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The author describes a thin-layer chromatographic method for the detection of small amounts of mineral oil and paraffin in foods. Fatty acids, glycerides, fat-soluble vitamins, sterols, and unsaturated hydrocarbons remain at the starting point. This method permits to detect as little as 0.2 mug of mineral oil or 20 mug of mineral oil/kg of food in low-fat products. 0.01% of mineral oil-like contaminants may be detected in fats.
The lipopolysaccharide (LPS) content of peritoneal fluids of BALB/c mice given mineral oil injections and of normal mice was measured. Peritoneal fluids were passed through DEAE-Bio-Gel columns to remove an inhibitor to the Limulus amebocyte lysate reaction and then were assayed for LPS by a spectrophotometric Limulus amebocyte lysate test. A highly significant difference between control animals and animals given mineral oil injections was found. A clear correlation between LPS concentration and time after first oil injection was shown. P-200 gel chromatography and heat stability of the active material were consistent with the behavior of LPS. The possible role of LPS in the pathogenesis of plasma cell tumor is discussed.
BACKGROUND: A retrospective cohort study of workers employed at a California aerospace company between 1950 and 1993 was conducted; it examined cancer mortality from exposures to the rocket fuel hydrazine. METHODS: In this study, we employed a job exposure matrix (JEM) to assess exposures to other known or suspected carcinogens-including trichloroethylene (TCE), polycyclic aromatic hydrocarbons (PAHs), mineral oils, and benzene-on cancer mortality (1960-2001) and incidence (1988-2000) in 6,107 male workers. We derived rate- (hazard-) ratios estimates from Cox proportional hazard models with time-dependent exposures. RESULTS: High levels of TCE exposure were positively associated with cancer incidence of the bladder (rate ratio (RR): 1.98, 95% confidence interval (CI) 0.93-4.22) and kidney (4.90; 1.23-19.6). High levels of exposure to mineral oils increased mortality and incidence of lung cancer (1.56; 1.02-2.39 and 1.99; 1.03-3.85), and incidence of melanoma (3.32; 1.20-9.24). Mineral oil exposures also contributed to incidence and mortality of esophageal and stomach cancers and of non-Hodgkin's lymphoma and leukemia when adjusting for other chemical exposures. Lagging exposure measures by 20 years changed effect estimates only minimally. No associations were observed for benzene or PAH exposures in this cohort. CONCLUSIONS: Our findings suggest that these aerospace workers who were highly exposed to mineral oils experienced an increased risk of developing and/or dying from cancers of the lung, melanoma, and possibly from cancers of the esophagus and stomach and non-Hodgkin's lymphoma and leukemia. These results and the increases we observed for TCE and kidney cancers are consistent with findings of previous studies.
We evaluated the survival and the morphological alteration of 70 strains of Paracoccidioides brasiliensis maintained in the Fungal Culture Collection of Institute Oswaldo Cruz and initially preserved by successive subculturing and later under mineral oil at room temperature from 1923 to 1992. Of the 70 strains preserved under mineral oil, 18 (26%) continued to be viable. The mycelia of the 18 viable strains and the mycelia of four representatives of the non-viable strains presented transitional micromorphology under mineral oil. Macroscopy and microscopy of the first subcultures of five of the seven strains, taken as random samples from the 18 viable strains and plated onto peptone-yeast extract-glucose agar, glucose-glycine-yeast extract agar and brain-heart infusion agar media at room temperature, revealed that all samples appeared to be in a transition phase (Y<-->M). These five strains were unable to grow and complete thermal dimorphism at a temperature of 37 degrees C. Only two strains were able to complete the entire dimorphic process. The period of preservation of these strains under oil was relatively short, i.e. 9 and 10 years. The results demonstrate that less widely spaced subculturing and more appropriate culture and environmental conditions are needed to preserve P. brasiliensis strains under oil.
The effect of two dietary treatments upon fecal excretion of Mirex was studied in rhesus monkeys dosed with 14C-Mirex. Administration of 5% mineral oil in the diet during the first month following dosing resulted in about 50% increase in fecal excretion of Mirex. The same treatment repeated 6 months after dosing triggered about a 400% increase in fecal excretion of Mirex. Subsequent dietary administration of cholestyramine resulted in a comparably small effect of fecal excretion of Mirex. The considerable difference in the ability of mineral oil to induce the effect during the first and sixth month after dosage is likely to be due to compartmental redistribution of Mirex. Mineral oil treatment appears to effect primarily the "very deep" compartment (fatty tissues) by enhancing intestinal elimination of Mirex.
Urine from workers of a cold-rolling steel plant exposed to mineral oils were tested for the mutagenic activity by the Salmonella/microsome assay, and for D-glucaric acid content as a measure of hepatic mixed-function oxidase activity. An occupationally unexposed group served as control. The biological monitoring phase followed an environmental phase carried out in the working environment that showed a substantially low mutagenic/carcinogenic risk for the exposed workers. Urine samples were collected before, during and after work. From the results it was observed that the urinary mutagenicity was detectable only with TA98 strain in the presence of enzymatic activation (+ S9 mix). Further addition of beta-glucuronidase did not give any enhanced mutagenic effects. There was a significant difference in urinary mutagenicity between the exposed and control workers. However, in both groups the highest mutagenicity data was found in smokers: both exposed smoking workers and smoking controls had significantly higher urine mutagenicity than the non-smoking exposed and control workers. The results suggested a synergistic effect of smoking with exposure to mineral oils: the mutagenicity of urine from exposed smokers was significantly higher than that of control smokers. There was no difference in urinary D-glucaric acid results between exposed and unexposed groups, however, smokers of both groups had a significant increase in D-glucaric acid excretion. The authors suggest that even for this workplace with its low mutagenic/carcinogenic risk, smoking could interact with the complex mixtures present in the environment, and thus modify urinary mutagenicity data.
Toxicity of emulsified trehalose-6,6'-dimycolate administered intravenously into mice depended on the size distribution of the mineral oil droplets. Emulsions containing the greatest number of the largest oil droplets were the most toxic. Emulsions of trehalose-6,6'-dimycolate made with peanut oil or with olive oil were less toxic than those made with mineral oil.
Dimethyl dioctadecyl ammonium bromide (DDA), a lipophilic quaternary amine, was evaluated in adult chickens for potentiation of immunological responses to subcutaneously administered inactivated Newcastle disease virus (NDV) vaccines. DDA enhanced humoral and cell-mediated immune (CMI) responses to levels which were significantly higher than those induced by the vaccine alone The haemagglutination inhibition antibody titers induced by DDA were slightly lower than those induced by mineral oil although neutralizing antibody titers seemed to be higher. DDA induced strong CMI (DTH and lymphocyte proliferation) responses, more than those induced by Freund's complete adjuvant and mineral oil. Both DDA and mineral oil induced comparable high levels of protection to challenge doses of 200,000 LD50 per chicken. No toxic effects or local tissue damage were observed in any of the inoculated chickens.
Steroid hormones, such as progesterone, oestrogen, androgen and meiosis activating sterols, are secreted from cumulus cells that are stimulated by gonadotrophins during maturation of oocytes in vitro. These steroid hormones may be absorbed by mineral oil or paraffin oil; however, in vitro maturation of pig oocytes is commonly performed using medium covered by oil. In this study, high concentrations of progesterone, oestradiol and testosterone were detected in the culture medium after pig cumulus-oocyte complexes (COCs) were cultured with FSH and LH for 44 h in medium without an oil overlay. However, high concentrations of these steroid hormones were not detected in medium when COCs were cultured with the mineral oil overlay. When high concentrations of these steroid hormones were secreted by COCs, germinal vesicle breakdown (GVBD) and the activation of p34(cdc2) kinase and mitogen-activated protein (MAP) kinase in oocytes occurred earlier in comparison with oocytes cultured in medium covered with mineral oil. Moreover, a decrease in p34(cdc2) kinase activity during meiotic progression beyond metaphase I was observed in oocytes cultured in conditions under which high concentrations of steroid hormones were secreted by COCs. In addition, the rate of development to the blastocyst stage after IVF was higher in oocytes matured in medium without an oil overlay. These adverse effects of oil may be explained by absorption by the oil of cumulus-secreted steroids or by the release of toxic compounds into the medium.
Seven days after dosing of two rhesus monkeys with 14C-DDT (50 mg/kg) per os, one monkey was put on a diet containing 5% mineral oil for 35 days, whereas the other animal served as control. During 5 weeks both urinary and fecal excretion of radioactivity was more than doubled in the treated as compared to the untreated animal. At the end of the treatment, concentration of DDT in adipose tissue of the mineral oil treated animal was about half of that found in the control. The data represent further support of previous reports that mineral oil reduces body burdens of refractory lipophilic chemicals.
Twelve mineral oils, originating from naphthenic and paraffinic stocks and variously refined, were evaluated for their potential to induce cutaneous neoplasia in female CF1 mice. The oils were applied to the shorn dorsal skin for up to 78 weeks, using several different treatment regimes. The sole acid/earth refined naphthenic spindle oil was a moderately potent cutaneous carcinogen. By comparison, the 11 oils, processed by other refining routes, were less carcinogenic or non-carcinogenic to murine skin. Two of the 11 oils were weak cutaneous carcinogens viz, a naphthenic spindle oil refined only by mild hydrotreatment and a paraffinic spindle oil refined by mild solvent extraction and 'Ferrofining'. All 9 remaining oils had been solvent-extracted as part of the secondary refining process; none induced malignant tumours, although solitary benign tumours of the treated site were recorded after exposure to 3 oils. The cutaneous carcinogenic potential of the test oils did not correlate well with their potential to induce epidermal hyperplasia at the treated site. Consequently, hyperplasia caused after short term exposure is of little value for distinguishing between carcinogenic and non-carcinogenic oils.
The effect of various dietary treatments on the fecal excretion of [14C]-hexachlorobenzene (HCB) was studied in rats and rhesus monkeys. Cholestyramine and sesame oil failed to influence fecal excretion of HCB and/or metabolites. However, dietary administration of n-hexadecane (5%) increased fecal excretion of radioactivity 4-13-fold in rats and rhesus monkeys. Similarly, mineral oil in the diet (5%) of rhesus monkeys elicited a 6-9-fold increase in fecal excretion of HCB and/or metabolites. As a result of the mineral oil treatment, and enhanced depletion of HCB from blood and also of the stored HCB from adipose tissue was observed. The concentration of HCB in the blood declined in accordance with decreasing storage levels of HCB in adipose tissue. The major site of elimination of HCB and/or metabolites seemed to be the intestine; in particular, the cecum and the colon ascendens. Both hexadecane and mineral oil appeared to stimulate specifically this elimination path way.
Subchronic 90-day feeding studies were conducted on four highly refined white mineral oils to determine any potential for toxicity in Long-Evans rats (20 per sex per dose level) and beagle dogs (4 per sex per dose level). Each oil was fed at dietary dose levels of 300 ppm and 1500 ppm (w/w). No treatment-related effects of toxicological importance were detected in daily observations of general health or in periodic assessments of food consumption and body weight, hematology, serum clinical chemistry, and urinalysis. Observations in dogs suggested that the white oils produced mild laxative effects. Gross and histopathologic examinations, as well as measurements of organ weights, did not reveal any macroscopic or microscopic changes which could be due to treatment. In addition, special staining by Oil Red O of liver, mesenteric lymph nodes, spleen, gastrointestinal tract, stomach, and kidneys indicated no evidence of oil or lipid deposition. A special re-examination of tissues from female and male rats, in response to more recent conflicting data from the Fischer 344 strain, found no histopathologic signs of macrophage accumulation and/or microgranuloma formation in liver, spleen, or mesenteric lymph nodes. These data indicate that repeated exposure to relatively high levels of white mineral oils in the diets does not produce significant subchronic toxicity in Long-Evans rats or beagle dogs.
Guinea pigs received skin application of petroleum-derived mineral oil distillate, containing about 10% of polycyclic aromatic hydrocarbons with the 4 hours exposure time everyday during 20 days. 100% distillate preparation and it's 50%, 3% or 0.5% solutions in furfurol and ethanol are used. It resulted in the distillate-dose-dependent cytochrome P-450 induction (1.38-2.23-fold) in liver of the all exposed groups of guinea pigs and in 20-60% decrease in microsomal and cytosol glutathione transferase activities in groups which received 50% and 3% mineral oil distillate solutions. Ratio values of cytochrome P-450 content level to glutathiontransferase activity level depended linearly on the distillate doses, and it increased 2.7-4.4-fold with the distillate concentration increasing in the preparation from 0.5% to 50%. Conclusion was made that with increasing distillate doses the process of polycyclic aromatic hydrocarbon activation with the genotoxic metabolite formation predominated over the process of those metabolite detoxication.
The toxicological databases for petroleum refinery products such as mineral oils, as well as for their potential contaminants and additives, were reviewed for human cases of poisoning by the oral route. The aim was to determine whether any overlooked adulterant in the oil implicated as the cause of the 1981 outbreak of Toxic Oil Syndrome (TOS) in Spain, may have been responsible for the unusual symptomatology characterizing this disease. The essential features of TOS were peripheral eosinophilia, pulmonary oedema and endothelial damage in the acute phase; myalgia, sensory neuropathy, hepatic injury, skin oedema and sicca in the intermediate phase; and peripheral neuropathy, muscle wasting, scleroderma and hepatopathy in the chronic phase. Of the more than 70 chemical entities and mixtures reviewed here, none had been reported as producing adverse toxic effects upon ingestion resembling the specific set of symptoms and progression that characterized TOS. Because of their viscosity, the most commonly recorded disease process associated with oral ingestion of petroleum refinery products was lipid pneumonia, implicating lung exposure via aspiration. The mineral oil additives and contaminants comprised a highly diverse range of chemical entities, producing a variety of symptoms in instances of poisoning. Specifically, no chemical entity amongst the refinery products, additives or contaminants was described as inducing a syndrome involving vasculitis accompanied by thrombotic events, along with immunological consequences (such as T-lymphocyte activation and cytokine release), as is considered to be the cellular basis of TOS.
The case of a 33 year old male is reported. Hepatic inflammation and scarring were associated with deposits of mineral oil in portal triads. This is believed to be the first reported case of hepatic damage resulting from mineral oil accumulation. Possible sources of the oil are considered.
Before spinning, jute and sisal fibres are treated with a batching oil commonly consisting of a raw mineral oil fraction. Such oil is transferred to foods packed into jute or sisal bags, i.e. primarily cocoa beans, hazelnuts, coffee, almonds, oil seeds, and rice. Concentrations in the foods easily exceed 100 mg/kg. Chocolate may be affected several-fold: cocoa beans as well as hazelnuts and almonds may be contaminated.
PURPOSE: Assisted reproductive technologies require the use of culture media for gametes and embryos. Culture media and conditions intended for use in human in vitro fertilization are tested prior to use by evaluating their ability to support normal development of mouse embryos. RESULTS: Development to blastocysts of two-cell mouse embryos was equivalent for embryos cultured in center well dishes alone (93 +/- 10%, mean +/- SD) and embryos cultured in center well dishes with an overlay of 1 ml of mineral oil (94 +/- 5%). In contrast, no development of two-cell-stage mouse embryos occurred in an embryotoxic medium when cultured in center well dishes. However, when this medium was covered with an overlay of mineral oil, development to blastocyst was no different than that of controls (96 +/- 5%). Similar results were found with cultures of one-cell-stage mouse embryos. CONCLUSION: These results indicate that in some circumstances the presence of mineral oil can significantly alter the outcome of embryo culture. Further, these results reinforce the necessity of directly testing the exact culture conditions to be used for assisted reproductive technologies.