Stress the silent killer

“Not everything that matters can be measured, and not everything that is measured matters.” – Elliot Eisner

Cardiovascular diseases (CVDs) are the number one cause of death globally. In 2008, more than 17 million people died from them. On a national level, based on the 2004-2005 National Health Survey, 3.7 million Australians are estimated to have existing cardiovascular problems; CVDs were the direct cause of 35% of total mortality in 2005, again the number one cause of death 1,2. This is despite the billions of dollars spent on medications to reduce the risk and intensity of cardiovascular diseases 3. CVD is no longer considered a disorder of lipid (fat) accumulation, but rather a disease process characterized by low-grade inflammation of the vascular (artery) lining and an inappropriate wound healing of the blood vessels. The answer is to treat the cause of inflammation not cholesterol.
A study in 2004 known as the INTERHEART study found that 90% of all myocardial infarctions (heart attacks) could be attributed to nine potentially modifiable risk factors 4,5. These factors include tobacco use, atherosclerosis, hypertension, diabetes, abdominal obesity, psychosocial factors, alcohol consumption, physical inactivity and poor diets 4,6.
Despite convincing evidence linking psychosocial factors such as chronic and acute stress to the risks of cardiovascular disease 7,8,9, there remains a lack of focus on stress reduction for the prevention and treatment of cardiovascular disease. Risk reduction for stress is low-cost, simple to administer, and “non-pharmaceutical” 10.
Stress is the failure of an individual to cope with an emotional or physical threat. It results in both psychological and physical effects on individuals by means of two main stress groups: acute stress and chronic stress. Chronic stress occurs from exposure to stressors such as family, society (traffic, population, etc.) and, almost all the time, the workplace. When the body is stressed, a large number of biological and chemical processes can occur that put the body at increased risk of CVD. Chemical mediators are released, which cause the prolonged activation of the sympathetic nervous system 7 and increase heart rate and blood pressure, which puts a lot of strain on the heart and cardiovascular system 11. Over time, the strain on the system leads to deterioration of the heart muscle, arteries and vessels 11. Chemical mediators can also result in sleep deprivation, elevated cortisol levels, elevated insulin and blood glucose levels and increases in ghrelin, the hormone that increases appetite 11.

Chronic stress, which is what we are often confronted with in our daily busy lives, plays a huge role in these increases, as it can cause the prolonged activation of the sympathetic nervous system 7. This results in an increase in blood pressure and heart rate, which remain elevated, leading to an increased risk of cardiovascular disease. In extreme circumstances this is also linked with endothelial dysfunction (inability of arteries to dilate) and possible necrosis of artery walls 7.
Stress increases the release of hormones like cortisol, adrenaline and noradrenaline, which act to increase the heart rate and contractile volume, as well as constricting arteries in the gastrointestinal tract, whilst dilating those in the periphery. Aldosterone and vasopressin, two lesser hormones in the stress response, are also released and act to increase blood volume through increased water retention. One of the functions of cortisol is to increase the concentration of fatty acids carried by lipoproteins and sugars in the bloodstream, leading to more damage to the arterial wall, producing excessive levels of cholesterol that may then bond to the artery walls (and lead to high cholesterol readings by your doctor), a process called atherosclerosis 12. Atherosclerosis is the process in which a blood vessel wall thickens due to a build-up of fatty substances. The combined effect of these hormones is a marked increase in blood pressure, which may over time result in damage to the vascular tissue in the form of small micro-tears in the vessel walls. These minute tears heal by bonding with molecules floating in the blood (that is, cholesterol acts as a Bandaid). This cholesterol then forms a hard fibrous plaque with calcium, which may build up over time, constricting blood flow in the artery. Stress also causes the blood to become stickier in preparation of potential injury, increasing the likelihood of an artery clogging blood clot 13. One study found that those who expressed feeling high levels of stress and despair had a 20% greater chance of developing atherosclerosis over a four-year period. This was the same magnitude of increased risk as seen in a pack-a-day smoker. Studies on animals have shown similar results. A study on hypertensive rats and normal rats found that the hypertensive rats suffering from stress had a higher rate of these events 14.
There is a large body of evidence demonstrating the relationship between increased stress and increased CVD. A study commenced before the terrorist attacks in the U.S. on September 11, 2001 examined the degree to which acute stress reactions as a result of the terrorist attacks could predict future cardiovascular outcomes through follow-up surveys over three years 15. In a sample of 2,592 adults, researchers found that the acute stress response was associated with a 53% increased incidence of cardiovascular ailments 15. Those individuals who had high levels of acute stress following the attacks also reported a two-fold increase in physician-diagnosed hypertension and a three-fold increase in other heart-related problems over the three-year period.
In a study of 11,119 patients found that those patients who had experienced a myocardial infarction reported a higher prevalence of all four stress factors: stress at home, stress at work, financial stress and major life events in the prior year 16. The study also found that the four stress factors worsened coronary atherosclerosis and endothelial dysfunction and increased inflammation 16.
The Whitehall II study found a 2.15-fold (215%) increased risk for cardiovascular disease in men who experienced a disparity between effort and reward at work 17. The study also concluded that high-risk individuals included those who were overcommitted at work, had poor promotion prospects, blocked or stalled careers as well as competitive and hostile work environments. Similarly, in a study of nearly two thousand male workers over a six-year period, researchers found that those who experienced chronic work-related stress were four times more likely to experience cardiovascular ailments 16. A study at the Beth Israel Deaconess Medical Centre in Boston found evidence that managers who fire someone run twice the usual risk of heart attack in the week following the dismissal; the greatest danger occurred to those who had conducted the firing while working under a high-pressure deadline. Another study found that chronic work stress and divorce increased the risk of cardiovascular mortality 17.
In a study of 791 patients, researchers reported that high-pressure deadlines increased the risk of heart attacks by 2.3 times within the seven days after the stress of the deadlines. Specific time pressures dramatically increase the risk of heart attack and early death. In a study of 60 women ages 30 to 45, researchers found that those under stress who secreted the highest levels of cortisol were also the ones who turned to high-fat foods in attempts to cope with their stress.
The results are similar for younger populations. In a study of 158 healthy adolescents who undertook self-report measures of chronic stress over 3.3 years, adolescents exposed to chronic, negative stressors that worsened over time demonstrated heightened cardiovascular risk 18. In a study investigating the responses of university students to stressful situations, researchers found that students exposed to stressful laboratory tasks displayed high levels of cardiovascular responses, which extended into a continued increase in blood pressure during instances of perceived stress in everyday life situations 19.
Being angry more than doubles the risk of cardiac arrest. In a study of 1,500 people who had suffered heart attacks who were surveyed and asked what their feelings were a few hours prior to the heart attack, it was found that the heightened risk appears to last for about two hours after the episode of anger.
Psychosocial stress also results in changes in physiological behaviours 5,7,11, which can put a person at increased risk of CVD. These behaviours include increased smoking and drinking, unhealthy eating and reductions in physical activity 20,21,22. In addition, chronic stress can lead to constrained appetites or overeating, leading to problems of anorexia or obesity 23. In extreme cases, anorexia or extreme weight loss can have an effect on heart rhythms and even lead to heart failure 2010, while overeating may lead to obesity that has significant health risks associated with coronary heart disease, hypertension and type 2 diabetes 25.
Stress is our great silent killer. Despite the growing body of evidence of this, we continue to focus on pharmaceutical treatments to reduce CVD and we continue to fail. The mechanisms behind stress being such a large contributing factor are now understood and numerous major studies have shown that the effects of chronic stress increase the risk from two to nine times. By contrast, medication to reduce cholesterol reduces the risk by 1% or 0.001 times (that is more than 2,000 times less important than stress). The next stage then is to invest in stress management practices. It’s that simple. Or is it?
1. NHMRC 2009
2. Bonthuis et al. 2010
3. Ademi et al. 2009
4. Yusef et al. 2004
5. Dimsdale 2008
6. Begg et al. 2008).
7. Rozanski et al. 1999
8. Black and Gabutt 2002
9. Siegrist 1995
10. Cade et al. 2010).
11. McEwen 2008
12. Brotman et al. 2007
13. Newton et al. 1990
14. Hallbäck and Folkow 2008
15. Holam et al. 2008
16. Rosengren et al. 2004
17. Dimsdale 2007
18. Low et al. 2009
19. Loft et al. 2007
20. Sturmer et al. 2006
21. Logan and Barksdale 2008
22. Hamer, Bates and Mishra 2011
23. Rutledge and Linden 1997
24. Bell 2010
25. Rapoport, Clark and Wardle 2000

Acknowledgements. Brigitta Curley, Amy Williams

Lead, A Toxic Case Study

Lead is the most widely used heavy metal and a deadly toxin that has become widespread in our modern world. Lead is a neurotoxin with a long history of causing damage to the human brain, from Roman times due to lead (Pb –Latin name plumbum) in drinking vessels, through eighteenth century ‘Devonshire colic’ where cider was poisoned with lead in its manufacture, to present day occupational exposure in the lead additive and battery manufacturing industry. Some historians put the demise of the Roman empire down to the high levels of lead in the aristocracy of Rome which may have contributed to madness such as Nero playing the fiddle as Rome burnt. Before the Industrial Revolution lead poisoning commonly occurred due to adulterated food or wine, or from occupational hazards such as mining or smelting.

Naturally lead is slowly released into the environment through the weathering of rocks, igneous (volcanic) activity and through radioactive decay of naturally occurring radon gas to form the isotope 210Pb. It is a heavy pliable and resistant to corrosion and weathering. These characteristics, as well as its plentiful and accessible supply and ease to smelt, have enabled humans to use it for thousands of years. Some lead artifacts have been dated back to 6500 BC. The Romans produced approximately 80,000 tons of lead annually and were known to increase the environmental lead approximately five times the background level, and as far back as 4,500 years ago in South East Asia, when methods of smelting for lead sulphide ores and cupellation of silver were developed, widespread atmospheric lead contamination occurred.

Lead is the only heavy metal whose open-ocean concentration has been measurably influenced by civilisation. The lead content of the open ocean (Mediterranean and Pacific) has increased 3 to 5 times since the introduction of lead-based gasoline additives and 10 times since pre-industrial times. The significance of these increases in global lead concentration is very difficult to assess. There is a growing concentration of lead found in the tissues of fish, especially shell fish, and in other food, but the effect on global ecosystem processes would be nearly impossible to assess as there are huge problems in determining what is ‘normal’ when the global ecosystem is now relatively drenched in lead compared with pre-industrial times. The extent of global lead is best seen in the fact that an emission product has been diluted into the open oceans and increased in concentration dramatically, yet most lead emissions do not normally reach the oceans but are deposited on the land, particularly in cities where most of us live.

Traditional uses of lead have included building, plumbing, printing, fishing, shooting and uses as weights with the additional present day use in radiation and electrical insulation, battery manufacture with various compounds of lead being used in paints, plastics, ceramics, glass and unfortunately petrol. Historically there have been three major sources of exposure of large populations to lead. Lead paint in older homes, lead in products like jewelry and crystal and lead added to petrol.

While lead was slowly removed from petrol over 25 years, it will remain as an environmental contaminant in the form of fine dust for many more decades and the controversy around it will last even longer. Lead was added to petrol as tetra ethyl and tetra methyl lead (two highly toxic forms) primarily to boost octane ratings. Lead was emitted to the atmosphere from motor vehicle exhausts as volatile lead compounds, unburnt tetra-ethyl lead and as particulates such as lead oxide. Around 70% of these particles are less than 0.1 micron in size which are easily dispersed over large distances and the size most dangerous to human health. Particles below 0.1 micron in size can pass into the lower parts of the lungs where they do most damage.

Automotive exhausts were the major contributors to lead emissions in most cities around the world, although other sources include paint and factory emissions. In the USA it is estimated that between 90 and 98 per cent of total lead emissions are from car exhausts and in Australia it has been estimated that about 98% of lead emissions came from lead in petrol, though the lead added to petrol only represented 14% of total lead usage.

Australia was one of the last developed countries to remove lead from petrol (almost 20 years after the USA). This was despite the toxic effects of lead being known as far back as the 1950s. Leaded petrol was phased out in Australia between 1986 and 2002. Australia has an influential lead industry (the largest lead mines in the world) that fought tooth and nail alongside the petrol industry and certain government departments to keep the lead in petrol. Shamefully, the health of the average person is usually not a consideration when weighed against the “health” of the economy when large amounts of money are at stake. The result of this reluctance to act means that even still many more Australians now have elevated levels of lead in their bodies and many children have been unnecessarily exposed to this toxic metal.

Although the amount of lead has decreased in road dust and soil lead is still found as a contaminant in the dust in our homes, usually near the entrance where it is brought in on people’s shoes. This contaminated dust will accumulate in carpets, where the possibility of it being ingested or being transferred to the skin is increased, especially if the dust particles are stirred. When we studied the amounts of lead in carpets we found the highest levels near the front door. The closer the house was to a busy road or a petrol station, the higher the level of lead.

Lead can cause very serious health problems, including damage to the nervous system, leading to behavioural changes and a decreased mental ability, inhibition of enzymes, interference with the growing foetus, colic, anaemia and kidney damage. Infants and young children are the groups most susceptible to lead exposure. Even at low levels, lead poisoning in children can cause significant IQ deficiencies, reading and learning disabilities, impaired hearing, reduced attention spans and hyperactivity and other behaviour problems. A lot like ADHD symptoms. Pregnant women poisoned by lead can transfer lead to the developing foetus, resulting in adverse developmental effects including increased levels of spontaneous abortion and still-born babies. One study found a strong correlation with prenatal lead exposure and violent offences and arrests later in life and lead exposure in utero will result in poor intellect in children, especially when exposed around 28 weeks of gestation when development is most crucial.

Schizophrenia has also been associated with exposure to lead in the foetus. In one study mothers with high‑lead blood samples were more than twice as likely to have children who later became schizophrenic. As a result they estimate that up to a quarter of the schizophrenia that developed in American urban centres in the 1950s and 1960s could be traced to lead pollution in the womb. Maybe the levels in Australia were even higher as a result of our lax controls.

Another sensitive issue is what levels of lead in the body are safe for kids. According to the grandfather of lead research Dr Needleman, ‘none’. Needleman had done literally decades of work on the toxic effects of lead on kids and had concluded there is no safe level and children are the most vulnerable to its toxic effects. However, as a result of the powerful lead industry the levels of lead acceptable in the blood were around 35ug/dl of blood. In the mid 80’s it was reduced to 25, then to 10 and now levels of 5 ug/dl or above are considered not acceptable. In one situation I was involved in however, the government officials tried to argue the child did not have a problem because the levels were 4.9 ug/dl. Clearly they were very good at reading numbers but not at understanding the effects of toxic chemicals such as lead and how standards should be used including how lead levels fluctuate in the blood and the effects of lead accumulation in the body.

Dust from lead-based paints continues to pose a health problem. Although these paints were banned from indoor use decades ago, people with older homes are still being exposed to lead dust, another legacy of complacent governments. More than 80 percent of homes built before 1978 contain lead paint. It was the primary component (up to 40 percent) of white paint in Australia until the 1960s. In homes built before 1950, white lead-based paints were used as undercoats on interior and exterior timbers and walls and as a prime coat for troweled lath and plaster walls and cement rendered surfaces. One study estimated that 38 million houses in the US had lead-based paint on their walls. How many in Australia? Since then, modern paints have turned from using lead based to titanium dioxide and latex products. Unfortunately lead based paints are still used in many developing countries.

Small quantities of dust are continually produced from lead paint, settling on indoor surfaces. During periods of home renovation, there is an increase in the number of cases of lead poisoning reported. Researchers have found the household dust of recently renovated homes contains lead levels of 12,600 mg/m2. This is thousands of times higher than the normal background level. In a recent incident, a family keen to renovate an older house was assured that the old paint on the outside of their home was not lead based. At the end of the first day of paint stripping, there was a layer of fine paint dust inside the home and in the new baby’s room. Fortunately the mother listened to her intuition and had the dust tested. It was laden with lead. In this case the family acted quickly to avert potentially grave health problems. It is essential to have paint tested before you remove it if you think there may be any possibility of it being lead based. This is simple and inexpensive as the test kits are available from any reputable hardware or paint shop. Don’t assume it will be fine. It is essential to test it and be sure. The best thing to do with most lead painted surfaces is to just paint over it. It will not be released with a few extra coats of paint over it.

Another concern is the use of lead in common consumer items. In particular the use of lead paint or contamination of children’s products and toys with lead. There is growing evidence and concern over the unregulated products coming into Australia from Asia. Many are made from cheaper metals and paints and may be contaminated or even used heavy metals such as lead and cadmium in their production. I have found jewelry with high concentrations of both lead and cadmium.

Ironically we add lead oxide to the molten glass to form lead crystal. The lead leaches out into liquids fairly rapidly but increases with alcoholic content and acidity. The longer the wine or drink is left in the crystal the higher the concentrations but it only takes a few minutes for the lead to begin leaching into the crystal. Lead may also be a lesser component of pewter but the same principles will apply for it migrating into foods and drink as crystal.

Lead also makes its way into cosmetics, particularly, hair dyes, eye shadow and lipsticks. Metal salts dyes, most commonly lead and bismuth (another toxic metal) salts, are used to create a reaction to dye the hair. Metal salts gradually darken the hair over time and are used in black-brown colours. Strangely lead salts have been approved as safe for use as hair dyes in the low concentrations. Remember, there is no safe level of lead, but for beauty’s sake it seems ok?

Lead in drinking water is not a new phenomenon as lead was historically used to make water pipes and has even been contributed to be a factor of the Roman Empire's demise. Although lead pipes are no longer produced, some older homes may still contain lead pipes and thus contaminate the drinking water. Lead in tap water may also increase due to leaching of lead-bearing materials such as solders.

Lead has also been found to accumulate in the soil of orchards where crop sprays containing lead compounds have been used such as apple and pear orchards sprayed with lead arsenate. The concern here is the encroaching urban sprawl as we build new homes on old horticultural or old industrial areas without anyone being the wiser on what is in the soils.

Whilst we have become smarter when dealing with lead, and it no longer affects our IQ, the possibility of future contamination still lingers as long as we accept it in our products. No level of lead, mercury or cadmium is acceptable, and therefore the only acceptable solution is to remove them from all environmental, household and personal care products.