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Getting Rocket Fuel out of Drinking Water: Another Step Forward in California

Gina Solomon

Posted January 6, 2011 in Health and the Environment

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California has been making some real progress on important drinking water issues in recent weeks. Last week I blogged about the newly proposed Public Health Goal (PHG) for cancer-causing hexavalent chromium in drinking water. Today, the State proposed a welcome new PHG for another important contaminant -- perchlorate. The new proposal – at 1 part per billion (ppb) – is significantly more stringent than the prior California standard of 6 ppb and is designed to protect infants and children.

Perchlorate is a toxic salt used in rocket fuel, fireworks, road flares and other explosives. Unlike hexavalent chromium, it’s not a potent carcinogen; instead its effects are much more subtle and insidious. Perchlorate blocks the uptake of essential iodine into the thyroid gland, thereby disrupting production of hormones essential for regulating human metabolism. In the fetus and infant, these hormones also have a key role in brain development. Oh, did I mention that perchlorate also blocks the movement of iodine across the placenta and also the delicate transportation mechanism that enriches breast milk with iodine?

The special susceptibility of young infants is the main reason why the new perchlorate PHG is lower than the last one. The prior regulation neglected to consider the breastfed infant, and also the significant water consumption of bottle-fed infants. In addition, people with nutritional iodine deficiencies are at much greater risk of adverse effects from perchlorate. That’s why getting enough dietary iodine – from seafood or (less ideally) from iodized salt – is so important for pregnant women and children.

There is no Federal drinking water standard for perchlorate. In April 2008, the EPA Science Advisory Board Drinking Water Committee (which I served on at the time) recommended that EPA prioritize perchlorate for a new standard. Instead, in late-2008, EPA under the Bush Administration proposed to not regulate this chemical at all. The Science Advisory Board responded with a strong letter stating that: “Given perchlorate's wide occurrence and well-documented toxicity to humans,” EPA should prioritize this chemical for regulation.

Since that time we have all simply been waiting.

We are still waiting for the long-overdue decision from U.S. EPA about whether they will even start the process of setting a drinking water standard for perchlorate. The EPA decision has been stalled awaiting approval in the Office of Management and Budget for more than three months. Since EPA hasn’t issued a new drinking water standard since the last century, it’s high time that the Feds get moving on this high-priority chemical.

Thankfully, California isn’t waiting.  California’s Office of Environmental Health Hazard Assessment (OEHHA) is showing scientific and policy leadership on this important issue. They deserve congratulations on their work so far, but the job isn’t done – California needs to move forward quickly to finalize an updated standard that protects infants and children.

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Larry LaddJan 9 2011 12:39 AM

I'm glad to see this public health goal adopted and hope both the US and the world at large follow California's example.

Comments on a couple of details in your post:

1. "Oh, did I mention that perchlorate also blocks the movement of iodine across the placenta" Yes, but they have found another iodide transporter in the placenta that perchlorate does not block.

2. Characterizing perchlorate in aqueous solution as "rocket fuel" is acceptable in public debate, but for roundabout reasons: When perchlorate displaces iodide it increases endogenous oxidative stress in the thyroid and possibly other iodide-concentrating tissues like the salivary glands, stomach, and bronchi. Oxygen radicals generated by our own metabolism are ameliorated by converting iodide I- to iodine I2, but perchlorate doesn't have this beneficial effect.

And yours truly isn't giving up until he finds a researcher who can rule out that environmentally relevant doses of perchlorate disable human beta defensin 2.

Thanks again for this write up, Gina.

John GibbsJan 9 2011 09:00 AM

A much more significant (but identical) problem for the state of California is nitrate in drinking water. Nitrate was regulated in the early 70's because of 'blue baby syndrome" but in the last decade, it has become apparent that nitrate has the same effects on iodine transport in the thyroid and placenta as perchlorate. The only difference is in potency and concentration. Nitrate is a few hundred times less potent than perchlorate but the legal limit for drinking water is over 300,000 ppb! See for an overview of the problem.

Larry LaddJan 9 2011 02:03 PM

"but in the last decade, it has become apparent that nitrate has the same effects on iodine transport in the thyroid and placenta as perchlorate."

Actually, that's been apparent since 1953.

Endocrinology. 1952 May;50(5):537-49.

The effect of certain anions upon the accumulation and retention of iodide by the thyroid gland.

PMID: 14936940 [PubMed - indexed for MEDLINE]

Endocrinology. 1953 May;52(5):568-74.

The effects of iodine, perchlorate, thiocyanate, and nitrate administration upon the iodide concentrating mechanism of the rat thyroid.

PMID: 13060263 [PubMed - OLDMEDLINE]

That's probably one reason perchlorate monitoring in groundwater started in my town the day the cease-fire took effect in Korea, but then stopped the week a missile unit took command of our local Air Force base in February, 1963.

In 1991 Aerojet used this comparison of nitrate and perchlorate to justify allowing up to 400 ppb perchlorate in my town's drinking water supply, the logic being if the competitive inhibition of iodide by nitrate at 40 ppm is legal, then similar levels of competitive inhibtion by perchlorate is legal. Of course, thyroid effects were never part of the toxicological evaluation of the nitrate MCL. Industry proponents argue that perchlorate and nitrate should be held to the same standard, knowing full well that alteration of the nitrate standard would create a political buzzsaw. I think there is some justification for regulating goitrogenic anions like perchlorate and nitrate as a group, and I have been making this argument to the US EPA since the late 1990s. But more research needs to be done to ascertain if the effects of these anions are truly identical. Thiocyanate, for example, is converted to sulfate within the thyroid and is not transported through the pendrin channel to the surface of the cell where the hydrogen peroxide (and thus the goitrogenic effect) is generated. I don't know if nitrate makes it to this sensitive spot in the thyroid or not. One thing I think does warrant re-examination of nitrate in drinking water is the likelihood that carcinogenic nitrosamines of all shapes and sizes co-occur with nitrate. That's why I am presently pushing for application of a total nitrosamine assay to the nation's drinking water supply.

Larry LaddJan 9 2011 02:42 PM

John, if you can experimentally establish that nitrate produces white matter in the male rat pup corpus callosum in the same manner as the study below, then we are talking turkey on perchlorate and nitrate having identical effects. While you are at it, please check to see if the new white matter has the cluster of differentiaiton 34 marker on it as a sign of stem cell origin. Thanks!

Int J Toxicol. 2005 Nov-Dec;24(6):451-67.

Refining the effects observed in a developmental neurobehavioral study of ammonium perchlorate administered orally in drinking water to rats. II. Behavioral and neurodevelopment effects.
York RG, Barnett J, Girard MF, Mattie DR, Bekkedal MV, Garman RH, Strawson JS.

Charles River Laboratories, Preclinical Services, 905 Sheehy Drive, Horsham, PA 19044, USA.

A developmental neurotoxicity study was conducted to generate additional data on the potential functional and morphological hazard to the central nervous system caused by ammonium perchlorate in offspring from in utero and lactation exposure. Female Sprague-Dawley rats (23 to 25/group) were given continuous access to 0 (carrier), 0.1, 1.0, 3.0, and 10.0 mg/kg-day perchlorate in the drinking water beginning 2 weeks prior to mating and continuing through day 10 of lactation for the behavioral function assessment or given continuous access to 0 (carrier), 0.1, 1.0, 3.0, and 30.0 mg/kg-day beginning on gestation day 0 and continuing through day 10 of lactation for neurodevelopment assessments. Motor activity was conducted on postpartum days 14, 18, and 22 and juvenile brain weights, neurohistopathological examinations, and regional brain morphometry were conducted on postpartum days 10 and 22. This research revealed a sexually dimorphic response, with some brain regions being larger in perchlorate-treated male rats than in comparable controls. Even so, there was no evidence of any obvious exposure-related effects on male rat brain weights or neuropathology. The most consistent exposure-related effect in the male pups was on the thickness of the corpus callosum, with both the right- and left-sided measures of the thickness of this white matter tract being significantly greater for the male pups in the 0.1 and 1.0 mg/kg-day exposure groups. The behavioral testing suggests prenatal exposure to ammonium perchlorate does not affect the development of gross motor movements in the pups.

PMID: 16393938 [PubMed - indexed for MEDLINE]

John GibbsJan 10 2011 12:38 PM

You are correct that in 1952 Wyngaarden et al established that nitrate and perchlorate share the same mechanism of action on the thyroid, differing only by potencies. Unfortunately this was long forgotten in the perchlorate risk assessment community by both EPA and OEHHA until Tonacchera et al published their 2004 study “Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter”. The relative potencies found in this study were robust and consistent with all of the prior published studies. Using the relative potencies from Tonacchera et al, the 10 ppm nitrate nitrogen standard is equivalent to 180 ppb perchlorate in terms of iodine uptake inhibition at the sodium iodide symporter. Those who are concerned about 1ppb perchlorate should be terrified about the nitrate in their drinking water!
With regard to the concern about “white matter in the male rat pup corpus callosum”, this issue was addressed in 2004 by the National Academies of Science Committee to Assess the Health Implications of Perchlorate Ingestion. Although this purported effect was the centerpiece of EPA’s 2002 draft risk assessment for perchlorate, the committee rejected this research in their 2005 report on the Health Implications of Perchlorate Ingestion (see They found that “the data are inadequate to determine whether or not a causal relationship exists between perchlorate exposure of pregnant rats and neurodevelopmental abnormalities in their pups, given the flaws in experimental design and methods in the studies conducted to evaluate that end point.” OEHHA did not use this flawed research in their PHG determination.

Larry LaddJan 10 2011 04:42 PM

"Unfortunately this was long forgotten in the perchlorate risk assessment community by both EPA and OEHHA" The common relationship between perchlorate and nitrate may have been ignored, but it wasn't forgotten. I used the Wyngaarden papers, and particularly the Wyngaarden, Stanbury, and Rapp diagram showing nitrate effects to introduce the perchlorate issue to Barbara Boxer's Sacramento office in 1997. When I mentioned the discrepancy between nitrate regulation and the proposed 30 ppb perchlorate reference dose at the 1999 perchlorate peer review, the reaction from EPA management was pensive. Steve Lamm was also there and duly noted my point. The Wyngaarden & Stanbury human research was the central study of the 1992 EPA reference dose literature review by Joan Strawson, although she did not include the Wyngaarden, Stanbury, and Rapp rat study that included nitrate. Joan also missed this very important study, given the proposed 4 ppb reference dose of 1992 was so low because of uncertainties about what caused the aplastic anemia in medicinal perchlorate doses:

Schweiz Med Wochenschr. 1968 Dec 21;98(51):2025-8.

[Erythema nodosum associated with a positive LE phenomenon and erythrocyte antibodies following perchlorate therapy].
[Article in German]

Beickert A, Heinicke HJ.

PMID: 4181403 [PubMed - indexed for MEDLINE]

Aplastic anemia in the context of elevated phospholipid antibodies sounds like a severe B-19 parvovirus infection to me, and that's what I warn people who have been exposed to perchlorate to look out for. When iodide deficiency, whether augmented by perchlorate or not, raises the vascular endothelial growth factor levels in the thyroid, the first pathogen that is going to get through those opened capillary tight junctions is the parvovirus, since it is the smallest virus known to infect humans.

As for the male rat pup white matter in the corpus callosum, there were a whole lot of well-educated people participating in the 2002 external peer review who did buy it. The EPA in that risk assessment also did not make a strong case for perchlorate's toxic effects in the skin not because the evidence isn't there, because it is. Any risk assessment for perchlorate that ignores halodermas in the spinosum layer of the skin is incomplete. At the 2002 external peer review though Annie Jarabek told me she was going to be able to get a drinking water standard for perchlorate on the thyroid hormone data alone. That hasn't turned out to be the case yet on the national level. The need to regulate perchlorate in drinking water is obvious -- if you want to continue generating billable hours for yourself over the next 6 years by haggling over the number for the drinking water MCL fine, because there are still data gaps and unanswered questions. But the decision to regulate perchlorate in drinking water is long overdue. God help us if OMB under Bill Daley overrides the EPA's decision to regulate perchlorate in drinking water -- it would be as if we are back in 1964 again.

John GibbsJan 10 2011 06:19 PM

Larry Ladd
I guess that I stand corrected again. I forgot your arguments regarding Wyngaarden & nitrate (although I was at the 1999 peer review meeting). I re-stumbled upon the nitrate-thiocyanate-perchlorate mechanism of action in 2003 while surfing PubMed in the middle of the night (I have insomnia). It turns out that thiocyanate (SCN-) also shares the common mode of action with nitrate and perchlorate – competitive inhibition of iodide uptake at the NIS. Thiocyanate, nitrate and perchlorate are all monovalent anions of similar size that can bind to the same site on the NIS as iodide, but with different potencies.

From an environmental standpoint, the cyanide (CN )content in water allowed by the EPA and California is worth consideration in these arguments. CN is rapidly ”detoxified” to thiocyanate (SCN-) once ingested. The current MCL for cyanide is 200 ppb … equivalent to 440 ppb thiocyanate (once “detoxified”). See ( Using the data developed by Tonacchera et al (which is consistent with the Wyngaarden data), the cyanide MCL allows the iodide uptake inhibition equivalence of well over 800 ppb perchlorate. Extensive peer reviewed literature has been published regarding thiocyanate and thyroid effects, which allows some quantitative comparison with perchlorate (see Gibbs JP. A Comparative Toxicological Assessment of Perchlorate and Thiocyanate Based on Competitive Inhibition of Iodide Uptake as the Common Mode of Action. Human & Ecological Risk Assess. 2006 Feb 12:157-173). If you are truly concerned about the perchlorate currently present in your drinking water, you should avoid all cruciferous vegetables and green leafy vegetables.

Larry LaddJan 11 2011 12:24 AM

"If you are truly concerned about the perchlorate currently present in your drinking water, you should avoid all cruciferous vegetables and green leafy vegetables." There is nothing new in what you offer here, John. I suggested to Aerojet's Suzanne Phinney in our very first meeting in 1997 that they come up with a broccoli serving equivalent in perchlorate dose units. The fact is I am not concerned about 1 or 2 ppb perchlorate in our drinking water in and of itself -- we stick very tightly to our 4 ppb perchlorate well shutdown level because it is an indicator, along with TCE and NDMA, for all kinds of other contaminants. I am open to the possibility that a 3 ppb detection of perchlorate in say, Hills IA, doesn't convey the same risk as 3 ppb from Aerojet because of the chemical complexity of the latter site. What I am adamant about, though, is that perchlorate at some level be regulated in drinking water. If Aerojet were transparent about all the nitrosamines, plasticizers, ethylene glycol, etc. I might, depending on how the science pans out, be willing to accept more perchlorate in our drinking water. But for starters you need to take a harder look at those male rat pup corpus callosums that includes some biochemical analysis between exposed and controls -- cd 34 is the first thing that comes to mind (if you will excuse the pun) in part because of the neural sheath tumors at the Whitaker Bermite site in Santa Clarita. And you need to better characterized perchlorate's immunotoxicity. I personally would start with salinity sensitive human beta defensin 2 and the interleukin 10 it induces. That is our concern in Rancho Cordova on the basis of a man who lost a lung to desert fever and a couple of juvenile osteomyelitis cases who were drinking 300 ppb clo4- -- all these ailments are related to interleukin 10 immunosuppression. Over at Whitaker Bermite again they had a lot of oral cancer, which is Il-10 promoted. Otherwise I can't in good conscience advise my neighbors to drink the stuff.

I'll finish by pointing out that at 1 ppb perchlorate we are talking about a public health goal, not an MCL. I tell my neighbors that public health goals are best used as yardsticks for relative toxicity between different chemicals, so 1 ppb perchlorate is about as toxic as 4 ppt arsenic or 3 ppt ndma. Heck we can't even measure to 4 ppt arsenic yet. And 1 ppb is how much perchlorate the South Koreans are finding in the ocean -- nobody is suggesting we try to remove perchlorate from the ocean. Public health goals are ideals. Fight all you want against a 1 ppb MCL, but at the present level of knowledge IMHO 1 ppb does seem to be an appropriate public health goal.

John GibbsJan 11 2011 09:10 AM

Larry, I am not aware of any new studies of relating perchlorate to effects on the immune system. The NRC reviewed all of the studies available in 2004 and concluded that “the data favor rejection of a causal relationship between perchlorate exposure and immunotoxicity."

Larry LaddJan 11 2011 10:41 AM

John, here is my notion of a sensitive individual for whom less than 6 ppb perchlorate might cause problems: Premature infant (perchlorate-excreting kidney pendrin not yet operating), with genetic disposition to high interleukin 10 production, who is being challenged by a respiratory infection and thus in need of effective human beta defensin 2 in their bronchial fluid. Since effective adhesion of hbd-2 to pathogens is salinity dependent, at some dose perchlorate should have an adverse effect. Bronchial fluid is also another example of how perchlorate and thiocyanate are not identical: thiocyanate and iodide are substrates of choice for various peroxidases used by the immune system, while unoxidizable perchlorate obviously cannot play that role.

Switching over to the B-19 parvovirus issue, I've suggested that the perchlorate-exposed infant populations used in the latest Steinmaus study also be checked for elevated incidence of non-immune fetal hydrops.

John GibbsJan 13 2011 12:26 PM

I think that we have strayed a bit too far from Gina's original arguments.

Comments are closed for this post.


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