However, far be it for me to simply criticize CR’s work without making the attempt to try and communicate health risk issues with heavy metals in protein powders more clearly.  So, I’ll take a run at talking about cadmium, because I kind of ran arsenic into the ground with the last post (Note that an expanded version of this post, providing a more detailed discussion of cadmium risks from protein powders, can be found here).

Cadmium is naturally occurring in soil and water, and can accumulate into the food chain.  For nonsmokers, dietary exposure to cadmium is the most likely route of exposure, with nuts, grains and vegetables providing the largest contributions to dietary exposure.  The toxic effects of cadmium on humans have been extensively studied, and evidence in humans indicates that the kidneys and bones are important target organs for cadmium toxicity.  Scientific studies of adverse effects to the kidney have been used by government agencies to estimate the limits on cadmium ingestion that do not have an appreciable risk of adverse effects; these limits are based on the most sensitive indication of adverse kidney effects, and include a margin of safety.  Authorities responsible for assessing the safety of dietary supplements, such as the U.S. Pharmacopeia (USP) use these very same limits.  The article in CR uses these USP limits to draw attention to cadmium levels in protein powders and drinks.

But is your risk from cadmium really different with protein powders?  In general, the amount of cadmium exposure and risk from protein powders used as meal replacements probably is not appreciably different from meals prepared from ordinary foods.  This is not to say that protein powders (or foods for that matter) are free of risk.  Some recent scientific papers (examples here and here) argue that the margins of safety on cadmium exposure are either very small or inadequate.  However, it is arguable that one’s risk is no different with or without protein powders or drinks in the diet (some of the homework supporting this assertion is here).

The article in CR could lead you to think that in general everyone using protein powders are at risk of kidney disease from cadmium.  There are people who are at increased risk of adverse effects from cadmium exposure: age, general health and nutritional status, whether one is a smoker (smoking makes a substantial contribution to cadmium exposure) and the presence of pre-existing kidney disease, are key risk factors.  I tried to think of an example of someone who might be at an increased risk of cadmium-related adverse effects from using protein powders.  Here’s what I came up with:

A skinny hard-gainer teen-aged kid who, in addition to consuming a lot of protein powder also eats a lot of spinach, sunflower seeds, whole-wheat bread and oatmeal.  He or she would either be employed or have well-off parents in order to afford all of the protein powder being consumed.  He or she also would have kidney problems related to diabetes or some other preexisting condition.  Bonus points for being a smoker.

Keep all of this up through middle-age, and this individual might be at an appreciable risk of kidney toxicity or osteoporosis from cadmium exposure.  The take-away point, for me at least, is that normally healthy people including protein powders and drinks in conjunction with a healthy diet (and not smoking. . .) shouldn’t appreciably be increasing exposure or risk from cadmium.

Ultimately, it’s up to you what you do to maintain and enhance your health.  What people need to do that is information that explains as clearly as possible what the risks from heavy metals might be, and provide the information balancing benefits versus risks of using protein powders.  The sound-bites that were supplied in the article in CR generally were pretty un-informative for users of protein powders about the relative benefits and risks.

However, far be it for me to simply criticize CR’s work without making the attempt to try and communicate health risk issues with heavy metals in protein powders more clearly.  So, I’ll take a run at talking about cadmium, because I kind of ran arsenic into the ground with the last post.

So, what’s the nature of the problem we are trying to address?  According to CR’s testing, a few protein powder products contain cadmium concentrations that are higher than the U.S. Pharmacopeia’s permitted daily exposure (PDE) limits.  We’ll defer for a moment the question of how much information CR’s testing actually provides about potential cadmium exposure from consuming protein powders – simply publicizing that any cadmium has been detected has been sufficient cause to elevate concerns about adverse health effects in the minds of consumers.

The toxic effects of cadmium on humans have been extensively studied.*   Humans consuming cadmium-contaminated rice in Japan have experienced adverse effects in the kidney and bones. Inhalation of cadmium by workers in certain industries has also been associated with kidney toxicity (inhalation by workers is associated with other effects such as lung diseases including lung cancer, but we’re interested in the risks from ingesting cadmium). There is conflicting evidence as to whether or not cadmium exposure produces high blood pressure in humans; cigarette smoking is an important source of cadmium exposure, but by itself may be a confounding factor. Excessive cadmium ingestion exposure in combination with low dietary intake of iron may be associated with anemia.

These pieces of information are useful in understanding the kinds of toxic effects that could be associated with cadmium exposure, based on what human populations have experienced in the past – typically from elevated levels of exposure.  However, these aren’t enough by themselves; there is additional information that needs to be considered to better understand how exposure under a specific circumstance (using protein powders, for example) could pose a health risk.

For example, elevated levels of exposure to cadmium are associated with an increased risk of kidney disease.  Lower levels of exposure do not produce observable kidney disease, but will be associated with an increased prevalence of abnormal biomarkers.  In this case, the abnormal biomarkers would be increased levels of certain low molecular-weight proteins in the urine.  These biomarkers are the earliest and most sensitive indications of changes in kidney functioning.  Some accumulation of cadmium in the kidney without apparent toxic effect is thought to be possible because cadmium in the kidney becomes bound to a protein called metallothionein.  However, when cadmium levels in kidney tissue become high enough, the amount of cadmium not bound to metallothionein becomes high enough to cause kidney toxicity.

Effects to the bone (osteoporosis, increase in bone fractures) were first observed in Japanese women living in areas with high cadmium contamination.  This was a disorder referred to as “itai-itai” (ouch-ouch) disease.  Other factors that may have been important in itai-itai disease included multiple pregnancies, poor nutrition (low calories, reduced calcium, protein, vitamin D, iron and zinc intakes).  The adverse effects in bones occur in the presence of kidney disease from cadmium exposure, and the kidney is thought by some to be a more sensitive target organ for cadmium toxicity.  Other researchers argue that effects to the bones, such as osteoporosis, occur at the same levels that produce kidney toxicity.  However, currently, the limits on cadmium exposure used to assess the risks of dietary intake consider the kidney to be the most sensitive target organ.

The excretion in the urine of biomarkers (low molecular-weight proteins) has been shown to increase due to cadmium-related alteration in kidney function; alteration in these biomarker levels is considered the most sensitive toxic effect from cadmium exposure.

This information has been used to identify a cadmium exposure level in humans associated with minimal health risks.

The Agency for Toxic Substances and Disease Registry (ATSDR) used a 10% increased risk of low molecular-weight proteinuria (proteinuria – excretion of excessive levels of protein in the urine) as an indication of cadmium-associated kidney toxicity.  Selection of the 10% value is based on a typical limit of detection for adverse effects in health effects studies.  ATSDR reviewed numerous scientific studies and estimated the cadmium dose in the body corresponding to the 10 percent increased risk of low molecular-weight proteinuria; that internal dose was estimated in those studies from the levels of cadmium measured in the urine of exposed persons (the researcher’s short-hand for describing this internal dose is the “urinary cadmium dose, 10%” or UCD10).

The next step is to estimate the daily intake rate of cadmium into the body that corresponds to the UCD10.  This uses the results from a “physiologically-based pharmacokinetic model” (the short-hand is “PBPK model”).  The PBPK model provides a mathematical description of the absorption, distribution throughout the body, accumulation in target organs and excretion of ingested cadmium.  The results from the PBPK model can then be used to relate the UCD10 to a daily intake rate over a lifetime.  That daily intake rate is known as the Minimal Risk Level (MRL).  The MRL is defined by ATSDR as: “an estimate of daily human exposure to a substance that is likely to be without an appreciable risk of adverse effects (noncarcinogenic) over a specified duration of exposure.”

This is the approach that U.S. Pharmacopeia (USP) used to develop its Permitted Daily Exposure (PDE) value for cadmium.  As USP described it:

Using data from select environmental studies examining the relationship of urinary cadmium and the prevalence of elevated levels of biomarkers of renal function ATSDR issued the provisional Minimal Risk Level (MRL) for chronic cadmium exposure. The 95% lower confidence limit of urinary cadmium dose corresponding to the probability to exceed in 10% the risk of low molecular weight proteinuria has been estimated as 0.5 ug/g creatinine, assuming accumulation over a 55-year period.  This value corresponds to an intake of 0.33 ug/kg/day in females, for which, applying a safety factor of 3 for human variability. ATSDR has set the MRL to 0.1 ug/kg/day.

The factor of 3 for human variability takes into consideration sensitive individuals (I talk more about sensitive individuals in a moment).  There are also a couple of critical assumptions to be aware of here.  First, the 95% lower confidence limit of the UCD10 is used to calculate the corresponding daily intake rate (i.e. the MRL).  The lower confidence limit provides for a more protective daily intake rate.  Second, the UCD10 is based on constant exposure to cadmium over a 55 year lifetime.  I come back to this latter point when discussing scenarios that may be associated with increased risks from cadmium exposure.

USP assumes that an individual with a 50 kg body weight (about 110 lbs) is exposed to the MRL of 0.1 ug/kg-day to calculate the PDE of 5 ug/day (0.1 x 50 = 5).

So far, we’ve identified the key adverse effects associated with cadmium ingestion, and we’ve quantitatively evaluated the levels that produce adverse health effects.  Recall from the previous post these were two of the three critical pieces of information needed to properly assess the health risks from heavy metals exposure.  The third piece of information is to explore the patterns and magnitude of human exposure to cadmium.

For nonsmokers, dietary exposure to cadmium is the most likely route of exposure.  Cadmium is naturally occurring in soil and water, and can accumulate into the food chain.  Cadmium levels in food can vary depending on the type of food, agricultural practices, the amount of atmospheric deposition (particles in air that deposit onto the ground) and industrial contamination in soil.  In general, leafy vegetables, grains, root vegetables and seeds (nuts and sunflower seeds) have higher levels of cadmium than other foods.  Organ meats such as liver and kidneys, and seafood, concentrate cadmium and therefore have relatively higher levels.  Dairy products, beef and poultry, and fruits have relatively lower levels of cadmium.

The Food and Drug Administration (FDA) performs laboratory analyses of metals in food as part of its Total Diet Study (TDS).  The TDS data might be a good way of comparing with other foods the cadmium concentrations reported in protein powders by CR; that is, if CR had actually reported concentration data (the problems with CR’s analytical results are a topic for another post).  CR’s lack of transparency in reporting metals data for protein powders makes it difficult to compare the risks relative to other foods.

Maybe there’s another way to get at this.  Based on food intake rates and concentrations in foods, a typical daily intake of cadmium for the U.S. population is estimated to be 18.9 micrograms per day or ug/day (note for the more scientific types: that statistic is the geometric mean).  According to CR’s data, cadmium exposures from protein powders and drinks range from 1.6 to 5.6 ug/day (based on the assumption that someone consumes three servings per day).  It could be difficult to argue that the cadmium intake is in addition to the daily intake from other foods; part of the criticism of protein powders is that they are consumed to the exclusion of other foods.   Without answering this question about how cadmium exposure from consumption of protein powders relates to cadmium exposure from all dietary sources, it is difficult to argue either that protein powders significantly increase one’s risk of adverse effects from cadmium OR do not increase one’s risk.

How about some examples?  I created some hypothetical healthy meals that people trying to get lean or stay lean might eat.  Using the TDS cadmium data (note for the nitpicking types, I just used the first quarter 2005 data – FDA samples foods quarterly as part of the TDS – I’m just trying to quickly get a rough indication of exposure here), I estimated the cadmium intake with these meals.  I’ll have to share the calculations in another post, because this is getting pretty long now by blog standards, and there are still a number of points that need to be made.  I present a range of estimated cadmium intakes, because of how the TDS reports non-detected analytical results.**  These examples are as follows:

• Breakfast consisting of two scrambled eggs, 1 cup of oatmeal and 6 oz of grapefruit: 1.07 to 1.21 ug cadmium.
• Snack consisting of 2 oz of peanut butter, two slices of whole-wheat bread and a banana: 2.05 to 2.4 ug cadmium.
• Dinner consisting of an 8 oz chicken breast, one cup of steamed broccoli and a cup of rice: 4.1 to 4.6 ug (the grains and veggies contained the higher concentrations of cadmium).
• A spinach salad with mushrooms, an ounce of shredded cheese, whole wheat croutons and Italian dressing weighs in at 4.8 to 4.9 ug – with most of the exposure coming from the vegetables.

As CR tells us, consuming three servings of protein drinks or protein powders corresponds to 1.6 to 5.6 ug of cadmium.  Eyeballing all of these numbers indicates they all (from the protein powders and example meals) fall within a narrow range – between 1 and 6 micrograms, and the exposures from the protein powders don’t look terribly distinguishable from the meals.  The point here is to not scare you about eating real food.  In a narrow sense, it’s probably correct that other sources of protein such as meat, milk and eggs provide lower exposures to cadmium.  However, if protein powders or drinks are being used as meal replacements, particularly if they are replacing consumption of grains, nuts and vegetables, then the difference in cadmium exposure with or without protein powders in the diet is probably insubstantial.

There are factors that could make an individual more susceptible to cadmium exposure than most, including age, general health and nutritional status, other sources of exposure to cadmium (for example, cigarette smoke), and exposure to other toxic substances – say mercury, for example.  These factors could affect how well cadmium is absorbed in the body, or could reduce the capacity to detoxify or excrete cadmium.  In addition, organ damage from preexisting diseases could affect cadmium toxicity.  Smoking substantially increases cadmium exposure.  Nutritional deficiencies, such as calcium or iron deficiencies, could increase cadmium absorption from the gastrointestinal tract – though this has not been demonstrated consistently in all of the pertinent studies.  Protein deficiencies could affect a person’s ability to detoxify cadmium.  Individuals with decreasing kidney function from unrelated causes – such as diabetes or aging – could be more sensitive to adverse effects from cadmium.

So, what kind of a scenario could we envision for an individual who could be at risk from ingesting cadmium in protein powders, if we overlay CR’s paradigm with some of the known risk factors.  What comes to mind for me is this:  a skinny hard-gainer teen-aged kid who, in addition to consuming a lot of protein powder also eats a lot of spinach, sunflower seeds, whole-wheat bread and oatmeal.  He or she would either be employed or have well-off parents in order to afford all of the protein powder being consumed.  He or she also would have kidney problems related to diabetes or some other preexisting condition.  Bonus points for being a smoker.  Keep all of this up through middle-age, and this individual might be at an appreciable risk of kidney toxicity or osteoporosis from cadmium exposure.

This in no way is being dismissive of the health risks from cadmium, though I hope it’s been a useful counterpoint to the faulty messages in CR’s article.  There are recent scientific papers (here, here and here) highlighting cadmium as a public health concern, noting that the most recent evidence suggests the margins of safety are very small or inadequate between levels that could begin to produce adverse effects and normal intakes from diet and smoking (so don’t smoke, already).  However, it’s important to keep in mind that the MRL (which again is the threshold for the most sensitive effects from a lifetime of cadmium exposure, reduced by an additional factor of three, and is also the number used by USP for assessing cadmium levels in diet supplements) is as protective as feasible, based on the available scientific information.  Would occasional fluctuations in exposure above that level cause harm?  That would depend – how large were the fluctuations, how often did they occur and did they occur to someone who is a sensitive individual, like a diabetic, a smoker or someone already experiencing kidney disease.  The take-away point from this analysis, for me at least, is that in normally healthy people including protein powders and drinks in conjunction with a healthy diet (and not smoking. . .) shouldn’t appreciably be increasing exposure or risk from cadmium.

Ultimately, it’s up to you what you do to maintain and enhance your health.  Some of the experts that CR interviewed did folks a disservice by saying in effect you shouldn’t consume protein powders because the heavy metals in them might increase the risk of adverse health effects; instead, they should have taken the time to explain to people as clearly as possible what those risks might be, and provide the information balancing benefits versus risks of protein powders – information that might be more useful in helping users make their own decisions about using these products.  But that’s a harder thing to do – the topic just doesn’t fit into a sound-bite, which is all that the authors allowed from these experts (I’ve expended about 2,800 words on it so far, and still have only scratched the surface).  The writers of the article in CR just didn’t try very hard, and the sound-bites they provided generally were pretty un-informative for users of protein powders about the relative benefits and risks.

Stay tuned.  I’ve got three more contaminants to go through.  The shorter version of this post minus the extended analysis can be found here.

Notes:

*Much of the discussion of cadmium-related adverse health effects in humans has been drawn from the ATSDR’s toxicological profile for cadmium.

**The TDS will report foods in which no cadmium was detected as zero mg/kg (milligrams of cadmium per kilogram of food).  However, the TDS also will report the “limit of detection” or LOD, which is the lowest concentration that the analytical method used on the food could detect.  So, if the TDS reports for whole milk a cadmium LOD of 0.002 mg/kg (or ug/g, microgram cadmium per gram of food), that means that cadmium intake associated with consuming an 8 oz cup of milk (226 grams) is probably less than 0.45 ug, though how much less might be difficult to say.   So, I reported a range of estimates – one without the LOD (foods reported as not detected are treated as zero) and one with the LOD (foods reported as not detected are assumed to have contamination at the LOD).  Again, this is a topic for a separate post.

CR’s article is a bit of a scattershot complaint about the nutritional benefits and health risks, much of which I’m not particularly disposed to address.  However, CR drew my attention by informing its readers how. . .

“[s]ome protein drinks can even pose health risks, including exposure to potentially harmful heavy metals, if consumed frequently.  All drinks in our tests had at least one sample containing one or more of the following contaminants: arsenic, cadmium, lead, and mercury.  These metals can have toxic effects on several organs in the body.”

“Harmful.”  “Contaminants.” ” Heavy metals.”  “Toxic effects.”  These are terms that I do not sling around with abandon.  And, from my perspective, people who read CR’s report about protein powders, at least the portion that discusses health risks from heavy metal contamination, will come away alarmed, confused, no better educated about this topic than when they picked up the article, and with no roadmap about what kinds of decisions they should make about using protein powders.

What CR did was to interview a few subject-matter experts, buy a handful of protein powder products and send them to an analytical laboratory for metals analyses, read some government reports, then drew their conclusions about the health risks from the metals detected in the protein powders and communicated those to their readers.  What could be so wrong about that?

I’ve found plenty of things to complain about, enough to fill several posts (welcome back to blogging. . .).  Let’s start by unpacking one of CR’s claims, and see what they’re really saying.

We found that three daily services of the ready-to-drink liquid EAS Myoplex Original Rich Dark Chocolate Shake provides an average of 16.9 micrograms (ug) of arsenic, exceeding the proposed USP limit of 15 ug per day.

Sounds dire.  But what’s that really mean?  Is that a lot of arsenic?  Are you putting your health in danger if you take in more arsenic than what’s in the USP limit?

CR benchmarks the risks from heavy metal contamination using limits developed by the U.S. Pharmacopeia (USP).  These are thrown out to the reader without providing any explanation as to what these limits signify, and particularly without noting that these limits are not arbitrary lines that define “safe” from “not safe”.  The USP proposed “permitted daily exposure” (PDE) for arsenic is based on a well-regarded epidemiological study of Taiwanese villagers exposed to high levels of arsenic in drinking water.  That study established a “no-observed-adverse-effect-level:” or NOAEL for significant adverse effect from long-term exposure which in this case were skin lesions and effects to blood vessels (hyperpigmentation, keratosis and possible vascular complications, according to the U.S. Environmental Protection Agency).

Toxicologists express the NOAEL as the amount of the toxic compound ingested per unit of body weight per day.  In the case of the Taiwanese epidemiological study, the NOAEL for arsenic exposure was 0.8 micrograms per kilogram of body weight per day or 0.8 ug/kg-day.  That no effect level is then reduced by a factor that accounts for uncertainties in the health effects information and to produce a level of exposure that protects sensitive individuals.  The value used to calculate the PDE is 0.3 ug/kg-day, is also used by other regulatory agencies such as EPA and the Agency for Toxic Substances and Disease Registry (ATSDR) to assess health risks from arsenic (EPA’s term for this value is the “Reference Dose” or RfD – we’ll come back to that later).  To calculate the PDE, USP assumes that a person exposed to arsenic weighs 50 kg or 110 pounds, to obtain the level of 15 ug/day cited in CR’s article.  The weight assumption is selected presumably because USP is trying to set a level that’s protective for everyone from scrawny teenagers to 300-pound defensive tackles.

So, is that a “safe” level?  Are you risking adverse effects if you consume more arsenic than15 ug/day?  CR’s presentation of the information implies that exposure to more than 15 ug/day is unsafe, but the real answer isn’t that clear-cut.  The RfD (which is used to develop USP’s limits) is a level described by regulatory agencies such as EPA as “likely to be without an appreciable risk of deleterious effects”.  Lower levels of exposure are not likely to be associated with health risks.  Correspondingly, as the level and frequency of exposures exceeding the RfD increase, the probability of adverse effects increases.  However, you can’t say categorically that any arsenic exposure above the RfD (or USP’s limits) will produce adverse health effects.

That’s probably a bit confusing and understandably so especially when readers haven’t been clued in about the imprecise nature of these health risk-based levels (you certainly won’t find a word about that in CR’s article).  One of the clues in deciphering this puzzle is in EPA’s definition of the RfD:  “an estimate (with uncertainty spanning perhaps an order of magnitude). . .”.  The purpose for that wording is to alert people to the fact that risk-based levels such as the RfD are imprecise – that’s the nature of science used to develop them.

Now, how can you be expected to judge what should be your level of concern about ingesting 16.9 ug/day of arsenic in your protein shakes when USP’s limit is 15 ug/day, when the authorities say there might be an order of magnitude range (from 4.5 to 45 ug/day – the math behind this range is a topic for another post) around USP’s limit for arsenic?  The answer is that the numbers comparison is only an approximate guide for judging the magnitude of risk associated with arsenic exposure.  It needs to be accompanied with other information to fully present and communicate the health risks.  And, this is information that CR didn’t include in its article.

The kinds of information needed to fully communicate risks would answer these questions:

• what is known about the capacity of a toxic chemical to cause adverse health effects in humans or laboratory animals;
• what is known about the quantitative relationship between exposure and adverse health effects (also known as the “dose-response relationship” – the RfD is an example of a quantitative dose-response relationship);
• what is known about the patterns and magnitude of human exposure?

In addition, there should be a discussion of uncertainty that addresses topics such as the quantity and quality of information used in assessing health risks, gaps in our knowledge about the chemical and assumptions made in estimating health risks.

It sounds like a lot of work, but assessing health risks, which is what CR’s article was doing, means presenting this information in a meaningful way that is transparent to the users.  Only then can the users, in this case people who are making decisions about buying and using protein powders, properly weigh the benefits versus the risks.

What’s one example of health risk information that should have accompanied the numbers comparison?  It might have been helpful if CR had mentioned that some forms of arsenic, and in particular the forms found in foods, are not known to pose a health risk to humans.  Arsenic in the environment occurs in ionic form (inorganic arsenic) and bound to organic molecules (organic arsenic).  Inorganic arsenic, and in particular trivalent arsenic, is of greatest concern for causing adverse health effects in humans.  Most organic arsenic compounds are not known to pose a health risks in humans; for example, the human body detoxifies inorganic arsenic by metabolizing it to an organic form.  In addition, arsenic is naturally occurring in soil, water and foods.  Typical intake of arsenic from ingestion of food and water is estimated to be 50 ug/day; however only 10 ug/day or less of that is considered to be inorganic arsenic – therefore, some of the arsenic you take in with foods is present as organic arsenic.  This distinction becomes important when you look at the laboratory analyses of the protein powder and shake products supplied by CR.

CR also doesn’t provide critical details about the laboratory analyses of the protein powders, such as whether or not the analytical method selected would distinguish from inorganic arsenic species from organic arsenic species.  USP’s proposed standard for heavy metals (they refer to them more correctly as ‘elemental impurities”) specifically states that “arsenic may be measured using a nonspeciation procedure under the assumption that all arsenic contained in the supplement is in the inorganic form.  When the limit is exceeded using a nonspeciation procedure, compliance with the limit for inorganic arsenic shall be demonstrated on the basis of a speciation procedure,” which is something CR doesn’t mention in its article.  In the article, CR makes the assumption that all of the arsenic found in the protein powders is inorganic arsenic which could be a human health risk, then doesn’t call readers’ attention to that assumption.  This potentially misleads readers about how much of a health risk is posed by arsenic in protein powders.

CR fails to provide any context regarding the levels of exposure and circumstances under which these heavy metals have been shown to produce adverse effects in humans.  I’ve focused on arsenic, but the same kind of story can be told for all of the metals mentioned in CR’s article – arsenic, cadmium, lead and mercury (I’ll try to provide more details in follow-up posts).

CR’s description of the risks from metals in protein powders fails because it is not transparent in presenting its data, methods and assumptions, and by starting out with a predetermined frame that protein powders are “bad” in general; featuring the heavy metal contamination is an eye-catching way of making that point.  I’m not an advocate for protein powders, but I am interested in using risk assessment in a manner that informs people and helps them make decisions about how to deal with health risks.

Here’s hoping that blogging resembling real environmental health science resumes soon.  My apologies for subjecting you to this.  I’m recovering from a head cold, and I’m overly preoccupied with the day job, and both seem to impede me from thinking very clearly.

The mixture of lectures, vendors, game rooms and people wandering about in costume made for a pleasant venue.  It was clear that my kids (kids, hah – they’re close to adults now) were in their element there – my son pondered attending a lecture presented by some science-fiction authors about writing about time travel; over the years we’ve had several discussions regarding the nature of time travel, after I had given him a copy of Michio Kaku’s Hyperspace.  Later, both of them sat in on a lecture on character development.  In that one, my daughter asked a question about how to make a whiny, angst-ridden, emo character interesting.  The participants struggled with that for a moment, until my son chimed in “like Anakin”, which provoked groans and chuckles from participants and the panel alike, but got the point across.

I couldn’t participate as much as I would have liked, since the whole work-life balance thing isn’t going so well right now. However, I attended a talk on protecting ourselves from collision with near-Earth asteroids. . . talk about a major environmental problem that is being almost totally ignored . . , which included on the panel Larry Niven, looking like the stereotypical grandpa of the “you kids get off my lawn” variety.  I quickly got bored and didn’t sit through the whole session, since it was focused on the cool technologies that in theory could be deployed to save the Earth from asteroid impaction.  I’m into cool technology as much as the next geek, but there’s the practical side of me who’s interested in hearing about the societal and technological changes involved in putting us on the path to achieve such a deployment (. . . boring. . .), and when are we going to pull our heads out of our asses and get on with it. . . .  Sorry, this isn’t intended to be a rant.  But the list of Manhattan Project-sized projects on the to-do list (manage climate change, achieve energy independence, preserve biodiversity, keep big rocks from dropping from orbit onto our heads) is starting to add up.

Attending a science fiction and fantasy con prompted me to think about the stories I’ve read with an environmental health theme.  There’s Norman Spinrad’s short story Carcinoma Angels, where the hero is a cancer victim who uses guided imagery to direct his own molecular and cellular defense mechanisms and save himself, but can’t wake from his drug-induced trance; John Brunner’s The Sheep Look Up, with it’s unsubtle message about unsustainable lifestyles including a scene in which hallucinogenic chemical warfare agents leaching into groundwater from the Rocky Mountain Arsenal make people in Denver crazy;  Cordwainer Smith’s short story The Crime and Glory of Commander Suzdal, with a planet where being female is carcinogenic, a foretelling of life with endocrine disruptors including a frank description of homosexual lifestyles (you see, everyone has to become male in order to survive. . .).  While it doesn’t harp on the subject, Kim Stanley Robinson’s Mars Trilogy does mention the problem with space travel of astronauts accumulating potentially life-shortening radiation doses, though he pulls out the plot device of anti-aging drugs to offset that problem and keep his characters into the multi-generational story.  I did enjoy the Mars Trilogy with it’s themes of ecological economics, and using the mission to Mars to give aerospace defense contractors something to do other than build implements of destruction.  Maybe this whole topic could be a workshop at next year’s con.

The investigators didn’t speculate about the policy implications of this work, but things that come to mind for me include better early detection of pre-cancerous conditions, genomic therapies that intervene on a macromolecular level and an airtight method for denying someone health insurance coverage for lung cancer treatment because of self-inflicted tobacco carcinogenesis.

One of the worrisome statements made in the discussion section was that, on average, lung cancer develops after 50 pack-years of smoking (where a pack-year is 7,300 cigarettes, representing the number smoked in a pack a day for a year), or an average of one mutation for every 15 cigarettes smoked, which could potentially transform a normal cell into a cancerous one that eventually clones into a tumor.

There are a couple of epidemiological modeling papers cited for that conclusion that should be looked in on later, but the 50 pack-years assessment provoked a bit of an oh-shit moment, because if I’m understanding the number properly, 50 pack-years is around a pack a day for one year; the dose-response relationship is cumulative, so the same risk would be associated with half a pack a day for two years, and so forth.  Tobacco contains a lot of other carcinogens other than mutagens, which initiate a carcinogenic response; these other carcinogens are promoters, which accelerate the growth and development of a tumor.  So, even if you’ve only currently a “light” smoker, you’re probably still screwing yourself health-wise; even if you quit years ago, you may have macromolecular or cellular injury now, that will eventually turn into lung cancer, but it just hasn’t progressed to the that you’re experiencing adverse effects.  It’s just another reason for not smoking at all or stopping at the earliest instance possible, in order to preserve your health (and insurance).

Pleasance, E.D. et al.  2009.  A small-cell lung cancer genome with complex signatures of tobacco exposure.  Nature.  463, 184-190 (14 January 2009)   http://www.nature.com/nature/journal/v463/n7278/full/nature08629.html

But sometimes, I get something mildly usable from it, at least enough to keep up the blogging rate.  Today’s example is a post in Huffpo about the city in the nation with the highest home foreclosure rate, along with 16% unemployment:  Stockton, CA.

I remember Stockton.  Thirty years ago, I lived in Sacramento just about an hour north of Stockton, first working for the State of California regulating pesticides, then working for a couple of environmental consulting firms.  I passed through Stockton more times than I can remember, on the way to the Bay Area – taking I-5 to I-205 and through the Altamont Pass was longer than I-80, but I would gladly drive the extra 70 miles, if I could go 80 mph all the way and avoid being stuck in traffic.  Stockton was also a waypoint when driving south to the San Joaquin Valley, to work sites where I could observe and monitor workers using pesticides, measuring their exposure and collecting data to figure out methods for reducing those exposures.

I was just starting to see the growth in the Valley towns when we left California – tens of thousands of people who bought homes in places such as Stockton, Modesto, Merced, Patterson, and commuted two-plus hours per day one way to jobs in the Bay Area.  I don’t think I have to read further to figure out what’s happened – the jobs in the Bay Area are starting to dry up, and there’s nothing locally to replace them. . . .

I’ve managed to miss all of this.  We left California in 1995 for opportunities elsewhere, and it feels as if we dodged a bullet.  It’s difficult for me to imagine what would be so desirable in a job that would make it worth driving 60 miles, one way in heavy traffic, while living in a garden spot such as Stockton.  Don’t get me wrong, I could live there, if I had a job in town.  Driving to Hayward to work every day?  No way.  But that’s me.  In the end, I’m relieved that we got out when we did.  California – forty million people can be wrong.

There have been several signal events related to formaldehyde which have occurred within the past few years.  Temporary housing units used by FEMA to house people rendered homeless from Hurricanes Katrina and Rita were found to have concentrations of formaldehyde in air at levels that were sufficiently high that public health officials were concerned about potential health risks to the occupants.  Recently published epidemiological studies of workers indicate that exposed to formaldehyde is associated with an increased incidence of leukemia (formaldehyde is already thought to be associated with an increased risk of nasal cancers in workers).  Senator David Vitter has held up nomination of a key EPA deputy administrator over the formaldehyde risk assessment, insisting that the risk assessment undergo review by the National Academy of Sciences, a step that would delay any regulation of formaldehyde emissions by a few years.  Finally, the California Air Resources Board finalized air toxics control measures for the manufacturing of some building materials containing formaldehyde.

Beyond the fact that formaldehyde has been recognized as a human cancer risk and a widespread indoor air contaminant for over two decades, an argument can be made that the existing regulatory frameworks will not produce real reductions in formaldehyde exposure for many years.  It is not simply a matter that more information is needed to make a decision.  Collecting and analyzing more information can in certain cases create more opportunities to create doubt and distraction.  The problem then is defining the kinds of information, messaging and framework that would mobilize enough power to effect changes; in this case, reengineering the manufacturing of building materials to “green” the formaldehyde out of them.

This involves either molding the views of decision makers or creating an enormous groundswell of public opinion. . . .   [To be continued]

However this does raise a good question about why, with the majority of the scientific community that is knowledgeable about the topic of climate change issuing alarms, is climate change risk communication so ineffective.  I look at climate change, and see nothing but ways to make capital flow so that lots of people can make money.  There’s some kind of a lesson about how being smart and committed about a topic isn’t necessarily enough to galvanize interest and concern about it.

As always, Peter Sandman has some sensible things to say about the problem of climate change apathy and precaution advocacy.  However, I recall a few months back something on his blog about him planning to retire soon.  I wonder who’s going to be picking up the slack here.