Rock bottom: can rocks in your dog’s water bowl protect your lawn?

Posted on 29 Oct, 2021 by katlday

$fractal image, featuring the hashtag #272sci$

Take a look at the Twitter hashtag #272sci

One quick thing before I dive into this month’s post: if you’re a Twitter user, check out my series of very tiny science tweets under the hashtag #272sci. The aim is to explain a science thing in one tweet – without using a thread – and it’s 272 because that’s the number of characters I have to use after including the hashtag and a space. So far I’ve covered leaf colours, frothy milk, caffeine and poisonous millipedes. There will be more to come!

Now, speaking of Twitter, a couple of weeks ago Prof Mark Lorch tweeted about Dog Rocks. Dog… what? I hear you ask (really quite understandably).

Well, it turns out that Dog Rocks are a product that you can buy, and that you put into your dog’s water bowl. Your dog then drinks the water that has been sloshing over the rocks, and, this is where we start to run into trouble, this is meant to have an effect on your dog’s urine. This, in turn, is supposed to protect any grass your dog might then pee on.

Dog urine damages grass

All right, so let’s start somewhere in the vague vicinity of some science: if you have a dog, or even if you’ve just spent some time with someone who has a dog, you’ve probably noticed that dog urine isn’t very kind to grass. Commonly, you see something like the photo here, that is, patches of yellow, dead grass, surrounded by quite luscious green growth.

Why is this? It’s because dog urine – like the urine of all mammals – contains urea, CO(NH₂)₂. Urea forms in the body when animals metabolise nitrogen-containing compounds, in particular, proteins. It’s essentially a way for the body to get rid of excess nitrogen.

People sometimes confuse urea with ammonia, for reasons that I’ll come to in a moment. But they’re not the same thing. Urea is odourless, forms a pH neutral solution and, if you extract it from the liquid in which it is dissolved, produces solid crystals at room temperature.

Pure ammonia, NH₃, by contrast, is a gas at room temperature (boiling point -33.3 ℃), forms alkaline solutions (with pH values greater than 7) and has that pungent ‘ngggh get it away from me!’ smell with which we’re probably all familiar.

Fresh urine contains urea, but little ammonia

Although these two substances aren’t the same, they are linked: many living things convert ammonia (which is very toxic) to urea (which is much less so) as part of normal metabolism. And it also goes the other way, in a process called urea hydrolysis. This reaction happens in urine once it’s out of the body, too, which is the main reason why, after a little while, urine starts to smell really, really bad.

Okay, fine, but what has this got to do with grass, exactly? Well urea (and ammonia, for that matter) are excellent sources of nitrogen. Plants need nitrogen to grow, but dog urine contains too much, and too much nitrogen is bad – in the same way that too much of pretty much anything nice is bad for humans. It damages the blades of grass and a yellowish dead spot appears, often ringed by some particularly lush grass that, being slightly outside the immediate target zone, caught a whiff of extra nitrogen without being overwhelmed.

Back to Dog Rocks. Interestingly, the website includes an explanation not unlike the one I’ve just given on their fact sheet. What it doesn’t do is satisfactorily explain how Dog Rocks are supposed to change the nitrogen content of your dog’s urine.

Dog Rocks are meant to be placed in your dog’s water bowl

The website says that Dog Rocks are “a coherent rock with a mechanically stable framework”. Okay… so… Dog Rocks won’t dissolve or break up in your dog’s water bowl. A good start. It goes on to say, “the rocks provide a stable matrix and a micro-porous medium in which active components are able to act as a water purifying agent through ion exchange” and “Dog Rocks will help purify the water by removing some nitrates, ammonia and harmful trace elements thereby giving your dog a cleaner source of water and lowering the amount of nitrates found in their diet.”

You’ll note they’re using the word nitrate. Nitrates are specifically compounds containing the NO₃^– ion, but I think they’re using the term in a more general way, to suggest any nitrogen-containing compound (including urea and ammonia). And by the way, nitrates are different from the similar-sounding nitrites, which contain the NO₂^– ion. Fresh urine from a healthy dog (or human, for that matter) shouldn’t contain nitrite. In fact, a dipstick test for nitrite in urine is commonly used to check for urinary tract infections, because it suggests bacteria are present.

Anyway, nitrates/nitrites aside, it’s the last bit of that claim which really makes no sense. Your dog is not ingesting anything like a significant quantity of nitrogen-containing compounds from its water bowl. Urea comes from the metabolic breakdown of proteins, and they come from your dog’s food.

Photo of puppies eating food that I totally picked because it's cute ;-)

The nitrogen-containing compounds in your dogs’ urine come from their food, not their water

It’s faintly possible, I suppose, that Dog Rocks might somehow filter out some urea/nitrates from urine. But then your dog would have to pee through the Dog Rocks and, honestly, if you can manage to arrange that, you might as well train your dog not to pee on your grass in the first place.

I suggest that there are three possible explanations for the positive testimonials for this product. 1) Owners who use it are inadvertently encouraging their dogs to drink more water, which could be diluting their urine, leading to less grass damage. 2) It’s all a sort of placebo effect: owners imagine it’s going to work, and they see what they’re expecting to see, or 3) they’re all made up.

You decide, but there is absolutely no scientifically-plausible way that putting any kind of rocks in your dog’s water bowl will do anything to stop dog pee damaging your grass. This is £15 you do not need to spend. But hey, you could avoid the money burning a hole in your pocket (see what I did there?) by buying me a coffee… 😉

Check out the Twitter hashtag #272sci here, and support the Great Explanations book project here!

Do you want something non-sciency to distract you from, well, everything? Why not take a look at my fiction blog: the fiction phial? You can also find me doing various flavours of editor-type-stuff at the horror podcast, PseudoPod.org – so head over there, too!

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Faking Lateral Flow Tests: the problem with pH

Posted on 6 Jul, 2021 by katlday

Fruit juices can be used to generate a fake positive on COVID-19 LFTs

On Thursday last week, I got a message from Prof Mark Lorch — my sometime collaborator on supercharacter-based ramblings.

“Have you seen the reports of kids fooling the Covid lateral flow tests and getting false +ve results by adding orange juice to the devices?” he wondered.

At this point, I had not – but I quickly got up to speed. Mark had previously made an excellent video explaining how lateral flow test (LFT) devices work, so it was just a case of working out, firstly, whether the false positives were reproducible, and secondly, speculating what, exactly, was causing them.

Thus ensued some interesting discussion which ultimately led to a couple of articles from Mark. One at The Conversation and another, slightly more recently, at BBC Future.

I won’t delve into LFT-related science, because Mark has covered it (really, check the video and those articles), but I am going to talk a little bit about pH – the scale chemists use to measure how acidic or alkaline solutions are – because as soon as news of this started to gain traction people, predictably, started trying it out themselves. And that was when things got really interesting.

The buffer included with LFTs is effective at neutralising the pH of solutions, for example, cola

Now, firstly, and importantly: the test kits come with a small vial of buffer solution. Buffers are substances which resist pH changes. As I’ve written before, our bodies naturally contain buffer systems, because keeping the pH of our blood and other body fluids constant is important. In fact, if blood pH varies even a little, you’re in all sorts of serious trouble (which is how we can be certain that so-called “alkaline” diets are a load of hooey). Anyway, the important message is: don’t mix any liquid you’re testing with the contents of that phial, because that will neutralise it.

If you want to try this for yourself, just drop the liquid you want to test directly into the window marked S on the test.

That out of the way, let’s get back to pH. It’s a scale, usually presented as going from 0–14, often associated with particular colours. The 0 end is usually red, the 7 in the middle is usually green, while the 14 end is usually dark blue.

These colours are so pervasive, in fact, that I’ve met more than one person with the idea that acids are red, and alkalis are blue. This isn’t the case, of course. The red/green/blue idea largely comes from universal indicator (UI), which is a mixture of dyes that change colour at different pH values. There’s also a common indicator called litmus (people sometimes mix up UI and litmus, but they’re not the same) which is also red in acid and blue in alkali.

Some species of hydrangea produce pink flowers in alkaline soil, blue in acid soil.

There are actually lots of pH indicators, with a wide variety of colour changes. Phenolphthalein, for example, is bright pink in alkali, and colourless in acids. Bromocresol purple (they have such easy-to-spell names) is yellow in acids, and violet-purple in alkalis.

Many plants contain natural indicators. Just to really mix things up, some species of hydrangea produce flowers that are blue-purple when they’re grown in acidic soil, and pink-red in alkaline conditions.

Bottom line? Despite the ubiquitous diagrams, pH has nothing to do with colour. What it is to do with is concentration. Specifically, the concentration of hydrogen ions (H⁺) in the solution. The more H⁺ ions there are, the more acidic the solution is, and the lower the pH. The fewer there are, the less acidic (and the more alkaline, and higher pH) it is.

In fact, pH is a log scale. When the concentration changes by a factor of 10, the pH changes by one point on the scale.

This means that if you take an acid with pH of 2, and you dilute it 1 part to 10, its pH changes to 3 (i.e. gets one point more alkaline, closer to neutral). Likewise, if you dilute an alkali with a pH of 10 by 1:10, its pH will shift to 9 (again, closer to neutral).

And what this means is that the pH of substances is not a fixed property.

Louder for anyone not paying attention at the back: the pH of substances is not a fixed property!

Yes, we’ve all seen diagrams that show, for example, the pH of lemon juice as 2. This is broadly true for most lemons, give or take, but if you dilute the lemon juice, the pH rises.

Apple juice dropped directly into the test window gives an immediate “positive” result.

I am by no means an expert in commercial, bottled lemon juice, but I reckon a lot of them have water added – which may well explain why @chrismiller_uk was able to get a positive result, while @BrexitClock, using a French bottle of lemon juice, couldn’t.

Mark and I concluded that the pH you need to aim for is probably around 3–4. Go too low, and you don’t get a positive (and you might wipe out the control line, too). Likewise, too high also won’t work.

Myself, I tried apple juice. I couldn’t find the indicator colour key for my indicator paper (I really must clear out the drawers one of these days) but it’s broadly the same as Mark’s cola photo, up above. In other words, the apple juice is about pH 3. And it gives a beautiful positive result, immediately.

One more interesting observation: Mark recorded some time-lapse video comparing orange juice to (sugar-free) cola. It shows the cola test line developing a lot more slowly. We’re not entirely sure why, but it may be pH again: orange juice almost certainly has a lower pH than cola.

For any parents reading this thinking we’re being terribly irresponsible, fear not: as Prof Lorch has made clear in his articles, you can identify a fake by waiting a few minutes and then dropping some of the buffer solution provided in the test window. As I said above, this will neutralise the pH, and the positive test line will disappear. Extra buffer won’t change a genuinely-positive test, because the antibodies bind very tightly (more technical info here). To quote Mark: “you’d need a swimming pool’s worth of buffer to have any chance of washing [the antibodies] off.”

Alternatively, you can just watch your teenager as they do their tests, and make sure they’re not getting up to anything nefarious…

Have you tried to trick an LFT? If you have, share your results! Look us up on Twitter: @chronicleflask and @Mark_Lorch or add a comment below. We’d love to see your photos!

One Flash of Light, One Vision: Carrots, Colour and Chemistry

Posted on 28 Feb, 2021 by katlday

“White” light is made up of all the colours of the rainbow.

Sometimes you have one of those weeks when the universe seems to be determined to yell at you about a certain thing. That’s happened to me this week, and the shouting has been all about light and vision (earworm, anyone?).

I started the week writing about conjugated molecules and UV spectrometry for one project, was asked a couple of days ago if I’d support a piece of work on indicators for the RSC Twitter Poster Conference that’s happening from 2-3rd March, and then practically fell over a tweet by Dr Adam Rutherford about bacteria that photosynthesise from infrared light in a hydrothermal vent*.

Oh well, who am I to fight the universe?

Light is awesome. The fact that we can detect it is even awesome-er. The fact that we’ve evolved brains clever enough built all sorts of machines to measure other kinds of light that our puny human eyes cannot detect is, frankly, astonishing.

The electromagnetic spectrum covers all the different kinds of light. (Image source)

Let’s start with some basics. You probably met the electromagnetic (EM) spectrum at some point in school. Possibly a particularly enthusiastic physics teacher encouraged you to come up with some sort of mnemonic to help you remember it. Personally I like Rich Men In Vegas Use eXpensive Gadgets, but maybe that’s just me.

The relevant thing here is that the EM spectrum covers all the different wavelengths of light. Visible light, the stuff that’s, well, visible (to our eyes), runs from about 400 to 700 nanometres.

A colour wheel: when light is absorbed, we see the colour opposite the absorbed wavelengths. (Image source)

Now, we need another bit of basic physics (and biology): we see light when it enters our eyes and strikes our retinas. We see colours when only certain wavelengths of light make it into our eyes.

So-called “white” light is made up of all the colours of the rainbow. Take one or more of those colours away, and we see what’s left.

For example, if something looks red, it means that red light made it to our eyes, which in turn means that, somewhere along the way, blue and green were filtered out.

(Before I go any further, there are actually several causes of colour, but I’m about to focus on one in particular. If you really want to know more, there’s this book, although it is a tad expensive…)

Back to chemistry. Certain substances absorb coloured light. We know them as pigments. Carrots are orange, for example, largely because they contain a pigment called beta-carotene (or β-carotene). This stuff appears, to our eyes, as red-orange, and the reason for that is that it absorbs green-blue light, the wavelengths around 400-500 nm.

β-Carotene is a long molecule with lots of C=C double bonds. (Image source.)

Why does it absorb light at all? Well, β-carotene is a really long molecule, with lots of C=C double bonds. These bonds form what’s called a conjugated system. Without getting into the complexities of molecular orbital theory, that means the double bonds alternate along the chain, and they basically overlap and… smoosh into one long thing. (Look, as the saying goes, “all models are wrong, but some are useful,” – it’ll do for now.)

When molecules with conjugated systems are exposed to electromagnetic light, they absorb it. Specifically, they absorb in the ultraviolet region – the wavelengths between about 200 and 400 nanometres. Here’s the thing, though, those wavelengths are right next to the violet end of the visible spectrum – that’s why it’s called ultraviolet after all.

Molecules with really long conjugated systems start to absorb in the coloured light region, as well. And because they’re absorbing violet and blue, possibly a smidge of green, they look… yup! Orangey, drifting into red.

So now you know why carrots are orange. Most brightly coloured fruit, of course, is that way to attract animals and birds to eat it, and thus spread its seeds. As fruit ripens, it usually changes colour, making it stand out better against green foliage and easier to find. This is the link with indicators that I mentioned at the start: many fruits contain anthocyanin pigments, and these often have purple-red colours in neutral-acidic environments, and yellow-green at the more alkaline end. In other words, the colour change is quite literally an indicator of ripeness.

But the bit of the carrot that we usually eat is underground, right? Not particularly easy to spot, and they don’t contain seeds anyway. Why are carrots bright orange?

Modern carrots are mostly orange, but purple and yellow varieties also exist.

Well, they weren’t. The edible roots of wild plants almost certainly started out as white or cream-coloured, as you might expect for something growing underground, but the carrots which were first domesticated and farmed by humans in around 900 CE were, most probably, purple and yellow.

As carrot cultivation became popular, orange roots began to appear in Spain and Germany in the 15th/16th centuries. Very orange carrots, with high levels of β-carotene, appeared from the 16th/17th centuries and were probably first cultivated in the Netherlands. Some have theorised that they were particularly selected for to honour William of Orange, but the evidence for this seems to be a bit slight. Either way, most modern European carrots do descend from a variety that was originally grown in the Dutch town of Hoorn.

In other words, brightly-coloured carrots are a mutation which human plant breeders selected for, probably largely for appearances.

But wait! There was an advantage for humans, too – even if we didn’t realise it straight away. β-carotene (which, by the way, has the E number E160a – many natural substances have E numbers, they’re nothing to be frightened of) is broken up in our intestines to form vitamin A.

Vitamin A is essential for good eye health.

Vitamin A, like most vitamins, is actually a group of compounds, but the important thing is that it’s essential for growth, a healthy immune system and – this is the really clever bit – good vision.

We knew that. Carrots help you see in the dark, right?

Hah. Well. The idea that carrot consumption actually improves eyesight seems to be the result of a World War II propaganda campaign. During the Blitz, the Royal Air Force had (at that time) new, secret radar technology. They didn’t want anyone to know that, of course, so they spread the rumour that British pilots could see exceptionally well in the dark because they ate a lot of carrots, when the truth was that those pilots were actually using radar.

But! It’s not all a lie – there is some truth to it! Our retinas, at the back of our eyes, have two types of light-sensitive cells. Cone cells help us distinguish colours, while rod cells help us detect light in general.

In those rod cells, a molecule called 11-cis-retinal is converted into another molecule called rhodopsin. This is really light-sensitive. When it’s exposed to light it photobleaches (stops being able to fluoresce), but then regenerates. This process takes about thirty minutes, and is a large part of the reason it takes a while for your eyes to “get used to the dark.”

Guess where 11-cis-retinal comes from? Yep! From vitamin A. Which is why one of the symptoms of vitamin A deficiency is night blindness. So although eating loads of carrots won’t give you super-powered night vision, it does help to maintain vision in low light.

Our brain interprets electrical signals as vision.

How do these molecules actually help us to see? Well, when rhodopsin is exposed to light, the molecule changes, which ultimately results in an electrical signal being transmitted along the optic nerve to the brain, which interprets it as vision!

In summary, not only is colour all about molecules, but our whole visual system depends on some clever chemistry. I told you chemistry was cool!

Just gimme fried chicken 😉

*Ah. I sort of ran out of space for the weird hydrothermal bacteria thing. At least one of the relevant molecules seems to be another carotenoid, probably chlorobactene. The really freaking amazing thing is that there seems to be an absorption at 775 nm, which is beyond red visible light and into the infrared region of the EM spectrum. Maybe more on this another day…

If you’re studying chemistry, have you got your Pocket Chemist yet? Why not grab one? It’s a hugely useful tool, and by buying one you’ll be supporting this site – it’s win-win! If you happen to know a chemist, it would make a brilliant stocking-filler! As would a set of chemistry word magnets!

Like the Chronicle Flask’s Facebook page for regular updates, or follow @chronicleflask on Twitter. Content is © Kat Day 2021. You may share or link to anything here, but you must reference this site if you do. If you enjoy reading my blog, and especially if you’re using information you’ve found here to write a piece for which you will be paid, please consider buying me a coffee through Ko-fi using the button below.

Want something non-sciency to distract you from, well, everything? Why not check out my fiction blog: the fiction phial.

Onerous ovens: why is cleaning the cooker such a chore?

Posted on 30 Nov, 2020 by katlday

As I write Thanksgiving was a few days ago, when most Americans traditionally cook a very large meal based around roasted turkey. Most Brits – and other countries of course – have the same thing coming up soon in the form of Christmas, and there are lots of other celebrations around this time of year that seem to feature cooking and food quite heavily.

Whatever your traditions, then, it’s a time when many of us frown critically at the dark, sticky depths of our oven and wonder if, perhaps, we should attempt to give it a clean. Or at least pay someone else to come and clean it.

Why is oven cleaning such a difficult and unpleasant job, anyway? It’s not that hard to clean other surfaces, is it? Why are ovens so particularly awful?

Well, to explain this, we first need to understand fats.

Fats vaporise during cooking.

Most of the grime in your oven is fat, combined with the carbonised remains of… something or other. The sorts of fats that are common in animal and plant products have boiling points around the 300 ^oC mark (animal fats typically having higher values than plant oils), but they start to form vapours at much lower temperatures, and certainly at typical cooking temperatures there’s plenty vaporised oil around. Besides, under typical conditions most oils will “smoke” – i.e. start to burn – long before they get close to boiling.

We’re all familiar with the idea that fats don’t mix well with water, and herein lies the problem: all that fatty gloop that’s stuck to the inside of your oven just doesn’t want to come off with standard cleaning methods, particularly when it’s built up over time.

Can chemistry help us here? What are fats, chemically? Well, they’re esters. Which may or may not mean anything to you, depending on how much chemistry you can remember from school. But even if you don’t remember the name, trust me, you know the smell. In particular, nail polishes and nail polish removers contain the simple ester known as ethyl acetate, otherwise known as ethyl ethanoate. (Some people say this chemical smells like pear drops which… only really helps if you know what pear drops smell like. Look, it smells of nail polish, okay?)

Fats are esters (image source)

Anyway, the point is that esters have a particular sequence of atoms that has a carbon bonded to an oxygen, which is bonded to another carbon, which is in turn double-bonded to oxygen. This is a bit of a mouthful, so chemists often write it as COOC. In the diagram here, oxygen atoms are red while carbon atoms are black.

There are actually three ester groups in fat molecules – which explains why fats are also known as triglycerides.

In terms of general chemistry, esters form when a carboxylic acid (a molecule which contains a COOH group) reacts with an alcohol (a molecule that contains an OH group). And this is where it all starts to come together – honest – because you’ve probably heard of fatty acids, right? If nothing else, the words turn up in certain food additive names, in particular E471 mono- and diglycerides of fatty acids, which is really common in lots of foods, from ice cream to bread rolls.

Glycerol is a polyol — a molecule that contains several alcohol groups (image source)

Well, this reaction is reversible, and as a result fats (which are esters, remember) break up into fatty acids and glycerol – which is a polyol, that is, a molecule with several alcohol groups. Or, to look at it the other way around: fats are made by combining fatty acids with glycerol.

And the reason it’s useful to understand all this is that the way you break up esters, and therefore fat, is with alkalis. (Well, you can do it with acid, too, but let’s not worry about that for now.)

Strong alkalis break up fats in a chemical reaction called hydrolysis — the word comes from the Greek for water (hydro) and unbind (lysis) and so literally means “split up with water”. Humans have known about this particular bit of chemistry for a long time, because it’s fundamental to making soap. As I said a few months ago when I was banging on about hand-washing, the ancient Babylonians were making soap some 4800 years ago, by boiling fats with ashes – which works because alkaline compounds of calcium and potassium form when wood is burnt at high temperatures.

The grime in ovens is mostly fat.

The really clever thing about all this is that two things are happening when we mix alkali with fat: not only are we breaking up the fat molecules, but also the substances they break up into are water-soluble (whereas fats, as I said at the start, aren’t). Which makes them much easier to clean away with water. Obviously this is the very point of soap, but it’s also handy when trying to get all that baked-on gunk off your oven walls.

Now, in theory, this means you could get some lye (aka sodium hydroxide, probably), smear it all over your oven and voilà. But I don’t recommend it, for a few reasons. Firstly, it’s going to be difficult to apply, since sodium hydroxide is mostly sold as pellets or flakes (it’s pretty easy to buy, because people use it to make soap).

Sodium hydroxide, sometimes called lye, is often sold in the form of pellets.

But, you say, couldn’t I just dissolve it in water and spray or spread it on? Yes, yes you could. But it gets really, really hot when you mix it with water. So you need to be incredibly careful. Because, and this is my next point, chemically your skin is basically fat and protein, and this reaction we’re trying to do on oven sludge works equally well on your skin. Only, you know, more painfully, and with scarring and stuff. In short, if you’re handing lye, wear good nitrile on vinyl gloves and eye protection.

Actually, regardless of how you’re cleaning your oven you should wear gloves and eye protection, because the chemicals are still designed to break down fats and so… all of the above applies. It’s just that specially-designed oven cleaners tend to come with easier (and safer) ways to apply them. For example, they might come as a gel which you can paint on, and/or with bags that you can put the racks into, and may also be sold with gloves and arm protectors (but rarely goggles – get some separately). They might also have an extra surfactant, such as sodium laureth sulfate, added to help with breaking down grease. The main ingredient is still either potassium hydroxide or sodium hydroxide, though.

Well, possibly, but also not really, if you’re sensible.

As an aside, it makes me smile when I come across an article like this which talks about the “serious” chemicals in oven cleaners and more “natural” ways to clean your oven. The “natural” ways are invariably weak acids or alkalis such as lemon juice or baking soda, respectively. They’re essentially ineffective ways of trying to do exactly the same chemistry.

And okay, sure, the gel and the bag and so on in the modern kits are newer tech, but the strong alkali? Nothing more natural than that. As I said at the start, humans have literally been using it for thousands of years.

A point which really cannot be repeated enough: natural does not mean safe.

Fumes can be irritating to skin, eyes and lungs.

Speaking of which, you will get fumes during oven cleaning. Depending on the exact cleaning mixture involved, these will probably be an alkaline vapour, basically (haha) forming as everything gets hot. Such vapour is potentially irritating to skin, eyes and lungs, but not actually deadly toxic. Not that I recommend you stick your head in your freshly-scrubbed oven and inhale deeply, but you take my point. It might give food a soapy, possibly bitter (contrary to what’s stated in some text books, not all alkalis taste bitter, but do not experiment with this) taste if you really over-do it.

In short, if you’re cleaning your oven yourself: follow the manufacturer’s instructions, make sure your kitchen is well-ventilated, leave the oven door open for a while after you’ve finished and, to be really sure, give all the surfaces an extra wash down with plenty of water.

Put the cleaning off until January – after all, the oven’s only going to get dirty again.

And that’s… it, really. Whether you’re cleaning your own oven or getting someone else to do it for you, the chemistry involved is really, really old. And yes, the chemicals involved are hazardous, but not because they’re not “natural”. Quite the opposite.

Or you could just leave it. I mean, it’s only going to get dirty again when you cook Christmas dinner, right?

Like the Chronicle Flask’s Facebook page for regular updates, or follow @chronicleflask on Twitter. Content is © Kat Day 2020. You may share or link to anything here, but you must reference this site if you do. If you enjoy reading my blog, and especially if you’re using information you’ve found here to write a piece for which you will be paid, please consider buying me a coffee through Ko-fi using the button below.

Want something non-sciency to distract you from, well, everything? Why not check out my fiction blog: the fiction phial.

Chemical connections: dexamethasone, hydroxychloroquine and rheumatoid arthritis

Posted on 16 Jun, 2020 by katlday

The chemical structure of dexamethasone (image from Wikimedia Commons)

It’s been widely reported today that a “cheap and widely-available” steroid treatment has been shown to be effective in patients suffering the most severe COVID-19 symptoms, significantly reducing the risk of death for both patients on ventilators and those on oxygen treatment.

Most of the reports have understandably focused on the medical aspects, but this is a chemistry blog (mostly) so *cracks chemistry knuckles* what is dexamethasone, exactly?

Its story starts a little over 60 years ago when, in 1958, a paper was published on “clinical observations with 16a-methyl corticosteroid compounds”. Bear with me, I shall explain. Firstly, corticosteroids are hormones which are naturally produced in our bodies. They do all sorts of nifty, useful things like regulate our immune response, reduce inflammation and help us to get energy from carbohydrates. Two of the most familiar names are probably cortisol and cortisone—both of which are released in response to stress.

The discovery of corticosteroids was an important one. So important, in fact, that a few years earlier, in 1950, Tadeusz Reichstein, Edward Calvin Kendall and Philip Showalter Hench had been awarded a Nobel Prize in Physiology and Medicine for “discoveries relating to the hormones of the adrenal cortex”.

The adrenal glands are two small glands found above the kidneys. The outermost part of these glands is called the adrenal cortex (“cortex” from the Latin for (tree) bark and meaning, literally, an outer layer). In the mid-1930s Kendall and Reichstein managed to isolate several hormones produced by these glands. They then made preparations which, with input from Hench, were used in the 1940s to treat a number of conditions, including rheumatoid arthritis.

This was hugely significant at the time, because until this point the treatments for this painful, debilitating condition were pretty limited. Aspirin was known, of course, but wasn’t particularly effective and long-term use had potentially dangerous side effects. Injectable gold compounds (literally chemical compounds containing Au atoms/ions) had also been tried, but those treatments were slow to work, if they worked at all, and were expensive. The anti-malarial drug, hydroxychloroquine (which has also been in the news quite a lot), had been tried as a “remittive agent”—meaning it could occasionally produce remission—but it wasn’t guaranteed.

Rheumatoid arthritis causes warm, swollen, and painful joints (image from Wikimedia Commons)

Corticosteroids were a game-changer. When Hench and Kendall treated patients with what they called, at the time, “compound E” (cortisone) there was a rapid reduction in joint inflammation. It still caused side effects, and it didn’t prevent joint damage, but it did consistently provide relief from painful symptoms.

Fast-forward to the 1958 paper I mentioned earlier, and scientists had discovered that a little bit of fiddling with the molecular structure of steroid molecules caused them to have different effects in the body. The particular chemical path we’re following here started with prednisolone, which had turned out to be a useful treatment for a number of inflammatory conditions. However, placing a methyl group (—CH₃) on the 16th carbon—which is, if you have a look at the diagram below, the one on the pentagon-shaped ring, roughly in the middle—changed things.

The steroid “nucleus”: each number represents a carbon atom (image from Wikimedia Commons)

In 1957, four different molecules with methyl groups on that 16th carbon were made available for clinical trial. One of them was 16a-methyl 9a-fluoroprednisolone, more handily known as dexamethasone.

(Quick aside to explain that on the diagram of dexamethasone at the start of this post, the methyl group on the 16th carbon is represented by a dashed wedge-shape. It’s a 2D diagram of a 3D molecule, and the dashed wedge tells us that the methyl group is pointing away from us, through the paper, or rather, screen. This matters because molecules like this have mirror image forms which usually have very different effects in the body—so it’s important to get the right one.)

Dexamethasone is on the WHO Model List of Essential Medicines

It turned out that dexamethasone had a much stronger anti-inflammatory action than plain prednisolone, and it was also more effective the other molecules being tested. It caused a bigger reduction in symptoms, at lower doses. A win all round. It did still have side effects—weight gain, skin problems and digestive issues—but these were no worse than other steroids, and better than some. In fact, salt and water retention were less with dexamethasone, which meant less bloating. It also seemed to have less of an effect on carbohydrate metabolism, making it potentially safer for patients with diabetes.

Skipping forward to 2020, and dexamethasone is routinely used to treat rheumatoid arthritis, as well as skin diseases, asthma, COPD and various other conditions. It is on the WHO Model List of Essential Medicines—a list of drugs thought to be the most important for taking care of the health needs of the population, based on their effectiveness, safety and relative cost.

In the wake of more and more evidence that COVID-19 disease was leading to autoimmune and autoinflammatory diseases, scientists have been looking at anti-inflammatory drugs to see if any of them might help. The Recovery Trial at the University of Oxford was set up to investigate a few different drugs, including hydroxychloroquine (there it is again) and dexamethasone.

It’s not a miracle cure but, in the most severe cases, dexamethasone—a cheap, 60+ year old drug—might just make all the difference.

And that brings us back to today’s news: in the trial, 2104 patients were given dexamethasone once per day for ten days and compared to 4321 patients who were given standard care. The study, led by Professor Peter Horby and Professor Martin Landray, showed that dexamethasone reduced the risk of dying by one-third in ventilated patients and by one fifth in other patients receiving only oxygen.

It’s not a miracle cure by any means: it doesn’t help patients who don’t (yet) need respiratory support, and it doesn’t work for everyone, but, if you find yourself on a ventilator, there’s a chance this 60+ year-old molecule that was first developed to cure rheumatoid arthritis might, just, save your life. And that’s pretty good news.

EDIT 17th June 2020: Chemistry World published an article pointing out that “the trial results have yet to be released leading some to urge caution when interpreting them” and quoting Ayfer Ali, a specialist in drug repurposing, as saying “we have to wait for the full results to be peer reviewed and remember that it is not a cure for all, just one more tool.

If you’re studying from home, have you got your Pocket Chemist yet? Why not grab one? It’s a hugely useful tool, and by buying one you’ll be supporting this site – it’s win-win!

Want something non-sciency to distract you from, well, everything? Why not check out my fiction blog: the fiction phial.

How are amber teething necklaces supposed to work?

Posted on 30 Sep, 2019 by katlday

Do amber beads have medicinal properties?

Amber, as anyone that was paying attention during Jurassic Park will tell you, is fossilised resin from trees that lived at least twenty million years ago (although some scientists have speculated it could be older). It takes the form of clear yellow through to dark brown stones, seemingly warm to the touch, smooth and surprisingly hard. It is certainly beautiful. But does it also have medicinal properties? And if it does, are they risk-free?

In 2016 a one year-old boy was found dead at his daycare centre in Florida. The cause of death was a necklace, which had become tangled and tightened to the point that he was unable to breathe.

Why was he wearing a necklace? Surely everyone knows that babies shouldn’t wear jewellery around their necks where it could so easily cause a terrible tragedy like this? No one needs a necklace, after all – it’s purely a decorative thing. Isn’t it?

Yes. Yes, it is. However, this particular type of jewellery was specifically sold for use by babies. Sold as a product that parents should give their children to wear, despite all the advice from medical professionals. Why? Because this jewellery was made from amber, and that’s supposed to help with teething pains.

Teething is a literal pain.

Anyone whose ever had children will tell you that teeth are basically a non-stop, literal pain from about 4 months onward. Even once your child appears to have a full set, you’re not done. The first lot start falling out somewhere around age five, resulting in teeth that can be wobbly for weeks. And then there are larger molars that come through at the back somewhere around age seven. Teenagers often find themselves suffering through braces and, even when all that’s done, there’s the joy of wisdom teeth still to come.

It’s particularly difficult with babies, who can’t tell you what hurts and who probably have inconsistent sleep habits at the best of times. Twenty sharp teeth poking through swollen gums at different times has to be unpleasant. Who could blame any parent for trying, well, pretty much anything to soothe the discomfort?

Enter amber teething necklaces. They’re sold as a “natural” way to soothe teething pain. They look nice, too, which I’m sure is part of their appeal. A chewed plastic teething ring isn’t the sort of thing to keep in baby’s keepsake box, but a pretty necklace, well, I’m sure many parents have imagined getting that out, running their fingers over the beads and having a sentimental moment years in the future.

Amber is fossilised tree resin.

So-called amber teething necklaces are made from “Baltic amber,” that is, amber from the Baltic region: the largest known deposit of amber. It is found in other geographical locations, but it seems that the conditions – and tree species – were just right in the Baltic region to produce large deposits.

Chemically, it’s also known as succinite, and its structure is complicated. It’s what chemists would call a supramolecule: a complex of two or more (often large) molecules that aren’t covalently bonded. There are cross-links within its structure, which make it much denser than you might imagine something that started as tree resin to be. Baltic amber, in particular, also contains something else: between 3-8% succinic acid.

Succinic acid is a dicarboxylic acid.

Succinic acid is a much simpler molecule with the IUPAC name of butanedioic acid. It contains two carboxylic acid groups, a group of atoms we’re all familiar with whether we realise it or not – because we’ve all met vinegar, which contains the carboxylic acid also known as ethanoic acid. If you imagine chopping succinic acid right down the middle (and adding a few extra hydrogen atoms), you’d end up with two ethanoic acid molecules.

Succinic acid (the name comes from the Latin, succinum, meaning amber) is produced naturally in the body where it is (or, rather, succinate ions are) an important intermediate in lots of chemical reactions. Exposure-wise it’s generally considered pretty safe at low levels and it’s a permitted food additive, used as an acidity regulator. In European countries, you might see it on labels listed as E363. It also turns up in a number of pharmaceutical products, where it’s used as an excipient – something that helps to stabilise or enhance the action of the main active ingredient. Often, again, it’s there to regulate acidity.

Basically, it’s mostly harmless. And therefore, an ideal candidate for the alternative medicine crowd, who make a number of claims about its properties. I found one site claiming that it could “improve cellular respiration” which… well, if you’ve got problem with cellular respiration, you’re less in need of succinic acid and more in need of a coffin. Supposedly it also relives stress and prevents colds, because doesn’t everything? And, of course, it allegedly relieves teething pains in babies, either thanks to its general soothing effect or because it’s supposed to reduce inflammation, or both.

Purporters claim succinic acid is absorbed through the skin.

The reasoning is usually presented like this: succinic acid is released from the amber when the baby wears the necklace or bracelet and is absorbed through the baby’s skin into their body, where it works its magical, soothing effects.

Now. Hold on, one minute. Whether this is true or not – and getting substances to absorb through skin is far less simple than many people imagine, after all, skin evolved as a barrier – do you really, really, want your baby’s skin exposed to a random quantity of an acidic compound? Succinic acid may be pretty harmless but, as always, the dose makes the poison. Concentrated exposure causes skin and eye irritation. Okay, you might say, it’s unlikely that an amber necklace is going to produce anywhere near the quantities to cause that sort of effect, but if that’s your logic, then how can it also produce enough to pass through skin and have any sort of biological effect on the body?

The answer, perhaps predictably, is that it doesn’t. In a paper published in 2019, a group of scientists actually went to the trouble of powdering Baltic amber beads and dissolving the powder in sulfuric acid to measure how much succinic acid they actually contained. They then compared those results with what happened when undamaged beads from the same batches were submerged in solvents, with the aim of working out how much succinic acid beads might conceivably release into human skin. The answer? They couldn’t measure any. No succinic acid was released into the solvents, at all. None.

Scientists submerged Baltic amber beads in solvents to see how much succinic acid they released.

They concluded that there was “no evidence to suggest that the purported active ingredient succinic acid could be released from the beads into human skin” and also added that they found no evidence to suggest that succinic acid even had anti-inflammatory properties in the first place.

So amber necklaces don’t work to relieve teething pains. They can’t. Of course, there could be a sort of placebo effect – teething pain is very much one of those comes-and-goes things. It’s very easy to make connections that just aren’t there in this kind of situation, and imagine that the baby is more settled because of the necklace, when in fact they might have calmed down over the next few hours anyway. Or maybe they’re just distracted by the pretty beads.

And, fine. If wearing the jewellery was really risk-free, then why not? But as the story at the start of this post proves, it is not. Any kind of string around a baby’s neck can become twisted, interfering with their breathing. Most necklaces claim to have some sort of “emergency release” mechanism so that they come apart when pulled, but this doesn’t always work.

Don’t fall for the marketing.

Ah, goes the argument. But it’s okay, because we only sell bracelets and anklets for babies. They don’t go around the baby’s neck. It’s completely safe!

No. Because I don’t care how carefully you make it: the string or cord could still break (especially if it’s been chewed), leaving loose beads to pose a serious choking hazard. Not to mention get jammed in ears or nostrils. Even if you’re with the baby, watching them, these sorts of accidents can happen frighteningly quickly. Letting a baby sleep with such an item is nothing short of asking for disaster, and no matter how good anyone’s intentions, babies do have a habit of dozing off at odd times. Will you really wake the child up to take off their bracelet? Every time?

In summary, don’t fall for the marketing. Amber necklaces may be pretty, but they’re not suitable for babies. The claims about succinic acid are completely baseless, and the risks are very real.

Like the Chronicle Flask’s Facebook page for regular updates, or follow @chronicleflask on Twitter. Content is © Kat Day 2019. You may share or link to anything here, but you must reference this site if you do. If you enjoy reading my blog, please consider buying me a coffee through Ko-fi using the button below.

The Chronicles of the Chronicle Flask: 2018

Posted on 28 Dec, 2018 by katlday

As has become traditional, I’m finishing off this year with a round-up of 2018’s posts. It’s been a good year: a few health scares which turned out to be nothing much to worry about, one which turned out to be a genuine danger, a couple of cool experiments and some spectacular shiny balls. So without further ado, here we go…

Things were a bit hectic at the start of this year (fiction writing was happening) and as a result January was quiet on the blog. But not on the Facebook page, where I posted a couple of general reminders about the silliness of alkaline diets which absolutely exploded, achieving some 4,000 shares and a reach (so Facebook tells me anyway) of over half a million people. Wow. And then I posted a funny thing about laundry symbols which went almost as wild. It’s a strange world.

February featured BPA: an additive in many plastics.

In February I wrote a piece about BPA (Bisphenol A), which was the chemical scare of the day. There’s always one around January/February time. It’s our penance for daring to enjoy Christmas. Anyway, BPA is a chemical in many plastics, and of course plastic waste had become – and remains – a hot topic. BPA is also used in a number of other things, not least the heat sensitive paper used to produce some shopping receipts. It’s not a harmless substance by any means, but it won’t surprise anyone to learn that the risks had, as is usually the case, been massively overstated. In a report, the European Food Safety Authority said that the health concern for BPA is low at their estimated levels of exposure. In other words, unless you’re actually working with it – in which case you should have received safety training – there’s no need to be concerned.

In March I recorded an episode for the A Dash of Science podcast, and I went on to write a post about VARD, which stands for Verify, Author, Reasonableness and Date. It’s my quick and easy way of fact-checking online information – an increasingly important skill these days. Check out the post for more info.

April ended up being all about dairy and vitamin D.

April was all about dairy after a flare-up on Twitter on the topic, and went on to talk about vitamin D. The bottom line is that everyone in the UK should be taking a small vitamin D supplement between about October and March, because northern Europeans simply can’t make vitamin D₃in their skin during these months (well, unless they travel nearer to the equator), and it’s not a nutrient we can easily get from our food. Are you taking yours?

May featured fish tanks, following a widely reported story about a fish-owner who cleaned out his tank and managed to release a deadly toxin that poisoned his entire family. Whoops. It turns that this was, and is, a real risk – so if you keep fish and you’ve never heard of this before, do have a read!

In June I wrote about strawberries, and did a neat experiment to show that strawberries could be used to make pH indicator. Who knew? You do, now! Check it out if you’re looking for some chemistry to amuse yourself over the holidays (I mean, who isn’t?). Did you know you can make indicators from the leaves of Christmas poinsettia plants, too?

Slime turned up again in July. And December. And will probably keep on rearing its slimy head.

July brought a subject which has turned up again recently: slime. I wrote about slime in 2017, too. It’s the gift that keeps on giving. This time it flared up because the consumer magazine and organisation Which? kept promoting research that, they claimed, showed that slime toys contain dangerous levels of borax. It’s all rather questionable, since it’s not really clear which safety guidelines they’re applying and whether they’re appropriate for slime toys. Plus, the limits that I was able to find are migration limits. In other words, it’s not appropriate to measure the total borax content of the slime and declare it dangerous – they should be looking at the amount of borax which is absorbed during normal use. Unless your child is eating slime (don’t let them do that), they’re never going to absorb enough borax to do them any harm. In other words, it’s a storm in a slimepot.

August was all about carbon dioxide, after a heatwave spread across Europe and there was, bizarrely, a carbon dioxide shortage which had an impact on all sorts of things from fizzy drinks to online shopping deliveries. It ended up being a long-ish post which spanned everything from the formation of the Earth, the discovery of carbon dioxide, fertilisers and environmental concerns.

September featured shiny, silver balls.

In September I turned my attention to a chemical reaction which is still to this day used to coat the inside of glass decorations with a thin layer of reflective silver, and has connections with biochemistry, physics and astronomy. Check it out for some pretty pictures of silver balls, and my silver nitrate-stained fingers.

In October I was lucky enough to go on a ‘fungi forage’ and so, naturally, I ended up writing all about mushrooms. Did you know that a certain type of mushroom can be used to make writing ink? Or that some mushrooms change colour when they’re damaged? No? You should go back and read that post, then! (And going back to April for a moment, certain mushrooms are one of the few sources of vitamin D.)

Finally, November ended up being all about water, marking the 235th anniversary of the day that Antoine Lavoisier formally declared water to be a compound. It went into the history of water, how it was proven to have the formula H₂O, and I even did an experiment to split water into hydrogen and oxygen in my kitchen – did you know that was possible? It is!

As December neared, the research for my water piece led me to suggest to Andy Brunning of Compound Interest that this year’s Chemistry Advent might feature scientists from the last 24 decades of chemistry, starting in the 1780s (with Lavoisier and Paulze) and moving forward to the current day. This turned out to be a fantastic project, featuring lots of familiar and not quite so-familiar scientists. Do have a look if you didn’t follow along during December.

And that’s it for this year. I hope it’s been a good one for all my readers, and I wish you peace and prosperity in 2019! Suggestions for the traditional January Health Scare, anyone? (Let’s hope it’s not slime again, I’m getting really tired of that one now…)

Like the Chronicle Flask’s Facebook page for regular updates, or follow @chronicleflask on Twitter. All content is © Kat Day 2018. You may share or link to anything here, but you must reference this site if you do.

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Toxins and tanks: could your fishtank really be deadly?

Posted on 7 May, 2018 by katlday

Could a deadly poison be lurking in your fish tank?

A few days ago I came across a news story: “Fish owner tells how cleaning out tank released deadly palytoxin that poisoned family and led to closure of entire street“. Now you have to admit, as titles go that’s pretty compelling.

To begin with, for some reason, I had it in my head that this happened in Australia (in my defence, that is where most of the really deadly stuff happens, right?). But no, this happened in the U.K. Not only that, but it was even in Oxfordshire, which is my neck of the woods.

The fish tank owner, a man named Chris Matthews, was actually an experienced aquarist. He knew about palytoxin – a poisonous substance which can be released by corals – and he was aware that it can be deadly if ingested. He also knew that it can cause serious skin irritation.

What he didn’t realise was that taking his pulsing xenia coral out of the tank could cause it to release the toxin into the air.

But before I talk about palytoxin, let’s just look at the word “toxin” for a moment. It has a specific meaning, and it’s often misused. As in many, many adverts. Here’s a recent one, but these easy to find – just put “toxin free” into the search engine of your choice.

In a way, this is quite funny. You see, “toxin” specifically refers to “a poison of plant or animal origin“. In other words, a naturally occurring poison*. There are lots and lots of naturally occurring poisons. Plants make them all the time, generally to ward off pests. Most essential oils can, at a high enough dose, be toxic. The hand cream in that picture contains peppermint oil. Peppermint is, of course, pretty safe – we’ve all eaten mints after all – but guess what? Take huge dose of it and it becomes a real problem. Now, I’m not for one second suggesting that hand cream is dangerous or harmful, but technically, it’s not “toxin free”.

Beauty products which contain only synthetic ingredients are, by definition, toxin-free.

Yes, the irony or this sort of marketing is that beauty products made out of entirely synthetic ingredients definitely will be toxin-free. Nothing natural = no toxins. Whereas anything made out of naturally occurring substances almost certainly isn’t, regardless of its spurious labelling.

Anyway, back to the palytoxin. It’s naturally occurring. And incredibly dangerous. More proof, as if we needed it, that natural doesn’t mean safe. Very often, in fact, quite the opposite. The human race has spent millenia working out how to protect itself from nature and all her associated nastiness (bacteria, viruses, extreme temperatures, poor food supply, predators…. the list is long and unpleasant) and yet for some reason it’s become fashionable to forget all that and imagine a utopia where mother nature knows best. Honestly, she doesn’t. Well, maybe she does – but being kind to human beings isn’t on her agenda.

Palytoxin is especially unpleasant. Indeed, it’s thought to be the second most poisonous non-protein substance known (there are some very impressive protein-based ones, though – botulinum toxin for one). The only thing which is more toxic is maitoxin – a poison which can be found in striated surgeonfish thanks to the algae they eat.

Palytoxin is a large molecule.

Palytoxin is a big molecule, technically categorised as a fatty alcohol. It has eight carbon-carbon double bonds, 40 hydroxy groups (phew) and is positively covered in chiral centres (don’t worry students: your teacher isn’t going to expect you to draw this one. Probably). Bits of it are water-soluble whilst other parts are fat soluble, meaning it can dissolve in both types of substance. Because it’s not a protein, heat doesn’t denature it, so you can’t get rid of this toxin with boiling water or by heating it. However, it does decompose and become non-toxic in acidic or alkaline solutions. Household bleach will destroy it.

It’s mostly found in the tropics, where it’s made by certain types of coral and plankton, or possibly by bacteria living on and in these organisms. It also turns up in fish, crabs and other marine organisms that feed on these things.

In fact, story time! There is a Hawaiian legend which tells that Maui villagers once caught a Shark God with a hunger for human flesh whom they believed had been killing their fishermen. They killed the Shark God and burned him, throwing the ashes into a tide pool. The ashes caused ugly brown anemones to grow. Later, the villagers discovered that blades smeared with these “limu” would cause certain death. So the anemones came to be known as “Limu Make O Hana” or Seaweed of Death from Hana. We now know that those brown ‘anemones’ are zoanthid corals, and the ‘certain death’ was due to palytoxin poisoning.

Zoanthids are a source of palytoxin.

People don’t suffer palytoxin poisoning very often. Most cases have been in people who’ve eaten seafood and, as here, aquarium hobbyists. In a few cases people have been exposed to algae blooms.

It’s really nasty though. Palytoxin can affect every type of cell in the body (yikes) and as a result the symptoms are different according to the route of exposure. Eat it and you’re likely to experience a bitter taste in your mouth, muscle spasms and abdominal cramps, nausea, lethargy, tingling and loss of sensation, slow heart rate, kidney failure and respiratory distress. It can damage your heart muscle; in the worst case scenario, it causes death by cardiac arrest.

On the other hand, if you inhale it, the symptoms are more likely to revolve around the respiratory system, such as constriction of the airways which causes wheezing and difficulty breathing. It can also cause fever and eye-infection type symptoms. Over time, though, the result is the same: muscle weakness and eventually, death from heart failure.

The respiratory symptoms from palytoxin are easily misdiagnosed: it looks like a viral or bacterial infection. In fact, our fish tank owner initially thought he had flu. It was only when everyone in the family got ill, even the dogs, that he realised that it must be poisoning. Fortunately, the emergency services took it seriously and sent both ambulance and fire crews to his house, as well as police. They closed the street and ensured that the poison was safely removed.

There is no antidote, but the symptoms can be eased by, for example, treatment with vasodilators. If the source of exposure is removed the victim is likely to recover over time. You’ll be pleased to hear that Chris Matthews, his family, and the firefighters who attended the scene, were checked over at hospital and appear to be okay.

If you’re an aquarium owner, how to you avoid getting into this kind of predicament? As Chris Matthews said, the coral he had, pulsing xenia, was “not expensive and a lot of people have it.”

Click the image to read safety guidelines from the Ornamental Aquatic Trade Association.

According to the Ornamental Aquatic Trade Association, the most important piece of safety advice is to only handle your marine creatures underwater and fully submerged. Don’t take them out of the tank unnecessarily, and if you do need to move them, use submerged plastic bags or a bucket, so that they stay underwater at all times. You should also wear strong rubber gloves, ideally gloves specifically designed for aquarium use (such as these). If you need to dispose of a rock which contains soft coral species, soak it in a bleach solution – one part household bleach to nine parts water – for several days before you intend to dispose of it. Leaving an untreated rock outside to dry will not make it safe – it could still be highly toxic. Finally, whilst activated charcoal can help to keep palytoxin out of the water, it may not be able to cope with large quantities, and it needs to be changed frequently.

Fish tank owner Chris also said: “The information is not readily available online in a way people can easily understand” and “I want to use this experience to educate people about the risks and the measures people need to take.” Hopefully this blog post (and all the associated news coverage) will help with that. Be careful with your corals!

* Note that while ‘toxin’ specifically refers to poisonous substances from plants and animals, this restriction doesn’t extend to the word “toxic”. The definition of that is “containing or being poisonous material” (regardless of whether it’s a naturally-occurring substance or not). So “non-toxic” labels are fine, if a little bit meaningless – no matter what the woo-pushing sites say, your hand cream really isn’t poisonous.

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Where did our love of dairy come from?

Posted on 14 Apr, 2018 by katlday

The popularity of the soya latte seems to be on the rise.

A little while ago botanist James Wong tweeted about the myriad types of plant ‘milk’ that are increasingly being offered in coffee shops, none of which are truly milk (in the biological sense).

This generated a huge response, probably rather larger than he was expecting from an off-hand tweet. Now, I’m not going to get into the ethics of milk production because it’s beyond the scope of this blog (and let’s keep it out of the comments? — kthxbye) but I do want to consider one fairly long thread of responses which ran the gamut from ‘humans are the only species to drink the milk of another animal’ (actually, no) to ‘there’s no benefit to dairy’ (bear with me) and ending with, in essence, ‘dairy is slowly killing us‘ (complicated, but essentially there’s very little evidence of any harm).

Humans have been consuming dairy products for thousands of years.

But wait. If dairy is so terrible for humans, and if there are no advantages to it, why do we consume it at all? Dairy is not a new thing. Humans have been consuming foods made from one type of animal milk or another for 10,000 years, give or take. That’s really quite a long time. More to the point (I don’t want to be accused of appealing to antiquity, after all), keeping animals and milking them is quite resource intensive. You have to feed them, look after them and ensure they don’t wander off or get eaten by predators, not to mention actually milk them on a daily basis. All that takes time, energy and probably currency of some sort. Why would anyone bother, if dairy were truly detrimental to our well-being?

In fact, some cultures don’t bother. The ability to digest lactose (the main sugar in milk) beyond infancy is quite low in some parts of the world, specifically Asia and most of Africa. In those areas dairy is, or at least has been historically, not a significant part of people’s diet.

But it is in European diets. Particularly northern European diets. Northern Europeans are, generally, extremely tolerant of lactose into adulthood and beyond.

Which is interesting because it suggests, if you weren’t suspicious already, that there IS some advantage to consuming dairy. The ability to digest lactose seems to be a genetic trait. And it seems it’s something to do, really quite specifically, with your geographic location.

Which brings us to vitamin D. This vitamin, which is more accurately described as a hormone, is a crucial nutrient for humans. It increases absorption of calcium, magnesium and phosphate, which are all necessary for healthy bones (not to mention lots of other processes in the body). It’s well-known that a lack of vitamin D leads to weakened bones, and specifically causes rickets in children. More recently we’ve come to understand that vitamin D also supports our immune system; deficiency has been meaningfully linked to increased risk of certain viral infections.

What’s the connection between vitamin D and geographic location? Well, humans can make vitamin D in their skin, but we need a bit of help. In particular, and this is where the chemistry comes in, we need ultraviolet light. Specifically, UVB – light with wavelengths between 280 nm to 315 nm. When our skin is exposed to UVB, a substance called 7-dehydrocholesterol (7-DHC to its friends) is converted into previtamin D3, which is then changed by our body heat to vitamin D₃, or cholecalciferol – which is the really good stuff. (There’s another form, vitamin D ₂, but this is slightly less biologically active.) At this point the liver and kidneys take over and activate the chloecalciferol via the magic of enzymes.

We make vitamin D in our skin when we’re exposed to UVB light.

How much UVB you’re exposed to depends on where you live. If you live anywhere near the equator, no problem. You get UVB all year round. Possibly too much, in fact – it’s also linked with skin cancers. But if you live in northerly latitudes (or very southerly), you might have a problem. In the summer months, a few minutes in the sun without sunscreen (literally a few minutes, not hours!) will produce more than enough vitamin D. But people living in UK, for example, get no UVB exposure for 6 months of the year. Icelanders go without for 7, and inhabitants of Tromsø, in Norway, have to get by for a full 8 months. Since we can only store vitamin D in our bodies for something like 2-4 months (I’ve struggled to find a consistent number for this, but everyone seems to agree it’s in this ballpark), that potentially means several months with no vitamin D at all, which could lead to deficiency.

In the winter northern Europeans don’t receive enough UVB light from the sun to produce vitamin D in their skin.

In the winter, northern Europeans simply can’t make vitamin D₃in their skin (and for anyone thinking about sunbeds, that’s a bad idea for several reasons). In 2018, this is easily fixed – you just take a supplement. For example, Public Health England recommends that Brits take a daily dose of 10 mcg (400 IU) of vitamin D in autumn and winter, i.e. between about October and March. It’s worth pointing out at this point that a lot of supplements you can buy contain much more than this, and more isn’t necessarily better. Vitamin D is fat-soluble and so it will build up in the body, potentially reaching toxic levels if you really overdo things. Check your labels.

Oily fish is an excellent source of vitamin D.

But what about a few thousand years ago, before you just could pop to the supermarket and buy a bottle of small tablets? What did northern Europeans do then? The answer is simple: they had to get vitamin D from their food. Even if it’s not particularly well-absorbed, it’s better than nothing.

Of couse it helps if you have access to lots of foods which are sources of vitamin D. Which would be… fatty fish (tuna, mackerel, salmon, etc) – suddenly that northern European love of herring makes so much more sense – red meat, certain types of liver, egg yolks and, yep, dairy products. Dairy products, in truth, contain relatively low levels of vitamin D (cheese and butter are better than plain milk), but every little helps. Plus, they’re also a good source of calcium, which works alongside vitamin D and is, of course, really important for good bone health.

A side note for vegans and vegetarians: most dietry sources of vitamin D come from animals. Certain mushrooms grown under UV can be a good source of vitamin D₂, but unless you’re super-careful a plant-based diet won’t provide enough of this nutrient. So if you live in the north somewhere or you don’t, or can’t, expose your skin to the sun very often, you need a supplement (vegan supplements are available).

Fair skin likely emerged because it allows for better vitamin D production when UVB levels are lower.

One thing I haven’t mentioned of course is skin-colour. Northern Europeans are generally fair-skinned, and this is vitamin D-related, too. The paler your skin, the better UVB penetrates it. Fair-skinned people living in the north had an advantage over those with darker skin in the winter, spring and autumn months: they could produce more vitamin D. In fact, this was probably a significant factor in the evolution of fair skin (although, as Ed Yong explains in this excellent article, that’s complicated).

In summary, consuming dairy does have advantages, at least historically. There’s a good reason Europeans love their cheeses. But these days, if you want to eat a vegan or vegetarian diet for any reason (once again, let’s not get into those reasons in comments, kay?) you really should take a vitamin D supplement. In fact, Public Health England recommends that everyone in the UK take a vitamin D supplement in the autumn and winter, but only a small amount – check your dose.

By the way, if you spot any ‘diary’s let me know. I really had to battle to keep them from sneaking in…

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Chemical du jour: how bad is BPA, really?

Posted on 13 Feb, 2018 by katlday

BPA is an additive in many plastics

When I was writing my summary of 2017 I said that there would, very probably, be some sort of food health scare at the start of 2018. It’s the natural order of things: first we eat and drink the calorie requirement of a small blue whale over Christmas and New Year, and then, lo, we must be made to suffer the guilt in January. By Easter, of course, it’s all forgotten and we can cheerfully stuff ourselves with chocolate eggs.

Last year it was crispy potatoes, and the year before that it was something ridiculous about sugar in ketchup causing cancer (it’s the same sugar that’s in everything, why ketchup? Why?). This year, though, it seems that the nasty chemical of the day is not something that’s in our food so much as around it.

Because this year the villain of the piece appears to be BPA, otherwise known as Bisphenol A or, to give it its IUPAC name, 4,4′-(propane-2,2-diyl)diphenol.

BPA is an additive in plastics. At the end of last year an excellent documentary aired on the BBC called Blue Planet II, all about our planet’s oceans. It featured amazing, jaw-dropping footage of wildlife. It also featured some extremely shocking images of plastic waste, and the harm it causes.

Plastic waste is a serious problem

Plastic waste, particularly plastic waste which is improperly disposed of and consequently ends up in the wrong place, is indisputably something that needs to be addressed. But this highlighting of the plastic waste problem had an unintended consequence: where was the story going to go? Everyone is writing about how plastic is bad, went (I imagine) editorial meetings in offices around the country – find me a story showing that plastic is even WORSE than we thought!

Really, it was inevitable that a ‘not only is plastic bad for the environment, but it’s bad for you, too!’ theme was going to emerge. It started, sort of, with a headline in The Sun newspaper: “Shopping receipts could ‘increase your cancer risk’ – as 93% contain dangerous chemicals also linked to infertility. Shopping receipts are, of course, not made of plastic – but the article’s sub-heading stated that “BPA is used to make plastics”, so the implication was clear enough.

Then the rather confusing: “Plastic chemical linked to male infertility in majority of teenagers, study suggests” appeared in The Telegraph (more on this in a bit), and the whole thing exploded. Search for BPA in Google News now and there is everything from “5 Ways to Reduce Your Exposure to Toxic BPA” to “gender-bending chemicals found in plastic and linked to breast and prostate cancer are found in 86% of teenagers”.

Yikes. It’s all quite scary. It’s true that right now you can’t really avoid plastic. Look around you and it’s likely that you’ll immediately see lots of plastic objects, and that’s before you even try to consider all the everyday things which have plastic coatings that aren’t immediately obvious. If you have young children, you’re probably drowning in plastic toys, cups, plates and bottles. We’re pretty much touching plastic continually throughout our day. How concerned should we be?

As the Hitchiker’s Guide to the Galaxy says, Don’t Panic. Plastic (like planet Earth in the Guide) can probably be summed up as mostly harmless, at least from a BPA point of view if not an environmental one.

BPA is a rather pleasingly symmetrical molecule with two phenol groups. (A big model of this would make a wonderfully ironic pair of sunglasses, wouldn’t it?) It was first synthesized by the Russian chemist Alexander Dianin in the late 19th century. It’s made by reacting acetone – which is where the “A” in the name comes from – with two phenol molecules. It’s actually a very simple reaction, although the product does need to be carefully purified, since large amounts of phenol are used to ensure a good yield.

It’s been used commercially since the fifties, and millions of tonnes of BPA are now produced worldwide each year. BPA is used to make plastics which are clear and tough – two characteristics which are often valued, especially for things like waterproof coatings, bottles and food containers.

The concern is that BPA is an endocrine disruptor, meaning that it interferes with hormone systems. In particular, it’s a known xenoestrogen, in other words it mimics the female hormone estrogen. Animal studies have suggested possible links to certain cancers, infertility, neurological problems and other diseases. A lot of the work is fairly small-scale and, as I’ve mentioned, focused on animal studies (rather than looking directly at effects in humans). Where humans have been studied it’s usually been populations that are exposed to especially high BPA levels (epoxy resin painters, for example). Still, it builds up into quite a damning picture.

BPA has been banned from baby bottles in many countries, including the USA and Europe

Of course, we don’t normally eat plastic, but BPA can leach from the plastic into the food or drink that’s in the plastic, and much more so if the plastic is heated. Because of these concerns, BPA has been banned from baby bottles (which tend to be heated, both for sterilisation and to warm the milk) in several countries, including the whole of Europe, for some years now. “BPA free” labels are a fairly common sight on baby products these days. BPA might also get onto our skin from, for example, those thermal paper receipts The Sun article mentioned, and then into our mouths when we eat. Our bodies break down and excrete the chemical fairly quickly, in as little as 6 hours, but because it’s so common in our environment most of us are continually meeting new sources of it.

How much are we getting, though? This is a critical question, because as I’m forever saying, the dose makes the poison. Arsenic is a deadly poison at high levels, but most of us – were we to undergo some sort of very sensitive test – would probably find we have traces of it in our systems, because it’s a naturally-occuring mineral. It’s nothing to worry about, unless for some reason the levels become too high.

When it comes to BPA, different countries have different guidelines. The European Food Safety Authority recommended in January 2015 that the TDI (tolerable daily intake) should be reduced from 50 to 4 µg/kg body weight/day (there are plans for a new assessment in 2018, so it might change again). For a 75 kg adult, that translates to about 0.0003 g per day. A USA Federal Drug and Administration document from 2014 suggests a NOAEL (no-observed-adverse-effect-level) of 5 mg/kg bw/day, which translates to 0.375 g per day for the same 75 kg adult. NOAEL values are usually much higher than TDIs, so these two figures aren’t as incompatible as they might appear. Tolerable daily intake values tend to have a lot of additional “just in case” tossed into them – being rather more guidance than science.

The European Food Standards Authority published a detailed review of the evidence in 2015 (click for a summary)

So, how much BPA are we exposed to? I’m going to stick to Europe, because that’s where I’m based (for now…), and trying to look at all the different countries is horribly complicated. Besides, EFSA produced a really helpful executive summary of their findings in 2015, which makes it much easier to find the pertinent information.

The key points are these: most of our exposure comes from food. Infants, children and adolescents have the highest dietary exposures to BPA, probably because they eat and drink more per kilogram of body weight. The estimated average was 0.375 µg/kg bw per day. For adult women the estimated average was 0.132 µg/kg bw per day, and for men it was 0.126 µg/kg bw per day.

When it came to thermal paper and other non-dietary exposure (mostly from dust, toys and cosmetics), the numbers were smaller, but the panel admitted there was a fair bit of uncertainty here. The total exposure from all sources was somewhere in the region of 1 µg/kg bw per day for all the age groups, with adolescents and young children edging more toward values of 1.5 µg/kg bw per day (this will be important in a minute).

Note that all of these numbers are significantly less than the, conservative, tolerable daily intake value of 4 µg/kg bw per day recommended by EFSA.

Here’s the important bit: the panel concluded that there is “no health concern for BPA at the estimated levels of exposure” as far as diet goes. They also said that this applied “to prenatally exposed children” (in other words, one less thing for pregnant women to worry about).

When it came to total exposure, i.e. diet and exposure from other sources such as thermal paper they concluded that “the health concern for BPA is low at the estimated levels of exposure”.

The factsheet that was published alongside the full document summarises the results as follows: “BPA poses no health risk to consumers because current exposure to the chemical is too low to cause harm.”

Like I said: Don’t Panic.

What about those frankly quite terrifying headlines? Well, firstly The Sun article was based on some work conducted on a grand total of 208 receipts collected in Southeast Michigan in the USA from only 39 unique business locations. That’s a pretty small sample and not, I’d suggest, perhaps terribly relevant to the readership of a British newspaper. Worse, the actual levels of BPA weren’t measured in the large majority of samples – they only tested to see if it was there, not how much was there. There was nothing conclusive at all to suggest that the levels in the receipts might be enough to “increase your cancer risk”. All in all, it was pretty meaningless. We already knew there was BPA in thermal receipt paper – no one was hiding that information (it’s literally in the second paragraph of the Wikipedia page on BPA).

The Telegraph article, and the many others it appeared to spawn, also weren’t based on especially rigorous work and, worse, totally misrepresented the findings in any case. Firstly, let’s consider that headline: “Plastic chemical linked to male infertility in majority of teenagers, study suggests”. What does that mean? Are they suggesting that teenagers are displaying infertility? No, of course not. They didn’t want to put “BPA” in the headline because that, apparently, would be too confusing for their readers. So instead they’ve replaced “BPA” with “plastic chemical linked to male infertility”, which is so much more straightforward, isn’t it?

And they don’t mean it’s linked to infertility in the majority of teenagers, they mean it’s linked to infertility and it’s in the majority of teenager’s bodies. I do appreciate that journalists rarely write headlines – this isn’t a criticism of the poor writer who turned in perfectly good copy – but that is confusing and misleading headline-writing of the highest order. Ugh.

Plus, as I commented back there, that wasn’t even the conclusion of the study, which was actually an experiment carried out by students under the supervision of a local university. The key finding was not that, horror, teenagers have BPA in their bodies. The researchers assumed that almost all of the teenagers would have BPA in their bodies – as the EFSA report showed, most people do. No, the conclusion was actually that the teenagers – 94 of them – had been unable to significantly reduce their levels of BPA by changing their diet and lifestyle. Although the paper admits the conditions weren’t well-controlled. Basically, they asked a group of 17-19 year-olds to avoid plastic, and worked on the basis that their account of doing so was accurate.

And how much did the teenagers have in their samples? The average was 1.22 ng/ml, in urine samples (ng = nanogram). Now, even if we assume that these levels apply to all human tissue (which they almost certainly don’t) and that therefore the students had roughly 1.22 ng per gram of body weight, that only translates to, very approximately, 1.22 micrograms (µg) per kilogram of body weight.

Wait a second… what did EFSA say again…. ah yes, they estimated total exposures of 1.449 µg/kg bw per day for adolescents.

Sooooo basically a very similar value, then? And the EFSA, after looking at multiple studies in painstaking detail, concluded that “BPA poses no health risk to consumers”.

Is this grounds for multiple hysterical, fear-mongering headlines? I really don’t think it is.

It is interesting that the teenagers were unable to reduce their BPA levels. Because it’s broken down and excreted quite quickly by the body, you might expect that reducing exposure would have a bigger effect – but really all we can say here is that this needs to be repeated with far more tightly-controlled conditions. Who knows what the students did, and didn’t, actually handle and eat. Perhaps their school environment contains high levels of BPA in dust for some reason (new buildings or equipment, maybe?), and so it was virtually impossible to avoid. Who knows.

In summary, despite the scary headlines there really is no need to worry too much about BPA from plastics or receipts. It may be worth avoiding heating plastic, since we know that increases the amound of BPA that makes its way into food – although it’s important to stress that there’s no evidence that microwaving plastic containers causes levels to be above safe limits. Still, if you wanted to be cautious you could choose to put food into a ceramic or glass bowl, covered with a plate rather than clingfilm. It’ll save you money on your clingfilm bills anyway, and it means less plastic waste, which is no bad thing.

Roll on Easter…

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the chronicle flask

Tales of interesting chemical tidbits

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Chemical du jour: how bad is BPA, really?

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