DEADLY GASES: Respiratory Consequences of Air Pollution

Sridhar Prasad, MD

In 1775, Percival Pott published a treatise on cancer of the scrotum, a disease entity almost solely linked to chimney sweepers. He elaborated two lines of evidence supporting the causal relationship between chimneys and scrotal cancer: the epidemiological observation that the tumor was almost exclusively noted in boys employed as chimney sweepers, as well as the observation that “the disease, in these people, seems to derive its origin from a lodgment of soot in the rugae of the scrotum.”[1] This description is widely credited as the first epidemiological observation linking an occupation to cancer. It is probably also one of the earliest observations linking air pollution with human disease. The prevalence of scrotal cancer did not decline until the 1940s, when heating shifted away from chimneys towards other technologies.

In December 1952, a dense smog descended on London, with “pea soup” air permeating the streets and into homes. This event probably was a consequence of industrial air pollution, cold weather, and “anti-cyclones” that prevented winds from dissipating the pollution.[2] The event, subsequently called “The Great Smog,” lasted four days, with a surge in mortality occurring in the months that followed. Initially, the excess mortality was thought to be limited to 3-4 months after the event, was attributed to influenza and other lung infections, and was thought to number 3,000 to 4,000 deaths. Subsequent analysis suggested that the footprint of excessive mortality lingered for a full year and carried a total tally as high as 12,000 attributable deaths. The ultimate outcome of The Great Smog was a persistent legislative interest in mandating clean air in industrialized nations.

Since these reports, it has become clear that the combustion of flammable substrates, so vital for our economy, leads to the elaboration of a host of different gases into the atmosphere, with far-reaching climate and health-related outcomes. Several of these gaseous pollutants have been linked to human disease.

The combustion of fossil fuels leads to the elaboration of five major classes of gaseous pollutants:

Carbon dioxide is the most well-known product of combustion and is a classic example of a greenhouse gas.

Carbon monoxide is a product of incomplete combustion and is directly toxic by binding to hemoglobin irreversibly and rendering it dysfunctional.

Sulfur oxides are the major causative agent of acid rain. The sulfur usually reflects impurities in the fuel source.

Nitrogen oxides are a consequence of the direct interaction between oxygen and nitrogen prevalent in the air at the high temperatures associated with combustion.

Fine particulate matter (FPM) reflects particles of liquid or solids, aerosolized into the air. These are further divided into 10µM size (FPM-10) and 2.5µM size (FPM-2.5). In general, particles larger than 10µM tend to be entrapped by the mucociliary system of the airways, and do not deposit in the small airways and microcirculation of the lungs.

The research predominantly links FPM and sulfur oxides to human disease and death. The other gases (nitrogen oxides, carbon dioxide and carbon monoxide) are often simultaneously produced with FPM and sulfur oxides, but the relationship between the other gases and human disease is not clearly shown.[3] Animal models suggest that all five gases can be linked to human disease, but human experiments have not confirmed this. Most measurements of air pollution levels, as performed by governmental organizations, focus on FPM and sulfur dioxides.

The mechanisms by which these gases cause death and disease are incompletely understood. The most common hypothesis is that inflammation occurs when the gases breach into the bloodstream. According to this hypothesis, the pollutants evade the mucociliary clearance system and deposit in the alveoli and small airways of the lungs. From there, they are absorbed into the bloodstream, where they are pro-inflammatory and can precipitate acute pro-coagulant and atherosclerotic events. Thus, acute air pollution exposure is linked to acute cardiac death. One study showed that when ambient South Boston FPM levels surged, there was a corresponding increase in local hospital admissions for acute myocardial infarction within 24 hours.[4]

Chronic exposure to FPM and sulfates has also been linked to increased mortality. This correlation was first characterized in a landmark study by Dockery et al.[5] The study followed 8,100 white men and women from six different cities prospectively over 16 years, with serial measurements of particulates and sulfates in their respective cities. The authors controlled for tobacco abuse, overweight, blood pressure, diabetes, gender and education. The final results showed a compelling independent increased risk of cardiopulmonary death, based on increased exposure to FPM and sulfates. The major causes of excessive mortality were lung cancer and cardio-respiratory disease.

Air pollution from combustion is the most common cause of death of children in developing countries. The combustion usually occurs in the context of burning fuel for cooking in enclosed and poorly ventilated informal structures, such as huts or shacks. The mechanism of lung injury is probably from deposition of particles in the small airways, with subsequent inflammatory response and airway inflammation.

Both acute and chronic exposure to air pollution have been linked to chronic lung disease. After massive exposure to dust and air pollution following the terrible events of Sept. 11, 2001, New York City firemen and emergency response workers suffered a 10% decline in lung function, compared to before the events. This decline continues to persist with serial measurements over seven years.[6]

Chronic exposure to increased air pollution has also been linked to decreased lung development in children. In one study, 1,700 children from 12 separate communities in Southern California were followed over eight years, with serial measurements of lung function as well as ambient pollution levels in their communities.[7] The findings showed a clear correlation between increased levels of pollutants and decreased development of lung function.

Fascinating studies in abatement of pollution show that a temporary decrease in air pollution can reduce acute illness. A Utah steel mill, for example, was shut down periodically during labor disputes between 1985 and 1988. Admissions to local hospitals for asthma and pneumonia decreased two- to threefold during the fall and winter, in both adults and children, when the mill was closed.[8] During the 1996 Olympic games in Atlanta, asthma hospitalizations and exacerbations in the city dropped by 40%; this drop correlated with a 22% reduction in traffic due to congestion-easing measures.[9]

The United States and other industrialized countries have tried to limit air pollution by tightening emission standards for cars and factories, among other measures. Increased energy efficiency and transition to cleaner energies such as solar power have also mitigated pollution. In addition, many polluting industries have shifted to poorer countries, as wealthier countries transition from manufacturing to services. In the United States, the reductions in air pollution from these factors have been linked with consistent declines in mortality. One study estimated that between the 1970s and the 1990s, decreased air pollution levels in the United States led to an increased life expectancy of 0.6 years, or roughly 15% of the total improvement in life expectancy over this time period.[10]

The optimal level of air pollution is not known. Clearly, a future without any air pollution is impractical, but finding the right balance between industry and public health continues to be a challenge for academics, policy makers and legislators. As clean technologies and alternative energies become cheaper and more plentiful, the trade-offs for this balance may be easier to make.

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Dr. Prasad is a pulmonologist and critical care specialist at Kaiser San Rafael.

Email: sridhar.k.prasad@kp.org

References

1. Brown JR, Thornton JL, “Percivall Pott and chimney sweepers’ cancer of the scrotum,” Br J Ind Med, 14:68-70 (1957).

2. Bell ML, et al, “Retrospective assessment of mortality from the London smog episode of 1952,” Enviro Health Perspec, 112:6-8 (2004).

3. Brunekreef B, Holgate ST, “Air pollution and health,” Lancet, 360:1233-42 (2002).

4. Peters A, et al, “Increased particulate air pollution and the triggering of myocardial infarction,” Circ, 103:2810-15 (2001).

5. Dockery DW, et al, “Association between air pollution and mortality in six U.S. cities,” NEJM, 329:1753-59 (1993).

6. Aldrich TK, et al, “Lung function in rescue workers at the World Trade Center after 7 years,” NEJM, 362:1263-72 (2010).

7. Gauderman WJ, et al, “Effect of air pollution on lung development from 10 to 18 years of age,” NEJM, 351:1057-67 (2004).

8. Pope CA, “Respiratory disease associated with community air pollution and a steel mill, Utah Valley,” Am J Pub Health, 79:623-628 (1989).

9. Friedman MS, e al, “Impact of changes in transportation and commuting behaviors during the 1996 Summer Olympic Games in Atlanta on air quality and childhood asthma,” JAMA, 285:897-905 (2001).

10. Pope CA, et al, “Fine-particulate air pollution and life expectancy in the United States,” NEJM, 360:376-386 (2009).