Another Reason to Avoid HFCS? Trying to Get a Handle on How Much Risk There Is

[Continued from previous posts, here and here.]

Making sense of what the risks are based on the available information about mercury contamination in high-fructose corn syrup (HFCS) is challenging because there is so little of it. And, I’m trying to get to some kind of blogging closure because there are other topics to move on to. However, before the news cycle leaves it completely behind, I wanted to explore further what kinds of risks there might be from consuming mercury in HFCS, because there doesn’t to seem to be a lot of risk information being provided.

The paper published by Dufault et al., 2009 used the maximum concentration of mercury detected in their samples of HFCS, 0.57 ug/g (parts per million), along with the assumption that an individual consumed 50 g/day HFCS from all sources of food, to calculate an intake rate for mercury of 28.5 ug/day. That 50 g/day ingestion rate was obtained from a study of the amount and sources of dietary fructose among US adults and children conducted as part of the third National Health and Examination Survey (NHANES).

The results from the dietary fructose study were that the mean consumption of fructose was estimated to be 54.7g/day across all age groups and accounted for 10.2% of total caloric intake. The mercury analytical data used to estimate the 28.5 ug/day intake rate was from samples of HFCS straight from the factory. This makes this mercury intake rate a theoretical upper bound, assuming that someone consuming their 54.7 g/day HFCS is getting it all the time from sources that are contaminated with the maximum concentrations reported in the study (0.57 ug/g, or parts per million). Also, in imagining what this exposure scenario looks like, I get the mental image of someone eating HFCS “straight”, and not in food products. In addition, 28.5 ug/day intake rate is appreciably higher than other estimates of total mercury intake rate (the EU estimates dietary inorganic mercury intake to be around 4 ug/day). HFCS being a dominant source of dietary mercury would be a startling finding.

In contrast, the study published directly by IATP (data presented here) used a “market basket” approach, and analyzed mercury concentrations in ready-to-eat foods. Those concentrations are much lower than found in “raw” HFCS from the factory. This is not unexpected, because HFCS will be blended in other ingredients, presumably uncontaminated or less contaminated with mercury, to make the ready-to-eat foods. The highest concentration in food reported by IATP was 350 ppt or parts per trillion (pg/g, or picogram per gram), while the highest concentration reported in HFCS syrup was 570,000 pg/g (0.57 ug/g x 1,000,000 pg/ug). Combining IATP’s residue data with the consumption rates for food groups from the FDA’s Total Diet Survey corresponding to the foods analyzed in IATP’s study gives much lower mercury intake rates associated with HFCS consumption.

The highest mercury intake rate calculated for the ready-to-eat foods is 0.032 ug/day, which is for males aged 14 to 16 (the calculations are here). This isn’t an aggregate exposure analysis because it focuses only on the foods analyzed by IATP and almost certainly neglects some sources of dietary mercury. It would seem implausible this estimated intake rate is neglecting 99.9% of the dietary mercury sources related to HFCS consumption, though someone with more refined tools (and more time, meaning someone getting paid to do it) needs to map the IATP residue data to some other databases, perhaps USDA’s table of foods with added sugars, to get an idea of the total dietary intake of mercury from HFCS consumption.

When the mercury intake rates are converted to a body weight basis then compared with EPA Reference Doses for either inorganic mercury or methylmercury, the results suggest that HFCS consumption is probably a small contribution to someone’s overall risk from exposure to mercury. Again, the caution with this analysis is that it doesn’t account for all dietary sources of inorganic mercury, but the results leave me with the sense that mercury exposure isn’t the best reason to avoid consuming HFCS.

Another Reason to Steer Away from HFCS? The Outdated Study

(Continuation from previous posts – here and here)

Well, I wanted to finish exploring the risks from potential mercury exposure in foods containing HFCS, to flesh out the somewhat cryptic posts I’ve been writing (you write long posts, you end up writing not very many of them). But tonight I have to stop and explore the pedigree of the data instead.

This came about because the Corn Refiners Association challenged the relevance of the mercury residue testing study of HFCS (high-fructose corn syrup) published earlier this week:

“This study appears to be based on outdated information of dubious significance. Our industry has used mercury-free versions of the two re-agents mentioned in the study, hydrochloric acid and caustic soda, for several years. These mercury-free re-agents perform important functions, including adjusting pH balances,” stated Audrae Erickson, President, Corn Refiners Association. “For more than 150 years, corn wet millers have been perfecting the process of refining corn to make safe ingredients for the American food supply.”

“It is important that Americans are provided accurate, science-based information. They should know that high fructose corn syrup is safe,” continued Erickson. “In 1983, the U.S. Food and Drug Administration formally listed high fructose corn syrup as safe for use in food and reaffirmed that decision in 1996.”

“High fructose corn syrup contains no artificial or synthetic ingredients or color additives and meets FDA’s requirements for the use of the term ‘natural.”

I’ll glide by for now the statement that HFCS meets FDA requirements for use of the term natural, which is no doubt accurate, but brings questions to mind about what “natural” really means.

The press release didn’t cite any product stewardship information which would support the assertion that caustic soda and hydrochloric acid used in food manufacturing is mercury-free. Maybe the individual manufacturers provide that information, but it sure seems like we have to search it out. . . . EPA states there are five operating mercury cell chlor-alkali plants in the U.S., with one of these plants planning to convert to non-mercury technology by 2012. Based on the most recently available industry census (2002), there are 40 alkali and chlorine manufacturing plants of all sizes in the U.S. Twenty of those facilities have 20 employees or fewer, so there is only a limited pool of facilities to supply the needs of a large food processing industry. I haven’t searched out international data on chlor-alkali manufacturing (look, the industry association should be doing this research, not me). If you make a chain of assumptions, it’s possible to assert that the corn refining industry uses mercury-free reagents, but right now, it doesn’t look supportable. The best course of action for the moment is to make the rebuttable presumption that the corn refining industry buys at least some reagents manufactured using a mercury cell chlor-alkali process to manufacture a couple of billion of dollars worth of HFCS each year, and that there could have been some mercury exposure (or continues to be some exposure) from HFCS and let’s continue assessing the health risks from potential mercury exposure.

Returning to risk assessment stuff now.

Another Reason to Steer Away from HFCS? Some Rough Calculations

(Continuation from a previous post)

[See the update from 1/31/2009, which corrects an error in the calculations in the original post]

Last night, I took a run at calculating the mercury exposure from IATP’s residue data, using the food ingestion rates from FDA’s Total Diet Study (TDS). I obtained a maximum intake rate similar to the recently published study (my value, 23.2 ug/day, DuFault et al., 2009, 28.4 ug/day), though they are basing their calculations on a total estimated intake of HFCS, while the result I obtained was for a single carbonated soft drink (I’ll be uploading the spreadsheet with the calculations shortly). I get a somewhat higher number when I add together all of the intakes from the TDS food items, but I’m confirming how TDS results are supposed to be presented before publishing a number. Doubtlessly, the estimates of exposure will be refined as more people weigh in on this topic.

For the sake of discussion, how does a mercury intake rate from 23 to 28 ug/day compare with other estimates? The European Union in its examination of dental amalgam exposure cites an inorganic mercury intake rate of 4.3 ug/day, so the findings for HFCS would seem to be a little unexpected. A better idea will come from a comparison with EPA’s oral Reference Dose.

More analysis forthcoming.

UPDATED 1/31/2009

I found an error while doing some more work with the spreadsheet. It was a units error: IATP reports their results in parts-per-trillion, which is also expressed as picograms per gram. I had originally expressed IATP’s results as nanograms per gram, three orders of magnitude higher. Picogram per gram is one trillionth of a gram, which is consistent wit parts per trillion. Serves me right trying to do analysis around the news cycle.

This changes my results by three orders of magnitude, so the mercury intake rate for a single carbonated beverage is 0.0232 ug/day, and is well below the published value. This makes more sense now – one product made from HFCS shouldn’t provide a dose comparable to the dose from total HFCS consumption. My apologies for any misinformation that has resulted.

PFOA Toxic Torts and the Future of Risk Assessment

Perfluorooctanoic acid (PFOA) has been used used to manufacture Teflon and other non-stick and stain-resistant products. It is highly persistent in the environment and bioaccumulates efficiently through the foodchain and into biota. Therefore, PFOA contamination has been found in drinking water and house dust, and has been detected in significant portion of human blood samples. PFOA affects primarily the liver and can cause developmental and reproductive toxic effects at relatively low dose levels in experimental animals. It’s increased tumor incidence in rats, mainly in the liver. Epidemiological studies in PFOA-exposed workers do not indicate an increased cancer risk. Some have shown associations with elevated cholesterol and triglycerides, or with changes in thyroid hormones, but overall there is no consistent pattern of changes. In recent studies, PFOA exposure of pregnant women, measured by maternal and/or cord serum levels was associated with reduced birth weight. The European Food Safety Authority (EFSA) noted that these observations could be due to chance, or to factors other than PFOA. EPA has recently developed a drinking water health advisory, based on reproductive effects in laboratory animals.

PFOA exposure has been the subject of multiple class-action lawsuits, filed on behalf of residents who have been exposed through contaminated groundwater. More information about the regulatory and litigation issues can be found on SKAPP’s web site. According to a January 20th news item published in the InsideEPA.com Risk Policy Report (“PFOA Rulings May Stymie Plaintiffs’ Use of EPA Risk Methods in Tort Suits”), Federal judges in West Virginia and New Jersey declined class-action status to plaintiffs seeking medical monitoring from DuPont due to contamination from perfluorooctanoic acid (PFOA). These rulings were based in part because the plaintiffs used EPA-backed risk assessment methods to argue their cases.

According to the West Virginia court, plaintiffs seeking medical monitoring must show significant exposure, meaning exposure to higher levels or for a longer duration than the general public. Next, plaintiffs must show they experience a significantly increased risk of contracting a particular disease relative to that in the absence of exposure. The court agreed with DuPont that the plaintiffs as a class could not show an increased health risk, because each class member’s risk would vary based on variations in PFOA exposure and variations in each individual’s background risk in the absence of PFOA exposure (background risk may vary from person to person depending on individual characteristics and habits). Rejecting class action status creates an obstacle in the plaintiffs obtaining reimbursement from DuPont for the costs of medical monitoring. Just this month, the federal district court in New Jersey rejected a similar class action suit against DuPont.

An interesting development was the courts analyses of the role and limitations of regulatory risk assessment. In the opinion of the West Virginia judge, risk assessments were of limited utility in a toxic tort case especially for the issue of causation. Risk assessments have largely been developed for regulatory purposes, and serve a protective function in identifying levels below which there is no appreciable risk to the general population; they do not provide information about actual risk or causation. Risk assessments use appropriately prudent assumptions when there are limited data, and therefore intentionally present the upper range of possible risks. Other court decisions are cited for rejecting the use of regulatory standards as measures of causation because their role is to reduce exposure to harmful substances, and for determining that upper-bound risk estimates developed with EPA risk methods appropriately overstate risks for regulatory purposes (where caution is warranted), but are inappropriate for determining whether medical monitoring should be instituted.

The New Jersey court observed there is a difference between a “safe” level for public policy and regulatory purposes and the “significant exposure” that creates excessive risk triggering medical monitoring, and also concluded that a risk assessment methodology “does not work in the tort litigation context”, where a plaintiff must prove there is an actual increased risk of disease in order to receive medical monitoring.

Several things come to mind about the implications of these rulings, beyond setting the bar higher for plaintiffs exposed to toxic substances to be able to get relief through class-action suits. They reinforce the conventional wisdom that regulatory risk assessments are highly conservative and that they overstate the health risks associated with exposure to toxic substances:

While risk assessment information about a chemical can be somewhat useful in a toxic tort case, at least in terms of setting reasonable boundaries as to the likelihood of causation, the impetus for the development of risk assessment has been the regulatory process, which has different goals. Because of their use of appropriately prudent assumptions in areas of uncertainty and their use of default assumptions when there are limited data, risk assessments intentionally encompass the upper range of possible risks.

This isn’t a uniformly held view. There is a compelling argument made that the relationship between uncertainty and conservatism in risk assessment is complex, and that the conventional wisdom includes several unstated assumptions such as there is some underlying “true” risk that could be reflected by a “best estimate” of risk but which is being overstated by the regulatory risk assessment, and that decisions to manage that “true” risk can be made an unbiased manner without consideration of issues such as trust or equity.

In addition, it is possible that our current concepts of risk assessment, which grew out of the National Research Council’s (NRC) “Red Book”, and further articulated in the NRC’s “Blue Book” and the Presidential/Congressional Commission on Risk Assessment and Risk Management, have been superseded by more recent thinking about what biomarkers and toxicogenomics might be saying about the relationships between exposure and adverse effects, how cumulative risk concepts affect our notions of what’s a significant risk and what’s causation, and how risk assessors, regulators and the public (and judges and attorneys) should interact in understanding risks and decisions made to manage them. In particular, the variability in exposure that the courts used to reject the class action status might very well be the key to identifying the individuals who are at risk. However you can’t identify them without a monitoring program which evaluates variability. I think there is more work to be done here to get to a satisfactory remedy.

EPA’s Draft Toxicological Review of PCE and (Once Again) What’s Wrong with Risk Assessment?

I wasn’t sure I was going to play in this sandbox again. I’m not really involved with volatile organic compound risk assessments anymore. I’ve expressed the opinion that what we need is not another toxicological assessment, but some action to replace the highest-exposure uses with some implementable alternatives. Outside of the workplace, perc isn’t terribly high on the list of environmental health hazards. But there is a framework in place for replacing it with lower-toxicity substitutes which could be template for other, more hazardous, compounds.

But instead, we have a draft toxicological assessment that is intended to provide toxicity values on EPA’s Integrated Risk Information System, which can then be used for risk assessments.

Just by eyeball, the estimated risks are similar to the last risk assessment conducted, done by Cal-EPA in the late 1990s. So, I’m not sure what’s been gained here – while it seems to be well-written, I’m wondering how this risk assessment is going to help us make faster or better decisions about managing PCE risks, given that it doesn’t say anything terribly different from what we knew a few years ago, and does not put much energy behind PCE risk-based decision making. In fairness, I should note that it’s not intended to be a policy document – its purpose is to make sure that good science and the right values are put up on IRIS.

At a high level, EPA’s assessment says that PCE is “likely to be carcinogenic” in humans by all routes of exposure and that the primary non-cancer toxic effects of PCE exposure in humans occur to the central nervous system, kidneys, liver and developing fetus. On the quantitative side, EPA judges the cancer potency of PCE to be slightly higher compared with its previous risk assessment, conducted in the late 1980s/early 1990s. Also, EPA judges PCE to pose slightly more of a non-cancer health risk, compared with previous assessments.

Once again, I’m wondering how we address what’s broken about risk assessment. I’m apparently not the only one:

However, risk assessment is at a crossroads. Despite advances in the field, risk assessment faces a number of significant challenges including lengthy delays in making complex decisions; lack of data leading to significant uncertainty in risk assessments; and many chemicals in the marketplace that have not been evaluated and emerging agents requiring assessment.

This is from the teaser from a forthcoming book from the National Academy of Sciences, Science and Decisions: Advancing Risk Assessment. This book promises to build off of the original framework for risk assessment, published in the book published in 1983 by the NAS, Risk Assessment in the Federal Government (also known as the Red Book). The Red Book established a framework for much of risk assessment as it is practiced today Science and Decisions, “embeds these concepts within a broader framework for risk-based decision-making.” Maybe it will contribute to “fixing” risk assessment. We’ll see. I’ve ordered a copy and will discuss it in a future post.

We Knew That

I just picked up an abstract from the open access journal Environmental Health which presents a review of cancer epidemiology studies at hazardous waste sites. Epidemiology is the science and art that attempts to identify the relationships between disease and environmental factors. Some of the most painstaking investigative work in science occurs in epidemiological investigations. A classic example is the investigation of occurrence of cholera in London, conducted by John Snow As a part of this investigation, Snow mapped the locations where cholera cases occurred along with the locations of the local water pumps, thus creating the story of “the pump handle”.

The conclusion from this study was that epidemiological investigations generally did not provide a lot of information about whether communities near hazardous waste sites experienced an increased cancer risk or not. Limitations in the study design and limited information regarding levels of exposure were cited as support for this conclusion.

This study was funded by the City of New York. Why the City of New York is interested in drawing attention to the limitations of hazardous waste epidemiology isn’t made clear. However, it isn’t really news that hazardous waste epidemiology is grossly imperfect. We knew that already back as 1991. What is surprising is how little appears to have changed in the intervening years.

Most of the studies reviewed in this recent paper were identified as ecological studies, which examine rates of diseases between different groups (i.e. a community using contaminated groundwater compared with a community using an uncontaminated supply). Detailed information on the health status of individuals or detailed exposure information generally is not part of an ecological study. An ecological study is most useful for generating hypotheses and scoping more detailed epidemiological studies. Limited modeling or sampling data were incorporated into these studies, particularly measurements at the locations where individuals were most likely to come into contact with hazardous waste contaminants.

There’s a whole litany of things that could be done better here. We’ve known about these for a long time, but haven’t bestirred ourselves to deal with them.

The exposure data for assessing hazardous waste site contaminants is very limited, but we can’t all be tobacco epidemiologists who get to work with human populations who dose themselves like they were laboratory animals. There hasn’t been enough emphasis on community-based participatory methods for increasing community cooperation with exposure studies, as well as not enough emphasis on risk communication to help explain that simply looking for exposure doesn’t necessarily mean there’s a significant risk. From personal experience, I am aware that residents get understandably edgy when you want to come in to collect air samples from inside their homes or soil samples from their yards. They naturally run to the conclusion that there must be a problem (if there wasn’t, we wouldn't be looking, right?). However, because risk assessors are unable to discuss exposure and health risk in simple English, decision makers really don’t have a clue about what’s really going on, and everyone is afraid to speak up without a bunch of hedging and qualifying when the lawyers are in earshot, the people who have the biggest need to understand what’s going on – the neighbors to a hazardous waste site – routinely don’t get a straight story.

There’s the two-part problem of the lack of conclusiveness of epidemiology, coupled with the extremely sensitive perceptions of risks, both of which contribute to the sense of anxiety and uncertainty in the neighbors of hazardous waste sites. Both parts, the relative risk of 2.0 as evidence of causation, and the excess lifetime cancer risk of 1 in 1,000,000 as a threshold of acceptable risk, do not appear to be grounded in any sort of public health reality. It’s an obscure point, which is the topic for another post (because this one’s getting too long. . .).

We don’t seem to have learned anything from epidemiology to better inform hazardous waste decision making. Therefore, we fall back on making cleanup decisions using the crudest of risk assessment methods, which either don’t address real and significant health risks, or are a wasteful expenditure of resources in relation to the amount of risk reduction that occurs.