Dear Editor:

The timely article by Blettner et al. [1] reports an association, albeit weak, between adverse health effects and a distance of < 500 m from mobile phone base stations. The authors state that this observation cannot be explained by participant attributions or concerns alone and conclude that “the worries and health complaints of people living close to mobile phone base stations need to be taken seriously.” While provocation studies have overall found no substantial evidence supporting electrohypersensitivity to short-term low-intensity electromagnetic field (LEMF) exposure [2], epidemiological studies involving longer-term exposures have consistently found an association between LEMF exposure and neurobehavioural symptoms [2]. The conclusion of Blettner et al. [1] is supported by such studies, which include independent reports from several countries [e.g., 2,3]. While the mechanism(s) by which base station EMFs might cause neurobehavioural symptoms remain(s) conjectural, it is notable that Science Magazine has recently acknowledged that there are several peer-reviewed papers from laboratories in at least seven countries showing that cell phone or similar LEMFs can, contrary to the expectations of such “non-ionizing” sources, damage or structurally modify DNA [4]. In the context of base station EMFs and cancer, only one study testing this association was found [5]. The authors reported a greater than 4-fold increased incidence of cancers among a cohort of 622 people living in the area near a base station for 3-7 years compared with a comparison cohort of 1222 people living more remotely. Although the particular medical logistics in the studied community leant themselves somewhat favorably to such a study and despite no other confounding variable(s) being identified by the authors, one or more confounders could not be excluded [5]. Phase 2 of the important study by Blettner et al. [1] may shed further light on any association between symptomatology and measured EMF exposure.

References:

1. Blettner M, Schlehofer B, Breckenkamp J, Kowall B, Schmiedel S, Reis U, Potthoff P, Schuez J, Berg-Beckhoff G. Mobile phone base stations and adverse health effects: Phase 1: A population-based cross-sectional study in Germany. Occup Environ Med 2008; Nov 18. [Epub ahead of print]

2. Roosli M. Radiofrequency electromagnetic field exposure and non- specific symptoms of ill health: A systematic review. Environ Res 2008; 107:277-87.

3. Abdel-Rassoul G, El-Fateh OA, Salem MA, Michael A, Farahat F, El- Batanouny M, Salem E. Neurobehavioral effects among inhabitants around mobile phone base stations. Neurotoxicology 2007; 28:434-40.

4. Khurana VG. Cell phone and DNA story overlooked studies. Science 2008. 322:1325.

5. Wolf R, Wolf D. Increased incidence of cancer near a cell-phone transmitter station. Int J Cancer Prev 2004; 1:123-128.

The author declares no competing interest, financial or otherwise.

Dear Editor,

As pointed out by the authors, the ultimate carcinogen in the occupational wood dust exposure is not known. It has been known that hardwood dust particles are much more harmful than those from softwood sources. Tannins are versatile markers for hardwood species (1) and their presence e.g. in the nasal lavage liquid can be used to quantitatively monitor the dust burden at the target site (2).

Shoemakers are another occupational group in an elevated risk for sinonasal adenocarcinoma. The common factor could be the use of plant tannins in the leather treatment. The leather dust tannin content in 24 shops in Lausanne corresponded to that of cherry tree dust (1).

1 Bianco MA, Savolainen H. Woodworkers´ exposure to tannins. J Appl Toxicol. 1994; 14: 293-295.

2 Mämmelä P, Tuomainen A, Vartiainen T, et al. Biological monitoring of wood dust exposure in nasal lavage by high-performance liquid chromatography. J Environ Monit. 2002; 4: 187-189.

There are several reasons for questioning the apparent conclusion reached by Mirabelli and colleagues (Mirabelli et al. 2008) that their data provide evidence for the mesothelioma-inducing potential of what they refer to as “tremolite-free chrysotile”. Most of the reasons may already be well-known to the authors. No longer a traditional follow-up of the cohort study to which they refer (Rubino et al. 1979; Piolatto et al. 1990; Silvestri et al. 2001), this account is essentially a case series assembled retrospectively, as best they could, unfortunately subject to several sources of bias, and analysed entirely without controls (or, as they acknowledge, even true estimates of exposed and unexposed populations). Information about “exposure” is incomplete and of doubtful reliability both for chrysotile and for fibrous amphibole and its analogues, including “tremolite” (which, unlike “balangeroite”, is not always, or even usually, “asbestos”; in the Jeffrey Mine in Québec for example it has been estimated that over 99% of the “tremolite” present is nonasbestiform (Williams-Jones et al. 2001)).

This is not the issue – the issue is whether or not the material present causes mesothelioma. For the “tremolite” levels present in some Quebec mines and the lungs of some Quebec miners and millers employed therein, we believe the case is proven (Case et al. 1997; McDonald, AD et al. 1997). There is strong evidence that it is true not only for male miners and millers, as well as factory workers using imported crocidolite in manufacture at one mine site proven not to contain that mineral. It is also true for women, without exception exposed in the highest tremolite area although shown in some cases by lung-retained fiber analyses and occupational histories to have had as well some occupational exposures to commercial amphibole (Case et al. 2002).

Similarly, in the cases reported by these authors (some of which they say were exposed to “tremolite”, without defining what they mean by that term mineralogically or any other detail), the amount of “balangeroite” reported by the authors to be “in the mine” is similar to the amount of “tremolite” (whether asbestiform or not) reported to be present in Thetford Mines locations in Québec. The difference is that, unlike tremolite, “balangeroite” has been classed as an “iron-rich asbestiform” fiber with structural, biochemical, and perhaps most important biodurability characteristics similar to crocidolite (Gazzano et al. 2005; Groppo et al. 2005; Turci et al. 2005). The authors appear to believe that the fact that balangeroite has not yet been “classed as a carcinogen” somehow absolves it. This is hardly a precautionary approach, and were it taken with richterite and/ or winchite, both unregulated amphiboles, the mesotheliomas in the workforce at Libby, Montana (McDonald, JC et al. 2004; Sullivan 2007) could be considered as much caused by ‘vermiculite’ as the authors appear to believe their cases are caused by chrysotile.

The most fundamental deficiency however is the complete absence of lung-retained fibre analyses. Such analyses have been performed by the authors in other locations (Barone-Adesi et al. 2008), so they have the capability and hopefully the plans to do this. Such analyses would almost certainly make clear whether and to what extent chrysotile alone or the specific amphiboles present are responsible, and lead to a better understanding of balangeroite’s toxicity, at least for mesothelioma. Certainly the Québec experience is instructive in that regard, in that our studies would not even have been thought of were it not for the discovery by other investigators that “tremolite” is selectively and preferentially retained in the lung (Pooley 1976; Rowlands et al. 1982); such is likely to be the case for balangeroite as well. Several of the Italian cases are quite recent, so lung tissue from biopsy (if adequate), surgical intervention with partial or total pneumonectomy, or autopsy may well be available. Even if not, broncho-alveolar lavage fluid from exposed individuals, or even sputum asbestos body content, which proved so useful in 70% of Libby workers (Sébastien et al. 1988) and was a better predictor of radiographic changes than was cumulative exposure, may be useful.

This is not simply an academic exercise: too many journals in occupational and environmental medicine and disease, public health science, epidemiology, and general medicine are so poorly equipped for peer review on mineralogical exposure parameters and assessment that some questionable aspects of papers in this area slip through the cracks. Perhaps the best-known example is the study by Yano and colleagues with the possibly misleading title “Cancer mortality among workers exposed to amphibole-free chrysotile asbestos” (Yano et al. 2001). Amphibole contamination was at the time of publication not assessed in the lungs of the victims but in four samples of “processed chrysotile” from “two mines” by methods not specified other than by “personal communication” with the scientist (Kohyama) who performed them, who is not an author of the paper. The authors were perhaps understandably not aware of the contemporaneous findings of (Tossavainen et al. 2001) who found tremolite in ten of ten samples from six Chinese mines, but noted that 71% of fibres found in the lungs of workers exposed to these were in fact anthophyllite, a fibre type only present (at the detection limit) in one of the ten bulk samples. Neither Dr. Yano nor Dr. Kohyama have yet updated the record with lung- retained fibre analysis information; only if and when they do will their work be reconciled with that of the Finnish investigators.

Given that chrysotile is also known at the very least to cause lung cancer, at sufficient dose and fiber length and often in interaction with smoking, do the details concerning the magnitude of the differential in fibre type risk for mesothelioma matter? We believe they do: Mesothelioma is the health outcome of greatest concern for low doses, and is therefore of greatest concern for public health. Regulatory agencies and other bodies charged with protecting the public depend on good science to determine where to spend their dollars in prevention and remediation. Ultimately, as such, they need the best information available. Given the hypothetical financial choice of, for example, exacting an adequate cleanup in Libby, Montana (where unregulated amphiboles are of great concern for mesothelioma), versus the two per cent of the surface area of the State of California covered with serpentine rock, we believe it is evident from the published work where the most effective use of resources should be placed.

REFERENCES

Barone-Adesi, F., D. Ferrante, M. Bertolotti, et al. (2008). "Long- term mortality from pleural and peritoneal cancer after exposure to asbestos: Possible role of asbestos clearance." Int J Cancer.

Case, B. W., M. Camus, L. Richardson, et al. (2002). "Preliminary findings for pleural mesothelioma among women in the Québec chrysotile mining regions." Ann. Occup. Hyg 46(S1): 128-131.

Case, B. W., A. Churg, A. Dufresne, et al. (1997). "Lung Fibre Content for Mesothelioma in the 1891-1920 Birth Cohort of Quebec Chrysotile Workers: A Descriptive Study." Ann Occup Hyg 41(S1): 231-236.

Gazzano, E., C. Riganti, M. Tomatis, et al. (2005). "Potential toxicity of nonregulated asbestiform minerals: balangeroite from the western Alps. Part 3: Depletion of antioxidant defenses." J Toxicol Environ Health A 68(1): 41-9.

Groppo, C., M. Tomatis, F. Turci, et al. (2005). "Potential toxicity of nonregulated asbestiform minerals: balangeroite from the western Alps. Part 1: Identification and characterization." J Toxicol Environ Health A 68(1): 1-19.

McDonald, A. D., B. W. Case, A. Churg, et al. (1997). "Mesothelioma in Quebec chrysotile miners and millers: epidemiology and aetiology." Ann Occup Hyg 41(6): 707-19.

McDonald, J. C., J. Harris and B. Armstrong (2004). "Mortality in a cohort of vermiculite miners exposed to fibrous amphibole in Libby, Montana." Occup Environ Med 61(4): 363-6.

Piolatto, G., E. Negri, C. La Vecchia, et al. (1990). "An update of cancer mortality among chrysotile asbestos miners in Balangero, northern Italy." Br J Ind Med 47(12): 810-4.

Pooley, F. D. (1976). "An examination of the fibrous mineral content of asbestos lung tissue from the Canadian chrysotile mining industry." Environmental Research 12: 281-298.

Rowlands, N., G. W. Gibbs and A. D. McDonald (1982). "Asbestos fibres in the lungs of chrysotile miners and millers--a preliminary report." Ann Occup Hyg 26(1-4): 411-5.

Rubino, G. F., G. Piolatto, M. L. Newhouse, et al. (1979). "Mortality of chrysotile asbestos workers at the Balangero Mine, Northern Italy." Br J Ind Med 36(3): 187-94.

Sébastien, P., B. Armstrong, B. W. Case, et al. (1988). " Estimation of amphibole exposure from asbestos body and macrophage counts in sputum: a survey in vermiculite miners." Ann Occup Hyg 32(S1): 195-201.

Silvestri, S., C. Magnani, R. Calisti, et al. (2001). "The experience of the Balangero chrysotile asbestos mine in Italy: Health effects among workers mining and milling asbestos and the health experience of persons living nearby." Canadian Mineralogist: 177-186.

Sullivan, P. A. (2007). "Vermiculite, respiratory disease, and asbestos exposure in Libby, Montana: update of a cohort mortality study." Environ Health Perspect 115(4): 579-85. Tossavainen, A., M. Kotilainen, K. Takahashi, et al. (2001). "Amphibole fibres in Chinese chrysotile asbestos." Ann Occup Hyg 45(2): 145-52.

Turci, F., M. Tomatis, E. Gazzano, et al. (2005). "Potential toxicity of nonregulated asbestiform minerals: balangeroite from the western Alps. Part 2: Oxidant activity of the fibers." J Toxicol Environ Health A 68(1): 21-39.

Williams-Jones, A. E., C. Normand, J. R. Clark, et al. (2001). "Controls of amphibole formation in chrysotile deposits: Evidence from the Jeffrey Mine, Asbestos, Quebec." Canadian Mineralogist: 89-104.

Yano, E., Z. M. Wang, X. R. Wang, et al. (2001). "Cancer mortality among workers exposed to amphibole-free chrysotile asbestos." Am J Epidemiol 154(6): 538-43.