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HLTH 340
Steve Mc Coll

Topic 5: Heavy Metals Part 2 Heavy metals as environmental health hazards  Alright, let's rap about heavy metals. Define them first. o Most "officially", we would say that heavy metals are metallic elements with high atomic weight and high density  For example: lead, mercury, cadmium, etc. o We have to be careful -- sometimes there are other types of metals classified as heavy metals which really aren't:  i.e. Arsenic -- listed as a heavy metal, but arsenic strictly speaking is not a metal at all but rather a metalloid -- a compound that in physical or chemical parlance strictly isn't a metal, but can act like one  Another set of compounds sometimes included here are the transition metals -- these are metals in the middle of the periodic table of the elements but are NOT heavy metals because:  They are not heavy  They participate in natural biological processes (think about iron and hemoglobin)  Chromium and nickel are also notable examples  Talk about how these heavy metals came about, and how this relates to our body's ability to deal with them. o OK, well firstly we don't mean to say that heavy metals never existed -- but it's just that when they DID exist naturally, they were always bonded to sulfide groups, which made them insoluble (thus they could not enter our bodies)  It is important to note here that the implication is that heavy metals had (and have) NO ROLE in biological systems  The other big implication is that the body does not know how to handle the heavy metals if they DO get in, and this is for the same reason -- just the fact that it never developed an evolutionary ability to deal with it o But we couldn't leave well enough alone: we started to mine these ores -- and get their pure forms -- separate out the sulfide groups -- create the metal and do various things with it -- then the metal is available in forms that ARE accessible to us -- and then that's when we get in trouble  In other words, we released metals from the geosphere into biosphere by anthropogenic activities  Talk about the longevity of heavy metals. o Well the thing is that as elemental contaminants, they cannot be destroyed  (This is as opposed to organic chemicals like pesticides or fungicides, which will break down gradually either in the external environment or the body) o We SHOULD say, though, that it is possible to have metal speciation between more toxic and less toxic forms High-risk Groups  What is the 90/10 rule? How do we get stuff like this? o It is that 90% of potential harm occurs in 10% of population -- or in other words, most environmental hazards disproportionately affect a small portion of the human population o We find out statistics like this by doing biomonitoring, which is monitoring the levels of chemicals in people's bodies  It can range from small research studies to large surveys (i.e. NHANES, which keeps track of 100 persistent chemicals)  Give a general overview of the two kinds of high-risk groups o Highly exposed groups: these groups have a greater exposure than most of population (e.g. 95th centile or +2 S.D.) o Highly susceptible groups: these groups incur a greater health risk than non- group members for a given exposure level  Discuss highly-exposed groups further. What are some things that we have to keep in mind with these guys? o Firstly, "high exposure" can happen in many ways but REPEATED CHRONIC exposure is the worst one (as opposed to, say, acute)  This is because repeated chronic exposure results in the accumulation of greater "body burden" (the total amount of these chemicals that are present in the human body at a given point in time) over prolonged time of exposure o Also, with these guys we have to be worried about co-exposure: exposure to more than one toxicant at a time  This is especially dangerous because the two toxicants could have interaction effects which are undetected if we are only studying one chemical at a time  Discuss highly susceptible groups further. Why are they so? o It is because they have weaker physiological defenses against toxic contaminants, and there are different reasons for this:  Inherited factors (gender, genetic)  Gender: for example, certain things only affect pregnant women  Genetics: 30,000 genes, about 10% play significant role in susceptibility to contaminants  Acquired factors (age, health status, nutrition, smoking, etc.)  Age: i.e. very young and very old are susceptible to air pollution  Health status: folks that have asthma suffer more from ozone  Nutrition: certain fruits and vegetables may confer protection against toxic substances  Smoking: smoking habits changes enzyme profiles in a bad way Body burden example: methyl mercury (MeHg)  Recall the graph which showed the body burden of MeHg. Describe it and state what it demonstrated. o Description:  The axises were [] of MeHg in blood and time (days)  There were lines indicating the increase of MeHg as a result of a meal consumption, but then also a thicker dashed line indicating the total MeHg (because multiple meals can add up) o Demonstrated:  We saw that blood concentration would peak just a few HOURS after a meal, but it took FIFTY DAYS for the concentration to return to 50% -- the implication that it is removed slowly, so it can build up  We also noticed that if you are exposed enough to the MeHg (say you are a fisher or a native Indian who eats it a lot) it is possible that MeHg would never return to zero  If you are not, then with enough time it will return to close enough to zero  This graph looked at blood levels, which means that the "dose type" it was looking at was "internal dose". What are the other two types of doses? For each of the dose types, how do we measure? o External dose: we would have to study the person's environment to know this o Internal dose: this is what BIOMONITORING is all about -- we find out how much is in the blood, for example (see reading for more on biomonitoring)  We look at blood, urine, feces, etc. o Effective dose: this is the amount which is actually able to get into its areas of effect and do something This is hard to know because it means we would have to (for example)  take liver samples, because that is one place where the mercury will travel from the blood in order to go wreak some havoc  However, note that with lead and other heavy metals, we CAN do this because we could take X-rays of people's bones and look at the lead content in there  This is however expensive and so the NHANES won't be doing it anytime soon  Also, NMR is used to some good effect here  What is found by these studies? o 90% of people have low body burden -- we're just concerned about the 10% Highly exposed groups - lead Talk about some of the different ways we can be highly exposed to lead.  o Inner city inhabitants (esp. low income) are exposed to...  Lead-based household paints (now banned)  Lead dust from automotive exhaust emissions (now banned)  Industrial emissions (lead refiners, smelters, battery recyclers, etc.) o Occupational exposure  Lead industry (i.e. smelters) workers have it on a large scale  Electronics and electronics recycling (lead in electrical solder) -- the places where computers, etc. are processed have lots of lead exposure  Notably this is mostly done in China or India, so the problem is there rather than here o Consumer products  Leaded glass (‘crystal’) containers: some crystal used to make glasses, etc. contains lead  PVC window blinds: sun degrades the plastic and PVC dust (containing LEAD) enters the air  Context: Vinyl (aka PVC) is used to make blinds  Children’s toys: lead is a very cheap, economical metal and so cheap toys from Asia, Eastern Europe may have a lot of lead! o Aboriginal people  They eat ‘country foods’ such as wild birds, fish who in turn have lead pellets from shotguns in their bodies  Gasoline abuse -- lead in snowmobile gasoline was banned, but Aboriginals continued using it History of lead in commercial use - gasoline and paints  How was leaded gas advertised? o They advertised leaded gas by saying that ethyl would give more horsepower and cause the engine to run smoother  How was paint advertised? o "If you love your children, you'll buy leaded paint - it allows you to wash and sanitize surfaces easily" Highly susceptible groups - lead  Name and discuss some groups of people that are highly susceptible to lead, and explain why. o Persons of young age: lead is neurotoxic (harms brain cells), and thus is especially harmful to the infant or child who is still growing their brain  Also, it is more bioavailable in younger children o Adult women: there are multiple categories here  Of childbearing age (risk to fetus)  All women (low calcium stores can cause lead to be absorbed more easily)  Post-menopausal women (bone loss) o Persons of poor nutritional status (we have discussed poor intake of calcium many times) o Persons where genetic polymorphism works against them: polymorphisms are subtle genetic variations in a given gene or trait which (in this case) make us more susceptible to some toxicant  On a molecular level, polymorphisms are caused by different alleles  Homozygous is when both alleles (one from each parents) are the same  Heterozygous is when they are different  Example: Blood types -- A, B, O -- these are all well known, and they result because different people have different alleles -- there is a POLYMORPHISM happening  Let's turn away from susceptible PEOPLE for a while, and concentrate on how the dose. What trends have we seen in this area, i.e. the relationship of dose to resulting illness? o At the very beginning, they had unsophisticated methods of determining lead toxicity: they would just go by whether the person was showing symptoms, which for various reasons is not the most dependable way to do things o At this time, we said that 30 ug/dL was a safe level of lead to have in our bodies o However, over last 30 years, toxicologists and epidemiologists discover that the harder they look, the more they find even small doses are likely to cause problems (ie: >10 ug/dl is unacceptable because it causes mild mental retardation in children) o Even a 10 ug might be pushing it when we realize that historically, 10 ug is a high level -- i.e. if we go back to prehistoric times before industry evolved, the level of lead in an aboriginal person/caveman would be 1 ug or less  Implication: even if we have 3 or 4 or 5 ug, that is still well above what our biological constitution is set up to manage b/c any dose of level has some risk Genetic susceptibility to lead toxicity  What are the two polymorphic things we will be discussing here? o VDR (vitamin D receptor protein) -- the protein that binds Vitamin D and thus allows it to exert its effect of synthesizing calcium channels o ALAD (alpha-aminolevulinic acid dehydratase) -- a protein in RBC's (erythrocytes) which binds to lead  Quickly review how al
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