Toxicity Of Hydrocarbons Research Articles

Levels and toxicity of polycyclic aromatic hydrocarbons in marine sediments

The occurrence of polycyclic aromatic hydrocarbons (PAHs) in the marine environment has attracted the attention of the scientific community, as these compounds are frequently detected in seawater and sediments at increasing levels and can have adverse health effects on marine organisms and humans. Several PAHs are potential human carcinogens and are included in the priority list of the European Union’s Water Framework Directive (2000/60/EC). Research regarding their environmental levels requires their determination by gas-chromatography and liquid-chromatography techniques, which have been developed and optimized, especially for marine-sediment samples. Results of sample analyses reveal the increasing occurrence of many species of PAHs worldwide, especially in marine sediments, where they finally accumulate, mostly in areas near intense industrial activities. In parallel, research on the toxicity of PAHs and their mixtures is continuing and is aiming to provide more insight into the health risks associated with the levels of PAHs in the environment.

Microarray analysis of polychlorinated biphenyl mixture–induced changes in gene expression among Atlantic tomcod populations displaying differential sensitivity to halogenated aromatic hydrocarbons

Several populations of fishes inhabiting contaminated Atlantic Coast estuaries exhibit resistance to early life-stage (ELS) toxicities induced by halogenated aromatic hydrocarbons such as coplanar polychlorinated biphenyls (PCBs). These toxicities include mortality, circulatory failure, edema, and craniofacial malformations. The mechanisms behind resistance to halogenated aromatic hydrocarbon toxicity in these populations are unknown. First and second generation Atlantic tomcod Microgadus tomcod embryos derived from the Hudson River ([HR]; New York, USA) population are highly resistant to PCB-induced cytochrome P4501A (CYP1A) expression and ELS toxicity when compared to embryos of Miramichi River ([MR]; New Brunswick, Canada) and Shinnecock Bay ([SB]; New York, USA) origin. The present study sought to identify novel genes involved in population differences in response to PCB exposure using custom microarrays. Microarray probes consisted of unsequenced inserts of randomly picked clones from a tomcod cardiac cDNA library. Tomcod embryos from three populations (HR, MR, and SB) were exposed to two doses of an environmentally relevant mixture of coplanar PCBs and screened for dose- and population-specific patterns of gene expression. Clones displaying significant differences between populations exposed to the high dose of PCBs were identified by DNA sequencing. Of the 28 identified nonribosomal protein clones, none displayed expression patterns highly similar to CYP1A (altered in MR and SB, but not in HR). However, several transcripts representing biomarkers of cardiomyopathy in mammals (cardiac troponin T2, cathepsin L, and atrial natriuretic peptide) were differentially altered among the three tomcod populations by PCBs. Although the present study did not identify any novel genes associated with PCB resistance in tomcod, several potential molecular biomarkers of PCB exposure were revealed.

Oil dispersion increases the apparent bioavailability and toxicity of diesel to rainbow trout (Oncorhynchus mykiss)

Diesel is a complex mixture containing polycyclic aromatic hydrocarbons, which persist after a spill, pass readily from water into tissues, and are toxic to early life stages of fish. The bioavailability and chronic toxicity of hydrocarbons dissolved into water from floating diesel (water-accommodated fraction) and chemically dispersed diesel (chemically enhanced water-accommodated fraction) were measured by the extent of ethoxyresorufin-O-deethylase (EROD) induction in juvenile rainbow trout (Oncorhynchus mykiss) and by the severity of blue sac disease in embryos. The water-accommodated fraction of floating diesel was virtually nontoxic to embryos at nominal concentrations up to 1,000 mg/L, causing only small weight changes. Liver EROD induction in juvenile trout was only observed at the highest nominal water-accommodated fraction concentration (10,000 mg/L). Chemical dispersion increased the bioavailability and toxicity of diesel to trout by 100-fold. Diesel chemically enhanced water-accommodated fraction induced EROD activity, caused blue sac disease, and impaired development and growth of embryonic trout at nominal concentrations as low as 10 mg/L; 88% mortality occurred at 100 mg/L. However, when total hydrocarbon concentrations were measured, differences between dispersed and undispersed diesel disappeared, with a median lethal concentration of 8 mg/L of total hydrocarbons and sublethal median effective concentrations ranging from 1.3 to 6.1 mg/L. Dispersion of diesel by high-energy mechanical mixing was recently reported to cause acute lethality to juvenile trout between 40 and 200 mg/L. Therefore, dispersion of oil by any means increases the bioavailability and apparent toxicity of diesel to fish embryos without changing the toxicity of its components. Nevertheless, in an actual spill, dispersion of diesel increases the effects of oil on fish populations.

Sublethal toxicity and biotransformation of pyrene in Lumbriculus variegatus (Oligochaeta)

The aim of this work was to study the toxicity and biotransformation of polyaromatic hydrocarbon (PAH) pyrene in the oligochaete aquatic worm, Lumbriculus variegatus. PAHs are ubiquitous environmental pollutants that pose a hazard to aquatic organisms, and metabolizing capability is poorly known in the case of many invertebrate species. To study the toxicity and biotransformation of pyrene, the worm was exposed for 15 days to various concentrations of water-borne pyrene. The dorsal blood vessel pulse rate was used as a sublethal endpoint. Pyrene biotransformation by L. variegatus was studied and the critical body residues (CBR) were estimated for pyrene toxicity. The toxicokinetics of pyrene uptake was evaluated. A combination of radiolabeled (14C) and nonlabeled pyrene was used in the exposures, and liquid scintillation counting (LSC) and high-pressure liquid chromatography were employed in both water and tissue residue analyses. The results showed that L. variegatus was moderately able to metabolize pyrene to 1-hydroxypyrene (1-HP), thus demonstrating that the phase-I-like oxidizing enzyme system metabolizes pyrene in L. variegatus. The amount of the 1-HP was 1-2% of the amount of pyrene in the worm tissues. The exposure to pyrene reduced the blood vessel pulse rate significantly (p<0.05), showing that pyrene had a narcotic effect. The estimated CBRs remained constant during the exposure time, varying from 0.120 to 0.174 mmol pyrene/kg worm wet weight. The bioconcentration factors (BCF) decreased as exposure concentration increased. It was suggested that the increased toxicity of pyrene accounted for the decrease in BCFs by lowering the activity of the organism.

Complexation of anthracene with folic acid studied by FTIR and UV spectroscopies

Toxicity and transformation process of polycyclic aromatic hydrocarbons (PAHs) is strongly depended on the interaction between PAHs and the coexisting compounds. Complexation between folic acid (FA) and a typical PAH, anthracene, was investigated using FTIR and UV spectra. Appearance of a new IR band at 2362 cm −1 demonstrates that NH 2–C N(1)– moiety on pterin (PT) ring in FA is protonated when anthracene is introduced. The shift of the characteristic IR band of the PT ring and the emergence of two charge transfer bands at 254 nm and 246 nm in UV difference spectra show the presence of π–π complexation between folic acid and anthracene. These experiments confirm that anthracene could combine with the pterin ring of folic acid through π–π donor–acceptor interaction (EDA) and induce the protonation process in FA upon strengthening electron accepting ability of PT ring.

Characteristics, toxicity, and source apportionment of polycylic aromatic hydrocarbons (PAHs) in road dust of Ulsan, Korea

This study identified concentrations, molecular distributions, toxicities, and sources of polycylic aromatic hydrocarbons (PAHs) in road dust from different areas of Ulsan, the largest industrial city in Korea. The total PAH concentrations in industrial areas were dependent on industrial emissions and vehicular exhaust, while those in urban areas were mainly dependent on traffic density, sampling site location, and accumulation of pollutants or road dust. The PAH concentration of each particle size group increased with decreasing particle size. This may be because of the higher surface area available for deposition or coating of PAHs in road dust with smaller particle sizes. The molecular distributions of PAHs among the sites in the petrochemical area and heavy traffic area were similar because of the similarities in their emission sources. The toxic equivalent concentrations (TEQs) of PAHs in the road dust ranged from 0.93 μg/g to 16.74 μg/g in industrial areas and from 4.37 μg/g to 68.84 μg/g in urban areas. The correlation coefficient of total PAH concentration and TEQ in urban areas was 0.98, which was much higher than that in industrial areas where it was 0.75. Principal component analysis showed that PAHs in road dust from Ulsan originate from four main sources: diesel vehicular emissions, oil combustion, gasoline vehicular emissions, and coal combustion.

Interfacial Approach to Polyaromatic Hydrocarbon Toxicity: Phosphoglyceride and Cholesterol Monolayer Response to Phenantrene, Anthracene, Pyrene, Chrysene, and Benzo[a]pyrene

Interactions of phenantrene, anthracene, pyrene, chrysene, and benzo[a]pyrene (polyaromatic hydrocarbons) with model phospholipid membranes were probed using the Langmuir technique. The lipid monolayers were prepared using 1,2-dipalmitoyl-sn-glycero-3-phosphocholine, 1,2-dipalmitoyl-sn-glycero-3-phosphoethanolamine, 1,2-dipalmitoyl-sn-glycero-3-phosphoglycerol, 1,2-dipalmitoyl-sn-glycero-3-phosphoserine, 1,2-myristoyl-sn-glycero-3-phosphoethanolamine, 1,2-dilauroyl-sn-glycero-3-phosphocholine, and cholesterol. Surface pressure and electrical surface potential were measured on mixed phospholipid/PAH monolayers spread on a pure water subphase. The morphology of the mixed monolayers was followed with Brewster angle microscopy. Polarization-modulation infrared reflection-absorption spectroscopy spectra obtained on DPPE/benzo[a]pyrene showed that the latter interacts with the carbonyl groups of the phospholipid. On the other hand, the activity of phospholipase A2 toward DLPC used as a probe to locate benzo[a]pyrene in the monolayers indicates that the polyaromatic hydrocarbons are not accessible to the enzyme. The results obtained show that all PAHs studied affect the properties of the pure lipid, albeit in different ways. The most notable effects, namely, film fluidization and morphology changes, were observed with benzo[a]pyrene. In contrast, the complexity of mixed lipid monolayers makes the effect of PAHs difficult to detect. It can be assumed that the differences observed between PAHs in monolayers correlate with their toxicity.

Modeling polycyclic aromatic hydrocarbon bioaccumulation and metabolism in time‐variable early life‐stage exposures

Recent laboratory investigations into the bioaccumulation and toxicity of polycyclic aromatic hydrocarbons (PAH) have focused on low-level, time-variable exposures to early life-stage fish. Polycyclic aromatic hydrocarbon body-burden residues reported in these studies were lower than critical body-burden residues predicted by the target lipid model (TLM). To understand this discrepancy, a time-variable uptake and depuration model of PAH bioaccumulation was developed. Kinetic constants were fit using measured exposure and tissue concentrations. The resulting lipid-water partition coefficients (K(LW)) were uncorrelated with the octanol-water partition coefficient (K(OW))--a qualitatively unrealistic finding considering that numerous studies have reported a positive correlation between the two. Because PAHs are known to be metabolized, the comparison of K(LW) with K(OW) suggests that metabolism may be occurring in early life-stage fish. Therefore, the uptake and depuration model was modified to include metabolism while assuming linearity of K(LW) with K(OW). Calculated metabolism rates were positively correlated with K(OW)--a finding qualitatively similar to those of other studies. The present study provides a reasonable explanation for the discrepancy between the TLM predictions and the measured toxic effect levels. Given the time-variable exposure concentrations, the maximum measured body burdens used to relate to toxic effects may be underestimated. In addition, the maximum body burden of parent PAH plus metabolites may be a better measure in relating tissue concentrations to toxic effects. Incorporating these refinements in relating body burdens to toxic effects may result in a better comparison between TLM predictions and measured effect levels.

Toxicity of four nitrogen-heterocyclic polyaromatic hydrocarbons (NPAHs) to soil organisms

The aims of this study were: (i) to investigate the toxicity of N-heterocyclic polyaromatic hydrocarbons (NPAHs) quinoline, acridine, phenazine, and 1,10-phenanthroline to the soil invertebrates Eisenia fetida, Enchytraeus crypticus, Folsomia candida, and Caenorhabditis elegans, (ii) to compare the toxicity of four NPAHs and the species sensitivity, and (iii) to discuss possible risks of these compounds in soils. Different toxicities were found for the tested NPAHs which might be partially explained by their structure and properties. Effect concentrations expressed as soil pore-water concentrations were related to log K ow, which indicated narcosis as the most probable mode of toxic action. The species sensitivity decreased in the rank: springtails >enchytraeids=earthworms> nematodes. Predicted no-effect concentration (PNEC) values were calculated for all tested species giving values from 0.5 to 6.8 mg/kg. It is unlikely that there is a risk for soil organisms in natural soils where lower NPAHs concentrations are expected.

Estrogenic status modulates aryl hydrocarbon receptor—mediated hepatic gene expression and carcinogenicity

Estrogenic status is thought to influence the cancer risk in women and has been reported to affect toxicity of carcinogenic polycyclic aromatic hydrocarbons (PAHs) in animals. The objective of this study was to examine the influence of estradiol (E2) on hepatic gene expression changes mediated by 7,12-dimethylbenz(a)anthracene (DMBA), a potent PAH. Sprague-Dawley rats were ovariectomized on postnatal day 50 and infused with E2 (5 mug/kg/day) or polyethylene glycol using osmotic pumps and 14 days later gavaged with DMBA (50 mg/kg) or sesame oil and killed 24 h thereafter. To understand the mechanism of DMBA-mediated hepatocarcinogenicity in the presence of E2, microarray analysis (Rat 230 2.0 Affymetrix-GeneChip) was performed. Two hundred and sixteen genes were downregulated; whereas, 106 genes were upregulated significantly (+/-1.5-fold, P < 0.05) by DMBA treatment. Hierarchical clustering revealed that the expression profile of 39 genes, regulated by DMBA, was significantly modified by E2 supplementation. Interestingly, 71 genes were uniquely modulated in the combined treatment of DMBA and E2, but not by either treatment alone. Results from chromatin immunoprecipitation assay demonstrate that in animals cotreated with E2 and DMBA, there was enhanced recruitment of estrogen receptor-alpha to the regulatory regions of CYP1A1 and aryl hydrocarbon receptor (AhR) genes compared with that observed in animals treated with DMBA alone. E2 supplementation leads to increased DMBA-induced CYP1A1 transcription, while the AhR gene was upregulated in the presence of E2 +DMBA only. Our data suggest that estrogenic status is (i) important in AhR regulation and can influence the effects of xenobiotics and (ii) may be an important factor in DMBA-mediated carcinogenicity.

Pneumatocele complicating acute hydrocarbon pneumonitis

We present the radiological images and clinical summary of a patient with hydrocarbon ingestion and aspiration complicated by the development of a large pneumatocele.

Ecotoxicological evaluation of polycyclic aromatic hydrocarbons using marine invertebrate embryo–larval bioassays

The toxicity of polycyclic aromatic hydrocarbons (PAHs) was determined using mussel, sea-urchin and ascidian embryo–larval bioassays. Fluorescent light exposure enhanced phenanthrene, fluoranthene, pyrene and hydroxypyrene toxicity in comparison with dark conditions, but not naphthalene and fluorene toxicity. The toxicity of PAHs was inversely related to their K OW values following QSAR models derived for baseline toxicity of general narcotics, whereas the obtained regression using toxicity data from photoactivated PAHs significantly departed from the general narcosis model. Also, the mixture toxicity of five PAHs to the larval growth of the sea-urchin was compared with predictions derived from the concentration addition concept, indicating less than additive effects. Finally, we compared our toxicity data with worst-case environmental concentrations in order to provide a preliminary estimate of the risk to the marine environment. Naphthalene, fluorene and pyrene are not considered to pose a risk to sea-urchin, mussel or ascidian larvae, whilst phenanthrene and fluoranthene may pose a risk for mussel and sea-urchin. Moreover, a higher risk for those species is expected when we consider the photoactivation of the PAHs.

A clinical decision rule for triage of children under 5 years of age with hydrocarbon (kerosene) aspiration in developing countries

Background. Unintended hydrocarbon ingestion is a common reason for pediatric hospitalization in the developing world. Objective. To derive a clinical decision rule, to identify patients likely to require a higher level facility (resource-requiring cases), that can be used at primary health care facilities with limited diagnostic and therapeutic resources. Methods. A prospective study of children 2 to 59 months old presenting to a poison treatment facility within 2 hours of oral hydrocarbon exposure. History and objective signs were recorded at admission and at 6, 12, 24 and, if present, 48 hours. Inclusion in the resource-requiring outcome group required: oxygen saturation <94%; any CNS depression; any treatment with (salbutamol); any care in the ICU; or death. Results. 256 met the inclusion criteria and completed the study. Of these, 170 had a course requiring resources unavailable at most primary health care facilities, and 86 did not. The presence of wheezing, any alteration in consciousness (lethargy or any restlessness), or a rapid respiratory rate for age (RR ≥50/min if age < 12mo, ≥ 40/min if age ≥ 12 mo) at presentation identified 167 of 170 of these patients (sensitivity 0.98). Thirty-six of 86 patients classified as non-resource requiring were correctly identified (specificity 0.42). No combination of clinical symptoms provided better discrimination while preserving sensitivity. Conclusions. This study suggests a triage decision rule based on the presence of wheezing, altered consciousness, or a rapid respiratory rate within 2 hours of hydrocarbon exposure. Such a rule requires validation in other settings.

Annetocin and TCTP expressions in the earthworm Eisenia fetida exposed to PAHs in artificial soil

The toxicity of sublethal polycyclic aromatic hydrocarbons (PAHs) levels in soils was assessed by testing their impact on expression of annetocin, a reproduction regulating gene, and translationally controlled tumor protein (TCTP), a tumorigenic response gene, in the earthworm Eisenia fetida cultured in artificial soil spiked with, phenanthrene (Phe), pyrene (Pyr), fluoranthene (Flu), or benzo( a)pyrene (Bap). Annetocin and TCTP were both up-regulated by 0.1 and 1.0 mg kg −1 benzo( a)pyrene and TCTP was down-regulated by 10.0 mg kg −1 phenanthrene. Weight loss and cocoon production of the worms were also analyzed. Only 10.0 mg kg −1 phenanthrene impacted earthworm weight loss significantly and no significant differences on cocoon production were observed. Our study indicated that the potential ecotoxicity of sublethal PAHs in soil should not be neglected and mRNA transcription level in earthworms was a more sensitive indicator of PAHs exposure than traditional indexes using cocoon production as endpoints and/or using the whole-organism as the test materials.

Successful outcome after intravenous gasoline injection

Gasoline, ingested intentionally or accidentally, is toxic. The majority of reported cases of gasoline intoxication involve oral ingestion or inhalation. Data are scarce on complications and outcomes following hydrocarbon poisoning by intravenous injection. Following a suicide attempt by intravenous self-injection of 10 ml of gasoline, a 26-year-old medical student was admitted to the intensive care unit (ICU) with hemoptysis, symptoms of acute respiratory failure, chest pain, and severe abdominal cramps. Gas exchange was severely impaired and a chest x-ray indicated chemical pneumonitis. Initial treatment consisted of mechanical ventilation, supportive hyperventilation, administration of nitrogen oxide (NO), and prednisone. Unfortunately, the patient developed multi-organ dysfunction syndrome (MODS) complicated by life-threatening severe vasoplegia within 24 hours after gasoline injection. High doses of vasopressors along with massive amounts of parenteral fluids were necessary. Despite fluid replacement, renal function worsened and required hemofiltration on 5 sequential days. After 12 days of intensive care management, the patient recovered completely and was discharged to a psychiatric care facility. Intravenous gasoline injection causes major injury to the lungs, the organ bearing the first capillary bed encountered. Treatment of gasoline poisoning is symptomatic because no specific antidote is available. Early and aggressive supportive care may be conducive to a favorable outcome with minimal residual pulmonary sequelae.

Crosstalk Between the Aryl Hydrocarbon Receptor and Hypoxia on the Constitutive Expression of Cytochrome P4501A1 mRNA

Endothelial cells are a target of halogenated aromatic hydrocarbon toxicity following aryl hydrocarbon receptor (AHR) activation. Further, evidence suggests that AHR has a physiological function in endothelial cells in the absence of exogenous ligands. Understanding these "normal" functions of AHR may help to reveal the mechanisms that contribute to the toxicity of xenobiotic ligands. Thus, this study focused on the crosstalk between hypoxia and AHR in the absence of exogenous ligands. Constitutive CYP1A1 mRNA was measured by real time PCR in human pulmonary microvascular endothelial cells exposed to hypoxia (1 or 2.5% O2), 25 nM AHR siRNA, 25 nM hypoxia-inducible factor (HIF)-2alpha siRNA, or their combinations. Hypoxia significantly induced known hypoxia-regulated genes, and this induction was highly attenuated by HIF-2alpha siRNA, suggesting that HIF-2alpha is a primary mediator of hypoxic responses in these cells. Hypoxia also significantly reduced CYP1A1 mRNA and this reduction was also attenuated by HIF-2alpha siRNA. As expected, AHR siRNA significantly reduced constitutive CYP1A1 mRNA. While the combination of hypoxia plus AHR siRNA reduced CYP1A1 mRNA more than either treatment alone, the reduction was less than additive, suggesting that hypoxia and AHR deficiency may share a common pathway in reducing CYP1A1 expression. Finally, hypoxia significantly reduced AHR mRNA and this reduction was completely prevented by HIF-2alpha siRNA. In conclusion, constitutive CYP1A1 mRNA expression is dependent on AHR and is reduced by hypoxia via a HIF-2alpha-dependent mechanism, which may be mediated by a HIF-2alpha-dependent reduction of AHR expression.

Supercritical carbon dioxide extraction as a predictor of polycyclic aromatic hydrocarbon bioaccumulation and toxicity by earthworms in manufactured‐gas plant site soils

The toxicity and uptake of polycyclic aromatic hydrocarbons (PAHs) by earthworms were measured in soil samples collected from manufactured-gas plant sites having a wide range in PAH concentrations (170-42,000 mg/kg) and soil characteristics. Samples varied from vegetated soils to pure lampblack soot and had total organic carbon contents ranging from 3 to 87%. The biota-soil accumulation factors (BSAFs) observed for individual PAHs in field-collected earthworms (Aporrectodea caliginosa) were up to 50-fold lower than the BSAFs predicted using equilibrium-partitioning theory. Acute toxicity to the earthworm Eisenia fetida was unrelated to total PAH concentration: Mortality was not observed in some soils having high concentrations of total PAHs (>42,000 mg/kg), whereas 100% mortality was observed in other soils having much lower concentrations of total PAHs (1,520 mg/kg). Instead, toxicity appeared to be related to the rapidly released fraction of PAHs determined by mild supercritical CO2 extraction (SFE). The results demonstrate that soils having approximately 16,000 mg rapidly released total PAH/kg organic carbon can be acutely toxic to earthworms and that the concentration of PAHs in soil that is rapidly released by SFE can estimate toxicity to soil invertebrates.

Photoinduced toxicity of the polycyclic aromatic hydrocarbon, fluoranthene, on the coral, Porites divaricata

The synergistic effect of ultraviolet radiation (UVR) and a polycyclic aromatic hydrocarbon (PAH) was tested on the coral Porites divaricata. Small branches were incubated in different concentrations of fluoranthene followed by exposure to ecologically relevant levels of natural solar radiation, with and without UVR. Exposure to the highest concentration of fluoranthene (60 μ g L− 1) resulted in decreased photochemical efficiency of corals exposed concomitantly to UVR but not in corals exposed to 60 μ g L− 1 fluoranthene without UVR. After 6 days, most coral samples that were exposed to fluoranthene and UVR bleached or died (78%) on the upper side of the branches. At 60 μ g L− 1 fluoranthene with UVR, 11 out of 12 samples died and the remaining sample bleached, much greater than the number of samples that bleached in manipulation or solvent controls. On the under side of the same samples, where the coral polyps are naturally protected from UVR, 11 out of 12 samples remained healthy and intact. The high UVR doses that shallow water dwelling corals receive combined with the results of this study show that photoinduced toxicity of PAHs is a stress factor that needs to be studied in more detail in coral reef ecosystems.

Mixtures of metals and polynuclear aromatic hydrocarbons elicit complex, nonadditive toxicological interactions in meiobenthic copepods

The acute toxicity of metal-polynuclear aromatic hydrocarbon (PAH) mixtures (i.e., Cd, Hg, Pb, fluoranthene, and phenanthrene) associated with sediments was assessed in two benthic copepods. Schizopera knabeni was exposed to sediment amended with single contaminants and mixtures. Adult S. knabeni were highly tolerant of single-contaminant exposures to phenanthrene, Cd, Hg, and Pb as well as a mixture of Cd, Hg, and Pb. Binary experiments revealed that although phenanthrene was synergistic with Cd and Hg, the phenanthrene-Cd synergism was much stronger (2.8 times more lethal than predicted). When a mixture of Cd, Hg, and Pb was combined with phenanthrene, a synergistic response was observed, eliciting 1.5 times greater lethality than predicted. A Cd-phenanthrene synergism in S. knabeni was also observed in aqueous exposures, suggesting that the interaction was related to a pharmacological insult rather than a sediment-related exposure effect. An antagonism between Cd, Hg, and Pb was indicated, and this antagonism may have moderated the Cd-phenanthrene synergism in mixtures containing Cd, Hg, Pb, and phenanthrene. Experiments with Amphiascoides atopus revealed that phenanthrene and fluoranthene were each synergistic with Cd in aqueous exposures. Our studies suggest that interactive toxicity among metal-PAH mixtures may be common among benthic copepods and that strong synergistic effects observed in binary mixtures may be moderated in more diverse contaminant mixtures. However, the strength of the observed synergisms raises concerns that established sediment quality criteria may not be protective for organisms jointly exposed to PAH and metals, especially Cd-PAH mixtures.

Toxic pneumonitis caused by inhalation of hydrocarbon waterproofing spray in two dogs

2 dogs were evaluated because of vomiting and lethargy (a Toy Poodle; dog 1) and acute respiratory distress, vomiting, and anorexia (a Chihuahua; dog 2). Dog 1 had been exposed to a commercial hydrocarbon waterproofing spray 24 hours before the development of clinical signs, and dog 2 was examined 18 hours after exposure to a waterproofing spray containing heptane, a highly flammable liquid hydrocarbon. In both dogs, major gastrointestinal tract abnormalities were ruled out but respiratory status worsened. Thoracic radiography revealed a diffuse interstitial pulmonary pattern, and hypoxemia was detected. Hospitalization for monitoring and care was required for both dogs. The dogs recovered with supportive care, which included administration of oxygen, fluids, and bronchodilators. Additionally, dog 1 received glucocorticoids via inhalation and supplemental enteral nutrition, whereas dog 2 was treated with an antimicrobial. The dogs of this report developed hydrocarbon pneumonitis following exposure to waterproofing sprays. Such sprays contain potentially toxic hydrocarbons. The severity of the adverse effects associated with exposure may have been amplified because the dogs were physically small and were exposed to a relatively large amount of aerosolized spray within small areas. Development of chemical pneumonitis in pet animals is best prevented by application of waterproofing sprays in well-ventilated or outdoor areas from which pets have been excluded. With prolonged hospitalization and considerable monitoring and care, affected dogs can recover from these exposures.