Lead is an old environmental metal which is presented everywhere and lead poisoning is an important health issue in many countries in the world including Iran. It is known as a silent environmental disease which can have life-long adverse health effects. In children, the most vulnerable population, mental development of children health effects is of the greatest influence. Low level lead exposure can significantly induce motor dysfunctions and cognitive impairment in children. The sources of lead exposure vary among countries. Occupational lead exposure is an important health issue in Iran and mine workers, employees of paint factories, workers of copying centers, drivers, and tile making factories are in higher risk of lead toxicity. Moreover lead processing industry has always been a major of concern which affects surface water, drinking waters, and ground waters, even water of Caspian Sea, Persian Gulf and rivers due to increasing the number of industries in vicinity of rivers that release their waste discharges into river or sea. In addition, lead contamination of soil and air especially in vicinity of polluted and industrialized cities is another health problem in Iran. Even foods such as rice and fishes, raw milk, and vegetables which are the most common food of Iranian population are polluted to lead in some area of Iran. Adding lead to the opium is a recently health hazard in Iran that has been observed among opium addicts. There are few studies evaluated current status of lead exposure and toxicity in the Iranian children and pregnant women which should be taken into account of authorities. We recommend to identify sources, eliminate or control sources, and monitor environmental exposures and hazards to prevent lead poisoning.

A Systematic Review of Aluminium Phosphide Poisoning: Every year, about 300,000 people die because of pesticide poisoning worldwide. The most common pesticide agents are organophosphates and phosphides, aluminium phosphide (AlP) in particular. AlP is known as a suicide poison that can easily be bought and has no effective antidote. Its toxicity results from the release of phosphine gas as the tablet gets into contact with moisture. Phosphine gas primarily affects the heart, lungs, gastrointestinal tract, and kidneys. Poisoning signs and symptoms include nausea, vomiting, restlessness, abdominal pain, palpitation, refractory shock, cardiac arrhythmias, pulmonary oedema, dyspnoea, cyanosis, and sensory alterations. Diagnosis is based on clinical suspicion, positive silver nitrate paper test to phosphine, and gastric aspirate and viscera biochemistry. Treatment includes early gastric lavage with potassium permanganate or a combination with coconut oil and sodium bicarbonate, administration of charcoal, and palliative care. Specific therapy includes intravenous magnesium sulphate and oral coconut oil. Moreover, acidosis can be treated with early intravenous administration of sodium bicarbonate, cardiogenic shock with fluid, vasopresor, and refractory cardiogenic shock with intra-aortic baloon pump or digoxin. Trimetazidine may also have a useful role in the treatment, because it can stop ventricular ectopic beats and bigeminy and preserve oxidative metabolism. This article reviews the epidemiological, toxicological, and clinical/pathological aspects of AlP poisoning and its management.

The molecular signaling pathways that lead to cell survival/death after exposure to organophosphate compounds (OPCs) are not yet fully understood. Mitogen-activated protein kinases (MAPKs) including the extracellular signal-regulated protein kinase (ERK), the c-Jun NH2-terminal kinase (JNK), and the p38-MAPK play the leading roles in the transmission of extracellular signals into the cell nucleus, leading to cell differentiation, cell growth, and apoptosis. Moreover, exposure to OPCs induces ERK, JNK, and p38-MAPK activation, which leads to oxidative stress and apoptosis in various tissues. However, the activation of MAPK signaling pathways may differ depending on the type of OPCs and the type of cell exposed. Finally, different cell responses can be induced by different types of MAPK signaling pathways after exposure to OPCs.

Aims: As an analgesic that acts upon the central nervous system (CNS), tramadol has gained popularity in treating moderate to severe pain. Recently, it has been increasingly reported as a drug of misuse with intentional overdoses or intoxications. This review focuses on tramadol intoxication in humans and its effects on different systems.Subject and method: This narrative review provides a comprehensive view of the pharmacokinetics, mechanism of action, and incidence of tramadol toxicity with an in-depth look at its side effects. In addition, the main approaches to the management of tramadol poisoning are described.Results: Tramadol poisoning can affect multiple organ systems: gastrointestinal, central nervous system (seizure, CNS depression, low-grade coma, anxiety, and over time anoxic brain damage), cardiovascular system (palpitation, mild hypertension to life-threatening complications such as cardiopulmonary arrest), respiratory system, renal system (renal failure with higher doses of tramadol intoxication), musculoskeletal system (rhabdomyolysis), endocrine system (hypoglycemia), as well as, cause serotonin syndrome. Seizure, a serious nervous disturbance, is more common in tramadol intoxication than with other opioids. Fatal tramadol intoxications are uncommon, except in ingestion cases concurrent with other medications, particularly CNS depressants, most commonly benzodiazepines, and ethanol.Conclusion: With the increasing popularity of tramadol, physicians must be aware of its adverse effects, substantial abuse potential, and drug interactions, to weigh its risk–benefit ratio for pain management. Alternative therapies might be considered in patients with a previous overdose history to reduce risks for adverse outcomes.