Cathleen Truong
May 21, 2015
Environmental Science
Period 3
Air Pollution Causes Lung Disease
Ackermann-Liebrich, U., Leuenberger, P., Schwartz, J., Schindler, C., Monn, C.,
Bolognini, G., ... & Zemp, E. (1997). Lung function and long term exposure to air
pollutants in Switzerland. Study on Air Pollution and Lung Diseases in Adults
(SAPALDIA) Team. American journal of respiratory and critical care medicine, 155(1), 122129.
In Switzerland, they analyzed and observed humans with lung diseases to find the explanation for
this health complication. From their studies, the causes for lung disease were from smoking cigarettes,
ozone, and air pollution. In conclusion, air pollution from fossil fuels was the main cause to human lungs
that included decrements in lung function parameters.
Brook, R. D., Franklin, B., Cascio, W., Hong, Y., Howard, G., Lipsett, M., ... & Tager, I.
(2004). Air pollution and cardiovascular disease A statement for healthcare professionals
from the expert panel on population and prevention science of the American Heart
Association. Circulation, 109(21), 2655-2671.
Air pollution as a heterogeneous, complex mixture of gases, liquids, and particulate matter, has
been studied as a consistent increased risk for cardiovascular disease in both, short-and-long term
exposure to our present-day concentrations of ambient particulate matter. Enhanced
coagulation/thrombosis, a propensity for arrhythmias, acute arterial vasoconstriction, systemic
inflammatory responses, and the chronic promotion of atherosclerosis were some of the plausible
mechanistic pathways that have been described. This is to provide health care professionals and
regulatory agencies to review air pollution and cardiovascular disease.
Bruce, N., Perez-Padilla, R., & Albalak, R. (2000). Indoor air pollution in developing
countries: a major environmental and public health challenge. Bulletin of the World Health
Organization, 78(9), 1078-1092.
Air pollution caused an increase of chronic constructive pulmonary disease and of acute
respiratory infections in childhood, the most important cause of death among children under 5 years of
age in developing countries. This has also caused low birth weight, increased infant and perinatal
mortality, pulmonary tuberculosis, nasopharyngeal, and laryngeal cancer, cataract, asthma and lung
cancer. Risk estimates are poorly quantifies and may be biased and indoor air pollution may be the reason
for 2 million excess deaths in developing countries with 4% of global burden of disease. Indoor air
pollution is a major global public health threat, requiring greatly increased efforts in the areas of research
and policy-making. Research of the effects should be paid more attention to, especially about tuberculosis
and acute lower respiratory infections.
Brunekreef, B., & Holgate, S. T. (2002). Air pollution and health. The lancet,360(9341),
1233-1242.
Pollutants being exposed, for example airborne participate matter and ozone are the causes to
respiratory and cardiovascular disease. For short-term studies are the day-to-day variations in air pollution
and health and long-term studies are followed cohorts of exposed individuals over time.
Devlin, R. B., McDonnell, W. F., Mann, R., Becker, S., House, D. E., Schreinemachers, D.,
& Koren, H. S. (1991). Exposure of humans to ambient levels of ozone for 6.6 hours causes
cellular and biochemical changes in the lung. American journal of respiratory cell and
molecular biology, 4(1), 72-81.
Many people are exposed to lower levels of ozone than this, but for periods of several hours.
Therefore, it is important to determine if a prolonged exposure to low levels of ozone is also capable of
causing cellular and biochemical changes in the lung. Bronchoalveolar lavage (BAL) was performed 18 h
after each exposure, and cells and fluid were analyzed. The BAL fluid of volunteers exposed to 0.10 ppm
ozone had significant increases in neutrophils (PMNs), protein, prostaglandin E2 (PGE2), fibronectin,
interleukin-6 (IL-6), and lactate dehydrogenase (LDH) compared with BAL fluid from the same
volunteers exposed to filtered air.
Dominici, F., Peng, R. D., Bell, M. L., Pham, L., McDermott, A., Zeger, S. L., & Samet, J.
M. (2006). Fine particulate air pollution and hospital admission for cardiovascular and
respiratory diseases. Jama, 295(10), 1127-1134.
Founded evidence of positive associations between day-to-day variation in PM concentration and
hospital admissions for all outcomes, except injuries, for at least 1 exposure lag. Largest effect was lag 0
for cardiovascular outcomes except ischemic heart disease with lag 2 of days. Lags 0 were respiratory
outcomes, 1 for COPD, and 2 for respiratory tract infections. Lag estimates were statistically significant
for heart failure.95% posterior intervals for distributed lag estimates reflect the restriction of the analysis
to 90 of the 204 counties with daily data. Concluding that the single lag models were also stratified by age
group at the lag with greatest effect. National average RR estimates were larger in the oldest
Hogg, J. C., Macklem, P. T., & Thurlbeck, W. M. (1968). Site and nature of airway
obstruction in chronic obstructive lung disease. New England Journal of Medicine, 278(25),
1355-1360.
Disease of small airways may be common to various chronic obstructive lung diseases. Because
Rp is normally so small, there may be considerable obstruction in peripheral airways that would affect
ventilation distribution and gas exchange but would have little effect on function tests designed to reveal
obstruction. When total airway resistance is elevated to a clinically detectable level by disease in the
small airways, obstruction is much more severe than is generally recognized.
Kampa, M., & Castanas, E. (2008). Human health effects of air pollution. Environmental
pollution, 151(2), 362-367.
Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to
broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in
exploring potential mechanistic pathways linking exposure and mortality.
KuÈnzli, N., Kaiser, R., Medina, S., Studnicka, M., Chanel, O., Filliger, P., ... & Sommer,
H. (2000). Public-health impact of outdoor and traffic-related air pollution: a European
assessment. The Lancet, 356(9232), 795-801.
Air pollution caused 6% of total mortality or more than 40 000 attributable cases per year. About
half of all mortality caused by air pollution was attributed to motorised traffic, accounting also for: more
than 25 000 new cases of chronic bronchitis (adults); more than 290 000 episodes of bronchitis (children);
more than 0·5 million asthma attacks; and more than 16 million persondays of restricted activities.
Leuenberger, P., Schwartz, J., Ackermann-Liebrich, U., Blaser, K., Bolognini, G., Bongard,
J. P., ... & Brutsche, M. (1994). Passive smoking exposure in adults and chronic respiratory
symptoms (SAPALDIA Study). Swiss Study on Air Pollution and Lung Diseases in Adults,
SAPALDIA Team. American journal of respiratory and critical care medicine, 150(5), 12221228.
The association of passive smoking exposure with dyspnea, wheeze, and asthma showed evidence
of a dose-dependent increase with hours per day of exposure, whereas association with symptoms of
bronchitis was stronger with years of exposure.
Peters, A., Döring, A., Wichmann, H. E., & Koenig, W. (1997). Increased plasma viscosity
during an air pollution episode: a link to mortality?. The Lancet, 349(9065), 1582-1587.
During the 1985 air pollution episode, an increased risk of extreme values of plasma viscosity
was observed in both men and women. Altered blood rheology due to inflammatory processes in the lung
that induce an acute-phase reaction might therefore be part of the pathological mechanisms linking air
pollution to mortality.
Pope, C. A., Burnett, R. T., Thurston, G. D., Thun, M. J., Calle, E. E., Krewski, D., &
Godleski, J. J. (2004). Cardiovascular mortality and long-term exposure to particulate air
pollution epidemiological evidence of general pathophysiological pathways of
disease. Circulation, 109(1), 71-77.
Vital status, risk factor, and cause-of-death data collected from American Cancer Society of the
Cancer Prevention II study, linked their data with United States metropolitan areas of air pollution.
Regression models from Cox Proportional Hazard were used to estimate air pollution (PM) mortality
relating to specific causes of death. Long-term PM were most strongly the causes of ischemic heart
disease, dysrhythmias, heart failure, and cardiac arrest. Cardiovascular causes of death are a 10-
μg/m3 elevation in fine PM and 8% to 18% increases in mortality risk. Larger risks are smokers relative to
nonsmokers, showing that respiratory disease are relatively weak associations. That being said, exposure
to fine PM imposes additional effects that are at least additive to, if not synergistic with smoking.
Samet, J. M., Marbury, M. C., & Spengler, J. D. (1987). Health effects and sources of
indoor air pollution. Part I. American Review of Respiratory Disease, 136(6), 1486-1508.
The health effects of indoor air pollution have been investigated with increasing intensity.
Consequently, a large body of literature is now available on diverse aspects of indoor air pollution:
sources, concentrations, health effects, engineering, and policy. Exposure to indoor air pollutants and
health effects are considered, with an emphasis on those indoor air quality problems of greatest concern at
present: passive exposure to tobacco smoke, nitrogen dioxide from gas-fueled cooking stoves,
formaldehyde exposure, radon daughter exposure, and the diverse health problems encountered by
workers in newer sealed office buildings.
Seaton, A., Godden, D., MacNee, W., & Donaldson, K. (1995). Particulate air pollution and
acute health effects. The Lancet, 345(8943), 176-178.
Epidemiological studies have proven that particulate air pollution is related to people with
respiratory diseases and also numerous deaths from cardiovascular and respiratory disease among older
people. The nature of the urban particulate cloud, containing 100000 nanometer-sized particles per mL
and including gravimetric concentration of only 100-200 μg/m3 of pollutant. Ultra-fine particles are able
to provoke alveolar inflammation, releasing mediators that are capable in susceptible individuals and
causing exacerbations of lung disease and increasing blood clots.
Vento, M., Moro, M., Escrig, R., Arruza, L., Villar, G., Izquierdo, I., ... & Asensi, M. A.
(2009). Preterm resuscitation with low oxygen causes less oxidative stress, inflammation,
and chronic lung disease. Pediatrics, 124(3), e439-e449.
Reducing adverse pulmonary adverse outcomes, oxidative stress, and inflammation in neonates of
24 to 28 weeks of gestation initially resuscitated with fractions of inspired oxygen of 30% or 90%.
Resuscitation of preterm neonates with 30% oxygen causes less oxidative stress, inflammation, need for
oxygen, and risk of bronchopulmonary dysplasia.