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PubMed1994

Nitrogen dioxide-induced acute lung injury in sheep.

Lung mechanics, hemodynamics and blood chemistries were assessed in sheep (Ovis aries) before, and up to 24 h following, a 15-20 min exposure to either air (control) or approximately 500 ppm nitrogen dioxide (NO2). Histopathologic examinations of lung tissues were performed 24 h after exposure. Nose-only and lung-only routes of exposure were compared for effects on NO2 pathogenesis. Bronchoalveolar lavage fluids from air- and NO2-exposed sheep were analyzed for biochemical and cellular signs of NO2 insult. The influence of breathing pattern on NO2 dose was also assessed. Five hundred ppm NO2 exposure of intubated sheep (lung-only exposure) was marked by a statistically significant, albeit small, blood methemoglobin increase. The exposure induced an immediate tidal volume decrease, and an increase in both breathing rate and inspired minute ventilation. Pulmonary function, indexed by lung resistance and dynamic lung compliance, progressively deteriorated after exposure. Maximal lung resistance and dynamic lung compliance changes occurred at 24 h post exposure, concomitant with arterial hypoxemia. Bronchoalveolar lavage fluid epithelial cell number and total protein were significantly increased while macrophage number was significantly decreased within the 24 h post-exposure period. Histopathologic examination of lung tissue 24 h after NO2 revealed patchy edema, mild hemorrhage and polymorphonuclear and mononuclear leukocyte infiltration. The NO2 toxicologic profile was significantly attenuated when sheep were exposed to the gas through a face mask (nose-only exposure). Respiratory pattern was not significantly altered, lung mechanics changes were minimal, hypoxemia did not occur, and pathologic evidence of exudation was not apparent in nose-only, NO2-exposed sheep. The qualitative responses of this large animal species to high-level NO2 supports the concept of size dependent species sensitivity to NO2. In addition, when inspired minute ventilation was used as a dose-determinant, a linear relationship between NO2 dose and lung resistance was found. The importance of these findings, NO2 dose-determinants, and the utility of sheep as a large animal inhalation model are discussed.

Administration, Inhalation↗

PubMed1989

Membrane perturbations and mediation of gap junction formation in response to taurine treatment in normal and injured alveolar epithelia.

Nitrogen dioxide is an air pollutant that causes pulmonary alterations. Employing light and transmission electron microscopy, we examined plastic sections and freeze-fracture replicas of alveolar epithelium of groups of hamsters exposed to nitrogen for 24 h to determine taurine-induced changes in intercellular junctions. Prior to exposure, one group of hamsters was given 0.5% taurine in their drinking water for 2 weeks. A second group of hamsters was given taurine-free water. The taurine-treated group was divided into three subgroups. The first subgroup was exposed to nitrogen dioxide at a concentration of 7 ppm for 24 h, the second subgroup was exposed to nitrogen dioxide at a concentration of 30 ppm for 24 h, and the third subgroup was exposed to normal room air for 24 h. The nontaurine-treated animals were similarly divided into three subgroups and treated as described above. The lungs of the hamsters exposed to nitrogen dioxide without the taurine pretreatment exhibited extensive inflammatory cell infiltration in the walls of the terminal bronchioles, alveolar ducts, and peribronchiolar alveoli. The degree of infiltration was proportional to the degree of nitrogen dioxide concentration. The taurine-treated animals exposed to nitrogen dioxide and the nontaurine-treated animals exposed to room aid did not show any inflammatory infiltrate. Freeze-fracture replicas of the tight junctional regions of the type I and type II pneumocytes revealed significant fragmentation in the nitrogen dioxide-exposed lungs. It was also observed that the tight junctions between the type I pneumocytes of the taurine-treated groups, whether exposed or not, revealed gap junction-like aggregates among the tight junction fibrils. The 30-ppm nitrogen dioxide exposed group exhibited larger and more frequent gap junctions between the pneumocytes than those observed in the 7-ppm nitrogen dioxide exposed group. The evidence suggests that taurine may have an effect on plasma membranes and intercellular communications. Changes in intercellular communication may contribute to decreased susceptibility to injury and increased pneumocyte survival.

Animals↗

PubMed1986

[National Observation Network for Air Pollutants. Measurements up to now--planned extensions].

Since 6 years a Swiss national emission monitoring network measures several air pollutants (sulfur dioxide, nitrogen oxides, ozone, carbon monoxide, suspended particulates, particle deposition and precipitations) at 8 sites with different pollution levels (Dübendorf, Zürich, Basel, Sion, Payerne, Lugano, Tänikon, Jungfraujoch). The emission concentrations of sulfur dioxide, nitrogen dioxide and ozone exceed the limit values proposed by federal legislation at several sites, though the monitoring stations are not located at sites with extreme exposure. At present the network is extended for two or three new stations in forests as a part of a Swiss research programme concerning air pollution and forest damages. A further extension of the NABEL will comprise improvements of the measuring programme at the existing stations as well as new stations.

Air Pollutants↗

PubMed1997

[Meta-analysis and dose-response functions of air pollution respiratory effects].

A Meta-analysis was conducted on 107 original epidemiological papers published between 1980 and 1993 on the respiratory health impact of suspended particles, sulfur dioxide, ozone and nitrogen dioxide. These are the usual air quality indicators that are monitored in urban ambient air. The range of exposures that were studied (averages and 90th percentiles are respectively up to 88, 83, 124 and 53 mu/m3 (averages) and 180, 147, 234 and 131 micrograms/m3 (90th percentile) for each of the four pollution indicators) allowed assessment of dose-response functions for irritative pulmonary conditions (cough and/or asthma episodes) and respiratory function (FEVI and peak expiratory flow). The dose-response functions seem linear in the range of observed concentrations, with nitrogen dioxide showing the least consistent association across different health indicators. When applied to exposures measured as a 100 micrograms/m3 increase of pollutant's concentrations compared to low background values, the average relative risks of airway irritation (cough and/or asthma épisodes) range, according to the pollutant, from 1.08 to 1.47; average relative decreases of respiratory function amount to 1.1 to 2.2%. The effects are most often stronger among young subjects. The results of this study, when applied to air pollution concentrations in the range of values that were observed in this study, should foster health risk assessment studies in places where population air pollution exposures are available.

Adult↗

PubMed2006

Bayesian modeling of air pollution health effects with missing exposure data.

The authors propose a new statistical procedure that utilizes measurement error models to estimate missing exposure data in health effects assessment. The method detailed in this paper follows a Bayesian framework that allows estimation of various parameters of the model in the presence of missing covariates in an informative way. The authors apply this methodology to study the effect of household-level long-term air pollution exposures on lung function for subjects from the Southern California Children's Health Study pilot project, conducted in the year 2000. Specifically, they propose techniques to examine the long-term effects of nitrogen dioxide (NO2) exposure on children's lung function for persons living in 11 southern California communities. The effect of nitrogen dioxide exposure on various measures of lung function was examined, but, similar to many air pollution studies, no completely accurate measure of household-level long-term nitrogen dioxide exposure was available. Rather, community-level nitrogen dioxide was measured continuously over many years, but household-level nitrogen dioxide exposure was measured only during two 2-week periods, one period in the summer and one period in the winter. From these incomplete measures, long-term nitrogen dioxide exposure and its effect on health must be inferred. Results show that the method improves estimates when compared with standard frequentist approaches.

Air Pollutants↗

PubMedDate not supplied

Domestic nitrogen oxide exposure, urinary nitrate, and asthma prevalence in preschool children.

A South Australian preschool study carried out in 1993 showed that the prevalence of respiratory symptoms was significantly associated with use of unflued gas appliances for cooking and heating. The authors sought to determine an association between domestic exposure to nitrogen dioxide and the excretion of total urinary nitrate and nitrite, and their association with asthma prevalence. The results indicated that the geometric mean concentrations of nitrogen dioxide were much higher in homes that had natural gas appliance(s) and other types of appliances (i.e., electric and solid fuel). Higher levels of nitrogen dioxide were found in homes of suburban areas with higher prevalence of asthma and respiratory symptoms. Nitrogen dioxide levels were lower in the summer, and there was a higher level in kitchens than in bedrooms. Urinary nitrate excretion was evaluated in 1,335 preschool children from the same sampling areas. No association existed between nitrogen dioxide levels and urinary nitrates, nor was there a relationship between urinary nitrates and asthma prevalence. These findings confirm that there is a positive association between nitrogen dioxide exposure from gas appliances and the prevalence of respiratory symptoms, but urinary nitrate is not a useful biomarker of exposure at these levels.

Air Pollution, Indoor↗

PubMed2003

Measuring reactive nitrogen emissions from point sources using visible spectroscopy from aircraft.

Accurate measurements of nitrogen dioxide (NO2), a key trace gas in the formation and destruction of tropospheric ozone, are important in studies of urban pollution. Nitrogen dioxide column abundances were measured during the Texas Air Quality Study 2000 using visible absorption spectroscopy from an aircraft. The method allows for quantification of the integrated total number of nitrogen dioxide molecules in the polluted atmosphere and is hence a useful tool for measuring plumes of this key trace gas. Further, we show how such remote-sensing observations can be used to obtain information on the fluxes of nitrogen dioxide into the atmosphere with unique flexibility in terms of aircraft altitude, and the height and extent of mixing of the boundary layer. Observations of nitrogen dioxide plumes downwind of power plants were used to estimate the flux of nitrogen oxide emitted from several power plants in the Houston and Dallas metropolitan areas and in North Carolina. Measurements taken over the city of Houston were also employed to infer the total flux from the city as a whole.

Air Movements↗

PubMed1995

Effect of nitrous acid on lung function in asthmatics: a chamber study.

Nitrous acid, a component of photochemical smog and a common indoor air pollutant, may reach levels of 100 ppb where gas stoves and unvented portable kerosene heaters are used. Nitrous acid is a primary product of combustion and may also be a secondary product by reaction of nitrogen dioxide with water. Because the usual assays for nitrogen dioxide measure several oxides of nitrogen (including nitrous acid) together, previous studies of indoor nitrogen dioxide may have included exposure to and health effects of nitrous acid. To assess the respiratory effects of nitrous acid exposure alone, we carried out a double-blinded crossover chamber exposure study with 11 mildly asthmatic adult subjects. Each underwent 3-hr exposures to 650 ppb nitrous acid and to filtered room air with three 20-min periods of moderate cycle exercise. Symptoms, respiratory parameters during exercise, and spirometry after exercise were measured. A statistically significant decrease in forced vital capacity was seen on days when subjects were exposed to nitrous acid. This effect was most marked at 25 min and 85 min after exposure began. Aggregate respiratory and mucous membrane symptoms were also significantly higher with nitrous acid. We conclude that this concentration and duration of exposure to nitrous acid alters lung mechanics slightly, does not induce significant airflow obstruction, and produces mild irritant symptoms in asthmatics.

Adolescent↗

PubMed1991

The effects of exercise on dose and dose distribution of inhaled automotive pollutants.

The purpose of this study was to determine how changes in ventilation rate and in the entry route of air pollutants into the respiratory tract (nose versus mouth breathing) affected the respiratory tract uptake and penetration of inhaled gaseous and particulate pollutants associated with automobile emissions. Experiments were performed with female beagle dogs exposed while standing at rest or while exercising on a treadmill at 5 km/hour and a 7.5 percent grade. Dogs were exposed to nitrogen dioxide at concentrations of 1 and 5 parts per million (ppm), to formaldehyde at 2 and 10 ppm, and to an aerosol of ammonium nitrate particles (0.3 micron mass median aerodynamic diameter) at 1 mg/m3. Total respiratory system uptake and effects on breath time, expired tidal volume, fractional expiration time, minute ventilation, respiratory gas exchange, ventilation equivalents for oxygen and carbon dioxide, and dynamic pulmonary resistance and compliance were measured in exercising and resting dogs exposed for two hours to 5 ppm nitrogen dioxide and 10 ppm formaldehyde in combination with 1 mg/m3 of ammonium nitrate particles. Regional penetration of pollutants through oral and nasal airways and pollutant uptake in the lung were measured in a separate group of six tracheostomized dogs standing at rest while being exposed to nitrogen dioxide, formaldehyde, and ammonium nitrate particles. Hypercapnic stimulation was used to modify ventilation rates in the tracheostomized dogs while pollutant penetration and uptake were measured. Dogs exposed to 5 ppm of nitrogen dioxide at rest tended to breathe more rapidly (p less than 0.05) and more shallowly (a nonsignificant trend) than dogs exposed to purified air. The changes observed were similar in direction, but of smaller magnitude, to changes observed when the same dogs were exposed during exercise to ozone at 0.6 ppm in a separate study. Rapid-shallow breathing was not observed when the dogs were exposed during exercise to 5 ppm nitrogen dioxide. Dogs exposed to a mixture of 10 ppm formaldehyde and 1 mg/m3 ammonium nitrate particles during exercise showed a shift to larger tidal volume breathing, but the response was much less pronounced than the slow-deep breathing pattern response observed in a separate study of dogs exposed to 10 ppm formaldehyde alone. The total respiratory system uptake of formaldehyde from the formaldehyde and ammonium nitrate mixture was larger than that measured for 10 ppm of formaldehyde alone in another exercise and exposure study.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1993

The identification of the allylic nitrite and nitro derivatives of methyl linoleate and methyl linolenate by negative chemical ionization mass spectroscopy.

The autoxidation of polyunsaturated fatty acids is initiated both in vivo and in vitro by nitrogen dioxide. The mechanism of the initiation process is believed to involve both addition reactions and hydrogen atom abstraction reactions, with hydrogen abstraction predominating at low levels of nitrogen dioxide. Therefore low levels of nitrogen dioxide should react with polyunsaturated fatty acids to give allylic derivatives; in an anaerobic system these derivations should be allylic nitro and nitrite compounds. Using negative methane chemical ionization mass spectrometry and other analytical techniques, we have identified these allylic nitrite and nitro compounds from the reactions of low levels of nitrogen dioxide with methyl linoleate and methyl linolenate in the absence of oxygen.

Chromatography, High Pressure Liquid↗

PubMed2004

Room chamber assessment of the pollutant emission properties of (nominally) low-emission unflued gas heaters.

UNLABELLED: Pollutant emissions from unflued gas heaters were assessed in CSIRO's Room Dynamic Environmental Chamber. This paper describes the chamber assessment procedure and presents findings for major commercial heaters that are nominally "low-emission". The chamber was operated at controlled conditions of temperature, humidity, ventilation and air mixing, representative of those encountered in typical indoor environments. A fixed rate of heat removal from the chamber air ensured that the heaters operated at constant heating rates, typically approximately 6 MJ/h which simulated operation of a heater after warm-up in an insulated dwelling in south-east Australia. The pollutants assessed were nitrogen dioxide, carbon monoxide, formaldehyde, VOCs and respirable suspended particulates. One type of heater was lower emitting for nitrogen dioxide, but emitted greater amounts of carbon monoxide and formaldehyde (the latter becoming significant to indoor air quality). When operated with low line pressure or slight misalignment of the gas burner, this heater became a hazardous source of these pollutants. Emissions from the heaters changed little after continuous operation for up to 2 months. PRACTICAL IMPLICATIONS: Unflued gas heaters have been popular as primary heating sources in Australian homes for many years due to their ease of installation and energy efficiency, with approximately 600,000 now installed in housing and schools. However, with concerns over potential health impacts to occupants, manufacturers have reduced the nitrogen dioxide emissions from unflued gas heaters in Australia over recent years. They have done so with a target level for nitrogen dioxide in indoor air of 300 p.p.b. This is somewhat higher than the ambient air (and WHO) guideline of 110 p.p.b. Several studies of child respiratory health show an impact of unflued gas combustion products. A full characterization of the combustion products is needed under conditions that simulate heater operation in practice-this study was undertaken to provide such characterization. Key findings are that the focus needs to be on total gas emissions (not just nitrogen dioxide), and that heater installation can be very sensitive to small faults which lead to very high levels of toxic pollutants. These findings have influenced current government proposals for emission limits for these heaters.

Air Pollution, Indoor↗

PubMed2005

Quercetin-dependent inhibition of nitration induced by peroxidase/H2O2/nitrite systems in human saliva and characterization of an oxidation product of quercetin formed during the inhibition.

Local pH in the oral cavity can decrease to below 7 at the site where acid-producing bacteria are proliferating. Effects of pH on nitration of 4-hydroxyphenylacetic acid were studied using dialyzed human saliva. Dialyzed saliva nitrated 4-hydroxyphenylacetic acid to 4-hydroxy-3-nitrophenylacetic acid in the presence of nitrite and H(2)O(2). The rate of the nitration was dependent on pH, and the maximal rate was observed between pH 5.5 and 7.2. The optimum pH seemed to reflect rates of formation of nitrogen dioxide and 4-hydroxyphenylacetic acid radicals. Quercetin inhibited the nitration. The quercetin-dependent inhibition might be due to scavenging of nitrogen dioxide and 4-hydroxyphenylacetic acid radicals, which were formed by salivary peroxidase-dependent oxidation of nitrite and 4-hydroxyphenylacetic acid, respectively, and competition with nitrite and 4-hydroxyphenylacetic acid for peroxidase in saliva. An oxidation product of quercetin was formed during inhibition of the nitration by quercetin. The oxidation product was identified as 2-(3,4-dihydroxybenzoyl)-2,4,6-trihydroxy-3(2H)-benzofuranone. This component could also be oxidized by salivary peroxidase and nitrogen dioxide radicals. The oxidation products were 2,4,6-trihydroxyphenylglyoxylic and 3,4-dihydroxybenzoic acids. On the basis of the results, the significance of quercetin for inhibition of nitrogen dioxide formation and for scavenging of nitrogen dioxide radicals in the oral cavity is discussed.

Humans↗

PubMed2002

Nitrous acid concentrations in homes and offices in residential areas in Greater Cairo.

Indoor and outdoor measurements of nitrous acid and nitrogen dioxide were conducted at four homes and two offices in residential areas in Greater Cairo during winter (2000-2001) and summer (2001) seasons. Indoor nitrogen dioxide concentrations were higher than outdoor levels at the four homes, whereas indoor concentrations of nitrogen dioxide were lower than outdoor levels at the two offices, during both seasons. Indoor nitrous acid concentrations were higher than outdoor levels at all homes and offices during the period of study. The mean indoor nitrous acid concentrations were 6.8 ppb and 3.67 ppb in the four homes, whereas they were 1.42 ppb and 1.24 ppb in the two offices, during the winter and summer seasons, respectively. Indoor/outdoor ratios of nitrous acid concentration were 6.94 in the winter and 5.03 in the summer for all of the homes. However, the ratios were 1.31 and 1.61 during the winter and summer seasons, respectively, for the two offices. Insignificant positive correlation coefficients were found between indoor and outdoor concentrations of nitrous acid at homes and offices. The maximum outdoor nitrous acid concentrations were recorded during the winter season. Significant positive correlation coefficients were found between nitrous acid and nitrogen dioxide and relative humidity in homes and offices. The ratios of nitrous acid to nitrogen dioxide concentrations ranged from 0.045 to 0.16, with a mean of 0.1, in the four homes, whereas the ratios ranged from 0.026 to 0.09, with a mean of 0.059, in the two offices.

Air Pollutants↗

PubMed1990

Methemoglobin formation in the blood of Japanese subjects and mice suffering from acatalasemia in response to methemoglobin inducers.

Hemolysates or erythrocytes prepared from Japanese normal and acatalasemic subjects were exposed to nitrogen monoxide or nitrogen dioxide, and methemoglobin formation was determined. Concentrations of methemoglobin in human and mouse acatalasemic hemolysates exposed to nitrogen monoxide or nitrogen dioxide were higher than those in the normal hemolysates. Results similar to Japanese acatalasemic hemolysates or erythrocytes were obtained with mouse hemolysates or erythrocytes. When acatalasemic mice were exposed to nitrogen monoxide, the methemoglobin concentration in the blood was higher than that in the normal mice. Similar results on methemoglobin formation were obtained after exposing mice to nitrogen dioxide, although the rate of methemoglobin formation was lower in the blood of nitrogen dioxide-exposed mice. The methemoglobin concentration in erythrocytes of acatalasemic mice after the addition of sodium nitrite was higher than that in red cells of normal ones. Methemoglobin concentration in the blood of mice receiving sodium nitrites in vivo was determined, and found that the methemoglobin concentration in the blood of acatalasemic mice was higher than that in the blood of normal ones. These results indicated that the formation of methemoglobin from hemoglobin with nitrogen monoxide, nitrogen dioxide and nitrite ion appears to be controlled by the blood catalase.

Animals↗

PubMed2004

Nitration of alkanes with nitric acid by vanadium-substituted polyoxometalates.

The nitration of alkanes by using nitric acid as a nitrating agent in acetic acid was efficiently promoted by vanadium-substituted Keggin-type phosphomolybdates such as [H4PVMo11O40], [H5PV2Mo10O40], and [H6PV3Mo9O40] as catalyst precursors. A variety of alkanes including alkylbenzenes were nitrated to the corresponding nitroalkanes as major products in moderate yields with formation of oxygenated products under mild reaction conditions. The carbon--carbon bond cleavage reactions hardly proceeded. ESR, NMR, and IR spectroscopic data show that the vanadium-substituted polyoxometalate, for example, [H4PVMo11O40], decomposes to form free vanadium species and [PMo12O40](3-) Keggin anion. The reaction mechanism involving a radical-chain path is proposed. The polyoxometalates initially abstract the hydrogen of the alkane to form the alkyl radical and the reduced polyoxometalates. The reduced polyoxometalates subsequently react with nitric acid to produce the oxidized form and nitrogen dioxide. This step would be promoted mainly by the phosphomolybdates, [PMo12O40](n-), and the vanadium cations efficiently enhance the activity. The nitrogen dioxide promotes the further formation of nitrogen dioxide and an alkyl radical. The alkyl radical is trapped by nitrogen dioxide to form the corresponding nitroalkane.

Journal Article↗

PubMed1996

Effects of nitrogen oxides on natural killer cells in glass craftsmen and braziers.

OBJECTIVES: To assess the effect of exposure to nitrogen oxides on peripheral blood natural killer cells. METHODS: Groups of glass craftsmen and braziers exposed to nitrogen oxides and non-exposed controls were studied. Air concentrations of nitrogen oxides were measured. Mononuclear cells isolated from peripheral blood samples were assayed for natural killer cell activity with K562 target cells in a 51Cr release assay and the percentage of natural killer cells (CD16) was measured by flow cytometry. RESULTS: Braziers were exposed to 1.2 ppm nitrogen dioxide and 8.6 ppm nitric oxide and glass craftsmen to 2.9 ppm nitrogen dioxide and 26.5 ppm nitric oxide. The natural killer cell activity of exposed workers was significantly lower than in non-exposed controls (P < 0.05 ANOVA Scheffe test). The percentage of natural killer cells in glass craftsmen was significantly greater than in controls (P < 0.05 ANOVA Scheffe test). Regression of natural killer cell activity against age, smoking habit, number of years worked and current exposure to nitrogen dioxide and nitric oxide gases was not significant. The percentage of natural killer cells was not significantly correlated with age, smoking habit, or numbers of years worked, but was significantly related to air concentrations of nitrogen dioxide (P < 0.01) and nitric oxide (P < 0.001). CONCLUSION: Natural killer cell activity and the percentage of natural killer cells in peripheral blood cells were altered in workers exposed to nitrogen oxides.

Adolescent↗

PubMed2002

Microbiological, biological, and chemical weapons of warfare and terrorism.

Microbiological, biological, and chemical toxins have been employed in warfare and in terrorist attacks. In this era, it is imperative that health care providers are familiar with illnesses caused by these agents. Botulinum toxin produces a descending flaccid paralysis. Staphylococcal enterotoxin B produces a syndrome of fever, nausea, and diarrhea and may produce a pulmonary syndrome if aerosolized. Clostridium perfringens epsilon-toxin could possibly be aerosolized to produce acute pulmonary edema. Ricin intoxication can manifest as gastrointestinal hemorrhage after ingestion, severe muscle necrosis after intramuscular injection, and acute pulmonary disease after inhalation. Nerve agents inhibit acetylcholinesterase and thus produce symptoms of increased cholinergic activity. Ammonia, chlorine, vinyl chloride, phosgene, sulfur dioxide, and nitrogen dioxide, tear gas, and zinc chloride primarily injure the upper respiratory tract and the lungs. Sulfur mustard (and nitrogen mustard) are vesicant and alkylating agents. Cyanide poisoning ranges from sudden-onset headache and drowsiness to severe hypoxemia, cardiovascular collapse, and death. Health care providers should be familiar with the medical consequences of toxin exposure, and understand the pathophysiology and management of resulting illness.

Bacterial Infections↗

PubMed1990

Respiratory health effects of the indoor environment in a population of Dutch children.

The effect of indoor exposure to nitrogen dioxide on respiratory health was studied over a period of 2 yr in a population of nonsmoking Dutch children 6 to 12 yr of age. Lung function was measured at the schools, and information on respiratory symptoms was collected from a self-administered questionnaire completed by the parents of the children. Nitrogen dioxide was measured in the homes of all children with Palmes' diffusion tubes. In addition, information on smoking and dampness in the home was collected by questionnaire. There was no relationship between exposure to nitrogen dioxide in the home and respiratory symptoms. Respiratory symptoms were found to be associated with exposure to tobacco smoke and home dampness. There was a weak, negative association between maximal midexpiratory flow (MMEF) and exposure to nitrogen dioxide. FEV1, peak expiratory flow, and MMEF were all negatively associated with exposure to tobacco smoke. Home dampness was not associated with pulmonary function. Lung function growth, measured over a period of 2 yr, was not consistently associated with any of the indoor exposure variables. The development of respiratory symptoms over time was not associated with indoor exposure to nitrogen dioxide. There was a significant association between exposure to environmental tobacco smoke in the home and the development of wheeze. There was also a significant association between home dampness and the development of cough.

Air Pollutants↗