Killer Tampons from Outer Space or Why We Don’t Hear About Toxic Shock Syndrome Anymore

5 minute read
Originally published here: https://mcgill.ca/oss/article/health-history/killer-tampons-outer-space-or-why-we-dont-hear-about-toxic-shock-syndrome-anymore

In the early 1980’s and 90’s toxic shock syndrome was on everybody’s mind. Its prevalence dominated headlines, inspiring fear in every tampon-using woman across North America. Young adults going through puberty were taught to watch out for toxic shock syndrome like it was hiding beneath every tampon wrapper.

My mom, going through puberty in the mid 80’s, was inundated with warnings to not leave tampons in too long and to always pay attention to new or unexplained rashes. But by the time I hit puberty in the early 2010’s the flood of warnings had slowed to a trickle. I was made aware that toxic shock syndrome was a risk, but also that it was rare, unlikely and treatable. Almost a decade later I don’t think I’ve heard the words toxic shock syndrome in years.

So what happened? How did people stop dying of toxic shock syndrome, or if they didn’t, why did we stop hearing about it?

What is toxic shock syndrome?

Toxic shock syndrome or TSS is an infection caused by Staphylococcus aureus, the same bacterium responsible for “staph infections” on the skin.S. aureusis normally present in human’s respiratory tracts and on their skin, but it’s what’s called an opportunistic pathogen. Given an opening (a compromised immune system or an injury on the skin),S. aureuswill infect its host, causing all sorts of nasty effects from pimples to pneumonia.

TSS is a condition resulting from an S. aureus infectionIt can occur because S. aureus contain what are called superantigensAntigens are substances that T-cells (a type of white blood cell and main player in our immune systems) bind to. Normally, some T-cells bind to antigens and then display them on their surface, to show other T-cells that the infection is being dealt with. Superantigens, however, skip this displaying step, causing more T-cells than usual (or necessary) to be activated.

These activated T-cells then go on to release cytokines, little proteins that cause inflammation. Normally, inflammation is actually a good sign. It’s the result of the body increasing blood flow to an injured area in order to heal it. But too many T-cells release too many cytokines which cause too much inflammation in a process called a cytokine storm. As the name suggests, it’s not good. Cytokine storms are associated with fevers, fatigue, nausea, rashes, diarrhea and dizziness, which are also the symptoms of TSS.

TSS is a tampon disease, right?

In 1983 over 2,200 cases of TSS were examined, and it was determined that 90% of the patients were menstruating when they fell ill. Of these menstruating patients, 99% of them were using tampons.

But TSS is not exclusive to tampons. It was first identified in five non-menstruating boys and girls in 1978. From 2001 to 2011 there were 11 cases of TSS associated with bandages used to treat burns in children, and in 2003, a man died as a result of TSS after having tattoo work done.

It’s estimated that 25-35% of TSS cases are unrelated to menstruation. These cases of nonmenstrual TSS can be caused by S. aureus or by Streptococcus pyogenes, and have a mortality rate 6 to 12 times higher than menstrual TSS. While the incidence of menstrual TSS has fallen sharply since its heyday in the 80s, the incidence of nonmenstrual TSS has remained essentially constant.

If nonmenstrual TSS is more prevalent and more dangerous, why do we only associate TSS with tampons?

Well for one, because the nonmenstrual TSS is still fairly rare. With an incidence rate of 2-4 cases per 100,000 people, nonmenstrual TSS is less common than dysentery (5.39 cases per 100,000) or Lyme disease (8.3 cases per 100,000).

Mostly, though, we don’t hear about nonmenstrual TSS because of the epidemic of menstrual TSS that took place in the early 80s.

Modern tampons were first patented in 1931, but not produced until Gertrude Tendrich bought the patent in 1933. They didn’t rise to mainstream popularity until WWII when women entering the workforce began to use them en masse.

Those tampons, marketed largely by the same brands as today (Tampax and o.b.), were made of cotton and rayon and were fairly similar to the tampons of today. One brand, however, decided to explore other materials to make their tampons more absorbent.

Rely tampons utilized compressed polyester beads and carboxymethylcellulose instead of cotton. These tampons were super-absorbent, holding nearly 20 times their own weight in blood, and opened inside the vagina to form a sort of cup to help prevent leakage. While these sound like fantastic features for a tampon, they turned out to also be fantastic features for a bacterial infection. 

Menstrual blood is not as acidic as the vagina normally, so during menstruation the pH of the vagina is raised, which can hinder its ability to kill bacteria. But that shouldn’t matter, so long as there are no cuts inside the vagina for bacteria to enter, right?

Well, the super-absorbent nature of Rely tampons meant that the vagina was left much dryer than usual. This caused tiny ulcerations to form when tampons were inserted or removed, giving bacteria the opening they needed. Couple this with the fact that people could leave Rely tampons in for longer (thereby maximizing the bacteria’s time to grow and infect) and you have the epidemic of TSS that occurred in 1980.

Rely tampons were recalled on September 22nd 1980, but cases of TSS kept occurring. It wasn’t until 1984 that researchers realized that TSS was associated with the use of any high absorbency tampon, cotton or polyester.

I don’t want TSS! What should I do?

First, don’t panic. TSS is really rare. While several high profile cases of TSS have occurred recently, the rates of TSS are lower than ever.

Tampon companies and government agencies have worked together to identify a strategy of use that minimizes your risk. Their recommendations are as follows:

  1. Use the lowest absorbency tampon that you can.
  2. Change your tampon every 4-8 hours.
  3. Wash your hands before inserting a tampon.
  4. Do not use tampons when you’re not on your period.

Can’t I just use a menstrual cup to avoid any risk of TSS?

Menstrual cups lessen the risk of TSS, but they don’t eliminate it. While it’s true they don’t absorb any blood, and therefore don’t cause vaginal dryness leading to ulcerations, they can be really difficult to put it, especially for new users, leading to scratches or cuts on the vaginal wall.

Case in point, a 37-year-old woman was diagnosed with TSS in 2015 after using a menstrual cup for the first time.

If you’re not going to change your tampon every 8 hours, you should consider a menstrual cup. They are approved by Health Canada to stay in the vagina for up to 12 hours at a time, making them great options for those who work 8-hour days or are just forgetful.

But do still remember to wash your hands before inserting the cup, and make sure to sanitize it between cycles.

If you’d like to learn more about TSS, click here for a short but very informative video.

Gaba Supplements: Glorious, Gimmicky or Just Garbage?

7 minutes read
Image created by Ada McVean
Originally posted here: https://mcgill.ca/oss/article/health/gaba-supplements-glorious-gimmicky-or-just-garbage

Take-home message:
– gamma-Aminobutyric acid (GABA) is a major neurotransmitter that regulates much of our brain function. It was previously thought that ingested GABA could not cross the blood-brain barrier, but new research suggests that it may be able to.
– Drugs that mimic the action of GABA are numerous, work in a variety of ways, and can have effects ranging from treating epilepsy to causing it.
– GABA supplements have shown some promise in early, small-scale studies, but a lot more research is needed to know if they truly help.

Lately, it seems that GABA supplements are being hawked on the corner of every pharmacy aisle and health food shelf. Marketed to promote relaxation, mental focus and sleep, GABA is even being sold by David’s Tea in the form of GABA guava tea. I found it while trying to buy some matcha powder. I don’t even like guava, never mind guava with a side of inflated claims.

While promotions by influencers like Olivia Culpoand Sarah Couture are pretty standard for any trendy supplement, (regardless of efficacy) the attention GABA has been given by known quacks like Dr. Oz,Joseph Mercola orMike Adams has left me wondering about the science behind, and evidence for, these supplements.

Let’s start with the basics: what is GABA?

gamma-Aminobutyric acid (also written as γ-aminobutyric acid) is a neurotransmitter, specifically the major inhibitory one in all mammal’s central nervous systems (CNS). That means that it’s a chemical that binds to nerve cell receptors and hinders their ability to receive, create or send messages to other nerve cells (neurons).

Functionally, GABA is incredibly important. A lack of GABA leaves your central nervous system with too many neuronal signals and causes conditions like epilepsyseizures or mood disorders. Meanwhile, too much GABA means not enough brain activity and can lead to hypersomnia or daytime sleepiness.

You can learn more about GABA in this lovely video, and more about neurotransmitters in general in this one, although I’ve said all you’ll need to know for this article.

GABAergic drugs

As the chief inhibitory neurotransmitter in the CNS, GABA and its receptors have been major targets for drug development. Drugs that activate GABA receptors (called agonists) or increase the receptors’ sensitivity to GABA (positive allosteric modulators) work to reduce the neuronal signals in the user’s brain, similar to what happens when you sleep. Logically, they include many common sedatives like barbital or Quaaludes, tranquillizers like ValiumAtivanor Xanax and the most commonly used sedative, alcohol.

GABA reuptake inhibitors like Deramciclane have similar effects, as they help to keep GABA in the vicinity of the receptors for longer.

On the flip side, substances that inhibit the activity of GABA (called antagonists) increase brain activity. That only sounds like a good thing. The results are less Scarlett Johansson in Lucy, more uncontrollable seizures and death.

GABA antagonists, like gabazine or bicuculline are only useful when studying seizures or to counteract overdoses of sedatives and tranquillizers. Some GABA antagonists are particularly scary poisons, causing death by disrupting the CNS’s control of basic body functions like breathing.

The class of drugs we’re most interested in, however, are GABA analogues. These molecules are structurally similar to GABA, though they have different targets of action. GABA analogues include some big names you’ve probably heard of: Lyrica and gabapentin.

While both Lyrica and gabapentin are prescribed to stop seizures, treat neuropathic pain, and anxiety disorders, gabapentin is additionally used for the prevention of migraines.

Gabapentin has been a constant in my life for a few years now, as my mother was prescribed it for diabetic neuropathic pain just a few years after my partner was prescribed it for near constant migraines. I’ve personally seen GABA to be quite effective in its on-label uses, as the evidence shows it to be, but it was recently at the heart of one of the largest court settlements in US history.

The manufacturers of gabapentin were found to have been marketing it extensively for off-label uses like the treatment of bipolar disorder, restless leg syndrome, hot flashes and stopping smoking. While off-label prescribing is not uncommon, and usually fairly safe, there is no evidence that gabapentin is effective for the bipolar disorder it was being prescribed to treat or some of the other conditions for which it’s being prescribed.

Presently gabapentin is again making headlines as its use as a recreational drug skyrockets. Many opioid users are misusing gabapentin to extend opioid highs or bypass drugs that block opioids effects, but its status as a non-controlled substance makes it difficult for law enforcement to control its unsanctioned use.

GABA and the Blood-Brain Barrier

GABA drugs are certainly useful, but why do we need all these GABA-receptor-activating or GABA-like molecules in the first place? Why not just give patients GABA?

We have a highly selective membrane that keeps our blood and cerebrospinal fluid (or brain juice, if you will) separate: the blood-brain barrier (BBB). Some molecules, like water, pass through it easily, other things, like bacteria don’t. This membrane also contains special channels to diffuse important molecules one way or the other, like glucose.

It’s a really important border, as drugs that cannot cross into the brain, or do so poorly, have much less of an effect than ones that do. For example, morphine can’t cross the BBB very well, but it’s close relative heroin can! Upon entry to the brain, heroin is converted into morphine, which is why heroin is so much more potent than morphine.

A 1958 study was the first to look at GABA’s relationship with the blood-brain barrier, and it found a lack of one: GABA could not cross the barrier. Later studies in ‘58‘71, and ‘88 confirmed the barrier’s impermeability to GABA. The evidence seems all but clear until you throw a few more studies into the mix. Studies done in ‘80‘81‘82 and ‘02 found that GABA did cross the blood-brain barrier, just in minuscule amounts.

Why the disagreement? Well, a few things. Some studies used a molecule just like GABA in lieu of GABA, assuming the 1 extra OH group featured on 3-hydroxybutyric acid wouldn’t make a difference, but it may have. Since many studies don’t report the type of GABA used, it’s hard to compare results. Some studies administered their GABA by injecting it straight into animal’s body cavities, others by injecting it into veins.

Most importantly, the BBB permeability of GABA has never been studied in humans!

What we do know is that human’s BBB contains transporters for GABA, implying that GABA can enter/exit the brain through these channels. In mice it was found that GABA was removed from the brain 17 times faster than it entered.

This could explain the conflicting study results. It may not be that GABA cannot enter the brain, but just that it’s removed from it very rapidly.

GABA as a Supplement

Even if it cannot cross the BBB however, GABA could still be affecting your brain.

The enteric nervous system (ENS) is the network of neurons that control your gastrointestinal system. The ENS contains many GABA receptors, and GABA itself, and is connected to the brain through the vagal nerve. It’s been proposed that ingested GABA is able to affect the body even without crossing the BBB through its interactions with the ENS.

We don’t know at this point how GABA is affecting the brain, but we have good evidence that it is. Several studies have shown reductions in markers of stress in patients given dietary GABA.

On their own the success stories from the consumers who buy GABA supplements are meaningless but taken along with the research findings, they may just show that there is something to these supplements.

We’ll need a lot more research to know for sure if GABA supplements are helpful or not. That being said, they are expensive (like most supplements) and if you’re not anxious, experiencing insomnia or very stressed out they’re probably not worth it. There don’t appear to be many side effects or drug interactions, but until more research is done I’d tread carefully.

I did ask my partner, who took gabapentin (a GABA analogue) for years if he ever experienced any focusing of his mind or relaxation as the GABA supplements claim. He said a definitive no.

Want a cheaper option for relaxation? Tea. You can even try some GABA tea, a strain of green tea specially fermented to accumulate GABA. Maybe I’ll pick some up… just not that guava flavoured stuff.

Are All Oils Essential? Are Essential Oils Even Oils?

Originally posted here: https://mcgill.ca/oss/article/health-you-asked/are-all-oils-essential-are-essential-oils-even-oils

Oils are defined as any net uncharged chemical substance that is a thick liquid at room temperature and is both hydrophobic (does not mix with water) and lipophilic (does mix with fats, or lipids). When we think of them, our minds tend to focus on the kitchen: olive, canola or peanut oil. But there are also oils in your garage (motor oil), bathroom (conditioner) and your art collection (oil paints).

Animal and vegetable oils are a mixture of triglycerides. A triglyceride is just three fatty acids held together by a molecule of glycerol, and they can be saturated or unsaturated. Saturated fats have the maximum number of carbon-hydrogen bonds, where unsaturated fats contain extra carbon-carbon bonds. These double bonds give unsaturated fats lower melting points, because the double bonds put kinks in their strands, preventing them from stacking nicely on each other.

Practically, this means that oils made mostly of unsaturated fats are liquids at room temperatures (like olive oil), and oils made mostly of saturated fats are solids (more commonly referred to simply as fats, like cocoa butter or lard).

So what about essential oils? The name is a bit misleading, since they aren’t oils in the classic sense, and aren’t essential in the same way essential amino acids are. They are hydrophobic, but unlike animal and vegetable oils, are not made of fatty acids. Their composition instead depends heavily on what plant it originated from. The “essential” in their name refers to the fact that the oil contains the essence of a plant, its fragrance.

Essential oils are often extracted via distillation (as shown in the infographic), but can also be physically squeezed out of some plants (like orange peels) or, in the case of flowers, extracted with a nonpolar solvent.

It’s easy to forget amid the many baseless health claims made for essential oils that they do have real purposes. Some, like clary and lemon oil, are used for flavouring. Others are used primarily for adding fragrance to cosmetics, foods or your home via a diffuser. Clove oil is used for euthanizing fish in labs, orange oil can repel ants, and eucalyptus oil is commonly used in cold remedies like vapour rub.

But just because most essential oils don’t help your health doesn’t mean they’re innocuous. Many are very flammable, with flashpoints as low as 50°C, others are photosensitizers and can make your skin more vulnerable to sun damage. Contact dermatitis from essential oils is fairly common, and there’s growing evidence that they can also affect hormone balances, particularly in young males. Several essential oils (including tea tree oil) are toxic to domestic animals, and while humans run little risk of achieving a toxic dose of most essential oils, there are exceptions. Cassia oil, derived from Chinese cinnamon, requires only 0.3 ml per kg of body weight to achieve dermal toxicity. That means that only 17 mL (little more than a tablespoon) of the oil applied to the skin could have tragic consequences.

So, all things considered, I’ll keep my vegetable oils for cooking and my essential oils strictly for smelling. Though I have always thought that coconut oil smells pretty nice.

Can Aspirin Help Remove Stains and Keep your Whites White?

Originally posted here: https://mcgill.ca/oss/article/can-aspirin-help-remove-stains-and-keep-your-whites-white

The internet is full of suggestions that Aspirin can be used to remove stains and get whiter whites. These sites don’t offer any mechanism of this bleaching of course, so I had to try it myself.

Rather than risk my real clothes tothis science experiment, I created some stains (tomato and espresso) on pieces of fabric taken from washcloths.

Every site had slightly different instructions, so I chose what seemed like the least nonsense filled options: Reader’s Digest and WikiHow. They both instructed me to soak my fabric in hot water in which I’d dissolved five 325 mg tablets of Aspirin, and leave it to soak. Since I foolishly bought 500 mg Aspirin (it was on sale!) I used 3.25 of my tablets. I ground them up, dissolved them in hot water, and added the fabric.

I also tested a more direct application to give the Aspirin the best chance of working. I ground up another 3.25 tablets, added a bit of water to make a paste, applied that directly to the stains, and let them sit.

While the experiments were brewing, I washed my control stains with ½cup of bleach (as per the instructions on the bottle) in the washer (on warm and “extra clean” settings).

Once a few hours had passed on the soaking and sitting stains, I washed them in the same way, without bleach, then hung them all on the line to dry. A few hours later I realized it had actually started raining, so I brought them inside and dried them in the dryer.

The waiting in this process gave me some time to do some math. 

Brand name Aspirin costs 7 cents per pill, making a single treatment of this method cost only 30 cents.

Pricing other stain removers is a bit more difficult. A rough estimate of the volume of one ‘spray’ from a spray bottle is 0.1 ml. If you used about 5 sprays to cover a stain the price per spot treatment would be about 0.0023 cents. So to make the Aspirin soak worth it, you’d need to be treating more than 13043 stains per load. Perhaps more directly comparable, Oxicleanpowder that is added to the laundry costs about 0.17 cents per load.

But, this is a good time to remember that even if the Aspirin is 13000 times more expensive than Shout, we’re talking about pennies here. They’re all dirt cheap. Cost is not the issuewith this method. The fact that it didn’t work is.

Neither the soak nor paste method worked as well as good, old-fashioned, bleach.

So why not?

Aspirin is the common name for acetylsalicylic acid (ASA). It’s a prodrug, meaning that the form it’s in while in pills is not the active form of the compound. ASA is absorbed into the bloodstreamin the stomach,and is then converted to salicylic acid(SA) (also known as salicylate) in the liver. It’s salicylic acidthat disperses through our bodies and causes the pain, inflammation and fever reductions we expect.

SA mainly binds and deactivates cyclooxygenase (COX) enzymes. These enzymes usually produce prostaglandins, pro-inflammatory hormones that help neurons detect pain, and thromboxanes, lipids that promote blood clotting. With fewer prostaglandins and thromboxanes, we feel less pain and blood clots are avoided. That’s why daily low dose aspirin is useful for avoiding heart attacks– it helps prevent the formation of blood clots that could block arteries.

ASA can be broken down by waterto form salicylic acid and acetic acid (vinegar). So it could be the acetylsalicylic acid, salicylic acid, acetic acid, or some other Aspirin ingredient that works as a bleaching agent. Bleaches can workeither by reducingthe molecule that gives something colour (giving it electrons),or by oxidizing it (taking electrons from it).

Luckily, scientists have a measure of how well an agent can reduce or oxidize its subject- reduction potential. The more negative a substance’s reduction potential, the better a reducing agent it is. For example, common bleach (sodium hypochlorite) works by oxidizing stain molecules and has a reduction potential of about +1.2, making it a pretty good oxidizing agent.

Salicylic acid and acetylsalicylic acid both have reduction potentials of about -0.49. Acetic acid breaks down into acetate ions in water and has a reduction potential of about -0.6. Those numbers just aren’t great. The evidence for bleaching properties just isn’t there.

And don’t forget the evidence of tomatoes and coffee that remains on my fabric.

You’re forgiven for believing in the aspirin bleaching method if you, like me, have used a lot of anti-acne products. Many of these products usesalicylic acidbenzoyl peroxide, or both, as their active ingredient. If you’ve ever applied a night cream and woken up to a bleached pillowcase, you know that some acne products cause bleaching of fabrics and hair. That’s because, unlike SA, benzoyl peroxidedoes have a strong bleaching effect, like most other peroxides. The two reagents are used so interchangeably and commonly in skin care products that it’s fairly easy to get them mixed up. Rest assured, a SA only cream won’t wreck your favourite bathrobe.

It also won’t get the lipstick stain out of it.

If You Have a Nut Allergy You Might Want to Check Your Shampoo Ingredients

Originally posted here: https://mcgill.ca/oss/article/you-asked/nut-allergies-and-shampoo

Nut allergies affect about 2% of the Canadian population and can be broken down into tree nut allergies (like almonds or cashews) and peanut allergies (peanuts aren’t actually nuts but legumes). These allergies are caused by ingesting or inhaling certain allergenic nut proteins, not all of which have been identified yet. So, if these proteins were present in oils made from nuts that are used in cosmetics like hand cream or shampoo, one could have a reaction to them.

If you’re allergic to peanuts, that’s likely all you’re allergic to. Numbers vary on the percentage of people allergic to peanuts that have cross-reactivity to other legumes like soy or tree nuts, but it’s not a majority. On the other hand, if you’re allergic to one kind of tree nut, chances are you’re allergic to several. You are likely, however, not allergic to coconut or nutmeg (though it’s a common misconception) as they are not nuts.

Studies have found that contact allergic reactions can occur due to exposure to allergens in cosmetics. But these reactions only occur if the relevant proteins are intact, so in general, the more processed and refined the cosmetic, the smaller the likelihood of a reaction.

Allergens in cosmetics can pop up more than you might expect. Peanut oil is often used under the name arachis hypogaea in shampoos and creams. Tree nut oils in cosmetics are downright common, with almond oilargan oil and shea butter being some common examples. Coconut oil is also growing in popularity lately, with many companies incorporating it into products in order to market them as ‘natural’. Looking in my bathroom I found six products containing peanut, tree nut or coconut oils.

Since every allergy is different it’s really best to evaluate your own situation. If you’re allergic to tree nuts but not coconut, look for coconut-based products. If you’re allergic to tree nuts and coconut, you might have to look for specialty products or make your own. Or, you might check the products you’ve already been using and realize that they contained your allergen, in which case you’re probably good to keep on using them.

How do fake nails work?

Originally posted here: https://mcgill.ca/oss/article/technology/chemistry-fake-nails

Fake nails come in two major varieties: acrylic and gel. Even this distinction, though, creates an element of confusion since both of these systems actually use acrylic products. All fake nail systems require certain compounds: monomers which, when activated by an initiator molecule, combine to form polymers, as well as catalysts to make the reaction go faster. If you’ve ever had fake nails (or seen someone else’s) you know that they’re pretty strong and durable, a feat all the more impressive when you realize they’re basically hardened goop.

What we call acrylic nails are created using a liquid and powder system. The powder is a mixture of polymers that carry the initiator molecules (often benzoyl peroxide which activates with body heat), and other things like pigments. The liquid contains the monomers that need to combine into polymers in order for the nails to ‘set’. These monomers are commonly ethyl methacrylate (EMA), though they used to be methyl methacrylate (MMA) before it was banned for damaging nail beds and causing finger damage!

The initiator molecules break apart with heat, creating free radicals that can energize the EMA monomers to combine and form long chains. These polymer chains wrap around the bead-like polymers from the powder, hardening and creating the strong fake nails. The ratio of powder to liquidused has a huge impact on the quality of the nail created, as you ideally want a homogenous distribution of polymers, which is only achieved when the powder and liquid are mixed in approximately equal proportions. This sounds pretty easy to do until you remember that nail techniciansonly have a few seconds after mixing these until they harden.

Enter gel nails, the low-odour, non-time-sensitive solution to acrylic nails. First invented in the 1980’s, these variations on fake nails use the basic chemistry of their acrylic forefathers with a few variations.

First, instead of EMA, they often use as their monomer urethane acrylate methacrylate (UAMA) (hence why calling gel nails “non-acrylic” is a misnomer). Second, to surpass the time sensitivenature of heat-activated initiators, they use a photo-activated initiator. These initiators absorb UV light from the little lamps you stick your hand into and use this energy to polymerize the monomers and set the nails. This means that the nail technician can keep reshaping the nails until lightis applied. This polymerization reaction isn’t quite as effective as the heat-activated one, though, so some of the monomers are pre-connected into what are called oligomers.

Gel nails have risen steeply in popularity for use in salons or at home due to their simpler application. Regardless of how you form the nails though, the last steps are almost always to buff off any bumps and paint them,a fun colour or not, before inevitably breaking one of them trying to open a pop can.