Disease relevance of Air Pollution

• Differences in rural and urban populations appear to be real and suggest the need to examine the factors of indoor and outdoor environments created by air pollution, crowding, and allergen exposure and the demands made on the immune system by frequency of challenge by respiratory tract infections [1].
• Proteins of natural latex can act as adjuvants and as antigens capable of eliciting immediate hypersensitivity, making their presence in particulate air pollution an important clinical issue [2].
• Daily mean hospital admissions for cardiovascular diseases, ischemic heart diseases (IHDs), and stroke in seven European areas (the cities of Birmingham, London, Milan, Paris, Rome, and Stockholm, and in The Netherlands) participating in the multicenter European study of air pollution (Aphea-II), were measured [3].
• There is consistency in the findings that relate the acute increases in urban air pollution (mainly the particulate matter) and the short-term health effects (i.e. mortality and hospital admissions) on patients suffering from chronic obstructive pulmonary disease (COPD) [4].
• Some of the risk factors for COPD are well-known and include smoking, occupational exposures, air pollution, airway hyperresponsiveness, asthma, and certain genetic variations, although many questions, such as why < 20% of smokers develop significant airway obstruction, remain [5].

Psychiatry related information on Air Pollution

• Non-occupational factors associated with these include age, sex, race, smoking, social class, alcohol consumption, diet, exposures in leisure time, exercise, atopy, heredity, personal hygiene, personality type, stress, past or predisposing illness or injury, weather/climate and air pollution [6].

High impact information on Air Pollution

• Polycyclic aromatic hydrocarbons (PAH), found in cigarette smoke and air pollution, interact with the aryl hydrocarbon receptor (Ahr) to cause reproductive defects [7].
• Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution [8].
• In the light of suggestions that outdoor air pollution can harm people with asthma, we investigated the effect of 1 h exposures to domestic concentrations of nitrogen dioxide on the airway response to house-dust mite (HDM) allergen in ten patients with mild asthma [9].
• Tropospheric O(3) and sulfate both contribute to air pollution and climate forcing [10].
• Environmental air pollution, childhood infections, and familial factors other than alpha-1 protease inhibitor deficiency appear to play only small roles [11].

Chemical compound and disease context of Air Pollution

• In a previous study at this Institute, inhaled sulfur dioxide (SO2) was shown to enhance the induction by inhaled benzo[a]pyrene (BaP) of squamous cell carcinoma (SQCA) of the respiratory tract of rats (S. Laskin, M. Kuschner, A. Sellakumar, and G. V. Katz, 1976, In "Air Pollution and the Lung," pp. 190-213) [12].

Biological context of Air Pollution

• Annual average exposures to particulate air pollution was associated with an increased risk of pulmonary exacerbations and a decline in lung function, suggesting a role of environmental exposures on prognosis in CF [13].
• Vanadium compounds present in air pollution particulate matter activate signal transduction pathways in pulmonary cell types leading to pathological outcomes including aberrant cell proliferation, apoptosis, and cytokine expression [14].
• CYP1A1 plays an important role in the metabolic activation of polycyclic aromatic hydrocarbons (PAH), carcinogenic components of air pollution [15].
• In populations exposed to air pollution episodes, blood viscosity, fibrinogen, and C-reactive protein (CRP) were higher [16].
• Effects of environmental exposures (smoking, air pollution, and diet) on CYP1A1 gene induction in placental tissue and the modulation of induction by the CYP1A1 MspI RFLP were evaluated in two groups from Poland: 70 mother-child pairs from Krakow, a city with elevated air pollution; and 90 pairs from Limanowa, a less polluted area [17].

Anatomical context of Air Pollution

• These include pulmonary function decrements, increased bronchial hyperresponsiveness, visits to emergency departments, hospital admissions, increased medication use and symptom reporting, inflammatory changes, interactions between air pollution and allergen challenges, and immune system changes [18].
• The ISR reveals that calf lung surfactant, Infasurf, exhibits remarkable fluidity, even when exposed to air pollution residual oil fly ash (ROFA), hydrogen peroxide (H2O2), or conditioned media from resting A549 alveolar epithelial cells (AEC) [19].
• Lipopolysaccharide (LPS), a major proinflammatory glycolipid component of the gram-negative bacterial cell wall, is one of the agents ubiquitously present as contaminant on airborne particles, including air pollution, organic dusts, and cigarette smoke [20].
• Thus, metals and transition metals could increase the level of allergen-mediated mast cell activation, which might be one of the mechanisms mediating exacerbation of allergen-driven asthma symptoms by air pollution [21].
• At the start of the pollen season, the NAL concentration of eosinophils and ECP in pollen-sensitised children was increased compared to winter, but their levels were not further affected by increased exposure to pollen or air pollution [22].

Associations of Air Pollution with chemical compounds

• OBJECTIVES: We evaluated the association between daily ambient air pollution levels (particle number concentration [PNC]--a proxy for ultrafine particles [diameter < 0.1 microm], mass of particles with diameter less than 10 microm [PM10]; CO, NO2, and O3) and the occurrence of fatal, nonhospitalized coronary events [23].
• Air pollution measurements (particulate matter less than 10 microns in diameter [PM10], nitrogen dioxide [NO2], sulfur dioxide [SO2], and ozone) and meteorologic data were collected in each community [24].
• To help assess short-term respiratory responses to summertime air pollution, we exposed 24 asthmatic volunteers aged 11-18 in a chamber to respirable acid aerosol (mass median aerodynamic diameter 0.66 micron) plus 0.3 ppm nitrogen dioxide (NO2) plus 0.2 ppm ozone (O3) [25].
• METHODS: Routine air pollution monitoring data for sulphur dioxide (SO2), nitrogen oxides (NOx), ozone (O3), carbon monoxide (CO), and particles with an aerodynamic diameter of 10 microm or less (PM10) were used [26].
• Air pollution studies have shown that nitric oxide (NO), a gaseous free radical, is a potent photosynthetic inhibitor that reduces CO2 uptake activity in leaves [27].

Gene context of Air Pollution

• Circulating levels of IL-1 beta, IL-6, and GM-CSF were elevated in subjects exposed to high levels of PM(10) during an episode of acute air pollution [28].
• The results of this study support TNF as a genetic factor for susceptibility to ozone-induced changes in lung function in humans, and has potential implications for stratifying health risks of air pollution [29].
• Expression of cyclooxygenase-2 (COX2), an inflammatory mediator, and accumulation of the 42-amino acid form of beta-amyloid (Abeta42), a cause of neuronal dysfunction, were measured in autopsy brain tissues of cognitively and neurologically intact lifelong residents of cities having low (n:9) or high (n:10) levels of air pollution [30].
• The results of this study suggest that adhesion molecules or chemokines are associated with asthma and that ICAM-1 may play an important role in the relationship between air pollution and the occurrence of asthma [31].
• Inhalation of urban particles results in higher circulating levels of the vasoconstrictor peptide endothelin-1 (ET-1), which may account for the adverse cardiovascular impacts associated with air pollution [32].

Analytical, diagnostic and therapeutic context of Air Pollution

• To date, animal models of pulmonary hypertension, bronchitis, asthma, and cardiovascular disease, but not emphysema, appear to exhibit greater susceptibility to air pollution particulate matter [33].
• Seasonal variation of asthma and allergic rhinitis. Consultation pattern in general practice related to pollen and spore counts and to five indicators of air pollution [34].
• OBJECTIVE: To assess the effects of exposure to low concentrations of carbon monoxide (CO), as commonly measured in atmospheric urban air pollution and certain occupational environments, on exercise performance and myocardial perfusion in young healthy men, and the possible need for tighter restrictions on ambient concentrations of CO [35].
• Health effects of air pollution due to coal combustion in the Chestnut Ridge Region of Pennsylvania: results of cross-sectional analysis in adults [36].
• Baseline measurements were performed during low air pollution levels (max. 24-h concentrations of SO2, O3 and NO2 were 55, 49 and 58 micrograms/m3, respectively) consisting of lung function measurements using spirometry and the forced oscillation technique (FOT) and the prevalence of respiratory symptoms, determined by a written questionnaire [37].

References