Elimination of pesticides in olive oil by refining using bleaching and deodorization.

The effects of the processing steps on some pesticides during physical refining of olive oil were determined. Oil samples were spiked with four types of pesticides, i.e. endosulfan (alpha-endosulfan, beta-endosulfan and endosulfan sulphate), simazine, oxifluorfen and diflufenican, and subjected to physical refining (bleaching and deodorization). The removal of contaminants by bleaching earths was compared using five types of commercial earths. Deodorization assays under laboratory (10 kg) and discontinuous pilot plant (200 kg) conditions at different temperatures and treatment times were carried out. Bleaching seemed effective only for the elimination of simazine. For removal of the other pesticides tested, a physical refining treatment was required at 240 degrees C in the deodorizing stage for different periods (1 h for diflufenican, oxifluorfen and alpha-endosulfan, 2 h for beta-endosulfan and 3 h for endosulfan sulphate).

Phenolic compounds in olive oils intended for refining: formation of 4-ethylphenol during olive paste storage.

The phenolic composition of "lampante olive oil", "crude olive pomace oil", and "second centrifugation olive oil" was characterized by high-performance liquid chromatography with UV, fluorescence, and mass spectrometry detection. The phenolic profile of these olive oils intended for refining was rather similar to that previously reported for virgin olive oil. However, a new compound was found in these oils, which is mainly responsible of their foul odor. It was identified as 4-ethylphenol by comparison of its UV and mass spectra with those of a commercial standard. Although 4-ethylphenol was discovered in all oils intended for refining, its presence was particularly significant in "second centrifugation olive oils", its concentration increasing with time of olive paste storage. Similar trends were observed for hydroxytyrosol, hydroxytyrosol acetate, tyrosol, and catechol, the concentration of these substances reaching values of up to 600 mg/kg of oil, which makes their recovery for food, cosmetic, or pharmaceutical purposes attractive.

Storage time and deodorization temperature influence the formation of aniline-derived compounds in denatured rapeseed oils.

In 1981 an epidemic, named Toxic Oil Syndrome, occurred in Spain as a result of ingestion of rapeseed oil denatured with 2% aniline, which had been imported for industrial use but was fraudulently diverted and processed for human consumption. Two groups of chemical compounds have been identified in the ingested toxic oil: fatty acid anilides and amino-propanediol derivatives. The objective of this work was to assess the effect of several refining process variables on the formation of 3-(N-phenylamino)-1,2-propanediol (PAP) esters. The amount of PAP esters in aniline-denatured oil increased dramatically when oil was heated from 250 degrees C to 300 degrees C. However, the ones formed when 300 degrees C was reached were lost during processing at that temperature. The level maintained during the operation time at 300 degrees C was higher in denatured samples stored for 3 weeks before refining than in denatured samples stored only for 1 week. Anilides were also analyzed. We found that anilides decreased very little with distillation time. In this paper we discuss the influence of storage time prior to refining and of elevated refining temperature, such as temperatures that might occur in close proximity to a deodorizer coil.

Pathology of "toxic oils" and selected metals in the MRL/lpr mouse.

The Toxic Oil Syndrome epidemic that occurred in Spain in 1981 and affected nearly 20,000 people was caused by ingestion of oil mixtures that contained analine-denatured rapeseed oil. To date, an animal model in which to identify the actual etiologic agents(s) and to investigate the pathogenesis of the disease has not been discovered. In this study, the MRL/lpr was used to assess the histopathological response of 3 "toxic oils" and 3 metals. The oils tested were a denatured rapeseed oil collected from a family who were affected by the Toxic Oil Syndrome epidemic in Spain (CO756) plus two synthesized oils (RSD and RSA). Female mice, 7 weeks of age, received an undiluted (neat) or a 1:10 diluted dose of each oil; mercury (50 ppm), cadmium (100 ppm), or lead (50 ppm). Half of each group was killed after 5 weeks of exposure and the remaining mice after 10 weeks of exposure. Body and organ weights (liver, kidney, thymus, and spleen) were recorded and selected organs were collected for histopathology. Ten weeks after treatment, body weights (BW) of the cadmium and lead groups were significantly suppressed, and the body weight of the C0756-neat group was significantly increased compared to their respective controls. Kidney/BW were decreased in the RSA-neat and RSA 1:10 groups after 10 weeks of exposure, and the kidney/BW in the mercury and cadmium groups were increased. Spontaneous development (12 weeks of age) and progression (17 weeks of age) of histopathological lesions are described for selected organs examined in the naïve mice as are changes that resulted from exposure to the "toxic oils" and metals. C0756-neat, mercury, and lead suppressed progression of the glomerulonephritis that normally occurs in the MRL/lpr mouse. Also of interest were lesions that included mononuclear cuffing of hepatic bile ducts, progression of the granulomas that formed in the renal glomeruli, vessels in the lymphoid organs that contained tightly packed lymphocytes, and the presence of plasma cells in the thymus. All 3 oils stimulated early development of the lymphoproliferative syndrome characteristic of the MRL/lpr mouse as demonstrated by an increase in the thymus/BW and spleen/BW ratios after 5 weeks of treatment. These data contribute to our knowledge of spontaneous disease progression in the thymus, spleen, lymph nodes, and kidneys in the MRL/lpr mouse and the effects of 3 different "toxic oils" and metals on the development and progression of those lesions.