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We previously investigated bladder cancer risk in a cohort of dyestuff workers who were heavily exposed to aromatic amines from 1922 through 1972. We updated the follow-up by 14 years (through 2003) for 590 exposed workers to include more than 30 years of follow-up since last exposure to aromatic amines. Expected numbers of deaths from bladder cancer and other causes were computed by use of national mortality rates from 1951 to 1980 and regional mortality rates subsequently. There were 394 deaths, compared with 262.7 expected (standardized mortality ratio = 1.50, 95% confidence interval = 1.36 to 1.66). Overall, 56 deaths from bladder cancer were observed, compared with 3.4 expected (standardized mortality ratio = 16.5, 95% confidence interval = 12.4 to 21.4). The standardized mortality ratio for bladder cancer increased with younger age at first exposure and increasing duration of exposure. Although the standardized mortality ratio for bladder cancer steadily decreased with time since exposure stopped, the absolute risk remained approximately constant at 3.5 deaths per 1000 man-years up to 29 years after exposure stopped. Excess risk was apparent 30 years or more after last exposure. © 2010 The Author. Published by Oxford University Press. All rights reserved.

False-positive results are inherent in the scientific process of testing hypotheses concerning the determinants of cancer and other human illnesses. Although much of what is known about the etiology of human cancers has arisen from well-conducted epidemiological studies, epidemiology has been increasingly criticized for producing findings that are often sensationalized in the media and fail to be upheld in subsequent studies. Herein we describe examples from cancer epidemiology of likely false-positive findings and discuss conditions under which such results may occur. We suggest general guidelines or principles, including the endorsement of editorial policies requiring the prominent listing of study caveats, which may help reduce the reporting of misleading results. Increased epistemological humility regarding findings in epidemiology would go a long way to diminishing the detrimental effects of false-positive results on the allocation of limited research resources, on the advancement of knowledge of the causes and prevention of cancer, and on the scientific reputation of epidemiology and would help to prevent oversimplified interpretations of results by the media and the public. © 2008 The Author(s).

OBJECTIVE: To examine cancer mortality in continuous glass filament workers. METHODS: A cohort of 936 continuous glass filament workers employed in a plant from northern Italy since January 1976 was followed-up through December 2003, for a total of 19,987 man-years. RESULTS: Overall, 144 deaths were observed compared with 160.8 expected based on regional death rates (standardized mortality ratio [SMR] = 0.90, 95% CI = 0.76 to 1.05). There were 53 deaths from all cancers (SMR = 1.01, 95% CI = 0.75 to 1.32), and 21 from lung cancer (SMR = 1.23, 95% CI = 0.76 to 1.89). There was no consistent relation with risk for age at first employment, time since first or last employment, or duration of employment for any of the causes considered. CONCLUSIONS: Although limited in size, this study provides no evidence that continuous glass filament workers experience a significant increased risk of cancer, including respiratory cancer. ©2009The American College of Occupational and Environmental Medicine.

European epidemiological studies on ambient air pollution and cancer published before December 2006 are reviewed, with focus on five analytic studies providing data on the association between various measures of particulate matter (PM) and lung cancer. A case-control study of 755 men who died from lung cancer in Trieste, Italy, reported that, compared with less than 0.18 g/m/day of deposition of particulate, the relative risk (RR) was 1.1 [95% confidence interval (CI): 0.8-1.5] for 0.18-0.30 and 1.4 (95% CI: 1.1-1.8) for more than 0.30 g/m/day. In the Netherlands Cohort Study on Diet and Cancer with 60 deaths from lung cancer, the RR was 1.06 (95% CI: 0.43-2.63) for an increase of 10 µg/m in black smoke. In the French Pollution Atmospherique et Affections Respiratoires Chroniques study cohort based on 178 deaths from lung cancer, the RR associated with an increase in exposure to 10 µg/m of total suspended particulate was 0.97 (95% CI: 0.94-1.01). A nested case-control study within the European Prospective Investigation on Cancer and Nutrition included 113 nonsmokers or exsmokers diagnosed with lung cancer and 312 controls. The RRs were 0.91 (95% CI: 0.70-1.18) for an increase in PM with diameter =10 µm (PM10) of 10 µg/m, and 0.98 (95% CI: 0.66-1.45) for exposure over 27 µg/m compared with less than 27 µg/m. In a Norwegian record linkage study, based on 1453 lung cancer deaths, no significant excess risk was found for men, and a modest association was observed for women. European studies of PM exposure and lung cancer do not show a clear association, but uncertainties remain for the measurement of exposure and latency. © 2008 Lippincott Williams & Wilkins, Inc.

Dear Sir, ’We derived our pooled risk estimate of mesothelioma from nonoccupational exposure to asbestos from a previous publication authored by some of us, in which the methods for the meta-analysis were described in detail (1). In addition to the summary relative risk, our estimate of the number of non-occupational mesothelioma cases was based on frequencies in the populations experiencing exposures comparable with those in which the relevant epidemiological studies have been carried out. This parameter is subject to great uncertainty, and as a result, we selected it in our commentary as an example of the possible lack of temporal correspondence between risk and exposure data. Mirabelli and Merler suggest a different approach to estimate the number of mesothelioma cases attributable to non-occupational exposure to asbestos, based on the reasonable assumption that all cases with a recorded exposure are attributable to it. Their results of the Italian mesothelioma registry are of interest, and a recent analysis of the same data reported that 4.2% of cases in the registry had environmental asbestos exposure (2). It should be kept in mind that, although all reasonable efforts should be made to reduce and eliminate environmental asbestos exposure, this would have a limited effect on the overall cancer burden. Mesothelioma accounts each year for 1000 cases out of 300 000 total cancer cases (0.3%) in a country such as Italy, and hence 10% of mesothelioma cases represent 0.03% of all cancer cases.

The definition of environment refers to external physical conditions that may affect human health (1), but the word is used in the medical literature with different connotations, both in English and in other languages. This generates confusion in the medical literature, when the role of environment is discussed in the context of disease etiology. In particular, research on the role of environment in human carcinogenesis suffers from this ambiguity. On the one hand, environment can encompass all non-genetic factors such as diet, lifestyle and infectious agents. In this broad sense, the environment is implicated in the causation of the majority of human cancers, as has been demonstrated since the 1960s (2). Such a broad meaning of the word environment is assumed when referring to gene–environment interactions . On the other hand, environmental factors can include only the (natural or man-made) agents and circumstances encountered by humans in their daily life, upon which they have no or limited personal control. In this sense, environmental factors are restricted to air, water, soil and food pollutants, including physical pollutants such as sources of ionizing radiation. These ambiguities in the terminology and the inconsistencies in the use of the vocabulary by cancer researchers contribute to public confusion regarding the role of the environmental causes of cancer. A distinction relevant to cancer prevention may be made between factors related to personal behaviors, lifestyle (e.g. tobacco smoking and alcohol drinking), involuntary exposures, such as those linked to air, water, soil or food pollutants, and occupation. It would be preferable to abandon the term environment and to use terms such as nongenetic or modifiable determinants of disease (broad sense of environment) and pollutants (narrow sense).

Authors’ Response From JOSEPH K MCLAUGHLIN,1,2 LOREN LIPWORTH,1,2 ROBERT E TARONE,1,2 CARLO LA VECCHIA,3,4 WILLIAM J BLOT1,2 and PAOLO BOFFETTA5