Tagged: shock

Pools: Safe Fun or Long Term Hazard?


This week’s question comes from Amy, who asks “I am a swim instructor and I’m curious what the long term effects of pool chlorine are.”

Well Amy, this is a very interesting question that I am sure most people who use pools regularly don’t consider. Before I get into the known effects, let’s first go over what chemicals they use.

Pools, as most people know, are most often sanitized by chemicals that contain chlorine. The unique, familiar smell of a pool in the summer comes directly from this and chloramines, products of a reaction between the chlorine and some organic molecules. But most people outside of the pool maintenance industry (or a particularly active do-it-yourself-er) aren’t aware of the variety of chemicals used to keep the pool clean and sanitary.

As far as I can find, most pools are sanitized by one of three salts: trichlor (sodium trichloroisocyanurate), dichlor (sodium dichloroisocyanurate), and cal-hypo (calcium hypochlorite). These salts are all used effectively as carriers for chlorine. Trichlor and dichlor react with water to release chlorine (Cl2) and cyanuric acid, which is the base chemical from which trichlor and dichlor are made. The cyanuric acid produced by this breakdown also protects the free chlorine from UV breakdown from sun exposure by weakly bonding to it. Unfortunately, this process also reduces the chlorine’s effectiveness and thus cyanuric acid levels must be monitored to ensure they don’t get too high. Trichlor and dichlor more slowly dissolve in water and are put in the floating canisters present in many home pools.

Cal-hypo is an older method of chlorination that is still used for both primary chlorination and for “shock” treatments that bring the chlorine levels up to required levels. It is less sophisticated than trichlor and dichlor and has no built in UV protection for the produced chlorine. This compound is used most often to “shock” pools with chlorine when they get too low because dichlor and trichlor dissolve too slowly.

On the whole, it appears that most professionally maintained outdoor pools one would encounter would more likely be primarily chlorinated with trichlor or dichlor. The choice between the three is not particularly important, but the attached sources should give a good idea if you’re interested. Regardless of the choice, chlorine levels in the pool should remain above roughly 1.5-3.0 parts per million (ppm) in order to effectively sanitize. This is approximately the same level as chlorinated drinking water.

Insofar as it relates to health, these chemicals are a mixed bag.

  • Cyanuric acid is considered non-toxic, with an LD50 of oral exposure of over 10,000mg/kg. LD50 is the dosage necessary to kill 50% (hence the 50 in LD50) 0f the subjects. Thus it would take over 10g per kg of weight to have a 50-50 chance of killing you; in other words, a standard 165lb (75kg) person would require a direct dose in excess of 750g or over 1.5lb. Longer exposure studies on rats show that it does not accumulate in the body and is effectively eliminated from the body within in a few hours. At the huge tested doses, far beyond the rate of any possible human pool exposure, the only reported complications were from cyanurate crystals forming in the bladder and causing an obstruction. There was no shown increase in cancer risk, birth defects, or organ damage.
  • Dichlor and trichlor (collectively tested and referred to as chlorinated isocyanurates), because they release cyanuric acid and chlorine, have effectively the same toxicity profile as cyanuric acid in water. Because the chlorine level is very small relative to the amount of water, skin irritation is the only significantly reported complication of long term exposure. According to a German environmental protection agency study, the margin of exposure rating, which measures the overall toxicity rating regardless of route of exposure, for each is over 8. For reference, triclosan (the anti-bacterial agent in hand soap) is a 9.6, sodium hypochlorite is 0.040, and the toxic fixative (allows for long term storage of organic material, ie. formaldehyde) glutardialdehyde is 0.49. Thus, it is reasonable to conclude these chemicals are theoretically safe even at levels much higher than present in a pool.
  • Hypochlorite salts (calcium, sodium, etc. hypochlorite) have a much different toxicity profile and thus present a much more risky exposure. As I mentioned above, the margin of exposure of sodium hypochlorite is over 200 times lower than the chlorinated isocyanurates and over 10 times lower than a toxic fixative. This means that they have a toxic exposure limit across all routes (ingestion, inhalation, and skin) that is much lower than even a toxic fixative. It is most dangerous through skin exposure, as it is corrosive and an irritant in higher concentrations. Luckily, these salts are used in very small amounts in pools, but it stands to reason that long term exposure to these compounds present a greater risk, especially to the skin, than with the chlorinated isocyanurates.
  • It is also worth noting that the formation of chloramines by any of these compounds have been thought to contribute to respiratory irritation and asthma in swimmers. However, this effect is normally associated with indoor pools, especially ones with poor ventilation.

In sum, it is clear that the use of chlorinated isocyanurates presents a much safer method of pool sanitation. Experimental evidence of minimal long term toxicity from doses much larger than would ever be found in a pool certainly supports this conclusion. It seems, then, that a properly treated and professionally maintained pool should not present a long term health hazard for those who use it, even those who do every day for multiple hours a day. If any, the greatest known risks are of skin irritation and, in the case of indoor pools, respiratory tract irritation.

Hope this helps, Amy! As always, feel free to submit your questions at the link above.

Till next time, abyssus abyssum invocat
















Lions, Tigers, and Bears, Oh My!: Allergies and Cross-Species Issues


First off, a huge thank you to everyone who has read, shared, submitted questions to, and commented on this thus far. I really appreciate the support I have received.

This week’s question comes from Aerin, who asked, “I’m allergic to cats. Does that mean I’d be allergic to tigers?” Well, after some detailed exploration of this topic, I found that the answer to this is “kind of.” Obviously, this is not a particularly impressive answer, so I will definitely explain what I mean in a little bit. But, before I get into that, this question brings up the larger question of how we get allergies in the first place. So I wish to begin with an overview of what allergies are and how they are produced in the body before then exploring Aerin’s question more in-depth.

Allergies are the body’s response to something foreign, called an allergen (or, more generally, an antigen). The dictionary defines allergens as things that cause allergies (shocker!). While not a particularly helpful definition, it is more telling that it seems on the surface. This broad definition demonstrates the wide variety of environmental elements to which the body can react. In theory, the body could produce an allergy response to just about anything, from avocados to pet dander to bee pollen to the detergent you use. Even foods you’re normally not allergic to may present allergens if they have been cross-bred or genetically altered. Some responses may be mild, others catastrophic.

Antibodies are protein structures secreted by immune cells called B cells that seek out specific epitopes (the part of the antigen that the antibody can bind to). B cells come in billions of varieties, producing a correspondingly wide array of antibodies to allow the body to recognize a large number of possible antigens and epitopes. There are five different types of antibiodies (or immunoglobulins, abbreviated Ig): IgA, IgD, IgG, IgM, and IgE. The particular one that concerns us here is IgE due to its role in the formation of the symptoms we most readily associate with allergies. More on that in a bit.

Once released by the B cells, antibodies themselves “tag” the antigen when they bind to said epitope, thus marking it for the body to destroy or at least attempt to eliminate. They can also be used to disable antigens in their own right (which is the foundation of monoclonal antibody therapy), but that is outside the scope of this discussion. These tags, if they successfully attach to an antigen, prompt the division of the successful B cell in preparation for the possibility of an antigenic invasion of some type as well as the stimulation of other immune cells to flock to the area. Once the reaction has subsided, the B cells created for this purpose largely die off, except for some, known as “memory B cells,” which stick around in the body in a state of ready alert to ward off any previously encountered threat. This is the basis of the “immunity” one gets from vaccines. Unfortunately, antibodies are not particularly selective in terms of their target. If the protein it seeks is found locally, antibodies can initiate a damaging response to the body itself. The exact mechanism of how this comes about is debated (B cells that damage the body aren’t supposed to survive), but this is thought to be the main source of autoimmune diseases like rheumatoid arthritis.

IgE itself is an important immunoglobulin because it is the only immunoglobulin that stimulates mast cells and basophils, cells that contain and release histamine. As you may have realized if you take Benedryl or Claratin (over the counter antihistamines), histamine is responsible for a vast majority of the physical symptoms felt during an allergic reaction, including runny nose, watery eyes, tightness in the chest, flushing of the skin, hives, and swelling. It causes the swelling by making the capillaries less water tight (increasing their “permeability”) as well as dilating (opening up) the blood vessels feeding them, which allows for immune cells in the blood to cross through more easily and in greater numbers in response to the antigen. This leakiness also allows fluid to flow from the capillary to the surrounding tissue, resulting in the characteristic swelling. If this release of fluid happens to an extreme degree, anaphylaxis can occur, causing throat swelling and shock (when blood pressure drops to dangerously low levels due to a loss of blood volume). Epinephrine, the medication contained in an Epi-Pen, acts to reverse the constriction of the lungs and dilation of blood vessels. This can quickly reverse the symptoms as the fluid drains back into the bloodstream.

So now that we have a general idea of how the allergy response works, let’s dive into Aerin’s question. As you may or may not know, “big” cats like tigers and lions are more distantly related to house cats than is commonly believed. Although house cats look very much like miniature, less ferocious versions of big cats, they are actually only related at the family level (Felidae). That means they aren’t just separate species, but in separate genera (Panthera for big cats and Felis for house cats) as well. This is a fair evolutionary spread, which contributes to the ambiguity of the question’s answer.

Just about the only conclusive journal article I could find that tackles this issue head on comes from the July 1990 issue of The Journal of Allergy and Clinical Immunology. In this article, the researchers investigated if the main house cat protein known to cause allergies in humans (Fel d I) is found in big cats as well by examining Fel d I-specific IgE response (as well as the more general IgG response) to big cat dander. Their results were mixed. Although they found the IgE reacted with the proteins found in the big cat dander, the amount of reaction was nowhere near that of Fel d I itself. The tiger dander specifically was found closely in line with the other big cats. Based on that data and the authors’ conclusions, it appears that tigers can prompt an IgE response in house cat-allergic people, however not with the same vigor. In other words, being allergic to house cats means you’ll likely feel something if you come in contact with big cat dander, but the severity will likely differ from the original allergy.

Thank you for the question, Aerin! Hope this response helps! If you want your question answered too, you can submit yours directly to me by selecting the “Submit Your Question” tab at the top of this page.

Till we meet again next week, “Live Long and Prosper.”




Thank you to MCAT studying and biology classes for endowing me with the knowledge to explain this without significant help. Who knew you’d actually be useful?