Documents bladder cancer 37 results

"Legal regulations of the work environment are probably regarded as the main tools for promoting prevention at the workplace. Legal regulations are expressed as occupational exposure limits, bans, and taxes. Taxes can be regarded as economic incentives as well, and other economic incentives are insurance systems for employers' and consumers' actions. The latter have been found to have profound effects regarding environmental issues and may also, in the future, be a powerful tool for workplace-related prevention. The research in this area is rather limited, but there are some research results that can be obtained from the area of environmental economics. This paper discusses some examples in which legal regulations, economic incentives, or both have been used. Legal regulations and market-based economic incentives may produce similar results, but the economic cost and political feasibility typically differ. This situation makes the selection and design of instruments an important field for future research."

"Background:Exposure to polycyclic aromatic hydrocarbons (PAHs) has been linked to bladder cancer.Objective:To evaluate the role of PAHs in bladder cancer, PAHs serum levels were measured in patients and controls from a case-control study.Methods:A total of 140 bladder cancer patients and 206 healthy controls were included in the study. Sixteen PAHs were analyzed from the serum of subjects by gas chromatography–mass spectrometry.Results:Serum PAHs did not appear to be related to bladder cancer risk, although the profile of contamination by PAHs was different between patients and controls: pyrene (Pyr) was solely detected in controls and chrysene (Chry) was exclusively detected in the cases. Phenanthrene (Phe) serum levels were inversely associated with bladder cancer (OR?=?0·79, 95%CI?=?0·64–0·99, P?=?0·030), although this effect disappeared when the allelic distribution of glutathione-S-transferase polymorphisms of the population was introduced into the model (multinomial logistic regression test, P?=?0·933). Smoking (OR?=?3·62, 95%CI?=?1·93–6·79, P<0·0001) and coffee consumption (OR?=?1·73, 95%CI?=?1·04–2·86, P?=?0·033) were relevant risk factors for bladder cancer.Conclusions:Specific PAH mixtures may play a relevant role in bladder cancer, although such effect seems to be highly modulated by polymorphisms in genes encoding xenobiotic-metabolizing enzymes."

"Objectives This study investigated associations between exposure to polycyclic aromatic hydrocarbons (PAH) and the incidence of lung, bladder, kidney, and pancreatic cancer among Norwegian aluminum plant workers.Methods Cancer incidence was investigated from 1953 to 1996 among 11 103 men employed for more than 3 years in the industry, giving 272 554 person-years during follow-up. A job exposure matrix was constructed to estimate exposure to particulate PAH and fluorides. The observed cases of cancer were compared with expected figures calculated from national rates. Dose-response relations were investigated by internal comparisons using Poisson regression and stratified analyses for standardized incidence ratio. Potential confounding by smoking was investigated in subanalyses restricted to 3 of the plants.Results The study showed an overall excess for bladder cancer, standardized incidence ratio 1.3 (95% confidence interval 1.1-1.5), which increased with increasing cumulative exposure to PAH and reached a relative risk of about 2 for the upper exposure category in the analysis with 30 years of lag time. There was no association between cumulative PAH exposure and lung cancer, but there were indications of an elevated risk of kidney cancer among the most heavily PAH-exposed persons in the analyses with a lag time of 30 years. For pancreatic cancer we found a higher incidence among the PAH-exposed persons than among the unexposed ones, but no clear dose-response association was found.Conclusions The study showed an association between bladder cancer and exposure to PAH, but gave no support to an association between PAH exposure and lung cancer in the primary aluminum industry."

Epidemiologic studies investigating the cancer risk associated with using metalworking fluids (MWFs) were reviewed. Results of a comprehensive, systemic survey of the epidemiologic evidence for occupational use of MWFs being associated with cancer of the skin and scrotum, larynx, rectum, pancreas, and bladder by NIOSH and which were included in a NIOSH criteria document for MWFs were presented. Specific studies covered included retrospective cohort mortality and cancer incidence studies of MWF exposed cohorts and associated nested case/control studies, proportionate mortality ratio (PMR) studies, and population based (PB) studies. A case/control study and a cancer incidence study and several case reports suggested MWFs, primarily straight oil MWFs, were associated with increased risk of skin and scrotal cancer. None of three PMR studies found an increased risk for skin and scrotal cancer. A number of cohort, PMR, and PB studies found increased risks for laryngeal and rectal cancer, especially for exposure to straight oil MWFs. Several cohort and PMR studies found increased risks for pancreatic cancer among MWF exposed workers. The strongest evidence was for grinding with synthetic MWFs and machining with straight oil MWFS. Some studies were inconsistent; for example, excess cancer risk was found in black, but not white, workers. One of six PMR studies and several PB case control studies found significant excess risks for bladder cancer after controlling for smoking. Neither of two cohort cancers found an elevated bladder cancer risk; however, both were based on small numbers. The route of MWF exposure was generally through dermal contact or inhalation; however, because of the large sizes of many airborne MWF droplets, gastrointestinal exposure may also have occurred. The authors conclude that increased risks for larynx, rectal, pancreatic, skin and scrotal, and bladder cancer were associated with the use of some types of MWFs. Because of the long latency period for solid organ tumors, the MWF exposures probably occurred before the mid 1970s. The risk of cancer from MWF exposures since the mid 1970s is undetermined because a definitive study of workers entering jobs with MWF exposure during this time period has not yet been performed.

"Ces recommandations de bonne pratique ont pour objectifs de proposer des outils et une méthodologie pour repérer des substances cancérogènes pour la vessie ou des situations exposant à ces cancérogènes, faciliter le recueil d'informations sur les expositions passées et actuelles, définir les modalités de surveillance pendant l'activité professionnelle et le suivi post-professionnel. Élaborées par la Société française de médecine du travail (SFMT) en partenariat avec plusieurs autres sociétés savantes, elles ont reçu le label de la Haute Autorité de santé et de l'Institut national du cancer en avril 2012. Sont reproduits ici le texte court, la fiche de synthèse et la fiche d'information pour le patient.Ces trois documents, ainsi que l'argumentaire et la fiche de synthèse des recommandations relatives aux cancers en général sont consultables sur le site de la SFMT : www.chu-rouen.fr/sfmt/pages/Recommandations.php"

"Our expanding capacity to detect human genetic susceptibility to various chronic diseases presents us with the opportunity to screen asymptomatic people for purposes of employment, insurance or credit. It also brings with it the responsibility of deciding the ethical and social value of such applications. This paper addresses scientific and ethical issues involved in the use of genetic screening techniques which intend to identify individuals that have more than average susceptibility to develop cancer from workplace chemical exposures. The case in point is the genetic polymorphism for N-acetyltransferase activity and the risk of bladder cancer in workers exposed to carcinogenic arylamines. The acetyltransferase polymorphism is related to the metabolic activation and deactivation of carcinogenic arylamines. Any genetic screening test for cancer susceptibility must be based upon sound science. For example, it must be demonstrated that a specific metabolic phenotype is a risk factor for cancer and, further, that the available tests accurately classify the subjects as to the phenotype. If there is a poor correspondence between phenotype and genotype, or a large intra-individual variability in phenotype, misclassification may result. Also, bias, arising as a consequence of enzyme induction by specific substrates, must be ruled out. Genetic screening of workers for susceptibility to cancer seems to us an ethically unacceptable and premature, application of the science."