Estimated exposure to microplastics through national and local brands of bottled water in Central India.

Microplastics (MPs) are ubiquitous pollutants that affect various environmental matrices, including air, water, soil, food, and beverages. In India, there is limited research on microplastics in bottled drinking water, which is a significant route of MP exposure to the human body. To date, the data on the occurrence of MPs in national and local bottled water brands have not been studied and compared. Therefore, the current study focuses on the contamination of MPs in bottled water from different national and local brands procured from the market of Nagpur, India. The MPs were observed in all the analyzed samples. It was observed that the local bottled water showed higher MP contamination compared to national bottled water, with MP concentrations of 212 ± 100 MPs/L and 72 ± 36 MPs/L, respectively. The MPs were identified and characterized using microscopic and attenuated total reflectance-fourier transform infrared spectroscopy (ATR-FTIR) analysis, revealing that the dominant MP particles were fragments (71%), followed by fibers (23%), and others (6%). Among the observed particles, 50% of particles were black colored, followed by transparent (16%), red (13%), orange (8%), green (3%), blue (5%), and yellow (5%). The predominant polymer types were polyethylene (PE) and polyethylene terephthalate (PET). Overall, the pollution load indices suggested a moderate level of contamination in bottled water samples. Furthermore, the estimated annual human exposure to MPs was calculated as 5186 ± 3751 p/kg-bw/year for children and 1482 ± 1072 p/kg-bw/year for adults, making it a significant route of human exposure to MPs.

Potential of Antarctic lipase from Acinetobacter johnsonii Ant12 for treatment of lipid-rich wastewater: screening, production, properties and applications.

The present study aimed to screen and optimize lipase production by the Antarctic strain Acinetobacter johnsonii Ant12 for lipid-rich wastewater treatment. Lipase production was successfully enhanced threefold through optimization of culture conditions. The optimum crude lipase activity was observed at 50 °C with high stability in a wide temperature range. The lipase also exhibited high activity and stability in the presence of solvents, metal ions, and surfactants. The crude lipase was used for the treatment of lipid-rich wastewater, which poses a significant challenge, as traditional removal methods are often inefficient or non-eco-friendly. In this study, bioaugmentation with Ant12 resulted in substantial lipid reduction in synthetic as well as real-world wastewater. Multiple linear regression analysis showed that lipid concentration and time were the most significant factors influencing lipid degradation. Bioaugmentation of real-world wastewater with Ant12 cells resulted in 84% removal of lipids in 72 h, while its crude lipase degraded 73.7% of lipids after 24 h. Thus, the specific rate of lipid degradation was higher for crude lipase (0.095/h) than the whole cell treatment (0.031/h). Economic analysis revealed that crude lipase production was much cheaper, faster and more eco-friendly than purified or partially purified lipase production, which justifies its use in wastewater treatment. The high activity of enzyme also implicates its application as a detergent additive. In our knowledge, it is the first study to establish A. johnsonii isolate from Antarctica for lipid-rich wastewater treatment.

Characterization and removal of microplastics in a sewage treatment plant from urban Nagpur, India.

Sewage treatment plant (STP) acts as a potential source of microplastic contamination in the environment. The presence of microplastics in the sewage treatment plant is reported over the globe in varying concentrations. Hence, the current study is intended to evaluate the presence and abundance of microplastics occurring in sewage treatment plants in India. The samples were processed through digestion and density separation, followed by microscopic and polymer identification through Fourier transform infrared spectroscopy. Also, different wastewater parameters were studied to analyze their influence. High microplastic concentrations were detected in the influent (1860 ± 265 MPs/L), which reduced by > 90%, to around 148 ± 51 MPs/L in the effluent. The concentration of microplastics in sewage sludge was 830 MPs/kg. The prominent plastic types identified include low-density polyethylene, polypropylene, polyurethane, polyvinyl chloride, and rayon. The smaller particles prevail in the effluent, releasing around 30 billion particles per day to the environment. This suggests that the current STP is efficient in removing the majority of the particles, but considerations are needed to avoid the ecological risks associated.

Mitochondrial dysfunctions elicited by solid waste leachates provide insights into mechanisms of leachates induced cell death and pathophysiological disorders.

Emissions (mainly leachates and landfill gases) from solid waste facilities are laden with mixtures of dangerous xenobiotics implicated with significant increase in various pathophysiological disorders including cancer, and eventual mortality of exposed wildlife and humans. However, the molecular mechanisms of solid waste leachates induce pathophysiological disorders and cell death are still largely unknown. Although, evolving evidence implicated generation of reactive oxygen species and oxidative stress as the possible mechanism. Recent scientific reports are linking reactive oxygen species and mitochondrial dysfunctions as the player mechanism in pathophysiological disorder and apoptosis induced by xenobiotics in solid waste leachates. This systematic review presents an explicit discussion of recent scientific findings on the structural and functional alterations in mitochondria induced by solid waste leachates as the molecular mechanisms plausibly responsible for the pathophysiological disorders, cancer and cell death reported in landfill toxicology and epidemiological studies. This review aims to increase scientific understanding on solid waste leachate induced mitochondria dysfunctions as the key player in molecular mechanisms of solid waste induced toxicity. The findings in this review were mainly from using primary cells, cell lines, Drosophila and fish. Whether the findings will similarly be observed in mammalian test systems in vivo and particularly in exposed humans, remained to be investigated. Improvement in technological advancements, enforcement of legislation and regulations, and creation of sophisticated health surveillance against exposure to solid waste leachates, will expectedly mitigate human exposure to solid waste emissions and contamination of the environment.

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 concentration, 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 components in PM2.5.

Landfill soil leachates from Nigeria and India induced DNA damage and alterations in genes associated with apoptosis in Jurkat cell.

Landfill soil leachates, containing myriad of xenobiotics, increase genotoxic and cytotoxic stress-induced cell death. However, the underlying mechanism involved in the elimination of the damaged cells is yet to be fully elucidated. This study investigated the apoptotic processes induced in lymphoma (Jurkat) cells by landfill soil leachates from Olusosun (OSL, Nigeria) and Nagpur (NPL, India). Jurkat was incubated with sub-lethal concentrations of OSL and NPL for 24 h and analyzed for DNA fragmentation and apoptosis using agarose gel electrophoresis and Hoechst 33258-PI staining, respectively. Complementary DNA expression profiling of some pro-apoptotic and anti-apoptotic genes regulating apoptosis was also analyzed using real-time PCR (RT-PCR) method. Agarose gel electrophoresis revealed DNA fragmentations in OSL and NPL-treated cells. Hoecsht-33258 - Propidium Iodide (PI) based apoptotic analysis confirmed apoptotic cell death in exposed Jurkat. RT-PCR analysis revealed different fold changes in the pro- and anti-apoptotic genes in OSL and NPL-treated Jurkat. There was significant increase in fold change of the up-regulated genes; apoptosis inducing factor mitochondrion-associated 2 (AIFM2), Fas-associated death domain (FADD), Caspase-2, Caspase-6, BH3 interacting domain death agonist (BID), tumor suppressor (p53), and BCL2 associated agonist of cell death (BAD) and down-regulation of apoptosis inhibitor 5 (API5). Results suggest that OSL and NPL elicited genotoxic stress-related apoptosis in Jurkat. The dysregulation in the expression of genes involved in apoptotic processes in wildlife and human exposed to landfill emissions may increase aetiology of various pathological diseases including cancer.

Environmental prevalence, fate, impacts, and mitigation of microplastics-a critical review on present understanding and future research scope.

Microplastics are considered to be ubiquitous and widespread emerging contaminants. They are persistent in the nature and pose considerable harm to the environment. Their omnipresence is documented in almost all aquatic habitats, several atmospheric and terrestrial environments, and also in human consumables. The objective of this review is to provide an overview of the environmental prevalence of the microplastics in all environmental compartments, and their possible adverse impacts. It also presents review of the studies conducted in India and the epitome of potential mitigation measures. The need and direction of future research are highlighted. The review will help in determining the exposure levels, environmental consequences, and risk estimations, and will guide the researchers and policymakers.

Burn to kill: Wood ash a silent killer in Africa.

Aside the emissions, burning of wood in traditional cookstoves (TCs) also generates substantial amount of ash containing hazardous pollutants such as polycyclic aromatic hydrocarbons (PAHs) and toxic metals. But, their concentrations in the ash, particularly in Africa where over 70% of the population utilize TCs, remain unknown. Here, we determined concentrations of sixteen PAHs and eleven heavy metals in ashes from twelve different African TCs, comprising six three-stone fires (TSFs) and six built-in-place cookstoves (BIPCs), burning common African wood species under real world situation. For each TC, ash samples were collected for six consecutive days (Monday-Saturday), and a total of seventy-two daily samples were collected from January-June 2019. Ash yields were measured gravimetrically, and concentrations of the pollutants were determined following standard analytical protocols. The results were used alongside secondary data (annual fuelwood consumption, African fuelwood densities, population proportion using fuelwood and surface human population density) to estimate annual tonnage, exposure potential and risk to health in Africa, using Monte Carlo simulation technique. The ash yields from all TCs studied exceeded 1% on dry weight basis, indicating that ash is a major waste by-product of wood combustion in TCs. TSFs produced more ash (5.7 ± 0.7%) than BIPCs (3.4 ± 1.0%). Concentrations of As, Cd, Hg and Pb in ashes were significantly higher (α = 0.05) for TSFs than BIPCs. In contrast, concentrations of PAHs were higher in ashes from BIPCs than TSFs. Assuming ash consumption rates range from 250 to 500 mg/day for young children weighing 10 to 30 kg, the upper dose (µg/kg-day) of Pb (0.2-3.9) or Σ16PAHs (0.02-0.34), for instance, surpasses the 0.3 µg/kg-day of Pb or PAH recognized as causing adverse effects in children, indicating a concern. The top five countries with the highest annual tonnage or exposure potential to toxic pollutants are Nigeria>Ethiopia>DR-Congo>Tanzania>Uganda, or Rwanda>Burundi>Uganda>Nigeria>Guinea-Bissau, respectively.

Induction of apoptosis in leukemic cells by the alkaloid extract of garden cress (Lepidium sativum L.).

OBJECTIVE: Garden cress (Lepidium sativum L.) is an important herb in traditional medicine used to improve production of breast milk in women and semen in men. In the present research the authors evaluated its ability to destroy leukemic cancer (Jurkat E6-1) cells, using the alkaloid extract of this plant. METHODS: Constituents of the alkaloid extract were analyzed by gas chromatography-mass spectrometry (GC-MS) and their cytotoxicity in leukemic cancer cells and healthy peripheral blood mononuclear cells (PBMCs) was assessed. Cell death via apoptosis was confirmed by DNA laddering, caspase-3 activity, annexin V-fluorescein isothiocyanate and mitochondrial toxicity assays. The specific course of gene activation in treated cells was determined through quantitative polymerase chain reaction (qPCR). RESULTS: GC-MS analysis identified six alkaloids and proto-alkaloids, namely, benzyl isothiocyanate (1), 2-ethoxy-4H-3,1-benzoxazin-4-one (2), (4R)-2-(2-aminophenyl)-4-phenyloxazoline (3), 5-acetyl-1,2-dihydro-6-methyl-2-oxo-4-phenyl-3-pyridinecarbonitrile (4), benzo[b][1,8]-naphthyridin-5(10H)-one,2,4,7-trimethyl (5) and 1,4-diaminoanthraquinone (6), in the alkaloid extract of L. sativum. Of these, compound 1 was previously identified in the seeds of L. sativum. Exposure to the alkaloid extract caused death of Jurkat E6-1 cells, with median lethal concentration (LC50) of 75.25 µg/mL. However, the alkaloid extract also showed a nontoxic and proliferative (1.6-fold) effect in healthy PBMCs. Further experiments performed with Jurkat cells at LC50 and sub-LC50 doses demonstrated DNA fragmentation, activation of caspase-3 and time-dependant phosphatidylserine translocation (apoptosis) from inner to outer cell membranes. Cell toxicity and assessment of adenosine triphosphate level, together with using qPCR to evaluate expression profile of major apoptosis genes, revealed that apoptosis may be induced by disruption in the mitochondrial outer membrane potential, through activation of extrinsic and intrinsic apoptosis pathways in Jurkat cells. CONCLUSION: The ability of the alkaloid extract of L. sativum seeds to induce apoptosis indicates a potential pharmacological use in cancer chemotherapy. The separation of individual active compounds and further in-depth exploration of the molecular mechanism of apoptosis may lead to novel chemotherapeutic compounds in our future antineoplastic research.

Molecular mechanism of apoptosis induction in Jurkat E6-1 cells by Tribulus terrestris alkaloids extract.

The present study demonstrates apoptosis-inducing potential and mechanism of action of Tribulus terristris alkaloid extract in Jurkat E6-1 cancer cell line. Liquid Chromatography-Mass Spectrometry and High Resolution-Mass Spectrometry analysis identified the presence of four N-feruloyltyramine derivatives, namely trans-N-feruloyl-3-hydroxytyramine (1), trans-N-coumaroyltyramine (2), trans-N-feruloyltyramine (3) and trans-N-feruloyl-3-ethoxytyramine (4) in the alkaloid extract. Compounds 2 and 3 have not been yet reported in the alkaloid extract of T. terristris. In silico analysis revealed therapeutic potential of N-feruloyltyramine derivatives and strong binding efficiency to both chains of Tumor Necrosis Factor Receptor 1. Treatment of alkaloids extract to Jurkat E6-1 clone induced dose-dependent cytotoxicity (LC50 140.4 µg mL-1). Jurkat cells treated with alkaloids extract at sub-lethal concentration showed DNA fragmentation, enhancement in caspase-3 activity and phosphatidylserine translocation (apoptosis indicator) compared to control cells. Gene expression analysis using Human Apoptosis RT2 Profiler PCR Array analysis upon alkaloid treatment was found to significantly alter expression of critical genes such as TNFR1, FADD, AIFM, CASP8, TP53, DFFA and NFKB1. These genes are predicted to mediate apoptotic cell death via both intrinsic and extrinsic apoptosis pathway. In summary, we report the identification of new N-feruloyltyramine derivatives from alkaloid extract of T. terristris fruit with probable anti-leukemic and pharmacological potential.

Simultaneous quantitative monitoring of four indicator contaminants of emerging concern (CEC) in different water sources of Central India using SPE/LC-(ESI)MS-MS.

Environmental occurrence of CECs poses a great threat to both aquatic life and human health. The aim of this study was to optimize and validate SPE/LC-(ESI)MS-MS method for simultaneous quantitative monitoring of two sub-classes of CECs (pharmaceuticals and hormones) and to estimate the concentrations of select CECs in environmental water samples. For all the tested analytes, recoveries in laboratory reagent water were greater than 81%. Average percent (relative standard deviation) RSD of the analytes in recovery, repeatability, and reproducibility experiments were ≤ 10%. Determination coefficients (r2) of primidone, diclofenac, testosterone, and progesterone were estimated to be 0.9979, 0.9972, 0.9968, and 0.9962, respectively. Limits of detection (LOD) for primidone, diclofenac, testosterone, and progesterone were 4.63 ng/L, 5.36 ng/L, 0.55 ng/L, and 0.88 ng/L, respectively. Limits of quantification (LOQ) for primidone, diclofenac, testosterone, and progesterone were 14.72 ng/L, 17.06 ng/L, 1.766 ng/L, and 2.813 ng/L, respectively. Average recoveries in environmental water and wastewater samples were greater than 74% and RSD were ≤ 7%. Trace levels (68.33-125.70 ng/L) of primidone were detected in four environmental water samples, whereas diclofenac was not detected in any of the tested sample. Trace levels of progesterone were observed in two environmental samples (16.64 -203.73 ng/L), whereas testosterone was detected in STP inlet sample (178.16 ng/L).

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

Exposure to PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) can elicit several types of cancer and non-cancer effects. Previous studies reported substantial burdens of PAH-induced lung cancer, but the burdens of other cancer types and non-cancer effects remain unknown. Thus, we estimate the cancer and non-cancer burden of disease, in disability-adjusted life years (DALYs), attributable to ambient PM2.5-bound PAHs exposure in Nagpur district, India, using risk-based approach. We measured thirteen PAHs in airborne PM2.5 sampled from nine sites covering urban, peri-urban and rural areas, from February 2013 to June 2014. We converted PAHs concentrations to benzo[a]pyrene equivalence (B[a]Peq) for cancer and non-cancer effects using relative potency factors, and relative toxicity factors derived from quantitative structure-activity relationships, respectively. We calculated time-weighted exposure to B[a]Peq, averaged over 30 years, and adjusted for early-life susceptibility to cancer. We estimated the DALYs/year using B[a]Peq exposure levels, published toxicity data, and severity of the diseases from Global Burden of Disease 2016 database. The annual average concentration of total PM2.5-bound PAHs was 458 ±â€¯246 ng/m3 and resulted in 49,500 DALYs/year (0.011 DALYs/person/year). The PAH-related DALYs followed this order: developmental (mostly cardiovascular) impairments (55.1%) > cancer (26.5%) or lung cancer (23.1%) > immunological impairments (18.0%) > reproductive abnormalities (0.4%).

The gains in life expectancy by ambient PM2.5 pollution reductions in localities in Nigeria.

Global burden of disease estimates reveal that people in Nigeria are living shorter lifespan than the regional or global average life expectancy. Ambient air pollution is a top risk factor responsible for the reduced longevity. But, the magnitude of the loss or the gains in longevity accruing from the pollution reductions, which are capable of driving mitigation interventions in Nigeria, remain unknown. Thus, we estimate the loss, and the gains in longevity resulting from ambient PM2.5 pollution reductions at the local sub-national level using life table approach. Surface average PM2.5 concentration datasets covering Nigeria with spatial resolution of ∼1 km were obtained from the global gridded concentration fields, and combined with ∼1 km gridded population of the world (GPWv4), and global administrative unit layers (GAUL) for territorial boundaries classification. We estimate the loss or gains in longevity using population-weighted average pollution level and baseline mortality data for cardiopulmonary disease and lung cancer in adults ≥25 years and for respiratory infection in children under 5. As at 2015, there are six "highly polluted", thirty "polluted" and one "moderately polluted" States in Nigeria. People residing in these States lose ∼3.8-4.0, 3.0-3.6 and 2.7 years of life expectancy, respectively, due to the pollution exposure. But, assuming interventions achieve global air quality guideline of 10 µg/m3, longevity would increase by 2.6-2.9, 1.9-2.5 and 1.6 years for people in the State-categories, respectively. The longevity gains are indeed high, but to achieve them, mitigation interventions should target emission sources having the highest population exposures.

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 (100µM) 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.

Application of cell-based assays for toxicity characterization of complex wastewater matrices: Possible applications in wastewater recycle and reuse.

Exposure to pre-concentrated inlet or outlet STP wastewater extracts at different concentrations (0.001% to 1%) induced dose-dependent toxicity in MCF-7 cells, whereas drinking water extracts did not induce cytotoxicity in cells treated. GC-MS analysis revealed the occurrence of xenobiotic compounds (Benzene, Phthalate, etc.) in inlet/outlet wastewater extracts. Cells exposed to inlet/outlet extract showed elevated levels of reactive oxygen species (ROS: inlet: 186.58%, p<0.05, outlet, 147.8%, p<0.01) and loss of mitochondrial membrane potential (Δψm: inlet, 74.91%, p<0.01; outlet, 86.70%, p<0.05) compared to the control. These concentrations induced DNA damage (Tail length: inlet: 34.4%, p<0.05, outlet, 26.7%, p<0.05) in treated cells compared to the control (Tail length: 7.5%). Cell cycle analysis displayed drastic reduction in the G1 phase in treated cells (inlet, G1:45.0%; outlet, G1:58.3%) compared to the control (G1:67.3%). Treated cells showed 45.18% and 28.0% apoptosis compared to the control (1.2%). Drinking water extracts did not show any significant alterations with respect to ROS, Δψm, DNA damage, cell cycle and apoptosis compared to the control. Genes involved in cell cycle and apoptosis were found to be differentially expressed in cells exposed to inlet/outlet extracts. Herein, we propose cell-based toxicity assays to evaluate the efficacies of wastewater treatment and recycling processes.

The health burden and economic costs averted by ambient PM2.5 pollution reductions in Nagpur, India.

National estimates of the health and economic burdens of exposure to ambient fine particulate matter (PM2.5) in India reveal substantial impacts. This information, often lacking at the local level, can justify and drive mitigation interventions. Here, we assess the health and economic gains resulting from attainment of WHO guidelines for PM2.5 concentrations - including interim target 2 (IT-2), interim target 3 (IT-3), and the WHO air quality guideline (AQG) - in Nagpur district to inform policy decision making for mitigation. We conducted a detailed assessment of concentrations of PM2.5 in 9 areas, covering urban, peri-urban and rural environments, from February 2013 to June 2014. We used a combination of hazard and survival analyses based on the life table method to calculate attributed annual number of premature deaths and disability-adjusted life years (DALYs) for five health outcomes linked to PM2.5 exposure: acute lower respiratory infection for children <5years, ischemic heart disease, chronic obstructive pulmonary disease, stroke and lung cancer in adults ≥25years. We used GBD 2013 data on deaths and DALYs for these diseases. We calculated averted deaths, DALYs and economic loss resulting from planned reductions in average PM2.5 concentration from current level to IT-2, IT-3 and AQG by the years 2023, 2033 and 2043, respectively. The economic cost for premature mortality was estimated as the product of attributed deaths and value of statistical life for India, while morbidity was assumed to be 10% of the mortality cost. The annual average PM2.5 concentration in Nagpur district is 34±17µgm-3 and results in 3.3 (95% confidence interval [CI]: 2.6, 4.2) thousand premature deaths and 91 (95% CI: 68, 116) thousand DALYs in 2013 with economic loss of USD 2.2 (95% CI: 1.7, 2.8) billion in that year. It is estimated that interventions that achieve IT-2, IT-3 and AQG by 2023, 2033 and 2043, would avert, respectively, 15, 30 and 36%, of the attributed health and economic loss in those years, translating into an impressively large health and economic gain. To achieve this, we recommend an exposure-integrated source reduction approach.

Chemical characterization of simulated landfill soil leachates from Nigeria and India and their cytotoxicity and DNA damage inductions on three human cell lines.

Landfill soils are sources of emerging carcinogens, teratogens and mutagens in the environment. There is inadequate information on its possible health risk and cytogenotoxicity. This study evaluated chemical characterization of four simulated landfill leachates with their cytotoxicity and DNA damage in human cells. Hepatocarcinoma (HepG2), lymphoma (Jurkat) and osteosarcoma (HOS) cells, incubated with 6.25, 12.5, 25, 50, 75 and 100% of Aba Eku (AEL), Olusosun (OSL), Awotan (AWL) and Nagpur (NPL) simulated leachates for 24 h, were assessed for cell viability using MTT assay and morphological alterations. DNA damage was also assessed after 24 h treatment of cells with sub-lethal concentrations of the leachates using comet assay. Metals and organic compounds in the soil leachates were determined using inductively coupled plasma-mass spectrometry (ICP-MS) and gas chromatography-mass spectroscopy (GC-MS) respectively. The leachates induced significant cytotoxicity in the treated cells with evidence of apoptosis; shrunken morphologies, detachment from the substratum and cytoplasmic vacuolations. Similarly, there was significant DNA damage induced in the treated cells, with increased Olive tail moment, tail length and % tail DNA. Jurkat was the most sensitive (Jurkat > HepG2 > HOS) to the cytotoxic and genotoxic effects of the leachates. All the analyzed metals except Cd, Fe, Zn and Mn were found at levels lower than standard allowable limits. 32, 17, 23 and 23 different PAHs and PCBs were detected in AEL, AWL, OSL and NPL respectively, at varying retention peak times. These toxic constituents induced the observed cytogenotoxicity in the cells and may suggest possible public health risk.

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 α-synuclein aggregation in the form of Lewy bodies in neuronal cells. Recent findings illustrate that manganese can cause overexpression of α-synuclein. α-Synuclein acts epigenetically via interaction with histone proteins in regulating apoptosis. α-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. This review presents the current state of findings in relation to role of epigenetic mechanism in manganese induced neurotoxicity, with a special emphasis on the development of Parkinson's disease.

Carvacrol induces mitochondria-mediated apoptosis in HL-60 promyelocytic and Jurkat T lymphoma cells.

The aim of the present study was to investigate the effect of carvacrol, a phenolic monoterpenoid on the induction of apoptosis in HL-60 (Human acute promyelocytic leukemia cells) and Jurkat (human T lymphocyte cells) cells. Carvacrol showed a potent cytotoxic effect on both cells with dose-dependent increase in the level of free radical formation as measured by an oxidation sensitive fluorescent dye, 2,7-dichlorodihydrofluorescein diacetate (H2DCFDA) levels. The reduction in the level of antioxidants such as catalase (CAT) and superoxide dismutase (SOD) (P<0.05) was observed in carvacrol-treated cells. The major cytotoxic effect appears to be intervened by the induction of apoptotic cell death as assessed by annexin-V labeling assay using flow cytometry. Western blot analysis showed that Bax expression was increased, whereas Bcl-2 expression was significantly decreased in carvacrol exposed HL-60 cells and Jurkat cells. Further studies revealed that the dissipation of mitochondrial membrane potential of intact cells was accompanied by the activation of caspase-3. Our results found that the potential mechanism of cellular apoptosis induced by carvacrol is mediated by caspase-3 and is associated with the collapse of mitochondrial membrane potential, generation of free radicals, and depletion of the intracellular antioxidant pool.

Biomass and lipid enhancement in Chlorella sp. with emphasis on biodiesel quality assessment through detailed FAME signature.

In this study, the concentrations of MgSO4, salinity and light intensity were optimised for maximum biomass productivity and lipid content in Chlorella sp. Lipid synthesized at varied experimental conditions was also assessed in detail for biodiesel properties through FAME analysis. FAMEs mainly composed of C16:0, C16:1(9), C16:3(7, 10, 13), C18:0, C18:1(11), C18:2(9, 12), C18:3(9, 12, 15). The optimum biomass productivity (372.50mgL(-1)d(-1)) and lipid content (32.57%) was obtained at MgSO4-150ppm; salinity-12.5ppm, and light intensity-25µmolm(-2)s(-1). However, at this condition the cetane number, a major biodiesel property was not complying with worldwide biodiesel standard. Therefore, further optimisations were done to check the suitability of biodiesel fuel. The optimum biomass productivity (348.47mgL(-1)d(-1)) and lipid content (12.43%) with suitable biodiesel fuel properties was obtained at MgSO4-50ppm, salinity-25ppm and light intensity-100µmolm(-2)s(-1). The validation experiments confirmed the closeness of predicted and measured response values.