Detrimental Effects Of Air Pollution Research Articles

Ambient and household air pollution: complex triggers of disease.

Concentrations of outdoor air pollution are on the rise, particularly due to rapid urbanization worldwide. Alternatively, poor ventilation, cigarette smoke, and other toxic chemicals contribute to rising concentrations of indoor air pollution. The World Health Organization recently reported that deaths attributable to indoor and outdoor air pollutant exposure are more than double what was originally documented. Epidemiological, clinical, and animal data have demonstrated a clear connection between rising concentrations of air pollution (both indoor and outdoor) and a host of adverse health effects. During the past five years, animal, clinical, and epidemiological studies have explored the adverse health effects associated with exposure to both indoor and outdoor air pollutants throughout the various stages of life. This review provides a summary of the detrimental effects of air pollution through examination of current animal, clinical, and epidemiological studies and exposure during three different periods: maternal (in utero), early life, and adulthood. Additionally, we recommend future lines of research while suggesting conceivable strategies to curb exposure to indoor and outdoor air pollutants.

Vanadate from air pollutant inhibits hrs-dependent endosome fusion and augments responsiveness to toll-like receptors.

There is a well-established association between exposure to air pollutants and pulmonary injuries. For example, metals found in ROFA (residual oil fly ash) increase susceptibility of mice as well as humans to microbial infections. In our research, we have found that vanadate substantially increased the response of several Toll-like receptors (TLRs) to stimulation with their ligands. Although vanadate caused generation of reactive oxygen species (ROS), the addition of ROS scavenger N-acetyl cysteine (NAC) had no effect on augmented lipopolysaccharide (LPS) stimulation. We further showed that vanadate inhibits endosome fusion. This effect was determined by measuring the size of endosomes, NF-κB activity and TLR4 degradation in Hrs (hepatocyte growth factor-regulated tyrosine kinase substrate) overexpressed cells. Moreover, we identified the role of Hrs phosphorylation in these processes. Based on our findings, we can conclude that vanadate potentiates TLR4 activity by increasing Hrs phosphorylation status, reducing the size of Hrs/TLR4-positive endosomes and impacting TLR4 degradation, thus contributing to the detrimental effects of air pollutants on human health.

A national case-crossover analysis of the short-term effect of PM2.5 on hospitalizations and mortality in subjects with diabetes and neurological disorders.

BackgroundDiabetes and neurological disorders are a growing burden among the elderly, and may also make them more susceptible to particulate air matter with aerodynamic diameter less than 2.5 μg (PM2.5). The same biological responses thought to effect cardiovascular disease through air pollution-mediated systemic oxidative stress, inflammation and cerebrovascular dysfunction could also be relevant for diabetes and neurodegenerative diseases.MethodsWe conducted multi-site case-crossover analyses of all-cause deaths and of hospitalizations for diabetes or neurological disorders among Medicare enrollees (>65 years) during the period 1999 to 2010 in 121 US communities. We examined whether 1) short-term exposure to PM2.5 increases the risk of hospitalization for diabetes or neurological disorders, and 2) the association between short-term exposure to PM2.5 and all-cause mortality is modified by having a previous hospitalization of diabetes or neurological disorders.ResultsWe found that short term exposure to PM2.5 is significantly associated with an increase in hospitalization risks for diabetes (1.14% increase, 95% CI: 0.56, 1.73 for a 10 μg/m3 increase in the 2 days average), and for Parkinson’s disease (3.23%, 1.08, 5.43); we also found an increase in all-cause mortality risks (0.64%, 95% CI: 0.42, 0.85), but we didn’t find that hospitalization for diabetes and neurodegenerative diseases modifies the association between short term exposure to PM2.5 and all-cause mortality.ConclusionWe found that short-term exposure to fine particles increased the risk of hospitalizations for Parkinson’s disease and diabetes, and of all-cause mortality. While the association between short term exposure to PM2.5 and mortality was higher among Medicare enrollees that had a previous admission for diabetes and neurological disorders than among Medicare enrollees that did not had a prior admission for these diseases, the effect modification was not statistically significant. We believe that these results provide useful insights regarding the mechanisms by which particles may affect the brain. A better understanding of the mechanisms will enable the development of new strategies to protect individuals at risk and to reduce detrimental effects of air pollution on the nervous system.

The Health Effects of Exercising in Air Pollution

The health benefits of exercise are well known. Many of the most accessible forms of exercise, such as walking, cycling, and running often occur outdoors. This means that exercising outdoors may increase exposure to urban air pollution. Regular exercise plays a key role in improving some of the physiologic mechanisms and health outcomes that air pollution exposure may exacerbate. This problem presents an interesting challenge of balancing the beneficial effects of exercise along with the detrimental effects of air pollution upon health. This article summarizes the pulmonary, cardiovascular, cognitive, and systemic health effects of exposure to particulate matter, ozone, and carbon monoxide during exercise. It also summarizes how air pollution exposure affects maximal oxygen consumption and exercise performance. This article highlights ways in which exercisers could mitigate the adverse health effects of air pollution exposure during exercise and draws attention to the potential importance of land use planning in selecting exercise facilities.

Allergic diseases and air pollution

The prevalence of allergic diseases has been increasing rapidly, especially in developing countries. Various adverse health outcomes such as allergic disease can be attributed to rapidly increasing air pollution levels. Rapid urbanization and increased energy consumption worldwide have exposed the human body to not only increased quantities of ambient air pollution, but also a greater variety of pollutants. Many studies clearly demonstrate that air pollutants potently trigger asthma exacerbation. Evidence that transportation-related pollutants contribute to the development of allergies is also emerging. Moreover, exposure to particulate matter, ozone, and nitrogen dioxide contributes to the increased susceptibility to respiratory infections. This article focuses on the current understanding of the detrimental effects of air pollutants on allergic disease including exacerbation to the development of asthma, allergic rhinitis, and eczema as well as epigenetic regulation.

Cool and dry weather enhances the effects of air pollution on emergency IHD hospital admissions

BackgroundAssociations between ambient pollution and cardiovascular morbidity including ischemic heart disease (IHD) have been confirmed. Weather factors such as temperature, season and relative humidity (RH) may modify the effects of pollution. We conducted this study to examine the effects of air pollution on emergency IHD hospital admissions varied across seasons and RH levels, and to explore the possible joint modification of weather factors on pollution effects. MethodsDaily time series of air pollution concentrations, mean temperature and RH were collected from IHD hospital admissions from 1998 to 2007 in Hong Kong. We used generalized additive Poisson models with interaction term to estimate the pollution effects varied across seasons and RH levels, after adjusting for time trends, weather conditions, and influenza outbreaks. ResultsAn increase in the detrimental effects of air pollution in cool season and on low humidity days was observed. In the cool and dry season, a 10μg/m3 increment of lag03 exposure was associated with an increase of emergency IHD admissions by 1.82% (95% CI: 1.24–2.40%), 3.89% (95% CI: 3.08–4.70%), and 2.19% (95% CI: 1.33–3.06%) for particles with an aerodynamic diameter less than 10μm (PM10), nitrogen dioxide (NO2), and ozone (O3), respectively. The effects of pollutants decreased greatly and lost statistical significance in the warm and humid season. ConclusionsWe found season and RH jointly modified the associations between ambient pollution and IHD admissions, resulting in increased IHD admissions in the cool and dry season and reduced admissions in the warm and humid season.

Season and humidity dependence of the effects of air pollution on COPD hospitalizations in Hong Kong

Associations between ambient pollution and respiratory morbidity including chronic obstructive pulmonary disease (COPD) have been confirmed. Weather factors, such as temperature, season and relative humidity (RH), may modify the effects of air pollution. This time series study was conducted to examine whether the effects of air pollution on emergency COPD hospital admissions in Hong Kong varied across seasons and RH levels, and explore the possible joint modification of season and RH on the effects of pollution. Data of daily air pollution concentrations mean temperature and RH, and COPD hospital admissions from 1998 to 2007 were collected. Generalized additive Poisson models with interaction terms were used to estimate the effects of pollution across seasons and RH levels. We observed an increase in the detrimental effects of air pollution in the cool season and on low humidity days. On the cool and dry days, a 10 μg m−3 increment of lag03 exposure was associated with an increase in emergency COPD admissions by 1.76% (95%CI: 1.19–2.34%), 3.43% (95%CI: 2.80–4.07%), and 1.99% (95%CI: 0.90–3.09%) for nitrogen dioxide (NO2), ozone (O3), and sulfur dioxide (SO2), respectively, all of which were statistically significantly higher than those on the other days. No consistent modification of weather factors was found for the effects of particles with an aerodynamic diameter less than 10 μm (PM10). The results suggested that season and RH jointly modified the effects of gaseous pollutants, resulting in increased emergency COPD hospitalizations on the cool and dry days.

The adverse effects of air pollution on the nervous system.

Exposure to ambient air pollution is a serious and common public health concern associated with growing morbidity and mortality worldwide. In the last decades, the adverse effects of air pollution on the pulmonary and cardiovascular systems have been well established in a series of major epidemiological and observational studies. In the recent past, air pollution has also been associated with diseases of the central nervous system (CNS), including stroke, Alzheimer's disease, Parkinson's disease, and neurodevelopmental disorders. It has been demonstrated that various components of air pollution, such as nanosized particles, can easily translocate to the CNS where they can activate innate immune responses. Furthermore, systemic inflammation arising from the pulmonary or cardiovascular system can affect CNS health. Despite intense studies on the health effects of ambient air pollution, the underlying molecular mechanisms of susceptibility and disease remain largely elusive. However, emerging evidence suggests that air pollution-induced neuroinflammation, oxidative stress, microglial activation, cerebrovascular dysfunction, and alterations in the blood-brain barrier contribute to CNS pathology. A better understanding of the mediators and mechanisms will enable the development of new strategies to protect individuals at risk and to reduce detrimental effects of air pollution on the nervous system and mental health.

City scale assessment model for air pollution effects on the cultural heritage

Damage caused to objects of cultural heritage is one of the most serious detrimental effects of air pollutants . Within the 6th Framework Programme of the EU, the CULT-STRAT project is an inter-agency, multi-disciplinary project that has integrated research and monitoring information to provide answers to policy and management questions, which relate the effects of air pollutants on heritage and the management options available to mitigate them. The overall aim of the project has been to assess and predict the effects of different pollutants on materials and objects of cultural heritage in a multipollutant scenario and to identify indicators and thresholds levels of pollutants. These have been used for development of management strategies for sustainable maintenance and preventive conservation of European Cultural Heritage and air quality policy from continental to local scale. The present paper reports one of the studies carried out in the CULT-STRAT project at city level and focused on the town of Madrid (Spain). Different maps are shown for the present and possible future scenarios (2010 and 2020): inventory of stock of cultural heritage for each selected material, concentration of selected pollutants (SO 2 , NO 2 , O 3 and PM 10 ), corrosion (cast bronze) and recession (Portland limestone), exceedance of tolerable degradation thresholds for each material and corrosion-cultural heritage overlapped maps. ► A methodology for the evaluation of Cultural Heritage at risk has been developed. ► A case-study focused on the city of Madrid, as example, is presented. ► Two materials have been considered: cast bronze and Portland limestone. ► Mainly, the effect of pollution reduction has been studied. ► Mapping: pollutants, corrosivity, exceedance and future scenarios.

Air pollution and infection in respiratory illness.

The detrimental effects of air pollution on health have been recognized for most of the last century. Effective legislation has led to a change in the nature of the air pollutants in outdoor air in developed countries, while combustion of raw fuels in the indoor environment remains a major health hazard in developing countries. The mechanisms of how these pollutants exert their effects are likely to be different, but there is emerging evidence that the toxic effects of new photochemical pollutants such as nitrogen dioxide are likely to be related to infection. This review discusses the relationship between air pollution and infection and will explore some of the mechanisms of how both could act synergistically to cause respiratory illnesses especially in exacerbating symptoms in individuals with pre-existing respiratory conditions such as asthma and chronic obstructive pulmonary disease.

The interaction between particulate air pollution and allergens in enhancing allergic and airway responses.

Although the detrimental effects of air pollution on human health have been brought widely to public notice, it appears that less attention has been given to the potential role of toxic air pollutants in the induction of allergic conditions such as asthma, rhinoconjunctivitis, and atopic eczema. A number of large epidemiologic studies have shown that people exposed to intense motor vehicle traffic and its associated emissions are at major risk for allergic symptoms, reduced lung function, and increased sensitization to common airborne allergens. Several laboratory-based studies have demonstrated that particulate air pollutants emitted from motor vehicles can induce allergic inflammation, enhance IgE responses, and increase airway hyperresponsiveness, which could provide an underlying mechanism for the increasing prevalence of allergic diseases. This article reviews the evidence that supports the causative link between particulate air pollution and the sharp increase in the prevalence of type I allergies in developed countries.

Particulate air pollution from motor vehicles: a putative proallergic hazard?

Air pollution generated from motor vehicle exhaust has become a major cause for scientific and public concern worldwide over recent years. The rapid and marked increase in the motor vehicle traffic and its associated emissions in urban areas have paralleled a sharp increase in the prevalence of allergic diseases such as asthma and rhinitis. Epidemiological studies have demonstrated a strong association between people living in close proximity to roads with high traffic density and increased allergic symptoms, reduced lung function and increased sensitization to common aeroallergens. Several laboratory-based studies have demonstrated that pollutants emitted from motor vehicles can induce allergic inflammation and increase airway hyperresponsiveness, which may provide an underlying mechanism for the increasing prevalence of allergic diseases. Although the detrimental effects of air pollution on human health have been brought to public attention, it appears that less attention has been given to the potential role of road traffic fumes in the induction of the allergic state. Legislators should consider pollutants emitted from motor vehicle exhausts as a potential pro-allergic hazard, before making important changes in environmental policy.

Continuing Lichen Recolonization in the Upper Ohio River Valley

Improvement in the air quality of the upper Ohio River valley has led to lichen recolonization at previously depauperate sites. Between 1973 and 1996 the number of corticolous macrolichen species in the area increased from 6 to 20. During the same time the mean species richness per site increased from 0.8 to 6.5. An indicator species, Flavoparmelia caperata, was absent from all study sites in 1973, but present at 27 of 28 study sites in 1996. Lichen studies performed over time provide a good tool to document air quality improvement, but a single study in a changing air quality environment may give problematic results. There are many published accounts of the detrimental effects of air pollution, especially sulfur dioxide, on lichen species distribution and community success (Ferry et al. 1973; Nash & Wirth 1988). Recently, however, industrial modernization and clean air legislation have led to decreases in sulfur emissions with concomitant decreases in ground-level SO2 concentrations both in North America and Europe. One source (Placet & Streets 1987) estimated that total SO2 emissions in the United States decreased from 26.8 million metric tons in 1975 to 21.2 million metric tons in 1985. There have been further decreases to 16.6 million metric tons in 1995 (USEPA 1996). Ohio has shown similar decreases in emissions with 2.99 million metric tons in 1975, 2.43 in 1985 and 1.90 in 1995. The upper Ohio River valley was once reputed to have the dirtiest air in the nation (Showman 1990). This area was heavily industrialized with coal-burning power plants, steel mills, foundries, and coking ovens. However, the region was severely affected by the economic recession in the late 1970s that led to the decline of the steel industry. Old plants were closed and others were upgraded and modernized. At the same time, clean air legislation led to particulate and gaseous emission controls on most electric power generation and industrial plants. This decrease in emissions had a dramatic effect on the ambient SO2 levels measured at upper Ohio River valley locations. Monitoring data (North Ohio Valley Air Authority, pers. comm.) show that in 1975, Steubenville, Ohio had an annual average SO2 concentration of 118 iggm-3. In 1985, this had almost halved to 60 agm-3, and by 1995 the value was further reduced to 34 agm-3. Likewise, East Liverpool, Ohio reported annual average SO2 concentrations of 120, 44, and 31 agm-3 during the same years. For comparison, the National ambient air quality standard (annual average) for SO2 is 80 Igm-3. Data from the several monitoring sites in the area consistently show a sharp decline from high to much lower values about 1981 (North Ohio Valley Air Authority, pers. comm.). Lichen studies in the upper Ohio River valley were first conducted in 1973 around Cardinal Power Plant, located just south of Steubenville, Ohio (Fig. 1). After the initial study, it was apparent that the regional SO2 background overwhelmed any contribution to ground-level concentrations by the power plant. Lichens were depauperate throughout a 570 km2 study area with no discernible differences between sites upwind and downwind from the Cardinal Plant. Studies were continued in order to monitor the impact of regional SO2 on lichens. Lichen re-surveys were performed in 1983, 1988, and then yearly to the present. Lichen improvement was first seen in 1988 and a note reporting this was published in 1990 (Showman 1990). The purpose of this paper is to describe lichen recolonization up to 1996 in greater detail, and to relate the observed changes in the lichen flora to potential associations with improved air quality over the same timespan.

Microbial transformations of some particulate pollution deposits in soils — A source of plant-available nitrogen and sulphur

Atmospheric pollution deposits, largely consisting of soot, were removed from sycamore leaves growing downwind of a coking plant, and added to soil. Increases in plant available S-ions (S2O32−; S4O62− and SO42−) and N (NH4+ and NO3−) occurred due to the action of soil microorganisms on the deposits. Although the detrimental effects of air pollution on plant growth have been previously emphasised, supply of nutrients resulting from the microbial transformation of particulate pollutants may prove important to the growth of pollution-resistant plant communities.

The Deterioration of Materials in Polluted Atmospheres

Abstract A brief summary of the chemical and physical aspects of polluted atmospheres. More specificially it deals with the detrimental effects of air pollutants on materials other than living tissue. In addition to corrosion of metallic surfaces, the physical and chemical principles involved in the damage to such materials as paint, glass, stone, rubber, and fibers by manmade air contaminants are discussed. 4.2.8