1. Infant and children

• World Health Organization: Air Pollution Exposure EQUALS Smaller Babies

The World Health Organization has released a new study of the correlation between PM2.5 pollution exposure during pregnancy and declining birth weights worldwide. Three million births over 14 global sites were studied. WHO recommends stricter air quality standards for the affected nations in the EU.

Air pollution has been associated with asthma prevalence. This study look at early-life exposures before the development of childhood asthma and many are limited to populations of mostly European descent. Using the largest pediatric gene environment study of asthma in Latinos and African Americans in the United States, this study found that exposure during infancy to NO2, a traffic-related air pollutant, was associated with increased risk for subsequent development of childhood asthma. The results suggest that air pollution may contribute to the higher prevalence of asthma, especially in some minority children exposed to higher levels of air pollution.

Katherine K. Nishimura, Joshua M. Galanter, Lindsey A. Roth, Sam S. Oh, Neeta Thakur, Elizabeth A. Nguyen, Shannon Thyne, Harold J. Farber, Denise Serebrisky, Rajesh Kumar, Emerita Brigino-Buenaventura8, Adam Davis, Michael A. LeNoir, Kelley Meade, William Rodriguez-Cintron, Pedro C. Avila, Luisa N. Borrell, Kirsten Bibbins-Domingo2,, Jose R. Rodriguez-Santana, _Saunak Sen, Fred Lurmann, John R. Balmes, and Esteban G. Burchard (2013) Am J Respir Crit Care Med Vol 188, Iss. 3, pp 309318, Aug 1.

Analyses of exposure outcome in this review demonstrated the importance of evaluating indoor home air pollution sources as risk factors for asthma morbidity. Results indicated indoor particulate matter (particularly the coarse fraction), NO2, and mouse allergen exposure are important determinants of asthma morbidity in urban environments. Avoidance of harmful exposures is a key component of national and international guideline recommendations for management of asthma. Guidelines identify PM and NO2 as pollutants of indoor air exposures may be indicated for children with uncontrolled asthma. These results suggest that modifying the indoor environment to reduce PM, NO2, and mouse allergen may be an important asthma management strategy.
Patrick N. Breysse, Gregory B. Diette, Elizabeth C. Matsui, Arlene M. Butz, Nadia N. Hansel, and Meredith C. McCormack (2010) Proc Am Thorac Soc Vol 7. pp 102106.

Ambient air pollution has been associated with several adverse respiratory health outcomes in children and adults. Bronchiolitis is the leading cause of hospitalization in the first year of life in North America, yet data regarding the role of ambient air pollution are few. This study provides evidence that traffic-derived, industrial point source, and wood smoke related exposures may increase the burden bronchiolitis in infants.
Catherine J. Karr, Paul A. Demers, Mieke W. Koehoorn, Cornel C. Lencar, Lillian Tamburic, and Michael Brauer (2009) Am J Respir Crit Care Med Vol 180. pp 9951001.

With substantial data from asthmatic and adult subjects, there are increasing evidence that short-term exposure to air pollution has a detrimental effect on respiratory morbidity. Studies in healthy populations, particularly infants, are scarce. Our study found a small but significant impact of moderate levels of air pollution on respiratory health in healthy infants. This was more pronounced in infants with pre-morbid lung function.
Georgette Stern, Philipp Latzin, Martin Roosli, Oliver Fuchs, Elena Proietti, Claudia Kuehni, and Urs Frey (2013) Am J Respir Crit Care Med Vol 187, Iss. 12, pp 13411348, Jun 15.

Long-term exposure to air pollutants is associated with a significant deficit in lung function growth in children.
Rosalba Rojas-Martinez, Rogelio Perez-Padilla, Gustavo Olaiz-Fernandez, Laura Mendoza-Alvarado, Hortensia Moreno-Macias, Teresa Fortoul, William McDonnell, Dana Loomis, and Isabelle Romieu (2007) Am J Respir Crit Care Med Vol 176. pp 377384.

his finding, in conjunction with significant associations between pollution and the volume- corrected measure, MMEF/FVC, indicates that long-term pollution exposure may affect the development of small airways in the lung. Further follow-up of CHS participants will allow determination of whether pollution-related deficits in lung function growth persist into adulthood, resulting in lower maximal attained lung function, and perhaps, leading to increased risk of respiratory illness.
W. James Gauderman, G. Frank Gilliland, Hita Vora, Edward Avol, Daniel Stram, Rob McConnell, Duncan Thomas, Fred Lurmann, Helene G. Margolis, Edward B. Rappaport, Kiros Berhane, and John M. Peters (2002) Am J Respir Crit Care Med Vol 166. pp 7684.

Exposure to ambient air pollution can exacerbate existing asthma. The role of exposure to ambient air pollution in the development of childhood asthma, allergy, and related symptoms found positive associations between traffic-related air pollution levels outside subjects homes, and the incidence and prevalence of asthma during the first 8 years of life. The results provide evidence that air pollution exposure may contribute to the pathogenesis of asthma in children.
Ulrike Gehring, Alet H. Wijga, Michael Brauer, Paul Fischer, Johan C. de Jongste, Marjan Kerkhof, Marieke Oldenwening, Henriette A. Smit, and Bert Brunekreef (2010) Am J Respir Crit Care Med Vol 181. pp 596603

Traffic-related exposures are associated with increased asthma severity. Traffic-related exposures are associated with increased airway inflammation and reduced lung volumes. Children with asthma are more susceptible than healthy control subjects.
Fernando Holguin, Silvia Flores, Zev Ross, Marlene Cortez, Mario Molina, Luisa Molina, Carlos Rincon, Michael Jerrett, Kiros Berhane, Alfredo Granados, and Isabelle Romieu; (2007) Am J Respir Crit Care Med Vol 176. pp 12361242, 2007

The data suggest that vitamin C and vitamin E supplementation above the minimum dietary requirement in children with asthma with low intake of vitamin E provides some protection against the acute effects of ozone on their lungs. It remains to be determined what is the optimal dose of antioxidant for adequate protection from ozone-induced lung injury and to what extent such supplementation would provide increased protection over that observed in subjects already considered to have a normal diet.
Isabelle Romieu, Juan Jose Sienra-Monge, Matiana Ramirez-Aguilar, Martha Maria Tellez-Rojo, Hortensia Moreno-Macias, Norma Isabel Reyes-Ruiz, Blanca Estela del Rio-Navarro, Maria Xo chitl Ruiz-Navarro, Gary Hatch, Ralph Slade, and Mauricio Hernandez-Avila (2002) Am J Respir Crit Care Med Vol 166. pp 703709.

2. Ultrafine Particles (UFP)

Airborne particulate matter (PM) has been linked to adverse human health effects, the relationship between PM and health varies seasonally and regionally, as does the particles chemical composition. This work provides evidence that the chemical composition of PM contributes to its toxicity. In places and during seasons when PM had higher fractions of nickel, vanadium, and elemental carbon, the risks of hospital admission associated with PM with aerodynamic diameter < 2.5 mm were higher.
Michelle L. Bell, Keita Ebisu, Roger D. Peng, Jonathan M. Samet, and Francesca Dominici (2009) Am J Respir Crit Care Med Vol 179. pp 11151120.

Short-term exposure to traffic pollution has been linked with cardiovascular diseases, which are characterized by a loss of blood DNA methylation. Changes in epigenetic markers, such as DNA methylation, may mediate environmental effects on human health. The data showed that blood leukocyte DNA methylation in sequences with widespread genomic representation decreases rapidly following peaks of higher ambient levels of traffic particles. These changes may contribute to produce environmental effects on human health.
Baccarelli, Wright, Bollati, et al.; (2009) Air Particles and DNA Methylation, Am J Respir Crit Care Med Vol 179. pp 572578.

A German study suggested that ultrafine particles may play a key role in the morbidity and mortality of inhaled air pollution. Inhaled ultrafine carbon particles are retained long term in the human lung and may accumulate. Mucociliary clearance does not remove all particles deposited in the airways and is impaired in smokers and in patients with chronic obstructive pulmonary disease.
Winfried Moller, Kathrin Felten, Knut Sommerer, Gerhard Scheuch, Gabriele Meyer3, Peter Meyer, Karl Haussinger, and Wolfgang G. Kreyling (2008) Am J Respir Crit Care Med Vol 177. pp 426432.

3) COPD, Lung, CHD

Researchers in Denmark found that long-term exposure to traffic-related air pollution increases the chance of developing COPD, especially in people with diabetes and asthma. They based their findings on a comparison of hospital discharge records for COPD patients and air pollution in Copenhagen and in Aarhus, two large cities in Denmark. The study, published in the American Journal of Respiratory and Critical Care Medicine, analyzed data over 35 years and included more than 57,000 people between the ages 50 and 64.

Similarly, researchers in Australia found that poor air quality can contribute to worsening COPD and possibly death. They compared air pollution in two towns in Australia, Launceston and Hobart, and analyzed mortality rates. They found that when residents of Launceston reduced smoke from burning organic materials such as wood, the number of deaths from COPD declined. The study was published in the British Medical Journal.

According to a study by U.S. researchers published in this week's PLOS Medicine, long term exposure to air pollution may be linked to heart attacks and strokes by speeding up atherosclerosis, or "hardening of the arteries".
Adar SD, Sheppard L, Vedal S, Polak JF, Sampson PD, et al. (2013) Fine Particulate Air Pollution and the Progression of Carotid Intima-Medial Thickness: A Prospective Cohort Study from the Multi-Ethnic Study of Atherosclerosis and Air Pollution. PLoS Med, DOI: 10.1371/journal.pmed.1001430

Patients released from the hospital following a heart attack are more likely to die over the following years if they go home to an area with higher levels of air pollution, according to a new study in the European Heart Journal." Patients released from the hospital following a heart attack are more likely to die over the following years if they go home to an area with higher levels of air pollution. By air pollution, the study refers specifically to particulate matter that's 2.5 micrometers in diameter (PM2.5). No significant results were found for larger particles or for the presence of nitrogen oxide in the air. But reducing the concentration of PM2.5 to a baseline level, absent human contributions, could reduce post-heart attack mortality by 12 percent, according to the authors. To arrive at this data, they followed over 150,000 patients in England and Wales, cross-referencing their health records with average air pollution levels for their postcode (that's British for zipcode). At the study's end, a quarter had passed away; the researchers estimate that 4,783 of those deaths occurred prematurely and can be attributed to the influence of air pollution.

European Heart Journal - http://eurheartj.oxfordjournals.org/content/early/recent

A Taiwan study suggests urban air pollution is associated with inflammation, oxidative stress, blood coagulation and autonomic dysfunction simultaneously in healthy young humans, with sulfate and O3 as two major traffic-related pollutants contributing to such effects. The mechanisms linking air pollution to cardiovascular diseases involve direct effects of air pollution on the lung and cardiovascular system and indirect effects mediated through pulmonary inflammation and oxidative stress.
Kai-Jen Chuang, Chang-Chuan Chan, Ta-Chen Su, Chung-Te Lee, and Chin-Sheng Tang (2007) Am J Respir Crit Care Med Vol 176. pp 370376.

What This Study Adds to the Field Portable air filters reduced indoor particulate air pollution, improved microvascular endothelial function, and reduced markers of systemic inflammation among healthy adults in a community heavily impacted by residential wood combustion. Exposure to particulate air pollution is associated with cardiovascular morbidity. One hypothesized mechanistic pathway involves oxidative stress, systemic inflammation, and endothelial dysfunction.
Ryan W. Allen, Chris Carlsten, Barbara Karlen, Sara Leckie, Stephan van Eeden, Sverre Vedal, Imelda Wong, and Michael Brauer (2011) Am J Respir Crit Care Med Vol 183. pp 12221230.

Members of the American Cancer Society Cancer Prevention Study II Cohort residing in California were subjected to precise exposure assignments at their home address using advanced exposure models. The study provides the first evidence that ozone is significantly associated with cardiovascular mortality, particularly from ischemic heart disease; shows a strong association between nitrogen dioxide (NO2) and lung cancer; and demonstrates that that fine particulate matter with aerodynamic diameter of 2.5 mm or less (PM2.5) and NO2 associate independently with premature death from all causes and cardiovascular disease. The findings from this study confirm earlier evidence on PM2.5 associations with mortality and expand the evidence base markedly on associations between ozone or NO2 and premature death.
Michael Jerrett, Richard T. Burnett, Bernardo S. Beckerman, Michelle C. Turner, Daniel Krewski, George Thurston, Randall V. Martin, Aaron van Donkelaar, Edward Hughes, Yuanli Shi, Susan M. Gapstur, Michael J. Thun, and C. Arden Pope III (2013) Am J Respir Crit Care Med Vol 188, Iss. 5, pp 593599, Sep 1.

The study adds to the evidence that elevated levels of ambient air pollution may cause systemic inflammatory and coagulation responses. These changes in blood markers could represent additional risk factors, which, in susceptible individuals, such as patients with CHD, could increase the likelihood of serious arterial vascular thrombotic events on exposure to high levels of air pollutants.
Regina Ruckerl, Angela Ibald-Mulli, Wolfgang Koenig, Alexandra Schneider, Gabriele Woelke, Josef Cyrys, Joachim Heinrich, Victor Marder, Mark Frampton, H. Erich Wichmann, and Annette Peters (2006) Am J Respir Crit Care Med Vol 173. pp 432441.

The carbonaceous core of environmental fine particulates has been shown to have adjuvant activity in allergic diseases. This study suggested Field Ultrafine carbon particle inhalation augments allergen induced lipid peroxidation and nuclear factor-kB activation in addition to lung inflammation, cytokine release, and airway hyperreactivity. Oxidative stress is central to this process.
Francesca Alessandrini , Ingrid Beck-Speier, Daniel Krappmann, Ingrid Weichenmeier, Shinji Takenaka, Erwin Karg, Bernhard Kloo, Holger Schulz, Thilo Jakob, Martin Mempel , and Heidrun Behrendt; (2009) Am J Respir Crit Care Med Vol 179. pp 984991.DOI: 10.1164/rccm.200807-1061OC on March 5, 2009.

Role of Oxidative Stress in Ultrafine Particle–induced Exacerbation of Allergic Lung Inflammation - https://www.atsjournals.org/doi/full/10.1164/rccm.200807-1061OC

The link between ambient particulate matter air pollution and cardiorespiratory mortality and morbidity is well established. Exposure to diesel exhaust causes a selective impairment of vascular endothelial function, which persists up to 24 hours after exposure. Adverse cardiovascular effects of combustion-derived pollution may be mediated through prolonged detrimental vascular effects.
Hakan Tornqvist, Nicholas L. Mills, Manuel Gonzalez, Mark R. Miller, Simon D. Robinson, Ian L. Megson, William MacNee, Ken Donaldson, Stefan Soderberg, David E. Newby, Thomas Sandstrom1, and Anders Blomberg (2007) Am J Respir Crit Care Med Vol 176. pp 395400