Prioritizing hazardous pollutants in two Nigerian water supply schemes: a risk-based approach

Objective To rank pollutants in two Nigerian water supply schemes according to their effect on human health using a risk-based approach. Methods Hazardous pollutants in drinking-water in the study area were identified from a literature search and selected pollutants were monitored from April 2010 to December 2011 in catchments, treatment works and consumer taps. The disease burden due to each pollutant was estimated in disability-adjusted life years (DALYs) using data on the pollutant’s concentration, exposure to the pollutant, the severity of its health effects and the consumer population. Findings The pollutants identified were microbial organisms, cadmium, cobalt, chromium, copper, iron, manganese, nickel, lead and zinc. All were detected in the catchments but only cadmium, cobalt, chromium, manganese and lead exceeded World Health Organization (WHO) guideline values after water treatment. Post-treatment contamination was observed. The estimated disease burden was greatest for chromium in both schemes, followed in decreasing order by cadmium, lead, manganese and cobalt. The total disease burden of all pollutants in the two schemes was 46 000 and 9500 DALYs per year or 0.14 and 0.088 DALYs per person per year, respectively, much higher than the WHO reference level of 1 × 10−6 DALYs per person per year. For each metal, the disease burden exceeded the reference level and was comparable with that due to microbial contamination reported elsewhere in Africa. Conclusion The estimated disease burden of metal contamination of two Nigerian water supply systems was high. It could best be reduced by protection of water catchment and pretreatment by electrocoagulation

The burden of disease attributable to ambient PM2.5-bound PAHs exposure in Nagpur, India

Polycyclic aromatic hydrocarbons (PAHs) bound to PM2.5 are genotoxic carcinogens that can also elicit non-cancer effects. Previous studies report substantial burdens of PAHs-related lung cancer, but no estimate for other cancer types or non-carcinogenic burden. Here, we assessed the burden of disease, in DALYs/person/year, attributable to thirteen priority PAHs in PM2.5 in Nagpur district, for several endpoints linked to benzo[a]pyrene, to inform policy decision-making for mitigation. We conducted detailed assessment of concentrations of PAHs in nine areas, covering urban, peri-urban and rural environments, from February 2013 to June 2014. PAHs concentrations were converted to benzo[a]pyrene equivalent concentration for cancer and non-cancer effects using relative potency factors and relative toxicity factors derived from quantitative structure-activity relationships, respectively. We derived severity for each endpoint using GBD 2016 dataset. The annual average concentration of total PAHs in Nagpur district was 458±246 ng/m3, and results in 0.011 DALYs/person/year (49,000 DALYs/year), much higher than the WHO reference limit of 1×10-6 DALYs/person/year. PAHs-related burden follow this order: developmental (mostly cardiovascular) impairment (55.1%) > cancer (26.5%) or lung cancer (23.1%) > immunological impairment (18.0%) > reproductive abnormally (0.4%). The estimated DALYs/person/year is high. Mitigation intervention should target combustion sources having the highest level of exposure

Influence of CO 2 concentration on carbon concentrating mechanisms in cyanobacteria and green algae: a proteomic approach

Carbon concentrating mechanisms play a vital role in photosynthesis in microalgae and cyanobacteria especially in the proper functioning of Rubisco and assimilation of carbon via the Calvin cycle. This study evaluates the role of carbon dioxide on carbon concentrating mechanism (CCM) in a cynaobacteria, Spirulina platensis and a microalga, Chlorella sp. 786. The study organisms were grown in both atmospheric (control sample, 0.035%) and high (exposed sample, 10%) CO2 concentrations. Second dimension (2D) electrophoresis revealed a huge difference in the protein profiles of both organisms suggesting the induction of CCM related proteins in the sample maintained at atmospheric CO2 concentration and the repression of CCM related proteins in the sample maintained at 10% CO2. Liquid chromatography-mass spectroscopy analysis revealed the presence of two important Ci transporter proteins in the control sample of S. platensis, namely ferredoxin-NADP+ reductase and ATP binding cassette (ABC) transport system protein. These proteins were only expressed in the control sample and were downregulated or not expressed at all in the exposed sample. Consequently, this study conclusively proves that CCMs are only inducted at low CO2 concentrations and are not functional at high CO2 concentration

Global DNA methylation profiling of manganese-exposed human neuroblastoma SH-SY5Y cells reveals epigenetic alterations in Parkinson’s disease-associated genes

Manganese (Mn) is an essential trace element required for optimal functioning of cellular biochemical pathways in the central nervous system. Elevated exposure to Mn through environmental and occupational exposure can cause neurotoxic effects resulting in manganism, a condition with clinical symptoms identical to idiopathic Parkinson’s disease. Epigenetics is now recognized as a biological mechanism involved in the etiology of various diseases. Here, we investigated the role of DNA methylation alterations induced by chronic Mn (100 µM) exposure in human neuroblastoma (SH-SY5Y) cells in relevance to Parkinson’s disease. A combined analysis of DNA methylation and gene expression data for Parkinson’s disease-associated genes was carried out. Whole-genome bisulfite conversion and sequencing indicate epigenetic perturbation of key genes involved in biological processes associated with neuronal cell health. Integration of DNA methylation data with gene expression reveals epigenetic alterations to PINK1, PARK2 and TH genes that play critical roles in the onset of Parkinsonism. The present study suggests that Mn-induced alteration of DNA methylation of PINK1–PARK2 may influence mitochondrial function and promote Parkinsonism. Our findings provide a basis to further explore and validate the epigenetic basis of Mn-induced neurotoxicity

Potential Role of Epigenetic Mechanism in Manganese Induced Neurotoxicity

Manganese is a vital nutrient and is maintained at an optimal level (2.5–5 mg/day) in human body. Chronic exposure to manganese is associated with neurotoxicity and correlated with the development of various neurological disorders such as Parkinson’s disease. Oxidative stress mediated apoptotic cell death has been well established mechanism in manganese induced toxicity. Oxidative stress has a potential to alter the epigenetic mechanism of gene regulation. Epigenetic insight of manganese neurotoxicity in context of its correlation with the development of parkinsonism is poorly understood. Parkinson’s disease is characterized by the �-synuclein aggregation in the form of Lewy bodies in neuronal cells. Recent fndings illustrate that manganese can cause overexpression of �-synuclein. �-Synuclein acts epigenetically via interaction with histone proteins in regulating apoptosis. �-Synuclein also causes global DNA hypomethylation through sequestration of DNA methyltransferase in cytoplasm. An individual genetic difference may also have an influence on epigenetic susceptibility to manganese neurotoxicity and the development of Parkinson’s disease. Tis review presents the current state of fndings in relation to role of epigenetic mechanism in manganese induced neurotoxicity, with a special emphasis on the development of Parkinson’s disease

decolorisation,biodegration and detoxificatio of benzidine based azo dye

The present study deals with the decolorisation,biodegration and detoxification of Direct Black-38,a benzidine based azodyes, by a mixed microbial culture isolated from an aerobic bioreactor treating textile wastewater. The studies revealed a biotransforma-tion of Direct Black-38 into benzidine and 4-aminobiphenyl followed by complete decolorisation and biodegradation of these toxic intermediates. From cytotoxicity studies, it was concluded that detoxification of the dye took place after degradation of the toxic intermediates by the culture

Can the Indian national ambient air quality standard protect against the hazardous constituents of PM2.5?

Globally, exposure to ambient fine particulate matter (PM2.5) pollution claims ~9 million lives, yearly, and a quarter of this deaths occurs in India. Regulation of PM2.5 pollution in India is based on compliance with its National Ambient Air Quality Standard (NAAQS) of 40 μg/m3 , which is eight times the revised global air quality guideline (AQG) of 5 μg/m3.But, whether the NAAQS provides adequate protection against the hazardous components in PM2.5 is still not clear. Here, we examined the risk to health associated with exposure to PM2.5–bound polychlorinated biphenyls (PCB), heavy metals and polycyclic aromatic hydrocarbons (PAHs) in an Indian district averaging below the NAAQS. The annual average concentrations of PM2.5 mass, Σ28PCB and Σ13PAHs were 34 ± 17 μg/m3, 21 ± 12 ng/m3 and 458 ± 246 ng/m3, respectively. Concentrations of As, Cr, Mn and Ni in PM2.5 surpassed the screening levels for residential air. Substantial level of risks to health were associated with exposure to dioxin-like PCBs (Σ12dlPCB), PAHs, As, Cr and Ni. The hazard index or lifetime cancer risk were 240, or 9 cases per 1000 population, respectively. The estimated risks to health through exposure to hazardous components, except Ni, were greatest in rural areas, having a lower average PM2.5 con�centration, than urban or peri-urban areas, suggesting higher toxicity potential of rural combustion sources. The large disparity between the estimated risk values and the acceptable risk level suggests that it would take a more stringent standard, such as the global AQG, to protect vulnerable populations in India from hazardous compo�nents in PM2.

Manganese exposure: linking down-regulation of miRNA-7 and miRNA-433 with α-synuclein overexpression and risk of idiopathic Parkinson's disease

Manganese is an essential trace element however elevated environmental and occupational exposure to this element has been correlated with neurotoxicity symptoms clinically identical to idiopathic Parkinson's disease. In the present study we chronically exposed human neuroblastoma SH-SY5Y cells to manganese (100 μM) and carried out expression profiling of miRNAs known to modulate neuronal differentiation and neurodegeneration. The miRNA PCR array results reveal alterations in expression levels of miRNAs, which have previously been associated with the regulation of synaptic transmission and apoptosis. The expressions of miR-7 and miR-433 significantly reduced upon manganese exposure. By in silico homology analysis we identified SNCA and FGF-20as targets of miR-7 and miR-433. We demonstrate an inverse correlation in expression levels where reduction in these two miRNAs causes increases in SNCA and FGF-20. Transient transfection of SH-SY5Y cells with miR-7 and miR-433 mimics resulted in down regulation of SNCA and FGF-20 mRNA levels. Our study is the first to uncover the potential link between manganese exposure, altered miRNA expression and parkinsonism: manganese exposure causes overexpression of SNCA and FGF-20 by diminishing miR-7 and miR-433 levels. These miRNAs may be considered critical for protection from manganese induced neurotoxic mechanism and hence as potential therapeutic targets