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P Kotin

Publications and source records attributed to P Kotin.

At least 19 recordsLinked to original sources
PubMed1999

Studies on the inhalation toxicology of two fiberglasses and amosite asbestos in the Syrian golden hamster. Part II. Results of chronic exposure.

Fiberglass (FG) is the largest category of man-made mineral fibers (MMVFs). Many types of FG are manufactured for specific uses building insulation, air handling, filtration, and sound absorption. In the United States, > 95% of FG produced is for building insulation. Several inhalation studies in rodents of FG building insulation have shown no indication of pulmonary fibrosis or carcinogenic activity. However, because of increasing use and potential for widespread human exposure, a chronic toxicity/carcinogenicity inhalation study of a typical building insulation FG (MMVF 10a) was conducted in hamsters, which were shown to be highly sensitive to the induction of mesotheliomas with another MMVF. A special-application FG (MMVF 33) and amosite asbestos were used for comparative purposes. Groups of 140 weanling male Syrian golden hamsters were exposed via nose-only inhalation for 6 h/day, 5 days/wk for 78 wk to either filtered air (chamber controls) or MMVF 10a, MMVF 33, or amosite asbestos at 250-300 WHO fibers/cm(3) with two additional amosite asbestos groups at 25 and 125 WHO fibers/cm(3). They were then held unexposed for 6 wk until approximately 10-20% survival. After 13, 26, 52, and 78 wk, various pulmonary parameters and lung fiber burdens were evaluated. Groups hamsters were removed from exposure at 13 and 52 wk and were held until 78 wk (recovery groups). Initial lung deposition of long fibers (>20 microm in length) after a single 6-h exposure was similar for all 3 fibers exposed to 250-300 fibers/cm(3). MMVF 10a lungs showed inflammation (which regressed in recovery hamsters) but no pulmonary or pleural fibrosis or neoplasms. MMVF 33 induced more severe inflammation and mild interstitial and pleural fibrosis by 26 wk that progressed in severity until 52 wk, after which it plateaued. While the inflammatory lesions regressed in the recovery animals, pulmonary or pleural fibrosis did not. A single multicentric mesothelioma was observed at 32 wk. No neoplasms were found in the remainder of the study. Amosite asbestos produced dose-related inflammation and pulmonary and pleural fibrosis as early as 13 wk in all 3 exposure levels. The lesions progressed during the course of the study, and at 78 wk severe pulmonary fibrosis with large areas of consolidation was observed in the highest 2 exposure groups. Progressive pleural fibrosis with mesothelial hypertrophy and hyperplasia was present in the thoracic wall and diaphragm in most animals and increased with time in the recovery hamsters. While no pulmonary neoplasms were observed in the amosite exposed hamsters, a large number of mesotheliomas were found; 25 fibers/cm(3), 3.6%; 125 fibers/cm(3), 25.9%; and 250 fibers/cm(3), 19.5%. For the 3 fiber types, the severity of the lung and pleural lesions generally paralleled the cumulative fiber burden, especially those >20 microm length, in the lung, thoracic wall, and diaphragm. They also inversely paralleled the in vitro dissolution rates; that is, the faster the dissolution, the lower were the cumulative lung burdens and the less severe the effects.

Animals↗
PubMed1985

Evaluation for compensation of asbestos-exposed individuals. I. Detection and quantification of asbestos-related nonmalignant impairment.

An objective method for measuring nonmalignant respiratory impairment caused by inhaled asbestos has been devised. Three standard physiologic tests (the forced vital capacity [FVC], the forced expiratory volume in 1 s [FEV1], the single-breath diffusing capacity for carbon monoxide [DCO]) and the posteroanterior chest roentgenogram are utilized. The age-, height-, and sex-specific normal ranges of the FVC%, the DCO%, and the FEV1/FVC% have been used in the method. The theory and rationale are described. The resulting algorithm can be presented using a nomogram. Data on 586 asbestos-exposed subjects were analyzed by the proposed method. Empirical evaluation showed the sensitivity to be greater than 90% in definitive diagnosis of asbestosis without airflow obstruction, and the specificity to be greater than 80% for those cases judged eligible for nomographic evaluation. Exceptions were found in 15 cases diagnosed clinically as asbestosis, none of whom had any evidence of pulmonary fibrosis. In addition, 50 cases diagnosed as "no asbestosis" did have evidence of pulmonary fibrosis and would have qualified for some compensation by the proposed method. In summary, this approach has been shown to yield a reliable final asbestos-related lung impairment index that, when taken together with individual societal data, can provide a reliable basis for determining compensation.

Aged↗
PubMed1985

Evaluation for compensation of asbestos-exposed individuals. II. Apportionment of risk for lung cancer and mesothelioma.

The incidence of lung cancer in the cigarette smoking population occupationally exposed to asbestos is inordinately high. A method for apportioning risk to these two agents has been developed. It utilizes degree of asbestos and smoking exposures; the time interval from onset and, where applicable, termination of both exposures; the time interval to diagnosis of lung cancer; and morphologic, physiologic, and radiological evidence of pulmonary fibrosis.

Adolescent↗
PubMed1985

Rewards for cancer control with use of biologic markers and end points.

The increasing availability of biologic markers and end points offers significant potential for improvement in cancer control. These tools are underutilized today, but it is clear that they can be major assets to pathologists, clinicians, epidemiologists, and ultimately to programs designed for preventive or therapeutic intervention in populations and individuals at high cancer risk.

Disease Susceptibility↗
PubMed1985

Asbestosis.

Explore the source record for details and available documents.

Asbestos↗
PubMed1976

Embryonal neoplasms in the opossum: a new model for solid tumors of infancy and childhood.

Opossums fed the chemical carcinogen ethyl nitrosourea early in postnatal life developed a variety of epithelial and mesenchymal embryonal neoplasms that were closely analogous, in morphology and biological behavior, to tumors of human infancy and childhood for which experimental models in laboratory animals are either imprecise or nonexistent. The embryonal tumors were found in association with, and occasionally at the same sites as, a limited number of malformations.

Animals↗