Adulterated Cooking Oils Research Articles

Identification of Adulterated Cooking Oil by Raman Spectroscopy

Identification of Adulterated Cooking Oil by Raman Spectroscopy

Systemic sclerosis: environmental and occupational risk factors.

There is growing concern about the association between systemic sclerosis and certain environmental and occupational risk factors, including exposures to vinyl chloride, adulterated cooking oils, L-tryptophan, silica, silicone breast implants, organic solvents, and other agents such as epoxy resins, pesticides, and hand/arm vibration. This article highlights the current medical research that has examined these associations in scleroderma-like disorders and in systemic sclerosis.

Eosinophilia-myalgia syndrome, toxic-oil syndrome, and diffuse fasciitis with eosinophilia

Eosinophilia-myalgia syndrome, a recently described illness, reached epidemic proportions in 1989 and was linked to the ingestion of L-tryptophan containing trace amounts of several contaminants. Eosinophilia-myalgia syndrome shares many clinical and pathologic similarities with toxic-oil syndrome, an epidemic linked to the ingestion of adulterated cooking oil that occurred in Spain in 1981, and to diffuse fasciitis with eosinophilia, a condition first described in 1974. Over the past year, much work has been done in understanding the etiology and pathogenesis of eosinophilia-myalgia syndrome and toxic-oil syndrome. Follow-up data detailing the long-term sequelae and mortality rates for these two conditions are becoming available. The results from these studies are reviewed in this paper.

Cyclooxygenase and lipoxygenase arachidonate metabolites synthesized by mouse peritoneal macrophages: in vitro effect of N-phenyllinoleamide from toxic oil samples.

N-phenyllinoleamide (NPLA) has been detected as extraneous compound in adulterated cooking oils associated with a unique epidemic disease known as the Toxic Oil Syndrome (TOS). In this communication we report on the action of NPLA on the endogenous cyclooxygenase and lipoxygenase arachidonate metabolism. Results show that mouse peritoneal macrophages (MPM) exposed to 1 mM NPLA for 2 h undergo significant increases of 6-keto prostaglandin F1a, prostaglandin E2, leukotriene B4, 12- and 15-hydroxyeicosatetraenoic acids. MPM prelabelled with 3H-AA showed an enhanced release when exposed to NPLA. Thus, it is concluded that NPLA potentiates AA release from cell membrane phospholipids and the subsequent cyclooxygenase and lipoxygenase oxidative metabolism of this precursor to various eicosanoids. This is in agreement with the implication of peroxidative process mediated by fatty acids anilides in TOS.

Isotype-restricted hyperimmunity in a murine model of the toxic oil syndrome.

The toxic oil syndrome is characterized by IgE elevation and eosinophilia, as well as scleroderma-like skin manifestations and other symptoms of autoimmune disease. Fatty acid anilides, found in large amounts in adulterated cooking oil, were suspected to be the etiologic agent in this disease. The capacity of oleic acid anilide to induce features of autoimmunity in vivo was investigated. B10.S mice were continuously treated i.p. with oleic acid anilide for 6 wk by using osmotic pumps. A significant increase in IgE and IgM serum levels was observed after 1 to 3 wk; subsequently five of six mice developed IgG1 levels 3.5- to 10-fold higher than the controls. Anilide-treated mice developed splenomegaly with a 2.1- and a 3.5-fold increase in IgM- and IgG-bearing splenocytes, respectively, and a 5.6- and 29-fold elevation in functional IgM- and IgG-secreting cells, respectively. Increased serum levels of predominantly IgM antibodies to histone, denatured DNA, and DNP as well as rheumatoid factor were detected. In vivo expression in the spleen of 10 cytokine genes was also examined, and mRNA encoding IL-1 beta and IL-6 were significantly elevated in splenocytes of anilide-treated mice. The enhanced Ig production suggests that anilide induced a cytokine-mediated polyclonal activation of B cells. Elicitation of IgM antibodies to denatured forms of autoantigens indicates that anilide treatment partially broke autoimmune tolerance in these mice. Anilide-treated mice may be a useful animal model for further exploring the mechanism and pathogenesis of systemic autoimmunity in the toxic oil syndrome.

Hepatic injury in the toxic epidemic syndrome caused by ingestion of adulterated cooking oil (Spain, 1981).

We describe the clinico-pathological characteristics of hepatic injury associated with the toxic-epidemic syndrome caused by the consumption of adulterated rapeseed oil. Of 842 toxic-epidemic syndrome patients admitted to our hospital between May, 1981, and January, 1982, 24.1% showed signs of liver involvement which was more frequent in women and in the fourth decade of life. No statistical significance was found in relation to alcohol consumption, treatment with potentially hepatotoxic antibiotics, or adult respiratory distress syndrome. Most (91.6%) patients with hepatic injury were asymptomatic; jaundice or abdominal pain was rarely noted. One patient died of acute liver failure following Budd-Chiari syndrome. Serum gamma-glutamyl transpeptidase activity was raised in all cases, alkaline phosphatase in 94.6%, and less frequently lactate dehydrogenase (80%), SGPT (84.7%), and SGOT (76%). Serum total bilirubin was usually normal (89.2%). The histologic lesion was similar to drug-induced cholestatic hepatitis. Lamellar inclusions, canalicular injury, giant mitochondria, and hyperplasia of the smooth endoplasmic reticulum were seen by electron microscopy. Ultrastructural signs of cholestasis were common (78.9%). The pathogenesis of this lesion is unknown; however, because of similarities with chlorpromazine-induced cholestatic hepatitis, we suggest that a combination of hypersensitivity and intrinsic hepatoxicity is a possible mechanism.