New Study Compares Air Pollution to “Smoking a Pack of Cigarettes per Day”

New Study Compares Air Pollution to “Smoking a Pack of Cigarettes per Day”

While we know that heart disease is the leading cause of death for both men and women, physicians still debate what causes atherosclerosis (hardening of the arteries). This “stiffening” gives rise to what we see clinically as heart attack, stroke, and peripheral vascular disease. Approximately one-half of all Americans have at least one of the following “key” risk factors of heart disease (CDC, 2011): 

  • High Blood Pressure
  • High LDL Cholesterol
  • Cigarette smoking

But these risk factors are an oversimplification. Recognizing that blood pressure, LDL-C, and smoking status weren’t enough to explain heart disease, researchers found that certain medical conditions and lifestyle choices also put people at a higher risk, including: 

  • Diabetes 
  • Overweight/Obesity 
  • Poor Diet 
  • Lack of Exercise
  • Excessive Alcohol Consumption

Even still, this is missing the bigger picture. Despite all the years and money spent in research, do we really believe we’re any closer to solving heart disease? 

In the U.S., someone has a heart attack every 34 seconds, and each minute, more than one person dies from a heart disease-related event (Heron, 2016). This equates to around 630,000 lives lost from heart disease each year, which is 1 in every 4 deaths (CDC & NCHS, 2017). With a cost of $200 billion each year—including health care services, medications, and lost productivity—, I argue that the U.S. is no closer to solving heart disease than when it started. 

Why? Because we are not thinking differently about this real crisis. First, heart disease does not discriminate. Heart disease is, in fact, the leading cause of death for people of most racial and ethnic groups in the United States, including African Americans, Hispanics, and whites. For Asian Americans, Pacific Islanders, American Indians, and Alaska Natives, heart disease is second only to cancer (Benjamin et al., 2017). More on this later…


Maybe 1 out of 4 of us are supposed to die from heart disease? Maybe that’s just the way it is. However, our genes haven't changed. Our environment has. Could it be that there is a profound mismatch between our polluted environment and previous circumstances that have produced the aberrant health outcomes we see today? The answer is yes.

Thinking differently, if you asked our ancestors what were life’s top two most vital elements, air and water would have been the unanimous answers. Without water, you would only survive for a few days. Without air, a few minutes.

Given these simple truths, wouldn’t it make sense that, because every person inhales thousands of gallons of air each day, air would be the greatest potential source of toxicant exposure known to humankind? 

As a dated example, we’ve known for generations that occupational exposure to air contaminated with chemical compounds in coal or radioactive dust can lead to black lung disease or lung cancer. The correlation was uncanny; hence, connections were made and occupational safety officers put in place systems and protocols to protect workers exposed to such hazardous air quality. More recently, similar protections were put in place after major cities’ air quality decreased due rising concentrations of gaseous lead found in gasoline exhaust. Unfortunately, lead-containing fuel is still sold for “off-road uses” to this day.

Sometimes we can’t see what’s around us. Out of sight, out of mind. This is why many of us assume that we can simply avoid poor air quality by refraining from occupational exposure or, at most, steering clear of tobacco use and second-hand smoke. But the truth is, even at home, the air you breathe inside is the same air you breathe outside. This is why we all have to care about air pollution.

Environmental Health Perspectives recently published a study that followed a sizable population (6,619 adults, between 45-84 years old) without cardiovascular disease or other health conditions to understand if there was an association between ground ozone exposure (i.e. vehicular exhaust emissions, smoke from nearby factories, etc.) and atherosclerosis. After almost a decade of follow-up, researchers found a strong association between long-term ozone exposure and an increased rate of carotid wall thickness progression and risk of new plaque formation (Wang et al., 2019). The carotid arteries are the two large vessels that supply blood to the head and neck. Injury here can have grave consequences.

What is Ground-level Ozone?

We essentially have two ozones: one in the sky that protects us and one on the ground made by humans. The ozone here on the ground is a powerful oxidizing agent. It is frequently referred to as “smog”, and is thought to be one of the most harmful air pollutants currently assessed by air quality standards in the U.S. and European Union (Wang et al., 2019). Ground-level ozone is produced via a complex set of chemical reactions triggered by sunlight and heat (EPA, 2013). Thus, as the planet gets warmer, we’re going to see a rise in cardiovascular events in polluted and non-polluted areas (remember, air travels across borders).

To make matters worse, ground-level ozone is not going anywhere. Over the past few decades, ground-level ozone has not markedly decreased in either the U.S. or Europe, and it will remain a persistent environmental health issue, by and large due to the projected increases in temperature related to global climate change (EEA 2015).

What Happens When You Breathe Ground-level Ozone?

According to the American Lung Association, ground-level ozone (i.e. gas molecules) likely damages lungs when inhaled. One suggested pathway is the production of reactive oxidative species (ROS) from the interaction of ozone with cellular membranes (i.e. lipids) in the lung. These ROS are then released into the circulatory system where they can damage other cells throughout the body. ROS propagates a systemic inflammatory response. It’s like a domino effect—a cascade of injury we can’t initially feel. Persistent exposure to ground-level ozone and/or repeated activation of this pathway is likely the mechanism that leads to the development of arterial injury (Cosselman et al., 2015).

This pathophysiologic story appears to play out similarly in both human and animal studies. In a mouse model, inhaled ozone increased plaque formation (atherogenesis), arterial wall dysfunction, oxidative stress, and mitochondrial DNA damage (Chuang et al., 2009). In young, healthy volunteers, exposure to outdoor ground-level ozone increased platelet activation, blood pressure, and vascular markers of inflammation relative to clean air, after controlling for the effects of PM2.5 and NO2 (Day et al., 2017).

Obviously, it would be incredibly unethical to expose populations of humans to varying degrees of toxic air; hence, much of what we know depends on associations between ambient air quality and human diseases. In addition to respiratory effects of long-term exposure to ground-level ozone (Jerrett et al., 2009), higher concentrations were associated with total mortality (Di et al., 2017) and cardiovascular mortality (Turner et al., 2016) and its subtypes, ischemic heart disease (Jerrett et al., 2013), cerebrovascular disease (Turner et al., 2016), and mortality risk among people with congestive heart failure (Zanobetti & Schwartz, 2011).

Putting it all together, simple risk factors like high blood pressure and high LDL-C are not accurately addressing the epidemic that is heart disease, especially when you consider the fact that almost 50% of patients experiencing heart attacks have normal lipid levels (Sachdeva et al., 2009). Something else is going on.

If you only reduce LDL, there's likely no benefit in reducing your risk of heart disease. If you reduce LDL and chronic inflammatory markers, you're likely to benefit. Inflammation is the differentiating variable. Atherosclerosis is NOT a disease of the lumen (the interior of the vessel), it is a disease of an inflamed vessel wall constantly under attack due to an environment that is not conducive to our cellular health. 

Read more about how to protect your lungs here: 

How To Keep Your Lungs Healthy and Respiratory Health

Dr. Bhandari and the Advanced Health Team Are Here to Support Your Health. Our team of experts work to help patients overcome life’s inflammatory battle, including persistent air pollution—even in a city like San Francisco! We can test patients’ industrial toxicants, and provide a personalized approach on how to effectively detoxify. Our expertise and two decades of clinical experience is proactively reversing heart disease. To book an appointment, contact Advanced Health or call 1-415-506-9393.

 

References

Benjamin, E. J., Blaha, M. J., Chiuve, S. E., Cushman, M., Das, S. R., Deo, R., ... & Jiménez, M. C. (2017). Heart disease and stroke statistics-2017 update: a report from the American Heart Association. Circulation, 135(10), e146-e603.

Centers for Disease Control and Prevention (CDC, 2011). Million hearts: strategies to reduce the prevalence of leading cardiovascular disease risk factors--United States, 2011. MMWR. Morbidity and mortality weekly report, 60(36), 1248.

Centers for Disease Control and Prevention, & National Center for Health Statistics. (CDC & NCHS, 2017). Multiple Cause of Death 1999-2015 on CDC WONDER Online Database, released December 2016. Data are from the Multiple Cause of Death Files, 1999-2015, as compiled from data provided by the 57 vital statistics jurisdictions through the Vital Statistics Cooperative Program.

Chuang, G. C., Yang, Z., Westbrook, D. G., Pompilius, M., Ballinger, C. A., White, C. R., ... & Ballinger, S. W. (2009). Pulmonary ozone exposure induces vascular dysfunction, mitochondrial damage, and atherogenesis. American Journal of Physiology-Lung Cellular and Molecular Physiology, 297(2), L209-L216.

Cosselman, K. E., Navas-Acien, A., & Kaufman, J. D. (2015). Environmental factors in cardiovascular disease. Nature Reviews Cardiology, 12(11), 627.

Day, D. B., Xiang, J., Mo, J., Li, F., Chung, M., Gong, J., ... & Zhang, Y. (2017). Association of ozone exposure with cardiorespiratory pathophysiologic mechanisms in healthy adults. JAMA internal medicine, 177(9), 1344-1353.

Di, Q., Wang, Y., Zanobetti, A., Wang, Y., Koutrakis, P., Choirat, C., ... & Schwartz, J. D. (2017). Air pollution and mortality in the Medicare population. New England Journal of Medicine, 376(26), 2513-2522.

European Environmental Agency (EEA, 2015). Air Pollution Due to Ozone: Health Impacts and Effects of Climate Change. Retrieved from: https://www.eea.europa.eu/data-and-maps/indicators/air-pollution-by-ozone-2/assessment.

Heron, M., & National Vital Statistics Reports. (2016). Deaths: Leading causes. National Vital Statistics Report, 65(5).

Jerrett, M., Burnett, R. T., Beckerman, B. S., Turner, M. C., Krewski, D., Thurston, G., ... & Gapstur, S. M. (2013). Spatial analysis of air pollution and mortality in California. American journal of respiratory and critical care medicine, 188(5), 593-599.

Jerrett, M., Burnett, R. T., Pope III, C. A., Ito, K., Thurston, G., Krewski, D., ... & Thun, M. (2009). Long-term ozone exposure and mortality. New England Journal of Medicine, 360(11), 1085-1095.

Sachdeva, A., Cannon, C. P., Deedwania, P. C., LaBresh, K. A., Smith Jr, S. C., Dai, D., ... & Fonarow, G. C. (2009). Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines. American heart journal, 157(1), 111-117.

Turner, M. C., Jerrett, M., Pope III, C. A., Krewski, D., Gapstur, S. M., Diver, W. R., ... & Burnett, R. T. (2016). Long-term ozone exposure and mortality in a large prospective study. American journal of respiratory and critical care medicine, 193(10), 1134-1142.

U.S. Environmental Protection Agency. (EPA, 2013). Integrated Science Assessment (ISA) for Ozone and Related Photochemical Oxidants. EPA/600/R-10/076F. Washington, DC:U.S. EPA.

Wang, M., Sampson, P. D., Sheppard, L. E., Stein, J. H., Vedal, S., & Kaufman, J. D. (2019). Long-Term Exposure to Ambient Ozone and Progression of Subclinical Arterial Disease: The Multi-Ethnic Study of Atherosclerosis and Air Pollution. Environmental health perspectives, 127(5), 057001.

Zanobetti, A., & Schwartz, J. (2011). Ozone and survival in four cohorts with potentially predisposing diseases. American journal of respiratory and critical care medicine, 184(7), 836-841.

Content Source

National Center for Chronic Disease Prevention and Health Promotion , Division for Heart Disease and Stroke Prevention

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