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R Saracci

Publications and source records attributed to R Saracci.

At least 55 records · Page 3Linked to original sources
PubMed1986

Ten years of epidemiologic investigations on man-made mineral fibers and health.

This paper introduces the reports that follow it in a supplement dealing with the extended follow-up of mortality and cancer incidence among workers in the man-made mineral fiber (MMMF) production industry in Europe, the largest international study of its kind thus far initiated. In addition it reviews the prior epidemiologic evidence on this subject, both in terms of the earlier results of the same study and the results of other studies on the long-term effects of occupational exposure to MMMF. The conclusion drawn from this prior evidence was that the possibility that some excess of lung cancer may be causally related to exposure to MMMF could not be ruled out of the range of reasonable interpretations. When the findings of the extended follow-up, which this paper introduces, are added to the existing evidence, the overall results were considered to endorse the indication that no adverse long-term health effects have been detectable in terms of mortality throughout almost all segments of the MMMF production industry and to support the inference that MMMF--as present in the environmental conditions of early slag-wool/rock-wool production--may have played a role in the causation of lung cancer.

Calcium Compounds↗
PubMed1985

Man-made mineral fibers and health. Answered and unanswered questions.

An overall assessment of the epidemiologic evidence from 23 published studies on workers' health in the industry producing man made mineral fibers (MMMF) (21 studies) and in the user industry (2 studies) is presented. Three major studies recently published, one cross-sectional and two of the historical cohort type, conducted in the producer industry, have been singled out for closer examination and discussion. The combined evidence from the epidemiologic studies indicates that causal associations between MMMF occupational exposure, as it occurred in past decades, and lung cancer and chronic respiratory diseases cannot be excluded, neither does it offer clear support for such associations. Experimental data indicate clearly that a fibrogenic effect can be obtained by the intratracheal administration of MMMF and a carcinogenic effect by the intratracheal, intrapleural, and intraperitoneal administration of MMMF, while no appreciably fibrogenic nor carcinogenic effects have been detected in inhalation experiments. While it can be stated that no long-term pathological effects have been observed in MMMF workers in the first 20 years or so after first employment, the key scientific issue of whether MMMF are fibrogenic and/or carcinogenic in man when inhaled remains still open.

Air Pollutants, Occupational↗
PubMed1985

[Markers of exposure and early lesions in cancer epidemiology].

The biological markers of risk can be separated into two categories: markers of exposure to a specific substance, based on several biochemical, physical and immunological methods (usually able to measure the absorbed dose); markers of early lesions which usually are not specific for a particular substance and do not estimate the dose of exposure. In epidemiological research on cancer etiology, biological markers have a different role according to whether cases are subjects with early lesions or with invasive cancers. The first approach has the advantage of shortening the observation time between exposure and the appearance of a biological effect. On the other hand, the biological relevance of the study could be limited due to the non univocal relation between early lesions and cancer. With the second approach, invasive cancer can be related to specific markers of exposure (this would permit to draw direct inference on disease etiology) or to markers of early lesions (etiological interpretation in this case would be less straightforward). The two approaches should be considered in the frame of two basic problems: What is the advantage of measuring exposure at the individual level? What is the advantage of a biological marker as compared to traditional epidemiological methods? With studies at the group level the correlation between exposure variables and disease frequency can be estimated. Nevertheless only studies at the individual level can exclude the fact that the observed correlation is due to an artefact. In this case we are left with the second question and many answers are possible.(ABSTRACT TRUNCATED AT 250 WORDS)

Carcinoma, Hepatocellular↗
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↗