One prospective epidemiologic study of asbestos cement workers with radiological small opacities has been cited as a rationale for attributing excess lung cancer to asbestosis. This approach could have considerable practical value for disease attribution in an era of decreasing exposure. However, a recent International Agency for Research on Cancer review concludes that the mechanism of production of asbestos-related lung cancer are unknown. Asbestosis, therefore, cannot be a biologically effective dose marker of lung cancer susceptibility. Asbestosis nonetheless would be useful in identifying asbestos-attributable lung cancer cases if it could be proven an infallible exposure indicator. In this study, we tested this hypothesis in the chrysotile miners and millers of Quebec, Canada. We examined exposure histories, autopsy records, and lung fiber content for 111 Quebec chrysotile miners and millers. If the hypothesis of an asbestosis requirement for lung cancer attribution were accurate, we would expect as asbestosis diagnosis to separate those with lung cancer and high levels of exposure from those with lower levels of exposure in a specific and sensitive manner. This is the first such study in which historical job-based individual estimates based on environmental measurements, lung fiber content, exposure timing, and complete pathology records including autopsies were available for review. We found significant excesses of lung tremolite and chrysotile and estimated cumulative exposure in those with lung cancer and asbestosis compared to those with lung cancer without asbestosis. However, when the latter were directly compared on a case-by-case basis, there was a marked overlap between lung cancer cases with and without asbestosis regardless of the measure of exposure. Smoking habits did not differ between lung cancer cases with and without asbestosis. In regression models, smoking pack-years discriminated between those with the without lung cancer, regardless of asbestosis status. Most seriously, the pathologic diagnosis of asbestosis itself seemed arbitrary in many cases. We conclude that although the presence of pathologically diagnosed asbestosis is a useful marker of exposure, the absence of this disease must be regarded as one of many factors in determining individual exposure status and disease causation.
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Occupational cancer research in the Nordic countries benefits from certain structural advantages, including the existence of computerized population registries, national cancer registries with high-quality data on cancer incidence, and a personal identification number for each inhabitant. This article outlines the utilization of this research infrastructure in Denmark, Finland, Iceland, Norway, and Sweden, together with research examples from the different countries. Future research on occupational cancer in this region requires that national legislation on electronic handling of sensitive personal information should not be stricter than the European Union Directive on individual protection with regard to personal data. A personal identification number is essential both for keeping up the high quality of data of the registers and for the high quality of the process of linking the different data sources together. Although previous occupational research has focused on male workers, a broader approach is needed in the future, including a study of how cancer risk in women may be affected by occupational activity and the question of possible cancer risk in offspring of men and women exposed to workplace carcinogens.
Ochratoxin A (OTA) is a nephrotoxin frequently contaminating grains. OTA inhalation during grain handling may therefore represent a health risk to farmers, and was the subject of this study. Airborne and settled grain dust was collected during grain work on 84 Norwegian farms. Climate and agricultural practices on each farm were registered. Penicillium spp., Aspergillus spp. and OTA in settled dust were measured. Settled dust contained median 4 microg OTA/kg dust (range 2-128), correlating with Penicillium spp. (median 40 cfu/mg; range 0-32000, rs =0.33; p
The presence of highly carcinogenic tobacco-specific nitrosamines (TSNA) in snuff has been a matter of serious concern. However, the levels of TSNA in such products may differ by orders of magnitude depending on origin and manner of processing, and the mere presence of such agents at low levels does hardly constitute a meaningful prerequisite for classifying all types of snuff as human carcinogens. Reviewing available epidemiological evidence, a wide discrepancy is found for estimated cancer risk associated with snuff dipping derived from on one hand previous investigations conducted in the United States and on the other from recent extensive Swedish epidemiological studies. In spite of the fact that approximately 20% of all grown-up Swedish males use moist snuff, it has not been possible to detect any significant increase in the incidence of cancer of the oral cavity or pharynx-the prevalence of which by international standards remains low in this country. Further, there is insufficient evidence for a causal link between the use of Swedish snuff and increased risk for cardiovascular disease. Dissimilarities in the content of TSNA in oral snuff products may represent one important reason for the different outcomes of the epidemiological surveys conducted in the United States and Sweden. Bioassays using pure TSNA in rodents appear to give exaggerated risk estimates for humans, a discrepancy that could be ascribed to species-related differences in the relation between exposure and DNA target dose and/or adduct repair rates, as well as to the presence of anticarcinogens in snuff. Although a small risk cannot be excluded, the use of smokeless tobacco products low in TSNA which now are available on the market entails a risk that at any rate is more than 10 times lower than that associated with active smoking. Nevertheless, due to the decisive role of potent TSNA in determining possible cancer risks in users of smokeless tobacco, and due to the fact that large variations in the concentrations may occur, adequate control measures should be taken to keep the levels of these nitrosamines in smokeless tobacco products as low as is technically feasible.
In these assessments of releases from copper smelters and refineries and from zinc plants as Priority Substances under the Canadian Environmental Protection Act (CEPA), available data were critically evaluated to determine if environmental exposure to selected components of these releases poses a risk to human health. The data on airborne levels of a variety of toxic substances near these facilities in Canada were obtained from the companies or provinces and systematically analyzed. Monitoring of ambient air near the Canadian copper smelters and refineries and zinc plants indicates that releases from these facilities result in increased potential for inhalation exposure of local human populations to several components of releases (As, Cd, Cr, Ni, Pb, SO(2) and PM(10)). Airborne levels in the vicinity of these metal-processing operations overlap those associated with cardiorespiratory effects for PM(10), and exceed health-based guidelines for SO(2) and, near some facilities, Pb. In addition, the margin between levels of As, Cd, Cr and Ni near these facilities in Canada and carcinogenic potency for each of these metals is relatively small near copper smelters, larger near copper refineries, and intermediate near zinc plants. On this basis, the risk to human health from environmental exposure to releases from these facilities is considered to be high compared with other Priority Substances assessed under CEPA, especially for facilities where copper is smelted.
The paper presents the exposure assessment method and quality control procedure used in an international, multi-centre case-control study within a joint Nordic and Italian cohort. This study was conducted to evaluate whether occupational exposure to carcinogens influenced the predictivity of high frequency of chromosomal aberrations (CA) in peripheral lymphocytes for increased cancer risk. Occupational hygienists assessed exposures in each participating country: Denmark, Finland, Italy, Norway and Sweden. The exposure status to a carcinogen or a clastogen was coded in the cohort according to the original CA studies at the time of CA testing, but not for the whole work life. An independent occupational hygienist coordinated harmonization of the assessment criteria and the quality control procedure. The reliability of the exposure assessments was calculated as deviation from the majority of the assessors, as Cohen's kappa and as overall proportion of the agreements. The reassessment of the exposures changed the exposure statuses significantly, when compared with the original cohort. Harmonization of the exposure criteria increased the conformity of the assessments. The prevalence of exposure was higher among the original assessors (the assessor from the same country as the subject) than the average prevalence assessed by the other four in the quality control round. The original assessors classified more job situations as exposed than the others. Several reasons for this are plausible: real country-specific differences, differences in information available to the home assessor and the others and misunderstandings or difficulties in translation of information. To ensure the consistency of exposure assessments in international retrospective case-control studies it is important to have a well-planned study protocol. Due to country-specific environments a hygienist from each participating country is necessary. A quality control study is recommended, to be performed as described, combined with round-table meetings to minimize information bias between the assessors.
In Sweden, snuff (locally known as snus), was introduced since the year 1637. Presently, Sweden has the highest per capita consumption and sale figures of snuff in the world, and the habit is becoming increasingly popular. Snus is manufactured into a dry form used in the nasal cavity and a moist form used in the oral cavity. Snus manufactured for oral use is a moist ground tobacco of Dark Kentucky or Virginia species mixed with an aqueous solution of water and other blending ingredients. This form of snuff is found in two types: (1) loose and (2) portion-bag-packed. These are the most widely used. The loose moist form (1-2 g a quid) is the most popular type consumed by 73% of the males, followed by the portion-bag-packed form (0.5-1 g a quid), consumed by 13% of the males, while 14% of the males are mixed users. The majority of snus users place the quid in the vestibular area of the upper lip, and the prevalence among persons 15 years of age or older in 15.9% among males and 0.2% among females. The pH of snus has declined from a previous range of 8-9 to a range of 7.8-8.5, moisture content ranges 35-60% and nicotine content is in the order of 5-11 mg/g dry wt tobacco-specific N-nitrosamines (TSNAs) in micrograms (N'-nitrosonornicotine: NNN 5-9; 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone: NNK 1-2; N'-nitrosoanatabine: NAT 2-5). In the Sudan, snuff, locally known as toombak, was introduced approximately 400 years ago. It is always processed into a loose moist form, and its use is widespread in the country. Tobacco used for manufacture of toombak is of the species Nicotiana rustica, and the fermented ground powder is mixed with an aqueous solution of sodium bicarbonate. The resultant product is moist, with a strong aroma, highly addictive and its use is widespread particularly among males. Its pH range is 8-11, moisture content ranges 6-60% and nicotine content is from 8 to 102 mg/g dry wt, and TSNAs contents in micrograms (NNN 420-1 550; NNK 620-7 870; NAT 20-290). Snus and toombak dippers develop a clinically and histologically characteristic lesion at the site of dipping. Probably due to control of the TSNAs in snus, this type of snuff is associated with a lower risk of cancer of the oral cavity (relative risk: RR 5-6-fold), whereas the risk for cancer of the oral cavity among toombak users was high (RR 7.3-73.0-fold). In conclusion, the two snuff products significantly differ in many aspects. Most notable differences are tobacco species, fermentation and ageing, nicotine and TSNAs content, pH, expression of the p53 tumour suppressor gene, and keratin types 13, 14, and 19. It was, therefore, the object of the present study to highlight the oral health hazards of toombak, and to compare it with snus regarding the aforementioned differences.