Environmental cadmium exposure: a possible factor in the pathogenesis of preeclampsia

Cadmium is a toxic metal, an environmental contaminant and a multi-organ poison which has been implicated in the derangement of a number of biological and molecular systems. Exposure to cadmium is a serious global health threat particularly in developing countries and pregnant women are at great risk, This is because they have increased gastrointestinal absorption and retention of cadmium and the tendency for increased risk of complications owing to its toxic effects. Preeclampsia is a pregnancy complication characterized by the development of onset of hypertension and significant proteinuria after 20 weeks of gestation or during labour and/or within 48 hours of delivery. This pregnancy-specific syndrome is a leading cause of maternal death particularly in developing countries. Several reports have provided evidence of remote association between preeclampsia and cadmium but the mechanism of the involment of this toxic metal in this disease is still surrounded with uncertainty. Some possible mechanistic pathways such as induction of oxidative stress, acting as an antimetabolite to zinc and deregulation of epigenetic mechanisms have been elucidated in this article may be interconnected, work synergistically or act independently. However, pertinent to understand them in a bid to possibly prevent the disease or forestall its devastating consequences. Environmental cadmium exposure may be considered a factor that merits further serious attention in the continuous search for the precise an etiology of preeclampsia particularly in developing countries that experience uncontrolled cadmium release into the environment.

Urinary calcium: a promising predictive biomarker for early recognition of environmental lead exposure in children

Background: In the continuous search for accessible, reliable and sensitive biomarkers for early detection of environmental lead exposure, authors determined the interaction between blood lead level (BLL), the conventional marker of lead exposure, and the indices of calcium and bone metabolism in children.Methods: This cross-sectional study involved 309 apparently healthy children from eight public primary schools in Ibadan, Nigeria who were classified as Elevated BLL (EBLL) and control based on standard cut-off for childhood BLL. BLL, serum Ca (tCa), phosphate, magnesium (Mg), 25-hydroxy-Vitamin D, alkaline phosphatase (ALP), urinary calcium (uCa) and urinary deoxypyridinoline (uDPD) were determined using AAS, HPLC and ELISA as appropriate. Bone-specific ALP (B-ALP) and ionized calcium (iCa) were calculated using standard formulae. Data analyses involved Student’s t-test, Pearson correlation and multivariate regression analysis. p<0.05 was considered statistically significant.Results: BLL and 25-OH-Vitamin D levels were increased in EBLL (0.4±0.1 µmol/L and 60.1±10.7 mmol/L) compared with control (0.2±0.0 µmol/L and 55.1±14.3 mmol/L) p <0.05. No significant differences existed in the levels of ALP, B-ALP, uCa, uDPD, tCa, iCa, phosphate and Mg in both groups (p>0.05). BLL had significant positive correlation with uCa (r=0.176, p=0.002) (p<0.05) but no significant correlation with uDPD, ALP, B-ALP, tCa, iCa, phosphate, Mg and 25-OH-Vitamin D (p>0.05). BLL could be accounted for by uCa by applying the equation, BLL=0.329+0.324uCa.Conclusions: Urinary calcium could be a promising predictive biomarker for early recognition of significant environmental lead exposure in children.

Toxicant-nutrient interaction as a veritable host resistance against chemical toxicity in the rapidly industrializing developing nations

Growing evidence indicates that chemical utilization including toxic waste in the developing countries is on the increase. These nations have limited facilities for sound chemical management involving production, use and disposal of chemicals with minimal adverse effects on human and environmental health. Though concerns are important to all nations, they appear particularly salient to the industrializing countries under pressures to achieve development and eradicate poverty yet with limited capacity for sound chemical management. This increases the risk of chemical toxicity, with consequences such as genotoxicity, cancer and teratogenicity. The growing chemical burden implies the need for an efficient and effective means of xenobiotic metabolism and host resistance. Relevant literature on nutrients and toxicants interaction in various search engines were reviewed. The possible role of host resistance, essentially involving nutritional modulation has been ignored. Nutrient-toxicant response pathways could be affordable strategies against excessive chemical exposure. Zinc, a prime micronutrient is an antioxidant [Cu-Zn superoxide dismutase (SOD)], component of p53, guardian of the genome; active in the repair of DNA damage and apoptosis; protective against carcinogenesis. Zinc also plays an important role in vitamin A metabolism, in turn important in differentiation and central to retinoids involved in gene expression. Zinc is important in all the stages of the cell cycle, derangement of which may be a pathway to carcinogenesis. Use of this and other protective nutrients including folate and selenium, among others, appears a veritable approach to improving host resistance against chemical toxicity and should be considered promising in developing nations

Oxidative Stress and Antioxidant Status in Nigerian E-waste Workers: A Cancer Risk Predictive Study.

Introduction: In Africa, Nigeria has been reported as the largest destination for unregulated volume of electronic waste (e-waste). Currently, e-waste management practices in Nigeria remain completely primitive, taking place essentially in the informal sector. Recent report indicates that the majority (88.8%) of Nigerian e-waste workers have exposure burden of ≥6 hours per day; ≥6 days per week, and reportedly worked without personal protective devices. These crude management practices enhance the workers’ exposure to electronic waste borne toxic and carcinogenic metals and chemicals through almost all body cavities. Objective: Concisely, this study aimed at evaluating the status of enzymatic and non-enzymatic oxidative stress biomarkers as cancer risk indices in Nigerians occupationally exposed to e-waste. Methods: Serum levels of malondialdehyde (MDA), uric acid (UA), albumin (ALB), total bilirubin (TBil) and conjugated bilirubin (Cbil.)] and activities of enzymatic antioxidants [glutathione reductase (Gr), catalase (Cat), superoxide dismutase (SOD) and glutathione peroxidase (GPx)] were determined in Nigerian e-waste workers (n=63) and in age-matched unexposed participants (n=41), using standard colorimetric methods. Results: Significantly elevated lipid peroxidation and raised uric acid levels were indicated in e-waste workers. Further to this, CAT, SOD and GPx were significantly reduced in e-waste workers compared with the unexposed human population. Comparatively different observations were not registered in the activity of GR and levels of ALB, TBil. and CBil. between exposed and unexposed participants. Conclusion: This study provides evidence that the oxidative stress observed in the studied population could be associated with occupational exposure to e-waste chemicals and may be a predictive mechanism for chemical carcinogenesis in Nigerians involved in primitive e-waste management.

Arsenic exposure and its health effects and risk of cancer in developing countries: micronutrients as host defence.

Arsenic (As) is a ubiquitous metalloid found in several forms in food and the environment, such as the soil, air and water. The predominant form is inorganic arsenic in drinking water, which is both highly toxic and carcinogenic and rapidly bioavailable. As is currently one of the most important environmental global contaminants and toxicants, particularly in the developing countries. For decades, very large populations have been and are currently still exposed to inorganic As through geogenically contaminated drinking water. An increased incidence of disease mediated by this toxicant is the consequence of long-term exposure. In humans, chronic ingestion of inorganic arsenic (> 500 mg/L As) has been associated with cardiovascular, nervous, hepatic and renal diseases and diabetes mellitus as well as cancer of the skin, bladder, lung, liver and prostate. Contrary to the earlier view that methylated compounds are innocuous, the methylated metabolites are now recognized to be both toxic and carcinogenic, possibly due to genotoxicity, inhibition of antioxidative enzyme functions, or other mechanisms. As inhibits indirectly sulfhydryl containing enzymes and interferes with cellular metabolism. Effects involve such phenomena as cytotoxicity, genotoxicity and inhibition of enzymes with antioxidant function. These are all related to nutritional factors directly or indirectly. Nutritional studies both in experimental and epidemiological studies provide convincing evidence that nutritional intervention, including chemoprevention, offers a pragmatic approach to mitigate the health effects of arsenic exposure, particularly cancer, in the relatively resource-poor developing countries. Nutritional intervention, especially with micronutrients, many of which are antioxidants and share the same pathway with As, appears a host defence against the health effects of arsenic contamination in developing countries and should be embraced as it is pragmatic and inexpensive.