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Biomedical subjects

P Boffetta

Publications and source records attributed to P Boffetta.

At least 235 records · Page 13Linked to original sources
PubMed1994

Biopersistence of respirable synthetic fibers and minerals: the point of view of the epidemiologist.

Biopersistence of fibers and minerals in human respiratory tissues is an important aspect of the toxicity of these agents. However, few data are available from human studies. Although a number of studies have measured the lung burden of asbestos and other minerals in exposed humans, few presented information relevant to biopersistence of these agents. The studies analyzing asbestos lung burden in workers at different intervals following cessation of exposure suggest a linear decrease in concentration over time, that is independent of duration of exposure. However, the available evidence on asbestos is too sparse to allow a firm conclusion; almost no data are available on other minerals.

Air Pollutants↗
PubMed1994

Secondary malignancies following cancer chemotherapy.

Many agents used in cancer chemotherapy are known carcinogens. However, few secondary malignancies have been definitely linked to chemotherapy, since studies on this problem are complicated by methodological problems. A causal relationship has been established between alkylating agents and leukaemia and between cyclophosphamide and bladder cancer. The risk of leukaemia peaks at 5-10 years after beginning of chemotherapy and declines steadily after its end. The interaction between chemotherapy and radiotherapy has not been fully clarified, nor has the leukaemogenic potency of individual drugs, although combinations without nitrogen mustard seem to entail a lower risk. Other tumours reported at increased incidence, in particular among Hodgkin's disease patients, for whom a carcinogenic effect of chemotherapy seems plausible, are non-Hodgkin's lymphoma and lung cancer. Other secondary solid tumors have also been reported, but for none of them an independent effect of chemotherapy has been demonstrated.

Antineoplastic Agents↗
PubMed1994

Mechanisms of the combined effect of asbestos and smoking in the etiology of lung cancer.

The joint effects of exposure to two known lung carcinogens, tobacco smoking and asbestos, are reviewed. The variable pattern of interaction--ranging from supramultiplicative to less than additive--may reflect the fact that both asbestos and smoking are complex carcinogens which can affect more than one stage of lung carcinogenesis. The joint effect of two such agents will depend on the relative magnitude of the effects at each stage. The epidemiologic evidence from studies of insulation workers with high exposures suggests an interaction that approximates the multiplicative model, indicating that each of the two factors has an independent action on the multistage process of carcinogenesis. Very limited information is available on the interaction between these two agents in causing specific histological types of lung cancer. Both tobacco smoke and asbestos fibers can be genotoxic and cytotoxic and cause proliferative lesions in the lungs. Tobacco smoke is known to contain carcinogens that bind to critical genes in DNA (deoxyribonucleic acid) and cause mutations. Asbestos fibers may cause chronic inflammation of the lungs, which releases various cytokines and growth factors, and therefore may provide a possible selective growth advantage for mutated cells.

Asbestos↗
PubMed1994

Pleural mesothelioma and asbestos exposure among Italian oil refinery workers.

OBJECTIVES: The association between asbestos exposure and risk of mesothelioma was studied among workers from two oil refineries located in the northern Italian cities of Genoa and La Spezia, given that previous cohort analyses revealed two clusters of mesotheliomas and that international cohort studies have so far not reported an excess of this neoplasm among oil refinery workers. METHODS: Men (N = 2300) who had been employed between 1914 and 1988 in two oil refineries located in northern Italy were studied. The follow-up covered the mortality of 639 white-collar and 1661 blue-collar from 1950 to 1991. RESULTS: Among the cases, the median duration of employment was 14.5 years, and the median time since first employment was 27.5 years. The job titles of the 10 men with pleural mesothelioma were maintenance worker (seven men), electrician (one man) and unspecified blue-collar worker (two men). Blue-collar workers experienced a significantly increased risk of pleural neoplasms, five deaths in each plant, in respect to both the provincial [standardized mortality ratio (SMR) 266] and national (SMR 1663) reference populations. The SMR, based on eight deaths, was 320 for workers with more than 10 years of employment and 20 years since first exposure. CONCLUSIONS: The results uphold the notion that exposure to asbestos in oil refineries causes pleural mesotheliomas. This is the first study to find an excess of pleural mesotheliomas among oil refinery workers exposed to asbestos.

Adult↗
PubMed1994

Occupational exposures to carcinogens in developing countries.

There have been very few studies of exposure to occupational carcinogens in developing countries, and even fewer studies of the health consequences of such exposures. However, all industrial chemicals, occupations and industrial processes classified by the International Agency for Research on Cancer (IARC) as Group 1 or Group 2A (carcinogenic or possibly carcinogenic to humans) have been described in developing countries, and there is growing concern that the health impact of many chemicals used in the developing world has been underestimated. In all regions a very large workforce is employed in the construction industry, in which substantial exposure to asbestos may occur, and there has been a rapid increase in production in countries such as Brazil and India. There is, for instance, a similar pattern for tyre production with a large increase in production in developing countries in the 1980s. Thus, the number of workers in industries entailing a carcinogenic risk is increasing in developing countries, partly as a result of the transfer of hazardous industry from industrialized countries. There is much that could be achieved in the prevention of occupational cancer in developing countries, and there have been a number of successful initiatives. However, the greatest progress in the prevention of occupational cancer in developing countries is most likely to come from political and economic changes.

Carcinogens↗
PubMed1994

Cancer.

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Agricultural Workers' Diseases↗
PubMed1994

Other diseases.

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Asbestosis↗
PubMed1994

Employment as hairdresser and risk of ovarian cancer and non-Hodgkin's lymphomas among women.

The incidence of ovarian cancer and non-Hodgkin's lymphomas (NHL) between 1971 and 1985 or 1987 has been studied on the basis of cancer registry data among women employed in hairdressing or related occupations at 1970 census in Denmark, Sweden, Norway, and Finland. Overall, the standardized incidence ratio (SIR) for ovarian cancer was 1.18 (95% confidence interval, 0.98 to 1.40). The increase was present among hairdressers from Denmark (SIR, 1.23) and Finland (SIR, 1.88); whereas hairdressers from Sweden and Norway had an incidence close to expectation (SIR 0.95 and 0.96, respectively). In three of the four countries, the SIR was higher in 1971 to 1975 than in later years. The SIR for NHL was 1.20 (0.84 to 1.66); an excess was seen in Denmark (SIR, 1.92) and a decrease was found in Sweden (SIR, 0.63). In previous studies, hairdressers have been reported to be at increased risk of ovarian cancer: this study adds some evidence in favor of the presence of an association. This study also offers some support to the hypothesis of an association between exposure to hair dyes and risk of NHL, that was reported among personal users from the United States. This study, however, strongly suggests that occupational cancer risk among female hairdressers depends on temporal and geographical factors.

Adult↗
PubMed1993

Tobacco smoking, alcohol drinking, and cancer of the oral cavity and oropharynx among U.S. veterans.

BACKGROUND: Independent carcinogenic effects of alcohol drinking and tobacco smoking as well as their interaction can be usefully studied in a population of heavy drinkers and smokers. METHODS: A hospital-based case-control study was conducted during 1972 to 1983 in a large Veterans hospital in East Orange, New Jersey. A total of 359 oral cavity-oropharynx cancer cases and 2280 controls were interviewed according to tobacco smoking, use of smokeless tobacco, alcoholic beverage, coffee and tea drinking, race, family origin, religion, and occupation as bartender. RESULTS: Odds ratio of oral cancer increased up to the level of 35 cigarettes per day and 21 whiskey equivalents per day: no further increase was found for higher level of exposure to either factor. A protective effect of quitting smoking was found, but the number of former smokers was small. No difference occurred in oral cancer risk according to type of alcoholic beverage drunk. An interaction effect compatible with a multiplicative model was found between the two exposures. Blacks were at lower risk than whites, and, in the latter group, individuals of Italian origin were at lower risk than individuals from northern or central European countries. CONCLUSIONS: Alcohol drinking and tobacco smoking were responsible for the majority of oral cancer cases in this population of US Veterans.

Adult↗
PubMed1993

[Passive smoking. Effects on health].

Passive smoking--also called involuntary or environmental smoking--is the exposure of non-smokers to the tobacco smoke released by smokers. The physico-chemical composition of tobacco smoke, and notably its contents in toxic and carcinogenic substances, is the same in the secondary stream between puffs as in the primary stream released by the smoker. The pathogenic effects of passive smoking are increasingly well known and accepted. A high incidence of respiratory tract infections and of chronic respiratory and asthmatic symptoms is observed in children. In adults, passive smoking seems to be one of the main risk factors for cardiovascular diseases. Its repercussions on the respiratory tracts is difficult to evaluate, but there are marked by an increase of respiratory symptoms and perhaps of chronic obstructive lung diseases. Finally, it is now recognized that passive smoking is a major risk factor for primary lung cancer in non-smokers exposed to tobacco smoke.

Adult↗
PubMed1993

Survival of breast cancer patients from Piedmont, Italy.

A population-based series of 4,764 women from Piedmont, Italy, who were diagnosed with breast cancer during 1979-81 and for whom information on social and demographic factors was available, was followed-up for mortality until 1986 or 1987. Relative survival rates at one, three, and five years were 94.6, 81.6, and 71.1 percent, respectively, and were similar to those of other European series. Women aged 40-49 years at diagnosis experienced a better survival than women in other age groups. The mortality was highest between one and four years after diagnosis, and lowest between five and seven years. Survival rates were lowest for women above the age of 80, and single women had a worse prognosis than married women. Women with less than seven years of education had nonsignificantly lower survival rates than more educated women. No difference in survival was found according to occupation, size of town of residence, place of birth, or type of hospital.

Adult↗
PubMed1993

Environmental tobacco smoke and the risk of cancer in adults.

The apparent effect of environmental tobacco smoke (ETS) exposure on cancer risk has become an important social and political issue. The risk of cancer in non-smokers is often the main reason for prohibiting or restricting smoking in public places. A number of epidemiological studies have shown an association between ETS exposure and lung cancer. However, the strength of this association has still to be estimated. Only a few studies have reported on ETS and cancer from sites other than the lung in adults. No definite conclusions can be drawn at present from a critical review of the epidemiological evidence, but the suggestion of an association is present for sinonasal cancer, while bladder cancer does not seem to be associated to ETS exposure. Positive studies are available for cancers from other sites, including the breast, the uterine cervix and the brain, but these are difficult to interpret.

Adult↗
PubMed1993

Mortality patterns and trends for lung cancer and other tobacco-related cancers in the Americas, 1955-1989.

Mortality from cancers of the oral cavity and pharynx, oesphagus, larynx and lung between 1955 and 1989 has been analysed for USA, Canada and 14 countries in Latin America. Among males, Uruguay, Cuba, Argentina and Puerto Rico have the highest rates for all sites, and Peru, Ecuador, Dominican Republic, Mexico and Colombia have the lowest rates. Among females, Cuba, Colombia and Puerto Rico rank high for all sites, and Mexico, Paraguay, Ecuador and Peru rank low. For both sexes, lung cancer mortality rates from the US and Canada are high, whereas rates from other sites are intermediate. An increasing trend in lung cancer mortality over time is shown in all countries except Cuba (no changes), Argentina, Paraguay and Peru (decreasing trend). In Latin America, the tobacco-related lung cancer epidemic is in its early phase among males, and very early phase among females.

Esophageal Neoplasms↗
PubMed1993

Development and use of a welding process exposure matrix in a historical prospective study of lung cancer risk in European welders.

A welding process exposure matrix has been developed relating 13 welding process-welded metal combinations to average exposure levels for total welding fumes, total chromium, chromium (VI) and nickel. Quantitative estimates were derived from consultation of literature sources and of some company data. This matrix was applied to the welding histories of 11,092 welders in the framework of an IARC multicentre study. When detailed welding history was not available at the individual level the average company welding practice profile was applied. No dose-response relationship emerged for lung cancer risk with cumulative dose of the carcinogens chromium (VI) and nickel for stainless steel welders. Dilution of the dose-response relationship could result from between-plant and within-plant variability, and exposure in jobs not accounted for in the study, but not from the partial use of company versus individual data. It is also possible that there is no increased risk related to chromium and nickel exposure in this group of workers. Matrix exposure estimates would need to be validated and the matrix possibly refined by comparison with a variety of comprehensive welding exposure data sets.

Air Pollutants, Occupational↗