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Biomedical subjects

S S Epstein

Publications and source records attributed to S S Epstein.

At least 19 recordsLinked to original sources
PubMed1990

The chemical jungle: today's beef industry.

In the absence of effective federal regulation, the meat industry uses hundreds of animal feed additives, including antibiotics, tranquilizers, pesticides, animal drugs, artificial flavors, industrial wastes, and growth-promoting hormones, with little or no concern about the carcinogenic and other toxic effects of dietary residues of these additives. Illustratively, after decades of misleading assurances of the safety of diethylstilbestrol (DES) and its use as a growth-promoting animal-feed additive, the United States finally banned its use in 1979 some 40 years after it was first shown to be carcinogenic. The meat industry then promptly switched to other carcinogenic additives, particularly the natural sex hormones estradiol, progesterone, and testosterone, which are implanted in the ears of more than 90 percent of commercially raised feedlot cattle. Unlike the synthetic DES, residues of which can be monitored and use of which was conditional on a seven-day preslaughter withdrawal period, residues of natural hormones are not detectable, since they cannot be practically differentiated from the same hormones produced by the body. The relationship between recently increasing cancer rates and the lifetime exposure of the U.S. population to dietary residues of these and other unlabeled carcinogenic feed additives is a matter of critical public health concern.

Animal Feed↗
PubMed1990

Industrial risk factors for colorectal cancer.

Colorectal cancer is the second most common malignancy in the United States, and its incidence rates have sharply increased recently, especially in males. Industrial exposures, both occupational and environmental, are important colorectal cancer risk factors that are generally unrecognized by clinicians. Migration studies have documented that colorectal cancer is strongly associated with environmental risk factors. The causal role of occupational exposures is evidenced by a substantial literature associating specific work practices with increased colorectal cancer risks. Industrially related environmental exposures, including polluted drinking water and ionizing radiation, have also been associated with excess risks. Currently, there is a tendency to attribute colorectal cancer, largely or exclusively, to dietary and other lifestyle factors, thus neglecting these industrially related effects. Concerted efforts are needed to recognize the causal role of industrial risk factors and to encourage government and industry to reduce carcinogenic exposures. Furthermore, cost-effective screening programs for high-risk population groups are critically needed to further reduce deaths from colorectal cancer.

Colorectal Neoplasms↗
PubMed1990

Corporate crime: why we cannot trust industry-derived safety studies.

The control of pesticides, as of all synthetic chemicals, in most industrialized countries relies heavily or even entirely on safety data supplied by the manufacturers. Such a regulatory system can only be effective if the companies conducting and reporting the studies honestly disclose any adverse findings. The record shows, however, that all too often company executives and their scientists knowingly suppress or manipulate information that could affect the licensing and sale of their products. A case in point is the gross manipulation of health and related data on the pesticides heptachlor and chlordane by the U.S. chemical company, Velsicol.

Chlordan↗
PubMed1990

Potential public health hazards of biosynthetic milk hormones.

The use of biosynthetic milk hormones raises fundamental ethical, social, and economic considerations, including the continued viability of the small family dairy farm and adverse veterinary effects. The past and expanding use of synthetic bovine growth hormone manufactured by the Agricultural Chemicals Division of Elanco (Eli Lilly and Co.) in conjunction with Dow Chemical Co. and Upjohn Co., and its methionyl analog, manufactured by American Cyanamid Co. and Monsanto Co., also poses significant potential public health hazards which have not so far been investigated. These concerns are exacerbated by the domination of synthetic hormone research by industry and its indentured academics, by failure of the industries concerned to disclose their unpublished data, by their manipulation of published data, and by refusal to label milk and meat from cows treated with biosynthetic hormones, and by denial of consumers' rights to know. These concerns are further exacerbated by the abdication of regulatory responsibility by the Food and Drug Administration and U.S. Department of Agriculture.

Animals↗
PubMed1990

Losing the war against cancer: who's to blame and what to do about it.

In 1971, the U.S. Congress launched a War on Cancer. Eighteen years and billions of dollars later, the United States is still in the grips of a cancer epidemic--and the number of victims grows every year. Much of the money has been squandered on a fruitless search for cancer "cures." Little has been done to prevent exposure to carcinogenic chemicals in the environment, despite ample evidence that chemical pollution of our air, water, food, and the workplace is the major cause of cancer. On the contrary, government, industry, and a small coterie of scientists have combined to stymie efforts to introduce preventive measures, such as strict pollution control standards. But cancer remains a preventable disease. It is up to citizens to push for action.

American Cancer Society↗
PubMed1990

Questions and answers on synthetic bovine growth hormones.

Questions are posed and answered on synthetic bovine growth (milk) hormones (s-BGH), covering a wide range of areas of critical international concern. These areas include: the data base on s-BGH; efficacy and benefits to the dairy industry; veterinary effects; public health effects; Food and Drug Administration approval; and the FDA review process.

Animals↗
PubMed1987

Leukemias and blood dyscrasias following exposure to chlordane and heptachlor.

We present 25 new cases of blood dyscrasia, including leukemias, production defects, and thrombocytopenic purpura, generally following home termite treatment with the chlorinated hydrocarbon pesticides chlordane and heptachlor (C/H). These newly reported cases are consistent with 34 previously published case reports associating blood dyscrasias with C/H exposure. Additionally, the newly reported leukemias are consistent with epidemiologic evidence of excess risk of leukemia and other cancers in C/H-exposed populations and with the carcinogenic action of C/H in animals. The importance of case reports in warning of the association of blood dyscrasias to C/H exposure is emphasized. Until the voluntary halt in production in July 1987, millions of homes in the United States were treated with chlordane and heptachlor for termites even though their agricultural uses were phased out in 1978, largely on the grounds of "imminent hazard" because of carcinogenicity. In view of the recognized myelotoxicity, carcinogenicity, and other chronic toxic effects of these pesticides, a national program for monitoring all homes treated is urgently needed to detect persistent contamination.

Anemia, Aplastic↗
PubMed1984

Irradiation of foods.

In the report "Communal nursing in Mexican free-tailed bat maternity colonies" by G. F. McCracken (9 Mar., p. 1090), table 1 was incorrectly printed. The correct table is reprinted below. [See Table 1. in Source PDF]

Food Irradiation↗
PubMed1982

Analyses of carcinogenesis dose-response relations with dichotomous data: implications for carcinogenic risk assessment.

Dose-response data from experimental and epidemiologic carcinogenicity studies were analyzed in attempts to resolve basic questions in extrapolating from high to low doses and assessing human risk. Four models (Weibull, Mantel-Bryan, Marshall-Groer, and Mancuso-Stewart) were fit to 46 sets of experimental and 4 sets of epidemiologic data by maximizing the likelihood function with a Rosenbrock hill-climbing algorithm. The models were compared as to their adequacy in describing the data and analyzed to determine the effect of carcinogen and breeding category, species, and spontaneous tumor incidence. The shapes of the dose-response curves were analyzed, and errors in risk estimation from linear extrapolation through the origin were calculated. All models were shown to fit the data and to be comparable in accuracy. The dose-response curves were generally "stretched out," particularly for outbred strains, with one or two orders of magnitude of dose increase required to increase the proportion of tumor responders from 10% to 70%. Linear extrapolation through the origin generally underestimated the response at low doses, frequently by several orders of magnitude. The power dependence of tumor incidence on dose was generally found to be of the order of unity, substantially less than assumed in most mathematical models.

Carcinogens↗
PubMed1981

Biosynthesis of dimethylnitrosamine in dimethylamine-treated mice after exposure to nitrogen dioxide.

These studies demonstrate the nitrosating potential of NO2 in vivo in ICR mice. Groups of mice were gavaged with 2 mg dimethylamine (DMA) and exposed to NO2 at levels from 0.04 to 44.5 ppm for periods up to 4 hours. Mice were individually frozen and blended to a powder, aliquots of which were homogenized in ice-cold dicholoromethane and 35% aqueous methanol. Concentrates of organic extracts were analyzed or dimethylnitrosamine (DMN) by a Thermal Energy Analyzer with a gas chromatograph interface. Biosynthesis of DMN was dose- and time-dependent with relation to NO2 exposure, reaching a maximum yield of 60-70 ng/mouse (0.0035% DMA conversion) at 2 hours. DMN biosynthesis was inhibited by sodium ascorbate and, more effectively, by ammonium sulfamate.

Animals↗
PubMed1980

Role of nitrogen dioxide in the biosynthesis of nitraosamines in mice.

Groups of three to four mice were gavaged with aqueous solutions of 2 milligrams of morpholine, after which they were exposed to nitrogen dioxide in inhalation chambers at concentrations of 0.2 to 50 parts per million for up to 4 hours. At sequential intervals during the exposure, mice were frozen and pulverized in liquid nitrogen, and the mice powder was extracted with ice-cold 35 percent aqueous methanol and dichloromethane; organic-phase concentrates were analyzed for N-nitrosomorpholine with a thermal energy analyzer interfaced to a gas chromatograph. The N-nitrosomorpholine yields, ranging up to about 2.3 micrograms per mouse, were time-dependent relative to the duration of exposure to nitrogen dioxide and dose-dependent relative to the concentrations of nitrogen dioxide; control levels (in mice that were gavaged with morpholine or distilled water and then exposed to air instead of nitrogen dioxide) were less than 5 nanograms per mouse. These preliminary studies demonstrate the in vivo nitrosating potential of nitrogen oxides.

Amines↗
PubMed1980

Kinetics of nitrosamine formation in mice following oral administration of trace-level precursors.

Groups of 3-5 Swiss CD1 mice were gavaged with aqueous solutions of sodium nitrite (250 micrograms), followed immediately by morpholine (5 micrograms) or dimethylamine (250 micrograms). At subsequent intervals, up to 30-60 min, mice were frozen, pulverized in liquid nitrogen and extracted with methylene chloride. Volatile nitrosamines were then quantitatively determined using a Thermal Energy Analyzer, interfaced to GC or HPLC. Biosynthesis of both N-nitrosodimethylamine (NDMA) and N-nitrosomorpholine (NMOR) showed a time-dependent increase for 3 and 9 min, respectively, followed by a steady decline. Levels of NDMA and NMOR were generally less than 0.1 ng/g in control mice gavaged with amine or nitrite alone. Zero-time recovery of NDMA and NMOR ranged from 50-70% and 70-90%, respectively. Biosynthesis of NDMA and NMOR was inhibited by prior administration of ascorbic acid, sodium ascorbate or ammonium sulfamate.

Administration, Oral↗