Face mask application as a tool to diminish the particulate matter mediated heavy metal exposure among citizens of Lucknow, India.

Traffic related fine particulate emissions, enriched in metal contents, are directly linked to respiratory disorders in human subjects. In view of the growing traffic related emissions in India, the present study was undertaken to estimate the heavy metal exposure among non-occupationally exposed two vehicle riders of Lucknow City and related health effects via application of face masks (FMs) fitted with cellulose nitrate filters and measuring the peak respiratory flow rate (PEFR). Carefully selected 200 volunteers (asymptomatic n=154 and symptomatic n=46) were advised to use FMs during their deriving time for 30 days and PEFR test was conducted on each subject at the beginning, i.e. 0 day, and at end of the study period, i.e. 30 days. On completion of the prescribed study period, filters from the used FMs were collected, acid leached and analyzed for Fe, Mn, Cu, Zn, Pb, Ni, Cr and Cd. Asymptomatic and symptomatic subject groups were further divided into two age groups of 15-40 years and 41-68. Pb, Cu and Cd were significantly higher in lower age group (15-40) of symptomatic group and Cr was in asymptomatic group. Negative associations were observed between metals viz. Pb (r=-0.39, p<0.001), Cd (r=-0.26, p<0.001), Fe (r=-0.37, p<0.001), Mn (r=-0.15, p<0.05) and the lung functioning. 30 days PEFR of all subjects were higher by nearly 10% than 0 day in all 200 samples irrespective of age and symptomatic nature of the subject. The improvement could also be due to metals and other organic species, not analyzed herein. Nevertheless the results indicate that FM usage has a role to play for immediate, if not ultimate, improvement in public health and need further studies.

Effects of sub-chronic low-level lead exposure on the homeostasis of copper and zinc in rat tissues.

Information about the health risks or the subtle adverse health effects that might be associated with low-level lead exposure on micronutrient metabolism are scarce in the literature. The present work investigated the subtle adverse health effects of exposure to progressively low levels of lead on the metabolism of two micronutrients, copper and zinc in different tissues of the rat. Rats were exposed to 200, 300 and 400 ppm lead in their drinking water for 12 weeks. Lead, copper and zinc concentrations were determined in blood, liver, kidney, heart, spleen and brain of the animals. While the imbalance in zinc metabolism was characterized by a deposition of zinc in the kidney and to a lesser extent in the heart of the animals, imbalance in copper metabolism was characterized by a depletion of blood and splenic copper concentrations as well as renal and cardiac accumulation of copper. Hepatic and brain copper and zinc contents, together with blood zinc were not affected by the 12-week lead exposure. A linear relationship was observed between lead dose and lead accumulation in the spleen, whereas a non-linear relationship was observed between lead dose and lead accumulation in blood, liver, kidney and heart. Our findings indicate that exposure to progressively low-level lead concentrations results in imbalance in copper and zinc in the organism and this might be a factor in propensity toward behavioral disorders observed in lead exposure.

Detoxification and antioxidant effects of curcumin in rats experimentally exposed to mercury.

Curcumin, a safe nutritional component and a highly promising natural antioxidant with a wide spectrum of biological functions, has been examined in several metal toxicity studies, but its role in protection against mercury toxicity has not been investigated. Therefore, the detoxification and antioxidant effects of curcumin were examined to determine its prophylactic/therapeutic role in rats experimentally exposed to mercury (in the from of mercuric chloride-HgCl(2), 12 micromol kg(-1) b.w. single intraperitoneal injection). Curcumin treatment (80 mg kg(-1) b.w. daily for 3 days, orally) was found to have a protective effect on mercury-induced oxidative stress parameters, namely, lipid peroxidation and glutathione levels and superoxide dismutase, glutathione peroxidase and catalase activities in the liver, kidney and brain. Curcumin treatment was also effective for reversing mercury-induced serum biochemical changes, which are the markers of liver and kidney injury. Mercury concentration in the tissues was also decreased by the pre/post-treatment with curcumin. However, histopathological alterations in the liver and kidney were not reversed by curcumin treatment. Mercury exposure resulted in the induction of metallothionein (MT) mRNA expressions in the liver and kidney. Metallothionein mRNA expression levels were found to decrease after the pre-treatment with curcumin, whereas post-treatment with curcumin further increased MT mRNA expression levels. Our findings suggest that curcumin pretreatment has a protective effect and that curcumin can be used as a therapeutic agent in mercury intoxication. The study indicates that curcumin, an effective antioxidant, may have a protective effect through its routine dietary intake against mercury exposure.

Evaluation of comparative effect of pre- and posttreatment of selenium on mercury-induced oxidative stress, histological alterations, and metallothionein mRNA expression in rats.

To evaluate the effect of pre- or posttreatment of selenium (6 micromol/kg b.w., single intraperitoneal injection) in mercury intoxication, rats were exposed to mercury (12 micromol/kg b.w., single intraperitoneal injection). Exposure to mercury resulted in induced oxidative stress in liver, kidney, and brain tissues. Marked changes in serum biochemical parameters together with alterations in histopathology and an induction in metallothionein-I and metallothionein-II mRNA expression in the liver and kidney were observed. Pretreatment with selenium to mercury-exposed animals had protective effect on the liver, whereas posttreatment had partial protection on restoration of altered oxidative stress parameters. In the kidney, pretreatment with selenium showed partial protection on restoration of altered biochemical parameters, whereas no protection was observed in posttreatment. The pretreatment with selenium resulted in restoration of mercury-induced metallothionein-I and metallothionein-II mRNA expression, which was completely restored in the liver whereas partial restoration was observed in the kidney. Posttreatment with selenium resulted in further induction in metallothionein-I and metallothionein-II mRNA expression in the liver and kidney. In the brain, selenium showed partial protection on alerted biochemical parameters. Results indicate that pretreatment with selenium is beneficial in comparison to posttreatment in mercury intoxication. Thus, dietary intake of selenium within safe limit may, therefore, enable us in combating any foreseen effects due to mercury exposure.

Role of vitamin E in preventing acute mercury toxicity in rat.

We have examined the effect of both pre- and post-treatment of vitamin E on mercury induced acute toxicity in rats. Mercury (12µmol/kg b.w., single intraperitoneal injection) resulted in oxidative injury and metallothionein mRNA expression together with alterations in tissue histology and accumulation of mercury in the body organs. The ameliorating potential of vitamin E (24µmol/kg b.w., single intraperitoneal injection) was observed in mercury administered rats. Our findings indicate that vitamin E provides complete protection from mercury toxicity in the liver with both pre- and post-treatments. As mercury is nephrotoxic and neurotoxic, it is interesting to note that post-treatment of vitamin E showed more protection in the kidney compared to pre-treatment. In brain tissue, partial protection was observed on oxidative stress parameters. Our results thus suggest that post-treatment with vitamin E could be more beneficial than pre- treatment in mercury intoxication.

Distribution, sources and characterization of polycyclic aromatic hydrocarbons in the sediment of the river Gomti, Lucknow, India.

Sediment samples were collected for PAHs analysis (upstream, midstream and downstream) from the bank of the river Gomti in Lucknow city, India during 2005-2007. Total concentration of the PAHs ranged from 0.068 to 3.153 microg/g dry weight. A correlation existed between the sediment organic carbon content (f(OC)) and the total PAHs concentration with a correlation coefficient (r(2)) of 0.788, suggesting that sediment organic carbon content played an important role in controlling the PAHs levels in the sediments. According to observed molecular indices, PAHs contamination in the river Gomti seems to be originated both from the high temperature pyrolytic process as well as from the petrogenic source, indicating a mixed PAH input pattern.

Lead-induced phospholipidosis and cholesterogenesis in rat tissues.

In order to investigate the effects of lead exposure on lipid metabolism, rats were exposed to 200, 300 and 400 ppm lead in their drinking water for 12 weeks. The lead exposure resulted in induction of phospholipidosis in kidney and brain of the animals. While renal phospholipidosis was accompanied with depletion of renal cholesterol, phospholipidosis in the brain was accompanied with enhanced cholesterogenesis and hypertriglyceridemia. Lead exposure also resulted in enhanced hepatic cholesterogenesis and this was accompanied with a decrease in triglyceride and phospholipid contents. While lead exposure did not affect erythrocyte phospholipids, there was a 37% increase in erythrocyte cholesterol in animals exposed to the 200 ppm lead dose. In the plasma, lead exposure resulted in a dose-dependent increase in free fatty acid concentration. Although phospholipids also decreased in the plasma as a result of lead exposure, the decrease was not dose-dependent. Lead exposure did not affect plasma and HDL cholesterol and triglyceride. A double fold increase in cholesterol/phospholipid ratio was observed in the brain of lead-exposed animals, whereas this ratio decreased in the kidney. Positive associations were observed between tissue cholesterol and phospholipids versus lead accumulation in blood, liver and kidney. In contrast however, negative associations were observed between tissue triglyceride and lead accumulation in liver and kidney. Our results suggest that induction of cholesterogenesis and phospholipidosis in tissues may be responsible for the subtle and insidious cellular effects of lead and that these cellular events may mediate the hepatotoxic, nephrotoxic and neurotoxic manifestations in lead intoxication.

Blood levels of polycyclic aromatic hydrocarbons in children of Lucknow, India.

Polycyclic aromatic hydrocarbons (PAHs) are compounds with two or more fused benzene rings produced by incomplete combustion of organic substances involved in natural and anthropogenic processes. Children are exposed to these compounds through inhalation, dietary ingestion, and, also, soil at the playground. It has been well established that PAHs have carcinogenic, mutagenic, and teratogenic effects. Considering possible health risks due to PAHs exposure among children, the present study was carried out in collaboration with the Pediatrics Department, King George's Medical University (KGMU), Lucknow, to determine its exposure in children by estimating blood PAHs levels. Due to the variable composition of PAHs mixtures emitted from different environmental sources, any single compound or metabolite may not be representative of all exposure conditions. For these reasons, the measurement of blood PAHs levels as a possible biomarker, especially of the EPA (Environmental Protection Agency, USA) priority list, has been proposed. Acenaphthylene, anthracene, phenanthrene, fluoranthene, naphthalene, pyrene, benzo(b)fluoranthene, benzo(k)fluoranthene, and benzo(a)pyrene were determined by HPLC-FD/UV. On the basis of the individual compound, the median (50th percentile) of naphthalene (19 ppb) was highest, however, benzo(a)pyrene (4.0 ppb) level was found to be lowest among all detected PAHs. The median level of total noncarcinogenic PAHs (113.55 ppb) was higher than the total carcinogenic PAHs (32.35 ppb) in blood samples of children. A significant correlation was found between period of time spent in the surrounding breathing zone of the cooking place and total noncarcinogenic PAHs (p < 0.05), while the blood carcinogenic PAHs level in children was found to be associated with lower status of their families (p < 0.05). It is speculated that there may be chances of health hazards through exposure to PAHs, those not yet declared hazardous and present at higher concentrations in the Indian environment. Further study with a larger sample size and accompanying environmental data is desired to validate the findings of this pilot study and strengthen the database of PAHs exposure in India.

Screening for mercury in aqueous environmental samples and urine samples using thin layer chromatography.

A method for screening based on thin layer chromatography (TLC) comprising silica gel 'G' as a stationary phase and benzene as a mobile phase was found to be most suitable for the detection of mercury in aqueous samples and spiked human urine, without digesting the samples. A broad range for the detection of mercury, from 20 microg/L (20 ppb) to 1000 mg/L (1000 ppm), was established, by optimizing the experimental conditions. In urine samples, mercury could be detected also, at levels as low as 50 microg/L (50 ppb) or above. Mercury was detected by complexation with dithizone followed by TLC, also in the presence of other heavy metals, including arsenic, cadmium, lead, copper, iron, zinc, and nickel. The method is simple, cheap, and has no interference of the matrix present in the natural water and aqueous industrial effluent samples obtained from the field. Further, no sophisticated instrument is needed for the detection of mercury.

Role of selenium in mercury intoxication in mice.

Studies were conducted to examine the effect of pre and post-treatment of selenium in mercury intoxication (20 micromole/ kg b.w. each given intraperitoneally) in mice in terms of lipid peroxidation (LPO), glutathione (GSH) content, activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and mercury concentration in liver, kidney and brain. No significant alteration was observed in all the organs examined after mercury or selenium treatment in LPO and GSH but administration of selenium (pre and post) resulted in an increase in the level of LPO and GSH. The activity of SOD was depleted in liver and kidney while that of GPx was lowered in liver of mercury exposed animals. Selenium administration resulted in restoration of the depletion of these enzymatic activities. The activity of CAT in liver and brain was enhanced both in mercury and selenium treated animals. Administration of selenium significantly arrested enhanced CAT activity. Kidney showed the highest mercury concentration among the organs examined. Administration of selenium resulted in further enhancement of mercury concentration in the tissues. An increase in selenium level in liver was observed after mercury treatment, which was also restored by mercury selenium co-administration. Our results indicate that the prooxidant effect of selenium was greater by its pretreatment.

Determination of total arsenic content in water by atomic absorption spectroscopy (AAS) using vapour generation assembly (VGA).

Analysis of arsenic in water is important in view of contamination of ground water with arsenic in some parts of the world including West Bengal in India and neighboring country Bangladesh. WHO has fixed the threshold for arsenic in drinking water to 10ppb (microg/l) level, hence the methodology for determination of arsenic is required to be sensitive at ppb level. Atomic absorption spectrophotometry with vapour generation assembly (AAS-VGA) is well known technique for the trace analysis of arsenic. However, total arsenic analysis [As(III)+As(V)] is very crucial and it requires reduction of As(V) to As(III) for correct analysis. As(III) is reduced to AsH3 vapours and finally to free As atoms, which are responsible for absorption signal in AAS. To accomplish this the vapour generation assembly attached to AAS has acid channel filled with 10 M HCl and the reduction channel with sodium borohydride. Further sample can be reduced either before aspiration for analysis, using potassium iodide (KI) or the sample can be introduced in the instrument directly and KI can be added in the reduction channel along with the sodium borohydride. The present work shows that samples prepared in 3 M HCl can be reduced with KI for 30 min before introduction in the instrument. Alternatively samples can be prepared in 6 M HCl and directly aspirated in AAS using KI in VGA reduction channel. The latter methodology is more useful when the sample size is large and time cycle is difficult to maintain. It is observed that the acid concentration of the sample in both the situations plays an important role. Further reduction in acid concentration and analysis time is achieved for the arsenic analysis by using modified method. Analysis in both the methods is sensitive at ppb level.