Archive for August, 2009
I lurk over at Scienceblogs, where some of the bloggers routinely express their outrage at particular leaders of the “autism community”, when those leaders speak out about vaccinations as a cause for the cases of autism observed in this country. That outrage stems from the unscientific nature of the anti-vaccination arguments, the public health risk created from certain infectious diseases if vaccination rates begin to fall, and the that fact that it appear to work – despite the wrongheadedness of it, the proponents of anti-vaccination are experiencing some success in getting their messages across in the mass media.
Ok, so maybe everyone knows this stuff already, and I’m just demonstrating a firm grasp of the obvious, but there may be a conceptual model which provides some understanding about why the anti-vaccination spokespeople are resonating, and the science bloggers. . . aren’t. Consider: if it’s selling, if you yell it loud and long enough, and if enough people start believing it, whatever “it” is becomes the truth regardless of what the facts are. Also, it helps if the spokespeople are appealing on camera and speak from their Gut (which if you allow it, passes for “common sense”).
I can’t take credit for that analysis, but have absorbed it from a recent reading of Charles Pierce’s new book. I’ll be optimistic that Pierce’s message is something the Sciencebloggers can absorb and use, because it sure seems that being rational, sensible and evidence-based just isn’t cutting it.
I don’t follow the Peak Oil debate closely enough to know who Michael Lynch is, beyond the fact that he was invited to write an op-ed in the New York Times about what a farce Peak Oil was, and that we’re not really running out of oil.
Reading that piece prompted a remembrance from about thirteen years ago. At the time, I was working on the RCRA corrective action for an oil refinery along the Gulf Coast. I had traveled to attend a meeting near the facility. During a break near the end of the day, I was chatting with one of the client’s technologists. He excused himself to go out and have a smoke. I went with him, bummed one and we continued talking. It was fall, and getting on towards sunset. Sunset was beautiful, all reds and oranges filtered through the crappy air quality and highlighting the cracking towers, flares and processing equipment in the background. Call it perverse but there was a sense of order at that moment, standing at the locus of ravening energy consumption and toxic hot spots, inhaling carcinogens and fine particulate matter.
We drifted on to the topic of oil depletion and the future of the energy business, and he expressed the opinion that we’re unlikely to ever run out of oil, which was understandable coming from a representative of the energy bidness. I replied yeah, we’ll probably pump 2% carbon dioxide into the air before we run out of oil. Both of us chuckled, then we stubbed out our cigs and went back into the meeting.
That was satire. Currently, a typical carbon dioxide concentration in the atmosphere is 384 parts-per-million (ppm), or 0.000384% in air. The IPCC predictions are that, with emissions unchecked, concentrations could rise to over 800 ppm, or 0.0008% by 2100; I linked that value from an article that’s skeptical of anthropogenic global warming just to show I’m not biased, and to present an example of really, really, really bad science journalism. Anyhow, 2% carbon dioxide, my untutored speculation, would be 20,000 ppm in air, which if we achieved that, would probably have sedentary unfit people and asthmatics breathing a little harder, render glaciers a distant memory and make Little Rock, Arkansas beachfront property. I’m not terribly interested in commenting on Mr. Lynch’s analysis, though I’m sure the Oil Drum is on it. However, there is a description of subsurface investigation pertinent to this matter which has stuck with me, though I can’t recall the source any longer, and which goes like this: trying to understand the Earth by boring holes in the ground is like trying to understand the stars by looking at them through a soda straw. . . . Readers who don’t know anything about geological uncertainty, in other words most of them, might be fooled into thinking he has a point, when he’s really just blowing smoke. The Peak Oil mavens might be as wrong as he says, though we don’t really know that, and that being the case, how do we want to roll the dice with regard to our oil policy? Actually, we’ve already decided that, by making our oil policy the same as our defense policy, and committing to fighting a combined resource and holy war in the Middle East. Unanswered in Mr. Lynch’s editorial is the why are we fighting and dying for oil, if it’s so plentiful?
This was a waste of time, but it’s off my chest, and I can now close the link to Mr. Lynch’s editorial and the New York Times op-ed page and move on. Besides, I needed a break from writing about endocrine disruptors, carcinogens and breast cancer.
[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. . . .
From a certain point of view (as Obi-Wan Kenobi might say), John Cloud’s article in TIME Magazine, “Why Exercise Won’t Make You Thin” is understandable. The man is a working writer who’s success is based on being dependable – being able to turn out a product of predictable quality and being able to stick to a schedule. That, from a certain point of view, his article resembles little more than a loosely fact-checked blog post, is more the responsibility of TIME’s editors. However, it would be too easy to chalk this article up to poor-quality writing and editing – far from it. Instead, I would argue that “Why Exercise Won’t Make You Thin” was precisely what TIME was looking for because it contained a message that resonates with a substantial potion of its readership; that message being “it’s not your fault that you’re overweight – exercise and self-control don’t work, and science has proved that”.
Cloud shows some surprise that exercise, at least the way he appears to define it, doesn’t fully offset the calories you take in, particularly if you’re trying to lose weight,
You might think half a muffin over an entire day wouldn’t matter much, particularly if you exercise regularly. After all, doesn’t exercise turn fat to muscle, and doesn’t muscle process excess calories more efficiently than fat does?
That last statement, in Cloud’s hands, becomes a strawman to be knocked down and so there is no exploration of how diet, exercise, muscle and fat are interrelated. No, exercise doesn’t turn fat into muscle. However, aerobic exercise in combination with a mild calorie deficit will burn fat. This combination by itself will also burn some muscle, so some strength training should accompany it to help you hold on to as much of your muscle mass as possible, while the fat burning is under way.
We now return to TIME:
Yes, although the muscle-fat relationship is often misunderstood. According to calculations published in the journal Obesity Research by a Columbia University team in 2001, a pound of muscle burns approximately six calories a day in a resting body, compared with the two calories that a pound of fat burns. Which means that after you work out hard enough to convert, say, 10 lb. of fat to muscle — a major achievement — you would be able to eat only an extra 40 calories per day, about the amount in a teaspoon of butter, before beginning to gain weight. Good luck with that.
Checking out this article, which is a review of the various methods for calculating resting energy expenditure (REE), does reveal as part of a conceptual model for REE that internal organs such as heart, kidneys, liver and brain have higher resting metabolic rates compared with skeletal muscle (13 kcal/kg-day) and body fat (4.5 kcal/kg-day). Checking the math indeed shows this to correspond to 6 kcal/day and 2 kcal/day (kcal = the “calorie” we hear about). However, for purposes of fat loss (hence weight loss), what we’re interested in is total energy expenditure which in the introduction to this article is described as the sum of five components: REE, physical activity-induced energy expenditure, thermic effect of food, facultative thermogenesis (energy expenditure in response to hot or cold conditions – sweating or shivering) and anabolism/growth. It’s the physical activity and the anabolism (muscle growth induced by strength training) that’s going to promote weight loss.
In the end, I can only say that John Cloud’s experience with weight loss seems to be completely different from mine. When I’m working on weight and fat loss (which isn’t continually), the strategy has been mild calorie reduction, food selections based on calculated macronutrient ratios (say 35%/35%/30% protein/carbs/fats) with a bias towards lean protein, vegetables, fruit, low glycemic index carbs, healthy fats such as fish and olive oil, combined with exercise intensity and duration along the American College of Sports Medicine recommendations (at least 150 minutes per week), mixing different modes of cardio with strength training including weight lifting. I can attest that this strategy has worked for me, allowing me to lose 50 lbs, keep it off for over eight years, and put me in striking distance of seeing my abs again. There are time sacrifices involved (you have to do some shopping and cooking), and I need to accommodate this within the schedule associated with being a success-addled corporate professional. However, I don’t regret one bit making fitness a goal in my life. I’m even starting to enjoy working out. One other thing I can recommend to John, beyond doing some weight training and paying closer attention to diet is to find a workout partner. Maybe his next article on exercise, fitness and diet might actually be informing and inspiring.
In my first quarter “Fate of Toxicants in the Environment” class (the classroom portion, not the second-quarter laboratory class from hell), we spent some time learning about petroleum refining, all of the organic chemical streams that were derived from petroleum, and how you could rank these by physical and chemical properties to determine where these would end up in the environment and how long they would persist. It helped me to cement the understanding of how tightly interwoven our society is with petroleum, a point that is being amplified right now as I re-read American Theocracy: The Peril and Politics of Radical Religion, Oil, and Borrowed Money in the 21stCentury by Kevin Phillips.
As a nod to Chris Jordan’s photographic essays on the costs and implications of overconsumption, a ScienceBlogger underwent a personal challenge to live a week without plastic, which provided a vivid reminder of plastic’s overwhelming presence in our lives. Will this get picked up in the mainstream media, so there can be more of a national conversation about why in an age of Peak Oil are we burning petroleum to drive cars when we should be conserving that oil so that we can have plastic? About why aren’t we being more thoughtful about closed cycles for production and consumption of plastic goods? Or, are we going to dismiss living sustainably as something that’s not practical, as has been done with the notion of exercising to lose weight?
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.
Disclosure statement: I’m a gym rat and I’m married to a fitness writer. My wife drew me into the fitness habit several years ago. In the intervening years I’ve gone from borderline obese, losing nearly 50 pounds and reducing my body fat several percent, to nearly normal body composition. This was accomplished primarily through a combination of diet, strength training and cardiovascular exercise. My perception of working out has evolved from a grim “something I have to do to keep from dying early” to something I’m getting a little bit of a kick out of.
Thus explains my barely concealed annoyance with John Cloud’s article in TIME Magazine, “Why Exercise Won’t Make You Thin”. Beyond the sweeping pronouncement that “exercise doesn’t work” because he can’t see any progress, there’s a deeper story in how scientific information is used to inform people on a policy issue – in this case, the role of diet and exercise in promoting wellness. Media outlets report on issues using drama and narrative structure, casting the participants in an event in terms of heroes and villains, for the sake of readability. However, the real world is complicated, and such a narrative structure can mislead readers by depicting events as having clear cause-and-effect relationships, when the real circumstances are not at all clear. When combined with the tendency to reinforce the status quo and to appeal to fairness (i.e. presenting both “sides” of an issue, regardless of how wrong one side might be), this thwarts the introduction of scientific thought into public discourse. In this case, the result is an article in a major media outlet that misinforms readers about the role and effectiveness of exercise in achieving and maintaining a healthy body composition.
John introduces the story with his workout experience, highlighted with the plaintive cry about why isn’t it making his gut go away. He observes that, “. . . like many other people, I get hungry after I exercise, so I often eat more on the days I work out than on the days I don’t,” and wonders if exercise could be keeping him from losing weight. I have to ask, what’s he eating after he exercises?
His thesis then is:
The basic problem is that while it’s true that exercise burns calories and that you must burn calories to lose weight, exercise has another effect: it can stimulate hunger. That causes us to eat more, which in turn can negate the weight-loss benefits we just accrued. Exercise, in other words, isn’t necessarily helping us lose weight. It may even be making it harder.
The underlying science he introduces as evidence of his point is a paper published by the Pennington Biomedical Research Center at Louisiana State University. In this study, the investigators examined compensatory mechanisms resulting from exercise which reduced or offset weight loss. The study was performed with sedentary, overweight or obese post-menopausal women who performed different levels of exercise under controlled conditions. The women were assigned to one of three groups of energy expenditure, 4, 8 or 12 kcal/kg-week for six months. All participants started at the lowest level; with the ones assigned to the higher groups ramping up to their designated level over the first 4 to 8 weeks. Relative perception of exertion was recorded, but not discussed in the paper, so we don’t get any sense to how hard the women felt they were working.
The investigators seemed to have measured everything that could have mattered in an exercise study. Actual measured weight loss was compared with predicted weight loss; predicted weight loss was based on the assumption that expending 7,700 kcal corresponded to 1 kg of weight. The difference between measured weight loss and predicted weight loss is termed “compensation” and is an important metric in the study. Body fat changes were measured with skinfold tests. Changes in waist circumference also were measured. Participants’ diets were documented by questionnaires, but other than reporting energy intake, diet was not analyzed in this study.
The results from the study were that women in the low (4 kcal/kg-week) and moderate (8 kcal/kg-week) groups experienced weight loss comparable to predicted weight loss. The highest energy expenditure group (12 kcal/kg-week) experienced less weight loss than was predicted. In the investigators’ terms, compensation was occurring at the high group which attenuated weight loss. All groups showed reduced waist circumference, including the controls, and body fat was consistent across all groups, controls included. The results don’t point to a “smoking gun” for why compensation occurred. The investigators observe that the methodology for estimating food consumption was not optimal for measuring small changes in energy intake, which is not a trivial uncertainty in this study. In the end, they speculate based the work of others that increased energy intake is the source of the produced weight losses that were less than predicted. It wouldn’t take much, really: the highest energy expenditure group (12 kcal/kg-week) corresponds to about 1,020 kcal/week. The 1,020 kcal/week energy burn corresponds to 145 kcal/day or about half of a Starbucks blueberry muffin. The investigators noted that about one fourth of the high group didn’t exhibit compensation (in other words, they lost as much or more weight than predicted), suggesting that the higher levels of exercise work for some individuals. They point to the Weight Control Registry which demonstrates that individuals who have lost a substantial amount of weight and maintained that weight loss typically get in 45 minutes or more of moderate exercise per day. There appears to be those who are not prone to compensation, or “who have developed strategies to combat compensation”. Such as being more thoughtful about what they eat while on a weight-loss program?
So what happens when this hits the mainstream media?
“’In general, for weight loss, exercise is pretty useless,’” says Eric Ravussin, chair in diabetes and metabolism at Louisiana State University and a prominent exercise researcher,” quoted by Cloud. However, a careful reading of the research paper cited at length in the TIME article, and produced by a colleague of Dr. Ravussin’s, doesn’t say that. The juxtaposition of that quote, without any other context, with a study cited as the “proof” (it isn’t really) misleads readers into thinking there is scientific evidence that “exercise doesn’t work”.
The findings were surprising. On average, the women in all the groups, even the control group, lost weight, but the women who exercised — sweating it out with a trainer several days a week for six months — did not lose significantly more weight than the control subjects did. (The control-group women may have lost weight because they were filling out those regular health forms, which may have prompted them to consume fewer doughnuts.) Some of the women in each of the four groups actually gained weight, some more than 10 lb. each.
First of all the control lost weight – an average of 0.9 kg (less than 2 pounds) over the course of six months. The investigators also observe that those control individuals who lost weight had lower energy intakes. The controls weren’t zero-exercise people either. Everyone in the study carried a step counter, and while the investigators didn’t explore this facet, it is likely that some of the control participants walked. The speculation that the control individuals reduced their energy intake because it was being monitored isn’t found in the paper. The most that the investigators say is that the food questionnaire has limitations, and that all the dietary results need to be interpreted with caution, which presumably applies to the exercise groups. Keep in mind that we’re talking about pretty mild exercise. These women pedaled recumbent bikes or walked leisurely on treadmills (they’re sedentary individuals, remember?). The exercise producing the highest energy expenditure corresponds to losing about a pound per month. The notion of the exercise groups “sweating it out with a trainer several days a week for six months” is laughable. While the imagery makes for a more vivid story, it distorts out of proportion what actually happened during the research. Finally, looking at the average weight losses out of context with all of the data further misleads readers. While there may have been no statistically significant differences in weight loss among the groups, controls included, examination of the frequency distributions seems to show that lower proportions of the exercise groups gained weight. Focusing only on the fact that some individuals gained weight is also misleading to readers. Nothing is mentioned in the TIME article about the investigators’ observations of individuals who might have developed strategies to overcome compensation.
This is enough for one day (there is other stuff to do, of course). But there is more to explore, such as the misleading stuff about the differences between muscle and fat, and the inappropriate use of the “self-control is like a muscle” metaphor. We’ll come back to this.
With all of the handwringing, I mean debate, about health care reform these, I wonder if anyone is going to get around to talking about and dealing with some of the underlying factors that would actually keep us from getting sick. Or, are the conversations going to continue to be about money and political power? Trying to do things to reduce the disease burden, which might correspondingly promote reform, doesn’t seem to be a prominent part of the discussion yet.
What prompted this line of thought was the announcement that David Michaels was being nominated as administrator of the Occupational Safety and Health Administration (OSHA). Dr. Michaels is an epidemiologist, and has prior experience with issues of protecting worker health. He will have a role in reducing the occupational disease burden, which indirectly may support health care reform.
How important is occupational disease? The annual burden of occupational disease mortality was estimated in 2003 by NIOSH researchers to be 49,000, with a range from 26,000 to 72,000. When added to the approximate 6,000 deaths from occupational accidents, work becomes the 8th leading cause of death in the U.S., after diabetes and ahead of motor vehicle accidents. The causes of deaths from occupational diseases were selected respiratory diseases, cancers, cardiovascular disease, chronic renal failure, and hepatitis. The annual cost of occupational illnesses and injuries has been estimated to be between $128 and $155 billion per year.
Something that might help reduce the occupational disease burden is to bring occupational exposure standards up to date, and make them relevant in light of today’s toxicological and epidemiological research.
The Occupational Safety and Health Administration (OSHA) is responsible for developing standards that will assure, “. . . that no employee will suffer material impairment of health or functional capacity even if such employee has regular exposure to the hazard. . . for the period of his working life.” In other words, achieving a safe and healthful workplace occurs through setting enforceable workplace standards that are based on allowable limits for worker exposure. OSHA hasn’t done a lot of exposure standards development in recent years. The easy answer would be to blame the G.W. Bush Administration business-friendly policies as the reason for this inaction. But exposure standards had been a problem long before the Bushies seized power.
OSHA sets enforceable Permissible Exposure Limits (PELs) which are regulatory limits on the amount or concentration of a hazardous substance that can be in the air in a workplace. When the OSH Act was enacted in 1970, OSHA needed PELs for lots of hazardous substances, right away. For this purpose OSHA reached out to use Threshold Limit Values (TLVs). TLVs are non-enforceable guidelines developed by the American Conference of Governmental Industrial Hygienists (ACGIH). TLVs “refer to airborne concentrations of substances, and it is believed represent conditions under which nearly all workers may be repeatedly exposed, day after day, without adverse effect”.
Years passed. TLVs were updated from time to time. The National Institute for Occupational Safety and Health began developing Recommended Exposure Limits (RELs), non-enforceable exposure limits similar in concept to TLVs. In 1989, OSHA tried to update its PELs, by adopting TLVs and RELs which presumably were based on more recent and better scientific data. That rule was thrown out of court in 1992 ironically in a suit brought by the AFL-CIO. The court directed OSHA to do risk assessments. . . on nearly 400 chemicals. So, the PELs returned to their obsolete, 1970 values (when OSHA was first enacted) which in many cases are based on even older science. With few exceptions, OSHA hasn’t attempted to promulgate new exposure standards, and Congress apparently hasn’t seen fit to push matters along, either.
The situation isn’t all bleak. TLVs have been updated, and while they are non-enforceable, the employers who are concerned about protecting the health of their workers have some better benchmarks than PELs. While NIOSH hasn’t been involved with standards development in awhile, EPA continues, slowly, to evaluate the dose-response of chemical substances through IRIS, the Integrated Risk Information System. Someday though, the EPA toxicologists and the industrial hygiene community will need to get on the same page regarding how to set thresholds of protectiveness – there are distinctly different philosophies used for the general public versus workers. That’s a topic for another day.
Looking at Dr. Michael’s biosketch, it’s apparent that the man knows something about exposure limits. Should his appointment be confirmed by the Senate, it will be interesting to see how he responds to the challenge of reforming PELs.
I’ll update this with links later. I’m tired, and there’s too much to do right now.