From the aChronic Disease Epidemiology Unit, Department of Epidemiology and Public Health, Swiss Tropical and Public Health Institute, Basel, Switzerland; and bDepartment of Epidemiology and Public Health, University of Basel, Basel, Switzerland.
Correspondence: Nicole Probst-Hensch, Unit Head Chronic Disease Epidemiology, Department of Epidemiology and Public Health, Swiss Tropical and Public Health Institute, Socinstrasse 57, P.O. Box, 4002 Basel, Switzerland. E-mail: firstname.lastname@example.org.
In September 2011, the United Nations General Assembly convened a “momentous and historical” high-level summit on noncommunicable diseases. The purpose was to identify priorities for action in fighting the steep global surge in noncommunicable diseases. There was general agreement that cardiovascular diseases, cancers, diabetes, and chronic lung diseases constitute the largest burden of morbidity and death, and that 4 major causes (tobacco, unhealthy diet, lack of physical activity, and harmful use of alcohol) should be a central target for prevention.1
Any public health expert would agree with the importance of these diseases, and with the dangers of those causal risk factors.2 But the UN′s focus on individual behavior and lifestyles leaves little room for risk factors that are not personally modifiable—factors such as environmental pollution, poverty, or genetic susceptibility.3 The UN′s strong focus on lifestyle is perhaps not surprising given the extensive research literature that has emphasized this aspect. However, targeting changes in individual behavior may not be enough.
PARTICULATE AIR POLLUTION, LUNG AND HEART DISEASE, AND INFECTION
Active and passive tobacco smoke, biomass-fuel smoke, and traffic-related air pollution have broad adverse health effects on the respiratory and cardiovascular system, as well as on cardiopulmonary mortality.2,4–7 Because the relation of these exposures with cardiovascular disease mortality is nonlinear, control efforts are particularly beneficial at lower levels of exposure. There is a strong argument for improving air quality early on in the combat against noncommunicable diseases.8
Furthermore, there is an interrelation among exposure to inhaled particles, noncommunicable diseases, and infections. Populations in economic transition often have had high exposure in utero and during childhood to smoke from biomass combustion (for cooking and heating). Early exposure to inhaled particles and fumes is associated with higher rates of acute, repeated, or chronic respiratory infections (for example, acute lower respiratory tract infections9 and tuberculosis [TB]10). Early childhood respiratory infections are in turn risk factors for chronic pulmonary diseases in adulthood.11 The lungs of people exposed in early life to indoor air pollution may become more susceptible to the adverse effects of smoking and traffic-related air pollution—for example, developing chronic obstructive lung disease (COPD) at an earlier age.
With rapid urbanization, many populations in low- and middle-income countries are going from high exposures to the products of biomass combustion in childhood to high adult exposures to traffic-related air pollution. Those moving into urban slums may experience a triple stress—facing the socioeconomic stress of poverty, the hazards of indoor air pollution from traditional cooking practices, and the hazards of outdoor air pollution from heavy traffic. Furthermore, social stress may amplify the adverse effects of air pollution.12 None of these hazards will be reduced with strategies (emphasized by the UN Summit) that focus on lifestyle.
PARTICULATE AIR POLLUTION, OBESITY, AND DIABETES
Both indoor and traffic-related air pollution may contribute to the obesity and diabetes epidemics in middle- and low-income countries. Tobacco smoking is an established cause of diabetes.13 Results from animal experiments and a limited number of epidemiologic studies suggest that air pollution may also contribute to adipose-tissue inflammation, obesity, insulin resistance, and diabetes,14–17 although more conclusive evidence is needed regarding air pollution effects at ambient levels. Pregnant women exposed to high levels of indoor smoke have increased risk of babies with low birth weight,4 and low birth weight is a hypothesized risk factor for obesity and diabetes in adulthood.18 Diabetes may also exacerbate the health effects of air pollution. Persons with diabetes have been reported to be more susceptible to the adverse health effects of ambient air pollution on cardiovascular morbidity.5
Inhaled pollutants from various sources may also threaten the control of TB, probably through chronic, low-grade inflammatory effects in the lung, adipose tissue, and circulation. To the extent that air particles can increase the risk of diabetes, this can also affect susceptibility to infectious diseases. Persons with diabetes are about 3 times more likely to develop pulmonary TB. TB may also be more likely to be undiagnosed or misdiagnosed in people with diabetes. Urbanization (and especially the crowded living conditions in urban slums) adds to this threat by increasing the likelihood for a TB infection and its progression to active disease.19–21
The complexity of the effects of inhaled particles and air pollution puts a question mark behind currently available estimates of burden of disease from air pollution and demonstrates the limitations of considering diseases in isolation from one another. Clearly, environmental exposures could make a substantial contribution to the disease burden from noncommunicable diseases.
THE CHALLENGE OF GLOBAL URBANIZATION
Noncommunicable diseases cannot be prevented with a focus only on personal habits. There must be attention to the structural and cultural barriers to healthy living, especially in rapidly growing urban areas (and especially in hot and humid climates) where it may be difficult to be physically active and to live a healthy family and community life.22 Since 2008, for the first time in history, more than half of the world's population is living in towns or cities. By 2025, there will be 27 cities with more than 10 million people—at least 21 of them in low- or middle-income countries.23 This rapid urbanization in itself contributes to the surge in noncommunicable diseases, for example through easier access to calorie-dense nutrition, tobacco, and sweetened and alcoholic beverages. Unless urban planning is made a central part of efforts to prevent noncommunicable diseases, many prevention strategies that target individual behavior will be in vain.
THE PROMISE OF -OMICS RESEARCH
The estimated disease burden due to environmental pollutants may be even larger in genetically susceptible subgroups. From an epidemiologic research perspective, we underscore the importance of studying the urban exposome24 and diseasome,25,26 making use of large cohort and biobank consortia for meta-analyses. These efforts may ultimately identify complex risk patterns defined by the interplay of endogenous (genes, epigenetic modifications, RNA expression, metabolites, proteins) and exogenous factors (environmental, social, lifestyle, urbanization, and other factors) that drive the epidemic of noncommunicable diseases. Considering internal biologic mechanisms through various -omics approaches may improve our understanding of causal risk factors, identify the biologically relevant internal doses for the most susceptible populations, and clarify the role of mechanisms (such as systemic inflammation or oxidative stress) and related pathways (such as cell proliferation and apoptosis) shared by different diseases.14 In fact, improved understanding of biologic mechanisms may be the most important public health contribution of the new -omics technologies.
In times of ever-cheaper, high-throughput technologies, it is important to keep in mind that the dramatic surge of noncommunicable diseases in the developing world over recent decades is due to external, modifiable causes. Furthermore, it has become evident over the past decade that the genes identified to date neither contribute much to disease prediction nor do they motivate healthier lifestyle behaviors.27 Common polymorphisms and loci identified through genome-wide association meta-analyses (GWAS) typically explain only 5% of phenotypic variability.28 This may in part reflect the fact that GWAS has largely ignored lifestyle and environmental risk factors. Several low- and middle-income countries are considering infrastructures for large-scale genetic testing.29 Internet-based gene testing companies are starting to collect consumer information beyond genes, but such broad data will not be sufficient to improve understanding of the complex interplay between genes and the environment.
Although lifestyle factors may “explain” a large portion of disease burden, the “preventability” of this burden is far from 100%, as is well known from smoking-prevention efforts. In contrast, many environmental hazards could be substantially and sustainably prevented—for example, by infrastructures providing clean water, by strict requirements for the best-available technologies to reduce emissions of vehicles and industries, or by occupational regulations to prevent harmful workplace exposures. In India, it has been estimated that environmental and occupational risk factors contribute 40% to the disease burden, with indoor and ambient risk factors being the major contributors.30 Strategies to prevent noncommunicable diseases must go beyond debates about lifestyle and genes and include the extent of disease due to factors such as environmental pollutants, social conditions, and occupational exposures—preventable factors, but only if we recognize the challenge.
2. WHO. Global Health Risks. Mortality and Burden of Disease Attributable to Major Selected Risks. Geneva: World Health Organization; 2009.
3. Probst-Hensch N, Tanner M, Kessler C, Burri C, Kunzli N. Prevention–a cost-effective way to fight the non-communicable disease epidemic: an academic perspective of the United Nations High-level NCD Meeting. Swiss Med Wkly. 2011;141:w13266.
4. Kim KH, Jahan SA, Kabir E. A review of diseases associated with household air pollution due to the use of biomass fuels. J Hazard Mater. 2011;192:425–431.
5. Brook RD, Rajagopalan S, Pope CA III, et al.. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association. Circulation. 2010;121:2331–2378.
6. Künzli N, Perez L, Rapp R. Air Quality and Health. Lausanne, Switzerland: European Respiratory Society; 2010.
7. WHO. Estimate on the Burden of Disease From Second Hand Tobacco Smoke. Geneva: World Health Organization; 2011.
8. Smith KR, Peel JL. Mind the gap. Environ Health Perspect. 2010;118:1643–1645.
9. Smith KR, McCracken JP, Weber MW, et al.. Effect of reduction in household air pollution on childhood pneumonia in Guatemala (RESPIRE): a randomised controlled trial. Lancet. 2011;378:1717–1726.
10. Lin HH, Ezzati M, Murray M. Tobacco smoke, indoor air pollution and tuberculosis: a systematic review and meta-analysis. PLoS Med. 2007;4:
11. de Marco R, Accordini S, Marcon A, et al.. Risk factors for chronic obstructive pulmonary disease in a European cohort of young adults. Am J Respir Crit Care Med. 2011;183:891–897.
12. Clougherty JE, Kubzansky LD. A framework for examining social stress and susceptibility to air pollution in respiratory health. Cien Saude Colet. 2010;15:2059–2074.
13. Willi C, Bodenmann P, Ghali WA, Faris PD, Cornuz J. Active smoking and the risk of type 2 diabetes: a systematic review and meta-analysis. JAMA. 2007;298:2654–2664.
14. Probst-Hensch NM. Chronic age-related diseases share risk factors: do they share pathophysiological mechanisms and why does that matter? Swiss Med Wkly. 2010;140:w13075.
15. Sun Q, Yue P, Deiuliis JA, et al.. Ambient air pollution exaggerates adipose inflammation and insulin resistance in a mouse model of diet-induced obesity. Circulation. 2009;119:538–546.
16. Kramer U, Herder C, Sugiri D, Strassburger K, Schikowski T, Ranft U, et al.. Traffic-related air pollution and incident type 2 diabetes: results from the SALIA cohort study. Environ Health Perspect. 2010;118:1273–1279.
17. Andersen ZJ, Raaschou-Nielsen O, Ketzel M, et al.. Diabetes incidence and long-term exposure to air pollution: a cohort study. Diabetes Care. 2012;35:92–98.
18. de Lauzon-Guillain B, Balkau B, Charles MA, Romieu I, Boutron-Ruault MC, Clavel-Chapelon F. Birth weight, body silhouette over the life course, and incident diabetes in 91,453 middle-aged women from the French Etude Epidemiologique de Femmes de la Mutuelle Generale de l'Education Nationale (E3N) Cohort. Diabetes Care. 2010;33:298–303.
19. Fisher-Hoch SP. Diabetes and tuberculosis: a twenty-first century plague? Int J Tuberc Lung Dis. 2011;15:1422.
20. Dooley KE, Chaisson RE. Tuberculosis and diabetes mellitus: convergence of two epidemics. Lancet Infect Dis. 2009;9:737–746.
21. WHO. Collaborative Framework for Care and Control of Tuberculosis and Diabetes. Geneva: World Health Organization; 2011.
22. Amiri P, Ghofranipour F, Ahmadi F, et al.. Barriers to a healthy lifestyle among obese adolescents: a qualitative study from Iran. Int J Public Health. 2011;56:181–189.
24. Peters A, Hoek G, Katsouyanni K. Understanding the link between environmental exposures and health: does the exposome promise too much? J Epidemiol Community Health. 2012;66:103–105.
25. Rappaport SM, Smith MT. Epidemiology: environment and disease risks. Science. 2010;330:460–461.
26. Barabasi AL. Network medicine–from obesity to the “diseasome”. N Engl J Med. 2007;357:404–407.
27. Marteau TM, French DP, Griffin SJ, et al.. Effects of communicating DNA-based disease risk estimates on risk-reducing behaviours. Cochrane Database Syst Rev. 2010:CD007275.
28. Seguin B, Hardy BJ, Singer PA, Daar AS. Genomic medicine and developing countries: creating a room of their own. Nat Rev Genet. 2008;9:487–493.
29. Manolio TA, Collins FS, Cox NJ, et al.. Finding the missing heritability of complex diseases. Nature. 2009;461:747–753.
30. Balakrishnan K, Ramaswamy P, Sambandam S, et al.. Air pollution from household solid fuel combustion in India: an overview of exposure and health related information to inform health research priorities. Glob Health Action. 2011;4.
About the Authors
NICOLE PROBST-HENSCH is Associate Professor in Epidemiology and Public Health at the University of Basel. Her research as Head of the Chronic Disease Epidemiology Unit at the Swiss Tropical and Public Health Institute focuses on noncommunicable diseases with a special focus on molecular mechanisms and genetic susceptibilities. NINO KÜNZLI is Professor in Epidemiology and Public Health at the University of Basel, Vice Director of the Swiss Tropical and Public Health Institute, and Head of the Department of Epidemiology and Public Health.