Introduction to India

Day 1:
We left for the Greenville airport at 7:30 on Thursday morning.  And didn't arrive in India until 4:00 Saturday morning.  Oh, the joys of flying.  First we had a 6 hour layover in the Dulles airport and I thought I might actually die of boredom.  Then we got diverted from landing in Chennai because a plane had skidded off the runway and they couldn't get it cleared in time.  So we took a surprise trip to Bangalore to get fuel.  And finally, 4 hours behind schedule, we landed in Chennai.  We didn't get to Madras Christian College until around 6, so we had a snack and Caitlin and I took a much needed nap.  (Which is why there are no pictures of me up yet, Megan).

After napping all morning, we wandered around campus.  We saw the trash heap.  That was lovely.  We also walked by the cricket fields and "we were so hot, we got whistled at" (quote courtesy of Caitlin).  The first of many whistles, I'm sure.  Later in the afternoon we went to a John Lennon tribute concert put on by the MCC students.  It was pretty awesome except I was so tired I almost fell asleep a few times.  And then we went to bed at 8:30 and slept for 11 1/2 hours.  "It was glorious" (also courtesy of Caitlin).  Except the bed feels like you're sleeping on a ream of paper.

Day 2:
After breakfast we all headed out to the market.  It reminded me a lot of markets in Malaysia except everything seems so much less permanent.  We saw some cows.  Traffic was scary - but kind of what I expected....crossing the street was....fun.  The best part was going in the air conditioned department store.  I forgot how awful the heat and humidity would be.  And how much I love air conditioning.  We came back from the market and Caitlin and I collapsed under the fan in our room.  In the afternoon we met our MCC "buddies" and they took us around campus.  Then we had dinner at the Principal's (aka the President of the college) house.

So to sum up: In the last two days, there's been lots of sleeping, we've taken a lot of showers, and we haven't done any homework.  Which, to borrow from Caitlin, is glorious.  

The Role of Selenium in Human Health

Humans contain roughly 20 mg of selenium distributed throughout the body (Combs, 2005).  The element is usually incorporated into proteins.  Due to the size similarities between selenium and sulfur atoms, selenium can be incorporated into amino acids, replacing the sulfur that naturally exists in sulfur-containing amino acids (Combs, 2005).  These selenoamino acids can then be integrated into a variety of proteins (Combs, 2005).  Two types of selenoamino acids exist.  Selenocysteine and selenomethionine are both incorporated into proteins, but only selenocysteine amino acids have a physiological function (Combs, 2005).  In the body selenium-containing proteins provide antioxidant protection, redox regulation, and thyroid hormone regulation (Combs, 2005).  The antioxidant properties of selenium are extremely important in counteracting diseases involving oxidative stress (Rayman, 2008).  Selenoproteins are also necessary to prevent neurological dysfunction and brainstem degeneration (Rayman, 2008).  

Selenium can play an influential role in a variety of health issues and disease states.  Studies have shown that addition of selenium in the diet can improve immune response even in healthy individuals (Rayman, 2008).  Through the use of animal models, researchers have shown that selenium supplementation may play an important role in preventing HIV from mutating to a more powerful and dangerous form, and it may be possible that supplementation is necessary because retroviruses deplete their host’s stock of selenium so they can incorporate it into their own selenoproteins (Rayman, 2008).  Selenium intake may also influence the reproductive health of men and women.  Men’s fertility can be improved and women’s risk of miscarriage and pre-eclampsia can be reduced by increasing selenium intake (Rayman, 2008).  Selenium may also have a role in the reduction of cancer risk.  Current research has suggested that selenium metabolites may prevent cancer by inducing apoptosis in cancerous cells and inhibiting tumor cell invasion (Combs, 2005; Rayman, 2008).  

The major species of selenium available in food determines what humans consume and accumulate within the body.  The available species of selenium also govern the element’s final destination and the body’s use of the element (Rayman, 2008).  For example, selenium obtained from broccoli (Se-methyl-selenocysteine) cannot accumulate in the tissues, nor does it have a significant physiological function (Rayman, 2008).  However selenomethionine which originates from cereals or yeast can accumulate in proteins and be stored for long periods of time, allowing it to be used to maintain selenium levels throughout the body (Rayman, 2008).

Selenium in humans may be derived from meat, shellfish, nuts, whole grains, beans, peas, lentils, or fortified breakfast materials (Combs, 2005).  Humans generally ingest selenium from plants.  The uptake of selenium by plants depends upon the amount present in the soil (Rayman, 2008).  The bioavailability of selenium to plants is controlled by concentration within the surrounding soil, pH and redox conditions, the amount of organic matter present, bacterial activity, and mineralogy among many other factors (Rayman, 2008).  Within the soil, selenium levels vary because organic matter, iron hydroxides, and clay minerals can bind selenium removing it from the cycle of uptake by plants (Rayman, 2008).  Additionally the particular species of selenium – determined by pH and redox conditions – present in soil affects the mobility of the element and bioavailability (Rayman, 2008).  Therefore high levels of selenium in soil do not always result in selenium-rich crops, because the element may not be present in a form that can be used by the plant (Rayman, 2008).  

Different plant species vary in the efficiency of their uptake of selenium.  Some plants that accumulate selenium in significant amounts include Brazil nuts, broccoli, cabbage, garlic, and onions, all of which can contain up to 40,000 μg Se/g dry weight (Rayman, 2008).  Cereals like wheat, oats, rye, and barley are non-accumulating crops; therefore they uptake relatively small amounts of selenium, no more than 100 μg Se/g dry weight (Rayman, 2008).  The amount of selenium present in foods varies by country and region from excessively toxic amounts to inadequate quantities.  Countries such as the United Kingdom, where selenium levels are low in plants, have begun supplementing animal feed with the element to increase human intake (Rayman, 2008).  

Humans can suffer from both a deficiency in selenium and an excessive intake of selenium.  Insufficient levels of selenium can cause cardiomyopathy, the deterioration of the heart muscle, possibly in conjunction with the mutated Coxsackie virus (Rayman, 2008).  This condition, known as Keshan disease, is mainly prevalent in north-east China, however the cardiomyopathy of some Western patients has been associated with a lack of selenium in the intravenous nutrients provided (Rayman, 2009).  Selenium toxicity is much less common than deficiency and symptoms of excessive selenium intake include hair loss, and brittle, thickened and stratified nails (Rayman, 2009).  Chronic ingestion of high levels of selenium may lead to skin rash, weakness, tingling sensation, and diarrhea (Combs, 2005).  Therefore selenium, like most nutrients must be consumed in the proper amounts or health problems could ensue.  However the determination of a recommended daily intake of selenium is difficult due to the numerous factors that influence regulation of the element (Rayman, 2009).  Advisory bodies must weigh both the benefits and the risks in order to determine an appropriate threshold level of intake.

References:

Combs, G.F. (2005) Geological Impacts on Nutrition. In Stone, D. Essentials of Medical Geology. Elsevier.

Rayman, M.P. (2008) Food-Chain Selenium and Human Health: Emphasis on Intake. British Journal of Nutrition. 100, 254-268.

Energy, Climate Change, and Health

          Energy production and use is both detrimental and beneficial to human health.  Although the availability of energy sources may provide electricity for cooking, communication, and industry, the process of producing energy can negatively affect a population through environmental pollution and hazards of the production process (Wilkinson, Smith, Joffe, and Haines, 2007).  Lack of energy security is a growing problem that, in addition to global climate change, will disproportionately affect the health of the poor, because the burden of reduced energy supply and climate change generally falls on those that are already lacking in resources (Wilkinson, et al., 2007).  For example, climate change may affect monsoon rainfall or glacial melt in India, thus changing the availability of water to populations – especially agricultural communities – that depend on it.

Due to India’s large population, the country contributes around 4% to global carbon emissions (Arora, Busche, Cowlin,  Engelmeier, Jaritz, Milbrandt, Wang, 2010).  Considering the vast number of health and environmental effects of climate change to due greenhouse gases, India has declared that it will not allow the country’s per capita greenhouse gas emissions to exceed that of an industrialized country.  Currently India emits around 1 ton of CO₂ per person compared to the 10-20 tons of CO₂ emitted per person in industrialized countries (Arora, et al., 2010).  These efforts are important when considering that the effects of climate change go beyond the immediate concerns of water, land, and air pollution.  Increasing temperatures that result from climate change may stimulate increased numbers of heat waves, which are extremely dangerous in all areas, developed or not, but especially of concern to countries where the ability to adapt to such temperature changes may be extremely restricted due to low income (Wilkinson, et al., 2007).  The world will probably also see an increase in the number of extreme weather events like severe storms, floods, and droughts (Wilkinson, et al, 2007).  Rising sea levels, a result of the melting of glaciers and expansion of the seas, will increase seawater intrusion into coastal freshwater and will result in the displacement of large coastal populations.  Additionally water, food, and vector-borne diseases might undergo changes in disease pattern and frequency (Wilkinson, et al., 2007).  

            Human energy use is almost exclusively focused on the use of fossil fuels as energy sources and there are extensive health risks associated with the extraction, production, and use of these fuels.  Of the total world energy use, about 80% is based on fossil fuels (Wilkinson, et al., 2007).  India accounts for 3.8% of the global consumption of energy, with the country’s focus being on coal and oil energy sources (Arora, et al., 2010).  

World Energy Use in 2001

Worldwide Consumption of Energy Sources by Country

Biomass fuel represents 10% of the world’s energy use and is extensively used as a traditional fuel source in developing countries (Wilkinson, et al., 2007).  Both fossil fuels and biomass contribute to substantial human health risk and the development and use of clean energy sources will be important in reducing both climate change and energy-related health hazards.  The combustion of biomass and fossil fuels results in airborne pollutants, which pose a significant risk at the household, community, regional, and global levels (Wilkinson, et al., 2007).   

Although fossil fuel combustion contributes the most to environmental pollution, the 2.4 million people worldwide who depend on biomass as a household energy source are more likely to suffer from pollution exposure due to biomass fuels (Wilkinson, et al., 2007).  In India, about 40% of the total energy supply consists of fuel such as wood and cow manure, which is mainly used in rural households for cooking and heating water since the availability of electricity in rural areas is low (Arora, et al., 2010).  Because the technology used to burn the fuel is not very advanced, a high concentration of smoke builds up indoors, often resulting in indoor air quality far worse than international standards on air pollution (Wilkinson, et al., 2007).  Chronic exposure to indoor air pollution results in a number of health issues including respiratory infections, lung and other cancers, tuberculosis, low birth weight babies, and potentially asthma and heart disease (Wilkinson, et al., 2007).  In southeast Asia, thirty-seven percent of the burden of disease can be attributed to indoor air pollution, especially among impoverished populations that cannot afford clean fuels and proper ventilation (Wilkinson, et al., 2007)

            India has begun using biogas to provide energy to small rural areas that are not connected to the grid and thus do not receive electricity.  Biogas is a product of the digestion of organic material like animal waste, crop residues, and industrial and domestic waste, a process which releases methane, a combustible gas (Arora, et al., 2010).  About four million family-size biogas-generating plants have been installed around the country and are used to provide energy for cooking and lighting in rural areas (Arora, et al., 2010).  Larger production plants can be installed to serve entire villages.  The majority of the biogas is generated from cattle manure, and given that India has 28% of the world’s cattle population, this alternative to biomass burning may be a highly useful and productive source of energy in rural areas (Arora, et al., 2010).

            There is no doubt that the development and distribution of energy sources that began during the industrial revolution has vastly improved the health of the world’s people.  However both the lack of clean energy and the climate change resulting from burning of fossil fuels can be detrimental to human health.  It is important that countries seek alternative fuel sources and improve existing energy technologies in order to ensure the health of their populations both today and for the future.

 References:

Wilkinson, P., Smith, K.R., Joffe, M., Haines, A.  (2007). A Global Perspective on Energy: Health Effects and Injustices. The Lancet 370(9591), 5-18.

Arora, D.S., Busche, S., Cowlin, S., Engelmeier, T., Jaritz, H., Milbrandt, A., Wang, S. (2010). Indian Renewable Energy Status Report.

 

The Epidemiological Transition in India

Recent evidence has emerged suggesting that developing countries are experiencing significant increases in non-communicable diseases (NCDs), especially among the poor and low-income populations (Shetty, 2002).  In developing countries about 40% of all deaths can be attributed to NCDs (Shetty, 2002).  Urban development and industrialization in these countries facilitate lifestyle and diet changes that can have a serious impact on populations that did not previously suffer from NCDs (Shetty, 2002).  India is no exception to these changes as it undergoes huge demographic transformations that vary across the states and regions.  An epidemiological transition is occurring as “complex changes in patterns of health, disease, and mortality” promote a shift from infectious diseases to non-communicable illnesses as the major driver for morbidity and mortality (Shetty, 2002).  India is currently undergoing this epidemiological transition and thus is dealing with both infectious disease at the poorest levels of society and chronic, non-communicable diseases in the upper levels of society. 

Some interesting studies have been done with migrant populations to understand the impacts that genetics and environment can have on an individual’s development of NCDs.  It has been shown that as migrants adopt the social and cultural lifestyles of their new environment, they develop disease patterns that resemble those of the local people (Shetty, 2002).  These environmental and behavioral changes may also expose pre-existing genetic disposition to certain NCDs that was not evident in the migrant’s previous lifestyle and location (Shetty, 2002).  Therefore the change in environment can have a direct impact on people who are intrinsically predisposed to have the illness.  For example, populations that have migrated to the United Kingdom from India have developed a high risk for coronary heart disease.  Despite the fact that the South Asian populations studied have plasma cholesterol levels below the national average in the UK and that their total and saturated fat intakes are no different from the national average, these people are at an increased risk for heart disease (Shetty, 2002).  This propensity to develop coronary heart disease may be due to a change in diet, lifestyle, or physical activity that occurred upon their migration to the UK (Shetty, 2002).  When ethnic populations have a disease-risk pattern that deviates from the indigenous population, it is likely that this variation is due to environmental aggravation of genetic predisposition (Shetty, 2002).  The increased risk of NCDs associated with migration is not just limited to international transitions, but may also be found in internal migration or areas undergoing urbanization (Shetty, 2002). 

Obesity and its related problems like high cholesterol are increasing in India due to the changing lifestyles and standards of living brought about by urbanization.  It is possible that malnourished children may be more at risk for obesity.  If a child undergoes several episodes of nutrient deprivation followed by rehabilitation, there may be a “discordance between linear growth and adipocyte development” that encourages the growth of fat cells at the expense of the child’s height, which is limited by the lack of nutrients (Shetty, 2002).  In addition childhood obesity is affected by decreased physical activity, especially in urban Indian cities where there is increased food intake along with an increase in sedentary lifestyles (Shetty, 2002).  Although adult obesity is less well studied, the Nutrition Foundation of India found that there were higher rates of obesity among the higher socio-economic classes and very low rates among the population living in urban slums (Shetty, 2002). 

The changing food consumption patterns in India are contributing to increasing prevalence of NCDs.  Although there has not been a significant increase in energy intake, there has been an increase in the amount of energy from fat that Indians are consuming (Shetty, 2002).  Between the years of 1975 and 1995, there was a decrease in the intake of cereal grains that was offset by the intake of milk products and animal fats (Shetty, 2002).  Traditionally pulses and legumes have been the source of protein in the Indian diet, but these animal proteins have superseded these foods (Shetty, 2002).

Chadha, Gopinath, and Shekhawat conducted a study to understand how the lifestyle, dietary, and physical activity patterns that accompany urbanization affected the prevalence of coronary heart disease in India (1997).  The study found that the prevalence of clinical coronary heart disease was 31.9 per 1,000 in urban areas compared to 5.9 per 1,000 in rural areas (Chadha, et al., 1997).  An examination of the risk factors for heart disease – hypertension, diabetes, obesity, family history, and smoking – shows that they follow the same pattern of high prevalence in urban areas (Chadha, et al., 1997). Sodium and alcohol consumption were also higher in urban than rural areas (Chadha, et al., 1997). 

The high rates of coronary heart disease risk factors in urban areas are most likely due to a sedentary lifestyle (Chadha, et al., 1997).  In contrast, rural men and women are more likely to be involved in the physical labor of agriculture (Chadha, et al., 1997).  A study cited by Chadha et al. found that urban populations were 2.5 times more likely to have coronary heart disease than rural populations (1997).  Chadha et al. also attribute the prevalence of coronary heart disease in urban populations to the considerable air pollution present in cities.  Pollutants like oxides of nitrogen, sulfur dioxide, and suspended particles are strong inducers of the buildup of fats and cholesterol in arteries (Chadha, et al. 1997).  This study of the increased prevalence of heart disease in urban areas is one example of the epidemiological transition occurring in India.  As more of the country urbanizes and populations change their lifestyles, there will be an increasing number of individuals suffering from chronic, non-communicable diseases, like heart disease.  

References:

Chadha, S.L., Gopinath, N., & Shekhawat, S. (1997). Urban-Rural Differences in the Prevalence of Coronary Heart Disease and its Risk Factors in Delhi. Bull. World Health Org. 76(1): 31-38. 

 

Shetty, P.S. (2002). Nutrition Transition in India. Public Health Nutrition 5(1A): 175-182. 

Nitrate Toxicity in Humans - Methemoglobinemia

Drinking water that contains high levels of nitrates can be toxic to humans.  Nitrate present in the environment comes from a variety of sources: 25% is derived from the atmosphere, while the rest comes from the geology of the area and human activities such as fertilizer use and ejection of sewage and industrial waste into water sources (Gupta, Gupta, Chhabra, Eskiocak, Gupta, and Gupta, 2008).  The nitrates present in humans result from consumption of meat, nitrate-rich vegetables and fruits, and water, but nitrate may also be produced by endogenous pathways (Gupta, et.al., 2008).   Excessive intake of nitrate is toxic to humans and may result in any number of health issues, including cancer, chronic diarrhea, detrimental changes in the respiratory and cardiovascular systems, and other effects (Gupta, et.al., 2008).

Consumption of excessive amounts of nitrates can also result in a condition known as methemoglobinemia, which starves the body’s tissues of oxygen.  As the body processes nitrate (NO₃^-), it is reduced to nitrite (NO₂^-) (Gupta, Gupta, Seth, Gupta, Bassin, and Gupta, 1999).  Therefore nitrate’s toxic effect depends on the amount present in potable water and on the reducing conditions present in an individual’s body (Gupta, et.al., 1999).  The reduction of nitrate is facilitated by bacteria that require a high stomach pH (pH greater than 4) in order to grow (Gupta, et.al., 2008).  Nitrate is reduced to nitrite in the oral cavity and intestinal tract, and upon reentering the bloodstream is converted back to nitrate (Gupta, et.al., 2008; Gupta et.al., 1999).  The process of converting nitrite in the blood back to nitrate directly oxidizes the ferrous ion (Fe²⁺) of hemoglobin to a ferric ion (Fe³⁺) to create methemoglobin (Gupta, et.al., 1999).  The image below shows the structure of hemoglobin, with the red and blue areas representing the different subunits of the protein.  The green structures represent heme groups, which contain the iron involved in the process described above.  The normal function of hemoglobin is to carry oxygen to various tissues throughout the body (Dugdale, 2010). 

The structure below is the most common type of heme group.

Methemoglobin has the same structure as that of hemoglobin.  The only exception is that the iron exists in a different oxidation state.  Upon oxidation to methemoglobin, the body naturally restores the hemoglobin through a process involving cytochrome b₅, an electron transport protein, as shown in the reaction below where Hb³⁺ is methemoglobin and Hb²⁺ is hemoglobin (Gupta, et.al., 1999).

 The enzyme cytochrome-b₅ reductase then restores the oxidized cytochrome b₅ to its original state (Gupta, et.al. 1999).  

In summary, ingested nitrate is converted to nitrite, which is then converted back to nitrate and in the process oxidizes hemoglobin to methemoglobin.  The methemoglobin is restored to hemoglobin by the protein cytochrome b₅.  Finally the cytochrome-b₅ reductase enzyme returns the now oxidized cytochrome b₅ to its previously reduced state.

In cases where nitrate levels are too excessive or the cytochrome-b₅ reductase system is weakened, the cytochrome-b₅ reductase enzyme reserves become exhausted and methemoglobin accumulates in appreciable levels in the blood (Gupta, et.al., 2008). The presence of high concentrations of methemoglobin in the blood can prevent oxygen from being delivered properly to tissues. When more than 10% of hemoglobin is present as methemoglobin, blue discoloration of the skin is evident, and if greater than 60% of hemoglobin has been oxidized, death results (Gupta, et.al., 1999).

Gupta, et.al. reported that the cytochrome-b₅ reductase system is able to accommodate and reduce amounts of methemoglobin in the blood until the levels of nitrate in drinking water reach about 95 mg/L (1999).  The activity of cytochrome-b₅ reductase then declines until it returns to normal levels at around 200 mg/L of nitrate in drinking water (Gupta, et.al., 1999).  This decline in cytochrome-b₅ reductase activity is correlated with an increase in nitrate concentration in the water and methemoglobin concentration in the blood (Gupta, et.al., 1999).  The enzyme’s ability to compensate for increasing levels of nitrate worked best for children age one to eighteen (Gupta, et.al., 1999).  Infants and adults in this study had poor cytochrome-b₅ reductase response to increasing levels of nitrate and methemoglobin, which may be due to the incomplete development of the reductase system in infants or a saturation of the system in adults (Gupta, et.al., 1999). Infants are also more likely to be affected by nitrate due to a higher stomach pH, which encourages growth of nitrate-reducing bacteria (Gupta, et.al., 2008).   

The World Health organization sets the maximum limit of nitrate ion in drinking water at 50 mg/L (Gupta, et.al., 1999).  The Bureau of Indian Standards sets the limit slightly lower at 45 mg/L (Gupta, et.al., 1999).  Despite the intentions of these regulatory institutions, people in India are still frequently exposed to levels of up to 500 mg/L of nitrate in their drinking water (Gupta, et.al., 1999).  The populations most affected by methemoglobinemia are infants and people older than 45 years (Gupta, et.al., 2008). 

Cleaning up the extremely high levels of nitrates present in drinking water is expensive and not cost-efficient (Gupta, et.al., 2008).  Since this is the case, governments need to focus on solutions that will decrease anthropogenic contributions to natural nitrate levels in water.  The use of nitrogen containing fertilizers should be reduced to keep too many nitrates from washing into drinking water sources (Gupta, et.al., 2008).  Individuals should also limit the use of antacids, as this will raise stomach pH and encourage the growth of nitrate-reducing bacteria (Gupta, et.al., 2008).  Governments must also focus on educating people on the health effects that can result from excessive nitrate consumption (Gupta, et.al., 2008).  Gupta, et.al. recommend that additional research needs to be done to better understand the toxicity of nitrate compounds and what levels of nitrate are safe for drinking water (2008).

           

References:

Gupta, S.K., Gupta, R.C., Chhabra, S.K., Eskiocak, S., Gupta, A.B., and Gupta, R. (2008). Health Issues Related to N Pollution in Water and Air. Current Science. 94(11): 1469-1477).

Gupta, S.K., Gupta, R.C., Seth, A.K., Gupta, A.B., Bassin, J.K., and Gupta, A. (1999). Adaptation of Cytochrome-b₅ Reductase Activity and Methaemoglobinaemia in Areas with a High Nitrate Concentration in Drinking-water.  Bull. WHO. 77(9): 749-753.

Dugdale, D.C. (2010). Hemoglobin. Medline Plus. http://www.nlm.nih.gov/medlineplus/ency/article/003645.htm

Image Sources:

http://en.wikipedia.org/wiki/Hemoglobin

http://en.wikipedia.org/wiki/Heme

Arsenic Contaminated Groundwater in West Bengal and Bangladesh

The presence of high levels of arsenic in the groundwater of West Bengal and Bangladesh has become a very serious health problem.  Recently there has been increased use of groundwater sources in an attempt to reduce the infectious diseases that result from bacteria-laden surface water (Sarkar 2009). Unfortunately the underground aquifers that supply this water for agriculture and domestic use are contaminated with arsenic.  When consumed over long periods of time, low levels of arsenic found in water and food can cause skin disorders, cancer, and cardiovascular disease (Dissanayake, Rao, and Chandrajith, 2010).  The World Health Organization recommends that drinking water contain less than 10 μg/L of arsenic, but arsenic concentration in the wells of West Bengal and Bangladesh is frequently above this level (Sarkar).  About half of the hand pumps and irrigation wells in these areas are contaminated (Sarkar).  In West Bengal, 95% of people extract their drinking water from the ground (Sarkar).  In the Murshidabad district of West Bengal 73% of irrigation wells and 62% of domestic wells are contaminated (Sarkar).  In Bangladesh only 20% of wells are characterized as arsenic free, and 97% of the population relies on 8.6 million tube wells, so the availability of clean drinking water is paramount (Dissanayake, Rao, and Chandrajith).

Potable water and food grown with arsenic contaminated water are the main sources of arsenic poisoning (Sarkar).  Food consumption accounts for 20-40% of human arsenic intake, with rice and vegetables grown underground being the most susceptible to retaining high levels of arsenic (Sarkar).  Because rice is a major dietary staple in these areas, arsenic poisoning is a wide-reaching problem.  Arsenic is even found in processed foods, because the manufacturing plants use groundwater without filtering it to remove the arsenic (Sarkar).  I thought this was an interesting example of the omnipresent character of water.  It affects our lives in countless ways, some obvious and some not.  Sarkar reported that studies have found a link between poor nutrition and the effect of arsenic intake.  Poor people who are unable to eat protein and nutrient rich foods are more likely to be affected by arsenic than the rich who can eat more protein, legumes, vegetables, and fruits (Sarkar).  The poor also suffer because they cannot afford the technology to filter the harmful substance out of their drinking water and because they do not receive adequate health care.  

Most arsenic found in groundwater naturally accumulates within the sediment of the aquifer (Dissanayake, Rao, and Chandrajith).  The arsenic in West Bengal and Bangladesh is thought to have originated in the rock formations of the Himalayas (Dissanayake, Rao, and Chandrajith).  It was probably transported via sedimentary particles traveling in rivers originating in the Himalayas, before settling in the aquifer (Dissanayake, Rao, and Chandrajith).  I found it really interesting and somewhat counterintuitive that the spatial distribution of arsenic within an aquifer can vary widely.  Normally I would expect the arsenic to be equally concentrated throughout the aquifer, but in reality water may have areas of very high arsenic concentration surrounded by spaces where low to no arsenic is present (Dissanayake, Rao, and Chandrajith).     

The aspect of this issue that most interested me was the mechanism of arsenic release within contaminated aquifers.  Generally arsenic within these wells exists in a form where it is adsorbed onto the surface of iron oxyhydroxide (FeOOH), which coats sedimentary particles (Nickson, McArthur, Ravenscroft, Burgess, Ahmed, 2000).  The reductive dissolution of arsenic-rich FeOOH is driven by bacteria, which degrade sedimentary organic matter (Nickson, et.al.).  In the degradation process bacteria consume dissolved oxygen and this loss of oxygen in the water produces a reducing environment (Nickson, et.al.).   Arsenic and iron are reduced and released to groundwater.  However, microbiological mediated reduction of iron oxyhydroxide only occurs after reducing conditions are reached and all free molecular oxygen and NO₃^-, which are more easily reduced than iron or arsenic, is reduced (Nickson, et.al.).  

Observable relationships between substances involved in this process allowed the authors to show that their proposed mechanism and conditions required for arsenic reduction were likely to accurately reflect the true arsenic release process. Water with high levels of dissolved oxygen has low levels of free arsenic (< 50 μg/L) because the presence of oxygen creates an oxidizing environment, and the arsenic remains adsorbed to the iron oxyhydroxide (Nickson, et.al.).  Only when bacteria consume the oxygen present does the system become a reducing environment.   

Wells with high levels of NO₃^- and almost no detectable amounts of dissolved arsenic indicate that reduction of arsenic and iron must not take place until the more easily reduced nitrate ions are removed from the system (Nickson, et.al.).

The reduction-oxidation reaction for this process (shown below) shows that bicarbonate ions are produced thus explaining why the concentration of bicarbonate ions is positively correlated to the concentration of arsenic in the well (Nickson, et.al.)

Although iron is also released in this process, Fe²⁺ levels are poorly coordinated to arsenic levels because the free iron tends to participate in further reactions (Nickson, et.al.).  

             There are many proposed solutions to the issue of arsenic contamination.   Nickson et.al. suggest that because dissolved arsenic is so closely associated with the presence of dissolved iron, it may be possible to remove arsenic by the aeration of iron rich water, which will precipitate FeOOH (Nickson, et.al.)  The precipitation of iron oxyhydroxide co-precipitates some of the arsenic from solution, so that it returns to an adsorbed state (Nickson, et.al.).  The solid could then be removed from the drinking water.  Other suggestions include placing shallow wells closer to the surface within a range that will maintain oxidizing conditions so that arsenic release is less likely (Dissanayake, Rao, and Chandrajith).  Sarkar recommends a long-term goal encompassing the reduction of groundwater dependence through better water management.  To provide safe drinking water in the short term, communities should consider investing in arsenic filters, although these require long-term maintenance and toxic waste disposal (Sarkar).  In addition to shallow wells, deep bore wells that draw water from below the level of arsenic contamination might be implemented (Sarkar; Dissanayake, Rao, and Chandrajith).  Other methods include collection of rainwater and filtration of river water (Sarkar).  Regardless of the solution chosen, government involvement in water management and community awareness and initiative are crucial to providing clean drinking water to these areas.

References: 

Dissanayake, C. B., Rao, C. R. M., and Chandrajith, R., (2010). Some Aspects of the Medical Geology of the Indian Subcontinent and Neighboring Regions. In Selinus, O., Finkelman, R. B., and Centeno J. A., (Eds.). Medical Geology: A Regional Synthesis. Springer.

Nickson, R.T., McArthur, J.M., Ravenscroft, P., Burgess, W.G., Ahmed, K.M. (2000). Mechanism of Arsenic Release to Groundwater, Bangladesh and West Bengal. J Appl Geochem. 15(4): 403-413.

Sarkar, A. (2009). Sustainable Solutions to Arsenic Contamination of Groundwater: The Ganga-Maghna-Brahmaputra Basin. In Pascual, U., Shah, A., and Bandyopadhyay, J., (Eds.). Water, Agriculture, and Sustainable Well-Being.