Environmental factors generally receive little attention concerning how they influence the development of cardiovascular disease yet they can play a major role. Large numbers of studies now implicate environmental toxins, particularly air pollution and persistent organic pollutants (POPs), in many of the risk factors associated with CVD, including high blood pressure, heart attacks, strokes and even Alzheimer's disease.
Considerable evidence exists to prove that air pollution contributes to inflammation and oxidation throughout the body and, in turn, leads to an increased risk of heart attack, stroke, heart failure and a number of chronic diseases including diabetes and asthma. Put simply, air pollution has a similar effect on blood vessels as smoking cigarettes. Air pollution from traffic and other sources is an established cause of premature mortality.(1) Acute events such as heart attack or stroke can be triggered by short-term exposure to air pollution.(2)
Exposure to air pollutants, particularly pollutants caused by motor traffic, increases the risk of a fatal heart attack.(3) These environmental agents can influence the heart, as they can change a person's heart rate and rhythm, alter the heart's excitability and the contractibility of heart muscle, and cause atherosclerosis.(4)
The association between air pollution and intima media thickness (IMT), an established marker of subclinical atherosclerosis, was reported for the first time in volunteers participating in two clinical trials in California.(5) Two population-based cross-sectional analyses (6) also reported associations between air pollution and IMT.
A study of 2,780 participants found indicators of air pollution nitrogen dioxide (25 µg/m3), traffic intensity on the nearest street (15,000 vehicles/day), and traffic load within 100 metres were associated with increased intima media thickness (IMT).(7)
Blood Pressure IncreaseMany observational studies in humans have found that within hours to days following exposure to air pollution, blood pressure increases. In animals, a 10 week study of hypertensive rats found that short-term exposure to air pollution elevates blood pressure in rats already predisposed to the condition.(8) Other studies have shown that diesel exhaust inhalation causes cardiovascular dysfunction including impaired vascular reactivity, increased blood pressure, and arterial stiffness. It is now well established that diesel exhaust inhalation disturbs normal vascular homeostasis and nitric oxide (NO) generation, which is involved in relaxing the artery wall muscles.(9)
Scientific studies have shown that air pollution is particularly hazardous to people with pre-existing cardiopulmonary diseases. Many studies already have linked fine particulate matter - which comes largely from vehicles and industries that burn fossil fuels - to heart risks and increased risk of premature death from cardiopulmonary disease,(10) including heart disease, insulin resistance (IR) and diabetes - all conditions that are characterised by inflammation.
Particulate air pollution can exacerbate an individual's risk of heart failure through a variety of mechanisms. Factors that enhance the clotting of blood are increased, as are fibrinogen levels and platelet aggregation. With particulate matter exposure, the viscosity of blood also increases. The variability of heart rate declines, which leads to arrhythmias. These factors may ultimately lead to an elevation in the incidence of heart disease.(11)
Diabetes RiskA number of studies have found a consistent and significant relationship between prevalence of type 2 diabetes and exposure to air pollution, especially ultrafine particulate matter.(12) Other studies have found that people who live in areas with high levels of traffic-related air pollution may face an increased risk of developing diabetes. After studying 52,000 residents of Denmark, researchers found that people living in urban areas with high levels of traffic pollution were four percent more likely to be diagnosed with diabetes than people living in neighbourhoods with cleaner air. The results suggest that air pollution may actually contribute to the development of diabetes. The link between long-term exposure to air pollution and diabetes also appeared to be greater in women. In an earlier study, the same researchers reported that people who live in areas with high levels of traffic-related pollution also might be at a slightly increased risk of dying from stroke.(13)
Metabolic SyndromeThose with enhanced susceptibility to the toxicity of air pollutants may include individuals with metabolic syndrome; the link between morbidity and mortality due to diabetes and exposure to ambient air pollution is well documented.(14) For example, exposure to PM2.5 (small particle matter less than 2.5 micron- 0.0025 mm) is associated with enhanced vascular reactivity (15) and cardiac function abnormalities (16) in diabetics. Acute cardiovascular responses to ozone (O3) exposure are also exaggerated, with increased heart rate (HR)(17) and decreased blood pressure (BP).(18) In addition, obesity and hypertension, common comorbidities of both metabolic syndrome and diabetes, are themselves susceptibility factors for adverse responses to PM2.5.(19) In epidemiological studies, elevated ambient concentrations of PM2.5 or carbon monoxide are linked to greater decreases in heart rate variability in metabolic syndrome subjects compared to healthy subjects.(20) In addition, small increases in urban ambient PM2.5 can decrease insulin sensitivity in healthy subjects,(21) suggesting that PM2.5 may contribute to the cause of metabolic syndrome or to the progression from metabolic syndrome to diabetes. Given the high prevalence of metabolic syndrome, the cardiovascular and metabolic health risk of exposure to ambient pollutants may be substantial.
Similar results have also been documented in animal studies. Rats that had induced metabolic syndrome (hypertensive and insulin resistant, and had elevated fasting levels of blood glucose and triglycerides) had more pronounced changes in heart rate and blood pressure compared to normal rats. The changes were also greater and more persistent, and lasted longer, in metabolic syndrome rats compared with those fed a normal diet.(22) These results in rodents suggest that people with metabolic syndrome may be prone to similar exaggerated blood pressure and heart rate responses to inhaled air pollutants.
Ultrafine particulates exposureAnimal studies have also found early exposure to ultrafine particulates led to the accumulation of abdominal fat, insulin resistance and increased inflammation in mice even if they ate a normal diet.(23) The study compared mice fed a high-fat diet with those fed a normal, healthy diet, and exposed some members of each group daily to ultrafine particulate matter. In the end, all of the mice exposed to air pollution, including those fed a normal diet, had increased abdominal and subcutaneous (under the skin) fat. These findings suggest that fine particulate pollution exposure alone, in the presence of a normal or high-fat diet, may lead to an increase in fat cell size and number, and also have a pro inflammatory effect. The data also suggest a high-fat diet may exacerbate the health effects of inhaled PM2.5; therefore obese people also appear to be at increased risk.
Breathing large particles, not just small (PM2.5), also seems to affect the heart. People in a rural community experienced changes in their blood pressure and heart rates when they inhaled unfiltered local air that contained large particles, mostly from windblown dust and soil. In a controlled laboratory study of 32 adults in a chamber, volunteers inhaling unfiltered air had increased blood pressure (both systolic and diastolic). Blood pressure increased linearly every 10 minutes, and the subjects' heart rates were elevated compared to the times they inhaled the filtered air.(24)
Animal studies link exposure to combustion hydrocarbon products from fossil fuels called PAHs (poly-aromatic hydrocarbons) to inflammation and subsequent development of diabetes mellitus. In addition, occupational studies suggest that exposure to PAHs may be associated with diabetes risk in humans. In a large US population-based study, researchers found a positive association between urinary biomarkers of PAH and diabetes mellitus. Compared to participants with the lowest PAH biomarkers, the risk of diabetes mellitus among those with the highest exposure was 3.1, or 310%, higher.(25) In another large observational study, researchers found exposure to PAHs was associated with increased heart rate variability.(26)
Persistent organic pollutantsIn recent years, studies have increasingly associated exposure to environmental pollutants such as persistent organic pollutants (POPs) like PCBs, dioxin and pesticides to cardiovascular problems, including high blood pressure, heart attack and diabetes. In one study of 1,016 adults aged 70 or older, seven of the POPs studied were significantly associated with the number of carotid arteries plaques, even after adjustment for multiple risk factors.(27) People with relatively high levels of certain pesticides in their blood have an increased risk of type 2 diabetes, particularly if they are overweight. In a study of approximately 2,000 older adults, the risk was higher among people with the highest levels of organochlorine pesticides in their blood. Those with levels in the top 10% were about twice as likely to have diabetes as their counterparts in the bottom 10%, but only in people who were overweight or obese. It seems that pollutants and body fat "may have a synergistic effect on the risk of type 2 diabetes."(28)
There is emerging evidence that exposure to persistent organic pollutants (POPs) also plays an important role in weight gain. Blood serum levels of POPs, such as polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and organochlorine pesticides have been associated with increasing body mass index, elevated triglyceride levels, abdominal obesity, and cardiovascular diseases.(29) In animal studies, POPs have been associated with body weight gain, insulin resistance, abdominal obesity, hepatosteatosis (fatty liver) and atherosclerosis.(30)
"Obesogens" (chemicals that increase the risk of obesity) are hypothesised to be environmental chemicals that promote obesity directly by increasing adipocyte size and/or number, or indirectly by altering metabolic homeostasis or interfering with regulation of appetite and satiety, suggesting that environmental chemicals can regulate lipid metabolism and adipogenesis, and thus promote obesity.(31)
Hexabromocyclododecane (HBCD) is an additive flame retardant used in the textile industry and polystyrene foam manufacturing. Because of its lipophilicity (ability to dissolve in fats) and persistency, HBCD accumulates in adipose tissue and thus has the potential to cause metabolic disorders through disruption of lipid and glucose homeostasis. Mice fed a diet high in HBCD (700 μg/kg) and medium-dose of HBCD (35 μg/kg) had markedly increased body and liver weight. This effect was more prominent in the high-dose group. The findings suggest that HBCD may contribute to the enhancement of diet-induced body weight gain and metabolic dysfunction through disruption of lipid and glucose homeostasis, resulting in accelerated progression of obesity.(32)
Weight Gain in ChildrenResearch also shows a link between prenatal exposure to persistent organic pollutants and weight gain in children.(33) Children exposed to certain persistent chemicals in the womb have a higher risk of being overweight. The results add to growing evidence that suggests POPs - by acting as endocrine disruptors - can influence weight gain. The developing foetus is exposed to POPs passed from the mother through the placenta. In a study of 344 children on island of Menorca, researchers found that both PCB and DDE exposure led to an increased risk of weight gain in children as assessed by BMI scores. The link between being overweight and PCB and DDE levels in cord blood was stronger in girls than boys. DDT was associated only with weight gain in boys, especially in children with average or above-average fat intakes. In some cases, children with higher POPs exposures were almost twice as likely to be overweight compared to children with lower exposures, depending on the pollutant and the child's gender.
Ubiquitous BPABisphenol A (BPA) is an industrial chemical that has become ubiquitous in its use in water bottles, food cans and even dental sealants. Higher levels of urinary Bisphenol A (BPA) are associated with cardiovascular disease, type 2 diabetes and liver-enzyme abnormalities. In a study, a very small increase in BPA concentration was associated with a 39% increased risk of cardiovascular disease (angina, coronary heart disease, or heart attack combined) and diabetes. Participants in the highest BPA concentration had nearly three times the risk of cardiovascular disease compared with those in the lowest concentration. Similarly, those in the highest BPA concentration had 2.4 times the risk of diabetes compared with those in the lowest. In addition, higher BPA concentrations were associated with clinically abnormal concentrations for three liver enzymes.(34)
Research has shown that BPA can interfere with cardiac rhythm. Parts-per-trillion concentrations of BPA triggered heart muscle cells to begin beating to their own internal drummers. BPA mimics the hormone oestrogen in the body. The researchers linked this finding to oestrogen's effect on calcium, which plays a pivotal role in heart-cell contractions. Both oestrogen and BPA - especially together - fostered a leakiness of calcium within female heart cells.(35) Researchers reported that delivering equal doses of oestrogen and BPA increased the cardiac effect more than would be the case from doubling the dose of either alone.
Since worldwide BPA production has now reached approximately seven billion pounds per year, eliminating direct exposures from its use in food and beverage containers will prove far easier than finding solutions for the massive worldwide contamination. Already many countries have taken steps to minimise BPA exposure.
DISCLAIMER: Dr Peter Dingle is a researcher, educator and public health advocate. He has a PhD in the field of environmental toxicology and is not a medical doctor.
1. Brook et al. 2010.
3 Karolinska Institute 2005.
4 Schwartz and Morris 1995.
5 Künzli et al. 2005.
6 Bauer et al. 2010; Diez Roux et al. 2008.
7 Rivera et al.; Künzli et al. 2010.
8 Sun et al. 2008.
9 Langrish et al. 2013.
10 Schwartz and Morris 1995.
12 Pearson 2010.
13 Diabetes Care, online November 10, 2011.
14 Ostro et al. 2006; Zanobetti and Schwartz 2011.
15 O'Neill et al. 2005.
16 Baja et al. 2010.
17 Hampel et al. 2012.
18 Hoffmann et al. 2012.
19 Dubowsky et al. 2006.
20 Min et al. 2009; Park et al. 2010.
235 Brook et al. 2013.
22 Wagner et al.
23 Arteriosclerosis, Thrombosis, and Vascular Biology; Rajagopalan 2014.
24 Brook et al. 2014.
25 Alshaarawy et al. 2013.
26 Feng et al. 2014.
27 Lind et al. 2011.
28 Airaksinen et al. 2011.
29 Ibid; Ha et al. 2007; Lee et al. 2012; Uemura et al. 2009.
30 Arsenescu et al. 2008; Ruzzin et al. 2010.
31 Hamilton 2002; Grün and Blumberg 2007; Newbold 2010.
32 Yanagisawa et al.
33 Valvi et al. 2011.
34 Melzer et al. 2008.
35 Yan et al. 2011; Yan et al. 2013; Gao et al. 2013.
Dr Peter Dingle (PhD) has spent the past 30 years as a researcher, educator, author and advocate for a common sense approach to health and wellbeing. He has a PhD in the field of environmental toxicology and is not a medical doctor. He is Australia’s leading motivational health speaker and has 14 books in publication.