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Kurt Straif

Publications and source records attributed to Kurt Straif.

18 recordsLinked to original sources

Field comparison of inhalable aerosol samplers applied in the european rubber manufacturing industry.

Several studies have been done in Europe to evaluate exposure to dust and fumes in the rubber industry. However, different aerosol sampling devices have been used which perform differently depending on the environmental conditions and particle size distribution. To compare measurements of rubber dust and fumes among countries and surveys we initiated a field comparison of personal inhalable samplers using a novel reference inhalable aerosol sampler (CALTOOL). Measurements were done in four factories in the Netherlands, Sweden, Poland and Germany in the mixing and milling and curing department. The Seven-hole sampler, PAS-6 sampler, Millipore (25 and 37 mm) cassette, IOM sampler and a Polish sampler were mounted on the reference CALTOOL device and used simultaneously. All samplers except the IOM sampler under-sampled inhalable dust. To compare measurements from different studies and countries, correction factors should be applied to all but the IOM sampler, which was the only sampler that performed similar to the CALTOOL sampler.

Aerosols↗

A database of exposures in the rubber manufacturing industry: design and quality control.

The concerted action EXASRUB was initiated to create a database management system for information on occupational hygiene measurements that could be used to develop exposure models in the European rubber manufacturing industry. Quality of coding was assessed by calculating percentages of agreement and Cohen's kappa statistics (kappa) for an intra- and inter-centre recoding of randomly selected subsets of the measurements. In a 6-month period, 59 609 measurements from 523 surveys in 333 factories from as early as 1956 to 2003 were coded. The database consists primarily of measurements of N-nitrosamines (36%), rubber dust (23%), solvents (14%) and rubber fumes (10%). Coding of epidemiologically relevant information was done consistently with inter-centre kappa between 0.86 and 1.00. For occupational hygiene information, values of kappa were estimated to be between 0.67 and 1.00. The proposed method resulted in a large quantity of exposure measurements with auxiliary information of varying completeness and quality. Analyses showed that coding of epidemiologically relevant information in such a multi-centre, multi-country study was coded consistently. Larger errors however, occurred in coding of occupational hygiene information. This was primarily caused by lack of information in the primary records of measurements, emphasizing the importance of having a universal system in place to collect and store measurement information by occupational hygienists for future use.

Chemical Industry↗

Epidemiologic review of marijuana use and cancer risk.

Marijuana is the most commonly used illegal drug in the United States and is considered by young adults to be the illicit drug with the least risk. On the other hand, marijuana smoke contains several of the same carcinogens and co-carcinogens as the tar from tobacco, raising concerns that smoking of marijuana may be a risk factor for tobacco-related cancers. We reviewed two cohort studies and 14 case-control studies with assessment of the association of marijuana use and cancer risk. In the cohort studies, increased risks of lung or colorectal cancer due to marijuana smoking were not observed, but increased risks of prostate and cervical cancers among non-tobacco smokers, as well as adult-onset glioma among tobacco and non-tobacco smokers, were observed. The 14 case-control studies included four studies on head and neck cancers, two studies on lung cancer, two studies on non-Hodgkin's lymphoma, one study on anal cancer, one study on penile cancer, and four studies on childhood cancers with assessment of parental exposures. Zhang and colleagues reported that marijuana use may increase risk of head and neck cancers in a hospital-based case-control study in the United States, with dose-response relations for both frequency and duration of use. However, Rosenblatt and co-workers reported no association between oral cancer and marijuana use in a population-based case-control study. An eightfold increase in risk among marijuana users was observed in a lung cancer study in Tunisia. However, there was no assessment of the dose response, and marijuana may have been mixed with tobacco. Parental marijuana use during gestation was associated with increased risks of childhood leukemia, astrocytoma, and rhabdomyosarcoma, but dose-response relations were not assessed. In summary, sufficient studies are not available to adequately evaluate marijuana impact on cancer risk. Several limitations of previous studies include possible underreporting where marijuana use is illegal, small sample sizes, and too few heavy marijuana users in the study sample. Recommendations for future studies are to (1) focus on tobacco-related cancer sites; (2) obtain detailed marijuana exposure assessment, including frequency, duration, and amount of personal use as well as mode of use (smoked in a cigarette, pipe, or bong; taken orally); (3) adjust for tobacco smoking and conduct analyses on nonusers of tobacco; and (4) conduct larger studies, meta-analyses, or pooled analyses to maximize statistical precision and investigate sources of differences in results. Despite the challenges, elucidation of the association between marijuana use and cancer risk is important in weighing the benefits and risks of medical marijuana use and to clarify the impact of marijuana use on public health.

Animals↗

Meeting report: summary of IARC monographs on formaldehyde, 2-butoxyethanol, and 1-tert-butoxy-2-propanol.

An international, interdisciplinary working group of expert scientists met in June 2004 to develop IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans (IARC Monographs) on formaldehyde, 2-butoxyethanol, and 1-tert-butoxy-2-propanol. Each IARC Monograph includes a critical review of the pertinent scientific literature and an evaluation of an agent's potential to cause cancer in humans. After a thorough discussion of the epidemiologic, experimental, and other relevant data, the working group concluded that formaldehyde is carcinogenic to humans, based on sufficient evidence in humans and in experimental animals. In the epidemiologic studies, there was sufficient evidence that formaldehyde causes nasopharyngeal cancer, "strong but not sufficient" evidence of leukemia, and limited evidence of sinonasal cancer. The working group also concluded that 2-butoxyethanol and 1-tert-butoxy-2-propanol are not classifiable as to their carcinogenicity to humans, each having limited evidence in experimental animals and inadequate evidence in humans. These three evaluations and the supporting data will be published as Volume 88 of the IARC Monographs.

Animals↗

Modification of breast cancer risk in young women by a polymorphic sequence in the egfr gene.

The regulation of the epidermal growth factor receptor (egfr) gene in human cancer is not yet fully understood. Recent data on a polymorphic CA repeat located at the 5'-regulatory sequence in intron 1 of the egfr gene [egfr CA simple sequence repeat (SSR) I] point to a possible inheritance of cancer risk associated with the egfr gene. Furthermore, we have detected frequent allelic imbalances restricted to the egfr CA SSR I in breast cancer tissue and nontumorous breast tissue adjacent to invasive and in situ breast cancer representing amplifications. Therefore, we conducted a population-based case-control study to assess the relationship between the egfr polymorphism and breast cancer risk. Cases with a first primary breast cancer by age 50 years and age-matched population controls provided information on known and suspected risk factors. The allelic length of the egfr CA SSR was determined in 616 cases and 1072 population-sampled controls. Genotypes were categorized for analysis by allele length. Multivariate logistic regression was used to compare genotype distributions, accounting for other risk factors, and to investigate gene-environment interactions. We found a modifying effect, albeit no main effect, of the allelic length of the egfr polymorphism on breast cancer risk. The presence of two long alleles (>/==" BORDER="0">19 CA) was associated with a significantly elevated odds ratio (OR) of 10.4 [95% confidence interval (CI), 1.85-58.70] among women with a first-degree family history of breast cancer (P = 0.015 for interaction). The risk increase associated with high red meat consumption (OR, 10.68; 95% CI, 1.57-72.58) and the protective effect of high vegetable intake (OR, 0.07; 95% CI, 0.004-1.07) was also most pronounced among carriers of two long alleles (>/==" BORDER="0">19 CA). The length of the egfr CA SSR may increase the risk for familial breast cancers, and its effect could be modulated by dietary factors.

Adult↗

Betel quid without tobacco as a risk factor for oral precancers.

The IARC monographs recently classified chewing betel quid without tobacco as a human carcinogen. Several studies in Taiwan have reported that betel quid without tobacco may increase the risk of oral precancers such as oral leukoplakia and oral submucous fibrosis. However in India, since most betel quid chewers prefer to add tobacco to the quid, the independent effect of betel quid on the risk of oral precancers is difficult to assess and has not yet been fully explored. We conducted a large case-control study in Kerala, India, including 927 oral leukoplakia cases, 170 oral submucous fibrosis cases, 100 erythroplakia cases, 115 multiple oral precancer cases and 47,773 controls. The focus of this reanalysis is on the minority of individuals who chewed betel quid without tobacco. Among nonsmokers and nondrinkers, chewing betel quid without tobacco conferred ORs of 22.2 (95%CI = 11.3, 43.7) for oral leukoplakia, 56.2 (95%CI = 21.8, 144.8) for oral submucous fibrosis, 29.0 (95%CI = 5.63, 149.5) for erythroplakia and 28.3 (95%CI = 6.88, 116.7) for multiple oral precancers, after adjustment for age, sex, education and BMI. Dose-response relationships were observed for both the frequency and duration of betel quid chewing without tobacco on the risk of oral precancers. In conclusion, our study supports the hypothesis that chewing betel quid without tobacco elevates the risks of various oral precancers.

Adult↗

The science and practice of carcinogen identification and evaluation.

Several national and international health agencies have established programs with the aim of identifying agents and exposures that cause cancer in humans. Carcinogen identification is an activity grounded in the scientific evaluation of the results of human epidemiologic studies, long-term bioassays in experimental animals, and other data relevant to an evaluation of carcinogenicity and its mechanisms. In this commentary, after a brief discussion of the science basis common to the evaluation of carcinogens across different programs, we discuss in more detail the principles and procedures currently used by the IARC Monographs program.

Biological Assay↗

Listing occupational carcinogens.

The occupational environment has been a most fruitful one for investigating the etiology of human cancer. Many recognized human carcinogens are occupational carcinogens. There is a large volume of epidemiologic and experimental data concerning cancer risks in different work environments. It is important to synthesize this information for both scientific and public health purposes. Various organizations and individuals have published lists of occupational carcinogens. However, such lists have been limited by unclear criteria for which recognized carcinogens should be considered occupational carcinogens, and by inconsistent and incomplete information on the occupations and industries in which the carcinogenic substances may be found and on their target sites of cancer. Based largely on the evaluations published by the International Agency for Research on Cancer, and augmented with additional information, the present article represents an attempt to summarize, in tabular form, current knowledge on occupational carcinogens, the occupations and industries in which they are found, and their target organs. We have considered 28 agents as definite occupational carcinogens, 27 agents as probable occupational carcinogens, and 113 agents as possible occupational carcinogens. These tables should be useful for regulatory or preventive purposes and for scientific purposes in research priority setting and in understanding carcinogenesis.

Carcinogens↗

Job titles and work areas as surrogate indicators of occupational exposure.

BACKGROUND: Job titles or work areas are often used as surrogate indicators of exposure in occupational epidemiological studies. In this article, we assess the validity and comparability of commonly used surrogate indicators. METHODS: We analyzed lung cancer mortality among a hypothetical and an actual cohort of rubber workers. Surrogate indicators of exposure were defined according to jobs in which workers were "only," "ever," "longest" or "last" employed, or in which they were employed at the "census" of the study. Occupational risks were estimated using standardized mortality ratios. Validity of surrogate indicators was assessed in the simulated data by comparison between estimated effects and the known underlying associations. Comparisons of surrogate indicators were conducted in both simulated and empirical data. RESULTS: Use of the definition "only" as the surrogate indicator gave valid but imprecise results. For all other definitions, we observed a moderate overestimation of risks in no-risk or low-risk jobs and attenuation of underlying dose-response relationships, without substantial differences among the applied definitions. CONCLUSIONS: Our results demonstrate a limitation of using surrogate indicators of exposure in occupational epidemiological studies. However, they suggest that the inconsistencies of published study findings in the rubber industry are unlikely to be attributable to the use of different surrogate indicators.

Cohort Studies↗