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Biomedical subjects

R Saracci

Publications and source records attributed to R Saracci.

At least 127 records · Page 7Linked to original sources
PubMed1981

Malignant mesothelioma and radiological chest abnormalities in two villages in Central Turkey. An epidemiological and environmental investigation.

A comparative epidemiological and environmental study in two neighbouring villages, Karain and Karlin, in Central Turkey showed an excess adult mortality, shortening of life expectancy, and an excess of pleural radiological abnormalities in Karain. This supports an earlier report of an endemic of pleural mesothelioma in the village. Concentrations of airborne respirable fibres were uniformly very low in Karlik and higher in some of the air samples from Karain, the fibres being similar in composition to those of erionite-a mineral of the zeolite family and the major contributor to the Karain clouds. This is compatible with the hypothesis of a causal association between endemic mesothelioma and inhalation of erionite fibres, but the fibre concentrations in all samples are so low as to leave in question the aetiological role of erionite. In addition to their local importance these results may have relevance for the wider scientific and public-health issue of long-term inhalation of mineral fibres at low concentrations.

Adolescent↗
PubMed1980

Long-term hazards of polychlorinated dibenzodioxins and polychlorinated dibenzofurans.

During January 10-11, 1978 in Lyon, France, a joint National Institute of Environmental Health Sciences/International Agency for Research on Cancer ad hoc Working Group considered and discussed the feasibility of coordinating epidemiological studies on the long-term hazards associated with the chlorinated dibenzo-p-dioxins and chlorinated dibenzofurans (PCDDs and and PCDFs). Nineteen invited scientists from eight countries presented introductory working papers summarizing the most up-to-date and relevant information available from their individual programs. This report represents the collective views and scientific opinions of the Working Group. The greater part of this document comprises epidemiological studies related to episodes of human exposures. The review begins with a brief section concerning possible routes of human exposure, an overview of the pertinent chemical characteristics, and the salient toxicological properties of the structurally similar PCDDs/PCDFs. The Working Group report ends with recommendations for future activities.

Abnormalities, Drug-Induced↗
PubMed1980

Time trends of primary liver cancer: indication of increased incidence in selected cancer registry populations.

Primary liver cancer (PLC) data from 30 selected cancer registries covering 37 populations in 18 countries were used to compare incidence rates in two periods (2-5 yr long) between 1956 and 1972. The median distance between central years of the two periods was about 8 years. Over this interval, all-ages incidence rates, standardized to world population, showed a statistically significant increase in 17 (45.9%) of the populations for males and in 10 (27.0%) for females. Corresponding figures for the 0- to 44-year age group were 4 (10.8%) for males and 7 (18.9%) for females. One statistically significant decrease was observed among the remaining populations. Over the whole set of 37 populations the median percent yearly increase was +3.7 for males and +6.7 for females (all ages) and +1.3 for males and +8.3 for females (ages 0-44 yr). The increase in PLC was most clearly identifiable in the populations of Kracow, Poland; Alberta, Canada; and Bombay, India; and in the Jewish population of Israel. Correlations between levels and/or changes of some variables (per capita income and calorie and alcohol consumption) and changes in PLC rates provided no consistent pattern of results. Changes in PLC mortality rates showed only a weak correlation with changes in PLC incidence rates, indicating the inadequacy of mortality data to describe PLC trends. Data on PLC incidence trends, as available from routine source, appeared insufficient to determine the role of diagnosis-registration changes in the observed increase and to exclude the contribution of etiologic factors.

Adolescent↗
PubMed1979

[Socioeconomic aspects of lung cancer].

The socio-economic aspects of lung cancer are briefly considered, first, with regard to the causes conditioning its occurrence and clinical progress. Tobacco smoking, occupational exposure and air pollution are (in decreasing order of importance) the main determinants of lung cancer occurrence, which differs as between social classes. Social class also appears to be related to clinical progress of the disease. The economic consequences of lung cancer may be tentatively estimated, for a country like Switzerland, at 40 million Swiss francs per year, a sum which can be greatly reduced if a sustained collective effort at prevention is implemented.

Air Pollution↗
PubMed1979

[Geographical pathology and the working environment (author's transl)].

The geographical, or, more generally, the topographical approach to health and disease has common and important applications in occupational health studies. Analysis of disease occurrence (prevalence and incidence) by area may be carried out at three levels of observation: within the working environment, when different areas usually correspond to different exposures to potentially noxious agents; in the locality where the working environment is situated, which may be affected, for example, by routine industrial discharges or by pollution following accidents; and in the region which includes the locality. Epidemiological tools for the spatial investigation of disease occurrence at each of these levels are reviewed and exemplified, and possible sources of confounding and bias (positive and negative) are emphasized. Attention is particularly drawn to "false negative" results arising in occupational studies because of dilution of an excess risk limited to only some of the workers operating in a defined area.

Environmental Exposure↗
PubMed1978

Evaluation of the carcinogenicity of chemicals: a review of the Monograph Program of the International Agency for Research on Cancer (1971 to 1977).

In 1971 the International Agency for Research on Cancer initiated a program on the evaluation of the carcinogenic risk of chemicals to humans, which concentrated on the production of monographs on individual chemicals. A review of this ongoing program is presented here as a contribution to the discussion of primary prevention of cancer. A total of 368 chemicals were evaluated in the first 16 volumes of the International Agency for Research on Cancer monographs. For 26 chemicals (or industrial processes), a positive association between exposure and the occurrence of cancer in humans was observed. For 221 chemicals, some evidence of carcinogenicity was found in at least one species of experimental animals. However, no evaluation of the carcinogenic risk of these chemicals to humans was made, either because no epidemiological studies or case reports were available or because the results of available human studies were inconclusive. For the remaining 121 chemicals, the available data were inadequate for an evaluation of the presence or absence of a carcinogenic effect in experimental animals or humans. The criteria on which the carcinogenicity of chemicals to humans and/or experimental animals was assessed, from the initiation of this program in 1971 until 1977, have recently been revised and are briefly discussed.

Animals↗
PubMed1977

Asbestos and lung cancer: an analysis of the epidemiological evidence on the asbestos-smoking interaction.

Three simple models for the asbestos-smoking interaction on human lung cancer production are considered. In the first model the excess incidence of lung cancer independently due to asbestos and to smoking adds together when both agents are present (additive model). In the second the addition of each one of the two agents produces an effect (increase in lung cancer incidence) which is proportional to the effect of the other (multiplicative model). In the third, asbestos can only increase lung cancer incidence in the presence of smoking. As previously found by other investigators, the additive model appears the least plausible in the light of the data from two published epidemiological studies. A discrimination between the other two models is attempted through a detailed analysis of the five published epidemiological studies today available which provide information on occupational asbestos exposure, smoking habits and lung cancer risk. Although the data do not allow a definitive discrimination, the multiplicative model appears to be more plausible, being also consistent with a multi-stage carcinogenic mechanism and with evidence from animal (rat) experiments. It is relevant both for biology and for public health that in this model asbestos and smoking are regarded as independently capable of producing lung cancer in humans and that they act synergistically when exposure to both occurs.

Air Pollutants↗