Beigmohammadi et al. reported a 40-year-old male with opium addiction history with a headache, nausea and abdominal pain, and weakness in his lower and upper extremities without a definitive diagnosis who was admitted in Intensive Care Unit (ICU). He did not have an occupational lead history in his past medical history. He had anemia, slightly elevated liver function tests, total bilirubin, and erythrocyte sedimentation rate. Electromyography and nerve conduction velocity results and neurologic examination were abnormal. His BLL was more than 200 μg/dL. He was treated with British Anti-Lewisite (BAL) and calcium disodium edetate CaNa₂ EDTA. Following ICU discharge, he was quadriplegic although BLL was decreased and all paraclinical findings were normal.[15]

Hayatbakhsh Abbasi et al. conducted a cross-sectional study to compare the serum lead levels between opium addicts (n = 50) and nonaddicts (n = 43). They were matched with sex and age. The serum level of lead in opium addicts was higher than nonaddicts.[16]

In another study which has been conducted by Salehi et al., they analyzed the BLL in opium addicts (n = 22) who used oral opium and control group (n = 22) which was matched with for age and sex. The BLL in opium addicts had a range of 7.2–69.9 μg/dL (mean of 21.9 ± 13.2 μg/dL). In control group, BLL was 4.1–17.4 μg/dL (mean of 8.6 ± 3.5 μg/dL). The result was statistically significant (P < 0.0001). In the patient group, BLL had a significant correlation with the amount of ingested opium (r = 0.65, P < 0.01). However, there was no significant correlation with duration of opium ingestion in the patient group. They concluded that screening of BLL should be considered in the treatment of opium addicts.[20]

Masoodi et al. (2006) showed that lead poisoning in three patients presented with diffuse abdominal pain, anemia, constipation, nausea, vomiting, and abnormal liver function tests. A history of oral consumption of opium was presented in all of the patients, and none of them reported known occupational lead exposure. Lead poisoning was confirmed by analysis of BLL. Ingestion of lead-contaminated opium was the cause of poisoning.[13]

Salman-Roghani and Foroozan reported a 46-year-old opium-addicted man with hepatobiliary tract problems. He complained of abdominal pain, constipation, weakness, and neurologic abnormalities (tremor and proximal weakness). BLL was 90 μg/dL, and the patient was treated with the diagnosis of lead toxicity.[21]

Verheij et al. described a case of the 40-year-old Iranian man anemia and abnormality in liver function tests with severe abdominal pain, In his past medical history, he was suffering from multiple sclerosis. The patient used opium as a painkiller, regularly. Basophilic stippling of erythrocytes proposed lead poisoning. In this patient, the probable source of poisoning was adulterated opium. BLL were strongly elevated (86 μg/dL). The authors showed lead-induced hepatotoxicity in the case. In the liver biopsy, pathologic findings of hepatotoxicity such as active hepatitis lymphocytic cholangitis, with steatosis, cholestasis and hemosiderosis have been reported in the patient. After chelating therapy, liver enzymes returned to normal, suggesting reversibility of the histological findings.[22]

Soltaninejad et al. in a descriptive and retrospective study presented 25 cases of lead poisoning who were admitted to a referral poison center in Tehran between the years 2002 and 2007. In seven patients, opium addiction was the only source of lead poisoning. None of them had a well-known occupational exposure to lead. The average age of the patients was 38.7 ± 9.3 years and the average BLL was 109 ± 37.6 μg/dL. Inhalation was the route of opium abuse in 4 patients. Others abused opium orally.[23]

Froutan et al. reported opium addicts with abdominal pain who were presented to the gastrointestinal center of a referral hospital in Tehran during 2008. Patients who had occupational exposure to lead were excluded from the study. During this period, 42 patients (all male) with an average age of 46.9 ± 10.1 years were included in the study. Average BLL was 51.17 ± 27.96 μg/dl. A total of 22 patients (52.6%) had lead poisoning. A significant relation was found between lead poisoning and mode of opium abuse. The relation between lead poisoning and duration of opium addiction was not observed. However, a statistically significant relation was found between lead intoxication and abnormal liver function tests, urine tests, electrocardiogram, presence of basophilic stippling, and hyperuricemia.[5]

Meybodi et al. demonstrated that of the 240 patients diagnosed with lead poisoning, 25 patients admitted to opium use. There were 24 (96%) men and one (4%) woman. The average age of the patients was 41.8 ± 13.5 years. The duration of addiction to oral opium differed widely (range 3 months to 40 years). BLL were 145 ± 61 (range: 61–323) μg/dL. There was no significant statistical correlation between the duration of addiction and BLL in addicted patients (r = −0.142, P = 0.54). The most common complaints were anorexia (96%), abdominal pain (92%), weight loss >10% within a 2-month period (84%), constipation (88%), and nausea (56%). The most common musculoskeletal complaint was muscle weakness (92%). Other complaints included wrist drop (4%), pain in the extremities (88%), paresthesia (56%), and reduced vision (20%) and hearing (8%). Three (12%) patients initially presented with acute abdomen (bowel obstruction and peritonitis).[24]

Amiri and Amini evaluated the BLL of 39 Iranian opium addicts and made a comparison with healthy individuals as a control group in a hospital in Tehran. All the cases were male. The addicts were used opium orally or by inhalation. The mean age was 48.6 ± 7.3 years. The control group (39 individuals) was matched with the addicts with regard to age and sex and with a mean age of 44.8 ± 5.6 years. The mean BLL was found to be significantly lower (P = 0.0001) in control group (16.70 ± 12.51 μg/dL) compared to addicts (57.04 ± 46.03 μg/dL). There was a significant difference (P = 0.0451) in BLL according to age. Furthermore, a tendency (P = 0.048) toward increasing BLL with respect to body mass index (BMI) was observed due to opium abuse, but there was no significant variation between BLL and BMI when the control group was considered (P = 0.35).[25]

Mokhtarifar et al. reported a 55-year-old man presented to the emergency department with abdominal pain, icterus, high serum alkaline phosphatase levels, and normocytic anemia. He had opium abuse history for 20 years. Clinical and paraclinical findings including the Burton's sign and generalized ileus on abdominal X-ray have been observed. BLL was 150 μg/dL. Investigation of the patient's history failed to reveal any exposure to lead. Magnetic resonance imaging and abdominal ultrasonography were performed for rule out the other reasons of cholestasis. Liver biopsy showed focal canalicular cholestasis and mild portal inflammation. The patient had severe nausea, vomiting, and a single generalized tonic–colonic seizure 4 days after admission. Neurologic evaluations including brain computed tomography scan, and magnetic resonance imaging, and magnetic resonance venography were normal. The patient was treated with CaNa₂ EDTA and BAL for five days. The patient's liver biochemical tests abnormality recovered. Gastrointestinal presentations subsided, and the patient was discharged with good condition.[26]

Domeneh et al. in a cross-sectional study among 86 opium addicts who were referred to five detoxification centers in Tehran, reported that BLL was higher in oral opium-dependent group (11.75 ± 6.06 μg/dL) than inhalation opium addict (7.07 ± 3.61 μg/dL) and healthy (6.05 ± 1.83 μg/dL) groups.[27]

Khatibi-Moghadam et al. reported that the mean value BLL in 40 opium addicts was 7.14 ± 1.41 μg/dL compared to 5.42 ± 1.46 μg/dL in healthy control group. The mean value of urine lead level was 2.62 ± 0.83 μg/dL and 2.50 ± 0.76 μg/dL in patient and control groups, respectively. They showed a significant correlation between BLL with duration of opium addiction.[28]

Azizi et al. reported a lead-intoxicated case in a 46-year-old Iranian man who resident in the UK with opium addiction history. He had a 4-day history of colicky abdominal pain and constipation and several weeks of irritability and malaise. He had smoked 10 g of opium per week for a year and a half. On examination, he had abdominal pain, nausea, vomiting, diffuse abdominal tenderness, and fecal loading. Furthermore, hemolytic anemia and basophilic stippling have been shown in hematologic tests. The patient's serum lead concentration was substantially elevated. After chelation therapy, he has recovered clinically and biochemically.[29]