ascorbic-acid and Carcinoma--Bronchogenic

In the first part of this study we have shown how the serum levels of four selected tumour markers, namely tissue polypeptide antigen (TPA), carcino-embryonic antigen (CEA), hyaluronic acid (HA) and ferritin, display patterns characteristic of mesothelioma (M) or bronchogenic carcinoma (BC) in asbestos-exposed workers, and we hypothesize that the differences in marker patterns correspond to differences in carcinogenesis mechanisms. In a preliminary study, we found these specific marker patterns in 5/19 exposed workers of whom only one demonstrated any radiological signs of disease. Thus these specific marker patterns may be early events, occurring long (possibly years) before the classical radiological signs of exposure to asbestos. Accordingly they afford an optimal opportunity for prevention which should be adapted to the carcinogenesis mechanism as it is revealed by the marker pattern; it is aimed at antagonizing free radical carcinogenesis in all persons with TPA levels in excess of 100 U/l or Ferritin in excess of 400 ng/ml, and at inhibiting chemical carcinogenesis in those having elevated CEA levels (over 3 ng/ml). The mechanisms involved in these inhibitory processes are described and discussed, as well as the practical implementations that proceed from them. A prevention trial is now being started among 300 active and retired workers of an asbestos-cement works in northern France; the design of the study is presented. This prevention programme should be maintained over many years and holds a strong potential for reducing the untoward effects of exposure to asbestos.

Topics: Acetylcysteine; Antigens, Neoplasm; Asbestos; Ascorbic Acid; beta Carotene; Biomarkers, Tumor; Carcinoembryonic Antigen; Carcinoma, Bronchogenic; Carotenoids; Cohort Studies; Ferritins; Humans; Hyaluronic Acid; Longitudinal Studies; Lung Neoplasms; Male; Mesothelioma; Middle Aged; Occupational Diseases; Occupational Exposure; Peptides; Riboflavin; Selenium; Tissue Polypeptide Antigen; Vitamin A; Vitamin E

Plasma and buffy-coat vitamin C were estimated in 158 samples from 139 lung-cancer patients, at all stages of the disease. Most samples showed hypovitaminosis C in both estimations: 64% had plasma, and 25% buffy-coat values below the thresholds for incipient clinical scurvy (0.3 mg% and 10 micrograms/10(8) cells respectively). Levels were diet-dependent and could be increased by oral supplements. Levels were low both in tumour-bearing patients and in those clinically free of disease after resection. The latter had particularly low values during the first 6 months, indicating the utilization of vitamin C in surgical repair. The vitamin C content of 13 primary lung tumours was assayed: tumours had a higher vitamin C content (mean 111.6 +/- 55.1 micrograms/g tissue) than normal lung (58.5 +/- 20.4 micrograms/g). Mononuclear cells from normal individuals show a higher vitamin C content than polymorphs, but in lung-cancer patients the expected correlation of buffy-coat vitamin C with the proportion of lymphocytes in peripheral blood was obscured by an inverse correlation in patients with relative lymphocytosis (greater than or equal to 25% lymphocytes), confirmed by an inverse correlation of the proportion of lymphocytes in peripheral blood with mononuclear-cell vitamin C in 14 patients in whom this was measured. These correlations were unaffected by controlling for plasma values, and indicate the utilization of vitamin C in lymphocyte-related anti-tumour mechanisms. Vitamin C is necessary for phagocytosis and for the expression of cell-mediated immunity. In view of the increasing circumstantial evidence that immune mechanisms exert some measure of control on tumour extension and metastasis in man, the effect of supplementation with vitamin C in lung-cancer patients on survival should be tested in a clinical trial.

Topics: Adult; Aged; Ascorbic Acid; Ascorbic Acid Deficiency; Carcinoma, Bronchogenic; Diet; Female; Humans; Immunity, Innate; Leukocyte Count; Leukocytes; Lung Neoplasms; Lymphocytes; Male; Middle Aged; Seasons

The dominant role of the physical and chemical environment in the development of cancer is challenged. Analyses of the etiology of skin, bladder, respiratory and gastric cancers are presented which demonstrate the considerable extent to which one's health status may modify the initiation and promotion of environmentally associated cancers. It is concluded that although environmental factors may initiate and/or promote 85 to 90 percent of all cancers this is misleading since it neglects the critical role of the individual's health status as a factor modifying carcinogenesis.

Topics: Ascorbic Acid; Benzopyrenes; Carcinogens, Environmental; Carcinoma, Bronchogenic; Diet; Humans; Hydrocarbons; Neoplasms; Neoplasms, Radiation-Induced; Racial Groups; Riboflavin; Skin Neoplasms; Smoking; Stomach Neoplasms; Ultraviolet Rays; Urinary Bladder Neoplasms; Vitamin A

Topics: Ascorbic Acid; Brain; Brain Damage, Chronic; Carcinoma, Bronchogenic; Dementia; Diagnosis, Differential; Drug Therapy; Geriatrics; Humans; Niacin; Psychotic Disorders; Schizophrenia; Urine