Other considerations about carcinogenicity of sulfur mustard

Abstract

Dear Editor in Chief,We read with great interest a recently published article byZafarghandi et al. [1] in Cancer Cause and Control journal.In this long-term follow-up cohort study, the incidence ofcancer in Iranian sulfur mustard (SM)-exposed veteranswas assessed and reported in comparison with a matchedcontrol group. They reported that the incidence of cancer inexposed cases was significantly higher than controls (theincidence rate ratio of cancer = 1.81, the age-adjustedincidence rate ratio = 1.64, and the hazard ratio was 2.02).They also finally concluded that ‘‘present study suggestscarcinogenesis of SM following acute exposure duringwar.’’ Though it is one of the rare and moreover interestingarticles in this field, we would like to draw the authors’attention to some points that can help to release a morevalid conclusion about the carcinogenicity of SM:1. It was approved that patients with chronic inflamma-tory diseases are susceptible to neoplasm [2, 3].Therefore, the role of chronic inflammatory conditions(bronchiolitis, bronchitis, dermatitis, recurrent pul-monary infections, etc.) should be considered in thesepatients [4]. It would be better concluded if findingswere reported and separated in terms of the presence orabsence of chronic inflammatory conditions in thesepatients.2. These patients have an imbalance in oxidant–antioxidantlevels in addition to increased levels of inflammatorysubstance. Therefore, some oxidative stressors such asNO may be escapes from cell defense due to decreasedlevels of antioxidant supply (such as NAD?)[5].Hereupon, these reactive oxygen species (such as NO)can damage DNA in long term [6]. On the other hand, itwas observed that DNA repair mechanisms are impairedin these patients [5, 6]. In addition to the abovemechanism, these patients use long-term medicationssuch as corticosteroid, which can make a defect in repairof damaged DNA [7] in addition to inhibition of p53-dependent apoptosis [8]. So, injured cells can progress toneoplasticcells.Therefore,thismechanismcanshednewlight on the molecular mechanisms by which chronicinflammatory disorders may initiate or enhance carcino-genesis in these cases [9]. Moreover, treatment can haveimpactonsomeneoplasm;itwasreportedthatpureriskofcancer increase in prolonged use of glucocorticoids andNSAIDs [10, 11]. Also, it was demonstrated that‘‘glucocorticoidsmay playa significantroleinregulatingtumor cells geneexpressionand cellgrowth’’ [12].It wasbetter if these results have been analyzed based ontreatment groups.3. It was constantly approved that chronic psychologicalstress (for example, PTSD in these patients) promotestumorigenesis. Feng et al. [13] showed that tumorigen-esis could be due to ‘‘the attenuation of p53 function asan important part of the underlying mechanism.’’Consistet with this issue, the mental health of veteranswhohavebeenexposedtoSMcouldbeaffectedbecauseof long-term adverse consequences [14]. Therefore, ifthe authors have compared SM-exposed case findings