise in cyp1a expression. The oil exposure led to only minor sublethal deformities in the upper jaw and otic vesicle. The findings suggest that lesser sandeel embryos are resilient to crude oil exposure. The lowest observed effect level documented in this study was 36 µg THC/L and 3 µg tPAH/L. The inclusion of these species-specific data in risk assessment models will enhance the precision of risk evaluations for the North Atlantic ecosystems.

Discovery of polycyclic aromatic acid metabolites in fish exposed to the petroleum compounds 1-methylphenanthrene and 1,4-dimethylphenanthrene.

Most of the polycyclic aromatic hydrocarbons (PAHs) in petroleum are alkylated (alkyl PAHs), still the metabolism of these alkyl PAHs to the expected acid products (polycyclic aromatic acids; PAAs) has yet to be demonstrated in oil-exposed fish. Should these compounds be discovered in fish as they have in ragworm, rodents, and humans, they could present an indicative biomarker for assessing oil pollution. In this study, the ability to biotransform alkyl PAHs to PAAs was examined on Atlantic haddock (Melanogrammus aeglefinus). Exposure to phenanthrene, 1-methyphenanthrene or 1,4-dimethylphenanthrene was performed via intraperitoneal injection. An Ion Mobility Quadrupole Time-Of-Flight Mass Spectrometer (IMS-Q-TOF MS) was used in exploratory analysis of extracted bile samples. Acquisition of four-dimensional information by coupling liquid chromatography with the IMS-Q-TOF MS and in-silico prediction for feature prioritization in the data processing workflow allowed several tentative identifications with high degree of confidence. This work presents the first detection of PAAs in fish and suggests the importance of investigating alkyl PAHs in ecotoxicological studies of oil-polluted fish environments.

Biological Responses of Pacific Herring Embryos to Crude Oil Are Quantifiable at Exposure Levels Below Conventional Limits of Quantitation for PAHs in Water and Tissues.

Pacific herring (Clupea pallasii), a cornerstone of marine food webs, generally spawn on marine macroalgae in shallow nearshore areas that are disproportionately at risk from oil spills. Herring embryos are also highly susceptible to toxicity from chemicals leaching from oil stranded in intertidal and subtidal zones. The water-soluble components of crude oil trigger an adverse outcome pathway that involves disruption of the physiological functions of cardiomyocytes in the embryonic herring heart. In previous studies, impaired ionoregulation (calcium and potassium cycling) in response to specific polycyclic aromatic hydrocarbons (PAHs) corresponds to lethal embryolarval heart failure or subtle chamber malformations at the high and low ends of the PAH exposure range, respectively. Sublethal cardiotoxicity, which involves an abnormal outgrowth (ballooning) of the cardiac ventricular chamber soon after hatching, subsequently compromises juvenile heart structure and function, leading to pathological hypertrophy of the ventricle and reduced individual fitness, measured as cardiorespiratory performance. Previous studies have not established a threshold for these sublethal and delayed-in-time effects, even with total (∑)PAH exposures as low as 29 ng/g of wet weight (tissue dose). Here, we extend these earlier findings showing that (1) cyp1a gene expression provides an oil exposure metric that is more sensitive than typical quantitation of PAHs via GC-MS and (2) heart morphometrics in herring embryos provide a similarly sensitive measure of toxic response. Early life stage injury to herring (impaired heart development) thus occurs below the quantitation limits for PAHs in both water and embryonic tissues as a conventional basis for assessing oil-induced losses to coastal marine ecosystems.

Co-Exposure of Phenanthrene and the cyp-Inducer 3-Methylchrysene Leads to Altered Biotransformation and Increased Toxicity in Fish Egg and Larvae.

Polycyclic aromatic hydrocarbons (PAHs) have frequently been suspected of governing crude oil toxicity because of similar morphological defects in fish. However, PAH concentrations are often not high enough to explain the observed crude oil toxicity. We hypothesize that one PAH can enhance the metabolism and toxicity of another PAH when administered as a mixture. Early life stage Atlantic haddock (Melanogrammus aeglefinus) were in this study exposed to phenanthrene in the presence and absence of 3-methylchrysene that is known to induce the metabolic enzyme cytochrome P450 1A via cyp1a gene expression. Uptake, metabolism, and multiple toxicity endpoints were then measured in a time-course study up to 3 days post-hatching. Passive dosing provided aqueous concentrations ≈180 µg/L for phenanthrene and ≈0.6 µg/L for 3-methylchrysene, which resulted in tissue concentrations ≈60 µg/g ww for phenanthrene and ≈0.15 µg/g ww for 3-methylchrysene. The low concentration of 3-methylchrysene led to the elevated expression of cyp1a but no toxicity. Levels of phenanthrene metabolites were 5-fold higher, and morphological defects and cardiotoxicity were consistently greater when co-exposed to both compounds relative to phenanthrene alone. This work highlights the metabolic activation of PAH toxicity by a co-occurring PAH, which can lead to excess toxicity, synergistic effects, and the overproportional contribution of PAHs to crude oil toxicity.

Cardiac toxicity of phenanthrene depends on developmental stage in Atlantic cod (Gadus morhua).

Complex mixtures like crude oil, and single components such as Phenanthrene (Phe), induce cardiotoxicity by interfering with excitation-contraction coupling. However, recent work has demonstrated that the timing of pollutant exposure during embryogenesis greatly impacts the degree of cardiac dysfunction caused. Here, we aimed to clarify the temporal dependence of Phe toxicity and the downstream effects of cardiac dysfunction using Atlantic cod (Gadus morhua). Phe (nominal concentration, 1.12 µmol/L), or the L-type­calcium channel blocker Nicardipine (Nic) (nominal concentration, 2 and 4 µmol/L), were individually applied to cod embryos either during cardiogenesis (early) or after the onset of cardiac function (late). Phe toxicity was highly dependent on the timing of exposure. Exposure after the onset of cardiac function (i.e. late) caused more severe cardiac and extracardiac abnormalities at 3 days post hatching (dph) than early exposure. Late Phe exposure resulted in a smaller ventricle, eliminated ventricular contraction, and reduced atrial contraction. In contrast, early Phe exposure did not have an effect on cardiac development and function. This temporal difference was not as evident in the Nic treatment. Early Nic exposure created similar morphological phenotypes to the late Phe exposure. The two treatments (early Nic and late Phe) also shared a cardiofunctional phenotype, comprised of eliminated ventricular, and reduced atrial, contraction. These data suggest that extracardiac abnormalities, such as the craniofacial deformities seen after late embryonic exposure to cardiotoxic oil components and mixtures, are mostly downstream effects of cardiac dysfunction.

Crude oil exposure of early life stages of Atlantic haddock suggests threshold levels for developmental toxicity as low as 0.1 µg total polyaromatic hydrocarbon (TPAH)/L.

Atlantic haddock (Melanogrammus aeglefinus) embryos bind dispersed crude oil droplets to the eggshell and are consequently highly susceptible to toxicity from spilled oil. We established thresholds for developmental toxicity and identified any potential long-term or latent adverse effects that could impair the growth and survival of individuals. Embryos were exposed to oil for eight days (10, 80 and 300 µg oil/L, equivalent to 0.1, 0.8 and 3.0 µg TPAH/L). Acute and delayed mortality were observed at embryonic, larval, and juvenile stages with IC50 = 2.2, 0.39, and 0.27 µg TPAH/L, respectively. Exposure to 0.1 µg TPAH/L had no negative effect on growth or survival. However, yolk sac larvae showed significant reduction in the outgrowth (ballooning) of the cardiac ventricle in the absence of other extracardiac morphological defects. Due to this propensity for latent sublethal developmental toxicity, we recommend an effect threshold of 0.1 µg TPAH/L for risk assessment models.

Alkyl-phenanthrenes in early life stage fish: differential toxicity in Atlantic haddock (Melanogrammus aeglefinus) embryos.

Tricyclic polycyclic aromatic hydrocarbons (PAHs) are believed to be the primary toxic components of crude oil. Such compounds including phenanthrene are known to have direct effects on cardiac tissue, which lead to malformations during organogenesis in early life stage fish. We tested a suite of 13 alkyl-phenanthrenes to compare uptake and developmental toxicity in early life stage haddock (Melanogrammus aeglefinus) embryos during gastrulation/organogenesis beginning at 2 days post fertilization via passive dosing. The alkyl-phenanthrenes were tested at their solubility limits, and three of them also at lower concentrations. Measured body burdens were linearly related to measured water concentrations. All compounds elicited one or more significant morphological defects or functional impairment, such as decreased length, smaller eye area, shorter jaw length, and increased incidence of body axis deformities and eye deformities. The profile of developmental toxicities appeared unrelated to the position of alkyl substitution, and gene expression of cytochrome 1 a (cyp1a) was low regardless of alkylation. Mortality and sublethal effects were observed below the expected range for baseline toxicity, thus indicating excess toxicity. Additionally, PAH concentrations that resulted in toxic effects here were far greater than when measured in whole crude oil exposures that cause toxicity. This work demonstrates that, while these phenanthrenes are toxic to early life stage fish, they cannot individually account for most of the developmental toxicity of crude oil, and that other compounds and/or mixture effects should be given more consideration.

Co-exposure to UV radiation and crude oil increases acute embryotoxicity and sublethal malformations in the early life stages of Atlantic haddock (Melanogrammus aeglefinus).

Crude oil causes severe abnormalities in developing fish. Photomodification of constituents in crude oil increases its toxicity several fold. We report on the effect of crude oil, in combination with ultraviolet (UV) radiation, on Atlantic haddock (Melanogrammus aeglefinus) embryos. Accumulation of crude oil on the eggshell makes haddock embryos particularly susceptible to exposure. At high latitudes, they can be exposed to UV radiation many hours a day. Haddock embryos were exposed to crude oil (5-300 µg oil/L nominal loading concentrations) for three days in the presence and absence of UV radiation (290-400 nm). UV radiation partly degraded the eggs' outer membrane resulting in less accumulation of oil droplets in the treatment with highest oil concentration (300 µg oil/L). The co-exposure treatments resulted in acute toxicity, manifested by massive tissue necrosis and subsequent mortality, reducing LC50 at hatching stage by 60 % to 0.24 µg totPAH/L compared to 0.62 µg totPAH/L in crude oil only. In the treatment with nominal low oil concentrations (5-30 µg oil/L), only co-exposure to UV led to sublethal morphological heart defects. Including phototoxicity as a parameter in risk assessments of accidental oil spills is recommended.

Photo-enhanced toxicity of crude oil on early developmental stages of Atlantic cod (Gadus morhua).

Photo-enhanced toxicity of crude oil is produced by exposure to ultraviolet (UV) radiation. Atlantic cod (Gadus morhua) embryos were exposed to crude oil with and without UV radiation (290-400 nm) from 3 days post fertilization (dpf) until 6 dpf. Embryos from the co-exposure experiment were continually exposed to UV radiation until hatching at 11 dpf. Differences in body burden levels and cyp1a expression in cod embryos were observed between the exposure regimes. High doses of crude oil produced increased mortality in cod co-exposed embryos, as well as craniofacial malformations and heart deformities in larvae from both experiments. A higher number of differentially expressed genes (DEGs) and pathways were revealed in the co-exposure experiment, indicating a photo-enhanced effect of crude oil toxicity. Our results provide mechanistic insights into crude oil and photo-enhanced crude oil toxicity, suggesting that UV radiation increases the toxicity of crude oil in early life stages of Atlantic cod.

Cardiac dysfunction affects eye development and vision by reducing supply of lipids in fish.

Developing organisms are especially vulnerable to environmental stressors. Crude oil exposure in early life stages of fish result in multiple functional and developmental defects, including cardiac dysfunction and abnormal and smaller eyes. Phenanthrene (Phe) has a reversible impact on cardiac function, and under exposure Phe reduces cardiac contractility. Exposure to a known L-type channel blocker, nicardipine hydrochloride (Nic) also disrupts cardiac function and creates eye deformities. We aimed to investigate whether cardiac dysfunction was the major underlying mechanism of crude oil-, Phe- and Nic-induced eye malformations. We exposed Atlantic haddock (Melanogrammus aeglefinus) early embryos to Nic and crude oil (Oil) and late embryos/early larvae to Phe exposure. All three exposures resulted in cardiac abnormalities and lead to severe, eye, jaw and spinal deformities at early larval stages. At 3 days post hatching, larvae from the exposures and corresponding controls were dissected. Eyes, trunk, head and yolk sac were subjected to lipid profiling, and eyes were also subjected to transcriptomic profiling. Among most enriched pathways in the eye transcriptomes were fatty acid metabolism, calcium signaling and phototransduction. Changes in lipid profiles and the transcriptome suggested that the dysfunctional and abnormal eyes in our exposures were due to both disruption of signaling pathways and insufficient supply of essential fatty acids and other nutrients form the yolk.

Differential developmental toxicity of crude oil in early life stages of Atlantic halibut (Hippoglossus hippoglossus).

To further understand the complexity of developmental toxicity of dispersed oil and importance of exposure timing on fish early life stages, Atlantic halibut (Hippoglossus hippoglossus) were exposed to environmentally relevant concentrations through two embryonic developmental windows: the first period occurred during the epiboly process (named as "early embryonic exposure") and the second period overlapped the ontogenesis and cardiogenesis processes (named as "late embryonic exposure"). Following 72 hour oil exposure, embryos were transferred to clean seawater and a toxicity screening was performed in the yolk-sac larvae until first-feeding stages (56 days). The current study demonstrated that the exposure timing is essential for the development of toxic effects of crude oil in Atlantic halibut. Neither embryonic exposures (early or late) showed notable acute toxicity during exposure, yet both showed global latent teratogenic effects during yolk sac stages. Fish exposed during organogenesis (late) displayed stronger and more severe toxic effects than fish exposed during epiboly process (early), including reduced condition, severe craniofacial deformities and cardiovascular disruptions. The uptake level of polycyclic aromatic hydrocarbons into larval tissue and metabolic activity were greater following the late embryonic exposure and remained high during the depuration period at the highest exposure concentration. Overall, the long yolk sac stage development timing of Atlantic halibut makes this species a good candidate for evaluation of embryonic crude oil toxicity and its mechanisms.

Untangling mechanisms of crude oil toxicity: Linking gene expression, morphology and PAHs at two developmental stages in a cold-water fish.

Early life stages of fish are highly sensitive to crude oil exposure and thus, short term exposures during critical developmental periods could have detrimental consequences for juvenile survival. Here we administered crude oil to Atlantic haddock (Melanogrammus aeglefinus) in short term (3-day) exposures at two developmental time periods: before first heartbeat, from gastrulation to cardiac cone stage (early), and from first heartbeat to one day before hatching (late). A frequent sampling regime enabled us to determine immediate PAH uptake, metabolite formation and gene expression changes. In general, the embryotoxic consequences of an oil exposure were more severe in the early exposure animals. Oil droplets on the eggshell resulted in severe cardiac and craniofacial abnormalities in the highest treatments. Gene expression changes of Cytochrome 1 a, b, c and d (cyp1a, b, c, d), Bone morphogenetic protein 10 (bmp10), ABC transporter b1 (abcb1) and Rh-associated G-protein (rhag) were linked to PAH uptake, occurrence of metabolites of phenanthrene and developmental and functional abnormalities. We detected circulation-independent, oil-induced gene expression changes and separated phenotypes linked to proliferation, growth and disruption of formation events at early and late developmental stages. Changes in bmp10 expression suggest a direct oil-induced effect on calcium homeostasis. Localized expression of rhag propose an impact on osmoregulation. Severe eye abnormalities were linked to possible inappropriate overexpression of cyp1b in the eyes. This study gives an increased knowledge about developmentally dependent effects of crude oil toxicity. Thus, our findings provide more knowledge and detail to new and several existing adverse outcome pathways of crude oil toxicity.

DNA damage and health effects in juvenile haddock (Melanogrammus aeglefinus) exposed to PAHs associated with oil-polluted sediment or produced water.

The research objective was to study the presence of DNA damages in haddock exposed to petrogenic or pyrogenic polyaromatic hydrocarbons (PAHs) from different sources: 1) extracts of oil produced water (PW), dominated by 2-ring PAHs; 2) distillation fractions of crude oil (representing oil-based drilling mud), dominated by 3-ring PAHs; 3) heavy pyrogenic PAHs, mixture of 4/5/6-ring PAHs. The biological effect of the different PAH sources was studied by feeding juvenile haddock with low doses of PAHs (0.3-0.7 mg PAH/kg fish/day) for two months, followed by a two-months recovery. In addition to the oral exposure, a group of fish was exposed to 12 single compounds of PAHs (4/5/6-ring) via intraperitoneal injection. The main endpoint was the analysis of hepatic and intestinal DNA adducts. In addition, PAH burden in liver, bile metabolites, gene and protein expression of CYP1A, GST activity, lipid peroxidation, skeletal deformities and histopathology of livers were evaluated. Juvenile haddock responded quickly to both intraperitoneal injection and oral exposure of 4/5/6-ring PAHs. High levels of DNA adducts were detected in livers three days after the dose of the single compound exposure. Fish had also high levels of DNA adducts in liver after being fed with extracts dominated by 2-ring PAHs (a PW exposure scenario) and 3-ring PAHs (simulating an oil exposure scenario). Elevated levels of DNA adducts were observed in the liver of all exposed groups after the 2 months of recovery. High levels of DNA adduct were found also in the intestines of individuals exposed to oil or heavy PAHs, but not in the PW or control groups. This suggests that the intestinal barrier is very important for detoxification of orally exposures of PAHs.

Expression and localization of the aryl hydrocarbon receptors and cytochrome P450 1A during early development of Atlantic cod (Gadus morhua).

The aryl hydrocarbon receptor (Ahr) is a ligand-activated transcription factor that mediates the toxicity of dioxins and dioxin-like compounds (DLCs) in vertebrates. Two clades of the Ahr family exist in teleosts (Ahr1 and Ahr2), and it has been demonstrated that Ahr2 is the main protein involved in mediating the toxicity of dioxins and DLCs in most teleost species. Recently, we characterized the Atlantic cod (Gadus morhua) Ahr1a and Ahr2a receptors. To further explore a possible subfunction partitioning of Ahr1a and Ahr2a in Atlantic cod we have mapped the expression and localization of ahr1a and ahr2a in early developmental stages. Atlantic cod embryos were continuously exposed in a passive-dosing exposure system to the Ahr agonist, benzo[a]pyrene (B[a]P), from five days post fertilization (dpf) until three days post hatching (dph). Expression of ahr1a, ahr2a, and the Ahr-target genes, cyp1a and ahrrb, was assessed in embryos (8 dpf and 10 dpf) and larvae (3 dph) with quantitative real-time PCR analyses (qPCR), while in situ hybridization was used to assess the localization of expression of ahr1a, ahr2a and cyp1a. Quantitative measurements showed an increased cyp1a expression in B[a]P-exposed samples at all sampling points, and for ahr2a at 10 dpf, confirming the activation of the Ahr-signalling pathway. Furthermore, B[a]P strongly induced ahr2a and cyp1a expression in the cardiovascular system and skin, respectively, of embryos and larvae. Induced expression of both ahr2a and cyp1a was also revealed in the liver of B[a]P-exposed larvae. Our results suggest that Ahr2a is the major subtype involved in mediating responses to B[a]P in early developmental stages of Atlantic cod, which involves transcriptional regulation of biotransformation genes, such as cyp1a. The focused expression of ahr1a in the eye of embryos and larvae, and the presence of ahr2a transcripts in the jaws and fin nodes, further indicate evolved specialized roles of the two Ahrs in ontogenesis.

Embryonic Crude Oil Exposure Impairs Growth and Lipid Allocation in a Keystone Arctic Forage Fish.

As Arctic ice recedes, future oil spills pose increasing risk to keystone species and the ecosystems they support. We show that Polar cod (Boreogadus saida), an energy-rich forage fish for marine mammals, seabirds, and other fish, are highly sensitive to developmental impacts of crude oil. Transient oil exposures ≥300 µg/L during mid-organogenesis disrupted the normal patterning of the jaw as well as the formation and function of the heart, in a manner expected to be lethal to post-hatch larvae. More importantly, we found that exposure to lower levels of oil caused a dysregulation of lipid metabolism and growth that persisted in morphologically normal juveniles. As lipid content is critical for overwinter survival and recruitment, we anticipate Polar cod losses following Arctic oil spills as a consequence of both near-term and delayed mortality. These losses will likely influence energy flow within Arctic food webs in ways that are as-yet poorly understood.

Accumulation and toxicity of monoaromatic petroleum hydrocarbons in early life stages of cod and haddock.

A multitude of recent studies have documented the detrimental effects of crude oil exposure on early life stages of fish, including larvae and embryos. While polycyclic aromatic hydrocarbons (PAHs), particularly alkyl PAHs, are often considered the main cause of observed toxic effects, other crude oil derived organic compounds are usually overlooked. In the current study, comprehensive two-dimensional gas chromatography coupled to mass spectrometry was applied to investigate the body burden of a wide range of petrogenic compounds in Atlantic haddock (Melanogrammus aeglefinus) and cod (Gadus morhua) embryos that had been exposed to sublethal doses of dispersed crude oil. Several groups of alkylated monoaromatic compounds (e.g. alkyl tetralins, indanes and alkyl benzenes), as well as highly alkylated PAHs, were found to accumulate in the fish embryos upon crude oil exposure. To investigate the toxicity of the monoaromatic compounds, two models (1-isopropyl-4-methyltetralin and 1-isopropyl-4-methylindane) were synthesized and shown to bioaccumulate and cause delayed hatching in developing embryos. Minor developmental effects, including craniofacial and jaw deformations and pericardial edemas, were also observed at the highest studied concentrations of the alkylindane.

Artificial turf: chemical flux and development of silicone wristband partitioning coefficients.

This work provides the first quantitative measure of in situ flux of semi-volatile contaminants on artificial turf fields. Passive samplers were used to identify gas-phase PAHs and OPAHs not previously reported associated with artificial turf. Utilizing a broad and targeted screen, we assess both artificial turf and from crumb rubber for 1,529 chemicals, including several with known health effects including benzo[c]fluorene. We also report the presence of 25 chemicals that have not yet been reported in artificial turf literature, including some with known effects on human health. This is the first report of bioavailable gas-phase PAH and OPAH concentrations on an outdoor field, to date gas-phase concentrations have only been reported from indoor facilities. Turf air and air were highly correlated at all three sites, and particularly at the recently-installed indoor site. Finally, thermal extraction and silicone passive samplers are highly suitable for larger-scale sampling campaigns that aim for less solvent and sample processing. We demonstrate for the first time that silicone passive samplers can be used to quantify volatile and semi-volatile organic chemicals from artificial turf. Co-deploying silicone passive samplers and conventional low density polyethylene, we develop partitioning coefficients that can be used for silicone passive air sampling environmental assessment.

Preparation and performance features of wristband samplers and considerations for chemical exposure assessment.

Wristbands are increasingly used for assessing personal chemical exposures. Unlike some exposure assessment tools, guidelines for wristbands, such as preparation, applicable chemicals, and transport and storage logistics, are lacking. We tested the wristband's capacity to capture and retain 148 chemicals including polychlorinated biphenyls (PCBs), pesticides, flame retardants, polycyclic aromatic hydrocarbons (PAHs), and volatile organic chemicals (VOCs). The chemicals span a wide range of physical-chemical properties, with log octanol-air partitioning coefficients from 2.1 to 13.7. All chemicals were quantitatively and precisely recovered from initial exposures, averaging 102% recovery with relative SD ≤21%. In simulated transport conditions at +30 °C, SVOCs were stable up to 1 month (average: 104%) and VOC levels were unchanged (average: 99%) for 7 days. During long-term storage at -20 °C up to 3 (VOCs) or 6 months (SVOCs), all chemical levels were stable from chemical degradation or diffusional losses, averaging 110%. Applying a paired wristband/active sampler study with human participants, the first estimates of wristband-air partitioning coefficients for PAHs are presented to aid in environmental air concentration estimates. Extrapolation of these stability results to other chemicals within the same physical-chemical parameters is expected to yield similar results. As we better define wristband characteristics, wristbands can be better integrated in exposure science and epidemiological studies.

Assessing soil-air partitioning of PAHs and PCBs with a new fugacity passive sampler.

Soil-air fluxes of polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs) were determined using a novel application of passive samplers to measure air and soil air, which is air in close proximity and in equilibrium with soil. Existing methods to measure flux of semi-volatile compounds between soil and air require collecting samples from the top soil layer. Yet, the top soil layer is hard to define and oversampling may misrepresent the exchangeable fraction. Alternatively, modified active samplers can measure soil air in situ, but require electricity while deployed. We present a new method to measure time-weighted averages of soil air concentrations in situ using passive sampling and requiring no electricity: a box is placed over low-density polyethylene passive samplers deployed 1cm above the soil. Passive air samplers were also co-deployed 1.5m above the soil to measure ambient air concentrations in three U.S. LOCATIONS: near a former PCB manufacturing facility in Anniston, Alabama; on a former creosoting and the current Wyckoff/Eagle Superfund site near Seattle, Washington; and near the site of a recent oil-train derailment and fire in Mosier, Oregon. Following n-hexane extraction, sampler extracts were analyzed for PAHs with gas chromatography-tandem mass spectrometry and PCBs with dual gas chromatography-electron capture detectors. PAHs were generally depositing at Anniston and Mosier sites, but volatilizing from soil in Wyckoff, the site with historically-contaminated soil. PCBs were detected most frequently at the Anniston site, although levels were lower than previous reports. Variability in concentration measurements was greater among soil air samplers than air samplers, likely due to soil heterogeneity. Environmental conditions under the novel soil air box did not substantially change soil-air partitioning behavior. This method of measuring soil air in situ will allow for understanding of source-sink dynamics at sites with recent and historical contamination, and where conventional sampling is challenging.

Silicone wristbands detect individuals' pesticide exposures in West Africa.

We detected between 2 and 10 pesticides per person with novel sampling devices worn by 35 participants who were actively engaged in farming in Diender, Senegal. Participants were recruited to wear silicone wristbands for each of two separate periods of up to 5 days. Pesticide exposure profiles were highly individualized with only limited associations with demographic data. Using a 63-pesticide dual-column gas chromatography-electron capture detector (GC-ECD) method, we detected pyrethoid insecticides most frequently, followed by organophosphate pesticides which have been linked to adverse health outcomes. This work provides the first report of individualized exposure profiles among smallholder farmers in West Africa, where logistical and practical constraints have prevented the use of more traditional approaches to exposure assessment in the past. The wristbands and associated analytical method enabled detection of a broad range of agricultural, domestic, legacy and current-use pesticides, including esfenvalerate, cypermethrin, lindane, DDT and chlorpyrifos. Participants reported the use of 13 pesticide active ingredients while wearing wristbands. All six of the pesticides that were both reportedly used and included in the analytical method were detected in at least one wristband. An additional 19 pesticide compounds were detected beyond those that were reported to be in use, highlighting the importance of measuring exposure in addition to collecting surveys and self-reported use records. The wristband method is a candidate for more widespread use in pesticide exposure and health monitoring, and in the development of evidence-based policies for human health protection in an area where food security concerns are likely to intensify agricultural production and pesticide use in the near future.