Asia Pacific Journal of Medical Toxicology
Volume:9 Issue: 1, Winter 2020

Inflammatory cell activation, oxidative stress and oxidative DNA damage have been associated with exposure to cement dust. Biomarkers of oxidative stress, oxidative DNA damage, inflammation and heavy metals were estimated in cement loaders. Ninety men (45 cement loaders and 45 controls) were recruited into this comparative cross-sectional study. Total antioxidant capacity (TAC), total plasma peroxides (TPP), malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NO) and uric acid (UA) were estimated by colorimetry, arsenic (As), chromium (Cr) and cadmium (Cd) by atomic absorption spectrophotometry and tumor necrosis factor alpha (TNF-α), 8-hydroxy-2-deoxyguanosine (8-OHdG) by enzyme linked immunosorbent assay.  Cement loaders had increased lipid peroxidation (MDA, TPP, OSI), inflammation (TNF-ɑ) and heavy metals (As, Cr) and lower antioxidants (UA, TAC, GSH) compared to controls (p<0.05). Increasing duration of exposure to cement dust was associated with higher lipid peroxidation, Cd, TNF-α and oxidative DNA damage (8-OHdG) (p<0.05). Negative correlation was observed between TAC and duration of exposure (r=-0.375, p=0.011) and positive correlations between TPP and duration of exposure (r=0.614, p=0.000), TNF-α and 8-OHdG (r=0.492, p=0.001) in cement loaders.  Chronic exposure to cement dust is associated with depletion of antioxidants, increased lipid peroxidation, oxidative stress, inflammation and oxidative DNA damage. These may be implicated in the development of chronic lung conditions.

Lead is a dangerous substance that can impact the blood components. Lead toxicity can cause imbalance in the homeostasis process of blood peripheral. The aim of this study is to search impact of lead exposure on peripheral blood parameter alterations among people around bus terminals in Yogyakarta. This study is a cross sectional research design with convenience sampling method. According to calculation of sample size, 72 respondents had fulfilled the inclusion criteria. The independent variable was lead exposure and dependent variables were peripheral blood parameters including leucocytes, erythrocytes, hemoglobin, and platelets. Lead exposure was measured by atomic absorption spectrophotometer (AAS) and peripheral blood parameters were measured by automatic hematology analyzer. Those variables were analyzed by linear regression. Based on Independent T Test was found aged > 40 yo correlated with leukocyte (P =0.029), male workers correlated with leukocyte, erythrocyte, hemoglobin, and platelet (P =0.025,0.006, 0.000, and 0.031, respectively), smoking 1 packed per week associated with hemoglobin (P =0.006) and settlement 500 meter around terminal associated with leukocyte, erythrocyte, hemoglobin and platelet (P =0.025, 0.006, 0.000, and 0.031, respectively). Linear regression can predict level of leukocyte (β=0.32; CI 95= -0.207 to 0.643, P =0.006), erythrocyte (β=0.3; CI 95=-0.269 to 0.29; P =0.009), hemoglobin (β=0.33; CI 95=0.042 to 0.211; P =0.004), and platelet (β=0.25; CI 95=-0.548 to 0.73; P =0.029).  Age > 40 years old associated with leukocyte; male gender associated with leukocyte, erythrocyte, hemoglobin, and platelet level, respectively; smoking 1 packed per week correlated with hemoglobin level; settlement 500 m around terminal associated with level leukocyte, erythrocyte, hemoglobin, and platelet level, respectively. Finally, level of lead can predict positively leukocyte, erythrocyte, hemoglobin, and platelet level respectively.

Hydrocarbon associated toxicity (HAT) is an emerging threat related to wide scale industrialization and easy access to hydrocarbon-containing chemical compounds. Hydrocarbons have a unique toxicological profile and the principles of managing related toxidromes are considerably different from other toxins. Case reports: Here, we present a case series and in-depth review of the existing literature to show the risks associated with these seemingly harmless chemicals, and the approved guidelines for treating exposed patients. In all three cases, the hydrocarbon was a diluent for a pesticide. The amount of pesticide ingested was nontoxic, while the hydrocarbons caused a dose-independent physical toxicity to the lungs.

Hydrocarbon associated toxicities often go unnoticed because of their usage as diluents for various other toxic chemicals. Their treatment usually differs from other toxins that may have been consumed with them, albeit in insignificant quantities.

Recognition of a hydrocarbon diluent in a consumed toxin marks the first step in the correct treatment. Correct labeling of chemical solutions containing hydrocarbons would go a long way in identifying these toxins.

Psyllium seeds, produced from Plantago ovata Forsk, are an herbal treatment generally used as a laxative. They also reportedly have lowering effects on some metabolic parameters such as blood glucose, lipids and uric acid. In this paper, we report the effect of this herbal medicine in reducing serum uric acid levels, without major adverse effects, in a hyperuricemic patient. Case report: A 51-year-old patient with a history of hyperuricemia (10.5 mg/dL in a recent measurement) gave consent to undergo a 40-day treatment using psyllium seeds with dosage of 83.3 mg/kg. Treatment was given in two 20-day courses: During the first course, the seeds were given daily and during the second course, the same dosage was given every other day. Serum uric acid levels decreased to 8.1 mg/dL and 6.8 mg/dL on the 20th and 40th days, respectively. No major adverse effects were observed, such as skin rashes, digestive disorders, muscular pain, allergic manifestations, abnormalities in liver and kidney function tests, and abnormalities in blood parameters. Psyllium seeds may be effective in reducing serum uric acid levels in hyperuricemia patients,  and major adverse effects are not expected to occur. These data can be used for further research and designing clinical trials.

Calcium channel blocker (CCB) toxicity is one of the most lethal and common drug overdoses encountered in the emergency department (ED). The toxicity of these drugs results from blockade of L-type calcium channels in smooth cells, myocardial cells, and beta cells of the pancreas. Severe toxicity can result in bradycardia, hypotension, hyperglycemia, metabolic acidosis, shock, cardiac arrest and death. According to the American Association of Poison Control Centers’ National Poison Data System’s annual report in 2015, cardiovascular medications were the fourth most common adult poisoning exposure and second most common cause of adult poisoning fatality in the USA. CCBs are responsible for a substantial portion of the mortality associated with cardiovascular medication overdose cases. Understanding the emergent management of CCB toxicity is essential. Treatment of patients with CCB overdose remains challenging especially in those with refractory hypotension and end organ dysfunction.

A 45-year-old male with massive amlodipine overdose presented to ED with syncope and severe hypotension. Intensive medical therapy (fluid resuscitation, inotropes, calcium gluconate, and hyperinsulinemia euglycemia therapy [HIET]) was initiated in the ED and continued in the Intensive Care Unit (ICU), and resulted in the patient’s total recovery, without any major complications. Fortunately, ECMO implantation (extracorporeal membrane oxygenation) was not required in this patient.

Urgent administration of fluids, calcium, vasopressors, and HIET therapy seem to be the most well validated initial approaches to CCBs overdose treatment. Our successful management strategy should serve as a good learning experience as well as a recommendation for managing such patients.

Cardiopulmonary arrest in the pediatric population due to methadone toxicity is not commonly reported. Severe methadone toxicity often involves respiratory depression with reports of orthostatic hypotension, due to vasodilation, and QTc prolongation.

A pair of toddler siblings presented in cardiopulmonary arrest due to methadone ingestion. They were successfully resuscitated with no significant neurobehavioral deficits despite a suspected prolonged “downtime.” After return of spontaneous circulation, the older sibling, a four-year old male, had electrocardiographs (ECGs) that were suggestive of sodium channel blockade. These changes were reversed following bicarbonate therapy.  The two-year old child’s ECGs did not show such changes.

There is no prior clinical literature on sodium channel blockade in methadone toxicity. The older sibling’s ECG findings and response to bicarbonate therapy appeared to be consistent with sodium channel blockade. There have been preclinical data that suggest methadone cardiotoxicity may involve cardiac sodium channels. Pharmacogenetic variations could also explain how these effects may selectively manifest.

Physicians should be aware of the possible toxicologic causes of cardiopulmonary arrest in the pediatric population. Pharmacogenetic variations may contribute to different clinical manifestations in methadone cardiotoxicity.

Plants have been used for the treatment of a wide range of conditions since ancient times but some have side effects and toxic effects that limit their use. Tribulus terrestris is traditionally used for lowering blood pressure, inhibiting kidney stone formation and inducing weight loss. In this case study, we present an Iranian woman who suffered from liver failure after using this plant.

A 31-year-old Iranian woman was admitted to Emam-Reza hospital due to epigastric pain radiating to back and shoulders, and  weakness, Malas,neusia and icterus. Upon admission,, her vital signs were normal. She had been consuming Tribulus terrestris as an herbal tea , several times a day for 2-3 months, in order to lose weight. Upon physical examination, the patient had generalized icterus and laboratory tests showed elevated transaminases, PT, and INR. Various causes of hepatic failure, such as viral hepatitis and autoimmune hepatitis, were ruled out and the only probable diagnosis was toxin-induced liver failure.

Herbal plants may have some beneficial medical effects but they can also cause toxicity. Consistent use and high dose of Tribulus terrestris may cause hepatic failure and death.