Archive for the ‘Risk Assessment’ Category
Consumer’s Reports published a report on health risks associated with protein powders, including a discussion of the risks associated with heavy metal contaminants found in some brands of powders. I’ve commented previously on the shortcomings in their reporting of the risks from the heavy metal contaminants, which I predict will do more to alarm and confuse people than inform them.
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).
Consumer’s Reports published a report on health risks associated with protein powders, including a discussion of the risks associated with heavy metal contaminants found in some brands of powders. I’ve commented previously on the shortcomings in their reporting of the risks from the heavy metal contaminants, which I predict will do more to alarm and confuse people than inform them (Note that a condensed version of this post without all of the geeky risk assessment talk can be found here).
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.
Consumer Reports seems to have stirred up some controversy over protein powders and drinks. These are staples in the fitness world, and while they’re not intended to be a substitute for real food, they are a convenient way to get some protein into you before a workout.
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.
Considered to be a probable human carcinogen through inhalation, formaldehyde for several years has been the subject of a risk assessment being conducted by EPA, as well as a candidate for development of emissions standards under the Clean Air Act. Formaldehyde is used in manufacturing of building materials, and the offgassing from new building materials is a source of formaldehyde exposure in indoor air for potentially millions of people.
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]
There’s no better way to start the New Year than getting a jump on it. I don’t know where I found this, but “Five Easy Lies” is a wonderful example of how to sow doubt and uncertainty about any set of data. I have written before about how sowing doubt and uncertainty with environmental data is a time-honored tradition of opponents of toxic substances regulation, climate change denialists or anyone desiring to use “too much uncertainty to make a decision” as a strategy for deferring any type of economically or politically painful decision. Stated more eloquently on SKAPP’s web site:
“Doubt is our product,” a cigarette executive once observed, “since it is the best means of competing with the ‘body of fact’ that exists in the minds of the general public. It is also the means of establishing a controversy.”
The lesson about how to talk about data that isn’t telling your story works better with the visuals (visit the site if you’re interested), but here’s a summary of the principles:
Select your cutoffs – focus on just the piece of the trend or the piece of the data set that’s most favorable to your side of the argument.
Talk about the trend of the trend – very useful for engaging people who are bad at math. If there is still an increasing (or decreasing) trend in the data that isn’t helpful to your side of the story, be sure to talk about the rate of the increase or decrease. If this fails, as the post notes, “[k]eep on differentiating until you find a curve that matches your needs.” If that fails, transform the data until is resembles something that’s helpful.
Talk about the different phases – focus on the changes in the data trends – any data set will have it’s moments when it will support your side of the story, even if the weight of evidence is against you. Make sure that noone looks closely at the magnitude of the different data trends.
Focus on outliers – there’s always a case that is not readily explainable based on the preponderance of the data, especially if it’s a noisy data set. This is more easily done if you ignore error bars or other measures of data uncertainty.
Sow confusion – combine any or all of the above to increase doubts about the data set.
I found this to be such a resonating statement:
Evidence is your friend. More evidence means more cutoffs to choose from, more trends to analyze, more phases to count, more outliers to discover, and more confusion to sow. Be careful to disguise the fact that you and not the data are the source of the confusion.
We’ll talk another time about how to criticize the methods use to collect environmental data, as a technique for sowing doubt.
Happy New Year.
Well, maybe a few. Such as the quote from the West Virginia woman. . .
How can we get digital cable and Internet in our homes, but not clean water?
. . . after having to treat her kid for skin lesions because he’s bathed in water contaminated with nickel, or get crowns on the teeth of another kid of hers after metals-contaminated drinking water has eroded the enamel off the kid’s teeth.
How about, “because we care more about digital cable and Internet than clean water”. How about, “because we’ve learned to not think of clean water as a right that we have to continue to fight for”. How about “because the political will which was around 40 years ago to give us the Clean Water Act and the Safe Drinking Water Act is has disappeared”. How about, “because we abrogate this responsibility for our health, leaving it in the hands of politicians and bureaucrats”.
The tone of the New York Times article implies that the government should be doing more, such as more stringent enforcement, or beefing up the resources of regulatory agencies. Helpfully, the article provides a database that allows readers to identify violations of Clean Water Act or Safe Drinking Water Act regulations in their area. There are similar products available from EPA such as EnviroFacts and the TRI database. However these all reflect operational and management metrics – how many permit violations have occurred or how many pounds of chemicals are emitted – which don’t really say anything about environmental conditions or the risks encountered by humans or the ecosystem. These still reflect the “command and control” style of environmental management which some in EPA through the Unfinished Business and Reducing Risk reports were considering to be obsolete as long as 20 years ago. Not addressed in the New York Times article is the idea that the existing command and control regulatory structure developed in the 1970s and 1980s NPDES, RCRA, Clean Air Act permitting and enforcement – is broken.
There is some recognition that a new framework for environmental protection is needed, which acknowledges that health and ecological risks are related to where a community is located, that multiple and overlapping sources of contaminant releases might affect members in that community, and that the best measure of risk is based on what types and levels of contaminants those individuals are exposed to. EPA has developed frameworks for community-based risk assessment and cumulative risk assessment, which acknowledge:
In many cases, human health often is directly related to where one lives. Certain communities, groups, or individuals within a community may be more at risk than others from multiple exposures to chemicals based on the location of a town; the individual’s location within a town; activities, such as commuting to work or school or exercising; dietary patterns of residents; or socioeconomic status. Focusing on the community provides a rational starting point for developing, evaluating, and applying cumulative risk tools to determine the risk of chemical mixtures.
Of course, characterizing risks with this framework involves more monitoring, particularly from the locations where the people or affected wildlife are located, possibly including biomonitoring using biomarkers and genomic markers. The current tools such as EnviroFacts and the TRI, which don’t really tell you anything about what you’re being exposed to aren’t what’s needed for community-based risk assessment. Also, the existing regulatory and legal framework, which is source- and industry-based, becomes an impediment to this very sensible risk-based approach. Who “owns” the liability and responsibility for what pollution? How do you prove that my releases (says the local chemical company) are producing your body burden? That regulatory framework is also going to become an impediment to implementing sustainable chemical production techniques (“green chemistry”), an initiative that also will revolutionize environmental protection.
Without a new paradigm in environmental protection that’s community-based, or oppressive enforcement of the current command and control regulatory framework, we’ll continue to have problems such as kids getting rashes and having their teeth fall from contaminated drinking water.
Enter data judo (to be continued).
Science-Based Medicine, a physicians’ group blog takes to task a recent documentary by the Canadian Broadcasting Corporation, “The Disappearing Male”, which mixes endocrine disruption science with overheated rhetoric to raise the question of the decline of the human species.
The post represents informed advocacy, and can scarcely be considered a full characterization of potential endocrine disruptor risks. While I have some minor disagreements with a few of its sources, overall it needs to be acknowledged as a welcome counterpoint in the endocrine disruption debate.
Science-Based Medicine: “The Disappearing Male – a Pinch of Science, a Pound of Speculation”.
[Note: this a series of posts stimulated by this recently-published research on breast cancer risks from multiple environmental contaminants. A previous post is here.]
I have been aware of initiatives to address endocrine disrupting chemicals, early-life exposure to environmental contaminants, and cumulative risk assessment but over the past few years hadn’t paid that much attention to them. While all of these topics had public health importance, and were beginning to turn into risk assessment guidance, regulatory agencies just haven’t been requiring them to be used for making decisions about the kinds of problems affecting my clients. So, they were more of an intellectual curiosity.
That might be changing. In 2005, EPA published guidelines for assessing susceptibility from early life exposure to carcinogens. In 2008, EPA updated the screening levels used for evaluating contaminant data at Superfund sites and incorporated the early life exposure guidelines for selected carcinogenic chemicals. Guidance on how to conduct cumulative risk assessments is steadily becoming more specific, and all of this represents a sea-change in how to perform risk assessments which the National Academy of Sciences says is overdue.
A recent review article argues there is substantial evidence that hormonal perturbations early in life (either in utero or during early development) are associated with increased disease susceptibility later in life, with two examples being prostate and breast cancer. The Endocrine Society has recently issued a scientific policy statement (news items here and here; link to the report here) identifying endocrine disruptors as a significant public health concern. The thrust of these stories is that professional societies are becoming involved not in just generating the science but in encouraging that it be used in policy making.
BPA, which was mentioned in the previous post, gets its own chapter in the Endocrine Society’s report. Low-dose exposure in rat fetuses to has resulted in alterations in mammary tissue. Higher dose prenatal exposures (i.e. where the pregnant females are dosed with BPA) increase the numbers of precancerous lesions in next-generation rats later in life. BPA increased mammary tumor incidence in animals when administered along with rodent carcinogens such as nitrosomethylurea and dimethylbenzanthracene. The Endocrine Society’s summary statement is:
These results indicate that perinatal exposure to environmentally relevant doses of BPA results in persistent alterations in mammary gland morphogenesis, development of precancerous lesions, and carcinoma in situ.
Or, exposure to levels of BPA, which you might normally encounter through your daily routine, might, if you’re pregnant, predispose your female child to an increased breast cancer risk. The Endocrine Society speculates that the increased incidence of breast cancer observed over the last 50 years might have been caused in part by exposure of women to endocrine-mimicking chemicals.
Of course, it’s risky to let yourself get tunnel-vision and focus on only one answer. In 2002, reports that post-menopausal hormone therapy posed an increased breast cancer risk resulted in a rapid decline in this kind of hormone use in women. The decline in hormone use is suspected to be a contributor to the subsequent decline in breast cancer rates. Would reducing BPA exposure in a systematic manner, also result in a decline in breast cancer rates? It would be hard to say – an epidemiological investigation of post-menopausal hormone therapy is a good deal simpler than investigating BPA; 93% of Americans have detectable levels of BPA in their bodies – where do you find a control population?
Not done yet. . . .
Bisphenol-a, used to manufacture polycarbonate including plastics for food and beverage containers, has been found to leach from those containers, is consumed by us and can be detected at trace levels in nearly everyone’s blood and urine. Bisphenol-a is hormonally active (otherwise known as an endocrine disruptor), and produces reproductive and developmental abnormalities in laboratory animals including changes in mammary glands. The kinds of changes observed in mammary tissue leads some to be concerned that bisphenol-a might pose some level of risk for breast cancer.
By itself, maybe the breast cancer risk from bisphenol-a (or BPA) by itself isn’t something a woman ordinarily needs to be concerned about. There isn’t any certainty about it, and the effects observed in lab animals are pretty subtle. But we’re not exposed to BPA by itself, but as mixtures of contaminants. Other chemicals that we’re commonly exposed to that are possible human carcinogens are polycyclic aromatic hydrocarbons (PAHs). PAHs are found in tobacco smoke, air pollutants, motor vehicle exhaust, particularly diesel, and some fried or smoked foods. One PAH, dimethylbenzanthracene (DMBA) reliably causes mammary cancer in a selected strain of rat, so that DMBA-rat system is used as an animal model for breast cancer research.
A study published a few months ago in Environmental Health Perspectives explored the hypothesis that exposure to BPA early in life would produce changes in mammary tissue, creating a predisposition for breast cancer. This study investigated the interaction between BPA and breast cancer risks by exposing newborn rats to BPA through lactation, then giving the young female rats oral doses of DMBA.
Those tending to be skeptical about environmental contaminant-disease trend relationships might be inclined to note that breast cancer incidence and mortality rates have declined over the past several years. When you browse the SEER statistics directly (breast, Figure 4.2), mortality hovers a little over 50 per 100,000, while incidence hovers around 300-350 per 100,000. While a decreasing trend is good news, a worthwhile question then is how many cases are too many? Note: yes, I know zero would be nice, but let’s stay in the real world for now. . . . The CDC reports that in 2005, about 186,000 women were diagnosed with breast cancer and 41,000 died from it. Aside from the financial and human costs, there is the issue that a substantial fraction of those cases may still be avoidable.
To be continued. . . .
I’m reading this paper in Environmental Health Perspectives, “Oral Exposure to Bisphenol A Increases Dimethylbenzanthracene-Induced Mammary Cancer in Rats”, which seems to provide an example of cumulative risk assessment at work. I hope to blog about it shortly. Cited in this paper is a review from several years back, “Models of breast cancer show that risk is set by events of early life: prevention efforts must shift focus”, where the abstract states that inherited genetic risk for breast cancer accounts for no more than 10-15% of all breast cancer cases, and explores the role of early-life exposure to carcinogens as a determinant of future cancer risk. The two ideas of cumulative risk (risks from multiple sources and multiple contaminants through multiple exposure pathways) and early-life exposure have taken root in risk assessment, a topic which I will have to return to some other day. Further bulletins as events warrant.