Monthly Archives: December 2014

Whole Foods Market Voluntarily Recalls Cut, Wrapped and Weighed Bleating Heart-Brand Cheeses in Arizona, California and Hawaii Because of Possible Health Risk

Whole Foods Market is recalling cheese sold in Arizona, California and Hawaii that came from its supplier Bleating Heart Cheeses because it has the potential to be contaminated with Listeria monocytogenes, an organism which can cause serious and sometimes fatal infections in young children, frail or elderly people, and others with weakened immune systems. Although healthy individuals may suffer only short-term symptoms such as high fever, severe headache, stiffness, nausea, abdominal pain and diarrhea, Listeria infection can cause miscarriages and stillbirths among pregnant women.

Oak Ridge officials are puzzled by failure of targets at Spallation Neutron Source

Oak Ridge National Laboratory’s Spallation Neutron Source, the premier source of pulsed experimental neutrons in the world, has been operating at reduced power due to the premature back-to-back failures of two of the target vessels that are the source of the facility’s experimental neutrons. Now down to a single spare target, the SNS will continue to operate at a reduced power level of 850 kW until April, soon after a new target is delivered, says Kevin Jones, SNS operations manager. At full power, the SNS operates at more than 1 MW.

Title: In Search of “Just Right”: The Challenge of Regulating Arsenic in Rice

Charles W. Schmidt, MS, an award-winning science writer from Portland, ME, has written for Discover Magazine, Science, and Nature Medicine.

Background image: © Koji Kitagawa/amanaimages/Corbis

About This Article open

Citation: Schmidt CW. 2015. In search of “just right”: the challenge of regulating arsenic in rice. Environ Health Perspect 123:A16–A19;

News Topics: Agriculture and Farming, Arsenic, Diet and Nutrition, Drinking Water Quality, Food Safety and Regulation, Laws, Regulations, and Policy, Risk Assessment, Soil Pollution, Standards

Published: 1 January 2015

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White and brown riceA regulation that’s too high may not adequately protect health, and a regulation that’s too low could be infeasible for producers to achieve.

© 145/Steve Outram/Ocean/Corbis

Rice, a dietary staple for millions of people around the world, is often contaminated with arsenic, a naturally occurring element in soils that can cause cancer and other health effects.1 Although other foods also contain arsenic, rice is unusually efficient at absorbing this element from soil; it can absorb up to 10 times more arsenic than other crops, such as wheat.2 Moreover, rice flour and syrup are used in many processed foods, including baby foods, so exposures aren’t limited to people eating the grain itself. It’s estimated that 95% of the average arsenic intake among Europeans comes from food, and half of that comes from rice and rice products.3 And in areas with high levels of arsenic in well water, the exposures via water and rice add up to a toxic double whammy.3

Mounting worries over arsenic in rice are now prompting calls for regulation. “We need to set strict standards for rice that will be meaningful in terms of reducing arsenic exposure through the diet,” says Andrew Meharg, a professor of biological sciences at Queens University Belfast in Ireland. “This is imperative to protect people with high rice consumption, including virtually all children, people living in South Asia, and those who eat a lot of rice for health reasons, such as gluten intolerance.”

But regulating a naturally occurring element in such a widely eaten food is no easy task. Arsenic levels can vary widely in rice from different countries and states, and among different rice cultivars, according to Aaron Barchowski, a professor of environmental and occupational health at the University of Pittsburgh. This raises difficult questions about how a regulated standard could be monitored and enforced.

Assessing the Threat

The U.S. Environmental Protection Agency (EPA) currently designates arsenic as a nonthreshold carcinogen, meaning that any dose, no matter how small, carries some cancer risk.4 Some scientists don’t agree—they say doses below a certain threshold won’t cause cancer, a debate that has yet to be resolved.5

In another area of uncertainty, Michael Crupain, director of food safety testing at the testing group Consumer Reports (CR), notes that scientists have not documented elevated rates of bladder and lung cancer—the more lethal malignancies with which arsenic in well water is most often associated6—in countries where rice is commonly eaten in large amounts. “Carefully designed studies investigating this question need to be conducted,” he says.

However, studies also reveal associations between arsenic and numerous health effects, including cardiovascular disease,7 lung disease,8 and impaired cognitive function,9 among many others. Barchowski explains that arsenic in small amounts stresses cells, making them prone to maladaptive reactions that promote disease over time.

Children in particular appear to be uniquely sensitive to low doses of arsenic.10 Investigators in both rural Bangladesh and the United States, for instance, have shown that fetal exposure to arsenic is associated with respiratory infections and diarrhea during infancy and early childhood.10,11,12

Moreover, cross-sectional epidemiological studies in Bangladesh and in Taiwan have connected early arsenic exposures with neuro­behavioral problems in school children and adolescents.1

While people can be assumed to drink water from the same well on a consistent basis, the amounts of arsenic ingested from food can be far more difficult to quantify, according to Habibul Ahsan, a professor of health studies, medicine, and human genetics at the University of Chicago. Dietary effects vary by whether the arsenic is organic or inorganic (the latter being more toxic) and by the amounts of arsenic in a given food, he says, and the absorption of arsenic from the gut into the bloodstream also varies by food type.

Barchowsky points out that rice and rice products contain many nutrients—for example, B vitamins and selenium—that can protect against the toxic effects of arsenic.13,14 “This greatly complicates assessing the real risk of eating rice with arsenic in it and is a point that is not raised often enough,” he says. “Eating a healthy balanced diet reduces risk.”

Moving toward a Standard

The U.S. Food and Drug Administration (FDA) has spent years grappling with the issue of arsenic in rice. It’s currently in the midst of a health risk assessment that officials say would help form the scientific basis for any future regulation. The agency currently advises parents to consider diversifying the grains they feed their infants and toddlers, and encourages all consumers to read products labels for rice-based ingredients, and to consume a variety of grains.15

In the meantime, Codex Alimentarius, a body coordinated by the Food and Agriculture Organization of the United Nations (FAO) and the World Health Organization (WHO) that develops international food standards, has proposed a maximum level of 0.2 mg/kg for inorganic arsenic specifically in white (or polished) rice.16 However, Codex recommendations are nonbinding—countries can adopt and enforce them at their own discretion. And some critics say the proposed rice standard, which was announced in July 2014, isn’t protective enough.

White rice makes up 79% of the international market.16 but the highest arsenic levels are consistently found in brown rice. That’s because rice kernels concentrate arsenic in the thin outer layer that gives brown rice its color and is removed to produce white rice.17 Organic brown rice syrup, a popular sweetener often touted as a healthier alternative to high-fructose corn syrup,18 has been found to contain a similar range of arsenic levels as brown rice grain.19

According to Angelika Tritscher, the coordinator for risk assessment and management with the WHO Department of Food Safety in Geneva, Codex attempted to set a standard for brown rice and proposed a value of 0.4 mg/kg, but could not reach agreement because of insufficient data on arsenic levels in brown rice occurring globally. The discussion of such a standard will be continued at the next meeting of the Codex Committee on Contaminants in food in March 2015.

Finding the Right Balance

Both the EPA and the WHO have adopted maximum limits of 10 µg/L for in­organic arsenic in drinking water.20,21 However, most countries do not currently regulate arsenic in rice. The European Union—which sets centralized food safety standards for its member countries—has come out in favor of the Codex white rice standard, but it has yet to endorse it as law.22 According to Meharg, the European Union also plans to adopt a value of 0.1 mg/kg that would be specific to inorganic arsenic in rice-based baby food.

Codex based its white rice standard on sampling data collected from ten countries in Europe, North America, and Asia. The intent was to set a level that would reduce arsenic exposure but that wouldn’t be so low that most countries wouldn’t be able to meet it. Otherwise, Tritscher explains, “The limit [would have been] hypothetical, with no practical relevance.” And the essential requirement for any arsenic regulation, she says, is that it can be enforced. Codex is developing additional guidance to help producers meet the standard.

Maximum inorganic arsenic levels in the submitted samples ranged between 0.16 and 1.8 mg/kg, but the mean values were all below 0.2 mg/kg.23 Thus, the 0.2-mg/kg value was selected in part because of its feasibility, with a relatively low exceedance rate of 2%. The official language used by Codex to describe the standard is that it is “a maximum level deemed to be as low as reasonably achievable.”24

That the standard is achievable is borne out by other sampling data. In 2012, for instance, CR tested 223 samples of rice and rice products purchased in the United States and found nearly all of them were below 0.2 mg/kg.25 The next year the FDA published an analysis of more than 1,300 samples26 and concluded that “the amount of detectable arsenic is too low in the rice and rice product samples to cause any immediate or short-term adverse health effects.”15 The next step, the agency said, is to learn more about the impact of long-term, low-dose exposures.15

Not Quite There

Meanwhile, the proposed Codex standard has come under attack by those who say it has no basis in health risk assessment. Meharg, for instance, champions a lower value of 0.1 mg/kg for all rice products, and an even lower value for products targeted at young children and babies, where he believes that 0.05 mg/kg is readily achievable. And Consumers Union (CU), the policy and advocacy arm of CR, has called on the FDA to adopt a standard of 0.12 mg/kg for both white and brown rice and rice products.27

Michael Klein, a spokesman for the Arlington, Virginia–based USA Rice Federation, agrees with how the Codex standard was derived. Setting it too low, he says, would have “wiped out the rice industries in some countries.”

But Meharg disagrees. “The standard should protect people’s lives and health, and as it is now, it doesn’t do that,” he says. “It gives no incentive to change agricultural practices or processing, and it justifies the status quo.”

According to Crupain, CU’s proposed standard of 0.12 mg/kg is based on a health risk assessment that assumes a nonthreshold dose response for cancer. “While it isn’t a threshold for safety, it does provide a reasonable and feasible starting place for a standard,” he says. He also says data from the FDA and CR indicate almost 90% of white rice and 28% of brown rice in the United States could meet this standard.

Other Solutions

The goal of reducing arsenic exposures from rice doesn’t lend itself to easy solutions. In a new report CR recommends that people limit their weekly rice consumption to just over 1 cup (uncooked) of rice produced in areas with lower detected levels of arsenic—specifically basmati rice from India, Pakistan, and California, and sushi rice from the United States.28 For rice from areas with higher arsenic levels, CR recommends limiting consumption to about half that amount for adults and one-quarter that amount for children.28

Scientists are also exploring other options that include breeding arsenic resistance into rice plants—some rice varieties absorb less arsenic than others, and studies so far suggest these traits can be successfully cross-bred into progeny.29 Soils can be inoculated with microbes that act to slow arsenic uptake through the roots, and likewise, rice can be genetically engineered in ways that prevent arsenic uptake, adds Barry Rosen, a professor of cellular biology and pharmacology at Florida International University. Rosen recently developed a transgenic rice plant that can methylate inorganic arsenic into less toxic organic forms.30 He says a commercially viable cultivar is still decades away.

Asked if genetic engineering poses acceptable solutions, Tritscher says, “We need to keep an open mind. … I would not exclude any reasonable option for improving the situation of arsenic in rice. But the safety of any new technology or agricultural procedure needs to be assessed first.”

Klein of the Rice Association is more skeptical. “Posed with a choice between [genetically engineered] rice and rice with arsenic in it, consumers may decide they just aren’t going to eat any rice,” he says. “And we think the nutritional benefits of eating rice outweigh the risk of exposure to trace amounts of arsenic.”

But simply avoiding rice isn’t feasible for people around the world who rely on the grain as a daily staple. Reducing their intake demands more fundamental changes in how rice is grown and processed—changes that likely won’t be undertaken until regulated standards compel them.


1. FAO and WHO. Safety Evaluation of Certain Contaminants in Food. Prepared by the Seventy-Second Meeting of the Joint FAO/WHO Expert Committee on Food Additives (JECFA). WHO Food Additives Series: 63. FAO JECFA Monographs 8. Rome, Italy:Food and Agriculture Organization of the United Nations; Geneva, Switzerland:World Health Organization (2011). Available: [accessed 19 December 2014].

2. Williams PN, et al. Greatly enhanced arsenic shoot assimilation in rice leads to elevated grain levels compared to wheat and barley. Environ Sci Technol 41(19):6854–6859 (2007); doi: 10.1021/es070627i.

3. EFSA Panel on Contaminants in the Food Chain (CONTAM). Scientific opinion on arsenic in food. EFSA J 7(10):1351 (2009); doi: 10.2903/j.efsa.2009.1351.

4. EPA. Integrated Risk Information System—arsenic, inorganic (CASRN 7440-38-2) [website]. Washington, DC:U.S. Environmental Protection Agency (updated 31 October 2014). Available: [accessed 19 December 2014].

5. Cohen SM, et al. Evaluation of the carcinogenicity of inorganic arsenic. Crit Rev Toxicol 43(9):711–752 (2013); doi: 10.3109/10408444.2013.827152.

6. NRC. Arsenic in Drinking Water: 2001 Update. Washington, DC:National Academies Press (2001). Available: [accessed 19 December 2014].

7. Moon KA, et al. Association between low to moderate arsenic exposure and incident cardiovascular disease. A prospective cohort study. Ann Intern Med 159(10):649–659 (2013); doi: 10.7326/0003-4819-159-10-201311190-00719.

8. Parvez F, et al. Arsenic exposure and impaired lung function. Findings from a large population-based prospective cohort study. Am J Respir Crit Care Med 188(7):813–819 (2013); doi: 10.1164/rccm.201212-2282OC.

9. Wasserman GA, et al. A cross-sectional study of well water arsenic and child IQ in Maine schoolchildren. Environ Health 13:23 (2014); doi: 10.1186/1476-069X-13-23.

10. Raqib R, et al. Effects of in utero arsenic exposure on child immunity and morbidity in rural Bangladesh. Toxicol Lett 185(3):197–202 (2009); doi: 10.1016/j.toxlet.2009.01.001.

11. Farzan SF, et al. In utero arsenic exposure and infant infection in a United States cohort: a prospective study. Environ Res 126:24–30 (2013); doi: 10.1016/j.envres.2013.05.001.

12. Rahman A, et al. Arsenic exposure in pregnancy increases the risk of lower respiratory tract infection and diarrhea during infancy in Bangladesh. Environ Health Perspect 119(5):719–724 (2011); doi: 10.1289/ehp.1002265.

13. Argos M, et al. Dietary B vitamin intakes and urinary total arsenic concentration in the Health Effects of Arsenic Longitudinal Study (HEALS) cohort, Bangladesh. Eur J Nutr 49(8):473–481 (2010); doi: 10.1007/s00394-010-0106-y.

14. Chen Y, et al. Arsenic exposure at low-to-moderate levels and skin lesions, arsenic metabolism, neurological functions, and biomarkers for respiratory and cardiovascular diseases: review of recent findings from the Health Effects of Arsenic Longitudinal Study (HEALS) in Bangladesh. Toxicol Appl Pharmacol 239(2):184–192 (2009); doi: 10.1016/j.taap.2009.01.010.

15. FDA. FDA Statement on Testing and Analysis of Arsenic in Rice and Rice Products. Silver Spring, MD:U.S. Food and Drug Administration (2013). Available: [accessed 19 December 2014].

16. Codex Alimentarius Commission. Report of the Eighth Session of the Codex Committee on Contaminants in Food; The Hague, The Netherlands; 31 March–4 April 2014. Rep14/CF. Rome, Italy:Food and Agriculture Organization of the United Nations; Geneva, Switzerland:World Health Organization (2014). Available: [accessed 19 December 2014].

17. Meharg AA, et al. Speciation and localization of arsenic in white and brown rice grains. Environ Sci Technol 42(4):1051–1057 (2008); doi: 10.1021/es702212p.

18. Jackson BP, et al. Arsenic, organic foods, and brown rice syrup. Environ Health Perspect 120(5):623–626 (2012); doi: 10.1289/ehp.1104619.

19. Signes-Pastor AJ, et al. Arsenic speciation in Japanese rice drinks and condiments. J Environ Monit 11(11):1930–1934 (2009); doi: 10.1039/B911615J.

20. EPA. Arsenic rule [website]. Washington, DC:U.S. Environmental Protection Agency (updated 12 August 2014). Available: [accessed 19 December 2014].

21. WHO. Guidelines for Drinking-Water Quality—Volume 1: Recommendations. Third Edition, Incorporating First and Second Addenda. Geneva, Switzerland:World Health Organization (2008). Available: [accessed 19 December 2014].

22. European Union. European Union Comments for the Codex Committee on Contaminants in Food, 8th Session, Agenda Item 6. Proposed Draft Maximum Levels for Arsenic in Rice (Raw and Polished Rice). The Hague, The Netherlands, 31 March–4 April 2014. Brussels, Belgium:European Union (17 March 2014). Available: [accessed 19 December 2014].

23. Codex Alimentarius Commission. Proposed Draft Maximum Levels for Arsenic in Rice (at Step 3). CX/CF 12/6/8. Rome, Italy:Food and Agriculture Organization of the United Nations; Geneva, Switzerland:World Health Organization (2012). Available: [accessed 19 December 2014].

24. Codex Alimentarius Commission. Proposed Draft Maximum Levels for Arsenic in Rice (Raw and Polished Rice). CX/CF 14/8/6. Rome, Italy:Food and Agriculture Organization of the United Nations; Geneva, Switzerland:World Health Organization (2014). Available: [accessed 19 December 2014].

25. Consumer Reports. Results of our tests of rice and rice products. Consumer Reports, online edition (November 2012). Available: [accessed 19 December 2014].

26. FDA. Analytical Results from Inorganic Arsenic in Rice and Rice Products Sampling, September 2013. Silver Spring, MD:U.S. Food and Drug Administration (2013). Available: [accessed 19 December 2014].

27. Consumers Union. CU Letter to the FDA Regarding Arsenic in Rice [website]. Yonkers, NY:Consumers Union (20 September 2012). Available: [accessed 19 December 2014].

28. Consumer Reports. Report: Analysis of Arsenic in Rice and Other Grains. Executive Summary. Yonkers, NY:Consumer Reports (2014). Available: [accessed 19 December 2014].

29. Norton GJ, et al. Variation in grain arsenic assessed in a diverse panel of rice (Oryza sativa) grown in multiple sites. New Phytol 193(3):650–664 (2012); doi: 10.1111/j.1469-8137.2011.03983.x.

30. Meng X-Y, et al. Arsenic biotransformation and volatilization in transgenic rice. New Phytol 191(1):49–56 (2011); doi: 10.1111/j.1469-8137.2011.03743.x.

Title: The WASH Approach: Fighting Waterborne Disease in Emergency Situations

Refugees collect water from a public tap stand in an Adjumani settlement. 
© Wendee Nicole

Rhino Camp, Arua District. Refugees in Uganda live on land donated by Ugandan nationals. Refugee families are given plots on which they can build temporary shelters and grow crops.
© Wendee Nicole

Oxfam staff members Tim Sutton (left) and Pius Nzuki Kitonyi (right) with the soon-to-be-repaired water pump in Adjumani. In disaster-affected situations, Oxfam takes a lead in delivering WASH-related services.
© Wendee Nicole

Hand-operated water pumps are a reliable source of precious water but require physical labor to get the water flowing.
© Wendee Nicole

The Swahili caption of this poster reads “How our water becomes contaminated.” This and other educational materials are available in multiple versions, customized for the various regions where open defecation is commonplace, including Africa, Latin America, the Caribbean, and South, South East, and South West Asia.
Source: Centre for Affordable Water and Sanitation Technology /

The foot-operated “tippy tap” provides a low-cost, low-tech, hands-free handwashing station.
© Wendee Nicole

Latrines can be a drastic and unwelcome departure for people who are accustomed to defecating in the open, and the public health benefits are not necessarily easy to sell.
© Wendee Nicole

The children of Rhino Camp celebrated Global Handwashing Day with songs, demonstrations, and a parade.
© Wendee Nicole

Background image: © Wendee Nicole

Wendee Nicole has written for Discover, Scientific American, and other magazines.

About This Article open

Citation: Nicole W. 2015. The WASH approach: fighting waterborne diseases in emergency situations. Environ Health Perspect 123:A6–A15;

News Topics: Community Health, Disaster Response, Drinking Water Quality, Infectious Disease, Infrastructure, International Environmental Health, Microbial Agents, Sanitation, Warfare and Aftermath, Water Pollution

Published: 1 January 2015

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To report this story, Wendee Nicole visited two refugee settlements in Northern Uganda, Arua District’s Rhino Camp and the settlements of Adjumani District. She celebrated Global Handwashing Day 2014 with dozens of young children at Rhino Camp.

“No water!” a young mother with short cornrowed hair says in her limited English, a worried look etched in her brow. She points to the spigots, dripping with the scant water remaining in the pipes.

It’s a sweltering October day just 3 degrees north of the Equator in Northern Uganda’s Adjumani District, where a dozen children and a handful of women have gathered at the public tap stand with their 20-liter jerrycans. They are among nearly 600,000 refugees who have walked hundreds of miles from South Sudan to neighboring countries, fleeing violence that began in December 2013.1 More than 66,000 men, women, and children have settled here, in camps in Adjumani District, with over 15,000 more in Arua District’s Rhino Camp.2

The tap stand has six spigots that, until a few days ago, supplied an ample supply of fresh water. “It was producing 140,000 liters of clean water, but two weeks ago the pump malfunctioned,” explains Tim Sutton, Oxfam’s WASH (Water, Sanitation, and Hygiene Promotion) interim team leader for the Adjumani and Arua settlements. Working under the aegis of the United Nations High Commission on Refugees (UNHCR) and Uganda’s Office of the Prime Minister Department of Refugees, Oxfam installed an electric generator in June 2014 that provides water for two of six refugee settlements in Adjumani District.

Although the refugees can still get water from hand-operated pumps on other boreholes, accessing them requires walking further distances and physical labor to prime the pump. Sutton reassures the young mother, his own brow furrowed with concern, “We are working on it.”

Sutton, who has engineered solutions for humanitarian crises around the world, knows well the importance of ready access to clean water. Most pressing, of course, is the need for drinking water. But the lack of water for washing also puts people’s lives at risk from waterborne illnesses spread by the fecal–oral route.

Fecal–oral diseases can proliferate rapidly, sometimes to epidemic proportions, when people in crowded conditions lack clean water for hygiene and sanitation.3 Among the agents involved are at least 20 viral, bacterial, and protozoan pathogens that cause diseases such as cholera, bacillary dysentery, and the relatively recently discovered hepatitis E.4,5

Aid groups are combating these pathogens with WASH, an integrated approach to disease prevention that ensures not only that people in emergency situations have water and sanitation infrastructure, but also that they practice behaviors that prevent disease.

The Threat of Diarrheal Diseases

Diarrhea may not seem deadly to Westerners who have access to improved sanitation. Nevertheless, it kills three-quarters of a million children every year, more than malaria, AIDS, and measles combined.6 The chief danger of diarrheal diseases is the loss of bodily fluids. “You get very weak within hours, and in fact you die of dehydration,” Sutton says. Worldwide, diarrheal diseases are the second leading cause of death of children under age 5 years6 and cause 40% of child deaths in the early stages of a humanitarian emergency, sometimes more.7

Disaster situations are prime settings for disease outbreaks: Limited water tends to go first to drinking and cooking, while hygiene gets short shrift, especially among people who are just being taught the connection between hygiene, sanitation, and health.8 “If it’s too far to walk, people will only collect a very small amount of water,” says Sutton. “They’ll use it for drinking and cooking and won’t have enough water to practice good hygiene.”

But access to water isn’t enough; health-protective behaviors are critically important. Worldwide, only 19% of people on average are estimated to wash their hands with soap after defecating (see table).9 Yet studies consistently show that handwashing with soap is effective at reducing diarrheal diseases; one systematic review of the literature estimated it reduces risk by 23–40%,9 while another estimated a 48% reduction.10

Although workers can install latrines and teach the value of handwashing and latrine use, only the refugees themselves can choose to change their behaviors. And that means changing social norms. Open defecation is common practice in developing nations. Handwashing is often done without soap,8 and cultural traditions such as eating with the hands and sharing plates can spread infectious diseases.11

“You need to understand the ‘F diagram,’” says Sutton, referring to the traditional schematic that sketches out all the fecal–oral disease transmission pathways (see figure). Feces, and whatever infectious agents are contained within it, can spread through fluids, fingers, flies, and the fields in which people defecate and/or grow crops. By not washing properly or keeping food in hygienic conditions, fingers, fluids, and flies can also contaminate food.11

Drinking, bathing, and cooking with unclean water sources can cause illness as well. Surface waters are likely to be contaminated with fecal pathogens, especially during the rainy season when rainwater washes feces into waterways.12

F diagramThe pathways of fecal–oral transmission all start with “F,” hence the name “F diagram.” Water, sanitation, and hygiene act as barriers to prevent contact with feces.

Joseph Tart/EHP

A “New” Hepatitis

Poor hygiene and fecal contamination were major factors in one of the world’s biggest outbreaks of hepatitis E, which began in October 2007 and persisted for a couple of years.13 This outbreak affected camps for internally displaced persons (IDPs) in Northern Uganda’s Kitgum District, infecting more than 10,000 people and killing 160, mostly pregnant women and young children. Other recent hepatitis E outbreaks have occurred among refugees and IDPs in Kenya, South Sudan, and Chad.

The term “hepatitis” refers to liver inflammation, most commonly caused by unrelated viruses A, B, C, D, and E as well as other hepatropic viruses. Hepatitis E is an emerging pathogen that, like hepatitis A, spreads by the fecal–oral route. It is particularly dangerous for pregnant women, especially in the third trimester. Recent data suggest hepatitis E could be responsible for approximately 10% of maternal deaths in Bangladesh.14

Hepatitis E was first described as “non-A, non-B hepatitis” in 1980.15 During a 1983 outbreak in Afghanistan, researcher Mikhail Balayan purposely exposed himself to the hepatitis E virus (HEV) to determine the causative agent of the illness. According to one account, “Though he wanted to bring samples back to his Moscow laboratory, he lacked refrigeration. So he made a shake of yogurt and an infected patient’s stool, drank it, went back to Moscow, and waited. When he became seriously ill a few weeks later, he started collecting and analyzing his own samples.”16

Balayan detected the novel virus by electron microscopy,17 and the single-stranded RNA virus was characterized in 1989 and sequenced in 1991.18 Hepatitis E is more common in the tropics and subtropics, particularly Asia and Africa. (Less relevant to refugee settlements, a swine HEV genotype that also infects humans is associated with illnesses in the industrialized world. This strain is transmitted by consumption of raw or undercooked pork sausage.19 There is evidence that incidence of HEV infection in industrialized nations is increasing.20,21)

Oxfam public health promoter Tracy Lamwaka trained and supervised volunteers in the Kitgum camps at the time of the outbreak there. “There was a lot of open defecation taking place,” Lamwaka says. “The water sources were also insufficient, and there was very poor food handling. There were so many people within the camp, it was very easy for [HEV] to spread.”

Oxfam engaged in hygiene education campaigns in the camps, training IDPs as “hygiene promoters” who educated their neighbors and kept an eye on sanitation in their camps. Each promoter monitored 20 households—checking, for instance, on whether people were washing their hands and utensils and whether anyone showed disease symptoms. The spread of HEV was brought under control but then spiked a second time.22

Until the Kitgum outbreak, most researchers believed HEV spread only through drinking contaminated water. But evidence from Kitgum suggested the virus may also spread directly from person to person. Eyasu Teshale, an epidemiologist with the U.S. Centers for Disease Control and Prevention, and colleagues reported in 2010 that “investigation did not reveal a clear continuing common source of infection necessary to sustain the epidemic for many months. Chlorination of drinking water had been implemented early in the epidemic, … and HEV RNA was not detected in borehole well water samples or from the nearest alternative source of drinking water.”22

If there were no secondary modes of transmission, Teshale explains, this outbreak would have been controlled with provision of safe and adequate drinking water. But it’s also too soon to definitively attribute cases to person-to-person transmission, he says.

If person-to-person transmission were to occur, it could potentially make hepatitis E much harder to contain. Rather than someone needing to drink contaminated water, they would only need to come in contact with a family member or a shared utensil carrying the virus.

“Our findings22 are from a unique setting, which since then has become a common setting for hepatitis E outbreaks in sub-Saharan Africa,” Teshale says. People in IDP or refugee camps are living in crowded conditions with poor environmental and household hygiene and inadequate water supply. “[T]he outbreak is sustained by the ongoing fecal contamination of water, food, water-collecting vessels, water and food, serving utensils, or the hands within the infected persons’ personal, social, or household contacts,” Teshale says. “Fecal excretion of HEV during illness is very high, allowing higher contamination risk.”

A Humanitarian Crisis

The broken pump at Adjumani is upsetting for the residents, and if it’s not fixed soon, the situation could rapidly develop into a health crisis. “It’s very serious,” Sutton says. But it is a relatively small setback compared with the humanitarian crisis in Kitgum or the situation a couple of years ago in Adjumani itself, when refugees first started arriving. 

“If you had been here at the beginning, it would have been very different,” says Sutton. “There were just tens of thousands of people. People were living outside. Land hadn’t been allocated to households. These camps are in the middle of the bush.”

Refugees are most vulnerable to waterborne diseases in the first stage of a crisis. “They’ve walked from South Sudan. Maybe the children are suffering a bit of malnutrition. There are no toilets. They’re doing a lot of open defecation,” says Sutton. “They’ve got no access to clean water or not enough access to clean water to practice good hygiene and to do basic domestic duties. So this is a precarious situation. You’ve got to get water to people immediately.”

Crisis management practices have changed over time. “Back in the eighties, we used to look at water on its own, and we used to look at sanitation on its own,” Sutton says. “And then we realized to have more health impact … we’ve got to start looking at things as a package.” The integrated WASH approach was born.

Oxfam and many other nonprofit entities adhere to the Sphere Project standards, which specify minimum requirements for water, sanitation, and shelter in humanitarian crises.23 Under these standards, people should have 7.5–15 liters of water per person per day for drinking, cooking, and hygiene; at a bare minimum, they should have 2–3 liters/person/day for drinking and food preparation. In Adjumani, the goal is to reach UNHCR’s higher standard of 20 liters/person/day24 within a couple of months, says Thurein Maung, the UNHCR WASH coordinator for the district.

In disaster-affected situations, Oxfam takes a lead in delivering WASH-related services. Often the first phase is hauling treated water to each settlement and filling large tanks from which refugees get water. Organizations also employ what they call a “sanitation ladder.” At the start of a crisis, the first step is to contain the spread of feces. Initially agencies may allocate specific fields or trench latrines for defecation. In addition, aid agencies may promote the so-called cat method, encouraging people to bury their feces. Moving up the next rung of the “ladder,” aid agencies install emergency slab latrines, often a plastic slab incorporating a drop hole that can be covered to keep flies and odor to a minimum.25 “Tippy taps” made of a jerrycan, some sticks, string, and a bar of soap make simple but effective handwashing stations.26

Getting People to Use Latrines

Teaching people to use latrines, wash with soap, or engage in other new behaviors takes time, says Oxfam public health engineer Pius Nzuki Kitonyi. “First we have a meeting so that we can hear their [views and priorities]. Then from there, we give them the information—‘This is what we intend to do.’ If it’s new, we tell them, ‘This will improve on what you have been doing.’ And then we start implementing.” Ideally, refugees themselves do some of the work, digging holes for latrines, trenches for water pipes, or clearing land for roads, in “pay for work” schemes that allow them to achieve some sort of socioeconomic independence, according to Oxfam.

In practice, getting people to use latrines—or other new behaviors—is hard when they have grown up with their own cultural beliefs. “Most of the [refugees], they …  go to the bush and do their stuff there,” explains Wilson Senyonyi, an Oxfam protection officer. “When pregnant mothers go to the latrines, they fear the child will just come out and fall into the pit.” These and other cultural beliefs can keep people from using modern latrines.

One technique used by UNHCR and its partners in refugee situations is called the Community-Led Total Sanitation (CLTS) approach.27 There are different steps involved in CLTS, including what Maung calls “the calculation of s—t.” In this exercise, a facilitator discusses how many grams of feces is produced by one person per day. The facilitator asks participants how many people there are and then calculates the total amount of feces in people’s living environment for a year or two.

Next, Maung says, “We ask them where those feces are. Before this exercise, the facilitator also walks with people through a community and identifies open defecation around the dwelling. We show them ‘you are living in s—t.’ It makes them uncomfortable. We bring a sense of shock or shame, while respecting the culture.”

The goal is to ignite awareness and a genuine desire for change in the community, and it works, Maung says—typically within a week people will begin building latrines or start using ones that are already there. But the effectiveness of CLTS largely depends on the skill of the facilitator, he adds.

In typical development projects, the activity requires people to use their own locally available building materials so they become invested in the process. Refugees have a different situation, however, so the process is adapted slightly. “Traditionally we don’t provide materials to construct the latrines, but in refugee situations, we create demand first, then provide materials,” Maung says; this encourages the refugees to use the facilities.

But does the mere presence of latrines and improved infrastructure really improve health outcomes? A team of researchers studied 100 villages in Odisha, India, some of which received latrines and some of which did not. They found no significant differences in diarrheal incidence or associated deaths, fecal contamination of water stored in households, contamination of the hands of mothers and children, malnutrition, or helminth worm infection between villages with and without additional latrines.28

“The lesson to draw is not that latrines don’t produce a benefit but the latrine programs weren’t properly implemented,” says Sandy Cairncross, a professor of environmental health at the London School of Hygiene & Tropical Medicine, who was not directly involved in the Odisha study. Public health improvement depends on changing people’s contact with to feces, he explains. And that requires changing behavior.

3-column tableGlobally, only 19% of people are estimated to wash their hands with soap after defecating, according to a systematic review of 42 studies on handwashing prevalence from around the world.9

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Encouraging Behavioral Change

Since the 1990s Cairncross and his collaborator at London School of Hygiene & Tropical Medicine, epidemiologist Val Curtis, have built their careers advancing the scientific basis for health education. Curtis calls herself a “disgustologist,” and her work focuses on understanding how health behaviors can be effectively changed. Specifically, she has shown that disgust is effective at getting people to avoid behaviors that contribute to disease.29

Curtis and Cairncross’s research has been funded, in part, by Unilever, which allowed them to bring private-sector marketing and advertising know-how to studying how best to promote health-protective behaviors.30 “Some whitecoat giving lectures to mothers with crying babies isn’t going to make an impact on anyone at all,” says Cairncross. “Telling people if they didn’t wash their hands they’ll get diarrhea and die—these doom-laden negative messages related to the threat to someone’s health don’t stop people doing unhealthy things or get them to do healthy things.”

On the other hand, he says, positive messages such as “If you wash hands with soap you’re a good mother” or “This is what all modern people are doing nowadays” or “It makes your hands taste nice when you eat your rice with your hands” are much more likely to inspire behavioral changes. “It’s not rocket science,” he says. “Advertisers have been doing this for years.”

But people also need repeat messages. Generally speaking, Cairncross says, people need to hear about washing their hands with soap about six times in a month before the message sticks.

To raise awareness among people in developing nations, the Global Public–Private Partnership for Handwashing with Soap started a campaign that includes Global Handwashing Day, celebrated October 15 around the world.31 At Arua’s Rhino Camp, dozens of children and their parents gathered to celebrate Global Handwashing Day 2014. Girls and boys sang songs and dramatized the importance of handwashing at critical times such as after using the toilet and before eating, as well as washing one’s head, feet, and body. Everyone marched around the open field before enjoying sodas and water—after washing their hands with soap. Community leaders from within the refugee settlements led the training of the children, along with various groups such as Oxfam and UNHCR.

Stabilizing the Crisis

With several months of hard work since the refugees began arriving here, the Adjumani and Arua settlements resemble traditional African villages. Latrines, boreholes, and roads have been built, and families have been assigned plots of land they can temporarily call their own. Before long, technicians repair the broken pump, and water soon returns to tap stands throughout the settlement.

Unlike a traditional refugee setting, where refugees live in tents in a fenced-off camp, those in Uganda live on land donated by Ugandan nationals through arrangement of the government, and refugee families are given plots on which they can build shelters and grow crops.32 The Ugandan government and UNHCR have a policy of devoting 70% of aid to refugees and 30% to nationals, according to Maung. This arrangement helps reduce resentment and also improves infrastructure that remains once refugees return home.

“We are in the process of transition from acute emergency to stabilized emergency,” says Maung, “but [there’s] quite a lot of work to be done in terms of operation and maintenance of WASH facilities to ensure sustainability.”

“There is not much data on long-term behavior change for handwashing with soap,” says Jelena Vujcic, an epidemiology researcher at the University of Buffalo.  Outstanding questions include how to make handwashing with soap a social norm in a way that’s culturally conscious and acceptable to a society, and which handwashing technologies support good handwashing practice and are acceptable to the communities that use them.

“Overall, there is a dearth of data on handwashing in emergencies,” Vujcic says. “There is no evidence on what works in emergencies to improve handwashing behavior.” But with no shortage of emergencies for UNHCR to attend to around the world, both humanitarians and epidemiologists will have their hands full for the foreseeable future—and hopefully those hands will be cleaned with soap.

Moving Beyond Camps
Refugees in settlement camps are supposed to stay put, but some return to their home country to visit family, or travel to cities. This can increase the risk of spreading disease. If a refugee comes down with a highly contagious and deadly disease, such as Ebola or Marburg, such movement could prove tragic—and the risks are real. In September 2014 a Ugandan died of Marburg hemorrhagic fever in a Kampala hospital,33 and in August 2014 an Ebola outbreak separate from the ongoing West Africa epidemic arose in Democratic Republic of Congo, killing 49.34 The U.S. Centers for Disease Control and Prevention declared the country Ebola-free on 21 November 2014.

Although Ebola and Marburg are not fecal–oral diseases per se, they can spread rapidly when people do not engage in hygienic behaviors, and as with any emergency situation, stopping an epidemic’s spread will ultimately depend on changing behaviors, and quickly. As one recent review stated, “The success of interventions to improve WASH practices ultimately rests on the ability to foster and maintain behaviour change at the individual, household, community, and structural levels.”35


1. UNHCR. South Sudan Situation [website]. Geneva, Switzerland:United Nations High Commissioner for Refugees (updated 25 November 2014). Available: [accessed 25 November 2014].

2. UNHCR. South Sudan Situation Rhino Camp [website]. Geneva, Switzerland:United Nations High Commissioner for Refugees (updated 8 June 2014). Available: [accessed 25 November 2014].

3. Nannyonga B, et al. The dynamics, causes and possible prevention of hepatitis E outbreaks. PLoS ONE 7(7):e41135 (2012); doi: 10.1371/journal.pone.0041135.

4. Curtis V, Cairncross S. Effect of washing hands with soap on diarrhoea risk in the community: a systematic review. Lancet Infect Dis 3(5):275–281 (2003); doi: 10.1016/S1473-3099(03)00606-6.

5. Khuroo MS. Discovery of hepatitis E virus—the untold story. JK Practitioner 11(3):291–294 (2004);

6. Liu L, et al. Global, regional, and national causes of child mortality: an updated systematic analysis for 2010 with time trends since 2000. Lancet 379(9832):2151–2161 (2012); doi: 10.1016/S0140-6736(12)60560-1.

7. Connolly MA, et al. Communicable diseases in complex emergencies: impact and challenges. Lancet 364(9449):1974–1983 (2004); doi: 10.1016/S0140-6736(04)17481-3.

8. Brown J, et al. Evidence Review and Research Priorities: Water, Sanitation, and Hygiene for Emergency Response. London, UK:Department for International Development (2012). Available: [accessed 25 November 2014].

9. Freeman MC, et al. Systematic review: hygiene and health: systematic review of handwashing practices worldwide and update of health effects. Trop Med Int Health 19(8):906–916 (2014); doi: 10.1111/tmi.12339.

10. Cairncross S, et al. Water, sanitation and hygiene for the prevention of diarrhoea. Int J Epidemiol 39(suppl 1):i193–i205 (2010); doi: 10.1093/ije/dyq035.

11. Choffnes ER, Mack A. Global Issues in Water, Sanitation and Health: Workshop Summary 2009. Washington, DC:National Academies Press (2014). Available: [accessed 25 November 2014].

12. Frumkin H (ed). Environmental Health: From Global to Local. San Francisco, CA:John Wiley & Sons (2010).

13. Teshale EH, et al. Hepatitis E epidemic, Uganda. Emerg Infect Dis 16(1):126–129 (2010); doi: 10.3201/eid1601.090764.

14. Labrique AB, et al. Hepatitis E, a vaccine-preventable cause of maternal deaths. Emerg Infect Dis 18(9):1401–1404 (2012); doi: 10.3201/eid1809.120241.

15. Khuroo MS. Study of an epidemic of non-A, non-B hepatitis: possibility of another human hepatitis virus distinct from post-transfusion non-A, non-B type. Am J Med 68(6):818–824 (1980);

16. NIAID. The Story of the Hepatitis E Vaccine [website]. Bethesda, MD:National Institute of Allergy and Infectious Diseases, National Institutes of Health (updated 30 August 2007). Available: [accessed 25 November 2014].

17. Balayan MS, et al. Evidence for a virus in non-A, non-B hepatitis transmitted via the fecal–oral route. Intervirology 20(1):23–31 (1983);

18. Tam AW, et al. Hepatitis E virus (HEV): molecular cloning and sequencing of the full-length viral genome. Virology 185(1):120–131 (1991); doi: 10.1016/0042-6822(91)90760-9.

19. Berto A. Hepatitis E virus in pork food chain, United Kingdom, 2009–2010. Emerg Infect Dis 18(8):1358–1360 (2012); doi: 10.3201/eid1808.111647.

20. Said B, et al. Hepatitis E virus in England and Wales: indigenous infection is associated with the consumption of processed pork products. Epidemiol Infect 142(7):1467–1475 (2014); doi: 10.1017/S0950268813002318.

21. Zaaijer HL. No artifact, hepatitis E is emerging. Hepatology; doi: 10.1002/hep.27611 [online 21 November 2014].

22. Teshale EH, et al. Evidence of person-to-person transmission of hepatitis E virus during a large outbreak in northern Uganda. Clin Infect Dis 50(7):1006–1010 (2010); doi: 10.1086/651077.

23. The Sphere Project. The Sphere Handbook: Humanitarian Charter and Minimum Standards in Humanitarian Response [website]. Bourton on Dunsmore, United Kingdom:The Sphere Project. Available: [accessed 25 November 2014].

24. UNHCR. Practical Guide to the Systematic Use of Standards & Indicators in UNHCR Operations. 2nd ed. Geneva, Switzerland:Division of Operational Services, United Nations High Commissioner for Refugees (February 2006). Available: [accessed 25 November 2014].

25. WHO. Sanitation and Hygiene Promotion: Programming Guidance. Geneva, Switzerland:Water Supply and Sanitation Collaborative Council and World Health Organization (2005). Available: [accessed 25 November 2014].

26. WMG. Build Your Own Tippy Tap [poster]. Tucson, AZ:Watershed Management Group. Available: [accessed 25 November 2014].

27. Kar K, Chambers R. Handbook on Community-Led Total Sanitation. Brighton, United Kingdom:Institute of Development Studies (March 2008). Available: [accesssed 25 November 2014].

28. Clasen T, et al. Effectiveness of a rural sanitation programme on diarrhoea, soil-transmitted helminth infection, and child malnutrition in Odisha, India: a cluster-randomised trial. Lancet Global Health 2(11):e645–e653 (2014); doi: 10.1016/S2214-109X(14)70307-9.

29. Curtis V, et al. Disgust as an adaptive system for disease avoidance behaviour. Philos Trans R Soc B Biol Sci 366(1563):389–401 (2011); doi: 10.1098/rstb.2010.0117.

30. Curtis VA, et al. Ethics in public health research. Masters of marketing: bringing private sector skills to public health partnerships. Am J Public Health 97(4):634–641 (2007); doi: 10.2105/AJPH.2006.090589.

31. PPPHW. Global Handwashing Day [website]. The Global Public–Private Partnership for Handwashing with Soap (2014). Available: [accessed 25 November 2014].

32. UNHCR. 2014 UNHCR Country Operations Profile—Uganda [website]. Geneva, Switzerland:United Nations High Commissioner for Refugees (undated). Available: [accessed 25 November 2014].

33. WHO. Marburg Virus Disease—Uganda [press release]. Geneva, Switzerland:World Health Organization (10 October 2014). Available: [accessed 25 November 2014].

34. Maganga GD, et al. Ebola virus disease in the Democratic Republic of Congo. New Engl J Med 371(22):2083–2091 (2014); doi: 10.1056/NEJMoa1411099.

35. Dreibelbis R, et al. The integrated behavioural model for water, sanitation, and hygiene: a systematic review of behavioural models and a framework for designing and evaluating behaviour change interventions in infrastructure-restricted settings. BMC Public Health 13:1015 (2013); doi: 10.1186/1471-2458-13-1015.

Trails Update – date posted Dec 31, 2014

Shoe transaction devices and hiking poles recommended. Before starting your hike, stop by the Backcountry Information Center for the latest trail conditions.

Hiking the Corridor? Be sure to visit the Trail Courtesy Practices That Leave No Trace webpage.

Hikers without a permit can stop by the Backcountry Information Center to request a last minute permit. Last minute permits and waitlist numbers are issued by the Backcountry Information Center, located inside the park. The South Rim Backcountry Information Center is open daily, year round, for walk-in visitors from 8 am to noon and 1-5 pm Mountain Standard Time. The North Rim Backcountry Information Center is open daily from mid-May to October 31 for walk-in visitors from 8 am to noon and 1-5 pm Mountain Standard Time.

Organized Group Rim-to-Rim and Extended Day Hike/Run: Any organized, noncommercial, group conducting rim-to-rim and extended day hiking and running, including rim-to-river-to-rim, and rim-to-rim-to-rim in the inner canyon is required to obtain a Special Use Permit from Grand Canyon National Park. The inner canyon is defined as the area below the Tonto Platform (Tipoff and Indian Garden) from the South Rim and below Manzanita Resthouse (Pumphouse Residence) from the North Rim. Any group, regardless of size, which has advertised to the general public, required individuals to sign up prior to participation, or that has an organizer who has been compensated for their services (including subsidized participation in the activity), is required to operate under a Special Use Permit. For more information visit

Title: ToxCast™ Wants You: Recommendations for Engaging the Broader Scientific Community

Carrie Arnold is a freelance science writer living in Virginia. Her work has appeared in Scientific American, Discover, New Scientist, Smithsonian, and more.

About This Article open

Citation: Arnold C. 2015. ToxCast™ wants you: recommendations for engaging the broader scientific community. Environ Health Perspect 123:A20;

News Topics: Chemical Testing, High-Throughput Screening, Research Issues and Initiatives

Published: 1 January 2015

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Since the U.S. Environmental Protection Agency (EPA) launched ToxCast™ in 2007, this chemical screening program has generated massive amounts of data. The main objective of ToxCast has been to help the agency prioritize chemicals for further review to meet different regulatory needs. But ToxCast may have much more to offer the broader research community—and the broader research community has much to offer ToxCast. A new commentary in this issue of EHP discusses two strategies for increasing engagement between ToxCast and researchers in disciplines beyond toxicology.1

Under the Toxic Substances Control Act, the EPA maintains an inventory of chemicals produced and processed in the United States. There are currently more than 84,000 chemicals on the inventory, and 500–1,000 additional chemicals are added each year.2

Two hands encircling a chemical structure ToxCast and the broader research community have much to offer one another on the quest to better understand the chemicals we use.

© 2014 James Steinberg c/o

But for most of these chemicals there are few or no toxicity data, and traditional toxicity testing is slow and expensive.3 Relying on traditional approaches alone, it would take decades to evaluate the tens of thousands of chemicals that lack adequate data to support regulatory action. “Concern is great that among the untested chemicals in wide use there may lurk currently undiscovered human toxicants,” says Philip Landrigan, a pediatric researcher at the Mount Sinai School of Medicine, who was not involved in the commentary.

The Tox21 consortium—which also includes the National Toxicology Program (NTP), the National Center for Advancing Translational Sciences, and the Food and Drug Administration—is a federal initiative aimed at focusing and speeding up this discovery process.4 ToxCast, short for Toxicity Forecaster, is one of the EPA’s main contributions to the Tox21 collaboration. ToxCast uses high-throughput in vitro screening to flag compounds that show signs of potential toxicity. These compounds are then prioritized for more in-depth study.5

In the new commentary, Jennifer McPartland, a health scientist at the Environmental Defense Fund, and colleagues suggest new approaches to broaden scientific engagement with ToxCast in particular and Tox21 overall. “We need more researchers to engage with the emerging data so that we are ultimately making better public health decisions,” McPartland says.

The authors point out that making better decisions depends in large part on the scientific integrity of the assays used in ToxCast (and other high-throughput in vitro initiatives) and the scientifically sound interpretation of the data those assays produce.1 This is where the larger community comes in. Kristina Thayer, director of the NTP Office of Health Assessment and Translation, explains, “The broader research community is well poised to do the orthogonal testing required to assess the utility of ToxCast predictions, which is needed to help with regulatory acceptance.” By “orthogonal testing,” she means the use of a different assay—usually one that is closer to the target physiological condition or using a different technology—to assess ToxCast results. (Thayer was not involved with the commentary.)

McPartland and colleagues first recommend using collaborative workshops to introduce ToxCast to a wider scientific audience.1 As an example of how this might work in practice, they point to a 2011 workshop conducted by the NTP in which experts from a spectrum of fields assessed the scientific literature and ToxCast data related to the role of chemical exposures in obesity and diabetes.6 The workshop gave NTP staff a chance to explain ToxCast to these researchers, who in turn provided expert analysis and feedback on the data produced by ToxCast. After the workshop, the NTP teamed up with some of the participants to discuss priority chemicals identified by ToxCast, which those participants might study in their own laboratories.1

Their second recommendation is to seek out mutually beneficial research partnerships like one established between Harvard and the EPA.1 Russ Hauser, an epidemiologist at Harvard School of Public Health, learned about ToxCast data when he served on an EPA Science Advisory Board. Hauser had been studying children with very early onset inflammatory bowel disease (VEO-IBD), which includes diseases such as Crohn’s disease and ulcerative colitis that are diagnosed in children under age 10.7 Together with EPA scientists, pediatric gastroenterologists, and pediatric immunologists, Hauser is co-leading a project using ToxCast data to identify environmental factors that may contribute to VEO-IBD.

“There’s no way we could measure the effects of dozens of chemicals in a human study,” Hauser says. “Our work wouldn’t be possible without ToxCast data.”

Tina Bahadori, director of the EPA’s Chemical Safety for Sustainability research program, says the agency has already been thinking along the same lines as McPartland and colleagues and is working toward implementing these recommendations. “This is exactly the feedback that we’re looking for,” says Bahadori, who was not involved with the commentary. “Not only is it useful, it also gives us the justification that’s needed to broaden our landscape and look at environmental and public health applications of these data from a broader vantage point than what we’re accustomed to.”


1. McPartland J, et al. Building a robust 21st century chemical testing program at the U.S. Environmental Protection Agency: recommendations for strengthening scientific engagement. Environ Health Perspect 123(1):1–5 (2015); doi: 10.1289/ehp.1408601.

2. EPA. TSCA Chemical Substance Inventory [website]. Washington, DC:U.S. Environmental Protection Agency (updated 13 March 2014). Available:​s/pubs/tscainventory/basic.html [accessed 4 December 2014].

3. Judson R, et al. The toxicity landscape for environmental chemicals. Environ Health Perspect 117(5):685–695 (2009); doi: 10.1289/ehp.0800168.

4. NTP. Tox21 [website]. Research Triangle Park, NC:National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health (updated 2 December 2014). Available:​ex.html [accessed 4 December 2014].

5. EPA. Toxicity Forecaster (ToxCast™) [fact sheet]. Washington, DC:U.S. Environmental Protection Agency (undated). Available:​actsheets/Tox_Cast_Fact_Sheet.pdf [accessed 4 December 2014].

6. Thayer KA, et al. Role of environmental chemicals in diabetes and obesity: a National Toxicology Program workshop review. Environ Health Perspect 120(6):779–789 (2012); doi: 10.1289/ehp.1104597.

7. Benchimol EI, et al. Incidence, outcomes, and health services burden of very early onset inflammatory bowel disease. Gastroenterology 147(4):803–813 (2014); doi: 10.1053/j.gastro.2014.06.023.

Title: Inner Workings of Arsenic: DNA Methylation Targets Offer Clues to Mechanisms of Toxicity

Lindsey Konkel is a Worcester, MA–based journalist who reports on science, health, and the environment.

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Citation: Konkel L. 2015. Inner workings of arsenic: DNA methylation targets offer clues to mechanisms of toxicity. Environ Health Perspect 123:A21;

News Topics: Arsenic, Epigenetics, Molecular Biology, Skin Health

Published: 1 January 2015

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Gene-Specific Differential DNA Methylation and Chronic Arsenic Exposure in an Epigenome-Wide Association Study of Adults in Bangladesh

Maria Argos, Lin Chen, Farzana Jasmine, Lin Tong, Brandon L. Pierce, Shantanu Roy, Rachelle Paul-Brutus, Mary V. Gamble, Kristin N. Harper, Faruque Parvez, Mahfuzar Rahman, Muhammad Rakibuz-Zaman, Vesna Slavkovich, John A. Baron, Joseph H. Graziano, Muhammad G. Kibriya, and Habibul Ahsan

Arsenic is a known human carcinogen,1 although it’s unclear how it causes cancer. Some studies have suggested that epigenetic modifications—specifically DNA methylation—may play a role in arsenic toxicity.2 In this issue of EHP, investigators identify gene-specific DNA methylation targets in white blood cells in a large study of Bangladeshi adults.3

In addition to cancer, chronic exposure to arsenic in drinking water has been associated with an increased risk of cardiovascular disease, peripheral neuropathy, respiratory diseases, and diabetes.4 Previous epidemiological studies probing DNA methylation and arsenic exposure have isolated methylation patterns within specific genes of interest,5,6 and a few have begun to assess epigenome-wide changes.7,8,9 The new study is the largest to date to investigate arsenic-related changes throughout the epigenome.

“Many of the genes we identified happened to be related to pathways that are associated with skin cancer, which was very relevant to the study population,” says lead author Maria Argos, an epidemiologist at the University of Illinois at Chicago. The researchers used blood and urine samples provided by more than 400 adults from rural Bangladesh with arsenical skin lesions—thickened or blackened areas of the skin that are associated with chronic arsenic exposure. People with arsenical skin lesions may be at an increased risk for developing skin cancer.10

Woman’s palm with arsenical skin lesionsSkin lesions can occur with any level of arsenic exposure but are most prevalent among people of South Asian descent, suggesting a genetic component.

© AP Photo/Pavel Rahman

Four gene loci showed significant changes in methylation status in relation to urinary arsenic concentration. Three of these also showed significant changes in relation to blood arsenic concentration. These four loci—sites in the genes PLA2G2C, SQSTM1, SLC4A4, and IGH—had not previously been associated with arsenic exposure.3

The researchers observed that several of the differentially methylated loci were associated with changes in gene expression levels in white blood cells.3 “The changes in gene expression that we observed make sense in the arsenic pathology that we see. These are good clues for exploring mechanism and prevention avenues,” says senior study author Habibul Ahsan, a medical epidemiologist at the University of Chicago.

For instance, PLA2G2C encodes lipid mediators with roles in inflammation, cell growth, and cell death,11 making them potentially important for cancer progression.3 Higher arsenic exposure was associated with decreased methylation levels at a locus of the SQSTM1 gene that has been implicated in a number of diseases, including cancer, obesity, insulin resistance, and neurodegenerative diseases.12

“The addition of gene expression data to DNA methylation data makes this study very unique and begins to suggest how some of the epigenetic changes may be linked to downstream health outcomes,” says Carmen Marsit, a molecular epidemiologist at the Geisel School of Medicine, Dartmouth College, who was not involved with the study.

The researchers identified methylation patterns in blood cells, but every tissue type in the body has a different methylation pattern. “We can’t necessarily say that the DNA methylation profile associated with arsenic exposure in blood would be the same as in skin or other tissues of the body,” Argos says.

The majority of study participants had higher levels of arsenic exposure than would typically be seen in the U.S. population, says Ahsan. And although skin lesions can develop at any level of arsenic exposure, he says, they are more widespread among people of South Asian descent, suggesting a genetic component. “It’s not clear yet how important a factor genetic variation may be in setting DNA methylation patterns,” Marsit says.

According to Argos, epidemiological studies may be able to use DNA methylation patterns in blood as a surrogate for past exposures to arsenic. Scientific research combining DNA methylation and gene expression data is a step toward doing more integrative molecular studies, she says. “We showed there is a lot to be learned by overlaying different types of molecular data.”


1. IARC. Arsenic, Metals, Fibres, and Dusts. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Volume 100 C: A Review of Human Carcinogens. Lyon, France:International Agency for Research on Cancer (2012). Available:​/vol100C/mono100C.pdf [accessed 5 December 2014].

2. Reichard JF, Puga A. Effects of arsenic exposure on DNA methylation and epigenetic gene regulation. Epigenomics 2(1):87–104 (2010); doi: 10.2217/epi.09.45.

3. Argos M, et al. Gene-specific differential DNA methylation and chronic arsenic exposure in an epigenome-wide association study of adults in Bangladesh. Environ Health Perspect 123(1):64–71 (2015); doi: 10.1289/ehp.1307884.

4. Navas-Acien A, et al. Arsenic exposure and type 2 diabetes: a systematic review of the experimental and epidemiologic evidence. Environ Health Perspect 114(5):641–648 (2006); doi: 10.1289/ehp.8551.

5. Engström KS, et al. Efficient arsenic metabolism—the AS3MT haplotype is associated with DNA methylation and expression of multiple genes around AS3MT. PLoS ONE 8(1):e53732 (2013); doi: 10.1371/journal.pone.0053732.

6. Intarasunanont P, et al. Effects of arsenic exposure on DNA methylation in cord blood samples from newborn babies and in a human lymphoblast cell line. Environ Health 11(1):31 (2012); doi: 10.1186/1476-069X-11-31.

7. Smeester L, et al. Epigenetic changes in individuals with arsenicosis. Chem Res Toxicol 24(2):165–167 (2011); doi: 10.1021/tx1004419.

8. Bailey KA, et al. Arsenic and the epigenome: interindividual differences in arsenic metabolism related to distinct patterns of DNA methylation. J Biochem Mol Toxicol 27(2):106–115 (2013); doi: 10.1002/jbt.21462.

9. Koestler DC, et al. Differential DNA methylation in umbilical cord blood of infants exposed to low levels of arsenic in utero. Environ Health Perspect 121(8):971–977 (2013); doi: 10.1289/ehp.1205925.

10. Rahman M, et al. Prevalence of arsenic exposure and skin lesions. A population based survey in Matlab, Bangladesh. J Epidemiol Community Health 60(3):242–248 (2006); doi: 10.1136/jech.2005.040212.

11. Dennis EA, et al. Phospholipidase a2 enzymes: physical structure, biological function, disease implication, chemical inhibition, and therapeutic intervention. Chem Rev 111(10):6130–6185 (2011); doi: 10.1021/cr200085w.

12. Geetha T, et al. Sequestosome 1/p62: across diseases. Biomarkers 17(2):99–103 (2012); doi: 10.3109/1354750X.2011.653986.

Title: “Exported” Deaths and Short-Term PM10 Exposure: Factoring the Impact of Commuting into Mortality Estimates

Julia R. Barrett, MS, ELS, is a Madison, WI–based science writer and editor. She is a member of the National Association of Science Writers and the Board of Editors in the Life Sciences.

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Citation: Barrett JR. 2015. “Exported” deaths attributable to short-term PM10 exposure: factoring the impact of commuting into mortality estimates. Environ Health Perspect 123:A22;

News Topics: Air Pollution, Cardiovascular Health, Exposure Science, Particulate Matter (PM), Respiratory Health

Published: 1 January 2015

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Commuting-Adjusted Short-Term Health Impact Assessment of Airborne Fine Particles with Uncertainty Quantification via Monte Carlo Simulation

Michela Baccini, Laura Grisotto, Dolores Catelan, Dario Consonni, Pier Alberto Bertazzi, and Annibale Biggeri

Exposure to coarse particulate matter (PM10) has been associated with increased mortality.1,2,3 Reliable health impact assessments are difficult, however, because existing exposure data may be incomplete, and exposures and effects alike typically are predicted rather than observed.4,5 A new report in EHP estimates mortality attributable to short-term PM10 exposure using sophisticated models to account for two of the chief obstacles to assessing health impact—namely, data uncertainty and mobility of the population.4

The study area in Lombardy is characterized by thermal inversions that trap air pollution at ground level within the highly populated Po River basin. Levels of PM10 in the basin often exceed guidelines set by the World Health Organization (WHO) and European Union (EU)—annual means of 20 μg/m3 and 40 μg/m3, respectively.4,6 For example, average annual concentrations in 2003–2006 reached 52.5 μg/m3 in the regional capital of Milan and 45.4 μg/m3 in other highly populated areas.6

Cars, motorbikes, trolleys, and pedestrians on the streets of MilanEvening rush hour in Milan, Italy.

© Peeter Viisimaa/

PM10 is a complex mix of small particles and adsorbed substances emitted by vehicles, industrial activities, and other sources.1 Inhalation of PM10 can trigger oxidative stress, inflammation, and other physiologic reactions,1 and both short- and long-term exposure have been associated with cardiac and respiratory morbidity and mortality.2 Although PM10 exposure plays a relatively small role in these conditions, many people are exposed, so the public health burden builds up.1,4

Individual monitoring is cost prohibitive, so PM10 exposure is typically estimated using data from monitoring stations, modeling, and satellite images.4 However, uncertainty surrounding the validity or meaning of these data can undermine the reliability of the resulting health impact assessments.5 In addition, exposure assessments typically have not accounted for PM10 exposure in multiple places. For instance, although some assessments are based on residential address, people who commute to work or school may spend a large part of their day in an area more polluted than their home neighborhood.7

To overcome these hurdles, the authors of the current study constructed models using existing data on total mortality, PM10 concentrations, PM10 health effects, and commuting patterns among towns in the Lombardy region of Italy. Uncertainty was incorporated for parameters including variability in exposure risk between larger municipalities and smaller, less well-characterized locations. The researchers applied statistical procedures, including Bayesian techniques and Monte Carlo simulations, to address the uncertainty and pull the data into sharper focus.

The researchers estimated that in 2007, 865 deaths in Lombardy were attributable to PM10 concentrations exceeding the WHO standard of 20 μg/m3, and 26% of those deaths were attributable to PM10 levels above the EU standard of 40 μg/m3. They further estimated that annual average PM10 levels of 20 μg/m3 or lower would have resulted in 311.4 fewer deaths, while annual average PM10 levels of 40 μg/m3 or lower would have prevented 189.4 deaths.4

The researchers partitioned the estimated deaths based on where exposure was predicted to have occurred.4 “We found the health impact of air pollution is not uniform in the region but is concentrated in the capital city and other major cities,” says coauthor Michela Baccini, an associate professor in the Department of Statistics, Informatics, and Applications “G. Parenti” at the University of Florence. “Moreover, we found that air pollution in the largest cities also has an impact on the health of commuters from other municipalities in the region.” In other words, people who lived in less-polluted areas could die of exposures received in more-polluted areas, which the authors referred to as “exported” deaths.

Potential weaknesses include the fact that people who are capable of commuting may be younger and healthier than average, so the authors’ use of mortality rates and effect estimates based on the general population may have inflated the apparent impact of commuting. They also did not consider the impact of commuting within cities but assumed all exposures within a municipality were the same.

The large credibility intervals reflect the level of uncertainty factored into the model. Nevertheless, the overall picture remains intact, even though the finer details may remain murky.

“It’s a very interesting paper and solid statistical work,” says Evangelia Samoli, an assistant professor in the Department of Hygiene, Epidemiology and Medical Statistics at the University of Athens Medical School, who was not involved with the study. “I believe the main advantage of the method is the health impact assessment at the municipality level as compared to previous approaches.” This kind of small-area estimation may not be useful for informing policies on a large scale, but it does highlight the magnitude and complexity of the problem, she says.

“Our research points out that in an interconnected world it is difficult to be immune from the negative effect of pollution,” says Baccini. “Even if our residence place is ‘clean,’ commuting to work and study places can expose us to air pollution. This highlights the need to develop adequate mobility planning, but also to better plan our lifestyle and the way we live in our cities.”


1. Anderson JO, et al. Clearing the air: a review of the effects of particulate matter air pollution on human health. J Med Toxicol 8(2):166–175 (2012); doi: 10.1007/s13181-011-0203-1.

2. Adar SD, et al. Ambient coarse particulate matter and human health: a systematic review and meta-analysis. Curr Environ Health Rep 1(3):258–274 (2014); doi: 10.1007/s40572-014-0022-z.

3. Samoli E, et al. Which specific causes of death are associated with short term exposure to fine and coarse particles in Southern Europe? Results from the MED-PARTICLES project. Environ Int 67:54–61 (2014); doi: 10.1016/j.envint.2014.02.013.

4. Baccini M, et al. Commuting-adjusted short-term health impact assessment of airborne fine particles with uncertainty quantification via Monte Carlo simulation. Environ Health Perspect 123(1):27–33 (2015); doi: 10.1289/ehp.1408218.

5. Mesa-Frias M, et al. Uncertainty in environmental health impact assessment: quantitative methods and perspectives. Int J Environ Health Res 23(1):16–30 (2013); doi: 10.1080/09603123.2012.678002.

6. Baccini M, et al. Health impact assessment of fine particle pollution at the regional level. Am J Epidemiol 174(12):1396–1405 (2011); doi: 10.1093/aje/kwr256.

7. Larssen S, et al. Estimating the Contribution of Commuting on Exposure to Particulate Matter in European Urban Areas. ETC/ACC Technical Paper 2012/2. Bilthoven, the Netherlands:European Topic Centre on Air Pollution and Climate Change Mitigation (March 2012). Available:​/ETCACM_TP_2012_2_PM_exposure_urban_comm​uting.pdf [accessed 9 December 2014].

Title: Potential Mitochondrial Toxicants: Tox21 Screen Identifies Chemicals of Interest

Carol Potera, based in Montana, also writes for Microbe, Genetic Engineering News, and the American Journal of Nursing.

About This Article open

Citation: Potera C. 2015. Potential mitochondrial toxicants: Tox21 identifies chemicals of interest. Environ Health Perspect 123:A23;

News Topics: Biochemistry, Chemical Testing, High-Throughput Screening, Molecular Biology

Published: 1 January 2015

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Related EHP Article

Profiling of the Tox21 Chemical Collection for Mitochondrial Function to Identify Compounds that Acutely Decrease Mitochondrial Membrane Potential

Matias S. Attene-Ramos, Ruili Huang, Sam Michael, Kristine L. Witt, Ann Richard, Raymond R. Tice, Anton Simeonov, Christopher P. Austin, and Menghang Xia

Mitochondria have many important functions, including production of adenosine triphosphate (ATP) to fuel cells and regulation of cell growth, signaling, differentiation, and apoptosis.1 Disrupted mitochondrial function raises the potential for health effects and in fact has been associated with cancer, diabetes, cardiovascular disease, and autism.2,3 In a study reported this month in EHP, investigators with the Tox21 consortium assessed the impact of more than 8,300 chemicals on mitochondrial activity.4

Tox21, short for Toxicology in the 21st Century, is a collaboration of federal entities including the National Toxicology Program, the Environmental Protection Agency, the Food and Drug Administration, and the National Center for Advancing Translational Sciences (NCATS). One product of Tox21 to date is a library of more than 10,000 chemical samples comprising 8,312 unique substances. These samples include industrial chemicals, consumer products, food additives, and human and veterinary drugs.5

Self-organizing map representing chemicals clustered based on structural similarityTest chemicals from the Tox21 library were arranged in 651 clusters based on structural similarity. Compared with the library overall, “enriched” clusters showed above-average evidence of harming mitochondria, reflected as a decrease in MMP. Identifying structural features associated with decreased MMP allows researchers to choose appropriate candidate chemicals for further research.

Source: Attene-Ramos et al. (2015)4

The Tox21 robotic system loads chemical samples and cells into 1,536-well microtiter plates; then the cells are scanned for specific changes.6 For the current study, researchers measured mitochondrial membrane potential (MMP) and intracellular ATP content in human hepatocellular carcinoma cells exposed to all 8,312 chemicals. Decreased MMP likely indicates harm to mitochondrial structure and activity, making this end point a good first step for flagging chemicals that interfere with mitochondrial bioenergetics. Changes to intracellular ATP content serve as a marker for both mitochondrial function and cell viability.4

Of the chemicals tested, 11% decreased MMP (but with no apparent effect on cell viability), 65% were inactive, and 3% increased MMP. The remaining 21% of the chemicals gave inconclusive results for a variety of reasons. Of these, 17% showed evidence of cytotoxicity.4

Some results paralleled previously identified mechanisms of toxicity for chemicals. For example, triethyltin bromide, which is already known to interrupt ATP production,7 also proved to be one of the most potent suppressors of MMP.4

Structure–activity relationship analysis gave clues about how other chemical may reduce MMP. Recurring structural features associated with decreased MMP included a substituted phenol moiety, a nitrobenzene core, and a thiazole substructure.4 “The cell model employed casts a broader net for defining mitochondrial toxicity to include targets beyond the electron transport chain,” says Kendall Wallace, a professor in the Department of Biomedical Sciences at the University of Minnesota, who was not involved with the study.

“We found several clusters not previously known to decrease MMP,” says senior author Menghang Xia, leader of the Systems Toxicology laboratory for the Tox21 program at NCATS. These included parabens with aliphatic side chains of varying lengths. “Their potency correlates with the length of the aliphatic side chain,” says Xia, suggesting these chemical structural features may predict mitochondrial damage. However, experimental research will be necessary to confirm this.

Craig Beeson calls Xia’s work “a tour de force that will go a long way to helping us better understand why so many different chemical classes exhibit mitochondrial damage.” The discovery that potency corresponded to small structural perturbations such as alkyl chain length in parabens is particularly exciting, says Beeson, an associate professor of drug discovery and biomedical sciences at the Medical University of South Carolina, who was not involved with the study.

Xia’s research team also evaluated the performance of the multiplex, high-throughput screening assay itself. “To decrease false-negative and false-positive rates, each chemical was tested in triplicate runs,” Xia explains. “We want to be certain that an inactive compound is accurately defined as inactive, and an active compound truly is active.” All the compounds were tested at 15 different concentrations.4

When comparing the multiple dose–response curves generated for each chemical, the mismatch rate was only 0.55% for MMP and 0.03% for ATP.4 “Our data quality from the primary screening was very high and reliable,” Xia says.

Now the team is further analyzing the chemicals that decreased MMP but did not change ATP content. Xia says these chemicals will be screened in rat and human hepatocytes to measure MMP changes. Some will also be tested in Caenorhabditis elegans (roundworms) and mitochondrial gene microarrays. The combined results will help guide the selection of compounds for in-depth animal studies.


1. McBride HM, et al. Mitochondria: more than just a powerhouse. Curr Biol 16(14):R551–R560 (2006); doi: 10.1016/j.cub.2006.06.054.

2. Pieczenik SR, Neustadt J. Mitochondrial dysfunction and molecular pathways of disease. Exper Mol Pathol 83(1):84–92 (2007); doi: 10.1016/j.yexmp.2006.09.008.

3. Napoli E, et al. Deficits in bioenergetics and impaired immune response in granulocytes from children with autism. Pediatrics 133(5):e1405–e1410 (2014); doi: 10.1542/peds.2013-1545.

4. Attene-Ramos MS, et al. Profiling of the Tox21 chemical collection for mitochondrial function to identify compounds that acutely decrease mitochondrial membrane potential. Environ Health Perspect 123(1):49–56 (2015); doi: 10.1289/ehp.1408642.

5. EPA. TOX21S: Tox21 Chemical Inventory for High-Throughput Screening: Structure-Index File [website]. Washington, DC:U.S. Environmental Protection Agency (updated 12 December 2013). Available:​s.html [accessed 16 December 2014].

6. EPA. The future of toxicity testing is here. Science Matters Newsletter 2(4) (August 2011). Available:​2011/toxicity.htm [accessed 16 December 2014].

7. Bragadin M, Marton D. A proposal for a new mechanism of interaction of trialkyltin (TAT) compounds with mitochondria. J Inorg Biochem 68(1):75–78 (1997); doi: 10.1016/S0162-0134(97)00011-1.

Hubble Sees an Ancient Globular Cluster

This image captures the stunning NGC 6535, a globular cluster 22,000 light-years away in the constellation of Serpens (The Serpent) that measures one light-year across.

Globular clusters are tightly bound groups of stars which orbit galaxies. The large mass in the rich stellar centre of the globular cluster pulls the stars inward to form a ball of stars. The word globulus, from which these clusters take their name, is Latin for small sphere.

Globular clusters are generally very ancient objects formed around the same time as their host galaxy. To date, no new star formation has been observed within a globular cluster, which explains the abundance of aging yellow stars in this image, most of them containing very few heavy elements.

NGC 6535 was first discovered in 1852 by English astronomer John Russell Hind. The cluster would have appeared to Hind as a small, faint smudge through his telescope. Now, over 160 years later, instruments like the Advanced Camera for Surveys (ACS) and Wide Field Camera 3 (WFC3) on the NASA/ European Space Agency (ESA) Hubble Space Telescope allow us to marvel at the cluster and its contents in greater detail.

European Space Agency
Credit: ESA/Hubble & NASA, Acknowledgement: Gilles Chapdelaine

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