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PubMed2006

Airway inflammation in iron ore miners exposed to dust and diesel exhaust.

The aim of the present study was to investigate if underground miners exposed to dust and diesel exhaust in an iron ore mine would show signs of airway inflammation as reflected in induced sputum. In total, 22 miners were studied, once after a holiday of at least 2 weeks and the second time after 3 months of regular work. Control subjects were 21 "white-collar" workers. All subjects completed a questionnaire regarding medical and occupational history, and underwent lung function testing and induced sputum collection. Total and differential cell counts and analyses of the fluid phase of the induced sputum were performed. Sampling of personal exposure to elemental carbon, nitrogen dioxide and inhalable dust was recorded. The average concentrations of inhalable dust, nitrogen dioxide and elemental carbon were 3.2 mg.m-3, 0.28 mg.m-3 and 27 microg.m-3, respectively. Miners had increased numbers of inflammatory cells, mainly alveolar macrophages and neutrophils, and increased concentrations of fibronectin, metalloproteinase-9 and interleukin-10 in induced sputum compared with controls. In conclusion, miners in an underground iron ore mine demonstrated persistent airway inflammation that was as pronounced after a 4-week holiday as after a 3-month period of work underground in the mine.

Adult↗

PubMed2004

Studies on photochemical reactions of air pollutants. XIV.Photooxidation of sulfur dioxide in air by various air pollutants.

Upon exposure to sunlight, or to artificial light at wavelengths longer than 290 nm, sulfur dioxide in air underwent oxidation to give sulfur trioxide in the presence of air pollutants such as biacetyl (2,3-butanedione), benzaldehyde and nitrogen dioxide, but not in their absence. Only nitrogen dioxide completely oxidized sulfur dioxide to sulfur trioxide.

Air Pollutants↗

PubMed2004

Effect of short-term exposure to low levels of gaseous pollutants on chronic obstructive pulmonary disease hospitalizations.

We examined the associations between gaseous pollutants and hospitalization for chronic obstructive pulmonary diseases (COPD) among elderly people living in Vancouver, British Columbia, Canada, a city in which ambient air pollution levels are relatively low. We regressed the logarithm of daily counts of acute COPD hospitalization during the 5-year period from 1994 to 1998 on the daily mean levels of each pollutant, after accounting for seasonal and subseasonal fluctuations, non-Poisson dispersion, and weather variables. Nitrogen dioxide and carbon monoxide were significantly associated with hospitalization for COPD, and the magnitude of effects was increased slightly with increasing days of exposure averaging, with the relative risk for a 7-day average being 1.11 (95%CI: 1.04, 1.20) and 1.08 (1.02, 1.13) for nitrogen dioxide and carbon monoxide, respectively. There was no significant association between either sulfur dioxide or ozone and COPD hospitalization. The combined relative risk for all four gaseous pollutants on COPD hospitalization was 1.21. The effects of gaseous pollutants on COPD hospitalization were not significant after adjustment for PM(10), although its inclusion did not have a marked effect on the point estimates for relative risks. Nitrogen dioxide has a significant impact on COPD hospitalization. Further studies are needed to separate the effects of single pollutants from the combined effects of the complex mixture of air pollutants in urban atmospheres.

Aged↗

PubMed1999

Peroxynitrite reaction with heme proteins.

We have reported that low levels of peroxynitrite (PN) can cause inactivation of the heme-thiolate protein prostacyclin (PGI2)-synthase by nitration of a tyrosine residue. To prove that iron catalysis is involved we studied the interaction of PN with microperoxidase and P450nor, a heme-thiolate protein of known structure. Spectral and kinetic analyses allow to conclude on a ferryl nitrogen dioxide complex as an intermediate which decomposes in the presence of an excess of PN under formation of dioxygen, nitrite, and nitrate. This occurs in a catalytic cycle which was more efficient with P450nor than with microperoxidase. If phenol was added to the reaction mixtures of PN and the ferric complexes the ratio of hydroxylated to nitrated phenols decreased compared to the metal-free system. Phenol competed with the formation of dioxygen indicating that the ferryl intermediate was involved in both pathways. One therefore can postulate that the ferryl complex reacts with phenol to give the phenoxyradical which is nitrated in the presence of nitrogen dioxide but does not give hydroxylated products as with metal-free PN. Alternately, the ferryl nitrogen dioxide complex can oxidize a second PN molecule to the radical, *OONO, which can decompose to dioxygen and NO. The latter forms N2O3, with the remaining *NO2 radical. A third pathway consists in the isomerization to nitrate which also is catalyzed by the heme proteins since the ratio of nitrite/nitrate does not change significantly during the catalytic reaction with excess of PN. Our data explain the mechanism of nitration of PGI2-synthase, suggest a role of P450nor as a PN scavenger, and favor heme-thiolate complexes for trapping PN.

Catalysis↗

PubMedDate not supplied

Traffic-related air pollution affects peak expiratory flow, exhaled nitric oxide, and inflammatory nasal markers.

The authors used a longitudinal observational design, with repeated measures, to study the association between traffic-related air pollutants (i.e., nitric oxide, nitrogen dioxide, carbon monoxide, and Black Smoke) and respiratory symptoms. Subjects (N = 82) attended an elementary school in either Utrecht (i.e., urban children) or Bilthoven (i.e., suburban children). These two geographic areas differed with respect to levels of Black Smoke (means = 53 microg/m3 and 18 microg/m3, respectively). Levels of nitric oxide, nitrogen dioxide, carbon monoxide, and Black Smoke were consistently higher in Utrecht than in Bilthoven (mean daily ratios were 8, 1.5, 1.8, and 2.7, respectively). The authors compared mean levels of short-term effects of the aforementioned air pollutants on suburban and urban children. Urban children had higher mean levels (p = .05) of interleukin-8 (32%), urea (39%), uric acid (26%), albumin (15%), and nitric oxide metabolites (21%) in nasal lavage than did suburban children. Peak expiratory flow, exhaled nitric oxide levels, and nasal markers were associated with levels of particulate matter with diameters less than or equal to 10 microm, Black Smoke, nitrogen dioxide, and nitric oxide. With respect to per-unit increases in air pollution, urban children had more increased peak expiratory flow, higher levels of exhaled nitric oxide, and more increased release of uric acid, urea, and nitric oxide metabolites than suburban children. In summary, urban children had increased levels of inflammatory nasal markers, and their responses were more pronounced than were the suburban children's responses to the same increments of air pollution.

Adolescent↗

PubMed2000

Nitrite as a substrate and inhibitor of myeloperoxidase. Implications for nitration and hypochlorous acid production at sites of inflammation.

Myeloperoxidase is a heme enzyme of neutrophils that uses hydrogen peroxide to oxidize chloride to hypochlorous acid. Recently, it has been shown to catalyze nitration of tyrosine. In this study we have investigated the mechanism by which it oxidizes nitrite and promotes nitration of tyrosyl residues. Nitrite was found to be a poor substrate for myeloperoxidase but an excellent inhibitor of its chlorination activity. Nitrite slowed chlorination by univalently reducing the enzyme to an inactive form and as a consequence was oxidized to nitrogen dioxide. In the presence of physiological concentrations of nitrite and chloride, myeloperoxidase catalyzed little nitration of tyrosyl residues in a heptapeptide. However, the efficiency of nitration was enhanced at least 4-fold by free tyrosine. Our data are consistent with a mechanism in which myeloperoxidase oxidizes free tyrosine to tyrosyl radicals that exchange with tyrosyl residues in peptides. These peptide radicals then couple with nitrogen dioxide to form 3-nitrotyrosyl residues. With neutrophils, myeloperoxidase-dependent nitration required a high concentration of nitrite (1 mM), was doubled by tyrosine, and increased 4-fold by superoxide dismutase. Superoxide is likely to inhibit nitration by reacting with nitrogen dioxide and/or tyrosyl radicals. We propose that at sites of inflammation myeloperoxidase will nitrate proteins, even though nitrite is a poor substrate, because the co-substrate tyrosine will be available to facilitate the reaction. Also, production of 3-nitrotyrosine will be most favorable when the concentration of superoxide is low.

Cells, Cultured↗

PubMed1989

Effects of inhaled acids on lung biochemistry.

Effects of respirable aerosols of sulfuric acid, ammonium sulfate, sodium sulfite, and ammonium persulfate on lungs of rats are reviewed. The literature regarding interactions between ozone or nitrogen dioxide and acidic aerosols (ammonium sulfate, sulfuric acid) is discussed. An unexpected interaction between nitrogen dioxide and sodium chloride aerosol is also discussed. An attempt is made to identify bases for prediction of how and when acid aerosols might potentiate effects of inhaled gases.

Acid Rain↗

PubMed2001

Effects of blasting fumes on exposure and short-term lung function changes in tunnel construction workers.

OBJECTIVES: This study attempts to determine the effects of exposure to blasting fumes and its influence on the lung function of tunnel workers. METHODS: Two groups of tunnel workers, one using ammonium nitrate fuel oil (ANFO) as the explosive and the other using size-sensitized emulsion (SSE), with 24 workers per group, were compared with a reference group (N=34) with low exposure. Spirometry was used to determine lung function. Personal exposure to total and respirable dust, alpha-quartz, volatile organic compounds, oil mist and vapors, formaldehyde, nitrogen dioxide, and carbon monoxide was measured. RESULTS: The ANFO workers were more exposed to all the agents than the reference group and more exposed than the SSE workers to all the agents except total dust and carbon monoxide. The SSE workers were significantly more exposed to total dust and alpha-quartz than the reference group. High peak exposures to nitrogen dioxide (up to 20 ppm) occurred for the ANFO workers in contrast to the SSE workers, whose exposure did not exceed 2 ppm. The lung function of the ANFO workers significantly decreased by 3% for forced vital capacity, 7% for forced expiratory volume in 1 second, and 8% for forced expiratory flow rate from 25% to 75% of the forced vital capacity over the 11-day period. The changes were reversible. There were no significant changes among the SSE workers and the outdoor workers. The ANFO workers had a significant decrease in FEV1.0 when compared with both the SSE and outdoor workers. CONCLUSIONS: Tunnel workers using ANFO explosive show a temporary reduction in lung function, whereas those using SSE do not. The most likely explanation for the observed changes is peak exposures to nitrogen dioxide.

Adult↗

PubMedDate not supplied

Pathogenesis of nitrogen dioxide-induced respiratory lesions in reference to respiratory clearance of inhaled particulates.

The pathogenesis of NO2-induced respiratory disease and the effect of NO2 on respiratory clearance of 51Cr2O3 were studied. Young adult female mice were exposed to a 51Cr2O3 aerosol, followed by a daily exposure to either 30 ppm NO2 for 2 wk or 60 ppm NO2 for 2 wk or a single exposure to 170 ppm NO2. Exposure to 30 ppm NO2 had a minimal histopathologic effect on respiratory tract tissue. Exposure to 60 ppm NO2 produced marked histopathologic effects, which were subsequently resolved. Exposure to 170 ppm NO2 produced permanent histopathologic lesions. In mice exposed to concentrations of NO2 that produced minimal histopathologic effects, respiratory clearance of 51Cr2O3 was similar to that in unexposed mice. When mice were exposed to concentrations of NO2 that produced permanent tissue damage, prolonged impairment of respiratory clearance of 51Cr2O3 was observed, despite resolution of edema produced by inhalation of NO2. At concentrations of NO2 that produced marked edema and histopathologic effects that were resolved despite repeated NO2 exposure, there was an initial marked impairment of respiratory clearance, then an accelerated rate of clearance, and finally a clearance rate similar to that of unexposed mice. The time during which accelerated clearance occurred was well correlated with the time at which the histopathologic lesions was observed to regress.

Animals↗

PubMed1986

Influence of exposure regimen on nitrogen dioxide-induced morphological changes in the rat lung.

Experiments were performed to study the influence of concentration, exposure pattern, and length of exposure on the degree and extent of morphological alterations in the NO2-exposed rat lung. Four weeks of continuous exposure to 20 mg NO2/m3 consecutively revealed damage and loss of cilia, replacement of desquamated type I pneumocytes by type II pneumocytes resulting in a cuboidal epithelial lining, an influx of alveolar macrophages, and hypertrophy and hyperplasia of the bronchiolar epithelium. The animals recovered almost completely from the induced lesions within 8 days. Continuous exposure to 1, 2.5, or 5 mg/m3 displayed minimal alterations in the 5 mg/m3 group. The effects increased with exposure time. Intermittent or continuous exposure to 20 mg NO2/m3 resulted in minor differences after 4 weeks. The onset of the lesions was delayed and the massive influx of alveolar macrophages in the continuously exposed animals failed to appear in the intermittently exposed animals. This work demonstrates that in subacute experiments: Concentration plays a more important role in inducing pulmonary lesions than exposure time when the product of concentration and time is kept constant. This effect is stronger during intermittent exposure than during continuous exposure. Continuous exposure seems to be a more important factor with regard to a macrophage response than intermittent exposure. The rat lung has a large capacity to repair almost completely from damage caused by short-term NO2 exposure.

Animals↗

PubMed2001

Atmospheric carbon dioxide concentration, nitrogen availability, temperature and the photosynthetic capacity of current-year Norway spruce shoots.

Branches of field-grown Norway spruce (Picea abies (L.) Karst.) trees were exposed to either long-term ambient or to elevated CO2 concentrations ([CO2]) using the branch bag technique. The light-saturated photosynthetic rates (A(max)) of current-year shoots differing in nitrogen (N) status were measured at various temperatures and at either ambient (360 micromol mol(-1), AMB) or elevated (ambient + 350 micromol mol(-1), EL) [CO2]. The value of A(max) was determined at various intercellular [CO2]s (A/Ci curves) and used to normalize photosynthetic rates to the mean treatment C(i) values, which were 200 micromol mol(-1) (AMB) and 450 micromol mol(-1) (EL), respectively. Needle N status and temperature strongly affected A(max). The response to N increased with temperature, and the photosynthetic temperature optimum increased with N status. This was assumed to be a result of reduced mesophyll CO2 conductance. The relative increase of Amax in the EL treatment compared to the AMB treatment varied from 15 to 90%, and increased with temperature, but decreased with N status. Nevertheless, the absolute photosynthetic response to EL increased with shoot N status. The relative increase in the instantaneous response of A(max) to elevated [CO2] was about 20% higher than the long-term response, i.e., there was downward acclimation in Amax in response to elevated [CO2]. The photosynthetic temperature optimum increased 4 degrees C with either a short- or a long-term increase in [CO2]. The bag treatment itself increased A(max) by approximately 16% and the temperature optimum of A(max) by approximately 3 degrees C.

Carbon Dioxide↗

PubMed1997

Biochemical detection of type I cell damage after nitrogen dioxide-induced lung injury in rats.

We have previously shown that injury to lung epithelial type I cells can be detected biochemically by measuring the airway fluid content of a type I cell-specific protein, rTI40, in a model of severe acute lung injury [M. C. McElroy, J.-F. Pittet, S. Hashimoto, L. Allen, J. P. Wiener-Kronish, and L. G. Dobbs. Am. J. Physiol. 268 (Lung Cell. Mol. Physiol. 12): L181-L186, 1995]. The first objective of the present study was to evaluate the utility of rTI40 in the assessment of alveolar injury in a model of milder acute lung injury. Rats were exposed to 18 parts/ million NO2 for 12 h; control rats received filtered air for 12 h. In NO2-exposed rats, the total amount of rTI40 in bronchoalveolar fluid was elevated 2-fold compared with control values (P < 0.001); protein concentration was 8.5-fold of control values (P < 0.001). The increase in rTI40 was associated with morphological evidence of injury to type I cells limited to the proximal alveolar regions of the lung. The second objective was to correlate the severity of alveolar type I cell injury with functional measurements of lung epithelial barrier integrity. NO2 inhalation stimulated distal air space fluid clearance despite a significant increase in lung endothelial and epithelial permeability to protein. These data demonstrate that rTI40 is a useful biochemical marker for mild focal injury and that exposure to NO2 alters lung barrier function. Taken together with our earlier studies, these results suggest that the quantity of recoverable rTI40 can be used as an index of the severity of damage to the alveolar epithelium.

Animals↗

PubMed2003

Exposure to air pollution during different gestational phases contributes to risks of low birth weight.

BACKGROUND: Although there have been growing concerns about the adverse effects of air pollution on birth outcomes, little is known about which specific exposure times of specific pollutants contribute to low birth weight (LBW). METHODS: We evaluated the relationships between LBW and air pollution exposure levels in Seoul, Korea. Using the air pollution data, we estimated the exposure during each trimester and also during each month of pregnancy on the basis of the gestational age and birth date of each newborn. Generalized additive logistic regression analyses were conducted considering infant sex, birth order, maternal age, parental education level, time trend, and gestational age. RESULTS: The monthly analyses suggested that the risks for LBW tended to increase with carbon monoxide (CO) exposure between months 2-5 of pregnancy, with exposure to particles <10 micro m (PM(10)) in months 2 and 4, and for sulphur dioxide (SO(2)) and nitrogen dioxide (NO(2)) exposure between months 3-5. CONCLUSIONS: This study suggests that exposure to CO, PM(10,) SO(2) and NO(2) during early to mid pregnancy contribute to risks for LBW.

Air Pollutants↗

PubMed1999

Effect of loratadine on nitrogen dioxide-induced changes in electrical resistance and release of inflammatory mediators from cultured human bronchial epithelial cells.

BACKGROUND: Recent studies have demonstrated that some antihistamines can attenuate histamine-induced release of inflammatory mediators from bronchial epithelial cells. OBJECTIVE: The purpose of study was to test the hypothesis that loratadine may influence pollution-induced inflammation of the airways by modulating epithelial membrane integrity and the synthesis and/or release of inflammatory mediators from airway epithelial cells. METHODS: We have cultured human bronchial epithelial cell (HBEC) cultures from surgical explants and investigated the effect of loratadine on NO2-induced changes in both electrical resistance of HBEC cultures and release of IL-8, RANTES, and soluble intercellular adhesion molecule-1 (sICAM-1) from these cells after exposure for 6 hours to either air or 400 ppb NO2. RESULTS: Exposure for 6 hours to NO2 significantly decreased the electrical resistance of HBEC cultures by 18.1% from baseline (P <.05). Incubation with 0.25 to 25 micromol/L loratadine did not alter the NO2-induced decrease in the electrical resistance of HBEC cultures. NO2 also significantly increased the release of IL-8 from a control value of 52.5 pg/microgram cellular protein to 81.9 pg/microgram cellular protein (P <.05), RANTES from a control value of 0.023 pg/microgram cellular protein to 0.062 pg/microgram cellular protein (P <.05), and sICAM-1 from a control value of 7.7 pg/microgram cellular protein to 16.3 pg/microgram cellular protein (P <.05). The NO2-induced release of all 3 mediators was significantly attenuated by incubation of HBECs with 25 micromol/L loratadine. Incubation with 2.5 micromol/L loratadine also significantly attenuated the NO2-induced release of RANTES and sICAM-1, but not IL-8. CONCLUSIONS: These results suggest that loratadine has the potential to reduce airway inflammation by modulating the release of inflammatory cytokines from airway epithelial cells.

Adult↗

PubMed2003

Relationship between air pollution and daily mortality in a tropical city: Kaohsiung, Taiwan.

Air pollution has been associated with daily mortality in numerous studies over the past decade. However, most of these studies were conducted in the United States and Europe, with relatively few done in Asia. In this study, the association between ambient air pollution and daily mortality in Kaohsiung, Taiwan, a large industrial city with a tropical climate, was investigated for the period 1994-2000 using a case-crossover analysis. This design is an alternative to Poisson time-series regression for studying the short-term adverse health effects of air pollution. The air pollutants examined included particulate matter (PM10), sulfur dioxide (SO2), ozone (O3), nitrogen dioxide (NO2), and carbon monoxide (CO). No significant effects were found between PM10 and SO2 exposure levels and respiratory-related mortality. The well-established link between air pollution levels and daily mortality may not be as strong in cities in tropical areas, although other factors such as differences in pollutant mixtures or underlying health of the population may explain the lack of a strong association in this study. Further studies of this type in cities with varying climates and cultures are needed.

Air Pollution↗

PubMed2007

Air quality assessment in Delhi: before and after CNG as fuel.

A number of policy measures have been activated in India in order to control the levels of air pollutants such as particulate matter, sulphur dioxide (SO(2)) and nitrogen dioxide (NO(2)). Delhi, which is one of the most polluted cities in the world, is also going through the implementation phase of the control policies. Ambient air quality data monitored during 2000 to 2003, at 10 sites in Delhi, were analyzed to assess the impact of implementation of these measures, specifically fuel change in vehicles. This paper presents the impact of policy measures on ambient air quality levels and also the source apportionment. CO and NO(2) concentration levels in ambient air are found to be associated with the mobile sources. The temporal variation of air quality data shows the significant effect of shift to CNG (Compressed Natural Gas) in vehicles.

Air Pollutants↗

PubMed2000

Impact to lung health of haze from forest fires: the Singapore experience.

OBJECTIVE: From late July to the beginning of October 1997, countries of Southeast Asia experienced severe smoke haze pollution from uncontrolled forest fires mainly in the Indonesian states of Kalimantan and Sumatra. In Singapore, the impact of the 1997 haze was felt in the period from the end of August to the first week of November 1997 as a result of prevailing winds. METHODOLOGY: The Ministry of the Environment monitors ambient air quality by a country-wide telemetric air quality monitoring and management network, with 15 stations located throughout the island, linked via a public telephone network to a central control station at the Environment Building. The monitoring methods used are the United States Environmental Protection Agency (USEPA) reference methods. The Pollutant Standards Index (PSI) developed by the USEPA is used for the reporting of daily air pollution concentrations. Intervals on the PSI scale are related to the potential health effects of the daily measured concentrations of the five major air pollutants: sulfur dioxide, particulate matter (PM10), nitrogen dioxide, ozone and carbon monoxide. Public sector health facilities which come under the Ministry of Health, have computerized patient care systems which enable the routine ongoing surveillance of disease conditions for the period of the haze. Attention during the period of the haze was focused on conditions related to health effects of the haze. Data sources for the monitoring of the lung health effects of the haze included morbidity from public sector outpatient care facilities, accidents and emergency departments, public sector inpatient care facilities and national mortality data. RESULTS: Findings from the health impact of the haze showed that there was a 30% increase in outpatient attendance for haze-related conditions. An increase in PM10 levels from 50 microg/m3 to 150 microg/m3 was significantly associated with increases of 12% of upper respiratory tract illness, 19% asthma and 26% rhinitis. Supplementary findings from scanning the electron microscopic sizing of the haze particles showed that 94% of the particles in the haze were below 2.5 microm in diameter. This was consistent with emissions from combustion sources originating over 500 km from Singapore. This has been of some concern because particles smaller than 2.5 microm in diameter can easily bypass normal body defence metabolism and penetrate deeply into the alveoli of the lungs. During the same period, there was also an increase in accident and emergency attendance for haze-related conditions. There was no significant increase in hospital admissions or in mortality. CONCLUSION: The present study found that the health effects from the 1997 smoke haze in Singapore were generally mild.

Air Pollutants↗

PubMed2000

Combined respiratory effects of cold air with SO(2) or NO(2) in repeated 10-minute exposures of hyperventilating guinea pigs.

Previous studies in asthmatic subjects and guinea pigs have demonstrated attenuation of bronchoconstriction in repeated exposures to clean cold dry air. In the present animal study, we have simulated short-lasting human exposures to subfreezing urban air containing sulfur dioxide (SO(2)) and nitrogen dioxide (NO(2)). The anesthetized, paralyzed, and mechanically ventilated guinea pigs had 4 consecutive 10-min exposures either to clean cold dry air or to cold air with graded concentrations of SO(2) (0-5 ppm) or NO(2) (0-4 ppm). Peak expiratory flow (PEF) and tidal volume (V(T)) were continuously measured both during and after highly controlled exposures. Bronchoalveolar lavage fluid (BALF) and histological samples were obtained after finishing the consecutive exposures. Cold air + SO(2) at 1 and 2.5 ppm (n = 12) produced immediate concentration-dependent increases in the lung function responses compared to the preceding single exposure to clean cold dry air in the same animals (DeltaPEF = -32.7 +/- 6.1% and -35.6 +/- 6.5% vs. -27.0 +/- 3.1%; DeltaV(T) = -22.4 +/- 4.4% and -28.3 +/- 4.7% vs. -18.1 +/- 2.9%). In a multivariate analysis, these responses were significantly larger than the attenuated lung function responses to the corresponding second and third clean cold dry air exposures (p <. 05). The fourth exposure to cold air + SO(2) at 5 ppm produced a smaller response (DeltaPEF = -25.3 +/- 4.8% and DeltaV(T) = -17.8 +/- 3.7%) than cold air with the lower SO(2) concentrations. Cold air + NO(2) at 1 and 2.5 ppm (n = 12) produced roughly similar lung function responses to the preceding single exposure to clean cold dry air in the same animals, and there was no significant attenuation of bronchoconstriction as with the consecutive exposures to clean cold dry air. The largest decreases in lung functions (DeltaPEF = -33.8 +/- 6.7% and DeltaV(T) = -26.2 +/- 6.8%) were recorded during the fourth exposure, which was to cold air + NO(2) at 4 ppm. In the cold air + SO(2) group, there was a significantly lower proportion of macrophages in the differential count of BALF white cells compared to the clean cold dry air group. In addition, there was eosinophilic infiltration within and below the tracheal epithelium in all guinea pigs exposed to either clean cold dry air, cold air + SO(2), or cold air + NO(2). In conclusion, the addition of moderate concentrations of SO(2) or NO(2) to clean cold dry air counteracted the attenuation of bronchoconstriction induced by repeated cold dry air exposures in guinea pigs. Cold air + SO(2) also decreased the proportion of macrophages in BALF white cells.

Air Pollutants↗