The following is a reprint of a letter from Dr. C. Arden Pope III addressing the recent controversy whether Beijing’s daily air pollution exposure PM2.5 is equivalent to 1/6 of a cigarette (my 2013 estimate, which you can read here, using Dr. Pope’s research), or to 38 cigarettes, as recently suggested by a new study with the accompanying media commentary and press releases by Dr. Richard Muller at Berkeley Earth. Dr. Muller, Dr. Pope and I have been corresponding via email this week and Dr. Muller has also already reviewed Dr Pope’s letter below and agrees with the general conclusions. Dr. Pope has given permission to publish this letter. I am preparing a blog article discussing this discrepancy but thought my readers should read this letter first.
You can skip to the “Discrepancy in excess risk…” section below to get to the most important parts, but otherwise the take-home message is, as Dr Pope says below, “air pollution is associated with a much higher excess risk and loss of life expectancy compared to cigarette smoking than would be expected based on the comparative dose of fine PM.” He offers three potential explanations for this discrepancy, all of which would require further research.
How can burden of disease from exposure to air pollution be comparable to cigarette smoking given enormous dose differences?
C. Arden Pope III, PhD
Mary Lou Fulton Professor,
Brigham Young University
Recent studies estimate the burden of disease from air pollution in some parts of the world (such as highly polluted cities in China) to be comparable with that from cigarette smoking. For example, the recent global burden of disease (GBD) estimated that 3.2 million deaths per year worldwide were attributed to ambient fine particulate matter (PM) air pollution (Lim et al. 2012). A recent study from Berkeley Earth (Rohde and Muller, 2015) estimates that in China alone fine PM air pollution contributes to approximately 1.6 million deaths (or roughly 17% of all deaths in China). These estimates of air pollution’s contribution to loss of life are comparable with, and for some areas, even greater than estimates from cigarette smoking. Is this possible given huge differences in dose to the body from mainstream tobacco smoke from active smoking versus breathing air pollution?
Doses of fine PM from different sources
Active cigarette smoking
When a smoker smokes a cigarette, the cigarette smoke, including fine PM and gases, are sucked through the tobacco rod and the filter. The fine PM from this cigarette smoke, excluding the nicotine and water, is commonly referred to as “tar”. A standardized smoking-machine test using the Federal Trade Commission (FTC) protocol has been used to estimate the doses (or yields) of tar and nicotine from various cigarettes. Sales-weighted tar yields, since the mid-1990s, based on this protocol have been approximately 12 mg (or 12,000 μg) per cigarette (National Cancer Institute 2001). A range of somewhat similar estimates of the dose of tar or fine PM come from multiple analyses (Martin et al. 1997; Djordjevic et al. 2000; Repace 2007). Cigarette yield estimates clearly depend on type of cigarette and other cigarette characteristics. Furthermore, the average daily dose of fine PM from active smoking is also highly dependent on more than just the cigarette yields estimates. Individual smoking patterns and habits play a critical role in determining actual fine PM exposures (National Cancer Institute 2001).
Ambient air pollution
The average daily dose of fine PM to the lung from breathing air pollution is dependent primarily on two factors: 1) the concentration of fine PM in the air being breathed (typically measured as in μg/m3 of fine PM) and 2) the daily inhalation rates (m3/day). Measured concentrations of long-term mean ambient fine PM range from as low as approximately 5 (or less) μg/m3 in very clean communities to as high as approximately 100 (or more) μg/m3 in highly polluted communities. Inhalation rates vary depending on age, sex, body size, activity levels and other factors, but estimates average volume of air inhaled by adults ranges from approximately 13 to 23 m3/day (Allan et al. 2008; Brochu et al. 2006; Layton 1993; Stifelman 2007; USEPA 1997). Assuming an inhalation rate of 18 m3/day, the approximate average dose of fine PM from air ambient air pollution could range from 90 μg (5 x 18) to 1,800 (100 x 18) μg per day.
Second hand smoke
Similar to exposures from ambient air pollution, the average daily dose of fine PM to the lung from breathing second hand smoke (SHS) is dependent primarily on two factors: 1) the average increase in concentration of fine PM from being exposure to SHS and 2) the daily inhalation rates (m3/day). There is limited information regarding the increase in concentrations of fine PM that comes from SHS, but one study suggests that homes with a smoker of one pack of cigarettes per day contributed about 20 μg/m3 to 24-hr indoor fine PM concentrations (Spengler 1991). Again, assuming an inhalation rate of 18 m3/day, the approximate average dose of fine PM from living with a smoker that smokes one pack of cigarettes per day would equal approximately 360 (20 x 18) μg per day.
Discrepancy in excess risk from smoking versus air pollution:
Comparing these estimated doses demonstrates that the doses of fine PM from air pollution or second-hand cigarette smoke are only a small fraction of the dose associated with active cigarette smoking. Yet, empirical studies of smoking indicate that smoking 20-40 cigarettes per day increases mortality risk by approximately 100 % (U.S. Department of Health and Human Services 2010; Pope et al. 2009; Pope et al. 2011) reducing life expectancy by approximately 8 years (Pope and Dockery 2013; Dockery and Pope 2014). Long-term exposure to fine particulate air pollution in highly polluted cities increases mortality risk by approximately 30% and reduces life expectancy by as much as approximately 3 years (Pope et al. 2002; Pope, Ezzati, Dockery 2009; Pope et al. 2011; Pope and Dockery 2013; Dockery and Pope 2014). Air pollution is associated with a much higher excess risk and loss of life expectancy compared to cigarette smoking than would be expected based on the comparative dose of fine PM.
It is informative to note that a similar dilemma also occurs for SHS exposures which are also only a small fraction of doses associated with active cigarette smoking. The excess risks of cardiopulmonary disease mortality from SHS (of about 20 to 30) are similarly disproportionately larger than would be expected based simple on comparative dose. In fact, the elevated fine PM exposures and excess mortality risks for SHS and air pollution are remarkably similar.
Potential explanations for this discrepancy
Supralinear exposure-response function
Recent studies that have integrated information from exposures to air pollution, SHS, and active smoking indicate that the exposure-response relationship, especially for cardiopulmonary diseases, is non-linear with a steep increase in risk at low exposures, flattening out at higher exposures (Pope et al. 2009; Pope et al. 2011; Burnett et al. 2014). There is evidence of a “saturation phenomenon” where relevant biological pathways for cardiopulmonary disease may be activated at low levels of exposure, and that increasing exposure further increases risk, but at a decreasing marginal rate.
Although the potential differential toxicity of fine particulate matter air pollution from various sources is not fully understood, fine PM from the burning of coal, diesel, and other fossil fuels as well as high temperature industrial processes may be more toxic than particles from the burning of tobacco. However, this potential explanation does not explain the disproportional excess risk from SHS and some have even suggested differential toxicity regarding SHS exposure versus mainstream exposures.
Ubiquitous exposure to air pollution
Essentially all individuals living in polluted communities are exposed, including the most vulnerable individuals such as infants, children, persons with existing coronary artery disease, chronic obstructive pulmonary disease, etc.
Combination of factors
It is likely that all three of the above potential explanations are relevant and play a role. Further discussion can be found in Pope et al. 2009; Pope et al. 2011; Burnett et al. 2014.
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U.S. EPA. 1997. Exposure Factors Handbook. EPA/600/C-99/001. Office of Research and development, Washington, DC, USA.
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