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R Saracci

Publications and source records attributed to R Saracci.

At least 19 recordsLinked to original sources
PubMed1992

Active and passive smoking and pathological indicators of lung cancer risk in an autopsy study.

OBJECTIVE: The association between involuntary smoking and lung cancer has been supported by most epidemiologic studies, but a number of authors and interest groups claim that the possibility of bias has not been excluded. Few autopsy-based studies have explored the role of active smoking and other exposures in lung carcinogenesis, and none has been previously done to examine the role of passive smoking. We have undertaken such an autopsy-based study in Athens, Greece. DESIGN: Lung specimens were taken at autopsy from 400 persons 35 years of age or older, of both genders, who had died within 4 hours from a cause other than respiratory or cancer in Athens or the surrounding area. For each person at least seven tissue blocks were taken from the main and lobar bronchi and at least five blocks from the parenchyma, including an average of about 20 smaller cartilaginous bronchi and membranous bronchioles. The specimens were examined without knowledge of the exposures of the particular subject in Turin, Italy. For 283 (71%) of the subjects the preservation of the bronchial epithelium was satisfactory for pathological examination, and for 206 among them (73%) an interview could be arranged with their next of kin, focusing on smoking habits of the deceased and their spouses, as well as other variables. The interviewers were not aware of the results of the pathological examinations. MAIN OUTCOME MEASURE: Specimens were examined for basal cell hyperplasia, squamous cell metaplasia, cell atypia, and (in membranous bronchioles and bronchiolo-alveolar airways) mucous cell metaplasia, ie, pathological entities that may be lung cancer risk indicators or epithelial, possibly precancerous, lesions (EPPL). The gland and wall thicknesses were also measured and their ratio calculated (Reid Index). RESULTS: In comparison with nonsmokers, EPPL values were significantly higher among current smokers and higher, but not significantly so, among former smokers. Furthermore, EPPL values were significantly higher among deceased nonsmoking women married to smokers rather than to nonsmokers. In this set of data neither occupation nor residence was associated with EPPL, but this could be due to the poor correlation of residential history with exposure to air pollution and the lack of adequate standardization of contemporary Greek occupations. The Reid Index was higher among smokers and former smokers in comparison with nonsmokers, among subjects with mainly urban residence in comparison with those with mainly rural residence, and among nonsmoking women married to smokers in comparison with those married to nonsmokers, but none of these differences was statistically significant. CONCLUSION: These results provide support to the body of evidence linking passive smoking to lung cancer, even though they are based on a study methodologically different from those that have previously examined this association.

Adult↗
PubMed1992

Soft-tissue sarcoma.

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Agricultural Workers' Diseases↗
PubMed1992

Carcinogen metabolism in human lung tissues and the effect of tobacco smoking: results from a case--control multicenter study on lung cancer patients.

Cigarette smoking is the strongest risk factor for lung cancer, but genetically determined variations in the activities of pulmonary enzyme that metabolize tobacco-derived carcinogens may affect individual risk. To investigate whether these enzymes (e.g., CYP1A-related) can serve as markers for carcinogen-DNA damage, lung tissue specimens were taken during surgery from middle-aged men with either lung cancer or non-neoplastic lung disease. Phase I [aryl hydrocarbon hydroxylase (AHH), ethoxycoumarin O-deethylase (ECOD)] and phase II (epoxide hydrolase, UDP-glucuronosyltransferase, glutathione S-transferase) enzyme activities, glutathione and malondialdehyde contents were determined in lung parenchyma and/or bronchial tissues; some samples were also analyzed for DNA adducts, using 32P-postlabeling. The data were then analyzed for the following: a) differences in metabolic profiles between bronchial and parenchymal lung tissue; b) the effect of recent exposure to tobacco smoke on enzyme inducibility and benzo[a]pyrene metabolism; c) differences in enzyme inducibility between lung cancer and non-lung cancer patients; d) the effect of smoking on metabolism of mutagens in vitro; e) pulmonary DNA adduct levels and AHH activity in lung parenchyma of smokers and ex-smokers; f) lipid peroxidation products in lung tissue from lung cancer and non-lung cancer patients, as related to smoking habits and degree of airway obstruction; and g) prognostic value of AHH pulmonary activity in lung cancer patients. The results demonstrate a pronounced effect of tobacco smoke on pulmonary metabolism of xenobiotics and prooxidant state and suggest the existence of a metabolic phenotype at higher risk for tobacco-associated lung cancer.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1992

Lung cancer mortality among workers in the European production of man-made mineral fibers--a Poisson regression analysis.

One hundred and eighty-one lung cancer deaths among workers during 301,085 person-years in European man-made mineral fiber production between 1930-1955 and 1982 were analyzed according to Poisson regression models including age, calendar period, country, and exposure variables. Time since first employment was the variable most strongly associated with lung cancer risk in both the rock-slag wool and glass wool subcohorts. Workers in the early technological phase were at higher risk than those in other categories, particularly in rock-slag wool production. No clear trend with duration of employment was suggested. No major changes occurred in the interpretation of the results when workers with less than one year of employment or less than 20 years since first exposure were excluded. The original results, based on analyses for standardized mortality ratios, were confirmed, and workers with a short duration of employment or a short time since first employment did not need to be excluded from the analysis.

Air Pollutants, Occupational↗
PubMed1991

Cancer mortality in workers exposed to chlorophenoxy herbicides and chlorophenols.

Epidemiological studies have revealed an increased risk of cancer, notably soft-tissue sarcomas and non-Hodgkin's lymphomas, in people occupationally exposed to chlorophenoxy herbicides, including those contaminated by 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD). We report here a historical cohort study of mortality in an international register of 18,910 production workers or sprayers from ten countries. Exposure was reconstructed through questionnaires, factory or spraying records, and job histories. Cause-specific national death rates were used as reference. No excess was observed in all-cause mortality, for all neoplasms, for the most common epithelial cancers, or for lymphomas. A statistically non-significant two-fold excess risk, based on 4 observed deaths, was noted for soft-tissue sarcoma with a standardised mortality ratio (SMR) of 196 and 95% confidence interval (Cl) 53-502; this was concentrated as a six-fold statistically significant excess, occurring 10-19 years from first exposure in the cohort as a whole (SMR = 606 [165-1552]) and, for the same time period, as a nine-fold excess among sprayers (SMR = 882 [182-2579]). Risks appeared to be increased for cancers of the testicle, thyroid, other endocrine glands, and nose and nasal cavity, based on small numbers of deaths. The excess of soft-tissue sarcomas among sprayers is compatible with a causal role of chlorophenoxy herbicides but the excess does not seem to be specifically associated with those herbicides probably contaminated by TCDD.

2,4,5-Trichlorophenoxyacetic Acid↗
PubMed1991

Is necropsy a valid monitor of clinical diagnosis performance?

OBJECTIVE: To improve the validity of comparisons between clinical and postmortem diagnoses when postmortem diagnosis is used to monitor clinical diagnosis performance. DESIGN: Analysis of elementary examples. MAIN OUTCOME MEASURES: Sensitivity and specificity of clinical and postmortem diagnoses and confirmation and agreement rates. Sensitivity and specificity permit valid comparisons of clinical and postmortem diagnoses among different procedures, sites, or times whereas agreement and confirmation rates may be misleading. Estimates of sensitivity and specificity, however, can be severely distorted by factors such as non-random selection of cases for necropsy or by unrecognised errors in postmortem diagnosis. Such distortion may be minimised by (a) estimating the likely magnitude of errors in postmortem diagnosis, (b) specifying standard conditions for performing necropsies, and (c) ensuring an unbiased sample of moderate size rather than a large biased sample. CONCLUSION: Sensitivity and specificity should be used as measures of agreement between clinical and postmortem diagnoses. IMPLICATION: Monitoring of clinical diagnosis performance by necropsy surveys requires ensuring accuracy of pathological examinations and validity of study design and analysis.

Autopsy↗
PubMed1991

Preventing war.

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Health Personnel↗
PubMed1991

Correlation of early pathological lesions in the bronchial tree with environmental exposures: study objectives and preliminary findings.

Lung specimens were taken at autopsy from 214 subjects aged 35 years and over who had died from nonpulmonary causes in Athens or the surrounding countryside. The samples were coded and examined for entities thought to be linked to environmental exposures, reflecting epithelial, possibly precancerous, lesions, as well as for morphological features, which were summarized using Reid's index. Of the 214 specimens, 142 were suitable for pathological examination. Next-of-kin of 101 of the dead people were identified and asked about the subject's exposure to active smoking, passive smoking, possible occupational hazards, dietary factors and proxy indicators of air pollution (residence). Preliminary analysis, controlling for age and sex, indicates that active smoking is related, although not statistically significantly, to both the Reid index (difference, 0.28, corresponding to a one-tailed p value of 0.07) and epithelial, possibly precancerous lesions (difference, 16.7, corresponding to a one-tailed p value of 0.09). Nonsignificant differences were found in the preliminary analysis of this ongoing study with respect to the other environmental factors examined.

Adult↗
PubMed1990

Possible prognostic value of pulmonary AH-locus-linked enzymes in patients with tobacco-related lung cancer.

As prognosis in breast cancer patients has been related to the AHH activity in their breast tissue, we have conducted a similar analysis on pulmonary drug metabolizing enzymes as prognostic markers for male lung cancer patients, primarily investigated for other reasons. A subset of 50 patients with lung cancer related to tobacco use, who had undergone thoracic surgery, was re-analyzed. The activity of parenchymal aryl hydrocarbon hydroxylase (AHH) and epoxide hydrolase (EH) that had been determined previously in homogenates of non-neoplastic surgical lung specimens, was used for comparisons of the patients' survival after surgery. When the crude mortality percentages at 1 and 2 years by AHH or EH activity, subdivided into quarters of the distribution, were calculated, a lower mortality was related to lower enzyme levels. Subjects in the 1st and 4th quarters of the distribution showed significant differences in their 1-year survival for AHH (p = 0.05) and EH (p less than 0.01) activities. This relationship could not be accounted for by age, cumulative lifetime smoking, recent or continuing smoking, stage or histological type of disease. Thus, the levels of pulmonary AHH and EH may have some prognostic significance in tobacco-related lung cancer.

Aryl Hydrocarbon Hydroxylases↗
PubMed1990

Passive smoking and diet in the etiology of lung cancer among non-smokers.

A case-control study was undertaken in Athens to explore the role of passive smoking and diet in the causation of lung cancer, by histologic type, in non-smoking women. Among 160 women with lung cancer admitted to one of seven major hospitals in Greater Athens between 1987 and 1989, 154 were interviewed in person; of those interviewed, 91 were life-long non-smokers. Among 160 identified controls with fractures or other orthopedic conditions, 145 were interviewed in person; of those interviewed, 120 were life-long non-smokers. Marriage of a non-smoking woman to a smoker was associated with a relative risk for lung cancer of 2.1 (95% confidence interval [CI] 1.1-4.1); number of cigarettes smoked daily by the husband and years of exposure to husband's smoking were positively, but not significantly, related to lung cancer risk. There was no evidence of any association with exposure to smoking of other household members, and the association with exposure to passive smoking at work was small and not statistically significant. Dietary data collected through a semi-quantitative food-frequency questionnaire indicated that high consumption of fruits was inversely related to the risk of lung cancer (the relative risk between extreme quartiles was 0.27 (CI 0.10-0.74)). Neither vegetables nor any other food group had an additional protective effect; furthermore, the apparent protective effect of vegetables was not due to carotenoid vitamin A content and was only partly explained in terms of vitamin C. The associations of lung cancer risk with passive smoking and reduced fruit intake were independent and did not confound each other.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1990

Exposure of nonsmoking women to environmental tobacco smoke: a 10-country collaborative study.

The interpretation and interpretability of epidemiologic studies of environmental tobacco smoke (ETS) depend largely on the validity of self-reported exposure. To investigate to what extent questionnaires can indicate exposure levels to ETS, an international study was conducted in 13 centers located in 10 countries, and 1,369 nonsmoking women were interviewed. The present paper describes the results of the analysis of self-reported recent exposure to ETS from any source in relation to urinary concentrations of cotinine. Of the total, 19.7 percent of the subjects had nondetectable cotinine levels, the median value was 6 ng/mg, and the cut-point of the highest decile was 24 ng/mg. The proportion of subjects misreporting their active smoking habit was estimated at between 1.9 and 3.4 percent, depending on whether cut-points of 50 or 100 ng/mg creatinine were used. Large and statistically significant differences were observed between centers, with the lowest values in Honolulu, Shanghai, and Chandigarh, and the highest in Trieste, Los Angeles, and Athens. Mean cotinine/creatinine levels showed a clear linear increase from the group of women not exposed either at home or at work, to the group of those exposed both at home and at work. Values were significantly higher for women exposed to ETS from the husband but not at work, than for those exposed at work but not from the husband. The results of linear regression analysis indicated that duration of exposure and number of cigarettes to which the subject reported being exposed were strongly related to urinary cotinine. ETS exposure from the husband was best measured by the number of cigarettes, while exposure at work was more strongly related to duration of exposure. After adjustment of number of cigarettes for volume of indoor places, a similar increase in cotinine (5 ng/mg) was predicted by the exposure to 7.2 cigarettes/8 h/40 m3 from the husband and 17.9 cigarettes/8 h/40 m3 at work. The results indicate that, when appropriately questioned, nonsmoking women can provide a reasonably accurate description of ETS exposure. Assessment of individual exposure to ETS should focus on daily duration and volume of indoor places where exposure occurred.

Adult↗
PubMed1990

The Po River Delta epidemiological study of obstructive lung disease: sampling methods, environmental and population characteristics.

A longitudinal study on chronic obstructive lung disease (AOD) has been started in the Po River Delta in northern Italy. The first cross-sectional study was conducted in this previously unpolluted rural area before the start of operation of a large thermoelectric power plant (2,649 megawatt). A significant output of air pollutants is expected. This will permit us to carry out a "natural experiment" to study the effects of air pollutants (SO2 and suspended particulates). A multistage stratified cluster design was chosen. Stratification was based on age and socio-economic characteristics (SES) of households, and was performed in two steps, using the different indices computed from the census data. Geographic zones represented four areas of different predicted pollution exposure, once the plant started operating. There were 3,289 subjects in the selected age group (8-64) who agreed to participate (78%); only 11% refused to participate. The participants were representative of the clusters and SES. Participants had slightly fewer employed males, who did not participate due to work. The stratification and staging method allowed us to keep an acceptable level of precision and efficiency in the sample. In fact age-related differences were not found among the SES strata and geographic zones; various socio-economic characteristics, verified from the questionnaire information, were consistent with the SES stratification. Differences between geographic zones were related to the number of households of different SES within clusters; however this reflects the characteristics of the general population in the area.

Air Pollutants↗
PubMed1990

The effect of involuntary smoking on the occurrence of chronic obstructive pulmonary disease.

One hundred and three ever-married women with newly diagnosed Chronic Obstructive Pulmonary Disease (COPD), who have never smoked, and 179 ever-married women who were visiting friends or relatives at the same hospital during the same period and have never smoked, were interviewed regarding the smoking habits of their husbands. There was statistically marginally significant difference between the COPD cases and the controls with respect to their husband's smoking habits. The association was irregular with respect to daily number of cigarettes smoked but there was a smooth dose response curve with respect to life long total number of cigarettes smoked, with women whose husband smoked more than 300 thousand cigarettes having a relative risk of 1.8 (90% confidence interval of 0.9-3.6) compared to women whose husband has never smoked. These findings, and converging related evidence, indicate that exposure to environmental tobacco smoke may be a risk factor for the development of COPD.

Adult↗