Daily Press Briefings : Daily Press Briefing: October 31, 2014

Jen Psaki
Spokesperson
Daily Press Briefing
Washington, DC
October 31, 2014

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TRANSCRIPT:


2:34 p.m. EDT

MS. PSAKI: Hi, everyone. Happy Halloween. I know it’s late today and it’s Halloween, so we can try to get through this rather quickly.

I have a couple of items for all of you at the top. Secretary Kerry will travel to Paris, Beijing, and Muscat from November 4th through the 12th. He will travel to Paris, France on November 4th through the 6th to meet with French Foreign Minister Fabius.

On November 7th through the 8th, he will lead the Department of State’s delegation to the APEC Ministerial Meeting. While in Beijing, Secretary Kerry will participate in a broad range of multilateral and bilateral meetings with officials from APEC-member countries in advance of President Obama’s visit to Beijing for the APEC Economic Leaders Meeting. APEC is the premier forum for facilitating economic growth, cooperation, trade, and investment in the Asia Pacific region. Promoting trade and investment in the Asia Pacific region remains a key component of the U.S. rebalance policy.

On November 9th and 10th, Secretary Kerry will travel to Muscat, Oman to participate in a trilateral meeting with Iranian Foreign Minister Zarif and EU High Representative Catherine Ashton as part of the EU-coordinated P5+1 nuclear negotiations with Iran. The Secretary will be accompanied by the former Deputy Secretary of State Ambassador Burns, Under Secretary of State for Political Affairs Wendy Sherman, Senior Advisor Jake Sullivan, and the U.S. negotiating team.

On November 10th through 12th, Secretary Kerry will return to Beijing to accompany President Obama during his visit to China to participate in bilateral meetings.

Two more items. We welcome news of an EU-brokered gas deal between Russia and Ukraine that will secure gas to Ukraine and ultimately the rest of Europe through the upcoming winter. The agreement is a positive step.

At the same time, we have grave concerns that separatists plan to go ahead with illegitimate and illegal elections in areas of eastern Ukraine on Sunday. The United States will not recognize the results. These elections violate the letter and spirit of the September 5th Minsk ceasefire agreement, which calls for elections in the east in line with the Ukrainian law on special status. Any moves to try to legitimize the results will undermine the Minsk agreement. We call on all nations to similarly reject the illegal effort and instead support the legal December 7th local elections.

We also condemn the burning of a historic movie theater in Kyiv yesterday that was screening an LGBT-focused movie. We call for a swift and transparent investigation into this repulsive act, which may also constitute a hate crime.

As part of the newly – finally, as part of the newly launched comprehensive partnership, the United States and Malaysia held the fourth senior officials dialogue October 30th through the 31st in Washington, D.C. Assistant Secretary Russel welcomed Malaysian MFA Deputy Secretary General Ramlan and an interagency delegation. The United States and Malaysia took the opportunity to discuss a wide range of bilateral, regional, and global issues and agreed to hold the fifth senior officials dialogue next year in Malaysia.

Very short final one: Secretary Kerry called Ibu Retno Marsudi on her appointment to be the new foreign minister in Indonesia. We look forward to working with the new working cabinet.

With that, Lara.

QUESTION: Thank you. I saw right before we came out the statement about executions in Anbar and wanted to talk a little bit about ISIL, both in Iraq and in Syria. One, what was your reaction to the new reports about the foreign fighter flow coming into Syria and Iraq, that the airstrikes have not seemed to stop these – this flow? And then also, I’m wondering if you saw the reports that some of the Peshmerga who went into Kobani over the last day or two have come out, and they’re saying that Turkey isn’t supporting them – if you have a reaction to that.

MS. PSAKI: Sure. Let me take the first one. As you know, cracking down on foreign fighters is one of the most important components of our effort to degrade and defeat ISIL. It’s one of the five elements of the coalition and something that we are working with every member of the coalition on. Over the past year, the Department of State has led interagency delegations to Western Europe, the Balkans, North Africa, and the Gulf to press for greater cooperation on – both bilaterally and regionally – on information sharing, border security, law enforcement, capacity building, and countering violent extremism. This engagement has directly resulted in steps such as stronger counterterrorism laws and arrests through the Balkans region, increased security cooperation in North Africa, terrorist financing reforms in the Gulf, and closer cooperations with Western European counterparts.

But we know that this is a long-term effort. Obviously, there are new laws and new steps that have put in place, but it’s going to continue to take some time. It’s positive that a number of countries in the region have taken steps to put new laws on the books, to take additional steps at their borders, and we’re going to continue to work with them, because we feel this is such a strong and important priority.

QUESTION: Do you have any explanation for why it’s starting to ramp up again now? There is some linkage to the airstrikes, the point being that the airstrikes hadn’t stopped this. I’m wondering if the airstrikes may have actually caused – been kind of a rallying cry for more to go, if there’s any analysis on that.

MS. PSAKI: I don’t think that’s our analysis. And I don’t think, as far as I read the story, that’s what the story said, but that’s not our analysis. Obviously, what I was getting at here is that there has been additional steps and additional actions by countries in the region to do more to crack down on foreign fighters. And we know that there have been – there has been a history where that has not been the case. That’s a positive step. Does that mean it’s resolved? Obviously, it’s not resolved. But we don’t have a new assessment of the numbers. I expect that’s something we may have soon.

QUESTION: Just to follow up on Lara’s question on the foreign fighters, you know the majority of these fighters come through Turkey. Why do you think the Turks are not really cracking down on foreign fighters? They have always – I mean, this is not something that has happened overnight. This is something chronic. It’s been going on for three and a half years.

MS. PSAKI: Well, Said, I’m not sure there’s evidence – or factual evidence to back that specifically up. I will say that this is one of the topics of discussion that the Secretary has had with his Turkish counterparts, that General Allen and Ambassador McGurk has discussed with them. Turkey has taken additional steps to crack down on foreign fighters. They have made a number of arrests over the course of the last several months. Is there more that needs to be done? Absolutely there’s more that needs to be done. And that’s part of the discussion that we’ll continue to have.

QUESTION: Do you think that Turkey has been looking the other way while these foreign fighters are going in?

MS. PSAKI: I think the fact that they have taken additional steps recently is evidence that they’re beginning to do more.

QUESTION: Like what? What are these steps?

MS. PSAKI: They’ve put laws on the books. They’ve made some arrests. They’ve done more on their borders.

QUESTION: But the border remains quite porous, in fact. And in fact, a lot of people go through – slip through that border.

MS. PSAKI: Well, there – I just said there are additional steps they’ve taken. I pointed you to those. And obviously there’s more that needs to be done.

QUESTION: Do you believe that Turkey has its own agenda in this scheme, in this big – in the scheme of things, I should say?

MS. PSAKI: We continue to believe that Turkey is not just a NATO ally, but they’re an important partner in this coalition. They’ve taken a range of steps. We’ll continue to discuss with them what more they can do.

QUESTION: Can you speak to my –

MS. PSAKI: Oh, sorry. What was your second question again?

QUESTION: — second question about Kobani? It was about the Peshmerga fighters who went into Kobani and who have come out. They’re saying that Turkey isn’t supporting them.

MS. PSAKI: Well, I know that there have been ongoing discussions on the ground between – that involve Turkey, of course, about moving the Peshmerga through. I remind you that Turkey is the one – is the country that said that they would be comfortable with having them come through, and they’ve actively talked about facilitating that. As – I think our last assessment of this – sorry, let me just pull this up. One moment.

QUESTION: Do you have any understanding of why – what’s your understanding of why the Peshmerga have come back out?

MS. PSAKI: I don’t have an independent analysis for you. I think we’ve seen that there has been some progress over the past couple of days in terms of who’s traveling in and out. I would point you to them for more specifics on that.

Do we have any more on this topic?

QUESTION: Yeah.

MS. PSAKI: Go ahead.

QUESTION: The French president has said today that he supports the conditions that the Turkish President Erdogan puts to join the coalition. How do you view this statement?

MS. PSAKI: I – can you give a little more context for what he means specifically by that?

QUESTION: We know that the Turkish president asked for the creation of a buffer zone and –

MS. PSAKI: And did the French president say specifically that he wants a buffer zone?

QUESTION: He said that he supports the conditions –

MS. PSAKI: And he said that in the past, too. I’m not sure that’s new.

QUESTION: No, he said it today, with the –

MS. PSAKI: Sure. I know, but I’m just getting that – the fact that France has said that they would support that in the past.

QUESTION: But he said that in the –

MS. PSAKI: Our position hasn’t changed on that. Turkey and France are important partners in the coalition. We continue to discuss with them, as we do with all of our partners, what ideas they may have about how to address the threat of ISIL. That’s an ongoing discussion.

QUESTION: But you disagree with the both of them?

MS. PSAKI: I think you’re familiar with our position.

QUESTION: But the conditions also that Turkey put down calls also for the removal of Assad and actually targeting Syrian forces and air assets, or air defense assets, and so on. So it’s a whole – it’s a package deal. It’s not just one thing.

MS. PSAKI: Well, Said, I think I’d point to the fact that Turkey has already made a range of contributions in all of the lines of effort. The United States and Turkey have a shared interest in defeating ISIL, seeing a political transition in Syria, and bringing stability to Iraq. Turkey also plays an important role in supporting international peace in many parts of the world. We’re working with them on all those objectives. Obviously, we don’t agree on every component, but they remain an important partner and we have the same – many of the same objectives we want to achieve.

Go ahead in the back.

QUESTION: Yes, please. Regarding the foreign fighters in ISIL, from your answer it’s not clear enough that – are you – are you agreeing or not agreeing with what was mentioned today in The Washington Post that their number is increasing or not? I mean, this is like a reality or just news story?

MS. PSAKI: Well, I don’t have an assessment from the United States Government on numbers. We’ve given numbers in the past that obviously comes out of other agencies. What I was pointing to is the fact that there are a range of steps that we have worked on diplomatically with a number of these countries on cracking down on foreign fighters, whether it’s putting new laws on the books, whether it’s doing more to crack down on borders. That’s one of the primary topics of discussion as it relates to the coalition.

QUESTION: The reason that I’m asking because at the beginning of the year it was mentioned the number of around five or six thousand, and then by July it reached more than 15,000 people from 80 countries. And when you say additional steps were taken by countries who are really concerned about or they have – they are concerned about the foreign fighters, do you have any assessment of these additional steps block some people from entering there, or it’s just like additional steps on the paper?

MS. PSAKI: Well, one, I’d say first on your first part, we have talked before in the past publicly about our assessment that ISIL can muster between 20,000 and 31,500 fighters across Iraq and Syria. That’s based on a review of all intelligence reports from May to August. And we saw an increase over the previous assessment, which is consistent with what we’ve been saying, which is that they grew in strength and numbers over the course of the early period of this year. We’ve seen specific impacts and countries – we’re working on an Iraq first strategy, which is something we’ve consistently talked about. We’ve seen the Iraqi Security Forces strengthen in some areas. We’ve seen efforts to try to take back some parts of territories. But this is going to be a long process, so I just don’t have a new assessment for you.

QUESTION: The other thing which is like always when this story or this issue is raised is based on the – one of the front line or the lines that you are fighting, which is propaganda war or what we can say deviating people from being misled by the ISIL message. Do you still believe there is a link between these two thing, I mean that the war of the – let’s say the war of ideas has to be done in order to stop these people from going there?

MS. PSAKI: Absolutely. The question of what is attracting individuals to join ISIL, to travel across borders is one that is key to us addressing the threat. And that’s why we’ve spent time and energy and the – of high-level State Department officials, including Under Secretary Stengel, to try to coordinate efforts to combat that.

QUESTION: I’m not trying to make the assessment of what you are doing of war of ideas, but generally people are linking between the increasing of the number and the Administration or generally the coalition failure in doing this war, I mean, properly or efficiently. Do you agree with that assessment?

MS. PSAKI: I would not. I think that there is a recognition that more needs to be done to take on ISIL messaging and that they have been effective in using online tools to recruit and to provide often misleading information out there. This is something – it’s not that the United States is the sole – will not be the sole owner of this. We will work with many countries in the region who have more impactful voices in the region to do that.

QUESTION: Do you think that –

QUESTION: Can I ask –

QUESTION: Oh, sorry.

MS. PSAKI: Yeah.

QUESTION: Can I go to Anbar?

MS. PSAKI: Sure.

QUESTION: Your statement about Anbar really quickly?

MS. PSAKI: Yes, yes.

QUESTION: I mean, I’m just reading over – as you know, this came out right before we –

MS. PSAKI: Yes.

QUESTION: — came here. And it just reminds me so much of what we saw in Iraq in 2006. And as the propaganda and the message of ISIL is kind of a “you’re either with us or you’re against us” type of thing, and so I wonder if that’s what was the circumstances for these executions of these Sunni militia tribesmen. I’m wondering if there’s anything more that the U.S. can do or plans to do to get the Sunni tribesmen to continue standing against ISIL in Anbar, which as you know – where the Sahwa beginning – the Awakening Council was, and such a turning point of that war.

MS. PSAKI: Well, I think, one, as – Secretary Hagel and Chairman Dempsey spoke a little bit to this yesterday, but we know that the Sunni tribes are going to have to be and will be a key part of any effort to defeat ISIL, and it’s also in their interests for the security of their provinces as well. It’s about, sure, what we’re doing, and Secretary – I mean – I’m sorry, Ambassador McGurk and General Allen have made efforts to meet with Iraqi leaders and, certainly, leaders of the Sunni tribes when they’ve been on the ground to engage them in this effort.

But it’s also about what the prime minister is doing, and how Prime Minister Abadi is engaging with officials. Just earlier this week, he met with a number of tribal leaders in Anbar to try to engage them in this effort to take on ISIL. I think we’ve felt from the beginning that unity and work across all of the parties in Iraq is the only way that they will be successful. So yes, you’re right there are, if you look back – although they’re entirely different scenarios. But certainly, we can look back and know that the Sunni tribes will play a key part in the success here. That’s why we’re working with the prime minister on this national guard plan which is beginning to be implemented. It’s going to take some time, and certainly, we recognize that.

QUESTION: How much time do you think it’ll take, and do you think those tribesmen are getting paid yet? Because that’s what a lot of that will come down to, is whether they’re getting paid.

MS. PSAKI: I don’t have an assessment of the time it will take. It’s probably more appropriate at DOD; I can check with them and see if they have any assessment of that. I know that we’ve started to start the implementation process of it – the Iraqis have.

QUESTION: But looking at the urgency of the situation – I mean, it all comes down to payments, because that’s what happened when Maliki stopped paying them after U.S. departure. Basically, they went back (inaudible).

MS. PSAKI: I’m familiar with the history, and obviously, incorporating them into the overarching work of the Iraqi Security Forces and ensuring they have the resources they need is certainly part of the factors.

QUESTION: And this – I’m sorry, one question on the national guard. Will this national guard include only Sunni – or will it include others, like the – perhaps incorporating the Shia militias?

MS. PSAKI: It will include – it’s about them all working together, Said.

Go ahead, Leslie.

QUESTION: Is your assessment of the situation – I mean, we know over the last few weeks you’ve been raising concerns about Anbar. I mean, is your assessment that this situation is grave now?

MS. PSAKI: Well, as you know, there have been – “ups and downs” is probably a too low-key way of stating it, but – in Anbar. And we’ve known – this is one of the reasons that there have been numerous airstrikes by the United States, by partner nations in Anbar province. And it’s something – it’s an area where we of course are watching closely, and we’re adapting our strategy as needed. But the province has been under severe threat since the beginning of this year, and the situation remains contested. So we’ve seen it have many ups and downs, and it’s one of the reasons it’s an area we’re especially focused on.

QUESTION: Jen –

MS. PSAKI: I think – let’s almost wrap this up so we can move to a new topic, but go ahead.

QUESTION: On Syria too, Secretary Kerry said yesterday answering a question, “In Iraq, if we didn’t get engaged, I don’t know where ISIL would be today – maybe in Baghdad. What would happen then with Assad and deterioration if ISIL commanded even more territory?” What did he mean by that, do you think?

MS. PSAKI: Well, he means that our engagement and work with the Iraqi Government – which, obviously, they were the leaders on – to form a new government, to have leadership that ruled in a more inclusive manner, to assess the Iraqi Security Forces, to build a coalition to take on airstrikes – or to take on ISIL with airstrikes and military action but also other components, has led to helping to push back ISIL from where it could have been. We’ll never – it’s hard to prove it, but I think there’s no question without these efforts, ISIL would’ve made more progress.

QUESTION: But in his words regarding President Assad that “what would happen then with Assad and deterioration if ISIL commanded” – did he mean that the U.S. doesn’t want Assad to fall to the benefit of ISIL and ISIL takes control?

MS. PSAKI: No, I think our position has been consistent. I don’t think he actually said exactly as you’ve said –

QUESTION: Yeah, this is from the transcript.

MS. PSAKI: I’m happy to look at the context, but I have to be honest with you: Our position has continued to be that we don’t see a place for Assad. He’s lost his legitimacy. I don’t think he was inferring that at all. He was making the point that without our effort and without our engagement, things would be far worse than they are today.

QUESTION: And there are news stories today too saying that the U.S. is in discussion with Saudi Arabia, Russia, and Iran on the future of the president, the Syrian president. Can you confirm these reports?

MS. PSAKI: Well, we’ve certainly been engaged with a range of countries to discuss how we can reach a political solution. We’re obviously not there at this point. As I mentioned a little bit earlier, we’re working on an Iraq first strategy. We’ve, of course, begun engaging militarily in Syria and otherwise. We all – we want to get to a political solution there, so it’s only natural we’d be talking to countries in the region about that.

QUESTION: Change topics?

MS. PSAKI: Sure.

QUESTION: So are you –

MS. PSAKI: Oh, go ahead.

QUESTION: — talking to Iran on Assad?

MS. PSAKI: Not more than you’re aware of, Lesley.

QUESTION: I was just – the alarm bells went off.

QUESTION: Can we go to –

MS. PSAKI: Sure. Go ahead.

QUESTION: Can we go to the Palestinian issue?

MS. PSAKI: Sure.

QUESTION: Okay. First of all, the Secretary Kerry called Abbas today, and can you share with us –

MS. PSAKI: Sure.

QUESTION: — if there’s a readout?

MS. PSAKI: You want a readout of –

QUESTION: Yes, right.

MS. PSAKI: And he also spoke with Prime Minister Netanyahu, I believe, it was last night. Let me just make sure.

QUESTION: Right.

MS. PSAKI: Here’s my little call cheat sheet. You just caught me. Okay.

QUESTION: Okay.

MS. PSAKI: Secretary Kerry spoke with Prime Minister Netanyahu last night and discussed the situation in Jerusalem and the importance of de-escalating tensions. The Secretary emphasized the importance of refraining from provocative actions and rhetoric and preserving the historic status quo on the Haram al-Sharif/Temple Mount. He also spoke with President Abbas this morning. He expressed his serious concern about the escalating tensions in Jerusalem. He stressed the importance of both sides taking steps to calm the situation, refrain from actions and rhetoric that could enflame the situation, and work cooperatively to lower tensions and discourage violence.

QUESTION: Are you doing anything else to lower tensions, I mean, other than just talking to the leaders?

MS. PSAKI: Well, certainly, talking to the leaders – and given Secretary Kerry’s strong relationship with them – we feel is an important component of what we’re doing. Obviously, on the ground, we’re continuing to encourage that directly with many counterparts in the Israeli Government and with the Palestinians as well.

QUESTION: And let me ask you: A Kuwaiti newspaper is saying that a high-level Palestinian delegation will be here on Monday. Can you tell us anything about that?

MS. PSAKI: Sure. Secretary Kerry will meet with Saeb Erekat on Monday, November 3rd. They plan to discuss the way forward for the Middle East, the situation in Gaza, and lowering tensions in Jerusalem.

QUESTION: Okay. And finally –

QUESTION: (Inaudible) delegation next week?

MS. PSAKI: I don’t have additional details on the delegation. I’d certainly ask the Palestinians that.

QUESTION: And finally, I wanted to ask you – I know that it’s not something –

QUESTION: Can we just stay on – is this still on Israel?

QUESTION: Yeah, yeah. I just want to – on the – the status of Jerusalem is going to be before the Supreme Court on Monday. I know this is just beginning.

MS. PSAKI: Mm-hmm.

QUESTION: I wonder if you had a chance to look at this issue and have anything else to add.

MS. PSAKI: Well, this is an ongoing legal proceeding, as you know, so I’m not going to have –

QUESTION: Right.

MS. PSAKI: — additional comment. We have filed – made numerous filings in this case, and certainly would refer you to those briefs for details of our positions. Obviously, the Department of Justice has the lead.

QUESTION: For Israelis that are born in Tel Aviv, does it say Tel Aviv, Israel?

MS. PSAKI: I would point you to the Department of Justice for –

QUESTION: Or does it say Israel? No, on the passports. This is a –

MS. PSAKI: I would point you to the Department of Justice –

QUESTION: — State Department issue, isn’t it?

MS. PSAKI: — for details on the case.

Go ahead.

QUESTION: Just back to the phone call with Prime Minister Netanyahu.

MS. PSAKI: Mm-hmm.

QUESTION: Could you say whether the issue of these comments, these un-named U.S. officials with the “chicken bleep” comments that – whether that came up and whether Secretary Kerry expressed any disappointment with them or that they don’t reflect –

MS. PSAKI: Let me check with him. I didn’t have a chance to ask him that question this morning.

QUESTION: Okay. Because there were some reports that, in fact –

QUESTION: Haaretz is reporting.

QUESTION: Yeah, he raised it and that Kerry kind of apologized for that –

MS. PSAKI: I wouldn’t be surprised if Kerry reiterated what he said many times publicly, which is that these don’t represent his views or the President’s views. But I’ll check with him.

QUESTION: But would you be surprised if he apologized to Prime Minister Netanyahu?

MS. PSAKI: I think he likely reiterated just as I said.

QUESTION: Jen –

QUESTION: Well, one more on Israel.

MS. PSAKI: Sure.

QUESTION: The Israeli finance minister vetoed today new spending on infrastructure for Jewish settlement in the West Bank. How do you view this step?

MS. PSAKI: I hadn’t seen that report. I’m happy to check on it.

Go ahead.

QUESTION: I just wanted to ask you again on the issue of someone – if a U.S. citizen was born or naturalized, let’s say, in Bombay, India. Does it say “India” or does it say “Bombay, India”?

MS. PSAKI: I’d have to check on that for you, Said.

QUESTION: Okay. Because, I mean, I want to ask about this issue –

MS. PSAKI: Said, I’m sorry. We have to move on because it’s Friday afternoon.

QUESTION: Burkina Faso?

MS. PSAKI: Okay. Let’s do Burkina Faso.

QUESTION: Was it a coup that happened today when the head of the armed forces took power?

MS. PSAKI: Well, we spoke about this a little bit yesterday. I don’t have a ton new. Obviously, we’re continuing to assess what’s happening on the ground. So I don’t have a new assessment or label at this point in time.

QUESTION: Well, when the military takes over for a government without a democratic election, is that a coup?

MS. PSAKI: Well, Elise, we look at every situation. We look at every situation and make sure we make an evaluation based on the circumstances on the ground.

QUESTION: Now, how do you anticipate that this will affect your significant security cooperation with Burkina Faso, because it is used as a hub to do counterterrorism activities in the area, particularly against AQIM.

MS. PSAKI: Sure. It’s just too early to assess that. We’re certainly concerned about unfolding events. We regret the violence and the loss of life and certainly call on all parties to avoid further violence and respect the constitutional process. But events are unfolding quickly and we are – continue to track them. I expect we’ll continue to have more to say as we know more.

QUESTION: I mean, is there any way – is there anything that you think needs to be – as they move forward, I mean, obviously whether you would advise or press them to move quickly with elections or to resolve this.

MS. PSAKI: Sure. Well, we have been in touch with senior officials in Burkina Faso, including with the president. We underscored our commitment to peaceful transitions of power through democratic elections and emphasized neither side should attempt to change the situation through extra-constitutional means. So obviously, we have concerns about what we’re seeing on the ground, but we’ve also spoken in the past and it continues to be our view that there are limitations – term limits in place for reasons. So we expressed both –

QUESTION: So you’re not calling for him to be reinstated?

MS. PSAKI: I think we’re calling – we’re conveying exactly as I said, and we’re looking – continuing to assess what’s happening there.

QUESTION: Well, but are you calling for him to be reinstated or not?

MS. PSAKI: I would have said if we were.

QUESTION: So that means no?

MS. PSAKI: I would have said if we were, Elise.

QUESTION: New topic?

MS. PSAKI: Let’s just finish this. Africa? Any more on Africa?

QUESTION: I have one on Africa.

MS. PSAKI: Okay, go ahead.

QUESTION: Actually, on Sudan. Was there a readout that you could give us between Secretary Kerry and the foreign minister of Sudan?

MS. PSAKI: Let me see if I have anything on that, Lara. I actually may. Hold on one second.

QUESTION: That’s what state media is reporting.

MS. PSAKI: Yes. I’m not – they did speak, but let me – I just – let me see if I have anything for you in terms of a readout of it. Why don’t we venture to get that to you after the briefing?

QUESTION: Okay, thank you.

QUESTION: New topic?

MS. PSAKI: Go ahead, Elliot.

QUESTION: Question on China?

MS. PSAKI: Sure.

QUESTION: Unrelated to Secretary Kerry’s trip. Sorry if – I don’t know if you already spoke to this; I apologize if you did.

MS. PSAKI: No, no.

QUESTION: Earlier in the week, Chinese Foreign Minister Wang Yi said that there would be an anticorruption treaty or a deal signed at the APEC meeting. I was wondering if you guys have received any details from the Chinese side about that accord, what would be in it, and what would be expected of the U.S. side on such a thing.

MS. PSAKI: I think he’s likely referring to something that might happen at the leader’s meeting, so I would –

QUESTION: Sure, yeah.

MS. PSAKI: — refer you to the White House for specifics on that. I don’t have any more details.

QUESTION: So you guys haven’t heard anything from –

MS. PSAKI: Obviously, we’re discussing with the White House and with the Chinese every component of the program, the agenda, and the deliverables, but I don’t have anything to preview for you.

QUESTION: Okay.

MS. PSAKI: Go ahead.

QUESTION: Mr. Robert Menendez, the chairman of the Senate Foreign Relations Committee, sent a letter to Vice President Biden and to the Secretary of State Kerry asking them to stop the blatant violation by Turkey against Cyprus. Do you agree with Mr. Menendez that what Turkey is doing is a violation of international law?

MS. PSAKI: Well, I’m certain we will reply to Chairman Menendez’s letter, as we always do. You’re familiar with our position on this issue, which certainly hasn’t changed. We continue to recognize the Republic of Cyprus’s right to develop its resources and its exclusive economic zones. We continue to support strongly the negotiation process conducted under UN Good Offices to reunify the island into a bi-zonal, bi-communal federation. But I don’t have anything new to preview for you.

QUESTION: Okay, can I have a follow-up?

MS. PSAKI: Sure.

QUESTION: In August Secretary Kerry asked China to freeze all provocation acts in South China Sea. What China did is – was what Turkey is doing today in Cyprus. He said, and I quote, “We need to work together to manage tension in the South China Sea.” You know the statement that – by Mr. Kerry. Why the State Department does not respond in the same way to the Turkey provocation in Cyprus?

MS. PSAKI: Because every –

QUESTION: What is the difference?

MS. PSAKI: — region and every conflict and every country is different. So I’m not going to have the same talking point for different countries or regions.

QUESTION: Another – different topic?

MS. PSAKI: Sure.

QUESTION: India. Quickly, I have two questions, please.

MS. PSAKI: Okay.

QUESTION: One: It’s been now one month since Prime Minister Modi was in Washington, and – at the State Department, of course. He made two points when he was here – one in New York when he said that every American will get Indian visa on arrival in India. Any comments on that, if U.S. is going to follow what he said? Because that means he was talking about people-to-people relations, opening the visa, Indian visa for the U.S. citizens.

MS. PSAKI: Well, as you know, Goyal, we’re big believers in people-to-people programs, and we’ve been working with India on certainly increasing visas. But I don’t have anything new to preview for you.

QUESTION: And second, when he was in Washington, before he left Washington, he spoke with the 500 Fortune companies at the U.S.-India Business Council, where he said that India will open for these American companies invest in India, and also make in India. So what he said, that he wants to work with the U.S. companies to have their – India’s doors will be open. So anything about that, if any request has come from the U.S. companies to invest in India or, like in the past, there were some problems about –

MS. PSAKI: Well, Goyal, I’ll just tell you it’s an ongoing discussion. We think India is a great market and one that we certainly believe is – there are opportunities for U.S. businesses –

QUESTION: And finally, one more quickly.

MS. PSAKI: I think we have to move on just because we don’t have unlimited time.

QUESTION: Thank you.

MS. PSAKI: Go ahead.

QUESTION: Jen, on the internal State Department memo about bringing non-U.S. citizens to the U.S. for Ebola treatment, our congressional sources have pushed back on your suggestion that the author of the Ebola memo was some mid-level official. Do you wish to clarify?

MS. PSAKI: I don’t.

QUESTION: Okay. One more on this: Our sources also insist that the memo was also sent to DHS to begin the interagency decision-making process. So folks on the Hill are saying your comment that it never went anywhere isn’t true. What’s your response?

MS. PSAKI: Well, I think the fact is it wasn’t – as I said the other day, it wasn’t – didn’t go through any of the typical process – internal process to senior decision makers. It wasn’t sent through any official interagency process. I can’t assess whether it was sent over an email or not. I don’t have any more information for you on that. But the bottom line is it’s irrelevant, as are their complaints, because this is not a policy we’re considering; it’s not one that we’re applying; it’s not one that we support. So it’s not a memo that is relevant at this point.

QUESTION: Yemen?

MS. PSAKI: Mm-hmm.

QUESTION: Reports that the Houthis have taken over Sana’a and have given President Hadi ten days to form a government.

MS. PSAKI: I’d have to check with our team. I hadn’t seen that report before I came out here.

QUESTION: Okay.

MS. PSAKI: But why don’t we get something around to all of you on it.

QUESTION: Okay. And then just a very fast follow-up –

MS. PSAKI: Sure.

QUESTION: Can you take it?

MS. PSAKI: Yeah. I’m happy to take it. We’ll get – we’ll take it and do a TQ.

QUESTION: Thanks. And just very quickly, there’s also – and you may be aware of this –

MS. PSAKI: Mm-hmm, sure.

QUESTION: — some work between Egypt, Saudi Arabia, and the UAE to create kind of a regional quick response force or regional force to respond to militant threats across the Mideast. I’m wondering if this is something that you all are aware of, and how realistic it is to create something like this.

MS. PSAKI: Sure. I think my – I think my counterparts at the Department of Defense spoke to this and the fact that we’re continuing to work with coalition partners, of which they are all members or partners, to determine how to best take on the threat of ISIL. So there’s just an ongoing discussion. I don’t have anything more for you in terms of what –

QUESTION: But this wouldn’t be necessarily ISIL. It’s for – it could be for Yemen, for example –

MS. PSAKI: Sure.

QUESTION: — or in Libya, for example. It’s just militancy response.

MS. PSAKI: I would point you to DOD. They’re the most appropriate outlet for that.

QUESTION: Well, I was just going to say, is that something that you would support without coordination with U.S. –

MS. PSAKI: I think we’d have to see what it is. It’s obviously just an initial report, and I’d point you to what my colleague at the Department of Defense said.

QUESTION: Boo.

MS. PSAKI: Hi, Jo.

QUESTION: Hi. Sorry for –

QUESTION: No, I’m sorry. Go on.

QUESTION: — running in and out.

MS. PSAKI: Did you say “boo”?

QUESTION: Yes. I thought we were done. (Laughter.)

QUESTION: Oh. Sorry, I cut off Arshad’s grand moment. (Laughter.)

Just a very quick question. I wanted to ask about an American guy called Robert Alan Black, who apparently has disappeared in Abu Dhabi. They believe he’s being held in jail, possibly for taking photos of the wrong things. Do you have any information about him?

MS. PSAKI: We are aware of the reports that a U.S. citizen has been detained in Abu Dhabi. We take our obligation to assist U.S. citizens overseas seriously. The U.S. Embassy in Abu Dhabi is providing all possible consular assistance, but I can’t provide any additional information.

QUESTION: Well, but wait a minute. You’re aware of the report and you’re providing consular assistance? Those two things are inconsistent. Has the gentleman been found and arrested or –

MS. PSAKI: We don’t have a Privacy Act waiver, Elise.

QUESTION: Okay.

MS. PSAKI: There’s not more I can share with all of you.

QUESTION: Okay.

MS. PSAKI: Do we have any more? All right. Happy Halloween, everyone.

QUESTION: Thank you.

(The briefing was concluded at 3:09 p.m.)

DPB # 186


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External links to other Internet sites should not be construed as an endorsement of the views or privacy policies contained therein.

Drinking Water Advisory for North Kaibab Trail – date posted Oct 31, 2014

The National Park Service is issuing a drinking water advisory for the following areas along the North Kaibab Trail, Manzanita Rest Area (Roaring Springs) and Cottonwood Campground within the backcountry at Grand Canyon National Park. Because of the detection of fecal indicators (E. coli), day hikers and backpackers should be self-sufficient and be prepared to carry or treat all drinking water. The rest of the park including South Rim Village, Desert View, Indian Garden, Phantom Ranch and North Rim Developed Area is not affected by this advisory and water is safe to drink.

News Release (www.nps.gov/grca/parknews/drinking-water.htm)

Official Advisory Notice (www.nps.gov/grca/parknews/upload/Boil-Water-Advisory-10-31-2014.pdf)

Safe Drinking Water Site Bulletin (www.nps.gov/grca/planyourvisit/safe-water.htm)

Development of Rapid Canine Fecal Source Identification PCR-based Assays

The extent to which dogs contribute to aquatic fecal contamination is unknown despite the potential for zoonotic transfer of harmful human pathogens. We used Genome Fragment Enrichment (GFE) to identify novel non-ribosomal microbial genetic markers potentially useful for detecting dog fecal contamination with PCR-based methods in environmental samples. Of the 679 sequences obtained from GFE, we used 84 for the development of PCR assays targeting putative canine-associated genetic markers. Twelve genetic markers were shown to be prevalent among dog fecal samples and were rarely found in other animals. Three assays, DG3, DG37, and DG72, performed best in terms of specificity and sensitivity and were used for the development of SYBR® Green and TaqMan® quantitative PCR (qPCR) assays. qPCR analysis of 244 fecal samples collected from a wide geographic range indicated that marker concentrations were below limits of detection in non-canine hosts. In addition, these markers were detected in five out of 18 urban stormwater samples, suggesting that they persist long enough under environmental conditions to be useful for water quality applications. These new assays will be useful to water resource managers who wish to use fecal source identification tools to help manage local water resources impacted by dog feces.

U.S. Condemns ISIL Executions in Anbar Province

We are deeply concerned by reports of mass executions of Sunni tribesmen in Anbar province by ISIL and strongly condemn the brutal actions that ISIL continues to perpetrate against the Iraqi people. One of the primary goals of ISIL is to sow fear into the hearts of all Iraqis and drive sectarian division among its people. We condemn these tactics in the strongest possible terms and stand in solidarity with the Iraqi people against these horrendous and senseless acts of violence. ISIL’s indiscriminate crimes prove, yet again, that it is targeting all Iraqis, regardless of faith or region.

The depravity of the reported executions of the Sunni tribesmen from the Albu Nimr tribe, and other Anbar tribes, reports of mass executions of Shiite prisoners in Mosul, the reports of a mass grave outside of Ramadi, and the continued persecution of other Iraqi minority groups, are further evidence of ISIL’s campaign of terror. Those individuals responsible for these horrendous acts of violence must be identified and held fully accountable.

ISIL does not represent the people of Iraq; they are murderers and terrorists, who do not govern, but bleed the country they occupy. It should also be clear that ISIL is not only a threat to the stability of Iraq, but a threat to the entire region. The international community, including prominent Islamic religious leaders, continues to condemn and reject ISIL’s unrelenting depravity and twisted ideology.

To stop ISIL’s campaign of terror and horror against the Syrian and Iraqi people, we remain steadfast in our efforts to work with the Iraqi Government and our regional partners and lead the international coalition to degrade and defeat ISIL. The United States will do its part to help Iraq move beyond this crisis and we urge all Iraqis to unite against this violence and continue to reject the path of hatred that ISIL represents.

- Source: state.gov

Hitachi Metals Ltd. Agrees to Plead Guilty for Fixing Prices and Rigging Bids on Automobile Parts Installed in U.S. Cars

Hitachi Metals Ltd., an automotive parts manufacturer based in Tokyo, Japan, and successor in interest to Hitachi Cable Ltd. (collectively Hitachi), has agreed to plead guilty and to pay a $1.25 million criminal fine for its role in a conspiracy to fix prices and rig bids for automotive brake hose installed in cars sold in the United States and elsewhere, the Department of Justice announced today. 

Estimating Personal Exposures from Ambient Air Pollution Measures – Using Meta-Analysis to Assess Measurement Error

Although ambient concentrations of particulate matter ? 10?m (PM10) are often used as proxies for total personal exposure, correlation (r) between ambient and personal PM10 concentrations varies. Factors underlying this variation and its effect on health outcome-PM exposure relationships remain poorly understood. The authors therefore conducted a systematic review of literature examining r, including fifteen studies (1990-2009) of 342 participants in five countries. The median (range) of r was 0.46 (0.13,0.72). There was little evidence of funnel plot asymmetry, but substantial heterogeneity of r, which increased 0.05 (95% confidence interval [CI]: 0.01,0.09) per 10µg/m3 increase in mean ambient PM10 concentration.

Title: Nutrient Pollution: A Persistent Threat to Waterways

John Manuel of Durham, NC, is a regular contributor to EHP and the author of The Natural Traveler Along North Carolina’s Coast and The Canoeist.

Background image: © Jodie Coston/Getty Images

About This Article open

Citation: Manuel J. 2014. Nutrient pollution: a persistent threat to waterways. Environ Health Perspect 122:A304–A309; http://dx.doi.org/10.1289/ehp.122-A304

News Topics: Agriculture, Drinking Water Quality, Fertilizer, Harmful Algal Blooms (HABs), Laws, Regulations, and Policy, Marine and Coastal Science, Sanitation, Water Pollution, Water Treatment

Published: 1 November 2014

PDF icon PDF Version (2.6 MB)

Drainage ditch winding through a field at sunsetPoint-source releases of nitrogen and phosphorus have declined dramatically since the 1970s, but nonpoint-source pollution continues to pose a significant threat to water quality.

© Sean Brubaker/Water Rights/Corbis

Passage of the Clean Water Act of 1972 brought many improvements to surface waters by curbing much of the toxic and organic pollution going into waterways. But 42 years later, we have yet to make significant reductions in two major pollutants in our rivers, lakes, and coastal sounds—the nutrients nitrogen and phosphorus. Although nitrogen pollution overall has gone down in U.S. streams and rivers since 2004, it remains a serious problem in many waterways, and phosphorus pollution has gone up significantly.1 The problem is especially challenging in that the deleterious effects of nitrogen and phosphorus often occur hundreds or thousands of miles from where the nutrients originate.

Why have these two nutrients proven so tough to get under control? And are current regulatory and programmatic efforts enough to turn this situation around?

Too Much of a Good Thing

The basics of nutrient pollution are simple enough. Nitrogen and phosphorus occur naturally in soil and water and, with respect to nitrogen, in the air we breathe. They also are added to the environment by humans, principally as fertilizers. These fertilizers enhance the growth not just of crops on land but also of algae and aquatic plants in the waters where they end up.2

Above certain levels, nitrogen and phosphorus cause algae to grow faster than ecosystems can handle. When algae die, the decomposition process consumes oxygen. Nutrient pollution also affects submerged aquatic vegetation, but in a different way: The nutrient-enriched sediment that comes off fields and impervious surfaces decreases the light available for these plants, and the shading leads to their death. Then they, too, consume oxygen as they decompose.3

Large algal blooms can entirely eliminate the oxygen in a body of water, a condition known as hypoxia that kills virtually all aquatic organisms unable to escape these so-called dead zones. According to an ongoing anaylsis by the Virginia Institute of Marine Sciences, the area of oceanic dead zones increased by one-third between 1995 and 2007.4 The hypoxic zone that forms in the Gulf of Mexico each summer varies in size from year to year but averages approximately 5,500 square miles, or roughly the size of the state of Connecticut.5

Toxins produced by harmful algal blooms (HABs) can also directly threaten human health. If ingested or contacted, these toxins can cause skin irritation, stomach cramps, vomiting, nausea, diarrhea, fever, headache, muscle and joint pain, blisters of the mouth, and liver damage.6 Local water treatment plants may not have the equipment necessary to rid drinking water of these toxins. In that case, the only safe course of action is to find other sources of drinking water for however long the toxin persists in the water supply, as was demonstrated in August 2014, when hundreds of thousands of Toledo residents found themselves without potable water.7 HABs can also have severe economic impacts on recreational and commercial fishing, business, and tourism. The U.S. Environmental Protection Agency (EPA) estimates that U.S. tourism alone loses close to $1 billion a year through losses in fishing and boating activities.8

Map of EPA ecoregions showing percentages of river and stream miles rated good, fair, and poor for phosphorus pollutionPhosphorus Pollution in U.S. Rivers and Streams

In six of the nine ecoregions defined by the EPA, phosphorus levels are consistently rated poor (i.e., high) in about a third or more of river and stream miles. The Northern Plains and the Northern Appalachians have the highest proportions of miles rated poor (84% and 71%, respectively). The Southern Plains ecoregion has the highest percentage of river and stream miles rated good (50%), with only 23% rated poor for phosphorus levels.

Source: EPA.1 Percents may not add up to 100% due to rounding.

According to the EPA’s latest National Rivers and Streams Assessment, some 40% of the nation’s river and stream length has elevated levels of phosphorus, and 28% has elevated levels of nitrogen, putting these waters at risk for poor quality as measured by their ability to support aquatic life.1 Where are the nutrients coming from? The principle source of phosphate and nitrogen is nonpoint-source pollution—the diffuse pollution from myriad inputs that accumulates into a problem at the watershed level.9

Although relative amounts vary from watershed to watershed, the fertilizer and animal waste that leach off farmed land generally contribute the most nonpoint-source nutrient pollution to U.S. waterways.10 Other nonpoint sources include stormwater runoff carrying lawn fertilizers and pet waste,11 and atmospheric deposition, much of it from vehicle exhaust and coal- and oil-burning power plant emissions.12

Individual farms also may be considered point sources of pollution, depending on what they directly discharge into waterways.13 Point sources of pollution are regulated by the federal government through the National Pollutant Discharge Elimination System and overall have dramatically reduced their releases of nutrients since the 1970s.14 However, wastewater contains large amounts of nitrogen and phosphorus from human waste, food, and some soaps and detergents, and not all of it is removed in the treatment process. Wastewater treatment plants with less advanced technology can therefore still be significant point-source contributors of nutrient pollution.15

The TMDL Approach

With such widespread pollution caused by so many different sources, it’s no wonder the United States is challenged politically, technologically, and financially to solve the problem of nutrient pollution. The Clean Water Act of 1972 and its various amendments set numeric limits for a variety of chemical pollutants emitted from point sources. However, phosphorus and nitrogen are not among the regulated chemicals. Furthermore, the law does not include regulation of nonpoint-source pollution.

Section 303(d) of the Clean Water Act does require states to submit a list of impaired and threatened waters within their jurisdiction and establish priorities for the development of total maximum daily loads (TMDLs) of pollutants for these water bodies. A TMDL is a calculation of the maximum amount of a pollutant that a water body can receive and still meet federal water quality standards. The TMDL is tailored to reflect how that specific water body is used. For example, a lake used for drinking water might have more stringent limits on phosphorus than one used just for recreation. Thus, while there are no overall federal limits on nitrogen or phosphorus pollution, these nutrients can be managed as part of a TMDL implementation plan.16

The TMDL approach was largely overlooked in the 1970s and 1980s as governments focused on bringing point sources into compliance with the Clean Water Act. More recently, however, attention has turned to the establishment of TMDLs to address other sources of pollution.

But the steps involved in developing a TMDL are time-consuming and costly. States must first identify waters not in compliance with the Clean Water Act, then prioritize water bodies for the development of TMDLs. Due to a lack of money and personnel, most state agencies are able to monitor only a small percentage of their waters consistently enough to detect water-quality problems.15

A third step involves developing a TMDL for each pollutant. This step can take years, especially for a large water body like the Chesapeake Bay, whose watershed encompasses 64,000 square miles in six states and the District of Columbia. Stakeholders in affected jurisdictions meet to hammer out goals, actions, and timetables. Proposed limits must be submitted to the EPA for approval. Planning for the Chesapeake Bay TMDL began in 2000 and was not approved by the EPA until December 2010.17 (The Bay TMDL is actually a combination of 92 smaller TMDLs for individual Chesapeake Bay tidal segments.16)

Map of EPA ecoregions showing percentages of river and stream miles rated good, fair, and poor for nitrogen pollutionNitrogen Pollution in U.S. Rivers and Streams

Many regions show less severe impacts from nitrogen than from phosphorus. The highest proportions of miles in poor condition for nitrogen are found in the Northern Plains (60%), the Temperate Plains (58%), the Northern Appalachians (42%), and the Xeric (36%). In four ecoregions (Coastal Plains, Southern Plains, Southern Appalachians, and Western Mountains) the majority of river and stream miles are rated good for nitrogen.

Source: EPA.1 Percents may not add up to 100% due to rounding.

Finally, the TMDL must be implemented. Again, this can take years following the EPA’s approval of a plan, with pollution reduction goals being targeted in stages. With respect to the Chesapeake Bay’s TMDL, 60% of the plan’s goal for reducing nutrients and sediment is anticipated to be met by 2017, and 100% should be met by 2025.18 As with most complex plans of this nature, however, actual implementation may take much longer, and the costs can be staggering. For instance, estimates for the state of Maryland to fully implement its portion of the Chesapeake Bay TMDL total $928 million for farmers, $2.37 billion for municipal wastewater systems, $7.39 billion for stormwater systems, and $3.72 billion for septic tank upgrades.19

Best Management Practices

TMDLs are not the only vehicle being used to address nutrient pollution. Federal programs including the Conservation Reserve Program (CRP), administered by the U.S. Department of Agriculture, provide direct rental payments to farmers who remove environmentally sensitive acreage from agricultural production and implement conservation practices.20 The EPA awards grants to states to build or upgrade wastewater treatment plants and to support various state-level nonpoint-source management programs.

Various best management practices (BMPs) are being employed to reduce nutrient pollution from urban sources. Technologies such as detention basins, constructed wetlands, vegetative swales, and bioretention facilities (e.g., rain gardens) can all be used to slow down stormwater and biologically degrade the nutrients before they reach waterways. Practices that reduce nutrient runoff from developed areas include leaf collection in the fall, bagging of dog waste, and prohibitions on phosphorus in lawn fertilizers.21 Agriculture employs a whole different array of proven BMPs ranging from planting cover crops in winter, to better timing and amounts of fertilizer application, to the establishment of vegetated buffers along streams.22

Yet, even after decades of research, much remains unknown about how phosphorus and nitrogen interact in the environment. For instance, recent studies in Lake Superior suggested that reducing phosphorus loads may actually lessen the ability of aquatic organisms to remove nitrogen from the water. The authors pointed out this should “in no way be considered as a rationale for relaxing [phosphorus] control measures.”23 Instead, they wrote, the results suggest more attention should be paid to controlling nitrogen in tandem with phosphorus—which will be challenging, they added, given that sources of nitrogen tend to be even more diffuse than those of phosphorus.22

With respect to farmers, the emphasis has been on use of incentives to encourage voluntary adoption of less-polluting practices. These approaches commonly use financial, educational, and technical assistance as a stimulus. However, surveys suggest that in key farming states such as Iowa, overall participation is low, and among farmers who do participate, the investment in conservation tends to be small.24 Referring to a 2011 poll of Iowa farmers, a report by the nonprofit Iowa Policy Project noted that 51% of respondents reported making no conservation expenditures in the past 10 years, and more than one-third were unaware of many of the conservation programs available in the state.25

The report authors further pointed out that farmers were enrolling fewer of their acres in the federal CRP. “Iowa CRP acres are decreasing, falling by almost one-fourth, from 1,970,486 acres in 2007 to 1,525,012 in 2012,” they wrote. “The drop in CRP enrollment has coincided with the ethanol boom and the rise in the price of corn, suggesting that the economic bottom line does affect a farmer’s willingness to adopt conservation measures. When [government] subsidies pay less than cash rent, the conservation practices disappear.”24

Map showing which states have numeric criteria for nitrogen and/or phosphorusStates with Numeric Criteria for Total Nitrogen (N) or Total Phosphorus (P)

This map shows a national summary of current numeric total nitrogen and total phosphorus EPA-approved criteria. More criteria are expected to be added in the near future, according to state-provided information. ”Watertypes” refers to three types of water bodies: lakes/reservoirs, rivers/streams, and estuaries.

Source: EPA28

Nutrient trading between point and nonpoint sources is an idea that is promoted as an alternative to cost-sharing. In this voluntary system, farmers accumulate and sell credits by implementing conservation measures that reduce nutrient loads. Wastewater treatment plants in the same watershed buy the credits from farmers instead of investing in new technology to meet federal requirements for reducing nutrient output.26

Nutrient trading has worked well in the Long Island Sound, where there are many wastewater treatment plants and farms in the same watershed.27 Patrick Parenteau, a professor of law and senior counsel to the Environmental and Natural Resources Law Clinic at Vermont Law School, notes this program currently operates between point sources, mainly publicly owned treatment works in Connecticut. “There has been talk about including nonpoint sources,” he says, “but it hasn’t gotten there yet.”

But in other watersheds such as the Maumee Valley in western Lake Erie, farms contribute vastly more nutrients than do the few wastewater treatment plants, so opportunities for trading are limited. Further, nutrient trading programs can be complex, and they take time to establish.

“There is a lot of both hope and frustration [among farmers] with nutrient trading,” says John Bell, government affairs counsel for the Pennsylvania Farm Bureau. “Pennsylvania set a reasonable set of ground rules for nutrient trading, but even with this, it’s hard for farmers to get enthusiastic because of the limited credit given to their conservation practices.” He explains that a farmer may implement a practice that reduces a hundred pounds of nitrogen at the stream flowing past his farm, but will only receive nutrient trading credit for the impact that action has in waters possibly hundreds of miles away. “Very few practices to reduce nonpoint-source pollution have an immediate impact on a watershed,” he says. “Often, the impacts are not measurable for a number of years after the [practice] was first implemented.”

Some experts believe that without setting numeric water-quality standards for nitrogen and phosphorus, efforts to combat nutrient pollution will fail. For now, almost half the states have established statewide numeric limits on nitrogen and/or phosphorus in at least some water bodies. Hawaii is the only state with a complete set of nitrogen and phosphorus criteria for all types of water bodies.28 Whether these states are able to maintain and enforce meaningful standards remains to be seen.


References

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2. EPA. Nutrient Pollution > The Problem [website]. Washington, DC:Office of Water, U.S. Environmental Protection Agency (updated 16 March 2014). Available: http://www2.epa.gov/nutrientpollution/pr​oblem [accessed 29 October 2014].

3. FWS. Submerged Aquatic Vegetation: Where Have All the Grasses Gone? [website]. Annapolis, MD:Chesapeake Bay Field Office, U.S. Fish and Wildlife Service (updated 28 January 2011). Available: http://www.fws.gov/chesapeakebay/cbsav.h​tml [accessed 29 October 2014].

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20. FSA. Conservation Reserve Program [website]. Washington, DC:Farm Service Agency, U.S. Department of Agriculture (updated 15 July 2014). Available: http://www.apfo.usda.gov/FSA/webapp?area​=home&subject=copr&topic=crp [accessed 29 October 2014].

21. EPA. Make Your Home the Solution to Stormwater Pollution. Washington, DC:U.S. Environmental Protection Agency (January 2003). Available: http://www.epa.gov/npdes/pubs/solution_t​o_pollution.pdf [accessed 29 October 2014].

22. Lilly JP. Soil Facts. Best Management Practices for Agricultural Nutrients. Raleigh, NC:North Carolina Cooperative Extension Service, North Carolina State University (undated). Available: http://www.soil.ncsu.edu/publications/So​ilfacts/AG-439-20/ [accessed 29 October 2014].

23. Finlay JC, et al. Human influences on nitrogen removal in lakes. Science 342(6155):247–250 (2013); doi: 10.1126/science.1242575.

24. ISU. Iowa Farm and Rural Life Poll. 2011 Summary Report. Ames, IA:Cooperative Extension Service, Iowa State University (2011). Available: http://www.soc.iastate.edu/extension/far​mpoll/2011/PM3016.pdf [accessed 29 October 2014].

25. Osterberg D, Kline A. Why Iowa’s Nutrient Strategy Falls Short Against Water Pollution. Iowa City, IA:The Iowa Policy Project (17 July 2014). Available: http://www.iowapolicyproject.org/2014Res​earch/140717-nutrient.html [accessed 29 October 2014].

26. Lal H. Nutrient credit trading—a market-based approach for improving water quality. In: Advances in Nitrogen Management for Water Quality (Delgado JA, Follett RF, eds.). Ankeny, IA:Soil and Water Conservation Society (2010). Available: ftp://ftp.wcc.nrcs.usda.gov/wntsc/mktBas​ed/nitrogenCreditTrading.pdf [accessed 29 October 2014].

27. Denny RC. Connecticut’s Nitrogen Trading Program. Hartford, CT:Department of Energy and Environmental Protection, State of Connecticut. Available: http://goo.gl/ipaIcm [accessed 29 October 2014].

28. EPA. Nutrient Pollution Policy and Data > State Development of Numeric Criteria for Nitrogen and Phosphorus Pollution [website]. Washington, DC:Office of Water, U.S. Environmental Protection Agency (updated 1 October 2014). Available: http://cfpub.epa.gov/wqsits/nnc-developm​ent/ [accessed 29 October 2014].

Title: Beyond Malnutrition: The Role of Sanitation in Stunted Growth

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

Background image: WHO

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Citation: Schmidt CW. 2014. Beyond malnutrition: the role of sanitation in stunted growth. Environ Health Perspect 122:A298–A303; http://dx.doi.org/10.1289/ehp.122-A298

News Topics: Children’s Health, Diet and Nutrition, Gastrointestinal Health, International Environmental Health, Microbial Agents, Musculoskeletal Health, Drinking Water Quality, Sanitation

Published: 1 November 2014

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Three Indian childrenWorldwide, stunting affects an estimated 165 million children under the age of 5. Nutritional interventions are only part of the solution.

© Roger Parkes/Alamy

Malnutrition in children can manifest in different ways; malnourished children can be underweight or obese, or their height can be stunted. Global health experts used to measure progress toward meeting childhood malnutrition goals on the basis of improvements in weight. But now stunting is the top priority. That’s because children who lose weight from a few days of being sick or hungry can readily gain it back, while the stunting that results from chronic malnourishment during early development has permanent consequences.1 More than merely a matter of appearance, stunting is a marker for an array of developmental problems, explains Reynaldo Martorell, a professor of international nutrition at Emory University. “The more stunted the child,” Martorell says, “the more likely it is that the brain, kidneys, and other organ systems will be affected.”

Studies have associated childhood stunting with IQ deficits, poor school performance, poverty, and higher risks for diabetes, heart disease, and stroke later in life.1,2,3,4 That’s both a health and an economic problem for affected countries, given how stunting impacts human capital and productivity.5 And although its prevalence is in steady decline—from 40% of children under age 5 in low-and middle-income countries in 1990 to 26% in 2011,6 mainly as a result of rising incomes and improved living standards—stunting remains pervasive. Worldwide, it’s estimated that 165 million children under age 5 are stunted, most of them in Africa and South and Central Asia.6 The number is expected to fall to 127 million by 2025, but that’s not enough to meet the goal of the World Health Organization (WHO) to reduce childhood stunting to 100 million cases by then.7

It has become clear that nutritional interventions are only part of the solution to stunted growth. In countries such as India, for instance, stunting occurs even among well-fed children, and that’s led investigators to consider other causes, especially poor sanitation and hygiene. Evidence shows that children who live without adequate sanitation, hygiene, and clean drinking water don’t grow as well as children who do. Meanwhile, more than 626 million people in India (nearly half the population) routinely defecate on the ground outdoors,8 and this practice has been proposed9 as an important cause of India’s stunting epidemic, which affected an estimated 48% of the country’s children as of 2005–2006.10

In somewhat newer thinking, researchers are exploring the possibility that poor hygiene and a lack of sanitation induce a gut disorder called environmental enteropathy (EE) that diverts energy from growth toward an ongoing fight against subclinical infection. Nutritionists are now collaborating with experts in a field known as water, sanitation, and hygiene (WASH), and their combined efforts are helping to galvanize regional programs to improve hygiene in countries afflicted with high stunting rates.

In November 2014, for instance, experts will convene in New Delhi, India, for a regional conference titled Stop Stunting: Improving Child Feeding, Women’s Nutrition, and Household Sanitation in South Asia. India’s new prime minister, Narendra Modi, has also spearheaded a campaign known as Swachh Bharat (Clean India)11 in part to eliminate open defecation in the country by 2019.12

The Historical View

Stunting has been observed for centuries, but it wasn’t until 1973 that the current standard definition for the term was introduced by the nutritionist John Waterlow, from the London School of Hygiene and Tropical Medicine. Writing in The Lancet, Waterlow distinguished between deficits in height-for-age, which he called stunting, and deficits in weight-for-height, or wasting.13 He also described wasting as “a fairly acute state of malnutrition,” whereas stunting was said to result from undernutrition over a long period, causing a “retardation in linear growth.”13

Waterlow quantified stunting in terms of standard deviations below the expected height for a given age. Today this metric is known as the height-for-age z (HAZ) score; stunted children are said to be at least 2 standard deviations below the age- and sex-specific median height as determined by the World Health Organization (WHO) Child Growth Standards.14

Bar charts illustrating trends in child stunting by UN regionTrends in child stunting by UN region (1990–2025)

Source: de Onis et al. (2013)7

These standards were developed using reference data collected through the Multicentre Growth Reference Study (MGRS), which the WHO conducted for nearly six years in six locations: Davis, California; Muscat, Oman; Oslo, Norway; Pelotas, Brazil; Accra, Ghana; and South Delhi, India. Growth measures were taken weekly during infancy, declining to monthly and then bimonthly as the children grew older to account for the especially rapid growth that occurs in babies. And importantly, measurements were made only of healthy, well-nourished, breastfed children from middle-class backgrounds, whose growth rates were assumed to be optimal and uncompromised by the effects of poverty.15

MGRS results published in 2006 produced a striking finding: Infants and young children follow similar growth patterns regardless of race or ethnicity.16 Maureen Black, director of the Division of Growth and Nutrition at the University of Maryland School of Medicine, explains that genetic differences that render some Arctic peoples short, for instance, and the Maasai of Kenya tall are expressed later in life. Black says that 97% of healthy young children should be of a height that falls within the HAZ’s statistical boundary. “So theoretically, just 3% of the child population should be less than two standard deviations shorter than the [median] HAZ,” she says. “But we see values much higher than that—in Bangladesh, for instance, nearly half the kids are stunted.”17

Beyond Nutrition

Nutritionists have tried dozens of approaches to prevent stunting, such as micronutrient supplements for pregnant women and children (especially growth promoters including iron, zinc, calcium, and folate); increased availability of fat-fortified commercial products such Nutributter and Plumpy’nut; a concerted push to encourage breastfeeding during the first six months of life; and efforts to improve the nutritional quality of the complementary foods babies eat while weaning.6

But Jean Humphrey, a professor of human nutrition at the Johns Hopkins Bloomberg School of Public Health, says none of these interventions has been able to eliminate stunting completely. At best, she says, they improve growth by about a third of the typical height deficit in stunted Asian and African children. “This tells us that dietary improvements are important but not sufficient,” she says. “If we really want to eliminate stunting, we need to do more.”

Meanwhile, mounting evidence has shown that poor hygiene and sanitation also constrain linear growth in children. One study found that Bangladeshi children who had access to clean drinking water, improved toilets, and facilities for handwashing with soap, for instance, had a roughly 50% improvement in HAZ scores compared with control children who didn’t.18 Similar results emerged from studies in Sudan19 and Mexico,20 yet it was unclear exactly why poor WASH would contribute to stunting and WASH improvements would help to ameliorate it.

World map showing prevalence of child stunting by countryStunting among children under age 5 years

Source: de Onis et al. (2013)7

Scientists at first hypothesized that children who live with poor hygiene become stunted because they have chronic diarrhea. A 2008 meta-analysis that pooled results from nine studies supported that hypothesis; the authors revealed a strong association between impaired linear growth and five or more episodes of diarrhea within the first two years of life.21 But in other studies, the evidence was less compelling. Researchers in Karachi, Pakistan, for example, found that handwashing by children and their parents was highly protective against diarrhea but had no effect on stunting.22

Investigations into potential links between diarrhea and stunting are ongoing. Meanwhile, researchers have increasingly turned their attention to the condition known as EE. This illness was first documented nearly 50 years ago, after military veterans and Peace Corps volunteers started coming home from South and Southeast Asia with an asymptomatic intestinal condition that looked like a mild form of celiac disease. Then known as tropical enteropathy, the disorder was seen initially on biopsy—intestinal linings tended to thin out and fill with inflammatory secretions. Experts describe people with EE as having “leaky guts,” and the disorder was eventually found to be pervasive in the developing world. Interestingly, EE generally resolves in people who relocate or return to developed countries.23

Exploring EE

EE isn’t easy to diagnose; biopsies are definitive but impractical for research, says Stephen Luby, a professor at Stanford University’s Freeman Spogli Institute for International Studies. Scientists generally rely on indirect approaches for diagnosing EE, the most common being a test of what’s called the lactulose:mannitol (L:M) ratio. To administer the test, which is also used to diagnose Crohn’s disease, scientists give children a drink that contains the two sugars lactulose and mannitol. Mannitol is a small sugar that is readily absorbed through the small intestine, while lactulose is a much larger sugar that is only partly absorbed. If the child’s intestine is abnormally permeable (“leaky”), then unusually large amounts of lactulose pass into the blood and are eventually excreted in urine. High lactulose levels in urine therefore predict EE, “but the test is hard to standardize and interpret,” Luby says. “Stunting is easy to measure; EE, not so much.”

Despite its limitations, the L:M ratio has provided much of the evidence in support of a role for EE in stunting. The most highly cited of these studies was published in 1991 by researchers who concluded that abnormal L:M ratios could explain nearly half the impaired growth observed in a group of Gambian children.24 Humphrey says the Gambian study was critical because it was the first to show that interventions to reduce clinical diarrhea could be highly successful without changing the incidence of stunting at all. In a followup study, the same research team linked impaired growth in Gambian infants to intestinal enteropathy and high levels of plasma immunoglobulins and endotoxin antibodies.25

Figure illustrating proposed pathogenesis associated with environmental enteropathyStunting among children under age 5 years

(a) In normal intestines, goblet cells secrete a layer of mucus that protects epithelial cells from exposure to bacteria. Macrophages protect against bacteria entering the lamina propria while minimizing tissue injury. Tight junctions are undisrupted. Villi are long and finger-like, separated by relatively shallow crypts.

(b) Recurrent gastrointestinal infection results in disruption of the mucus layer and loss of barrier function. Luminal bacteria bind to dendritic cells and intraepithelial lymphocytes (IELs) on the epithelial surface. The immune response engages, and the intestine becomes more permeable as a result of IEL activation. Increased pathogenic infiltration into the lamina propria results in a cycle of inflammation that ultimately changes the architecture of the intestine, with increased IELs and lymphocytic infiltration in the lamina propria, as well as villus atrophy and crypt hyperplasia.

Figure reprinted from Korpe and Petrie (2012).30 Caption adapted by EHP.

According to Humphrey, ingested microbes, once they pass through a leaky gut into the blood stream, set off a continual low-level immune reaction. She says this reaction drains off energy and nutrients that children would otherwise need to grow to their full potential. “The immune response in EE is lifesaving, but it’s also metabolically expensive,” she says. Humphrey now believes that diarrhea is a minor contributor to stunting when compared with EE, which she calls a “chronic immune-activating disorder that chips away at growth and affects kids on a population level.”

Luby points out that in extreme cases, chronic diarrhea and EE might go hand in hand, making it difficult to tease out their individual effects. But he adds that a number of different organisms can infect the intestinal tract and cause gut dysfunction without inducing diarrhea. Specific causative bacterial agents in EE remain unknown, Luby says, but preliminary investigations in Bangladesh found that children with access to better hygiene had fewer intestinal pathogens, lower L:M ratios, less immune stimulation, and better linear growth.18

Two major randomized studies, each funded by the Bill and Melinda Gates Foundation, are now investigating the potential role of EE in childhood stunting. Humphrey leads one of them—the Sanitation, Hygiene, Infant Nutrition Efficacy (SHINE) Project26—which is under way in Zimbabwe. The study is comparing growth outcomes in relation to measures of gut function among villagers at two locations. One of the villages has access to latrines, treated drinking water, and programs to limit exposure to fecal microbes, while the other does not. The second study, known as WASH Benefits, is co-directed by Luby. It is now under way at multiple sites in Bangladesh and Kenya.27 Like SHINE, the WASH Benefits study will measure EE markers in relation to stunting, among many other end points. Villagers in both Bangladesh and Kenya have been randomized to a variety of interventions involving water quality, sanitation, handwashing, and nutrition.

Cultural Barriers

Luby says subjects in the WASH Benefits study have been highly cooperative. The team had extensive anthropological support, he says, and “when walking into villages during unannounced visits we see chlorine in drinking water, soap in the washing stations; all our indicators are way above benchmark.” Yet Luby concedes that the cooperation seen in research settings might not carry through in a real-world intervention. When it comes to fighting stunting, he says, it’s easier for health groups to dispense micronutrient tablets than it is to change an entire community’s drinking water, sanitation, and handwashing behavior.

Other researchers echo similar views. Francis Ngure, an independent consultant and researcher at Cornell University, found that even though soils ingested by infants and toddlers crawling on dirt floors in rural Peru were often highly contaminated with chicken feces and fecal bacteria, villagers generally were unable or unwilling to take steps to limit their exposure. According to Ngure, villagers more often said they couldn’t afford to keep poultry in cages and that they preferred the taste of free-range chicken meat and eggs. Similarly, confining children to clean play spaces elicited negative reactions from villagers in Zimbabwe, who felt they interfered with cultural concepts of play.22

Sue Coates, chief of the WASH Section with the United Nations Children’s Fund India, adds that when it comes to stopping open defecation in India, toilet construction isn’t the main problem. “The real problem is promoting a social demand for initial and sustained toilet use,” she says. It would be like telling Americans or Europeans they should now defecate in the street, she explains. “We’re overlaying our belief system, norms, and mindsets on others, and this is a very complex development scenario to tackle,” Coates says.

For the Indian government’s new Swachh Bharat campaign, which launched in October 2014, frontline health workers are trying to associate toilet use with dignity, especially for women and girls.28 UNICEF and other groups are also urging a link between infant and child care and the need for mothers to wash their hands with soap before engaging in breastfeeding and complementary feeding by equating hand hygiene with better nutrition and child growth.29

Maintaining this trend is both a health and an economic imperative for developing countries. Stunted children will likely never reach their full potential as productive members of their own societies, emphasizes Mercedes de Onis, coordinator of the Growth Assessment and Surveillance Unit in the WHO Department of Nutrition. “But stunting isn’t something you can address with a silver bullet,” she says. “It has divergent components, and what causes it in one location may not be what causes it in another. There’s a lot we can do, but ultimately stunting is tied to poverty. And eradicating poverty isn’t easy.”


References

1. Hoddinott J, et al. Adult consequences of growth failure in early childhood. Am J Clin Nutr 98(5):1170–1178 (2013); doi: 10.3945/ajcn.113.064584.

2. Grantham-McGregor S, et al. Developmental potential in the first 5 years for children in developing countries. Lancet 369(9555):60–70 (2007); doi: 10.1016/S0140-6736(07)60032-4.

3. Carba DB, et al. Early childhood length-for-age is associated with the work status of Filipino young adults. Econ Hum Biol 7(1):7–17 (2009); doi: 10.1016/j.ehb.2009.01.010.

4. Hoddinott J, et al. The economic rationale for investing in stunting reduction. Mat Child Nutr 9(suppl 2):69–82 (2013); doi: 10.1111/mcn.12080.

5. Adair LS, et al. Associations of linear growth and relative weight gain during early life with adult health and human capital in countries of low and middle income: findings from five birth cohort studies. Lancet 382(9891):525–534 (2013); doi: 10.1016/S0140-6736(13)60103-8.

6. Maternal and Child Nutrition Study Group. Executive Summary of The Lancet Maternal and Child Nutrition Series. Oxford, United Kingdom:Elsevier Inc. (6 June 2013). Available: http://download.thelancet.com/flatconten​tassets/pdfs/nutrition-eng.pdf [accessed 29 October 2014].

7. de Onis M, et al. The World Health Organization’s global target for reducing childhood stunting by 2025: rationale and proposed actions. Mat Child Nutr 9: suppl26–26 (2013); doi: 10.1111/mcn.12075.

8. WHO. Water Sanitation Health: Fast Facts [website]. Geneva, Switzerland:World Health Organization (2014). Available: http://www.who.int/water_sanitation_heal​th/monitoring/jmp2012/fast_facts/en/ [accessed 29 October 2014].

9. RICE. The Nutritional Value of Toilets: How Much International Variation in Child Height Can Sanitation Explain? Amston, CT:Research Institute for Compassionate Economics, Inc. (2013). Available: http://riceinstitute.org/wordpress/resea​rch/?did=13 [accessed 29 October 2014].

10. DHS Program. Where We Work: India [website]. Rockville, MD:The Demographic and Health Surveys Program, ICF International (2014). Available: http://dhsprogram.com/Where-We-Work/Coun​try-Main.cfm?ctry_id=57&c=India [accessed 29 October 2014].

11. PM launches Swachh Bharat Abhiyaan. Narendramodi.in (2 October 2014). Available: http://www.narendramodi.in/pm-launches-s​wachh-bharat-abhiyaan/ [accessed 29 October 2014].

12. HP sets 2019 as deadline to make state open defecation free. Hindustan Times, online edition (26 October 2014). Available: http://goo.gl/r7je7P [accessed 29 October 2014].

13. Waterlow JC. Note on the assessment and classification of protein-energy and malnutrition in children. Lancet 302(7820):87–89 (1973); doi: 10.1016/S0140-6736(73)93276-5.

14. WHO. The WHO Child Growth Standards [website]. Geneva, Switzerland:World Health Organization (2014). Available: http://www.who.int/childgrowth/en/ [accessed 29 October 2014].

15. WHO Multicentre Growth Reference Study Group WHO Child Growth Standards based on length/height, weight and age. Acta Pediatr Suppl 450:76–85 (2006); doi: 10.1080/08035320500495548.

16. WHO Multicentre Growth Reference Study Group Assessment of differences in linear growth among populations in the WHO Multicentre Growth Reference Study. Acta Paediatr Suppl 450:56–65 (2006); doi: 10.1080/08035320500495514.

17. Helen Keller International. Bulletin No. 7: Bangladesh. The Food Security and Nutrition Surveillance Poject (FSNSP)–Round 1: January 2010–April 2010. Gulshan, Dhaka, Bangladesh:Helen Keller International, Bangladesh (2010). Available: http://goo.gl/PqTQuN [accessed 29 October 2014].

18. Lin A, et al. Household environmental conditions are associated with enteropathy and impaired growth in rural Bangladesh. Am J Trop Med Hyg 89(1):130–137 (2013); doi: 10.4269/ajtmh.12-0629.

19. Merchant AT, et al. Water and sanitation associated with improved child growth. Eur J Clin Nutr 57(12):1562–1568 (2003); doi: 10.1038/sj.ejcn.1601725.

20. Allen LH, et al. The Collaborative Research and Support Program on Food Intake and Human Function: Mexico Project: Final Report. Storrs, CT:Department of Nutritional Sciences, University of Connecticut.

21. Checkley W, et al. Multi-country analysis of the effects of diarrhoea on childhood stunting. Int J Epidemiol 37(4):816–830 (2008); doi: 10.1093/ije/dyn099.

22. Ngure FM, et al. Water, sanitation, and hygiene (WASH), environmental enteropathy, nutrition, and early child development: making the links. Ann NY Acad Sci 1308:118–128 (2014); doi: 10.1111/nyas.12330.

23. Lindenbaum J, et al. Subclinical malabsorption in developing countries. Am J Clin Nutr 25(10):1056–1061 (1972); PMID: 4562265; http://ajcn.nutrition.org/content/25/10/1056.long.

24. Lunn PG, et al. Intestinal permeability, mucosal injury, and growth faltering in Gambian infants. Lancet 338(8772):907–910 (1991); doi: 10.1016/0140-6736(91)91772-M.

25. Campbell DI, et al. Growth faltering in rural Gambian infants is associated with impaired small intestinal barrier function, leading to endotoxemia and systemic inflammation. J Nutr 133(5):1332–1338 (2003); http://www.ncbi.nlm.nih.gov/pubmed/12730419.

26. NIH. SHINE Sanitation, Hygiene, Infant Nutrition Efficacy Project [clinical trial]. Bethesda, MD:National Library of Medicine, National Institutes of Health (updated 19 June 2013). Available: http://clinicaltrials.gov/show/NCT018249​40 [accessed 29 October 2014].

27. Arnold BF, et al. Cluster-randomised controlled trials of individual and combined water, sanitation, hygiene and nutritional interventions in rural Bangladesh and Kenya: the WASH Benefits study design and rationale. BMJ Open 3:e003476. (2013); doi: 10.1136/bmjopen-2013-003476.

28. UNICEF. WASH and Women [website]. New York, NY:United Nations Children’s Fund (updated 30 April 2003). Available: http://www.unicef.org/wash/index_womenan​dgirls.html [accessed 29 October 2014].

29. UNICEF and EU. Multi-sectoral Approaches to Nutrition: The Case for Investment by Public Health, Water, Sanitation, and Hygiene. New York, NY and Brussels, Belgium:United Nations Children’s Fund and the European Union (undated). Available: http://www.unicef.org/eapro/Brief_Health​Nutrition.pdf [accessed 29 October 2014].

30. Korpe PS, Petrie WA Jr. Environmental enteropathy: critical implications of a poorly understood condition. Trends Mol Med 18(6):328–336 (2012); doi: 10.1016/j.molmed.2012.04.007.

Title: PCBs and Impaired Cochlear Function in Children: Comparing Pre- and Postnatal Exposures

Julia R. Barrett, MS, ELS, a Madison, WI–based science writer and editor, has written for EHP since 1996. 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. 2014. PCBs and impaired cochlear function in children: comparing pre- and postnatal exposures. Environ Health Perspect 122:A310; http://dx.doi.org/10.1289/ehp.122-A310

News Topics: Children’s Health, Persistent Organic Pollutants (POPs), Polychlorinated Biphenyls (PCBs), Sensory Health

Published: 1 November 2014

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Prenatal and Postnatal Serum PCB Concentrations and Cochlear Function in Children at 45 Months of Age

Todd A. Jusko, Renata Sisto, Ana-Maria Iosif, Arturo Moleti, Soňa Wimmerová, Kinga Lancz, Juraj Tihányi, Eva Šovčíková, Beata Drobná, L’ubica Palkovičová, Dana Jurečková, Kelly Thevenet-Morrison, Marc-André Verner, Dean Sonneborn, Irva Hertz-Picciotto, and Tomáš Trnovec

High stability, the quality that made polychlorinated biphenyls (PCBs) so useful in hundreds of industrial and commercial applications during the mid-1900s, has ensured the compounds’ continuing presence in the environment despite decades of banned and restricted use.1 This class of more than 200 structurally related chemicals has been linked to both cancer and noncancer outcomes,1 and some studies suggest prenatal or early-life exposure to PCBs may adversely affect the auditory system.2,3 A new study reported in EHP specifically links postnatal—but not prenatal—PCB exposure with impaired cochlear function.2

The cochlea, an extremely sensitive organ in the inner ear, converts soundwave vibrations to nerve impulses transmitted to the brain. Cochlear damage can impair hearing and is a well-known side effect of certain antibiotics and chemotherapeutic drugs.4 Rodent studies have shown that PCBs, too, can affect the cochlea, leading to hearing loss.5 Some human studies have reported associations between PCB exposure and hearing impairment, particularly in children,6,7 although others have found no such association.8

Micrograph of cochlear hair cellsClusters of hair cells populate the cochlea and detect sounds transmitted to the inner ear.

© David Spears FRPS FRMS/Corbis

The current study focused on mother–infant pairs from an ongoing birth cohort study in eastern Slovakia. Study participants enrolled during hospital stays for childbirth in 2002–2004. Maternal and cord blood samples were collected for PCB and lipid measurements, and children underwent blood tests at 6, 16, and 45 months of age. At 45 months, the children also underwent otological and auditory testing, including an assessment of distortion product otoacoustic emissions (DPOAEs), a measure of cochlear function.

Health records provided information on the children’s births and subsequent medical visits. Mothers completed questionnaires at study enrollment and at the 16- and 45-month followup visits, providing sociodemographic information and data on lifestyle, diet, medical history, and other factors that could affect their children’s health and hearing. A total of 351 children were included in the study.

Blood tests measured 15 PCB congeners, but analyses focused on PCB-153, which was detected in nearly all samples and closely correlated with total PCB concentrations. An inverse relationship existed between decreased DPOAE amplitude (a marker of diminished cochlear function) and postnatal serum PCB concentrations, with the strongest association observed for cumulative levels of PCBs. The authors suggest this could indicate that duration of exposure, rather than timing, is most important for cochlear development. No association was observed between prenatal PCB exposure and decreased DPOAE amplitude.2

The PCB-associated decrease in DPOAE amplitude was not large.2 “Certainly, the hearing impairment would be subclinical,” says study coauthor Tomáš Trnovec, a professor of environmental medicine at Slovak Medical University in Bratislava. However, the cochlea is vulnerable to any number of environmental insults, including noise, organochlorine pesticides, and drugs, among others, Trnovec says. “The combined effect of these factors is completely unknown,” he says, adding that “under different settings and other data treatment … a prenatal exposure effect cannot be excluded.”

It’s also unknown whether effects persist and whether continued exposure (combined with other stressors) builds on early damage. “In my opinion, PCB ototoxicity may be involved in the pathogenesis of hearing impairment in the adult population,” says Kyoung-Bok Min, an assistant professor in occupational and environmental medicine at South Korea’s Ajou University School of Medicine, who was not involved in the study. Min and colleagues recently reported an association between PCB serum levels and increased prevalence of hearing impairment in adults who participated in the National Health and Nutrition Examination Survey.9 “Further epidemiologic studies are needed in terms of whether the impact of exposure to PCBs on cochlear function changes throughout the life span of the human,” he says.

In addition, Susan Schantz, a professor of veterinary biosciences and psychology at the University of Illinois at Urbana–Champaign, raises the possibility of potential impacts beyond hearing. “One of the things that really interests me—and that I don’t know the answer to—is what does that kind of a decrease [in DPOAE amplitude] mean? Would it be enough to have subtle impacts on language acquisition in children?” asks Schantz, who was not involved in the study. Previous PCB cohort studies have shown an adverse impact on cognitive function, including verbal abilities.10 “I’ve always wondered whether subtle changes in hearing could be affecting language development, and then that could be affecting verbal abilities,” Schantz says.

The new study features a particularly strong design based on multiple PCB measurements in a well-characterized population. However, it did not account for potential effects of co-contaminants, which may produce damage when combined with other exposures.11 “I think it’s very interesting that they’re seeing reductions to amplitudes related to postnatal exposure,” says Schantz. “That’s not what I would have predicted based on the animal research, but I think it’s very interesting and potentially important.”


References

1. EPA. Polychlorinated biphenyls (PCBs) [website]. Washington, DC:U.S. Environmental Protection Agency (updated 25 June 2014). Available: http://www.epa.gov/epawaste/hazard/tsd/p​cbs/index.htm [accessed 24 October 2014].

2. Jusko TA, et al. Prenatal and postnatal serum PCB concentrations and cochlear function in children at 45 months of age. Environ Health Perspect 122(11):1246–1252 (2014); doi: 10.1289/ehp.1307473.

3. Trnovec T, et al. Serum PCB concentrations and cochlear function in 12-year-old children. Environ Sci Technol 44(8):2884–2889 (2010); doi: 10.1021/es901918h.

4. Tabuchi K, et al. Ototoxicity: mechanisms of cochlear impairment and its prevention. Curr Med Chem 18(31):4866–4871 (2011); doi: 10.2174/092986711797535254.

5. Powers BE, et al. Developmental exposure to PCBs, MeHg, or both: long-term effects on auditory function. Environ Health Perspect 117(7):110–1107 (2009); doi: 10.1289/ehp.0800428.

6. Grandjean P, et al. Neurobehavioral deficits associated with PCB in 7-year-old children prenatally exposed to seafood neurotoxicants. Neurotoxicol Teratol 23(4):305–317 (2001); doi: 10.1016/S0892-0362(01)00155-6.

7. Trnovec T, et al. Exposure to polychlorinated biphenyls and hearing impairment in children. Environ Toxicol Pharmacol 25(2):183–187 (2008); doi: 10.1016/j.etap.2007.10.030.

8. Longnecker M, et al. In utero exposure to polychlorinated biphenyls and sensorineural hearing loss in 8-year-old children. Neurotoxicol Teratol 26(5):629–637 (2004); doi: 10.1016/j.ntt.2004.04.007.

9. Min J-Y, et al. Serum polychlorinated biphenyls concentrations and hearing impairment in adults. Chemosphere 102:6–11 (2014); doi: 10.1016/j.chemosphere.2013.11.046.

10. Boucher O, et al. Prenatal exposure to polychlorinated biphenyls: a neuropsychologic analysis. Environ Health Perspect 117(1):7–16 (2009); doi: 10.1289/ehp.11294.

11. Poon E, et al. Effects of developmental exposure to polychlorinated biphenyls and/or polybrominated diphenyl ethers on cochlear function. Toxicol Sci 124(1):161–168 (2011); doi: 10.1093/toxsci/kfr214.

Title: Thinking One Step Ahead: Strategies to Strengthen Epidemiological Data for Use in Risk Assessment

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

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Citation: Arnold C. 2014. Thinking one step ahead: strategies to strengthen epidemiological data for use in risk assessment. Environ Health Perspect 122:A311; http://dx.doi.org/10.1289/ehp.122-A311

News Topics: Research Issues and Initiatives, Risk Assessment

Published: 1 November 2014

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Evaluating Uncertainty to Strengthen Epidemiologic Data For Use in Human Health Risk Assessments

Carol J. Burns, J. Michael Wright, Jennifer B. Pierson, Thomas F. Bateson, Igor Burstyn, Daniel A. Goldstein, James E. Klaunig, Thomas J. Luben, Gary Mihlan, Leonard Ritter, A. Robert Schnatter, J. Morel Symons, and Kun Don Yi

Risk assessment is a cornerstone of environmental health research and policy making.1 A commentary in this issue of EHP presents a set of recommendations and guidelines to help researchers more effectively characterize uncertainty in epidemiological findings.2 Not only will this provide more transparency for the science itself, says coauthor Jennifer Pierson, a scientific program manager at the ILSI Health and Environmental Sciences Institute, it should also lead to more sound policies when those findings are integrated into risk assessments.

“Risk assessment is nothing magical; it’s a process to guide decision making. As with any kind of scientific question, it’s important to know how certain we are of our data,” says Thomas Burke, director of the Johns Hopkins Risk Science and Public Policy Institute, who was not involved with the commentary. “We can’t ever fully eliminate uncertainty, but we can describe it and put bounds around it with statistics.”

DAG superimposed over a crowded thoroughfareDirected-acyclic graphs (DAGs) can be an effective way to visualize relationships between the variables in a study.

© Joseph Tart; Tomislav Pinter/Shutterstock

Experimental data have traditionally formed the basis for most human health risk assessments, but increasingly regulators are recognizing the value of epidemiological data for this purpose. “Different types of studies, like toxicology studies in animals and epidemiological studies in humans, can help compensate for each other’s inherent weaknesses,” says Michael Dourson, director of Toxicology Excellence for Risk Assessment, a public health organization located in Cincinnati, Ohio. Dourson was not involved with the commentary.

In October 2012 Pierson and colleagues convened a workshop with more than 30 environmental health researchers to develop recommendations for characterizing uncertainty in epidemiological studies. Their recommendations and guidelines form the basis of the new commentary.

To Pierson, one of the most important first steps is to get study authors out of their respective silos. “Oftentimes, the epidemiologists don’t work with the toxicologists, who don’t work with the risk assessors,” she says. By working together from the earliest planning stages of a study, researchers can pool their knowledge to limit uncertainty through study design, rather than scrambling to fix problems at the end.

Addressing uncertainty is critical when writing up results so that policy makers can factor it into their appraisal of the literature. Pierson and colleagues recommend that investigators assess and comment on the uncertainty in their findings using a tiered system developed by the National Research Council. This system enables policy makers to rate the quality of epidemiological data and how well study findings can be generalized to larger populations. This further allows them to weigh the uncertainties from different studies based on the quality of research, creating more accurate and nuanced risk assessments. For authors, applying the system to their own work can point to areas where uncertainty can benefit from further analysis.2

Validation studies and sensitivity analyses of epidemiological data, combined with a better understanding and disclosure of the sources of uncertainty, can help authors explore such areas. These methods can transform the discussion of uncertainty from its usual qualitative form3 into a quantitative measurement. This allows scientists to clearly communicate their results and accompanying uncertainties in the numbers-driven language of policy makers.2

“You need to communicate what you’ve done, and you’ve got to be able to state your results in a way that managers can get their head around,” Dourson says.

The authors of the commentary recommend several more techniques to more clearly and accurately present data. Among others, they suggest the use of directed-acyclic graphs as a way to visualize the sometimes complex relationships among confounders. They also emphasize the need to distinguish between correlation and causation in describing study results, to ensure scientists and policy makers don’t draw incorrect conclusions about risk.


References

1. National Research Council. Science and Decisions: Advancing Risk Assessment. Washington, DC:The National Academies Press (2009).

2. Burns CJ, et al. Evaluating uncertainty to strengthen epidemiologic data for use in human health risk assessments. Environ Health Perspect 122(11):1160–1165 (2014); doi: 10.1289/ehp.1308062.

3. Jurek AM, et al. Exposure-measurement error is frequently ignored when interpreting epidemiologic study results. Eur J Epidemiol 21(12):871–876; doi: 10.1007/s10654-006-9083-0.

Title: More Fat, Less Bone? Flame Retardant May Deliver a One–Two Punch

Wendee Nicole was awarded the inaugural Mongabay Prize for Environmental Reporting in 2013. She writes for Discover, Scientific American, National Wildlife, and other magazines.

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Citation: Nicole W. 2014. More fat, less bone? Flame retardant may deliver a one–two punch. Environ Health Perspect 122:A312; http://dx.doi.org/10.1289/ehp.122-A312

News Topics: Children’s Health, Dust, Flame Retardants, Musculoskeletal Health, Obesity

Published: 1 November 2014

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Ligand Binding and Activation of PPARγ by Firemaster® 550: Effects on Adipogenesis and Osteogenesis in Vitro

Hari K. Pillai, Mingliang Fang, Dmitri Beglov, Dima Kozakov, Sandor Vajda, Heather M. Stapleton, Thomas F. Webster, and Jennifer J. Schlezinger

Firemaster®550 (FM550) was introduced in 2003 as an alternative to the toxic, persistent flame retardant pentabromodiphenyl ether, for use in mattresses, couches, and other items containing polyurethane foam.1 FM550 contains a mixture of brominated phthalates and organophosphates. In 2013 a groundbreaking study found that pre- and postnatal exposure to FM550 was associated with increased anxiety, obesity, and early-onset puberty in rats, raising concern over the continued use of these chemicals.2 In this issue of EHP, a team of investigators report further evidence that components of FM550 may act as environmental obesogens, stimulating adipogenesis (fat formation) at the expense of bone health.3

Using computer modeling and receptor binding and activity assays, the authors of the current study found that the phosphate components of FM550 bound to and activated peroxisome proliferator–activated receptor γ, the master regulator of adipogenesis. The brominated components of FM550 did not. Using multipotent mesenchymal stromal cells from rats, they also showed that FM550 and its constituent triphenyl phosphate (TPP) stimulated formation of fat cells.3

Fingertip smudged with dust, inlaid with the molecular structure for TPPHouse dust can be a major source of exposure to flame retardants.

Finger: © Gunnar Pippel/Shutterstock; TPP molecule: Pillai et al. (2014)3

When stem cells differentiate into fat cells, they do so at the expense of bone and cartilage formation.4 In this study, both FM550 and TPP suppressed osteogenesis in bone marrow cultures, with FM550 suppressing activity more than TPP alone.3 The authors hypothesize that environmental obesogens could be contributing to the growing prevalence of osteoporosis worldwide.5

House dust contains high levels of organophosphate flame retardants, and their metabolites are ubiquitous in human urine.6 The authors estimated that young children could ingest 120 μg/day TPP from indoor exposure to dust alone.3

“The effects shown in this paper occur at significantly higher exposures; thus, at present exposure levels there seems to be a margin of safety,” says Jerry Heindel, a health scientist administrator at the National Institute of Environmental Health Sciences, which supported the study in part. “However, if exposure increases due to increased use of FM550, the margin of safety could be eroded.”

According to Barbara Corkey, director of the Obesity Research Center at Boston University School of Medicine, the new study is important to the field “because FM550 is one of thousands of chemicals that have appeared in our environment since the obesity epidemic began. The important question this study raises is how many of the other thousands of compounds that have not been tested [may] also have a small effect on obesity.” Corkey was not involved in the research.

“This is the first study to provide evidence that an organophosphate-based flame retardant could contribute to bone loss,” says coauthor Jennifer Schlezinger, an associate professor of environmental health at Boston University School of Public Health. Although the idea that environmental chemicals could be contributing to the obesity epidemic is gaining ground,4 “few people think about what the consequences of environmental nuclear receptor ligands may be in the bone,” Schlezinger says.

Other research has found that the anti-diabetes drug rosiglitazone both increases the risk of bone fracture and acts as an obesogen,7 and tributyltin has been shown to induce adipogenesis and suppress osteogenesis.8 Arsenic and lead also may inhibit bone formation.9,10 “Each time I find that a chemical can suppress bone formation I become more intrigued and concerned with the idea that common environment contaminants are contributing to the onset or exacerbation of osteoporosis,” Schlezinger adds.

“This is a good study because it is comprehensive, asking the same question multiple times with different assays,” says Heindel. “These data match the physiology, as TPP … is structurally similar to tributyltin, which causes these same effects but at lower doses.”

The next steps will involve an expanded, improved risk assessment to the human population, Heindel says. “It is highly likely that similar effects will be seen in humans, as all these same pathways exist,” he says. “Indeed, tributyltin has been shown to affect human mesenchymal stem cells in the same manner as rodent stem cells used here.”11


References

1. Stapleton HM, et al. Alternate and new brominated flame retardants detected in U.S. house dust. Environ Sci Technol 42(18):6910–6916 (2008); doi: 10.1021/es801070p.

2. Patisaul HB, et al. Accumulation and endocrine disrupting effects of the flame retardant mixture Firemaster 550® in rats: an exploratory assessment. J Biochem Mol Toxicol 27(2):124–136 (2013); doi: 10.1002/jbt.21439.

3. Pillai HK, et al. Ligand binding and activation of PPARγ by Firemaster® 550: effects on adipogenesis and osteogenesis in vitro. Environ Health Perspect 122(11):1225–1232 (2014); doi: 10.1289/ehp.1408111.

4. Janesick A, Blumberg B. Endocrine disrupting chemicals and the developmental programming of adipogenesis and obesity. Birth Defects Res C Embryo Today 93(1):34–50 (2011); doi: 10.1002/bdrc.20197.

5. Sànchez-Riera L, et al. The global burden attributable to low bone mineral density. Ann Rheum Dis 73(9):1635–1645 (2014); doi: 10.1136/annrheumdis-2013-204320.

6. Meeker JD, et al. Urinary metabolites of organophosphate flame retardants: temporal variability and correlations with house dust concentrations. Environ Health Perspect 121(5):580–585 (2013); doi: 10.1289/ehp.1205907.

7. Kahn SE, et al. Rosiglitazone-associated fractures in type 2 diabetes: an analysis from A Diabetes Outcome Progression Trial (ADOPT). Diabetes Care 31(5):845–851 (2008); doi: 10.2337/dc07-2270.

8. Kirchner S, et al. Prenatal exposure to the environmental obesogen tributyltin predisposes multipotent stem cells to become adipocytes. Mol Endocrinol 24(3):526–539 (2010); doi: 10.1210/me.2009-0261.

9. Beier EE, et al. Heavy metal lead exposure, osteoporotic-like phenotype in an animal model, and depression of Wnt signaling. Environ Health Perspect 121(1):97–104 (2013); doi: 10.1289/ehp.1205374.

10. Wu CT, et al. Effects of arsenic on osteoblast differentiation in vitro and on bone mineral density and microstructure in rats. Environ Health Perspect 122(6):559–565 (2014); doi: 10.1289/ehp.1307832.

11. Chamorro-García R, et al. Transgenerational inheritance of increased fat depot size, stem cell reprogramming, and hepatic steatosis elicited by prenatal exposure to the obesogen tributyltin in mice. Environ Health Perspect 121(3):359–366 (2013); doi: 10.1289/ehp.1205701.

Title: Focusing on the AhR: A Potential Mechanism for Immune Effects of Prenatal Exposures

Lindsey Konkel is a Worcester, MA–based journalist who reports on science, health, and the environment. She is an editor for Environmental Health News and The Daily Climate.

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Citation: Konkel L. 2014. Focusing on the AhR: a potential mechanism for immune effects of prenatal exposures. Environ Health Perspect 122:A313; http://dx.doi.org/10.1289/ehp.122-A313

News Topics: Dioxins and Furans, Immunity, Molecular Biology

Published: 1 November 2014

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Effects of Developmental Activation of the AhR on CD4+ T-cell Response to Influenza Virus Infection in Adult Mice

Lisbeth A. Boule, Bethany Winans, and B. Paige Lawrence

Epidemiological studies suggest that prenatal and early-life exposures to certain chemicals can influence immune system function later in life.1 However, the mechanisms by which these changes may occur remain unknown. In this issue of EHP, researchers report an altered immune response to influenza virus infection in adult mice that had been exposed prenatally to 2,3,7,8-tetrachlordibenzo-p-dioxin (TCDD), revealing a novel cellular target of developmental exposures.2

“Researchers have been demonstrating for a number of years that the developing immune system is uniquely sensitive to chemical exposures,” says Dori Germolec, leader of the Systems Toxicology Group at the National Institute of Environmental Health Sciences. “This study provides a mechanistic framework that may help us understand why this is the case.” Germolec was not involved in the current study.

Micrograph of influenza A virionsA new study of influenza A (shown) and TCDD provides a mechanistic framework that may help researchers understand how certain chemical exposures affect the developing immune system.

© Eye of Science/Science Source

Previous epidemiological studies have reported that maternal and cord blood levels of polychlorinated biphenyls and dioxins corresponded with decreased immune response to routine vaccinations3 and increased respiratory infections in children.4 The new study is thought to be the first to demonstrate that CD4+ T cells—immune cells that are critical in the creation of effective responses to both vaccinations and infections—are functionally altered after developmental exposure to a member of the same family of chemicals as those measured in the epidemiological literature.

TCDD is a bioaccumulative by-product of industrial processes such as waste incineration and pesticide production.5 The compound has been shown in human and animal studies to alter transcription of genes by binding to the aryl hydrocarbon receptor (AhR).1

The researchers exposed pregnant female mice to an environmentally relevant dose of TCDD (1 μg/kg body weight). At age 6–8 weeks, the adult offspring were infected with influenza A virus.

CD4+ T cells have the ability to differentiate into distinct subsets of immune cells in response to infection. Compared with mice born to untreated mothers, mice exposed to TCDD in utero showed a reduced frequency of four subsets of conventional helper CD4+ T cells, which are responsible for enhancing the antiviral immune response. Additionally, says senior study author B. Paige Lawrence, an immunotoxicologist at the University of Rochester, “we saw an increase in the proportion of regulatory T cells, which put the brakes on an immune response.”

To test whether developmental exposure to TCDD caused intrinsic changes in the ability of CD4+ T cells to differentiate, the researchers transferred purified cells from exposed offspring into unexposed mice. They observed a reduction in the number of T helper cells responding to influenza virus infection when the cells came from exposed mice. Additionally, exposed mice had two- to three-fold fewer B cells, which are responsible for the antibody response, than control mice.2 The changes persisted, suggesting that “developmental exposure to chemicals may change epigenetic programming of the immune cells, such that their response to infection is durably altered,” Lawrence says.

Future studies will explore whether changes in immune function can be transferred to future generations of offspring. “The idea that you can expose a pregnant mouse to an environmental chemical like a dioxin during pregnancy and have that adversely impact the immune response [of its offspring] to influenza later in life has profound consequences for public health,” says Michael Laiosa, an environmental health scientist from the Zilber School of Public Health, University of Wisconsin–Milwaukee, who was not involved in the study. Laiosa notes it’s not clear whether all chemicals that bind the AhR would have the same effect as TCDD, which is one of the most potent agents known to act on that receptor.

New evidence in mice suggests that brominated dioxin-like compounds that bind to the AhR also affect immune function.6 If similar immunomodulatory effects occur in humans, we may not be recognizing the impact these bioaccumulating compounds have on the overall burden of disease, particularly in groups with higher exposures, Germolec says.

Previous studies investigating the impact of chemical exposures on the human immune system have focused largely on antibody levels.3,7,8 This new work “has implications for examining how early-life exposures affect immune function in the human population, where antibody responses are often the sole measurement,” the authors wrote.2 Indeed, Lawrence now hopes to turn this new knowledge toward studying human populations. She says, “This tells us we should also be looking more closely at the function of different cell types and what those cells contribute to the immune response—not just measuring the level of antibodies produced.”


References

1. Winans B, et al. Environmental toxicants and the developing immune system: a missing link in the global battle against infectious disease? Reprod Toxicol 31(3):327–336 (2011); doi: 10.1016/j.reprotox.2010.09.004.

2. Boule LA, et al. Effects of developmental activation of the AhR on CD4+ T-cell response to influenza virus infection in adult mice. Environ Health Perspect 122(11):1201–1208 (2014); doi: 10.1289/ehp.1408110.

3. Heilmann C, et al. Serum concentrations of antibodies against vaccine toxoids in children exposed perinatally to immunotoxicants. Environ Health Perspect 118(10):1434–1438 (2010); doi: 10.1289/ehp.1001975.

4. Dallaire F, et al. Effects of prenatal exposure to polychlorinated biphenyls on incidence of acute respiratory infections in preschool Inuit children. Environ Health Perspect 114(8):1301–1305 (2006); doi: 10.1289/ehp.8683.

5. CDC. Fourth National Report on Human Exposure to Environmental Chemicals. Atlanta, GA:U.S. Centers for Disease Control and Prevention (2009). Available: http://www.cdc.gov/exposurereport [accessed 20 October 2014].

6. Frawley R, et al. Relative potency for altered humoral immunity induced by polybrominated and polychlorinated dioxans/furans in female B6C3F1/N mice. Toxicol Sci 139(2):488–500 (2014); doi: 10.1093/toxsci/kfu041.

7. Hochstenbach K, et al. Toxicogenomic profiles in relation to maternal immunotoxic exposure and immune functionality in newborns. Toxicol Sci 129(2):315–324 (2012); doi: 10.1093/toxsci/kfs214.

8. Stølevik SB, et al. Prenatal exposure to polychlorinated biphenyls and dioxins from the maternal diet may be associated with immunosuppressive effects that persist into early childhood. Food Chem Toxicol 51:165–172 (2013); doi: 10.1016/j.fct.2012.09.027.

Title: Anthony (Tony) McMichael: 1942–2014

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Citation: Ebi KL, Butler C. 2014. Anthony (Tony) McMichael: 1942–2014. Environ Health Perspect 122:A290; http://dx.doi.org/10.1289/ehp.122-A290

Published: 1 November 2014

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Anthony McMichael

Is the role of epidemiology essentially reactive? Is it limited to helping society understand and tidy up its public health messes after they occur and, thus, to reducing the likelihood of recurrence? Hopefully not. Rather, as the scale of humankind’s impact on large biophysical systems increases, triggering unfamiliar global-scale environmental changes, epidemiologists should acquire new skills in anticipatory, scenario-based, health risk assessment.

Anthony J. McMichael

[Prisoners of the proximate: loosening the constraints on epidemiology in an age of change. Am J Epidemiol 149(10):887–897 (1999)]

Photo: Kristie L. Ebi

Anthony (Tony) McMichael died 26 September 2014 in Canberra, Australia, at the age of 71. McMichael graduated in medicine from the University of Adelaide in 1967 and earned a PhD from Monash University in 1972, where he was the first doctoral student in epidemiology. He recognized and coined the term “healthy-worker effect” while doing postdoctoral research at the University of North Carolina at Chapel Hill. After returning to Australia, he worked in the field of nutrition and health with the Commonwealth Scientific and Industrial Research Organisation (CSIRO) before being recruited as the Foundation Chair in Occupational and Environmental Health at the University of Adelaide. He was a professor of epidemiology at the London School of Hygiene and Tropical Medicine from 1994 to 2001 and directed the Australia National University National Centre for Epidemiology and Population Health from 2001 to 2006. McMichael held a National Health and Medical Research Council Australia Fellowship, Australia’s most prestigious award for excellence in the fields of health and medical research. In 2011, he was made an Officer of the Order of Australia and was elected to the U.S. National Academy of Sciences. At his death, he held honorary positions at the University of Copenhagen and the London School of Hygiene and Tropical Medicine, and he was a long-standing advisor to the World Health Organization. He also was a Fellow at Chatham House on Global Health Security and a Fellow of the Australian Academy of Technological Sciences.

McMichael was a pioneer in developing research on the health risks and burdens of global climate change and other large-scale environmental changes. His book Planetary Overload: Global Environmental Change and the Health of the Human Species (1993) established global environmental change as a public health issue. He worked tirelessly to promote understanding of the challenges humans are creating through patterns of development, paying particular attention to the risks for highly vulnerable populations. He urged epidemiologists to, in his words, escape “the prison of the proximate”; that is, in the study of population health, epidemiologists should look beyond individual-level risk factors to the roles of social and ecologic systems. In other work, he examined how the long-term record of climatic trends and fluctuations affected human health, well-being, and survival. He was also involved in developing approaches to study the roles of urban settlements, food production and consumption patterns, transportation, and energy use, among others, as determinants of environmental sustainability.

McMichael made significant contributions across a wide range of public health issues, including smoking, cancer, nutrition, infectious diseases, and the effects of lead on cognitive development. In an eminent and productive career, he published more than 300 peer-reviewed papers and 160 book chapters, coedited 9 books, and wrote 2 books, with a third nearly complete. McMichael retired from Australia National University in 2012. That same year, a Festschrift was held to commemorate his career; the associated book (Health of People, Places and Planet. Reflections Based on Tony McMichael’s Four Decades of Contribution to Epidemiological Understanding) will be published in 2015.

Upon meeting McMichael, one would not perceive that he was a scientific giant, providing insights that will continue to inform research and policy for years to come. He was the most humble and gracious of men, and a kind and thoughtful friend and mentor to many people worldwide. He willingly answered questions, shared references and slides, and provided guidance on epidemiological approaches for studying complex issues.

He had a delightful sense of humor. The opening of his keynote address to the International Epidemiological Association’s 20th World Congress on Epidemiology in Anchorage, Alaska, in August 2014 was typical: After graciously thanking his hosts for the invitation, he looked at his notes and said he should have listened to his wife and cleaned his glasses.

Tony McMichael’s scientific contributions, although legendary, do not give a sense of who he was—and that is what everyone who had the privilege of working with him will remember.

McMichael is survived by his wife Judith Healy, his daughters Anna and Celia, four grandchildren, and his brothers Philip and Robert.

Title: Transparency of Values in Science: Elliott and Resnik Respond

1Michigan State University, East Lansing, Michigan, USA; 2National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA

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Citation: Elliott KC, Resnik DB. 2014. Transparency of values in science: Elliott and Resnik respond. Environ Health Perspect 122:A291–A292; http://dx.doi.org/10.1289/ehp.1408936R

E-mail: kce@msu.edu

This letter is the work product of an employee of the National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH). However, the statements, opinions, or conclusions presented here do not necessarily represent the statements, opinions, or conclusions of the NIEHS, NIH, or the U.S. government.

The authors declare they have no actual or potential competing financial interests.

Published: 1 November 2014

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We thank Schwartz for his thoughtful comments, which provide an opportunity for us to clarify some of the points in our commentary, in which we called for greater transparency about the values that influence policy-relevant research (Elliott and Resnik 2014). His first concern is that even though we call for employing different standards of evidence in various social contexts, the evidence itself remains the same. We agree; in our commentary we were not claiming that the evidence itself changes but only that the form of evidence required for different decisions depends on the social context. Nevertheless, it is important to recognize that although the evidence itself does not change, it has to be interpreted and weighed, and many contemporary science policy disputes stem from disagreements about how to do so (Douglas 2012). Therefore, our view is that conflicts over public policies often stem from value judgments about both the nature of the evidence and standards of evidence. We agree with Schwartz about the solution: Transparency is essential. The more scientists acknowledge the assumptions and values that influence their interpretations of evidence and their decisions about how to weigh it, the better.

Schwartz’s second point is that it is problematic for us to treat tort law and chemical regulations as equivalent contexts, in which weaker standards of evidence can appropriately inform policy. We agree that different standards of evidence may be appropriate in the two contexts. However, we caution against equating the standards of evidence expected in tort law with those expected in more traditional scientific contexts. The tort system requires only a preponderance of evidence (> 50% likelihood) to win a case; this is much weaker evidence than scientists typically demand when presenting or publishing results, and confusion about these differing standards has led to significant legal controversies (Cranor 2006).

Schwartz’s third point is that other conflicts of interest, such as “ideological ties to advocacy organizations,” are important to disclose in addition to financial ties to industry. We heartily agree; indeed, in our commentary (Elliott and Resnik 2014) we stated that “Disclosures of competing financial interests and nonfinancial interests (such as professional or political allegiances) also provide opportunities for more transparent discussions” (Elliott and Resnik 2014). One of the aims of our commentary was to encourage more careful thinking about how to promote transparency regarding a wide range of different factors that could influence scientists’ reasoning, including ideology. Nevertheless, there are at least two reasons that financial connections to industry groups should continue to receive careful attention: a) Advocacy organizations typically have much fewer resources than industry to generate policy-relevant research that serves their interests (Elliott 2011); and b) a large body of evidence indicates that industry funding has important effects on research outcomes, whereas there is less information about how ideological ties affect research (e.g., Lundh et al. 2012).

Schwartz’s fourth concern is that it is important to think about risk–benefit relationships when applying science to public policy. This is a very good point, but it needs to be considered in conjunction with the fact that scientists’ values and assumptions may influence their assessments of the evidence. It would be ideal if scientists could provide perfectly unbiased risk assessments to policy makers, who could then evaluate the risks versus the benefits in order to make policy decisions. Unfortunately, this picture is unrealistic; scientists’ views about the benefits associated with new technologies likely have implicit influences on their risk assessments. For example, evidence from the literature on risk perception indicates that people’s perceptions of risk are influenced by a number of factors, including the voluntariness of the risks, the fairness of their distribution, their familiarity, and the perceived benefits associated with them (Fischhoff et al. 1981). Scientists are subject to these same influences, especially when they have limited data or are forced to weigh multiple forms of evidence (Cooke 1991). This provides further support for our central claim, namely, that scientists should explore ways to acknowledge the values that may influence them rather than denying the presence of these influences.


References

Cooke R. 1991. Experts in Uncertainty: Opinion and Subjective Probability in Science. New York:Oxford University Press.

Cranor C. 2006. Toxic Torts: Science, Law, and the Possibility of Justice. New York:Cambridge University Press.

Douglas H. 2012. Weighing complex evidence in a democratic society. Kennedy Inst Eth J 22(2):139–162.

Elliott K. 2011. Is a Little Pollution Good for You? Incorporating Societal Values in Environmental Research. New York:Oxford University Press.

Elliott KC, Resnik DB. 2014. Science, policy, and the transparency of values. Environ Health Perspect 122:647–650; doi: 10.1289/ehp.1408107.

Fischhoff B, Lichtenstein S, Slovic P, Keeney D. 1981. Acceptable Risk. Cambridge, UK:Cambridge University Press.

Lundh A, Sismondo S, Lexchin J, Busuioc OA, Bero L. 2012. Industry sponsorship and research outcome. Cochrane Database Syst Rev 12:MR000033; doi: 10.1002/14651858.MR000033.pub2.