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Occup Environ Med. 2007 May; 64(5): 352.
PMCID: PMC2092543

Causal relationship between trichloroethylene exposure and non‐Hodgkin's lymphoma

Mandel et al's1 interesting literature review on trichloroethylene (TCE) exposure and non‐Hodgkin's lymphoma (NHL) has serious limitations.

First, there are three alternative descriptions of their stratification of group 1 studies: (1) population source (multiple industries vs only aerospace); (2) outcome (incidence vs mortality); and (3) location (European vs US). It would have been helpful to have specified a priori the interpretive advantages and disadvantages of each rather than focusing on population source.

Second, in their cohort analyses, they combine incidence and mortality data. Several assumptions the authors have not justified are implicit: (1) exposure to TCE confers quantitatively similar risks for incidence and mortality; (2) temporal changes in risk occur equally in incidence and mortality; (3) because mortality lags incidence, exposure to TCE must have been relatively constant in each study longitudinally (even though technological improvements probably decreased exposure); and (4), although they state, “The increases for NHL in the general population over the past several decades have been for both morbidity and mortality” (p 20), surveillance, epidemiology and end results data show that incidence increased more than mortality (fig 11),), especially in white men (fig 22),), resulting in a nearly two‐thirds increase in percentage surviving at least 5 years from 1960 to 1995 (from 31% to 51% in white men).2

figure om29629.f1
Figure 1 Surveillance, epidemiology and end results annual incidence and mortality data
figure om29629.f2
Figure 2 Surveillance, epidemiology and end results annual incidence and mortality data for white men only

Third, although the authors conclude that, “…there is insufficient evidence to suggest a causal link between TCE and NHL [abstract]”, all eight group I studies showed increased risks, with two being statistically significant, and all four summary risk estimates were increased, with three being statistically significant. Group I comparisons of highest and lowest, cumulative, and duration of, exposures show similar patterns. Group II data are less compelling, although the case–control data show some support.

In summary, contrary to Mandel et al's conclusions, the results, which extend our work,3,4 provide increasing support for a causal relationship between TCE and NHL.


1. Mandel J H, Kelsh M, Mink P J. et al Occupational trichloroethylene exposure and non Hodgkin's lymphoma: a review and meta‐analysis. Occup Environ Med 2006. 63597–607.607 [PMC free article] [PubMed]
2. Ries L A G, Harkins D, Krapcho M. et al SEER cancer statistics review, 1975–2003. Bethesda, MD: National Cancer Institute, 2006, (accessed 22 Feb 2007)
3. Wartenberg D, Reyner D, Scott C S. Trichloroethylene and cancer: the epidemiologic evidence. Environ Health Perspect 2000. 108(Suppl 2)161–176.176 [PMC free article] [PubMed]
4. Wartenberg D, Scott C S. Carcinogenicity of trichloroethylene [letter]. Environ Health Perspect 2002. 110A13–A14.A14 [PMC free article] [PubMed]

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