Subject(s)
Causality , Adult , Aged , Alcohol Drinking , Anilides/poisoning , Animals , Case-Control Studies , Chi-Square Distribution , Child , Female , Humans , Lung Neoplasms/etiology , Male , Myocardial Ischemia/epidemiology , Myocardial Ischemia/prevention & control , Oleic Acids/poisoning , Risk , Risk Factors , Sex Factors , Smoking/adverse effects , Syndrome , Time FactorsABSTRACT
The toxic oil syndrome (TOS) was caused by the ingestion of an adulterated rapeseed oil containing oleic acid anilide (OAA). It was characterized by lethal symptoms in the acute phase and by symptoms of idiopathic autoimmune diseases in the chronic phase. The pathogenetic mechanisms remain unclear. In a murine model of TOS we demonstrate strain-dependent effects on the immune system after treatment with OAA intraperitoneally. While C57BL/6 (H-2b) mice develop a polyclonal B cell activation without disease symptoms, most A/J (H-2a) mice suffer an acute lethal wasting disease. These differences are reflected in the splenic cytokine gene expression and secretion and in the Ig production. Increased IgE serum levels and reduced TNF-beta mRNA suggest a Th2 cell response in C57BL/6 mice. In A/J mice, splenocytes express IL-1alpha, IL-10, and IFN-gamma mRNA in vivo and secrete high levels of TNF-alpha in vitro. These observations resemble the human condition in TOS with development of either an acute lethal disease or a chronic autoimmune-like disease. As in other chemical-induced reactions genetic susceptibility seems to be important.
Subject(s)
Anilides/poisoning , Autoimmune Diseases/chemically induced , Cytokines/biosynthesis , Immunoglobulin E/blood , Oleic Acids/poisoning , Wasting Syndrome/chemically induced , Animals , Autoimmune Diseases/genetics , Autoimmune Diseases/immunology , Cells, Cultured , DNA Damage , Disease Models, Animal , Disease Susceptibility , Female , Interferon-gamma/biosynthesis , Interferon-gamma/genetics , Interleukin-1/biosynthesis , Interleukin-1/genetics , Interleukin-10/biosynthesis , Interleukin-10/genetics , Lymphotoxin-alpha/biosynthesis , Lymphotoxin-alpha/genetics , Male , Mice , Mice, Inbred C57BL , Mice, Inbred Strains , Plant Oils/poisoning , RNA, Messenger/analysis , Spleen/immunology , Splenomegaly/chemically induced , Splenomegaly/immunology , Tumor Necrosis Factor-alpha/biosynthesis , Tumor Necrosis Factor-alpha/genetics , Wasting Syndrome/genetics , Wasting Syndrome/immunologyABSTRACT
A histopathological study was made of Clara cells in lungs from mice intoxicated by sc injections of linoleylanilide dissolved in olive oil (20% w/v) at doses of 1,000, 2,500 or 4,000 mg/kg administered at 500 mg/kg on 2, 5 or 8 occasions, respectively. Cells were evaluated for biotransformation capacity. Morphological alterations included degeneration processes in the Clara cells that correlated with the doses administered. The observed lesions were very similar to those caused by xenobiotics with pneumotoxic capacity due to their biotransformation to electrophilic intermediates. The changes observed in Clara cells under our experimental conditions may reflect the activity of reactive catabolites from oleoanilides.
Subject(s)
Anilides/poisoning , Linoleic Acids/poisoning , Lung/drug effects , Anilides/metabolism , Animals , Cytoplasmic Granules/ultrastructure , Linoleic Acids/metabolism , Lung/pathology , Lung/ultrastructure , MiceSubject(s)
Anilides/toxicity , Water Pollutants, Chemical/toxicity , Water Pollutants/toxicity , Anilides/analysis , Anilides/poisoning , Animals , Dose-Response Relationship, Drug , Guinea Pigs , Lethal Dose 50 , Maximum Allowable Concentration , Mice , Rats , Skin Absorption/drug effects , Time Factors , Water Pollutants, Chemical/analysis , Water Pollutants, Chemical/poisoningABSTRACT
In May 1981 a new disease, with epidemic characteristics, appeared in Spain. Initially it was thought that an infectious agent was responsible for the disease, a theory that was later discarded when the disease was found to be associated with the ingestion of adulterated olive oil contaminated with potentially toxic chemicals. More than 20 000 people have been affected, and whilst official reports put the death toll at 250, the true figure may exceed 300. The disease is multi-systemic in presentation, affecting several organs and systems of the body. The disease has a poor prognosis in its chronic stages, which affect approximately 10% of victims, and its ultimate natural history is still to be observed. The pathogenesis of the disease remains to be elucidated, despite considerable efforts already made in this direction.
Subject(s)
Brassica , Oils/poisoning , Anilides/poisoning , Autoantibodies/immunology , Disease Susceptibility , HLA Antigens/immunology , Humans , Immunoglobulin E/immunology , Mycotoxins/poisoning , SyndromeABSTRACT
In a survey of occupationally acquired disease in workers at a pesticide plant, we found that 11 (11%) of 102 workers had been hospitalized for illness related to chemical exposures; highest hospitalization rates occurred in packaging (27%), production (22%), and maintenance (9%) workers. Commonest causes of hospitalization were intoxication by the carbamate pesticide methomyl [1-(methylthio)ethylideneamino methyl carbamate], a reversible cholinesterase inhibitor, and methemoglobinemia following exposure to 3,4-dichloroaniline. On clinical evaluation, five (46%) of 11 packaging workers, the group with the highest exposure to methomyl, had experienced blurred vision or pupillary constriction. Seventeen (61%) of 28 production workers with exposure to dichloroaniline and propanil (3'4'-dichloropropionanilide) had chloracne, an acne-form dermatosis caused by the contaminant tetrachlorazobenzene in propanil and dichloroaniline. The chloracnegenic potentials of propanil and dichloroaniline were verified by rabbit ear tests. These findings reemphasize the hazards inherent in the the manufacture and formulation of pesticides and herbicides.
