Sulfur mustard is an alkylating agent that reacts with ocular, respiratory, cutaneous, and bone marrow tissues, resulting in early and late toxic effects. We compare these effects based on the experience in Iranian veterans exposed to the agent during the Iran-Iraq conflict . The first clinical manifestations of sulfur mustard poisoning occurred in the eyes with a sensation of grittiness, lacrimation, photophobia, blepharospasm, and corneal ulceration. Respiratory effects appeared as rhinorhea, laryngitis, tracheobronchitis, and dyspnoea. Skin lesions varied from erythema to bullous necrotization. Initial leukocytosis and lymphopenia returned to normal within four weeks in recovered patients, but marked cytopenia with bone marrow failure occurred in fatal cases. Late toxic effects of sulfur mustard were most commonly found in lungs, skin and eyes. Main respiratory complications were chronic obstructive pulmonary disease, bronchiectasis, asthma, large airway narrowing, and pulmonary fibrosis. Late skin lesions were hyperpigmentation, dry skin, atrophy, and hypopigmentation. Fifteen of the severely intoxicated patients were diagnosed with delayed keratitis, having corneal vascularization, thinning, and epithelial defect. Respiratory complications exacerbated over time, while cutaneous and ocular lesions decreased or remained constant. Both the severity and frequency of bronchiectatic lesions increased during long-term follow-up. The only deteriorating cutaneous complication was dry skin. The maximum incidence of delayed kaeratitis was observed 15 to 20 years after initial exposure. Being suggested as the main cause ofassociated with malignancies and recurrent infections, natural killer cells were significantly lower 16 to 20 years after intoxication.

Sulphur mustard (SM) is regarded as one of the most important agents of chemical warfare because of its simple and cheap chemical synthesis that makes it readily available for both terrorist and military use. SM acts as an alkylating agent that induces disruption of nucleic acids and proteins, impairing cell homeostasis and eventually causing cell death. It rapidly reacts with ocular, respiratory and cutaneous tissues, as well as bone marrow and the mucosal cells of the gastrointestinal tract, resulting in several devastating long-term effects on human health, many of which are not clinically or pathologically well defined. In light of the possible threat of SM use against military and civilian populations, physicians should be aware of its grave effects and knowledgeable how to care for its victims. The pattern of immediate and long-term toxic effects following exposure to SM is reviewed in this article with special references to the recent data available from over 100,000 chemical casualties incurred during the Iran-Iraq conflict.

Sulphur mustard (SM) is an alkylating chemical warfare agent that was widely used during the World War I and in the Iran-Iraq conflict. Delayed complications of SM in different organs and their severity correlations have not previously been reported. Dermatological, ophthalmological, neurological and respiratory examinations, as well as spirometry, gasometry, high resolution computed tomography scanning of the chest, electromyography, nerve conduction velocity, cell blood counts, flow-cytometric analyses, and measurement of serum immunoglobulins and complement factors were performed on all severely SM poisoned veterans in the province of Khorasan, Iran. Haematological and immunological studies were also performed on a control group consisting of 35 healthy male subjects. The severity of dermal, ocular and respiratory complications were classified into four grades and their correlations with each other as well as with the haematological and immunological parameters were determined, using Spearman's rank correlation test. Forty male patients (aged 43.8 +/- 9.8 years) with confirmed SM poisoning 16-20 years after the exposure were studied. The most common complications were found in the lungs (95%), peripheral nerves (77.5%), skin (75%), and eyes (65%). WBC, RBC, haematocrit (HCT), IgM, C3, and the percentages of monocytes and CD3+ lymphocytes were significantly (P < 0.042) higher and the percentage of CD16 + 56 positive cells was significantly (P = 0.006) lower in the patients than in the control group. The severity of respiratory complications revealed a significant correlation with the severity of ocular complications (r = 0.322, P = 0.043), as well as with the haemoglobin (r = 0.369, P = 0.024) and HCT (r = 0.470, P =0.003). Although late complications of SM poisoning in the skin, eyes, and respiratory system are mainly due to its direct toxic effects, the neuromuscular, haematological and immunological complications are probably the result of systemic toxicity.

Drugs and chemicals are almost easily available in Iran. Natural toxins as poisonous plants and animals also exist in most parts of the country. Therefore, acute poisonings, either intentional or accidental and also drug abuse/addiction are common in Iran. In spite of these difficulties there is no center for poison control and surveillance in this country to gather information and analyse data. The files of a systematic randomised ten percent of all hospital-referred poisoned patients from 21 March 1993 to 20 March 2000 in Imam Reza (p) University Hospital of Mashhad (71589 cases) were screened retrospectively. Young adults (40.3%) and school children (22.9%) were the most vulnerable group. Mean age was 22.3 (S.D. 14.38) years with a minimum of less than one and a maximum of 98 years old. A female predominance was found (53.4%). Intentional poisoning was more common (54.4%) than accidental exposures (45.2%). Fourteen cases were classified as criminal poisoning. 79.7% of exposures were via ingestion, followed by dermal exposures (14.1%), and inhalation (6.2%). The majority (83.7%) of patients were from urban areas. Most patients (68.6%) were treated in the Emergency Toxicology Clinic and discharged, 19.2% were temporarily hospitalized and 11.3% were hospitalized for 24 hr. Main groups of poisons were pharmaceuticals (61.4%), chemicals (22.8%), and natural toxins (16.6%). The overall number of poisoned patients was higher in spring and summer (62.8%). In conclusion, acute poisonings, particularly self-poisonings, are common in Iran. Since medical documentation is not routinely provided in this country the results of this retrospective study can be used for surveillance. Establishment of fluent data gathering and analysis within the local health system are challenges for the future.

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SM causes delayed destructive lesions in the ocular surface and cornea, leading to progressive visual deterioration and ocular irritation. Late complications of SM poisoning in the eyes, respiratory system and skin are mainly due to SM's local irritant effects.

Organophosphorous (OP) Nerve agents (NAs) are known as the deadliest chemical warfare agents. They are divided into two classes of G and V agents. Most of them are liquid at room temperature. NAs chemical structures and mechanisms of actions are similar to OP pesticides, but their toxicities are higher than these compounds. The main mechanism of action is irreversible inhibition of Acetyl Choline Esterase (AChE) resulting in accumulation of toxic levels of acetylcholine (ACh) at the synaptic junctions and thus induces muscarinic and nicotinic receptors stimulation. However, other mechanisms have recently been described. Central nervous system (CNS) depression particularly on respiratory and vasomotor centers may induce respiratory failure and cardiac arrest. Intermediate syndrome after NAs exposure is less common than OP pesticides poisoning. There are four approaches to detect exposure to NAs in biological samples: (I) AChE activity measurement, (II) Determination of hydrolysis products in plasma and urine, (III) Fluoride reactivation of phosphylated binding sites and (IV) Mass spectrometric determination of cholinesterase adducts. The clinical manifestations are similar to OP pesticides poisoning, but with more severity and fatalities. The management should be started as soon as possible. The victims should immediately be removed from the field and treatment is commenced with auto-injector antidotes (atropine and oximes) such as MARK I kit. A 0.5% hypochlorite solution as well as novel products like M291 Resin kit, G117H and Phosphotriesterase isolated from soil bacterias, are now available for decontamination of NAs. Atropine and oximes are the well known antidotes that should be infused as clinically indicated. However, some new adjuvant and additional treatment such as magnesium sulfate, sodium bicarbonate, gacyclidine, benactyzine, tezampanel, hemoperfusion, antioxidants and bioscavengers have recently been used for OP NAs poisoning.

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