The article claims that because influenza vaccines have 25 ug of thimerasol, they exceed the EPA exposure limit by a factor of 250 times. He then goes on to claim that if someone gets annual vaccinations for 10 years they’d exceed the limit by 2500 times. The exposure limit he is talking about is the US EPA chronic oral reference dose of 0.1 ug per kilogram body weight per day for methylmercury.

Even ignoring the fact that thimerasol (ethylmercury) is much less toxic than methylmercury and has a much shorter half-life in the body, and therefore using the methylmercury reference dose is completely inappropriate, and also ignoring the fact that very few flu vaccines have that much thimerasol, the author doesn’t seem to get either the “per kilogram body weight” part or the “lifetime average” part.

Assuming someone gets 1 flu shot per year, the actual chronic dose would be 0.068 ug per day thimerasol. We still have to adjust for body weight though. Even an infant weighing only 5 kg (which since the vaccine isn’t given to babies under 6 months is pretty low) would have an annual dose-equivalent of 0.014 ug/kg/day – about an order of magnitude below this “limit”, and it drops over time as the person’s body weight increases, so the lifetime average exposure would end up about an order of magnitude or so below that (2 orders of magnitude below the limit). So even if you consider ethylmercury to be as toxic as methylmercury (which it isn’t), you still end up about 100 times below the US EPA limit, or 10 times below even if you don’t amortize over a lifetime and just look at infant exposure.

In reality you shouldn’t even be comparing an acute (short-term) dose to a reference dose based on average lifetime exposure, but if you’re going to do that at least get the math right. It’s apparent that Anthony Gucciardi is completely without a clue on this subject (and from a quick look also on the other topics he writes about) and that “the Canadian” is not even remotely credible as a source of news. The flu vaccine is quite safe.

First off, to have a human health risk, you have to have a few conditions met. The first is obviously that you have to have a potentially harmful chemical. Since any chemical, whether natural or synthetic, is potentially harmful at some dose, that one is kind of a given. The second condition is that chemical must get to where humans can be exposed. The third is that humans have to be exposed to enough of the chemical to have a potential for adverse health effects.

When oil is inside a pipeline there isn’t really any potential for exposure. So what happens when oil is released during a pipeline rupture?

When oil is released from a pipeline, it spreads out in the surrounding soil. How far it goes depends on the size of the rupture and how much time passes before it is noticed, the type of oil in the pipeline, and the geology. Most underground spills don’t go a huge distance, but can travel over tens of metres in some cases. Surface spills can travel further since they aren’t as confined, and spills into a water body can potentially travel fairly long distances.

When oil is present in soil, there are basically three things that can happen to it over the short term. The first is being physically bound to the soil; most of the heavier hydrocarbons end up in this state. The second is to enter a vapour form and become airborne; this really only happens to significant extents for fairly light hydrocarbons that might be found in light crude oil, for example. The third is to be dissolved into water between the soil pores, which could eventually move towards the water table – again mostly for light hydrocarbons. Oil spilled on the surface or in water is more likely to end up in vapour or dissolved phases than an underground spill.

So what is the potential for human exposure? The hydrocarbons bound to the soil are pretty much going to stay put, possibly degrading slowly over time (or until remediated); really the only potential for exposure is if a person comes into direct contact with the contaminated soils near the pipeline, and even then risks aren’t generally that high except in the case of something like children playing in the contaminated soil. There is also potential exposure if food crops are grown directly in the contaminated soil, though most petroleum hydrocarbons don’t bioaccumulate to a huge extent since they’re metabolized. Overall there are some localized risks, but once the contamination is identified they can generally be managed fairly readily.

Hydrocarbon compounds in the vapour phase are obviously more mobile, but at the same time they tend to break down fairly quickly in air. The biggest concerns are compounds like benzene which can be present at significant concentrations in light oils, but between the degradation in air, dilution due to air movement, and limited quantities of the volatile compounds, risks are fairly localized and short-term, unless there is a building such as a house on top of or within a few metres of the contamination (which wouldn’t be allowed in most places). Heavier oil mixtures or bitumen don’t have a lot of the light-end hydrocarbons that can enter air.

The portion that is dissolved in soil pore water is probably the portion with the biggest human health risk if it can enter an aquifer used for drinking water. Again this is really only an issue for light-end hydrocarbons; heavier hydrocarbons don’t really move very far and aren’t very soluble. This is really only an issue if there is a shallow aquifer used for drinking water that isn’t geologically isolated from the oil contamination. One of the concerns raised about the Keystone XL pipeline is the potential for impacts to the Ogallala Aquifer, which according to the Wikipedia entry ranges from 30 m to 122 m below the soil surface. I’ve seen soil and groundwater investigations from a lot of oil spills, and even spills of very light oil mixtures don’t travel more than a few metres downward. In the case of the Keystone pipeline the product would be bitumen (which is very insoluble and immobile), the shallowest depth is 30 m and surface recharge to the aquifer is known to be very slow, so there isn’t really any possibility of a pipeline break resulting in bitumen contaminating the aquifer. There are some more volatile compounds used to dilute bitumen for transport, but these compounds are more volatile and have a fairly short environmental life; vertical migration velocities are not high enough for these compounds to travel downwards 30 m before they degrade unless there’s some sort of conduit for them; in my experience it’s fairly rare for them to be found more than about 5 or 6 m below ground surface from a pipeline spill.

The biggest risks to human health occur when a pipeline release occurs into a surface water body, particularly if that surface water body is used as a source of drinking water or for recreational use, since in that case the oil is potentially released directly into the water. This is where efforts should be focused in my opinion – reducing unnecessary surface water crossings, and ensuring that when pipelines do cross surface water bodies that protective measures are taken and proper monitoring is in place.

A CFL typically contains about 4 mg of mercury (according to US EPA); a lot of newer CFLs contain 1 mg or less. I’ll look at the worst-case exposure, so let’s go with 4 mg of mercury in a bulb. In reality that mercury isn’t going to all be in the air right away – the evaporation rate of mercury is about 56 micrograms per hour per square centimetre – but figuring out the rate at which it enters the air requires assumptions about the area covered by the spilled mercury, temperature, pressure, etc. To keep things simple and to make sure I’m considering the absolute worst case, I’ll assume that all of that mercury instantly volatilizes.

After the mercury is released into the air, two things are going to happen. First, it will spread out, occupying a larger volume of air. Second, air movement in and out of the room will remove mercury over time. So let’s look at a couple of specific scenarios:

1. Let’s assume that right after the bulb breaks a person bends down to pick up the pieces. To keep the math simple I’ll say the mercury has spread into a volume of 1 m3 at this stage – large enough that the person’s head is within the affected volume and representing pretty much a worst-case exposure. In reality the mercury concentration within this 1 m3 volume would be highest right next to the floor (presuming the broken bulb is on the floor) and decreasing as you go up, but again to keep it simple and look at an absolute worst-case I’ll simplify things and pretend the mercury is evenly mixed over that entire 1 m3. The resulting concentration would be 4 mg mercury per m3 air. This concentration would not last very long at all and represents a worst-case instantaneous exposure.

2. If the CFL bulb broke in a fairly standard-sized bedroom (around 3 m x 3 m x 2.4 m, or 21.6 m3 – I’ll round down to 20 m3), then over time the mercury would mix throughout the volume of the room, with an average concentration of 4/20 = 0.25 mg/m3. However, air is also going to move in and out of the room (and the house). Even at the low end in winter with windows closed, an air exchange rate of about 1 air change per 3 hours is fairly conservative, so about 1/3 of the mercury would be removed after every hour. Therefore after 1 hour the concentration would be 0.17 mg/m3, after 2 hours it would be 0.11 mg/m3, after 3 hours it would be 0.074 mg/m3, and so on.

These concentrations are probably unrealistically high, since I’ve assumed all of the mercury instantly volatilized. A more realistic concentration would consider the evaporation rate (56 μg/h/cm2). The volume of 4 mg mercury would be about 0.0003 cm3; if it formed a hemispherical drop (probably a reasonable approximation) the exposed surface area would be about 0.017 cm2. Assuming room temperature and sea-level atmospheric pressure, the concentration in the bedroom would peak at about 0.0003 mg/m3 (again based on mixing throughout the bedroom; concentrations would be higher if you put your head right next to the mercury on the floor).

So now we have a very conservative prediction of how much mercury could be in the air under worst-case conditions. What does this mean in terms of potential for effects? The infamous National Post story I mentioned above talked about a Maine Department of Environmental Protection employee comparing concentrations measured in a bedroom to a state exposure limit of 0.0003 mg/m3. This exposure limit is actually the US Environmental Protection Agency “reference concentration” (RfC). However, if a Maine DEP employee really was using this value here, that employee is utterly incompetent or at least unqualified for that sort of assessment – it is a completely inappropriate value to use. The RfC is a conservative estimate of the average concentration you could be breathing in over your entire life without expecting any adverse effects. I’ve seen some other evaluations use occupational exposure limits – again this isn’t ideal, since they’re based on a worker being exposed every day over their working career.

The Agency for Toxic Substances and Disease Registry compiled data on short-term exposures to mercury vapours. The data on short-term human exposures are fairly limited, but measurable effects were associated with very high mercury exposures (of the cases where concentrations were known, they exceeded 40 mg/m3). There are also some animal studies using short-term exposures; generally effects were only observed at concentrations above about 27 mg/m3. The one exception is developmental toxicity; there were a couple of animal studies showing that when pregnant rats were exposed to concentrations as low as about 0.05 mg/m3 over 6 or 7 days at a key stage of foetal brain development, their offspring were hyperactive and showed effects on spatial learning.

Overall, a broken CFL bulb won’t result in mercury concentrations in air anywhere near as high as the concentrations at which effects on humans or even animals have been observed. However, given that mercury is a known developmental toxin, and since concentrations could be higher very close to the spill or after disturbance (e.g. during cleanup), it’s probably not a bad idea for pregnant women to avoid cleaning up broken CFL bulbs if possible; there probably wouldn’t be an effect but it doesn’t hurt to err on the side of caution if possible.

The commenter I mentioned at the beginning of this post mentioned a different scenario where her husband drove in a car for 3 months in winter with a case of broken bulbs. A study of air exchange rates of stationary vehicles suggests between 1 and 3 exchanges per hour with windows closed and no ventilation, or between 1.8 and 3.7 exchanges per hour with windows closed and the fan on recirculation; a compact car has an interior volume of about 3 m3. If the case had 12 CFLs, that would be a total of 48 mg of mercury potentially released; if it was released all at once this would result in an initial concentration of about 16 mg/m3 which would rapidly decrease. Again this mercury probably would not be volatilized to the air all at once though. Rather mercury would be released gradually over time. It’s honestly almost impossible to calculate the likely concentrations, particularly without knowing things like the temperature, how the car was used, etc. If we assume room temperature (e.g. the heater was on) and that each bulb resulted in a hemispherical mercury drop as described above, then a concentration as high as about 0.004 mg/m3 could be calculated, but there are so many assumptions and unknown variables that I wouldn’t want to rely on that number. The concentration probably isn’t in the range where short-term effects are likely, but there are so many unknowns I wouldn’t feel comfortable making predictions about long-term effects, particularly if the driver was spending long periods of time in the car.

In case anyone is wondering, yes, I do plan to get back to talking about actual science in the near future. We get about two months a year of nice weather here, so I’ve been trying to enjoy the outdoors as much as possible before going back into winter hibernation mode. On top of that I’ve recently agreed to take on a new teaching gig on the side (as if I didn’t have enough on my plate already) and am trying to get everything ready before the semester starts in September. I should be able to get to some more substantive posts soon though.

This is the reason why I and many other science bloggers use a pseudonym. Mr. Daniels reportedly owns Captiva Pharmaceuticals – another company to avoid doing business with for ethical people.

Boiron are snake-oil salesmen on a grand scale, with annual sales exceeding half a billion Euros (about $735 million) according to their financial reports. Spread the word, and especially don’t buy anything from them.

So what’s the concern with cadmium, and is it really more toxic than lead? Read on…

Cadmium in its metal form is a silver-white metal that is very soft and malleable. It isn’t normally found as a pure metal naturally, but rather as a component of zinc ores. Canada is one of the largest producers of cadmium, primarily in Ontario, Quebec and New Brunswick, with most of it being exported. It is used in batteries, coatings, pigments, as a plastic stabilizer, and in various metal alloys, and can be found in many common consumer products. Cadmium isn’t a very large component of natural soils, and most cadmium in the environment is a result of human activity.

The main health effect from cadmium discussed in media reports is cancer, and cadmium is classified as a confirmed human carcinogen by the International Agency for Research on Cancer (their old assessment is here; it is currently being updated). The primary cancer effect from cadmium is lung cancer from occupational exposures to cadmium fumes and dust, however, which isn’t really relevant for the general population. There isn’t really any evidence of cadmium causing cancer in humans from ingestion, although there is some limited evidence in animal studies that suggests it could be associated with leukaemia, testicular cancer and prostate cancer, but only in animals with low dietary zinc intake.

The most important effect outside of occupational exposures is actually kidney damage, which has been observed both in humans and in animal studies. Health Canada currently suggests a maximum chronic cadmium intake of 1 microgram per kilogram body weight per day (μg/kg/d) from oral (ingestion) exposure. Similarly, the US Environmental Protection Agency has an oral reference dose (essentially the maximum dose which, over a lifetime of continuous exposure, is not expected to result in adverse effects) of 1 μg/kg/d from food or 0.5 μg/kg/d from water.

Everyone is exposed to some cadmium, mostly from food, although tobacco smoke can also be a major source. For most people the typical exposure doesn’t exceed these recommended limits, but it can be fairly close, particularly for young children; for example, it has been estimated that a typical Canadian toddler has an exposure of about 0.74 μg/kg/d (mainly from food). These exposure estimates do not include exposures from consumer products such as children’s jewelry, however, so even a small amount of additional exposure is considered to be a concern.

As for whether cadmium is more toxic than lead – that’s far from resolved. There’s still a lot of debate about lead toxicity, and in particular its effects on brain development in young children, with some people arguing that there may not be a “safe” dose. Neither of these substances should really be in children’s jewelry.

So, what can you do to minimize exposure? The best thing right now is just to avoid really cheap children’s jewelry, particularly anything from dollar stores (which are notorious for having unsafe products); definitely don’t let young children who might be more inclined to put it in their mouths have it.

Yes, I’ve been pretty slack about posts lately – summer is pretty short here so I should spend the time outside rather than sitting at my computer.

Now more technical information about the IARC evaluation is available, published in the Lancet; while it still isn’t the full IARC technical monograph (which we probably won’t see for several months at least) it does provide a bit more insight into the basis for the IARC classification. At virtually the same time, another analysis of the same data by the International Commission for Non-Ionizing Radiation Protection (ICNIRP) Standing Committee on Epidemiology has been published, which concluded that “the accumulating evidence is increasingly against the hypothesis that mobile phone use can cause brain tumours in adults.” Which of these two apparently conflicting conclusions should we believe?

First a look at the IARC evaluation, as summarized in the Lancet. As expected, the evaluation relies primarily on the INTERPHONE case-control study, which looked at cell phone use (based on recall) in 2708 people with glioma and 2972 controls, and found that for most groups there was no increased risk of glioma (in fact reduced risk in most cases – though as discussed below this is likely a study design artifact), except for the group with the highest cell phone use (>1640 hours of use) which showed an increased risk of glioma, with some suggestion of an increased risk on the side of the head and in the part of the brain where exposure would be highest. Similar results were reported in a Swedish pooled analysis.

The IARC Working Group acknowledged that both of these studies are susceptible to bias, but overall believed that the results “could not be dismissed as reflecting bias alone, and that a causal interpretation between mobile phone RF-EMF exposure and glioma is possible.” On this basis they found there is “limited evidence in humans” for carcinogenicity, although this was not unanimous and some members of the Working Group found the data to be inadequate. They also reviewed animal studies; the available chronic animal studies did not show an increased cancer risk from RF-EMF; a few studies showed an increased cancer risk from a combined exposure to RF-EMF and a known carcinogen but the meaning of that isn’t clear. They also concluded there was only “weak” evidence of a mechanism for RF-EMF to cause cancer. The combined result was classification of RF-EMF as “possibly carcinogenic to humans”, which as I have previously noted would not normally result in regulatory agencies treating it as a carcinogen.

The ICNIRP evaluation also looked at the INTERPHONE study. They found several issues in the study design, including evidence that people’s memory of their cell phone usage was generally biased, and people with lower cell phone use who didn’t have glioma were more likely to refuse to participate in the study; these biases are believed to be the cause for the reported lower glioma risks in low/moderate cell phone users than people who didn’t use cell phones at all. They found data suggesting that people had better recall of the number of calls made than the amount of time they spent on their cell phones, and found that if number of calls was used instead of total hours spent on the phone there was no indication of increased risk of glioma. There was also no increased risk observed for those who had used cell phones the longest. They also noted that the INTERPHONE study showed that individuals who had a very high usage over the past 1 to 4 years had a higher risk than those with similar total usage and more than 10 years of use, which is the opposite of the trend that would be expected for most carcinogens (though a possible alternative explanation is that cancer risk is more a function of the intensity of exposure than cumulative dose).

They found data on where in the brain the tumours were reported to also be subject to bias and to be very inconsistent.

The ICNIRP evaluation also considered the data on brain cancer incidence in several countries with reliable records, including Nordic Countries, Switzerland and the US; in all cases there has been no indication of an increase in brain tumour incidence (as I discussed previously, the trend is the same in Canada).

Overall ICNIRP concluded that the combined evidence suggests that there is no significant increase in adult brain tumours within 10 to 15 years of cell phone use, but noted that there are no data on the risk of childhood tumours.

These two evaluations do not really contradict each other as much as it might seem. Neither give a clear black and white conclusion – both show that the available studies have significant flaws and biases that make it difficult to draw solid conclusions. The two evaluations were done using a different approach; IARC looked at the evidence within a specific framework and set of rules for comparison with other evaluations, while ICNIRP looked at the overall weight of evidence and tried to make general conclusions.

Both evaluations acknowledge some major shortcomings in the data. In particular, cell phone use has only really been widespread for about 10 years, and some cancers may take longer than that to develop. There also aren’t any good data for risks to children, who might be expected to be more sensitive due to thinner skulls and still-developing brains.

Overall, I stand by my original conclusion that there is no reason to panic unless brain cancer incidence rates start to increase, but at the same time if you’re an extremely heavy user of cell phones it probably wouldn’t hurt to take at least minimal precautions. Also of note, the IARC evaluation mentions that the electromagnetic field exposure from newer 3G phones (or from Bluetooth headsets) is about 100 times lower than for traditional cell phones, which means that even if the amount of cell phone usage continues to increase, exposure will likely decrease.

Baan, R., Grosse, Y., Lauby-Secretan, B., El Ghissassi, F., Bouvard, V., Benbrahim-Tallaa, L., Guha, N., Islami, F., Galichet, L., & Straif, K. (2011). Carcinogenicity of radiofrequency electromagnetic fields The Lancet Oncology, 12 (7), 624-626 DOI: 10.1016/S1470-2045(11)70147-4

Swerdlow, A.J., Feychting, M., Green, A.C., Kheifets, L., & Savitz, D.A. (2011). Mobile Phones, Brain Tumours and the Interphone Study: Where Are We Now? Environmnetal Health Perspectives DOI: 10.1289/ehp.1103693

First, a bit of background. As described in the US National Toxicology Program’s (NTP) 12th Report on Carcinogens, the main evidence supporting this classification is from human occupational studies. Specifically, there have been several studies showing higher rates of nasopharyngeal cancer and sinonasal cancer (basically cancers of the upper part of the throat and nasal cavity, respectively) among industrial workers with high levels of formaldehyde exposure. These cancers are fairly rare in the general population, and the incidence of these cancers has been shown to increase at higher levels of formaldehyde exposure. It has also been shown that formaldehyde can cause damage to DNA in nasal tissues, showing that there is a plausible mechanism by which formaldehyde can cause these cancers. These data alone are pretty much a slam-dunk argument that show formaldehyde can cause cancer in humans, despite claims from the American Chemistry Council that the classification is not warranted.

There is also some evidence of formaldehyde being associated with blood-related cancers such as leukemia, although the evidence is a bit more mixed there. There are also animal studies showing evidence of carcinogenicity from both inhalation and oral (in water) exposures.

Just because a substance is capable of causing cancer doesn’t automatically mean that it will have an effect on the general population, however. The studies showing human carcinogenicity are all involving people with abnormally high exposures, including various industrial workers and embalmers. To determine the likelihood of formaldehyde causing cancer in humans, we need to consider both its potency as a carcinogen and the amount of exposure.

Everyone is exposed to formaldehyde. It is in the air we breathe, the water we drink (whether from a municipal system or bottled water), and the food we eat. It is also produced naturally within the human body as part of our metabolism. Based on data published by the World Health Organization, typical concentrations in outdoor air are on the order of about 10 μg/m3 (micrograms formaldehyde per cubic meter of air), and concentrations in indoor air are on the order of about 30 μg/m3. Concentrations in water can be around 20 μg/litre. Overall, the NTP concluded that typical exposures include about 0.5 to 2.0 mg (milligrams) each day from air, while the exposure from water would probably work out to about 0.03 mg each day. Higher exposures can occur from tobacco smoke, particularly second-hand smoke. Exposures can also occur from various consumer products, including an estimated exposure of 0.1 mg from applying hand creams or suntan lotion. The amount of formaldehyde found in blood in humans from natural metabolic processes is about 2 to 3 μg/g, which would work out to about 150 to 200 mg in an average sized adult.

The World Health Organization looked at the risk of getting cancer from typical formaldehyde exposures. They concluded that the risks of getting cancer from typical exposures are extremely low – less than 2.7 cases in 100,000,000 people (generally anything less than 1 in 1,000,000 is considered to be negligible), based primarily on nasal cancers. This evaluation suggests that normal exposures to formaldehyde are not likely to be a concern for the general population. The total amount of formaldehyde exposure is also generally much less than the amount of formaldehyde naturally present in the body, again suggesting fairly limited risk. The main risks are associated with occupational exposures.

Despite the low risks, many regulatory agencies handle confirmed human carcinogens differently than other chemicals. This means that some form of regulatory action may be required to manage risks from the substance. This is particularly true for chemicals such as formaldehyde that can directly damage DNA. Typically these actions involve the development of a risk management plan to minimize exposures and phase out unnecessary uses (e.g. uses where another, less harmful chemical could be used without significant economic consequences).