Occupational exposure to solvents and risk of lymphoma subtypes: results from the Epilymph case–control study

Abstract

This analysis of a large European dataset confirms a role of occupational exposure to solvents in the aetiology of B-NHL, and particularly, CLL. It is suggested that benzene is most likely to be implicated, but we cannot exclude the possibility of a role for other solvents in relation to other lymphoma subtypes, such as follicular lymphoma. No association with risk of T-cell lymphoma and Hodgkin's lymphoma was shown.

Comparison of hospitalization among German coastal and deep sea fishermen

“…In view of the known high tobacco consumption among fishermen (Casson et al 1998;Hansen and Jensen 1998;Mastrangelo et al 1995;Oldenburg et al 2008;Rafnsson and Gunnarsdottir 1995), an elevated SHR for respiratory cancer was indeed expected. In addition, in spite of the assumed moderate exposure to exhaust gases on deck of fishing vessels, it cannot be excluded that these emissions (containing benzene, toluene, xylene) might have contributed to the observed elevated risk for respiratory cancer and also to non-Hodgkin lymphoma (Cocco et al 2010). …”

The mystery of chronic lymphocytic leukemia (CLL): Why is it absent in Asians and what does this tell us about etiology, pathogenesis and biology?

“…Several other risk factors for CLL in persons of predominately European descent are reported including tobacco use (see below), some chemicals, herbicides (such as found in Agent Orange), benzene and other aromatic hydrocarbons, and ionizing radiations [114][115][116][117][118][119][120][121].…”

CYP2E1 epigenetic regulation in chronic, low-level toluene exposure: Relationship with oxidative stress and smoking habit

“…The meaning of this relation could also be interpreted based on the following facts: a) age is the most known risk factor for cancer (Vineis and Wild, 2014), and b) GSTP1 promoter is hypermethylated in some cancers, although this phenomenon has been claimed recently more as a secondary effect, rather than a causal event (Pellacani et al, 2014). Then it can be proposed that the possible effect of age on GSTP1 promoter demethylation is a precondition to develop the carcinogenic effect attributable to toluene exposure, as claimed in some epidemiological studies (Breccia et al, 2012;Cocco et al, 2010;Costantini et al, 2008;Jung et al, 2007).…”

“…Human and cell-culture studies have implicated oxidative stress, inflammation and induction of apoptosis in toluene induced toxicity (Haro-García et al, 2012;Sarma et al, 2011;Mögel et al, 2011;Kim et al, 2011). Toluene has also shown genotoxic effects (Moro et al, 2012;Cassini et al, 2011;Rekhadevi et al, 2010;González-Yebra et al, 2009) and an increased risk of developing hematologic malignancies (Breccia et al, 2012;Cocco et al, 2010;Costantini et al, 2008;Jung et al, 2007). Toluene biotransformation takes place in the liver by the cytochrome P450 2E1 (CYP2E1) isoform, producing mainly hippuric acid, which is excreted in urine (Nakajima and Wang, 1994).…”