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Biomedical subjects

H Vainio

Publications and source records attributed to H Vainio.

At least 55 records · Page 3Linked to original sources
PubMed2000

Pregnancy outcome of personnel in Swedish biomedical research laboratories.

Possible hazardous effects of laboratory work on the reproduction outcomes of female laboratory personnel in Sweden from 1990 to 1994 were investigated in a questionnaire-based study (n = 1052) by comparison with personnel in non-laboratory departments. The individual woman constituted the primary sampling unit, with her pregnancies defined as the unit of analysis. Allowance for dependence between different pregnancies of the same woman was considered by applying random effect models. With regard to spontaneous abortions, no elevated odds ratio was found for laboratory work in general, but an odds ratio of 2.3 and a 95% confidence interval of 0.9 to 5.9 (n = 856) was connected to working with chloroform. The odds ratio for large for gestational age infants in association with the mother's laboratory work was 1.9 (confidence interval, 0.7 to 5.2). The result with regard to spontaneous abortion partly supports previously reported increased risks of miscarriage related to laboratory work with solvents.

Abortion, Spontaneous↗
PubMed2000

Non-steroidal anti-inflammatory drugs and chemoprevention of cancer.

Aspirin and other NSAIDs are showing promise in the chemoprevention of colorectal cancer. Ongoing trials will eventually provide still lacking information about the optimum dose and treatment duration. NSAIDs may also help to lower the risk of cancer in other organs such as the oesophagus, and possibly breast, stomach, and lung. The chemoprevention by NSAIDs should be seen not as the sole method of prevention, but as an additional tool which will be accompanied by other approaches such as stopping smoking, limiting alcohol consumption, and eating more fruits and vegetables. The chemoprevention by NSAIDs needs also to be balanced against the risks of toxicity (particularly in the stomach) and the other beneficial effects such as prevention of cardiovascular morbidity and mortality. Some of the NSAID induced gastric ulceration and bleeding will most likely be avoided by adopting the use of cyclooxygenase-2 (COX-2) selective NSAIDs, which will selectively inhibit COX-2 while sparing COX-1.

Adult↗
PubMed2000

Steroid metabolism gene CYP17 polymorphism and the development of breast cancer.

The potential role of the polymorphism in the CYP17 gene was evaluated in a case-control study with 483 incident breast cancer patients and 482 population controls, all of homogenous Finnish origin. Our data disagree with the earlier suggestions that the minor A2 variant of CYP17 would pose an increased risk for developing advanced breast cancer. In contrast, a tendency of inverse association was found for premenopausal women carrying the A2 allele containing genotypes with a multivariate adjusted odds ratio of 0.58 approaching statistical significance (95% CI, 0.31-1.07). Agreeing with previous observations, the protective effect of later age at menarche (> or =13 years) was mainly limited to women with A1/A1 genotype, although this could only be seen in premenopausal women (odds ratio, 0.34; 95% CI, 0.15-0.76). Similarly, we found a remarkably lower risk for premenopausal women with at least one child (odds ratio, 0.22; 95% CI, 0.07-0.62) to be mainly attributable to the A1/A1 genotype. CYP17 genotypes may thus modify individual breast cancer proneness in certain subpopulations, although they appear not to have any major modifying role in the risk of this malignancy overall. Because these findings are based on relatively small numbers in stratified analysis, they should, however, be interpreted with caution before being confirmed in future studies.

Adult↗
PubMed2000

Cancer-preventive effects of sunscreens are uncertain.

Provocative findings have been published suggesting that the use of sunscreens may promote skin cancer. A recent meeting of international experts on the use of sunscreens and skin cancer was held at the International Agency for Research on Cancer in Lyon. The workshop concluded that the topical use of sunscreens reduces the risk of sunburn and that sunscreens probably prevent squamous-cell carcinoma of the skin when used mainly during unintentional sun exposure. No conclusion could be drawn about the cancer-preventive activity of topical sunscreens against basal-cell carcinoma and cutaneous melanoma. The use of sunscreens can extend the duration of intentional sun exposure, such as sunbathing. Such an extension may increase the risk for cutaneous melanoma. The workshop warned against relying solely on sunscreens for protection from ultraviolet radiation.

Basal Cell Carcinoma↗
PubMed1999

Ovarian cancer and occupational exposures in Finland.

BACKGROUND: No single occupational or environmental agent has been established as causing ovarian cancer, existing studies often being based on ecologic or proportional mortality data in which potential confounders related to reproductive history have not been taken into account. METHODS: This study linked 324 job titles of occupationally active Finnish women (n = 892,591) at 1970 census with incidence of ovarian cancer (Finnish Cancer Registry, 5,072 cases) during 1971-1995 (over 15 million person-years). The job titles were converted into indicators of exposure to 33 agents, using a national job-exposure matrix based on measurements and surveys (FINJEM). Poisson regression analyses were performed with stratification by birth cohort, follow-up period, and socioeconomic status, and adjusted for mean number of children, mean age at first delivery, and turnover rate for each job title. RESULTS: We found indications of elevated risks for aromatic hydrocarbon solvents (standardized incidence ratio 1.3 (95% CI 1.0-1.7), leather dust (1.4; 0.7-2.7), man-made vitreous fibers (1.3; 0.9-1.8), and high levels of asbestos (1.3; 0.9-1.8), and diesel (1.7; 0.7-4.1), and gasoline (1.5; 1.0-2.0) engine exhausts). Previously reported findings for hairdressers and women in the printing industry were supported in our data, but not for women in dry cleaning jobs. CONCLUSIONS: Given the various drawbacks in linkage studies and job-exposure matrices, the excesses found in this study need confirmation in individual-level studies.

Adult↗
PubMed1999

Modulation of genotoxic and related effects by carotenoids and vitamin A in experimental models: mechanistic issues.

The mechanisms involved in the modulation of genotoxic and related effects by carotenoids and vitamin A were inferred from a critical review of an ad hoc constructed database. Almost 500 results were generated in experimental models evaluating the activity of 32 structurally, metabolically and functionally related nutrients, including beta-carotene and 26 other carotenoids, retinol, retinal, all-trans-retinoic acid and retinyl esters. As many as 67 experimental test systems, either in vitro or in vivo, used a variety of cellular targets and/or end-points suggestive of distinctive mechanisms of action. The bulk of available data support the view that carotenoids and vitamin A do not induce genotoxic effects per se. Even in the absence of any genotoxic agent, these nutrients appeared, on the contrary, to display some mechanisms which play protective roles in tumor promotion and progression, such as inhibition of N-myc gene expression resulting in antiproliferative effects, up-regulation of cell-to-cell communication, an increase in connexin 43 gene expression, a decrease in the 'spontaneous' cell transformation frequency and induction of differentiation in vitro. A large number of studies investigated the modulation by carotenoids and vitamin A of genotoxic and related effects produced by 69 genotoxicants, including biological agents, physical agents, chemical compounds and complex mixtures. In spite of some discrepant data, the general trend was that both carotenoids and vitamin A are poorly effective in acting as nucleophiles, nor do they appear to substantially interfere with the induction or repair of DNA damage produced by direct-acting agents. In contrast vitamin A and carotenoids, irrespective of their provitamin A role, in most studies inhibited those genotoxicants which require metabolic activation to electrophilic derivatives in either bacterial or mammalian cells. Coupled with biochemical data, the distinctive patterns observed with genotoxic agents belonging to different chemical classes suggest a complex modulation of both phase I and phase II enzymes involved in the metabolism of xenobiotics. Furthermore, carotenoids and vitamin A shared other protective mechanisms, such as scavenging of genotoxic oxygen species, modulation of signal transduction pathways, inhibition of cell transformation induced by physical and chemical agents, and facilitation of intercellular communication inhibited by genotoxic compounds. Therefore, carotenoids and vitamin A appear to work via multiple mechanisms, which would support a potential protective role in cancer initiation and in the pathogenesis of other mutation-related diseases. These conclusions are consistent with the recognized cancer-preventive activity of these nutrients in certain animal models and with the evidence provided by observational epidemiological studies, which suggested cancer-protective effects at many sites as related to their dietary intake or plasma levels. However, all these lines of evidence and mechanistically based premises contrast with the unexpected outcome of recent clinical intervention trials, which raised the concern that supplemental use of beta-carotene and vitamin A may increase the risk of lung cancer amongst high risk individuals such as tobacco smokers and asbestos-exposed workers.

Animals↗
PubMed1999

Lung cancer and past occupational exposure to asbestos. Role of p53 and K-ras mutations.

Studies on somatic mutations in lung cancers associated with cigarette smoking and asbestos exposure are few. We investigated prevalence of mutations in the p53 and K-ras genes in lung tumors from smokers with and without asbestos exposure at work. For K-ras mutations, the study was an extension of an earlier analysis. Nearly all of the 105 consecutive patients examined were smokers and had non-small-cell carcinoma of the lung with squamous-cell carcinoma or adenocarcinoma histology. Exposure to asbestos was estimated by pulmonary fiber counts and occupational histories. A pulmonary burden of >/= 1 x 10(6) asbestos fibers per gram of lung tissue, indicating work-related exposure, was found in 32% of the patients for whom fiber-analysis data were available (33 of 102 patients, all men). The statistical analysis showed pulmonary fiber count as the only significant predictor of adenocarcinoma histology, in contrast to squamous-cell carcinoma (smoking-adjusted odds ratio [OR] 3.0, 95% confidence interval [CI] 1.1 to 8.5). The frequency of p53 mutations was 39% (13 of 33) among the asbestos-exposed cases, as compared with 54% (29 of 54) among the nonexposed cases; the difference was not significant, however. In male ever-smokers, a long duration of smoking was associated with p53 mutation (OR 3.2, 95% CI 1.2 to 8.8). In adenocarcinoma, p53 mutations were less prevalent (10 of 30, 33%) as compared with squamous-cell carcinoma (28 of 46, 61%; P = 0.02), whereas a strong and significant association was found between adenocarcinoma and K-ras mutation (OR 37, 95% CI 5.8 to 232, adjusted for smoking and asbestos exposure). Asbestos exposure alone was not significantly associated with increased occurrence of K-ras mutations. In conclusion, the results may primarily reflect the observed excess of adenocarcinoma in the asbestos- exposed patients, and hence the decrease in p53 mutations and increase in K-ras mutations.

Adenocarcinoma↗
PubMed1999

From in utero and childhood exposure to parental smoking to childhood cancer: a possible link and the need for action.

The objective of the present work is to critically summarize published studies and reassess the state of knowledge on a highly controversial topic: the potential association between prenatal exposure to passive smoking as well as maternal active smoking and postnatal exposure to environmental tobacco smoke (ETS) and enhanced incidence of childhood cancer. Elements to be considered include the substantial proportion of pregnant women who remain smokers, the widespread nature of exposure to ETS during pregnancy as well as during childhood, the known toxicology of tobacco smoke, and in particular sidestream smoke, characterized by a rich carcinogen content, the specific metabolism of foetuses and new-borns and finally the amount of epidemiologic data already available. We conducted a thorough review of the literature to identify studies either exclusively dealing with the effects of passive smoking on the occurrence of childhood cancers or more generally etiologic studies of cancer, be it overall or site-specific. We identified close to 50 publications presenting pertinent results from epidemiological investigations and about 50 more on mechanisms and metabolism, smoking in pregnancy and exposure to ETS as well as selected reviews and commentaries. Collaborative epidemiological studies were conducted in the United Kingdom (UK), USA, Sweden, Netherlands and internationally (France, Italy). In addition, other studies were also available from the USA, UK, Canada, Australia, Sweden, Italy, Denmark and People's Republic of China. The vast majority were case-control studies dealing with all cancers, leukaemia and lymphomas, central nervous system (CNS) tumours, Wilms' tumour, retinoblastoma, neuroblastoma, hepatoblastoma, rhabdomyosarcoma, bone and soft tissues tumours, germ cell tumours, as well as specific histological types of leukaemias, lymphomas or CNS tumours. No strong association between maternal smoking in pregnancy and/or exposure to ETS and childhood cancer is found. Yet, several studies found slightly increased relative risks, generally smaller than 1.5, i.e. the order of magnitude associated with some recognized hazards of exposure to ETS (1.2 to 1.3 for adult lung cancer and cardiovascular diseases). Tumours most often found associated with maternal smoking in pregnancy or ETS exposure are childhood brain tumours and leukaemia-lymphoma, with risks up to two or greater in selected studies. In a few studies, risks associated with paternal smoking are higher than the maternal ones. This evidence from human studies coupled with demonstration of genotoxic effects on the foetus of exposure to metabolites of tobacco smoke, and demonstrable presence of adducts should lead to strong recommendations aiming at fully protecting foetuses, new-borns and infants from tobacco smoke.

Brain Neoplasms↗
PubMed1999

Chemoprevention of cancer: a controversial and instructive story.

Increased intake of fruits and vegetables seems to be one of the simplest means of decreasing the risk for cancer. Cancer-preventive effects of fruits and vegetables have been observed in epidemiological studies, which could not, however, distinguish the effects of the various ingredients. Antioxidant defence has been proposed as a mechanism of chemoprevention, although inconclusive results have been obtained. The results of randomized intervention trials have shown that beta-carotene supplements are of limited value and may even be deleterious. Vitamins are a good marker of the ingestion of fruits and vegetables, and vitamin E (alpha-tocopherol) is a lipid-soluble antioxidant which can scavenge free radicals. It has no significant effect on the risk for lung cancer of long-term smokers in an intervention trial, but it decreased both the incidence of and mortality from prostate cancer; however, there was a 50% increase in the occurrence of cerebral haemorrhage among the men given vitamin E. Aspirin and aspirin-like drugs appear to decrease the risk for intestinal tumours; the mechanism of action appears to involve diminishing prostaglandin production due to inhibition of cyclooxygenases. Dietary fibre has been linked to a reduced risk for colorectal cancer in many observational studies, but opposite findings were reported recently. In order to resolve these paradoxes, we need to understand better the underlying biology, develop mechanistic hypotheses and test them in clinical trials in humans. Until that time, we should confine any premature enthusiasm for chemopreventive micronutrient supplementation.

Animals↗
PubMed1999

Promise of molecular epidemiology--epidemiologic reasoning, biological rationale and risk assessment.

Molecular epidemiology has emerged as a natural outgrowth of attempts to apply information derived from the explosion in molecular biology to disease in human populations. The incorporation of biomarkers into classical epidemiologic designs holds the promise of unraveling mechanisms, elucidating gene-environment interactions, and dissecting heterogeneity. The primary interest of molecular epidemiology is in the identification of factors in the physical and social environment which affect the risk for disease and which are amenable to preventive intervention. The explosion in molecular technology has not, however, resulted in radical, widespread improvements in epidemiologic results and therefore has led to a sense of frustration in the public health community. As experience accumulates, there is new appreciation that attention to study design, infrastructure, and biomarker validation can improve the results.

Biomarkers↗
PubMed1999

Simian virus 40 (SV40)-like DNA sequences not detectable in finnish mesothelioma patients not exposed to SV40-contaminated polio vaccines.

Occupational asbestos exposure can be demonstrated in 80% of mesothelioma cases. A possible role of simian virus 40 (SV40) in the etiology of mesothelioma was raised because several studies reported the presence and expression of SV40-like DNA sequences in human mesotheliomas. It is also known that expression of SV40 large T antigen inhibits cellular Rb and p53. This suggests that SV40 might render infected cells more susceptible to asbestos carcinogenicity. The SV40-like sequences are suggested to have arisen from contaminated polio vaccines. Millions of people in the United States and most European countries were inoculated with SV40-contaminated polio vaccine in 1955-1963. However, in Finland, where polio vaccination started in 1957, no SV40-contaminated vaccine was used. We used a polymerase chain reaction-based method to test for the presence of SV40-like sequences in DNA extracted from the frozen tumor tissues of 49 Finnish mesothelioma patients, most of whom had been occupationally exposed to asbestos. All of the Finnish tumor tissues tested negative for SV40-like sequences. The results suggest that the SV40-like sequences detected in mesothelioma tissue in some previous studies may indeed originate from SV40-contaminated polio vaccines. It is a matter of speculation whether the absence of SV40 infection has contributed to the relatively low incidence of mesothelioma in Finland (1/10(5) in 1990-1995).

Adult↗
PubMed1999

An international evaluation of the cancer preventive potential of vitamin A.

The IARC convened a Working Group of experts in May 1998 to evaluate the cancer preventive potential of vitamin A and to compile the third volume of the IARC Handbooks of Cancer Prevention. The handbook is intended to provide a comprehensive review of the relevant information in the published scientific literature through April 1998 on the role of vitamin A in cancer prevention. The focus of this critical review and commentary is on retinol and the retinyl esters. Much of the scientific literature in this field overlaps with studies involving vitamin A metabolites, vitamin A precursors, and studies of total dietary vitamin A (which is a combination of preformed vitamin A and its precursors), so work from this wide range of research is included in this review when it is deemed relevant to our understanding of the effects of retinol or retinyl esters on cancer development. The observed effects of preformed vitamin A on cell and organ culture, on animal models, in dietary observational epidemiological studies, and in human intervention studies was reviewed in the meeting. In summary, there is little evidence that vitamin A intake has any substantial cancer-preventive effects.

Animals↗
PubMed1998

Use of biomarkers--new frontiers in occupational toxicology and epidemiology.

The incorporation of biomarkers into occupational toxicology and epidemiology some 25 years ago marked a turning-point for the discipline. The advances in molecular biology have provided new tools. At first, the major interest was in biomarkers of exposure, borrowing concepts from pharmacology, then it moved from the external estimates of exposure to internal measures of dose, and ultimately, to markers of target dose. Concerted efforts to measure carcinogens at the molecular level, e.g. DNA adducts, occupied a substantial fraction of the biomarkers work. In parallel, more quantitative and more sensitive end-points for etiological studies were sought earlier. Again, with advancing techniques in cytogenetics, extensive studies were conducted on such markers as sister chromatid exchanges (SCEs), micronuclei and other changes deemed to represent genomic damage. However, these types of end-points were quite unspecific for application to new hazards of uncertain human carcinogenic potential. Recent work focusing on more specific early-effect markers such as certain oncogenes and tumour-suppressor genes have substantial promise as shown by work with aflatoxins and vinyl chloride. Such studies have also enhanced mechanistic insight. The advances in molecular genetics have led to an upsurge in interest in most susceptibility factors, and identification of polymorphisms of various enzymes has become possible. Ongoing search for 'ultra-high risk' individuals may be fruitful, but probably only relevant to a small segment of potentially exposed populations. Factors associated with a small differential risk, however theoretically or mechanistically important, offer only little practical use.

Biomarkers↗