BackgroundThis study assessed lead, cadmium, and nickel level in food crops, fruits and soil samples from Ohaji and Umuagwo and Owerri in South Eastern Nigeria and estimated the potential health risks of metals. Samples were washed, oven-dried at 70–80°C for 24 h and powdered. Samples were digested with perchloric acid and nitric acid. Metals were analysed with Unicam Atomic Absorption Spectrophotometer.ResultThe concentration of Pb, Cd, and Ni in Ohaji exceeded the maximum allowable concentrations for agricultural soil as recommended by EU. Lead, Cd, and Ni in the food crops were highest in Oryza sativa, Glycine max, and Pentabacta microfila respectively. Highest levels of Pb, Cd, and Ni, in fruits were detected in Canarium schweinfurthii, Citrus reticulata, Ananas comosus respectively. The true lead and cadmium intake for the rice based meal were 3.53 and 0.034 g/kg respectively. Whereas the true intake of lead and cadmium for the cassava based meal were 19.42 and 0.049 g/kg respectively.ConclusionLocal food stuff commonly available in South Eastern Nigeria villages may contribute to the body burden of heavy metal. This is of public health importance.

The last few decades have seen a rise in the use of herbal supplements, natural products, and traditional medicines. However, there are growing concerns related to the safety and toxicities of these medicines. These herbal medicines are associated with complications such as liver damage with a high incidence of mortalities and morbidities. Clinical manifestations range from asymptomatic cases with abnormal liver functions tests to sudden and severe liver failure necessitating liver transplantation. This work aimed to review the etiology, risk factors, diagnosis, clinical manifestations and selected clinical case reports of herbal hepatotoxicity in developing nations. PubMed and Google Scholar searches were undertaken to identify relevant literature. Furthermore, we scanned the reference lists of the primary and review articles to identify publications not retrieved by electronic searches. Little data exists on clinical cases of herb-induced liver injury in some developing countries such as Nigeria, as most incidences are either not reported to health care providers or reports from hospitals go unpublished. Studies in Nigeria have highlighted a possible correlation between use of herbs and liver disease. In Uganda, and association between the use of traditional herbal medicine with liver fibrosis in HIV-infected and non-HIV patients was demonstrated. Reports from China have revealed incidences of acute liver failure as a result of herbal medicine use. The actual incidence and prevalence of HILI in developing nations remain largely unknown due to both poor pharmacovigilance programs and non-application of emerging technologies. Improving education and public awareness of the potential risks of herbals and herbal products is desirable to ensure that suspected adverse effects are formally reported. There is need for stricter regulations and pre-clinical studies necessary for efficacy and safety.

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This review updates our knowledge on clinical food-drug interactions with emphasis on mechanism and clinical implications. Results obtained from literature search identified interactions with selected foods/herbs generated from in vivo and in vitro studies. For example, interaction studies in humans revealed a reduction in the bioavailability of mercaptopurine when taken concurrently with substances containing xanthine oxidase (eg, cow milk); a reduction in the bioavailability of quinine with Garcinia kola; increased bioavailability/toxicity of felodipine, nifedipine, saquinavir, sildenafil with grape juice; increased bioavailability of felodipine, cisapride with red wine and diminished bioavailability of fexofenadine with apple. Pharmacokinetic and/or pharmacodynamic mechanisms are implicated in many of these interactions. By evaluating the dietary patterns of patients and use of prescribed medications, health professionals will be well informed of potential interactions and associated adverse effects.

Ibuprofen is an effective, cheap, and frequently used non-steroidal anti-inflammatory drug. The present study investigated the dose-and time-dependent effects of ibuprofen on hepatic, renal, and hematological functions in rats. Groups of rats (n=6) were given ibuprofen (20, 40 mgkg -1 day -1 ) for 7, 14 or 28 days; or vehicle (control), orally. Blood samples were obtained, and hematological indices and biochemical markers of hepatic and renal functions were measured. Ibuprofen significantly increased, P < 0.001 serum alkaline phosphatase level at all doses and durations of exposure. Serum uric acid level was dose-and time-dependently decreased by ibuprofen, but alanine transaminase was increased, P < 0.05 by ibuprofen, only at 40 mgkg -1 and following subchronic (28 days) exposure. In addition, at 40 mgkg -1 , ibuprofen increased creatinine and urea levels at all durations of exposure; but at 20 mgkg -1 , creatinine and urea were increased only in rats that were exposed for 28 days. Furthermore, subchronic exposure of 40 mgkg -1 ibuprofen increased, P < 0.01 WBC count, but it caused no significant effect on WBC at the lower durations of exposure and dose. Also, while RBC and hematocrit were not affected, ibuprofen significantly, P < 0.01,P < 0.001 decreased platelet counts in all treated rats except those that were exposed for 7 days. The implication of this research is that chronic use of ibuprofen could affect hepatic, renal and hematological functions in the rat; and duration of exposure may promote ibuprofen toxicity relative to dose.

This paper reported available studies on blood lead level of childbearing age in Sub-Saharan African women. PubMed and Google scholar databases were searched for original articles reporting blood lead levels of women of childbearing age in Sub-Saharan Africa. Searches were not limited to year of study but limited to studies published in English Language. Data were extracted and synthesized by estimating the weighted mean of the reported blood lead levels. Fifteen papers fulfilled the inclusion criteria. Mean blood lead levels of women in the studies ranged from 0.83 to 99 μg/dl. The overall weighted mean of blood lead levels was 24.73 μg/dl. The weighted mean from analyses of data on blood lead levels of pregnant women alone was 26.24 μg/dl. Identified sources of lead exposure included lead mine, informal lead-acid battery recycling, leaded gasoline and piped water. Elevated BLLs were associated with incidence of preeclampsia, hypertension, and malaria. Important contributing factors for elevated blood lead levels (BLL) in these women include poverty, high environmental lead burden, low awareness on lead exposure hazards and lack of regulation for lead in consumer products. BLLs of women of childbearing age in SSA are unacceptably high. There is need therefore, for aggressive programs to address lead exposure in this population.