Severe Coal Tar Sealcoat Runoff Toxicity to Fish Is Prevented by Bioretention Filtration

Coal tar sealcoats applied to asphalt surfaces in North America, east of the Continental Divide, are enriched in petroleum-derived compounds, including polycyclic aromatic hydrocarbons (PAHs). The release of PAHs and other chemicals from sealcoat has the potential to contaminate nearby water bodies, reducing the resiliency of aquatic communities. Despite this, relatively little is known about the aquatic toxicology of sealcoat-derived contaminants. We assessed the impacts of stormwater runoff from sealcoated asphalt on juvenile coho salmon (<i>Oncorhynchus kisutch</i>) and embryo-larval zebrafish (<i>Danio rerio).</i> We furthermore evaluated the effectiveness of bioretention as a green stormwater method to remove PAHs and reduce lethal and sublethal toxicity in both species. We applied a coal tar sealcoat to conventional asphalt and collected runoff from simulated rainfall events up to 7 months postapplication. Whereas sealcoat runoff was more acutely lethal to salmon, a spectrum of cardiovascular abnormalities was consistently evident in early life stage zebrafish. Soil bioretention effectively reduced PAH concentrations by an order of magnitude, prevented mortality in juvenile salmon, and significantly reduced cardiotoxicity in zebrafish. Our findings show that inexpensive bioretention methods can markedly improve stormwater quality and protect fish health

Severe Coal Tar Sealcoat Runoff Toxicity to Fish Is Prevented by Bioretention Filtration

Coal tar sealcoats applied to asphalt surfaces in North America, east of the Continental Divide, are enriched in petroleum-derived compounds, including polycyclic aromatic hydrocarbons (PAHs). The release of PAHs and other chemicals from sealcoat has the potential to contaminate nearby water bodies, reducing the resiliency of aquatic communities. Despite this, relatively little is known about the aquatic toxicology of sealcoat-derived contaminants. We assessed the impacts of stormwater runoff from sealcoated asphalt on juvenile coho salmon (<i>Oncorhynchus kisutch</i>) and embryo-larval zebrafish (<i>Danio rerio).</i> We furthermore evaluated the effectiveness of bioretention as a green stormwater method to remove PAHs and reduce lethal and sublethal toxicity in both species. We applied a coal tar sealcoat to conventional asphalt and collected runoff from simulated rainfall events up to 7 months postapplication. Whereas sealcoat runoff was more acutely lethal to salmon, a spectrum of cardiovascular abnormalities was consistently evident in early life stage zebrafish. Soil bioretention effectively reduced PAH concentrations by an order of magnitude, prevented mortality in juvenile salmon, and significantly reduced cardiotoxicity in zebrafish. Our findings show that inexpensive bioretention methods can markedly improve stormwater quality and protect fish health

Observed relationship between log <i>K</i>_OW and rate of decline in body burden concentration from day 3 to day 9 during exposure of crude oil exposed haddock embryos.

<p>The fitted line shows a third-degree polynomial fit for 3–6 ring compounds (blue circles). 2-ring PAHs (red circles) showed a linear increase with increasing log <i>K</i>_OW.</p

Relative body burden (%) of select 2–6 ring PAHs and alkyl PAHs in larvae of cod exposed to ~9 μg/L tPAH, haddock exposed to WSF and haddock exposed to ~9 μg/L tPAH who hatched in the tank and that was dechorionated.

<p>NAP = naphthalene, FLU = fluorene, DBT = dibenzothiophene, PYR = pyrene, CHR = chrysene.</p

Deviation in body burden (pg/embryo) of PAHs and alkyl PAH groups between day 9 and day 3 for an intermediate exposure concentration (~3 μg/L tPAH).

<p>Negative values indicate a decline in body burden of the compound group between the two time points. NAP = naphthalene, FLU = fluorene, DBT = dibenzothiophene, PYR = pyrene, CHR = chrysene.</p

Relative body burden (%) of select 2–6 ring PAHs and alkyl PAHs in larvae of cod exposed to ~9 μg/L tPAH, haddock exposed to WSF and haddock exposed to ~9 μg/L tPAH who hatched in the tank and that was dechorionated.

<p>NAP = naphthalene, FLU = fluorene, DBT = dibenzothiophene, PYR = pyrene, CHR = chrysene.</p

Total PAH body burden (including alkyl clusters) measured in cod and haddock eggs at day 3 and day 9 of exposure.

<p>Total PAH body burden (including alkyl clusters) measured in cod and haddock eggs at day 3 and day 9 of exposure.</p

Coefficient of determination (R2) as a function of log KOW for the fit of a linear relationship between cyp1a induction and single compound body burdens.

<p>Coefficient of determination (R2) as a function of log KOW for the fit of a linear relationship between cyp1a induction and single compound body burdens.</p

Confirmation of Stormwater Bioretention Treatment Effectiveness Using Molecular Indicators of Cardiovascular Toxicity in Developing Fish

Urban stormwater runoff is a globally significant threat to the ecological integrity of aquatic habitats. Green stormwater infrastructure methods such as bioretention are increasingly used to improve water quality by filtering chemical contaminants that may be harmful to fish and other species. Ubiquitous examples of toxics in runoff from highways and other impervious surfaces include polycyclic aromatic hydrocarbons (PAHs). Certain PAHs are known to cause functional and structural defects in developing fish hearts. Therefore, abnormal heart development in fish can be a sensitive measure of clean water technology effectiveness. Here we use the zebrafish experimental model to assess the effects of untreated runoff on the expression of genes that are classically responsive to contaminant exposures, as well as heart-related genes that may underpin the familiar cardiotoxicity phenotype. Further, we assess the effectiveness of soil bioretention for treating runoff, as measured by prevention of both visible cardiac toxicity and corresponding gene regulation. We find that contaminants in the dissolved phase of runoff (e.g., PAHs) are cardiotoxic and that soil bioretention protects against these harmful effects. Molecular markers were more sensitive than visible toxicity indicators, and several cardiac-related genes show promise as novel tools for evaluating the effectiveness of evolving stormwater mitigation strategies

Acute Embryonic or Juvenile Exposure to <i>Deepwater Horizon</i> Crude Oil Impairs the Swimming Performance of Mahi-Mahi (Coryphaena hippurus)

The <i>Deepwater Horizon</i> incident likely resulted in exposure of commercially and ecologically important fish species to crude oil during the sensitive early life stages. We show that brief exposure of a water-accommodated fraction of oil from the spill to mahi-mahi as juveniles, or as embryos/larvae that were then raised for ∼25 days to juveniles, reduces their swimming performance. These physiological deficits, likely attributable to polycyclic aromatic hydrocarbons (PAHs), occurred at environmentally realistic exposure concentrations. Specifically, a 48 h exposure of 1.2 ± 0.6 μg L^–1 ΣPAHs (geometric mean ± SEM) to embryos/larvae that were then raised to juvenile stage or a 24 h exposure of 30 ± 7 μg L^–1 ΣPAHs (geometric mean ± SEM) directly to juveniles resulted in 37% and 22% decreases in critical swimming velocities (<i>U</i>_crit), respectively. Oil-exposed larvae from the 48 h exposure showed a 4.5-fold increase in the incidence of pericardial and yolk sac edema relative to controls. However, this larval cardiotoxicity did not manifest in a reduced aerobic scope in the surviving juveniles. Instead, respirometric analyses point to a reduction in swimming efficiency as a potential alternative or contributing mechanism for the observed decreases in <i>U</i>_crit