Comparative acute toxicity of shale and petroleum derived distillates

In anticipation of the commercialization of its shale oil retorting and upgrading process, Unocal Corp. conducted a testing program aimed at better defining potential health impacts of a shale industry. Acute toxicity studies using rats and rabbits compared the effects of naphtha, Jet-A, JP-4, diesel and "residual" distillate fractions of both petroleum derived crude oils and hydrotreated shale oil. No differences in the acute oral (greater than 5 g/kg LD50) and dermal (greater than 2 g/kg LD50) toxicities were noted between the shale and petroleum derived distillates and none of the samples were more than mildly irritating to the eyes. Shale and petroleum products caused similar degrees of mild to moderate skin irritation. None of the materials produced sensitization reactions. The LC50 after acute inhalation exposure to Jet-A, shale naphtha, (greater than 5 mg/L) and JP-4 distillate fractions of petroleum and shale oils was greater than 5 mg/L. The LC50 of petroleum naphtha (greater than 4.8 mg/L) and raw shale oil (greater than 3.95 mg/L) also indicated low toxicity. Results demonstrate that shale oil products are of low acute toxicity, mild to moderately irritating and similar to their petroleum counterparts. The results further demonstrate that hydrotreatment reduces the irritancy of raw shale oil.     

Toxicity of five shale oils to fish and aquatic invertebrates

The chemical composition and toxicity of three shale crude oils (Tosco, Paraho, and Geokinetics), a hydrotreated oil (Paraho HDT), and a refined shale oil (Paraho JP-4) were assessed to determine the potential hazards to native fish species and food chain organisms posed by accidental spills of such materials. Colorado squawfish (Ptychocheilus lucius), fathead minnow (Pimephales promelas), cutthroat trout (Salmo clarki), and colonies of aquatic invertebrates were exposed to the watersoluble fractions of the shale oils for 96 hr to determine concentrations lethal to 50% of the exposed organisms (LC-50). The behavior of surviving fish was also measured to determine the sublethal influences of exposure. The composition of the five water-soluble fractions was similar to that of the crude and refined shale oils from which they were made. Hydrotreated and refined oils contained fewer aromatic compounds than the crude shale oils. The cutthroat trout, a species endemic to oil shale regions, was less tolerant of shale oil exposure than the other species tested; the LC-50 concentrations were 1.8 mg/L Geokinetics, 2.1 mg/L Tosco, and 1.3 mg/L Paraho. Exposure to concentrations of one-half to one-eighth those causing mortality reduced the swimming capacity of squawfish and significantly impaired their ability to capture prey. The number of invertebrate taxa, species, and organisms colonizing plate samplers declined with increasing oil concentration. The generaBaetis andIsoperla were most sensitive to shale oil exposure; significant mortality occurred at the lowest concentration (0.5–0.7 mg/L) tested for each shale oil.     

Effect of hydrotreatment on the photomutagenicity of shale oil

Dimethyl sulfoxide extracts of a parent crude and a hydrotreated Paraho shale oil were tested in Salmonella to detect the presence of direct acting mutagens, promutagens, which are converted by liver enzymes to direct acting mutagens, and photomutagens, which photosensitize Salmonella to mutation by fluorescent light. Direct acting mutagens were not detected in extracts of either shale oil. Both photomutagens and promutagens were detected in the parent crude, but only photomutagens were detected in the hydrotreated material. These results suggest that the photomutagens and promutagens were effected differently by hydrotreatment and that the two types of mutagens are to some degree different chemical entities. Both the crude and hydrotreated shale oils are reported to be carcinogenic in mouse skin, and our results of photomutation testing more closely parallel the carcinogenicity of the shale oils than do our results of testing with enzymatic activation.     

Effect of drilling fluid systems and temperature on oil mist and vapour levels generated from shale shaker

Workers in the drilling section of the offshore petroleum industry are exposed to air pollutants generated by drilling fluids. Oil mist and oil vapour concentrations have been measured in the drilling fluid processing areas for decades; however, little work has been carried out to investigate exposure determinants such as drilling fluid viscosity and temperature. A study was undertaken to investigate the effect of two different oil-based drilling fluid systems and their temperature on oil mist, oil vapour, and total volatile organic compounds (TVOC) levels in a simulated shale shaker room at a purpose-built test centre. Oil mist and oil vapour concentrations were sampled simultaneously using a sampling arrangement consisting of a Millipore closed cassette loaded with glass fibre and cellulose acetate filters attached to a backup charcoal tube. TVOCs were measured by a PhoCheck photo-ionization detector direct reading instrument. Concentrations of oil mist, oil vapour, and TVOC in the atmosphere surrounding the shale shaker were assessed during three separate test periods. Two oil-based drilling fluids, denoted 'System 2.0' and 'System 3.5', containing base oils with a viscosity of 2.0 and 3.3-3.7 mm(2) s(-1) at 40°C, respectively, were used at temperatures ranging from 40 to 75°C. In general, the System 2.0 yielded low oil mist levels, but high oil vapour concentrations, while the opposite was found for the System 3.5. Statistical significant differences between the drilling fluid systems were found for oil mist (P = 0.025),vapour (P < 0.001), and TVOC (P = 0.011). Increasing temperature increased the oil mist, oil vapour, and TVOC levels. Oil vapour levels at the test facility exceeded the Norwegian oil vapour occupational exposure limit (OEL) of 30 mg m(-3) when the drilling fluid temperature was ≥50°C. The practice of testing compliance of oil vapour exposure from drilling fluids systems containing base oils with viscosity of ≤2.0 mm(2) s(-1) at 40°C against the Norwegian oil vapour OEL is questioned since these base oils are very similar to white spirit. To reduce exposures, relevant technical control measures in this area are to cool the drilling fluid <50°C before it enters the shale shaker units, enclose shale shakers and related equipment, in addition to careful consideration of which fluid system to use.     

Polycyclic aromatic primary amines as determinant chemical mutagens in petroleum substitutes

Petroleum crude oils and coal- and shale-derived petroleum substitutes have been separated by chemical class and the class fractions have been subjected to bacterial mutagenicity testing. Alkaline constituents of the petroleum substitutes are found to make major contributions to their mutagenicities. High-resolution chromatographic and spectroscopic analysis of alkaline subfractions enriched in mutagenic activity show the causative agents to be polycyclic aromatic primary amines. The amines may be responsible for the increased biological activity of coal- and shale-derived petroleum substitutes relative to petroleum.     

Carcinogenic potential of hydrotreated petroleum aromatic extracts

Five experimental petroleum extracts were produced from luboil distillates derived from Middle East paraffinic crude by solvent extraction and severe hydrotreatment. The polycyclic aromatic content (PCA) of the extracts was determined by dimethyl sulphoxide extraction and ranged from 3.7-9.2% w/w. The five extracts were evaluated for their potential to induce cutaneous and systemic neoplasia in female mice derived from Carworth Farm No 1 strain (CF1). The test substances were applied undiluted (0.2 ml per application) to the shorn dorsal skin twice weekly for up to 78 weeks, with 48 mice in each treatment group and 96 in the untreated control group; two further groups, each of 48 mice, were similarly treated either with a non-hydrotreated commercial aromatic extract (PCA content, 19.7% w/v) or with a low dose of benzo(a)pyrene (12.5 micrograms/ml acetone). The mice were housed individually in polypropylene cages in specified pathogen free conditions. The incidence of cutaneous and systemic tumours was determined from histological analysis of haematoxylin and eosin stained tissue sections. The results were correlated with the PCA content of the extracts and compared with those from female mice exposed to a non-hydrotreated commercial aromatic extract. Four of the hydrotreated extracts were carcinogenic for murine skin; the two products with the lower PCA contents were less carcinogenic than the products with the higher PCA contents and all were less carcinogenic than the commercial extract. One extract with the lowest PCA content was non-carcinogenic. Thus refining by severe hydrotreatment was an effective method of reducing the carcinogenic potential of petroleum aromatic extracts. Although other physicochemical properties may influence the biological activity of oil products, the PCA content determined by dimethyl sulphoxide extraction may be a useful indicator of the potential of oil products to induce cutaneous tumours in experimental animals. There was no evidence that the commercial or hydrotreated extracts increased the incidence of systemic neoplasms when applied twice weekly to the dorsal skin.     

Carcinogenic potential of hydrotreated petroleum aromatic extracts.

Five experimental petroleum extracts were produced from luboil distillates derived from Middle East paraffinic crude by solvent extraction and severe hydrotreatment. The polycyclic aromatic content (PCA) of the extracts was determined by dimethyl sulphoxide extraction and ranged from 3.7-9.2% w/w. The five extracts were evaluated for their potential to induce cutaneous and systemic neoplasia in female mice derived from Carworth Farm No 1 strain (CF1). The test substances were applied undiluted (0.2 ml per application) to the shorn dorsal skin twice weekly for up to 78 weeks, with 48 mice in each treatment group and 96 in the untreated control group; two further groups, each of 48 mice, were similarly treated either with a non-hydrotreated commercial aromatic extract (PCA content, 19.7% w/v) or with a low dose of benzo(a)pyrene (12.5 micrograms/ml acetone). The mice were housed individually in polypropylene cages in specified pathogen free conditions. The incidence of cutaneous and systemic tumours was determined from histological analysis of haematoxylin and eosin stained tissue sections. The results were correlated with the PCA content of the extracts and compared with those from female mice exposed to a non-hydrotreated commercial aromatic extract. Four of the hydrotreated extracts were carcinogenic for murine skin; the two products with the lower PCA contents were less carcinogenic than the products with the higher PCA contents and all were less carcinogenic than the commercial extract. One extract with the lowest PCA content was non-carcinogenic. Thus refining by severe hydrotreatment was an effective method of reducing the carcinogenic potential of petroleum aromatic extracts. Although other physicochemical properties may influence the biological activity of oil products, the PCA content determined by dimethyl sulphoxide extraction may be a useful indicator of the potential of oil products to induce cutaneous tumours in experimental animals. There was no evidence that the commercial or hydrotreated extracts increased the incidence of systemic neoplasms when applied twice weekly to the dorsal skin.     

A 90-day toxicity study of the effects of petroleum middle distillates on the skin of C3H mice

Petroleum middle distillates (PMDs) elicit skin tumors in mouse epidermal carcinogenesis studies. The response is characterized by a long latency with only a small percentage of animals developing tumors. Although the carcinogenic activity of certain other petroleum hydrocarbons largely depends upon the presence of polycyclic aromatic hydrocarbons (PAHs), many PMDs contain relatively low concentrations of PAHs. PMDs are also irritating to mouse skin, and chronic irritation may be involved in the development of skin tumors. This study was conducted to investigate the patterns of cutaneous irritation elicited by topical application of PMDs having compositional differences. The three PMDs selected for study were a steam cracked gas oil (SCGO), a lightly refined paraffinic oil (LRPO), and a jet fuel (JF). Male C3H/HeNCr1BR mice (25/group) were treated topically (37.5 microliters 2x/week for 13 weeks) with 10%, 50% or 100% (undiluted) concentrations of each PMD. Catalytically cracked clarified oil (CCCO, 10%), a potent carcinogen to mouse skin, was also tested. The vehicle was a noncarcinogenic mineral oil with a viscosity of 90 SUS. Cutaneous changes were evaluated by gross observations and light microscopy. Cutaneous irritation was the only significant toxic response in this study. Neither the vehicle nor any of the 10% PMD concentrations produced significant cutaneous irritation. The 10% CCCO and 50% PMD treatments all elicited slight to moderate proliferative and inflammatory changes in mouse skin. Ulcers were also observed microscopically in mice treated with 10% CCCO and 50% SCGO. The 100% SCGO treatment produced evidence of necrosis on Days 1-7 but not later in the study despite continued treatment. In contrast, the irritating effects of 100% LRPO were not evident until 2-3 weeks of study, and at study completion were characterized by moderately severe inflammatory and proliferative changes. The effects of 100% JF were qualitatively similar to 100% LRPO but less marked. Thus, the SCGO caused a different pattern of cutaneous responses than either LRPO or JF. The possible relationships of these cutaneous changes to epidermal carcinogenesis are being studied further.     

Development and application of an oil toxicity and exposure model,OilToxEx

An oil toxicity and exposure model (OilToxEx) was developed and validated for estimation of impacts to aquatic organisms resulting from acute exposure to spilled oil. Because oil exposure is shorter than the time required for equilibrium between the organism and the water to be reached, the time and temperature dependence of toxicity is addressed. Oil toxicity is a function of aromatic composition and the toxicity of individual aromatics in the mixture. Lethal concentration to 50% of exposed organisms (LC50), as a function of octanol-water partition coefficient (Kow), and an additive model are used to estimate the toxicity of monoaromatic and polycyclic aromatic hydrocarbon mixtures in water-soluble fractions (WSF) and oil-in-water dispersions (OWD) of oil. The toxicity model was verified by comparison with oil bioassay data where the exposure concentrations of aromatics were measured. The observed toxicity in the bioassays could be accounted for by the additive narcotic effects of the dissolved aromatics in the exposure media. Predicted LC50s were compared to those calculated from measured concentrations after spills to verify the exposure model for field conditions. These results indicate that the additive toxicity and exposure model may be used to estimate toxicity of untested oils and spill conditions.     

Toxicity of jet fuels to several terrestrial insects

The acute toxicity of a variety of Air Force jet fuels was evaluated for several terrestrial insects. The most toxic fuel was a shale-derived JP-8. In general, shale fuels were more toxic than their petroleum-derived counterparts. The order of decreasing susceptibility to the current standard Air Force fuel, petroleum-derived JP-4, was earwigs, rice weevils, flour beetles, lady beetles, tenebrionid beetles, and cockroaches. However, species response varied with different jet fuel types.     

Petroleum mineral oil refining and evaluation of cancer hazard

Petroleum base oils (petroleum mineral oils) are manufactured from crude oils by vacuum distillation to produce several distillates and a residual oil that are then further refined. Aromatics including alkylated polycyclic aromatic compounds (PAC) are undesirable constituents of base oils because they are deleterious to product performance and are potentially carcinogenic. In modern base oil refining, aromatics are reduced by solvent extraction, catalytic hydrotreating, or hydrocracking. Chronic exposure to poorly refined base oils has the potential to cause skin cancer. A chronic mouse dermal bioassay has been the standard test for estimating carcinogenic potential of mineral oils. The level of alkylated 3-7-ring PAC in raw streams from the vacuum tower must be greatly reduced to render the base oil noncarcinogenic. The processes that can reduce PAC levels are known, but the operating conditions for the processing units (e.g., temperature, pressure, catalyst type, residence time in the unit, unit engineering design, etc.) needed to achieve adequate PAC reduction are refinery specific. Chronic dermal bioassays provide information about whether conditions applied can make a noncarcinogenic oil, but cannot be used to monitor current production for quality control or for conducting research or developing new processes since this test takes at least 78 weeks to conduct. Three short-term, non-animal assays all involving extraction of oil with dimethylsulfoxide (DMSO) have been validated for predicting potential carcinogenic activity of petroleum base oils: a modified Ames assay of a DMSO extract, a gravimetric assay (IP 346) for wt. percent of oil extracted into DMSO, and a GC-FID assay measuring 3-7-ring PAC content in a DMSO extract of oil, expressed as percent of the oil. Extraction with DMSO concentrates PAC in a manner that mimics the extraction method used in the solvent refining of noncarcinogenic oils. The three assays are described, data demonstrating the validation of the assays are shown, and test results of currently manufactured base oils are summarized to illustrate the general lack of cancer hazard for the base oils now being manufactured.     

Morbidity survey of U.S. oil shale workers employed during 1948-1969

The health status of 325 oil shale workers employed at the Anvil Points, Colorado, demonstration facility from 1948 to 1969 was evaluated. As a comparison population, 323 Utah coal miners frequency matched for age were studied. The prevalence of respiratory symptoms among oil shale workers who smoked were similar to the coal miners who smoked, although nonsmoking oil shale workers had fewer symptoms compared to nonsmoking coal workers. Four cases of skin cancers were found on the oil shale workers and eight cases in the controls. Similar numbers of nevi, telangiectasiae, possible pitch warts, pigment changes (solar/senile lentigo), and papillomata (seborrheic keratoses and skin tags) were seen in both groups, while actinic keratoses were more frequent in the oil shale workers. The prevalence of actinic keratoses was significantly associated with oil shale work after allowing for age, sun exposure, and other exposures. The prevalence of pulmonary cytology metaplasia was associated with years of production work in oil shale among both smokers and exsmokers. More of the oil shale workers had atypical cells in the urine, but the excess was mostly found among exsmokers. Although these workers had short-term and limited oil shale exposure work exposure, we recommend that medical surveillance of oil shale workers consider the skin, respiratory, and urinary systems for special observation.     

Specific in vitro toxicity of crude and refined petroleum products: 3. Estrogenic responses in mammalian assays

Current petroleum risk assessment considers only narcosis as the mode of action, but several studies have demonstrated that oils contain compounds with dioxin-like, estrogenic or antiestrogenic, and androgenic or antiandrogenic activities. The present study is the third in a series investigating the specific toxic effects of 11 crude oils and refined products. By employing recombinant mammalian cells stably transfected with the human estrogen receptor alpha (ERα) or beta (ERβ), and expressing the luciferase protein (ERα-U2OS-Luc and ERβ-U2OS-Luc assay), the estrogenicity or antiestrogenicity of oils was studied. All oils, except for two refined oils and one crude oil, induced estrogenic responses. The calculated estrogenic potencies of the oils were six to nine orders of magnitude lower than the potency of 17β-estradiol (E2). Upon coexposure to a fixed concentration of E2 and increasing concentrations of oils, additive, antagonistic, and synergistic effects were revealed. One nautical fuel oil was tested in the human breast carcinoma cell line MCF-7, in which it induced cell proliferation up to 70% relative to the maximal induction by E2. At its minimum effect concentration of 25?mg/L, the oil was also capable of inducing mRNA expression of the estrogen-dependent protein pS2 by a factor of two. The present results indicate that oils naturally contain potentially endocrine-disrupting compounds that are able to influence the estrogenicity of other compounds and may cause biological responses beyond receptor binding.     

Respiratory symptoms,ventilatory impairment,and bronchial reactivity in oil mist-exposed automobile workers

Studies concerning the respiratory effects of oil mists are sparse and contradictory. The aim of this study was to determine the respective effects of occupational exposure to straight cutting oils and soluble mineral oils on the prevalence of respiratory symptoms, ventilatory impairment, and bronchial reactivity. The population study consisted of 308 male workers of a large French car-making plant, including 40 subjects chronically exposed to straight cutting oils (group S), 51 subjects chronically exposed to soluble mineral oils (group E), 139 subjects with chronic dual exposure to straight cutting oils and soluble mineral oils (group D), and 78 unexposed assembly workers used as a control group (group C). Worker evaluation included a standardized questionnaire, measurement of pulmonary function, and a methacholine challenge. Oil mist concentration at the work place was determined by gravimetric analysis. The arithmetic mean concentration was 2.6 ± 1.8 mg/m³. The geometric mean concentration was 2.2 pm 1.9 mg/m³. The prevalence of respiratory symptoms did not differ significantly among the four groups. However, the subjects exposed to straight cutting oils (group S + group D) had a significantly higher prevalence of chronic cough and/or phlegm than the others (group E + group O): 25.7% vs. 16.3% (p = 0.048). Furthermore, the prevalence of cough and/or phlegm increased significantly (p = 0.03) with increasing duration of exposure to straight cutting oils after adjustment on smoking categories. Lung function tests did not differ significantly among the four groups but we observed a significant decrease of forced expiratory volume in 1 see (FEV₁), forced expiratory flow during the middle half of forced vital capacity (FEF_25-75), and maximal flow rate at 50% and 25% of exhaled forced vital capacity (V₅₀ and V₂₅) according to duration of exposure among smokers exposed to straight cutting oils, suggesting a synergistic effect of tobacco and insoluble oils. No effect of exposure to mineral oils on bronchial reactivity was demonstrated. It is concluded that despite low levels of pollution by oil mists, the present study has shown tenuous adverse chronic effects of straight cutting oils on respiratory symptoms and lung function. However, no adverse effect of soluble mineral oils was demonstrated. These results suggest that threshold limit values for mineral oils should be reassessed.     

Immunological and respiratory changes in tea workers

Immunological status and respiratory function were studied in 26 female nonsmokers employed in processing different types of tea. Skin tests with tea-allergens demonstrated the highest percentage of positive reaction to sage (45%), gruzyan (40%), mentha (35%), and dog rose (10%). Among 17 skin-tested control workers, 23% had positive skin reaction to sage, 19% to gruzyan tea, 20% to mentha and 11% to dog rose and Indian teas. Serum levels of total IgE were increased in 27% of the tea workers and in 7% of the control subjects. Prevalence of almost all chronic respiratory symptoms was higher in tea workers with positive skin tests than in those with negative skin tests to tea allergens. Tea workers with positive skin tests to tea allergens had larger mean acute reduction over the Monday workshift in flow rates (MEF50%: -11.9%; MEF25%: -20.6%) than in those with negative skin tests (MEF50%: -5.7%; MEF25%: -16.7%), thus suggesting an obstructive effect mostly located in smaller airways. Bronchoprovocation testing with different tea allergens provoked acute reductions of ventilatory capacity in four out of six subjects tested. Relative fall over a 90-min post exposure was greater in MEF25% (ranging from 13% to 67%) than in MEF 50% (ranging from 9% to 45% of the control values).     

Contrasting Mercury Bioavailability in the Marine and Fluvial Dominated Areas of the Jaguaribe River Basin,Ceará, Brazil

Solar radiation exposure can increase the toxicity of bioaccumulated oil compounds in a diversity of aquatic species. We investigated the photoenhanced toxicity of weathered South Louisiana crude oil in sediment and water accommodated fractions (WAF) to larval zebrafish. Larvae were first exposed for 24 h to one of six treatments: no oil (sediment or water), 7.5 g oil/kg sediment, oil-only WAF, oil WAF plus the dispersant Corexit 9500A, or dispersant alone. Larvae were then exposed to high or low levels of sunlight in control water for 3 or 3.5 h. Hydrocarbon concentrations were measured in exposure media, including alkanes, polycyclic aromatic compounds and total petroleum hydrocarbons. Significant phototoxicity was observed in larvae exposed to oiled sediment, oil-only WAF, and oil plus dispersant WAF. The results indicated that petroleum from the northern Gulf of Mexico can be phototoxic to larval fish exposed to oil in either the water column or sediment.     

The systemic toxicity of Prudhoe Bay crude and other petroleum oils to CD-1 mice

CD-1 mice were given oral doses of 0–16 ml/kg/ day for five days of Prudhoe Bay (PBCO), South Louisiana and Arabian Light crude oils, Bunker C oil (BCO), mineral oil (MO) and corn oil. Minor decreases in packed cell volume and increases in mean corpuscular hemoglobin concentration occurred after ingestion of crude oils and BCO. Dietary depletion of vitamin E and selenium failed to enhance hematological changes. Pronounced liver enlargement and atrophy of thymus and spleen accompanied ingestion of all petroleum oils except MO and were shown to be dependent on dose of PBCO. Concentration of RNA and total RNA were increased while total DNA, but not concentration of DNA, was increased in enlarged livers. Liver enlargement was attributed primarily to hyperplasia with an additional contribution due to hypertrophy. The severe hemolytic anemia reported in marine birds that ingested PBCO was not reproduced in mice. Liver enlargement and lymphoid tissue atrophy were similar to those reported in other species exposed to petroleum oils.     

Suppression of avian hepatic lipid metabolism by solvent extracts of garlic: impact on serum lipids

The effects of garlic on lipid metabolism were examined in White Leghorn pullets that had been fed for 4 weeks either a control diet based on corn and soybean meal or an experimental diet containing either 3.8% garlic paste, a solvent extract (petroleum ether, methanol and water in sequence) of garlic paste, the residue or commercial garlic oil. Significant decreases in hepatic 3-hydroxy-3-methylglutaryl-CoA reductase (79-83%), cholesterol 7 alpha-hydroxylase (43-51%), fatty acid synthetase (17-29%) and in representative pentose-phosphate pathway (23-39%) activities accompanied the feeding of the petroleum ether-, methanol- and water-soluble fractions of garlic. Garlic paste and oil also suppressed these activities. Significant decreases in serum lipids occurred in response to the feeding of these garlic fractions: serum total cholesterol by 20-25%, low density lipoprotein cholesterol by 28-41% and triglycerides by 10-26%; but high density lipoprotein cholesterol failed to respond to these treatments. The residue remaining after solvent fractionation had little influence on these parameters. These findings were substantiated by a second study in which pullets of a commercial broiler line were fed the garlic fractions. The results confirm that garlic oil and odorous components of garlic lower cholesterol levels. An odorless water-soluble component of garlic also has this effect. The mechanism of the hypocholesterolemic action is at the level of the suppression of cholesterol biosynthesis.     

Comparative toxicity of four chemically dispersed and undispersed crude oils to rainbow trout embryos

The chronic toxicity of crude oil to fish embryos depends on the chemical constituents of the test oil and on factors that control the exposure of embryos to those constituents. The partitioning of chemicals from oil to water depends on the surface area of oil exposed to water and thus on the susceptibility of oil to be dispersed into droplets. The chronic toxicity of four different crude oils to embryos of rainbow trout (Oncorhynchus mykiss) was measured by exposure to the water-accommodated fraction (WAF; no droplet formation) and to the chemically enhanced WAF (CEWAF) of each oil. When effects were compared with the amount of WAF or CEWAF added to test solutions, chemical dispersion increased toxicity dramatically, by >35 to >300-fold, with the smallest difference measured for the lightest and least viscous oil. When effects were compared with measured concentrations of oil in test solutions, there were no differences in toxicity between WAF and CEWAF treatments, indicating that chemical dispersion promoted droplet formation and the partitioning of hydrocarbons from oil to water. On a dilution basis, the differences in toxicity among the four oils were correlated with the concentrations in oil of polynuclear aromatic hydrocarbons (PAH), particularly those with three to five rings, and with their viscosity, an index of dispersibility. However, when PAH concentrations were measured in solution, toxicity did not vary substantially among the four oils, suggesting that the PAH of each oil had equivalent toxicities and that differences in toxicity represented differences in dispersability.     

Respiratory toxicology of mineral oils in laboratory animals

Early subchronic and chronic inhalation toxicology studies on various petroleum mineral oils and formulated lubricants supported the ACGIH TLV of 5 mg/m(3) for mineral oil mist. Additional subchronic studies with aerosolized mineral base oils and lubricants during the last 15 years demonstrated that exposures to aerosols of mineral base oils (often >100 mg/m(3)) resulted mainly in concentration-related accumulation in the lung of alveolar macrophages laden with oil droplets. Inflammatory cells were observed with higher aerosol concentrations, consistent with the clinical literature from highly exposed workers. These pulmonary changes appeared to be a nonspecific response to the presence of deposited aerosol. Studies on sensory irritation during exposures of lab animals to mineral oils indicate possible effects only with very high aerosol concentrations. Coupled with changes in refining to remove carcinogenic polynuclear aromatic hydrocarbons from mineral oils several decades ago, this information indicates that current aerosols of mineral oils have a profile of low toxicity from acute to long-term exposures. Available information suggests that additives in some formulated products and/or maintenance of mineral-based metalworking fluids may play a much more significant role in potential health effects.