The seasonal influenza (flu) vaccine is designed to protect against the three or four influenza viruses research indicates are most likely to spread and cause illness among people during the upcoming flu season. Flu viruses are constantly changing, so the vaccine composition is reviewed each year and updated as needed based on which influenza viruses are making people sick, the extent to which those viruses are spreading, and how well the previous season’s vaccine protects against those viruses.
More than 100 national influenza centers in over 100 countries conduct year-round surveillance for influenza. This involves receiving and testing thousands of influenza virus samples from patients. The laboratories send representative viruses to five World Health Organization (WHO) Collaborating Centers for Reference and Research on Influenza, which are located in the following places:
- Atlanta, Georgia, USA (Centers for Disease Control and Prevention, CDC);
- London, United Kingdom (The Francis Crick Institute);
- Melbourne, Australia (Victoria Infectious Diseases Reference Laboratory);
- Tokyo, Japan (National Institute for Infectious Diseases); and
- Beijing, China (National Institute for Viral Disease Control and Prevention).
Twice a year, the World Health Organization (WHO) organizes a consultation with the Directors of the WHO Collaborating Centers, essential regulatory laboratories and representatives of key national laboratories and academies. They review the results of surveillance, laboratory, and clinical studies, and the availability of vaccine viruses and make recommendations on the composition of the influenza vaccine. These meetings take place in February for selection of the upcoming Northern Hemisphere’s seasonal influenza vaccine and in September for the Southern Hemisphere’s vaccine. WHO recommends specific vaccine viruses for inclusion in influenza vaccines, but then each country makes their own decision about which viruses should be included in influenza vaccines licensed in their country.
In the United States, the Food and Drug Administration (FDA) makes the final decision about vaccine viruses for influenza vaccines to be sold in the U.S. Information about circulation of influenza viruses and available vaccine viruses is summarized and presented to an advisory committee of the FDA in February each year for the U.S. decision about which viruses to include in the upcoming season’s vaccine.
What are the main factors that influence which viruses are selected for use in vaccine production?
The influenza viruses in the seasonal flu vaccine are selected each year based on surveillance data indicating which viruses are circulating and forecasts about which viruses are the most likely to circulate during the coming season. The degree of similarity between available vaccine viruses and circulating viruses also is important. Vaccine viruses must be similar to the influenza viruses predicted to circulate most commonly during the upcoming season. Another important practical factor in the recommendation about what viruses to include in a flu vaccine is whether or not there is a good vaccine virus available; that is, a virus that could be used in vaccine production and which would likely protect against the viruses likely to circulate during the upcoming season. Vaccine viruses must be isolated and grown in chicken eggs. They also must be tested and available in time to allow for production of the large amount of vaccine virus needed to make vaccine. Occasionally, a suitable vaccine virus cannot be identified or developed in time to be included in the upcoming season’s vaccine.
Why is it sometimes difficult to get a good vaccine virus for vaccine production?
There are a number of factors that can make getting a good vaccine virus for vaccine production challenging, including both scientific issues and issues of timing. Currently, influenza vaccine viruses must be grown in eggs per FDA regulatory requirements. However, some influenza viruses, like H3N2 viruses, grow poorly in eggs, making it difficult to obtain candidate vaccine viruses.
In terms of timing, in some years certain influenza viruses may not appear and spread until later in the influenza season, making it difficult to prepare a candidate vaccine virus in time for vaccine production. This can make vaccine virus selection very challenging.
What is CDC’s Influenza Division’s role in vaccine virus selection?
As one of five WHO Collaborating Centers, CDC’s Influenza Division receives and tests thousands of influenza viruses from around the world each year and collaborates with other WHO Collaborating Centers and National Influenza Centers in the bi-annual seasonal vaccine virus selection process for the Southern and Northern Hemispheres. CDC plays a major role in testing and identifying new strains of influenza viruses through their global surveillance activities and then preparing candidate vaccine viruses. The Influenza Division provides this information to the directors of other WHO Collaborating Centers, essential regulatory laboratories and representatives of key national laboratories and academies and then participates in discussions regarding which viruses will be recommended for inclusion in flu vaccines. CDC also presents information to FDA’s advisory committee for their decision making and helps to identify vaccine viruses.
CDC’s Influenza Division collects and reports information on influenza activity in the United States each week. Laboratory studies of circulating influenza viruses allow CDC to evaluate how close a match there is between viruses in the vaccine and circulating viruses each season. Antigenic characterization is one process that can give an indication of the flu vaccine’s ability to produce an immune response against the influenza viruses circulating in people. Genetic characterization also can inform decision-making for vaccine virus selection. CDC also conducts studies to determine the effectiveness of the seasonal vaccine against circulating viruses. For more information, see Vaccine Effectiveness – How Well Does the Flu Vaccine Work? For more information about CDC’s surveillance and to access the weekly reports, visit Flu Activity and Surveillance.
What happens after a recommendation has been made about which viruses should be included in the seasonal flu vaccine?
As soon as a recommendation has been issued about what viruses should be included in the vaccine, private sector manufacturers begin the process of producing vaccine. In fact, some manufacturers may start growing one or more viruses for the vaccine even before a WHO or FDA decision is made based on what they think may be the recommended vaccine viruses. This allows manufacturers more time to make vaccine for the fall; the more time a manufacturer has to make vaccine, the greater the number of doses that can be produced.
How long does it take to manufacture seasonal influenza vaccine?
It takes at least six months to produce large quantities of influenza vaccine. For vaccine to be delivered in time for vaccination to begin in the fall, manufacturers may begin to grow one or more of the vaccine viruses in January based on their best guess as to what viruses are most likely to be included in the vaccine. For information about flu vaccine production, see How Influenza (Flu) Vaccines Are Made.
By: Megan Pond
It’s September. Where I live, September is the month that remains warm, but the evenings often cool down, warning of the impending weather-change about to come. In turn this is also when flu shot signs and tables with bored looking nurses and boxes full of needles join Halloween decorations as they make their seasonal debut into stores. “Flu Shots Now Available” signs begin to dot big box stores’ message boards and cheap signs stuck in the grass that wave back and forth in the wind. Flu vaccines are a huge market for these stores. It creates a big source of income at the best time of the year, so it’s only natural that they would try and advertise the heck out of them. It often brings me to ask myself, “What are they more worried about? My health? Or their pocketbook?”
Flu vaccine debates on the internet also make their yearly appearance and will continue for the next several months. There, I find many false statements regarding the flu vaccine and influenza itself being swept throughout cyberspace. Let’s identify some of these myths.
Myth #1: There’s No Thimerosal (or Mercury) in the Flu Shot Anymore.
First, I would like to direct you to two articles: Vaccine Ingredients – A Comprehensive Guide and Is There Thimerosal in the Flu Vaccine? If you click on the first link, you can scroll down to the section that explains a little more about thimerosal and mercury in vaccines. Here’s a quick summary of the articles’ findings.
According to the CDC, vaccines labeled “thimerosal-free” often have a little asterisk next to those words which lead you to something like: “This vaccine has ‘trace’ amounts of thimerosal, which the FDA says is equivalent to thimerosal-free products.” If we look closer into “thimerosal-free” vaccines, we will actually find that there is still a toxic amount of mercury contained in them.
There are two kinds of flu shots given. One contains 25 mcg of mercury (in the form of thimerosal with is 50% mercury. There is 50mcg of thimerosal in this flu shot) and is often given as the “regular” flu shot to those with no special circumstances. The other kind of flu shot is labeled “thimerasol-free” (containing less than 3mcg of mercury) and is given to young children and pregnant women.
If we look at “safe” and “un-safe” levels of mercury, per the FDA, we find this:
2 ppb is the maximum amount of mercury that deems water “safe” for drinking
Anything over 200 ppb mercury is considered TOXIC [source – EPA]
After doing some math [you can check my math in the article: Vaccine Ingredients – A Comprehensive Guide], we find this:
There is up to 300 ppb mercury is in the “thimerosal-free” flu vaccine.
There is 25,000 ppb mercury given in the flu shot containing 25 mcg of thimerosal as a preservative.
No matter how you cut it, flu vaccines contain toxic amounts of mercury. So yes, the flu vaccines still DOES contain thimerosal. The claim that there is “no thimerasol” in the flu vaccine is a complete fallacy, which leads to the next myth.
Myth #2: Sure, the Flu Vaccine Might Contain Thimerosal, but 25mcg is a Safe Amount. Pregnant Women Can Even Eat Up to 25 mcg of Mercury Contained in Fish.
I have heard this countless times. First, I would like to point out that pregnant women do not get the flu vaccine containing thimerosal as a preservative. They receive the vaccine falsely claiming to be “thimerosal-free.” It really should be called, “thimerosal decreased, but still overly toxic.” From the above statement, we have people running around thinking it’s safe to not only eat 25 mcg of mercury, but also to inject 25 mcg of thimerosal into their body (thimerosal is 50% mercury).
There have never been any real studies done on pregnant women and the effects of eating fish-contained mercury. What information has been gathered is mainly based on trial and error. Some doctors urge their pregnant patients to completely steer clear of fish altogether because of the mercury content, while others advise pregnant women to eat “low mercury fish” once or twice a week. According to the 2010 Dietary Guidelines for Americans, eating 8-12 ounces of low mercury fish per week is safe for pregnant women. The FDA (Federal Drug Administration) and EPA (Environmental Protection Agency) say up 12 ounces per week is safe. The Mayo Clinic says to limit albacore tuna, chunk white tuna and tuna steak to 6 ounces per week. [source Mayo Clinic]
So then we have to ask: What is considered low mercury fish?
According to the FDA: shrimp, crab, salmon, pollock, catfish, cod, tuna, and, tilapia are considered low mercury fish. Tuna contains the highest amount of mercury in the low mercury fish category. [source FDA.gov]
Which leads us to: How much mercury is in fish?
Using tuna as an example, which contains the highest amount of mercury in the low mercury fish category, we find out it contains approximately 128 ppb mercury. All of the other low mercury fish are lower than that. The fish containing the highest amount of mercury, tilefish, has 1,450 ppb mercury — very understandable that pregnant women and children are urged to not eat high mercury fish. [source FDA.gov]
Now we’ll look at how many micrograms of mercury is in a serving of fish, again using tuna as an example. Three oz. of tuna is considered 1 serving, so that means a pregnant woman can safely eat 1 serving of tuna 4 times a week, according to the Dietary Guidelines for Americans. If we look at the current amount of mercury in fish (because it changes from year to year), we see that there are approximately 13.32mcg of mercury in 12 ounces of tuna, which equates to 3.33mcg per serving. The amount of mercury in tuna sits between 12-14mcg per 12 ounces every year, and has never been recorded as going over 14mcg. [source EPA]
Therefore, we can safely come to the conclusion that the FDA standard for mercury consumption in pregnant women is a maximum of 14mcg in one week, not the 25mcg that floats around on message boards. Consuming 25mcg of mercury in fish would almost double the amount the FDA considers safe for pregnant women.
I would also like to point out that *INGESTING* mercury is very different than *INJECTING* it straight into your muscle or blood stream. Ingesting small amounts of mercury is considered safe because it goes through a number of natural filtration systems in our body before it reaches the blood stream. Studies suggest that eating higher amounts of mercury (anything over 200ppb) can be toxic because a small amount of mercury is able to reach the blood stream and can cause neurological disorders, immune disorders, and other significant problems. A very in-depth study done by the University of Calgary showed that even small amounts of mercury reaching the brain cannot only halt neuron growth, but it actually causes the neuron growth to *reverse*. Neurons are integral cell bodies and nerve processes in our brains. Unlike other body cells, neurons stop reproducing shortly after birth. Because of this, some parts of the brain have more neurons at birth than later in life because neurons die and cannot be replaced. [source University of Calgary] [source]
By injecting mercury instead of ingesting it, you are essentially by-passing your inner filtration systems. All of the mercury in a vaccine enters the blood stream, which leads straight to the brain. Remember that toxic amounts of mercury is considered anything over 200ppb, and the amount of mercury in a “thimerosal-free” flu vaccine is 300 to 600 ppb – the vaccine most commonly used contains 50,000 ppb. When you ingest mercury, the amount that reaches your blood stream is much less than the actual amount you consumed. When you vaccinate, the entire amount of mercury reaches your blood stream.
So here’s the point: when we combine the information from Myth #1 and Myth #2, even the FDA and EPA standards for INGESTION (over an entire week) of mercury are significantly lower than the amount in even the “thimerosal-free” vaccines – which are given all at once – and are outrageously lower than the 25mcg flu vaccine which, of course, is also given all at once.
Myth #3: Last Year I Got the Flu and I Threw Up Three Times a Day and was Constantly in the Bathroom with Diarrhea! There’s No Way I’m Skipping my Shot This Year!
Many people, after experiencing a rough weekend of throwing up and diarrhea, come back to work and say they had an awful flu. This is a common misconception. The “stomach flu” is different from “the flu” that we vaccinate for. The flu shot is ineffective against “stomach flu.”
The flu vaccine guards against “the flu.” Flu is short for Influenza. Many interchange the word “flu” to also mean “stomach flu,” which in fact is not a flu at all. Many describe having the flu as being a “cold from Hell.” Symptoms generally include fever, runny nose, head congestion, body and muscle aches, fatigue, dry cough, and sore throat. It’s definitely not fun to have and will often keep you in bed, depending on how healthy your immune system is. Influenza is caused by a virus – meaning antibiotics are not affective against killing it. With the influenza virus – as well as any other virus – you generally have to “wait it out” and let your body take care of killing the virus.
The “stomach flu” is scientifically called gastroenteritis and is caused by a virus, parasite, or bacteria. The symptoms include stomach cramps, nausea, vomiting, and diarrhea and is usually caused by eating contaminated food or drinking contaminated water. Conditions such as lactose intolerance or food allergies can also cause gastroenteritis. [source Web MD]
Myth #4: If I Get a Flu Shot, I Won’t Get the Flu! (And My Body Will Be Healthier and Stronger to Boot!)
There are several different strains of influenza that cause a human to get “the flu.” There are 3 different classifications, or genuses, of Influenza: Influenza A, Influenza B, and Influenza C. Each genus has several different serotypes (or several different flus), under each classification. Influenza A has been shown to affect humans the most and has 10 known serotypes, and the CDC suspects that there are over 100 different serotypes of Influenza A. Considering that only a small percentage of people are actually tested in one year to find out what kind of flu they contracted, it is impossible to know just how many different serotypes of Influenza there are. Most people that get the flu don’t go to the doctor or hospital, and even those that are hospitalized are not commonly tested. [source Wiki]
According to the CDC:
There are several reasons why someone might get flu-like symptoms even after they have been vaccinated against the flu.
- People may be exposed to an influenza virus shortly before getting vaccinated or during the two-week period that it takes the body to gain protection after getting vaccinated. This exposure may result in a person becoming ill with flu before the vaccine begins to protect them.
- People may become ill from other (non-flu) viruses that circulate during the flu season, which can also cause flu-like symptoms (such as rhinovirus).
- A person may be exposed to an influenza virus that is not included in the seasonal flu vaccine. There are many different influenza viruses that circulate every year. The flu shot protects against the 3 viruses that research suggests will be most common. Unfortunately, some people can remain unprotected from flu despite getting the vaccine. This is more likely to occur among people that have weakened immune systems. However, even among people with weakened immune systems, the flu vaccine can still help prevent influenza complications. [source CDC.gov]
Reports of “getting the flu” after vaccination is common. Immediately following vaccination, the body’s immune system is weakened. During that time of weakened immunity, it is common for someone to more easily contract a flu virus (or any other kind of virus), even one that the vaccine prevents against considering that it takes up to 2 weeks for the body to create enough antibodies to prevent future illness from the strains contained in the vaccine.
So how many strains are contained in this year’s vaccine?
Three. H1N1, H3N2, and an Influenza B serotype called Brisbane. [source CDC.gov]
How are the strains chosen for the current year’s vaccine?
The most popular strains from the previous year become the blueprint for the current year’s vaccine. However, according to the CDC, the most popular strains of influenza change on a yearly basis. My red flag just went up! If the flu vaccine for this year is made from the previous year’s most popular strains, and they change yearly, doesn’t that mean this year’s “most popular strains” will likely be different? My internal compass says yes. Hence, the vaccine with last year’s most popular strains will be grossly ineffective this year.
“The viruses used in making seasonal flu vaccines are chosen each year based on information collected over the previous year about which influenza viruses are spreading.” [source flushotstogo.com]
One interesting fact about this year’s flu vaccine (2011-2012) is that it’s EXACTLY the same vaccine as last year’s. Nothing has been changed, yet the medical community and the government are recommending that even if you had this vaccine last year, you should still get it this year because it “wears off” in just a matter of months. HUH?! Flu vaccines are made exactly the same way as all the other vaccines we give our children: Inactivated virus, preservatives, chemicals, etc… except this is the ONLY vaccine they admit lasts for “just a couple of months.” Shouldn’t that mean that other vaccines are just as ineffective? We give those to our children and they’re supposed to last for up to 10 years after the whole series is completed. If I knew how to raise one eyebrow, I would do that now.
Myth #5: The Flu Vaccine Has Saved Countless Lives.
Influenza vaccines have been around since 1945. Just before the flu season of 2003-2004 the CDC recommended for the first time that children younger than 60 months (5 years) and older than 6 months receive an annual flu vaccination. About this time is when the fad of getting a flu vaccine became common for not only children under 5, but for everyone over 5 as well. [source CDC.gov] [source vaccineinformation.org]
The following is a list of different years and the number of flu associated deaths in children reported to the CDC:
- 1999-2000 -36 deaths [source]
- 2000-2001 -30 deaths [source] 17% decrease
- 2001-2002 – 25 deaths [source] 17% decrease
- 2002-2003 – 29 deaths [source] 16% increase (This is the last year that the flu vaccine was considered “unsafe” by the CDC for children under 5 – now let’s watch the increase of deaths after the CDC recommends all children age 6 months to 5 years be vaccinated for Influenza.)
- 2003-2004 – 153 [source] 427% increase
- 2004-2005 — 47 deaths [source] 69% decrease
- 2005-2006 – 46 deaths [source] 3% decrease
- 2006-2007 – 68 deaths [source] 48% increase
- 2007-2008 – 88 deaths [source] 29% increase
- 2008-2009 – 133 deaths [source] 51% increase
- 2009-2010 – 282 deaths [source] 112% increase
- 2010-2011 – 115 deaths [source] 59% decrease
The number of children dying from the flu has risen *drastically* since the CDC recommended children under 5 receive the flu vaccine. There has been an average of67% increase of flu-associated death in children since the CDC recommended children under 5 receive the flu vaccine.
According to research presented at the 105th International Conference of the American Thoracic Society in San Diego, children who get the flu vaccination have a 3 times greater risk for hospitalization:
They found that children who had received the flu vaccine had three times the risk of hospitalization, as compared to children who had not received the vaccine. In asthmatic children, there was a significantly higher risk of hospitalization in subjects who received the TIV (Stands for Trivalent Influenza Vaccine – a.k.a. the flu shot), as compared to those who did not. [source Sciencedaily.com]
So in essence, parents who vaccinate their children against the flu are increasing the hospitalization risk for their child!
”The number of deaths attributed to influenza over the years is always averaged at 36,000 per year in the United States, and that number is still often used. This number, as many people found out, was completely false and misleading.
Their claim that 36,000 Americans die from the seasonal flu is classic deception & fear mongering propaganda. Most of those deaths, as you can see by the breakdown chart below, resulted from bacterial pneumonia triggered by the Flu. And the age bracket for most victims is 65 and over. But the Flu itself is relatively innocuous by comparison, and actual flu death figures are statistically minor. The who base Flu death averages not on the Influenza totals but on the combined Pneumonia & Influenza totals are overcoming a serious political challenge: convincing the public of the urgency to be vaccinated when the crisis is no longer perceived to be real. Without that advantage of fear, given all that we have learned about the lack of efficacy & dangers inherent to the shots, the entire Flu Vaccine Industry might very well collapse.
INFLUENZA: ACTUAL NUMBER OF DEATHS CATALOGED IN THE US
2002 – 727
2003 – 1,792
2004 – 1,100
2005 – 1,812
PNEUMONIA: ACTUAL NUMBER OF DEATHS CATALOGED IN THE US
2002 – 64,954
2003 – 63,371
2004 – 58,564
2005 – 61,189
PNEUMONIA & INFLUENZA: ACTUAL NUMBER OF DEATHS CATALOGED
2002 – 65,681
2003 – 65,163
2004 – 59,664
2005 – 63,001
The CDC and the World Health Organization (WHO) converts numbers from the third set; based on yearly fluctuations they arrive at 36,000.” [Joel Lord in VRM: “One For All” Universal Flu Vaccine – 21st Century Genetic Roulette Part 1; Founder of the VRM]
So when you hear the number of flu related deaths per year, remember that it’s a complete estimation. The WHO and the CDC take the numbers of not only those individuals with confirmed influenza cases, but also those individuals that have not been tested to see whether or not they had influenza but died from pneumonia. They’re taking a complete guess and assuming that about half of the individuals that died from pneumonia developed pneumonia because they contracted influenza as well, which may or may not be true. You’ll also see that, despite a consecutive increase of flu vaccinations each year, the number of influenza AND pneumonia cases remain about the same.
At the end of all of this, we find that the Flu vaccine is dangerous and essentially ineffective. So that means we must be doomed to live in a never-ending cycle of possibly contracting the yearly flu?
Not so. Studies have shown that adequate amounts of Vitamin D during the flu months (when Vitamin D levels are at their lowest) can prevent people from contracting influenza up to 100% of the time!! And even if your Vitamin D levels aren’t as high as they need to be to completely prevent the flu, even higher than average levels of Vitamin D can greatly minimize the symptoms of the flu if you catch it. This is one of the only safe and natural ways to prevent the flu or lessen flu symptoms. [source Naturalnews.com][source medicalnewstoday.com] [source mercola.com] [source University of Cambridge Medical Journals]
Along with adequate amounts of Vitamin D, studies show that regular visits to a chiropractor can have significant affects on immune system health and development. The Journal of Pediatric, Maternal & Family Health issued a release on May 04, 2009 with the headline “Flue Prevention Plan Should Include Chiropractic,” urging people to include chiropractic during this most recent flu scare. In this report, it states:
People of all ages are encouraged to add chiropractic to their strategy for warding off and fighting the flu and its effects swine flu or otherwise. Spinal adjustments can have a positive effect on immune function according to a growing number of researchers who are exploring the common denominators in disease processes, and the role of the nervous, immune, and hormonal systems in development of immune related illnesses. [source]
During the Spanish Influenza outbreak in 1918 in Davenport, Iowa, 50 medical doctors cared for 4,953 cases of the Spanish flu, and 274 of their patients died. In the same city, 150 chiropractic doctors, including students and faculty of the Palmer School of Chiropractic, treated 1,635 Spanish Flu patients where only 1 patient died.
Outside Davenport, chiropractors in Iowa cared for 4,735 Spanish Flu sufferers with only six deaths – one out of 866. In Oklahoma, out of 3,490 flu patients receiving the benefits of chiropractic care, only seven people died.
National figures for the United States show that 1,142 chiropractic doctors treated a total of 46,394 flu patients during the 1918 Spanish Flu outbreak, with a mortality rate of only 54 patients – one out of every 859, or less than 0.12 percent.
In sharp contrast, the mortality rate from Spanish flu in regular US hospitals generally ranged from 30 to 40 percent. For one hospital in New York, the mortality rate was 68 percent! [source][source]
The main threats to human health from heavy metals are associated with exposure to lead, cadmium, mercury and arsenic. These metals have been extensively studied and their effects on human health regularly reviewed by international bodies such as the WHO. Heavy metals have been used by humans for thousands of years. Although several adverse health effects of heavy metals have been known for a long time, exposure to heavy metals continues, and is even increasing in some parts of the world, in particular in less developed countries, though emissions have declined in most developed countries over the last 100 years. Cadmium compounds are currently mainly used in re-chargeable nickel–cadmium batteries. Cadmium emissions have increased dramatically during the 20th century, one reason being that cadmium-containing products are rarely re-cycled, but often dumped together with household waste. Cigarette smoking is a major source of cadmium exposure. In non-smokers, food is the most important source of cadmium exposure. Recent data indicate that adverse health effects of cadmium exposure may occur at lower exposure levels than previously anticipated, primarily in the form of kidney damage but possibly also bone effects and fractures. Many individuals in Europe already exceed these exposure levels and the margin is very narrow for large groups. Therefore, measures should be taken to reduce cadmium exposure in the general population in order to minimize the risk of adverse health effects. The general population is primarily exposed to mercury via food, fish being a major source of methyl mercury exposure, and dental amalgam. The general population does not face a significant health risk from methyl mercury, although certain groups with high fish consumption may attain blood levels associated with a low risk of neurological damage to adults. Since there is a risk to the fetus in particular, pregnant women should avoid a high intake of certain fish, such as shark, swordfish and tuna; fish (such as pike, walleye and bass) taken from polluted fresh waters should especially be avoided. There has been a debate on the safety of dental amalgams and claims have been made that mercury from amalgam may cause a variety of diseases. However, there are no studies so far that have been able to show any associations between amalgam fillings and ill health. The general population is exposed to lead from air and food in roughly equal proportions. During the last century, lead emissions to ambient air have caused considerable pollution, mainly due to lead emissions from petrol. Children are particularly susceptible to lead exposure due to high gastrointestinal uptake and the permeable blood–brain barrier. Blood levels in children should be reduced below the levels so far considered acceptable, recent data indicating that there may be neurotoxic effects of lead at lower levels of exposure than previously anticipated. Although lead in petrol has dramatically decreased over the last decades, thereby reducing environmental exposure, phasing out any remaining uses of lead additives in motor fuels should be encouraged. The use of lead-based paints should be abandoned, and lead should not be used in food containers. In particular, the public should be aware of glazed food containers, which may leach lead into food. Exposure to arsenic is mainly via intake of food and drinking water, food being the most important source in most populations. Long-term exposure to arsenic in drinking-water is mainly related to increased risks of skin cancer, but also some other cancers, as well as other skin lesions such as hyperkeratosis and pigmentation changes. Occupational exposure to arsenic, primarily by inhalation, is causally associated with lung cancer. Clear exposure–response relationships and high risks have been observed.
Although there is no clear definition of what a heavy metal is, density is in most cases taken to be the defining factor. Heavy metals are thus commonly defined as those having a specific density of more than 5 g/cm3. The main threats to human health from heavy metals are associated with exposure to lead, cadmium, mercury and arsenic (arsenic is a metalloid, but is usually classified as a heavy metal).
Heavy metals have been used in many different areas for thousands of years. Lead has been used for at least 5000 years, early applications including building materials, pigments for glazing ceramics, and pipes for transporting water. In ancient Rome, lead acetate was used to sweeten old wine, and some Romans might have consumed as much as a gram of lead a day. Mercury was allegedly used by the Romans as a salve to alleviate teething pain in infants, and was later (from the 1300s to the late 1800s) employed as a remedy for syphilis. Claude Monet used cadmium pigments extensively in the mid 1800s, but the scarcity of the metal limited the use in artists’ materials until the early 1900s.
Although adverse health effects of heavy metals have been known for a long time, exposure to heavy metals continues and is even increasing in some areas. For example, mercury is still used in gold mining in many parts of Latin America. Arsenic is still common in wood preservatives, and tetraethyl lead remains a common additive to petrol, although this use has decreased dramatically in the developed countries. Since the middle of the 19th century, production of heavy metals increased steeply for more than 100 years, with concomitant emissions to the environment (Fig. 1).
At the end of the 20th century, however, emissions of heavy metals started to decrease in developed countries: in the UK, emissions of heavy metals fell by over 50% between 1990 and 20001.
Emissions of heavy metals to the environment occur via a wide range of processes and pathways, including to the air (e.g. during combustion, extraction and processing), to surface waters (via runoff and releases from storage and transport) and to the soil (and hence into groundwaters and crops) (see Chapter 1). Atmospheric emissions tend to be of greatest concern in terms of human health, both because of the quantities involved and the widespread dispersion and potential for exposure that often ensues. The spatial distributions of cadmium, lead and mercury emissions to the atmosphere in Europe can be found in the Meteorological Synthesizing Centre-East (MSC-E) website (http://www.msceast.org/hms/emission.html#Spatial). Lead emissions are mainly related to road transport and thus most uniformly distributed over space. Cadmium emissions are primarily associated with non-ferrous metallurgy and fuel combustion, whereas the spatial distribution of anthropogenic mercury emissions reflects mainly the level of coal consumption in different regions.
People may be exposed to potentially harmful chemical, physical and biological agents in air, food, water or soil. However, exposure does not result only from the presence of a harmful agent in the environment. The key word in the definition of exposure is contact2. There must be contact between the agent and the outer boundary of the human body, such as the airways, the skin or the mouth. Exposure is often defined as a function of concentration and time: “an event that occurs when there is contact at a boundary between a human and the environment with a contaminant of a specific concentration for an interval of time”3. For exposure to happen, therefore, co-existence of heavy metals and people has to occur (see Chapter 1).
Occurrence, exposure and dose
Cadmium occurs naturally in ores together with zinc, lead and copper. Cadmium compounds are used as stabilizers in PVC products, colour pigment, several alloys and, now most commonly, in re-chargeable nickel–cadmium batteries. Metallic cadmium has mostly been used as an anticorrosion agent (cadmiation). Cadmium is also present as a pollutant in phosphate fertilizers. EU cadmium usage has decreased considerably during the 1990s, mainly due to the gradual phase-out of cadmium products other than Ni-Cd batteries and the implementation of more stringent EU environmental legislation (Directive 91/338/ECC). Notwithstanding these reductions in Europe, however, cadmium production, consumption and emissions to the environment worldwide have increased dramatically during the 20th century. Cadmium containing products are rarely re-cycled, but frequently dumped together with household waste, thereby contaminating the environment, especially if the waste is incinerated.
Natural as well as anthropogenic sources of cadmium, including industrial emissions and the application of fertilizer and sewage sludge to farm land, may lead to contamination of soils, and to increased cadmium uptake by crops and vegetables, grown for human consumption. The uptake process of soil cadmium by plants is enhanced at low pH4.
Cigarette smoking is a major source of cadmium exposure. Biological monitoring of cadmium in the general population has shown that cigarette smoking may cause significant increases in blood cadmium (B-Cd) levels, the concentrations in smokers being on average 4–5 times higher than those in non-smokers4. Despite evidence of exposure from environmental tobacco smoke5, however, this is probably contributing little to total cadmium body burden.
Food is the most important source of cadmium exposure in the general non-smoking population in most countries6. Cadmium is present in most foodstuffs, but concentrations vary greatly, and individual intake also varies considerably due to differences in dietary habits4. Women usually have lower daily cadmium intakes, because of lower energy consumption than men. Gastrointestinal absorption of cadmium may be influenced by nutritional factors, such as iron status7.
B-Cd generally reflects current exposure, but partly also lifetime body burden8. The cadmium concentration in urine (U-Cd) is mainly influenced by the body burden, U-Cd being proportional to the kidney concentration. Smokers and people living in contaminated areas have higher urinary cadmium concentrations, smokers having about twice as high concentrations as non-smokers4.
Inhalation of cadmium fumes or particles can be life threatening, and although acute pulmonary effects and deaths are uncommon, sporadic cases still occur9,,10. Cadmium exposure may cause kidney damage. The first sign of the renal lesion is usually a tubular dysfunction, evidenced by an increased excretion of low molecular weight proteins [such as β2-microglobulin and α1-microglobulin (protein HC)] or enzymes [such as N-Acetyl-β-D-glucosaminidase (NAG)]4,,6. It has been suggested that the tubular damage is reversible11, but there is overwhelming evidence that the cadmium induced tubular damage is indeed irreversible4.
WHO6 estimated that a urinary excretion of 10 nmol/mmol creatinine (corresponding to circa 200 mg Cd/kg kidney cortex) would constitute a ‘critical limit’ below which kidney damage would not occur. However, WHO calculated that circa 10% of individuals with this kidney concentration would be affected by tubular damage. Several reports have since shown that kidney damage and/or bone effects are likely to occur at lower kidney cadmium levels. European studies have shown signs of cadmium induced kidney damage in the general population at urinary cadmium levels around 2–3 μg Cd/g creatinine12,,13.
The initial tubular damage may progress to more severe kidney damage, and already in 1950 it was reported that some cadmium exposed workers had developed decreased glomerular filtration rate (GFR)14. This has been confirmed in later studies of occupationally exposed workers15,,16. An excess risk of kidney stones, possibly related to an increased excretion of calcium in urine following the tubular damage, has been shown in several studies4.
Recently, an association between cadmium exposure and chronic renal failure [end stage renal disease (ESRD)] was shown17. Using a registry of patients, who had been treated for uraemia, the investigators found a double risk of ESRD in persons living close to (<2 km) industrial cadmium emitting plants as well as in occupationally exposed workers.
Long-term high cadmium exposure may cause skeletal damage, first reported from Japan, where the itai-itai (ouch-ouch) disease (a combination of osteomalacia and osteoporosis) was discovered in the 1950s. The exposure was caused by cadmium-contaminated water used for irrigation of local rice fields. A few studies outside Japan have reported similar findings4. During recent years, new data have emerged suggesting that also relatively low cadmium exposure may give rise to skeletal damage, evidenced by low bone mineral density (osteoporosis) and fractures18–20.
Animal experiments have suggested that cadmium may be a risk factor for cardiovascular disease, but studies of humans have not been able to confirm this4. However, a Japanese study showed an excess risk of cardiovascular mortality in cadmium-exposed persons with signs of tubular kidney damage compared to individuals without kidney damage21.
The IARC has classified cadmium as a human carcinogen (group I) on the basis of sufficient evidence in both humans and experimental animals22. IARC, however, noted that the assessment was based on few studies of lung cancer in occupationally exposed populations, often with imperfect exposure data, and without the capability to consider possible confounding by smoking and other associated exposures (such as nickel and arsenic). Cadmium has been associated with prostate cancer, but both positive and negative studies have been published. Early data indicated an association between cadmium exposure and kidney cancer23. Later studies have not been able clearly to confirm this, but a large multi-centre study showed a (borderline) significant over-all excess risk of renal-cell cancer, although a negative dose–response relationship did not support a causal relation24. Furthermore, a population-based multicentre-study of renal cell carcinoma found an excess risk in occupationally exposed persons25. In summary, the evidence for cadmium as a human carcinogen is rather weak, in particular after oral exposure. Therefore, a classification of cadmium as ‘probably carcinogenic to humans’ (IARC group 2A) would be more appropriate. This conclusion also complies with the EC classification of some cadmium compounds (Carcinogen Category 2; Annex 1 to the directive 67/548/EEC).
Occurrence, exposure and dose
The mercury compound cinnabar (HgS), was used in pre-historic cave paintings for red colours, and metallic mercury was known in ancient Greece where it (as well as white lead) was used as a cosmetic to lighten the skin. In medicine, apart from the previously mentioned use of mercury as a cure for syphilis, mercury compounds have also been used as diuretics [calomel (Hg2Cl2)], and mercury amalgam is still used for filling teeth in many countries26.
Metallic mercury is used in thermometers, barometers and instruments for measuring blood pressure. A major use of mercury is in the chlor-alkali industry, in the electrochemical process of manufacturing chlorine, where mercury is used as an electrode.
The largest occupational group exposed to mercury is dental care staff. During the 1970s, air concentrations in some dental surgeries reached 20 μg/m3, but since then levels have generally fallen to about one-tenth of those concentrations.
Inorganic mercury is converted to organic compounds, such as methyl mercury, which is very stable and accumulates in the food chain. Until the 1970s, methyl mercury was commonly used for control of fungi on seed grain.
The general population is primarily exposed to mercury via food, fish being a major source of methyl mercury exposure27, and dental amalgam. Several experimental studies have shown that mercury vapour is released from amalgam fillings, and that the release rate may increase by chewing28.
Mercury in urine is primarily related to (relatively recent) exposure to inorganic compounds, whereas blood mercury may be used to identify exposure to methyl mercury. A number of studies have correlated the number of dental amalgam fillings or amalgam surfaces with the mercury content in tissues from human autopsy, as well as in samples of blood, urine and plasma26. Mercury in hair may be used to estimate long-term exposure, but potential contamination may make interpretation difficult.
Acute mercury exposure may give rise to lung damage. Chronic poisoning is characterized by neurological and psychological symptoms, such as tremor, changes in personality, restlessness, anxiety, sleep disturbance and depression. The symptoms are reversible after cessation of exposure. Because of the blood–brain barrier there is no central nervous involvement related to inorganic mercury exposure. Metallic mercury may cause kidney damage, which is reversible after exposure has stopped. It has also been possible to detect proteinuria at relatively low levels of occupational exposure.
Metallic mercury is an allergen, which may cause contact eczema, and mercury from amalgam fillings may give rise to oral lichen. It has been feared that mercury in amalgam may cause a variety of symptoms. This so-called ‘amalgam disease’ is, however, controversial, and although some authors claim proof of symptom relief after removal of dental amalgam fillings29, there is no scientific evidence of this30.
Methyl mercury poisoning has a latency of 1 month or longer after acute exposure, and the main symptoms relate to nervous system damage31. The earliest symptoms are parestesias and numbness in the hands and feet. Later, coordination difficulties and concentric constriction of the visual field may develop as well as auditory symptoms. High doses may lead to death, usually 2–4 weeks after onset of symptoms. The Minamata catastrophe in Japan in the 1950s was caused by methyl mercury poisoning from fish contaminated by mercury discharges to the surrounding sea. In the early 1970s, more than 10,000 persons in Iraq were poisoned by eating bread baked from mercury-polluted grain, and several thousand people died as a consequence of the poisoning. However, the general population does not face significant health risks from methyl mercury exposure with the exception of certain groups with high fish consumption.
A high dietary intake of mercury from consumption of fish has been hypothesized to increase the risk of coronary heart disease32. In a recent case-control study, the joint association of mercury levels in toenail clippings and docosahexaenoic acid levels in adipose tissue with the risk of a first myocardial infarction in men was evaluated33. Mercury levels in the patients were 15% higher than those in controls (95% CI, 5–25%), and the adjusted odds ratio for myocardial infarction associated with the highest compared with the lowest quintile of mercury was 2.16 (95% CI, 1.09–4.29; P for trend = 0.006).
Another recent case-control study investigated the association between mercury levels in toenails and the risk of coronary heart disease among male health professionals with no previous history of cardiovascular disease. Mercury levels were significantly correlated with fish consumption, and the mean mercury level was higher in dentists than in non-dentists. When other risk factors for coronary heart disease had been controlled for, mercury levels were not significantly associated with the risk of coronary heart disease34.
These intriguing contradictory findings need to be followed up by more studies of other similarly exposed populations.
Occurrence, exposure and dose
The general population is exposed to lead from air and food in roughly equal proportions. Earlier, lead in foodstuff originated from pots used for cooking and storage, and lead acetate was previously used to sweeten port wine. During the last century, lead emissions to ambient air have further polluted our environment, over 50% of lead emissions originating from petrol. Over the last few decades, however, lead emissions in developed countries have decreased markedly due to the introduction of unleaded petrol. Subsequently blood lead levels in the general population have decreased (Fig. 2).
Occupational exposure to inorganic lead occurs in mines and smelters as well as welding of lead painted metal, and in battery plants. Low or moderate exposure may take place in the glass industry. High levels of air emissions may pollute areas near lead mines and smelters. Airborne lead can be deposited on soil and water, thus reaching humans via the food chain.
Up to 50% of inhaled inorganic lead may be absorbed in the lungs. Adults take up 10–15% of lead in food, whereas children may absorb up to 50% via the gastrointestinal tract. Lead in blood is bound to erythrocytes, and elimination is slow and principally via urine. Lead is accumulated in the skeleton, and is only slowly released from this body compartment. Half-life of lead in blood is about 1 month and in the skeleton 20–30 years35.
In adults, inorganic lead does not penetrate the blood–brain barrier, whereas this barrier is less developed in children. The high gastrointestinal uptake and the permeable blood–brain barrier make children especially susceptible to lead exposure and subsequent brain damage. Organic lead compounds penetrate body and cell membranes. Tetramethyl lead and tetraethyl lead penetrate the skin easily. These compounds may also cross the blood–brain barrier in adults, and thus adults may suffer from lead encephalopathy related to acute poisoning by organic lead compounds.
The symptoms of acute lead poisoning are headache, irritability, abdominal pain and various symptoms related to the nervous system. Lead encephalopathy is characterized by sleeplessness and restlessness. Children may be affected by behavioural disturbances, learning and concentration difficulties. In severe cases of lead encephalopathy, the affected person may suffer from acute psychosis, confusion and reduced consciousness. People who have been exposed to lead for a long time may suffer from memory deterioration, prolonged reaction time and reduced ability to understand. Individuals with average blood lead levels under 3 μmol/l may show signs of peripheral nerve symptoms with reduced nerve conduction velocity and reduced dermal sensibility. If the neuropathy is severe the lesion may be permanent. The classical picture includes a dark blue lead sulphide line at the gingival margin. In less serious cases, the most obvious sign of lead poisoning is disturbance of haemoglobin synthesis, and long-term lead exposure may lead to anaemia.
Recent research has shown that long-term low-level lead exposure in children may also lead to diminished intellectual capacity. Figure 3shows a meta-analysis of four prospective studies using mean blood lead level over a number of years. The combined evidence suggests a weighted mean decrease in IQ of 2 points for a 0.48 μmol/l (10 μg/dl) increase in blood lead level (95% confidence interval from −0.3 points to −3.6 points)35.
Acute exposure to lead is known to cause proximal renal tubular damage35. Long-term lead exposure may also give rise to kidney damage and, in a recent study of Egyptian policemen, urinary excretion of NAG was positively correlated with duration of exposure to lead from automobile exhaust, blood lead and nail lead36.
Despite intensive efforts to define the relationship between body burden of lead and blood pressure or other effects on the cardiovascular system, no causal relationship has been demonstrated in humans35.
Using routinely collected data on mortality (1981–96), hospital episode statistics data 1992–1995 and statutory returns to the Health and Safety Executive (RIDDOR), one death and 83 hospital cases were identified37. The authors found that mortality and hospital admission ascribed to lead poisoning in England were rare, but that cases continue to occur and that some seem to be associated with considerable morbidity.
Blood lead levels in children below 10 μmg/dl have so far been considered acceptable, but recent data indicate that there may be toxicological effects of lead at lower levels of exposure than previously anticipated. There is also evidence that certain genetic and environmental factors can increase the detrimental effects of lead on neural development, thereby rendering certain children more vulnerable to lead neurotoxicity38.
IARC classified lead as a ‘possible human carcinogen’ based on sufficient animal data and insufficient human data in 1987. Since then a few studies have been published, the overall evidence for lead as a carcinogen being only weak, the most likely candidates are lung cancer, stomach cancer and gliomas39.
Occurrence, exposure and dose
Arsenic is a widely distributed metalloid, occurring in rock, soil, water and air. Inorganic arsenic is present in groundwater used for drinking in several countries all over the world (e.g. Bangladesh, Chile and China), whereas organic arsenic compounds (such as arsenobetaine) are primarily found in fish, which thus may give rise to human exposure40.
Smelting of non-ferrous metals and the production of energy from fossil fuel are the two major industrial processes that lead to arsenic contamination of air, water and soil, smelting activities being the largest single anthropogenic source of atmospheric pollution41. Other sources of contamination are the manufacture and use of arsenical pesticides and wood preservatives.
The working group of the EU DG Environment concluded that there were large reductions in the emissions of arsenic to air in several member countries of the European Union in the 1980s. In 1990, the total emissions of arsenic to the air in the member states were estimated to be 575 tonnes. In 1996, the estimated total releases of arsenic to the air in the UK were 50 tonnes42.
Concentrations in air in rural areas range from <1 to 4 ng/m3, whereas concentrations in cities may be as high as 200 ng/m3. Much higher concentrations (>1000 ng/m3) have been measured near industrial sources. Water concentrations are usually <10 μg/l, although higher concentrations may occur near anthropogenic sources. Levels in soils usually range from 1 to 40 mg/kg, but pesticide application and waste disposal can result in much higher concentrations40.
General population exposure to arsenic is mainly via intake of food and drinking water. Food is the most important source, but in some areas, arsenic in drinking water is a significant source of exposure to inorganic arsenic. Contaminated soils such as mine-tailings are also a potential source of arsenic exposure40.
Absorption of arsenic in inhaled airborne particles is highly dependent on the solubility and the size of particles. Soluble arsenic compounds are easily absorbed from the gastrointestinal tract. However, inorganic arsenic is extensively methylated in humans and the metabolites are excreted in the urine40.
Arsenic (or metabolites) concentrations in blood, hair, nails and urine have been used as biomarkers of exposure. Arsenic in hair and nails can be useful indicators of past arsenic exposure, if care is taken to avoid external arsenic contamination of the samples. Speciated metabolites in urine expressed as either inorganic arsenic or the sum of metabolites (inorganic arsenic + MMA + DMA) is generally the best estimate of recent arsenic dose. However, consumption of certain seafood may confound estimation of inorganic arsenic exposure, and should thus be avoided before urine sampling40.
Inorganic arsenic is acutely toxic and intake of large quantities leads to gastrointestinal symptoms, severe disturbances of the cardiovascular and central nervous systems, and eventually death. In survivors, bone marrow depression, haemolysis, hepatomegaly, melanosis, polyneuropathy and encephalopathy may be observed. Ingestion of inorganic arsenic may induce peripheral vascular disease, which in its extreme form leads to gangrenous changes (black foot disease, only reported in Taiwan).
Populations exposed to arsenic via drinking water show excess risk of mortality from lung, bladder and kidney cancer, the risk increasing with increasing exposure. There is also an increased risk of skin cancer and other skin lesions, such as hyperkeratosis and pigmentation changes.
Studies on various populations exposed to arsenic by inhalation, such as smelter workers, pesticide manufacturers and miners in many different countries consistently demonstrate an excess lung cancer. Although all these groups are exposed to other chemicals in addition to arsenic, there is no other common factor that could explain the findings. The lung cancer risk increases with increasing arsenic exposure in all relevant studies, and confounding by smoking does not explain the findings.
The latest WHO evaluation40 concludes that arsenic exposure viadrinking water is causally related to cancer in the lungs, kidney, bladder and skin, the last of which is preceded by directly observable precancerous lesions. Uncertainties in the estimation of past exposures are important when assessing the exposure–response relationships, but it would seem that drinking water arsenic concentrations of approximately 100 μg/l have led to cancer at these sites, and that precursors of skin cancer have been associated with levels of 50–100 μg/l.
The relationships between arsenic exposure and other health effects are less clear. There is relatively strong evidence for hypertension and cardiovascular disease, but the evidence is only suggestive for diabetes and reproductive effects and weak for cerebrovascular disease, long-term neurological effects, and cancer at sites other than lung, bladder, kidney and skin.
Recent data indicate that adverse health effects of cadmium exposure, primarily in the form of renal tubular damage but possibly also effects on bone and fractures, may occur at lower exposure levels than previously anticipated. Many individuals in Europe already exceed these exposure levels and the margin is very narrow for large groups. Therefore, measures should be taken to reduce cadmium exposure in the general population in order to minimize the risk of adverse health effects.
The general population does not face a significant health risk from methylmercury, although certain groups with high fish consumption may attain blood levels associated with a low risk of neurological damage to adults. Since there is a risk to the fetus in particular, pregnant women should avoid a high intake of certain fish, such as shark, swordfish and tuna. Fish, such as pike, walleye and bass, taken from polluted fresh waters should especially be avoided.
There has been a debate on the safety of dental amalgams and claims have been made that mercury from amalgam may cause a variety of diseases, but to date no studies have been able to show any associations between amalgam fillings and ill health.
Children are particularly vulnerable to lead exposure. Blood levels in children should be reduced below the levels so far considered acceptable, recent data indicating that there may be neurotoxic effects of lead at lower levels of exposure than previously anticipated. Although lead in petrol has dramatically declined over the last decades, thereby reducing environmental exposure, there is a need to phase out any remaining uses of lead additives in motor fuels. The use of lead-based paints should also be abandoned, and lead should not be used in food containers. In particular, the public should be aware of glazed food containers, which may leach lead into food.
Long-term exposure to arsenic in drinking water is mainly related to increased risks of skin cancer, but also some other cancers, and other skin lesions such as hyperkeratosis and pigmentation changes. Occupational exposure to arsenic, primarily by inhalation, is causally associated with lung cancer. Clear exposure–response relationships and high risks have been observed.