Environmental Toxins and Cardiovascular Disease
Joseph Pizzorno, ND
Introduction
The incidence of virtually every chronic disease in almost every age group has increased relentlessly the past half century. A growing body of research has now documented that much, if not most, of this increase is due to the increasing levels of toxic metals and chemicals in the environment. Heavy metals (eg, cadmium, lead, and mercury), meta-metals (eg, arsenic), nonpersistent chemical toxins (eg, PAHs [polyaromatic hydrocarbons], VOCs [volatile organic compounds], glyphosate, organophosphate pesticides), persistent chemical toxins (DDT [dichlorodiphenyltrichloroethane], PCBs [polychlorinated biphenyls], air pollutants (particulate matter, ozone, sulfur, and nitrogen oxides), and several other less pervasive, but still important, classes of toxicants, have all been shown to increase cardiovascular disease (CVD) and many other diseases as well as risk of death. These toxicants contaminate air, water, health and beauty aids, food, packaging, pharmaceuticals, house and yard chemicals—in other words every human contact with the environment.
Everyday exposure to many of these is common, but making the problem far more challenging is that many of them have very long half-lives in humans. Although simple avoidance is critical, substantial skill and effort are needed to help facilitate excretion of the persistent organic pollutants (POPs). The long lifetimes of lead in the body is well known. But far less recognized is that many of these new-to-nature molecules were specifically designed to be difficult to detoxify by biological systems. Particularly problematic for humans are the halogenated compounds. Without intervention, molecules like DDT and PCBs have half-lives measured in years to even decades, causing continuous, unrelenting, cumulative damage. A key reason so much disease occurs later in life is that these long half-lives result in progressively higher body levels as age increases.
This chapter focuses on the worst of the toxicants shown to induce CVD, where they come from, how their body load is assessed, and key strategies for increasing excretion from the body. Well recognized toxins like smoking are addressed elsewhere. Those who want to dive more deeply into the huge role of environmental toxins in chronic disease are encouraged to read Crinnion and Pizzorno, Clinical Environmental Medicine, Elsevier, 2018.
Cardiovascular Diseases Caused or Aggravated by Environmental Toxicants
The key toxicants for each cardiovascular dysfunction/disease are listed alphabetically to avoid misplaced concreteness. Although some toxicants are clearly worse than others, there is huge variability according to each person’s biochemical individuality, nutritional status, and exposure to other toxicants. Another challenge is that research on chronic, low level exposure to toxicants and disease risk as well as mechanisms of damage is still at an early stage. Some toxicants may appear worse simply because they have been subjected to more research or, like lead, have been damaging humans for much longer. This list includes those toxicants that increase disease risk at least 20% and have substantial research support. Also, of substantial significance is the fact that people are rarely exposed to a single toxicant. Because the average person is exposed to multiple toxins, their damaging effects are amplified (Table 34.1).
The Worst Cardiotoxins
Air Pollution (Indoor and Outdoor)
Inexplicably, the American Heart Association (AHA) website does not list air pollution as a significant modifiable cause of heart disease. An AHA expert panel published in 2004 the following1:
Table 34.1 DAMAGING EFFECTS OF MULTIPLE TOXINS | |
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Short-term exposure to elevated particular matter (PM) significantly contributes to increased acute cardiovascular mortality, particularly in certain at-risk subsets of the population.
Hospital admissions for several cardiovascular and pulmonary diseases acutely increase in response to higher ambient PM concentrations.
Prolonged exposure to elevated levels of PM reduces overall life expectancy by a few years.
A more recent expert panel report in 2015 added further support to the problem of air pollution and CVD2:
“There is now abundant evidence that air pollution contributes to the risk of cardiovascular disease and associated mortality, underpinned by credible evidence of multiple mechanisms that may drive this association. In light of this evidence, efforts to reduce exposure to air pollution should urgently be intensified and supported by appropriate and effective legislation.”
Another significant risk factor for CVD is solvent exposure such as found in beauty salons. The regular exposure experienced by salon workers causes an elevation in C-reactive protein (CRP) and 8-hydroxy deoxyguanosine (8-OHdG), indicating both inflammation and oxidative stress.3 These are nonpersistent toxicants as demonstrated by dramatic decreases in these measures on days when the salons were not working. CRP levels average 10.9 mg/dL when working but only 1.1 mg/dL when not working. 8-OHdG shows the same results, dropping from 4.5 to 0.6 ng/mL. This benefit from decreasing solvent exposure was significant, although VOC levels in the air dropped only from 75 to 44 ppb. Of concern is that their exposure was still significant away from their salon exposure.
This may be explained by the research on home use of indoor freshening sprays. Their use showed loss of heart rate variability proportionate to the frequency of use, with damage showing up at just one use a week.4 The same loss of heart rate variability was found with use of cleaning sprays and other home scented products.
Arsenic
According to the latest Centers for Disease Control and Prevention report, arsenic levels in the general US population are well into the toxic damage range (Fourth National Report on Human Exposure to Environmental Chemicals, Updated Tables, January 2019 https://www.cdc.gov/exposurereport/index.html). In general, the threshold for toxic effects is considered 10 µg/L of urine. As can be seen in Table 34.2, approximately 40% of the population exceeds this threshold.
Although most arsenic research is based on urinary levels, toenail arsenic is a better reflection of long-term exposure because of its short (2-4 days) half-life. Several studies have clearly demonstrated that blood pressure increases in proportion to arsenic levels.5 The STRONG heart study of Native Americans found a strong association between urinary arsenic and heart disease. Urinary arsenic levels of 15.7 µg/g creatinine compared with 5.8 µg/g creatinine had a 65% increased risk of CVD, 71% increased risk of coronary heart disease, and over threefold increased risk of stroke.6
Bisphenol A
BPA levels increase dramatically simply by eating food or drinking soy milk stored in cans. This is well demonstrated by the following figure. Compared with fresh lentil soup, one
12-oz serving daily for 1 week increases BPA levels 12-fold.7 Drinking just 6 oz of soy milk from cans rather than glass increases BPA levels by 16-fold and was shown to increase systolic blood pressure by approximately 4.5 mm Hg8 (Figure 34.1). Bisphenols are ubiquitous and damaging in many ways. Unfortunately, even just maternal exposure to BPA increases a child’s future risk for hypertension.9
12-oz serving daily for 1 week increases BPA levels 12-fold.7 Drinking just 6 oz of soy milk from cans rather than glass increases BPA levels by 16-fold and was shown to increase systolic blood pressure by approximately 4.5 mm Hg8 (Figure 34.1). Bisphenols are ubiquitous and damaging in many ways. Unfortunately, even just maternal exposure to BPA increases a child’s future risk for hypertension.9
Table 34.2 URINARY TOTAL ARSENIC (2009-2010), CAS NUMBER 7740-38-2, GEOMETRIC MEAN AND SELECTED PERCENTILES OF URINE CONCENTRATIONS (IN µG/L) FOR THE US POPULATION FROM THE NATIONAL HEALTH AND NUTRITION EXAMINATION SURVEY | ||||||||||||||
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NHANES PBA levels between 2003 and 2006 was used to compare self-reporting of CVDs with urinary BPA levels showed statistically significant risk.10 Table 34.3 shows the odds ratio per standard deviation for various CVDs, after adjusting for all other CVD risk factors. One of the problems with statistically eliminating standard risk factors is that many of these are actually also caused by BPA as well as other common toxicants. Nonetheless, the results are clear (Table 34.4).
Utilizing these data, the 25% of the population with a urinary BPA level of 3.70 to 5.50 were 34% more likely to have some form of CVD. Those in the 95th percentile would have doubled risk. A study in the United Kingdom compared adults without coronary artery disease with those with severe coronary artery disease and found a mean urinary BPA of 1.28 ng/mL in the former and 1.53 ng/mL in the latter.11 Those with higher urinary BPA are 43% more likely to have severe CAD. However, I cannot help but wonder if the latter group spent more time receiving medical procedures that entailed fluids from PBA–contaminated medical tubing. At this time, such medical BPA exposure has only been documented as problematic in neonates. Risk of developing CAD over 10 years was shown in a large European study to correlate with BPA levels.12 A study in Swedish showed a similar positive association between BPA and carotid atherosclerosis.13
 Figure 34.1 Storing food in cans greatly increases bisphenol A levels. |
Cadmium
Cadmium is a serious persistent metal toxin that concentrates in the kidneys. Primary sources are cigarette smoking and nonorganic soy products. The threshold for increased disease risk is 0.40 µg/g. As can be seen from the following table, greater than 30% of population exceeds this level (Table 34.5).
Table 34.3 INCREASED RISK OF CARDIOVASCULAR DISEASE BY STANDARD DEVIATION OF BPA | ||||||||||||
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Table 34.4 URINARY LEVELS OF BISPHENOL A (BPA) IN NHANES 2002-2006 (IN NG/ML) | ||||||||||||||||||||||||
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Lead
The good news is that lead levels are going down as shown in the following table (Table 34.6). Public health measures to decrease environmental toxins have clearly worked. The bad news is that there is still enough lead in the general population to increase the risk of many diseases, especially cardiovascular. And because lead is stored primarily in bone, older people losing bone are at increased risk of toxicity.
Lead causes cardiovascular damage in many ways. This is also covered in standard medical textbooks. Typical examples are elevation of blood pressure by causing renal damage, reduction of available nitric oxide, oxidative damage, increase in circulating vasoconstrictive prostaglandins, and alterations to the renin-angiotensin system.16
As the general population levels have decreased, so has the ratio of increased risk of those in the highest quartiles. For example, women in the top quartile of NHANES 1988 to 1994 had an 8.1 OR of both systolic and diastolic hypertension.17 But NHANES 2003 to 2010 analysis found only a slight nonsignificant association between hypertension and blood lead.18
Table 34.5 BLOOD CADMIUM (2009-2010), CAS NUMBER 81271-94-5, GEOMETRIC MEAN AND SELECTED PERCENTILES OF BLOOD CONCENTRATIONS (IN µG/L) FOR THE US POPULATION FROM THE NATIONAL HEALTH AND NUTRITION EXAMINATION SURVEY | ||||||||||||||
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Methyl Mercury
All forms of mercury are toxic, and humans are regularly exposed to many of them. The methyl form may be the most damaging, but the other forms are toxic in many ways as well (Table 34.7).
Because the intake of high-omega-3 fish has been shown to decrease CVD, fish is now a commonly recommended dietary intervention.21 Unfortunately, some of these fish are also heavily contaminated with the very toxic methyl mercury, which negates many of the benefits.22 NHANES 1999 to 2000 showed that, for each 1.3 µg/L increase in mercury, the systolic blood pressure increased almost two points.23 One of the earliest manifestations is elevation of blood pressure.24
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