Toxicity vesus Sensitization as a factor in building construction and maintenance

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Reply to Tony et al. on the topic of toxicity - my participation is sporadic due to homelessness and also because my priorities for the use of my time goes first to survival and then to patient advocacy needs. Sorry for the inconvenience and thank you for your patience. This subject of toxicity is relevant to this list as many, if not most trade materials are toxic by definition and by necessity. That is not a bar to their use. However, many are more toxic than is safe for use in any structure while others are far more toxic than is necessary for long durations. This is likely for the sake of efficiency, cosmetic effect and/or because they are cheaper to use. Few, if any, are pre-tested to determine what gasses and particulates are produced into confined spaces (and in estimated amounts), as a result of usage so that consumers have an opportunity to make informed choices while workers have an

understanding of the risks inherent in acute and chronic exposures. I am not referring to mold or mycotoxins although there will be some overlap. I also reject ‘odor’ tests as any indication of toxicity since it is merely a perceptual assessment (highly variable between subjects) and is unreliable as a means of determining when hazardous emissions from materials are absent or negligible. I use the term ‘perception’ in its scientific sense referring to an individual’s recognition of sensory input - not their belief’s about that awareness. Thresholds will differ widely for awareness of sensory input and even more widely for its recognition (individual can determine the source/type of input). A threshold is the amount of a stimulus required to be perceived 50 percent of the time it is presented. Adverse effects often occur prior to perception and recognition of emissions. Sensory adaptation also leads individuals to stop recognizing input after

awhile for both physiological and psychological reasons and the sense that an odor has dissipated is not always reliable. My concern is about toxicity and not allergenicity. Allergy infers adverse responses to materials which are otherwise of a benign nature like pollen or wheat, when encountered in normal concentrations. Directing attention solely to overall issues of sensitization (more diverse than classic allergy), merely directs attention away from the multiple hazards of toxicity from volatile and semi-volatile substances, and other airborne contaminants. The term ‘sensitive’ is used and misused frequently, usually to derail conversation or single out those who are harmed as being unavoidably damaged due to some defect in their wiring. They are also consigned to the category of 'acceptable risks' if blame is not rightly placed upon the materials to which they were exposed. This is not a denial of the multiple processes

involved in sensitization but a statement that ‘toxicity’ is far broader than that and applicable to the entire population. In other words, Socrates did not die of an allergic reaction to hemlock. I am concerned with medical events and not court proofs, for purposes of this discussion. ________________________________________ http://www.nlm.nih.gov/medlineplus/mplusdictionary.html defines poison as1 : a substance that through its chemical action usually kills, injures, or impairs an organism 2 : a substance that inhibits the activity of another substance or the course of a reaction or process Everyone is harmed by exposure to toxic chemicals because they are incompatible with human biochemistry. This can happen via direct actions upon biological structures such as the way in which ethylene glycol can damage kidneys, or chlorinated solvents damage liver cells (see http://www.haz-map.com/heptox1.htm ). Hyper-activation of nerve cell transmission by neurotoxins will damage or kill those cells. Pesticides do this in a variety of ways such as organophosphates which stop the production of inhibitory enzymes at the synaptic level. Pyrethroid insecticides directly interfere with the functions of sodium ion channels on nerve axons. Toxic chemicals can cause genetic (DNA) mutations which lead to cancer. Acquired gene mutations are more frequently than inherited ones, according to the American Cancer

Society. So we see primary damage from toxic exposures. Next, damage to any particular cell or organ will also lead to a cascade of events which will impede physiological processes involving multiple body systems. For example, endocrine functions regulate multiple events from thyroid function to reproductive abilities. The body has uniform ways of dealing with the removal of toxicants upon detection, which depends upon the amount and type of invasive substances through one or more routes of absorption. This activation of defenses has adverse consequences for the individual in that activities devoted to removal of foreign toxicants is in outright competition with processes normally devoted to homeostasis (anti-aging, maintenance of normal functions of digestion, vascular function etc.). We have natural defenses to rid us of those toxins produced during basic functions like

digestion (sulfites and aldehydes), muscle activity leaching waste products like lactic acid and many other examples. However, the same enzymes required for detoxification of naturally occurring toxins (e.g. methylation turning toxic sulfites into sulphates and antioxidants; oxidation of ‘bad’ lipids by paroxonase), are 'hijacked' to process the synthetic toxicants introduced into the environment. This means that exposure can leave you with depleted resources and impair many other bodily functions dependent upon the processes relying upon the availability of those resources. That is a sign of toxicity whether or not it meets criteria for any of the numerous forms of sensitization. It further explains why exposures affect so many diverse systems, confusing doctors and interfering with the accurate estimation of the amount and frequency of toxic injury in the population. The pool of detoxification resources (not to be

confused with the immune system), varies widely across and within individuals throughout life. This variability automatically makes some people more ‘sensitive’ (I prefer the term ‘prone’) to differing degrees and types of harm resulting from exposures. Some people are also more likely to perceive (be aware of) adverse symptoms based upon experience gained from repeatedly suffering adverse effects paired with the detection of certain odors in the environment. These people may be referred to as ‘odor’ sensitive but it is more of a learning process with regard to olfactory cues. The terms 'odor' and 'smell' are often used to downplay the need to recognize such cues as tangible fumes comprised of real particles that can be harmful when absorbed. I have read a number of product MSDS sheets which stated that a single exposure can result in lowered tolerances for future

contact. This does not mean that sensitization is the only cause for this. It can also be referring to the mechanism which leads to depletion of resources as with cholinesterase inhibition once exposed to OP pesticides. However, studies are showing that exposures lead to alteration of DNA cause the expression of normal gene functions to be disrupted. This prevents cells from receiving signals indicating they need to be activated or inhibited at appropriate intervals. This is well illustrated with the hormonal influences of endocrine disrupting chemicals. This influence upon estrogen regulation harms women, fetuses and reduces male fertility. A miscarriage can result from improper signaling and altered hormonal balances. Still another major factor in toxic exposure is inflammation, known to cause multiple disease processes and cancer. The physiological stress of

acute and/or chronic exposures have widespread effects across systems. Here are two good descriptions of such effects: http://www.som. tulane.edu/ classware/ pathology/ medical_patholog y/inflammation/http://www.nature. com/bjp/journal/ v147/n1s/ full/0706400a. html Currently, issues of dose-response relationships have ruled the way in which contaminants are assessed, approved and used in society. This brings is based in outdated science using the rule that 'the dose makes the poison', a sixteenth century concept elucidated by Paracelsus. Current thinking on this issue is found in these easy to read

references: http://www.actionbioscience.org/environment/trautmann.html The Dose Makes the Poison; Or Does It? Trautmann, Ph.D., directs Cornell University’s Environmental Inquiry Program http://www.ourstolenfuture.org/NewScience/lowdose/2007/2007-0525nmdrc.html Does the Dose Make the Poison by Theo Colburn et al http://www.protectingourhealth.org/corethemes/lowdose/doseresponse.htm The

Collaborative on Health and the Environment - Does the Dose Make the Poison? Cause and effect relationships are not as simple as they were before the chemical revolution. Poisons are well known to have been prominent in ancient times, be it the hemlock that Socrates drank, the lead poisoning that contributed to the fall of the Roman Empire or mercury from mining projects. Even for these well known poisons, the conceptual framework fails to account for cumulative exposure effects. The new model is best illustrated in consideration of endocrine disruptors where low dosages have been found to be more bio-active than higher ones. The dose/response model remains popular as it is industry friendly. However, the EU is now proceeding with a modified precautionary principle, understanding that the cost of the old premise is bankrupting societies which pay for the medical

expenses of all their citizens. The reason the US finally limited tobacco use in the workplace was because taxpayers were footing much of the bill for related ailments in non-smokers (cancer, COPD, vasculitis, cardiac anomalies, asthma etc). It wasn’t out of concern for the sickened bystanders. The Paracelsus model is insufficient to rely upon in modern society, unless you are speaking about substances which are benign in their habitual concentrations in the environment. A benign substance will become toxic to organisms when taken in excessive amounts such as too much water disrupting the environments on either side of cell membranes. However, to compare the toxicity of water with that of ethylene glycol is a distraction from responsibility and reason. One chooses to ingest water and can self-regulate the amount swallowed. You can’t do that in your office or classroom by deciding not to inhale. A poison is always a poison in some fashion, as discussed above. The dose merely aids in predicting or explaining the type and degree of harm it does to an individual assuming you know the characteristics of the substance, its biochemical meanderings through the human system and particular aspects of an affected individual that result in more or less harm. This refers to gender, genes, weight, age, concurrent exposures, health and so forth. Individual differences play a role in determining the degree of harm suffered. but not always in the expected order of 'more exposure' means 'more harm'. It has been shown that endocrine disrupting chemicals have had greater adverse effects in small doses which sneak under the radar of the immune/detox system. The use of smaller particles can result in higher absorption rates for the substances. Nano particles more easily penetrate our largest protective organ, the skin, than larger particles of poisons. Ultra low volume

sprays of malathion, used in mosquito abatement are more easily lodged in bronchioles of the lungs and therefore more rapidly absorbed than larger particles in higher concentration sprays. Most relevant today, and a large part of why dose/response figures are useless, is that combinations of chemicals act in completely unpredictable ways. Animal studies have replicated the kind of harm common to the brains of Gulf War vets when rats are given the same combinations of drugs and pesticide exposures as the troops experienced (protective drugs against chemical attack, DEET and pyrethroids in high concentrations). Damage is higher for troops with lower amounts of paroxonase enzyme but not across the board. Such enzyme activity wasn't even baselined so depletion may account for much of that phenomenon. Combined chemicals are more likely to cross the blood brain barrier, according to research at Duke U and Southwestern U. Industry makes use of the relationships between chemicals to alter their actions in products. When pyrethroid pesticides were substituted for OPs, presumably because they are 'less toxic' (many OPs have been banned in recent years), this assumption is based only upon testing of the active ingredients (e.g. cypermethrin). However, the marketed formulations usually contain a synergist chemical called PBO or piperonyl butoxide. This increases the toxicity of the formulation up to a factor of ten, but is not a consideration in marketing approvals offered by the EPA. Methods of applying chemicals are another way industry gets around restrictions upon toxicity levels. The use of misters to apply pesticides (now outlawed in NY state) whereby repeated release into the environment occurs every fifteen minutes (varies by appliance), completely prevents any control of amount introduced to an area regardless of inhabitants.

These devices are not regulated by EPA. Air freshener misters are very common as well as plug-ins, although I don't see any data regarding the steady increase in accumulated VOCs resulting from their use! To conclude this lay summary, the only way to increase the safety of indoor air is to measure the contaminants typically found during and after construction. Analysis of the results can then be used to alter either the composition or the selection of particular materials which most contribute to toxic effects upon inhabitants and workers. By measuring drop off rates, workers will know when to cease using protective gear and better able to estimate appropriate re-entry times for tenants after renovations are completed. Measurement can lead to accurate warnings on labels allowing consumers to make informed choices. More importantly, related illnesses will be recognized and treated

appropriately by medical personnel. Barb Rubin