Ghanei Mostafa, Poursaleh Zohreh, Harandi Ali Amini, Emadi Seyed Emad, Emadi Seyed Naser
Research Center of Chemical Injuries, Baqiyatallah University of Medical Sciences, Mollasadra St, Tehran, Iran.
Cutan Ocul Toxicol. 2010 Dec;29(4):269-77. doi: 10.3109/15569527.2010.511367. Epub 2010 Sep 24.
Sulfur mustard (2,2-dichlorodiethyl sulfide, SM) is one of the vesicant classes of chemical warfare agents that causes blistering in the skin and mucous membranes, where it can have lingering long-term effects for up to ten years (1). SM was employed extensively by the Iraqi army against not only Iranian soldiers but also civilians between 1983 and 1988, resulting in over 100,000 chemical casualties. Approximately 45,000 victims are still suffering from long-term effects of exposure (2,3). More than 90% of the patients exposed to SM exhibit various cutaneous lesions in the affected area. The human skin can absorb approximately 20% of the SM through exposure. Up to 70% of the chemical is concentrated in the epidermis and the remainder in the basement membrane and in the dermis (4).Sulfur mustard exists in different physical states. The liquid form of SM evaporates slowly in cold weather and can penetrate through the clothing, thereby increasing exposure. However, the gas form readily diffuses in the air and it can be inhaled, leading to systemic absorption. In addition, warm temperatures are ideal conditions that liquid SM present in the clothing of the exposed individual could be converted to gas form. SM-induced clinical cutaneous symptoms include itching and burning. Other clinical findings include erythema or painless sunburn, bulla, hypo- and hyper pigmentation in both exposed and unexposed areas (5,6) The mechanism and biochemical cascade of SM-induced cutaneous manifestations are not completely understood but several published pathways support many of the know facts. Our current understanding fails to explain the time interval between the acute chemical exposure and the late-onset and delayed tissue damage (7,8). The aim of this article is to review the acute and long-term cutaneous findings resulting from SM exposure. Also, cellular and molecular mechanism involved in SM-induced skin pathology have been discussed.
硫芥(2,2-二氯二乙硫醚,SM)是一类糜烂性化学战剂,可导致皮肤和黏膜起泡,其长期影响可持续长达十年(1)。1983年至1988年间,伊拉克军队广泛使用硫芥,不仅针对伊朗士兵,也针对平民,造成了超过10万例化学中毒伤亡。约4.5万名受害者仍在遭受接触硫芥的长期影响(2,3)。超过90%接触硫芥的患者在受影响区域出现各种皮肤损伤。人体皮肤通过接触可吸收约20%的硫芥。高达70%的化学物质集中在表皮,其余分布在基底膜和真皮中(4)。硫芥有不同的物理状态。硫芥的液体形式在寒冷天气中蒸发缓慢,可穿透衣物,从而增加接触风险。然而,气体形式在空气中容易扩散,可被吸入,导致全身吸收。此外,温暖的温度是使暴露个体衣物中存在的液体硫芥转化为气体形式的理想条件。硫芥引起的临床皮肤症状包括瘙痒和灼痛。其他临床发现包括红斑或无痛晒伤、水疱、暴露和未暴露区域的色素减退和色素沉着(5,6)。硫芥引起皮肤表现的机制和生化级联反应尚未完全了解,但一些已发表的途径支持了许多已知事实。我们目前的理解无法解释急性化学暴露与迟发性和延迟性组织损伤之间的时间间隔(7,8)。本文的目的是综述硫芥暴露导致的急性和长期皮肤表现。此外,还讨论了硫芥诱导皮肤病理的细胞和分子机制。