We read with great interest the recent publication by Boers et al (2010), in which they presented updated mortality results from an occupational cohort of Dutch chlorophenoxy herbicide manufacturing workers. The previous follow-up from this cohort (Hooiveld et al, 1998) reported a statistically significant dose-related increase in mortality from ischemic heart disease (IHD) with increasing levels of modeled TCDD exposure. The relative risks in the medium and high TCDD exposure categories compared to the low category were 1.5 (95% CI 0.7-3.6) and 2.3 (95% CI 1.0-5.0), respectively (Hooiveld et al, 1998). The earlier study was cited in our recent literature review of cardiovascular disease mortality in relation to dioxin exposure (Humblet et al, 2008).

In the present publication (Boers et al, 2010) the authors concluded that the observed associations between occupational exposure and IHD were attenuated compared with those found in their previous analysis. However, in their recent paper they did not present the updated results for IHD from the analysis of modeled TCDD. The authors explained that they did not use the earlier TCDD model approach because it was available only for one of the two factories in the study, and furthermore was based on a small number of blood samples. These considerations notwithstanding, we believe that it would be important to provide the updated modeled TCDD results both for IHD and all circulatory disease. At a minimum it would provide comparability with the previous findings from their study. Furthermore, future literature reviews on cardiovascular disease and TCDD would then be able to include this information, providing guidance for future dioxin risk assessments. This is especially important since the suggestion of an increased IHD risk persisted in the updated results that were presented, i.e. a statistically non-significant increased IHD relative risk of 1.6 (95% CI 0.72-3.55) among the workers exposed to a 1963 accidental release of dioxins. These workers would be expected to be among the highest exposed of all the workers.

O Humblet, R Hauser

Correspondence to: Mr. O Humblet, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA; ohumblet@hsph.harvard.edu

References

Boers D, Portengen L, Bueno-de-Mesquita HB, Heederik D, Vermeulen R. Cause-specific mortality of Dutch chlorophenoxy herbicide manufacturing workers. Occup Environ Med. 2010 Jan;67(1):24-31.

Hooiveld M, Heederik DJ, Kogevinas M, Boffetta P, Needham LL, Patterson DG Jr, Bueno-de-Mesquita HB. Second follow-up of a Dutch cohort occupationally exposed to phenoxy herbicides, chlorophenols, and contaminants. Am J Epidemiol. 1998 May 1;147(9):891-901.

Humblet O, Birnbaum L, Rimm E, Mittleman MA, Hauser R. Dioxins and cardiovascular disease mortality. Environ Health Perspect. 2008 Nov;116(11):1443-8.

Conflict of Interest:

None declared

Dear Editor,

This carefully conducted study (1) points at the kidney as a potential target of toxicity of phenoxy acids in a chronic occupational exposure.

This is biologically plausible as the phenoxy acids are inhibitors of chloride channels in renal tubular cells (2) which leads to alterations in the excretion of urinary electrolytes (3).

Thus, it is entirely possible that the chronic dysfunction can lead to renal problems.

1 Boers D, Portengen L,Bas Bueno-de-Mesquita H, et al. Cause-specific mortality of Dutch chlorophenoxy herbicide manufacturing workers. Occup Environ Med 2010; 67: 24-31

2 Savolainen H. New uses for old urine tests. Brit J Ind Med 1989; 46: 361-363

3 Manninen A, Kangas J, Klen T, Savolainen H. Exposure of Finnish farm workers to phenoxy acid herbicides. Arch Environ Contam Toxicol 1986; 15: 107-111

Conflict of Interest:

None declared