Understanding the importance of key risk factors in predicting chronic bronchitic symptoms using a machine learning approach.

BACKGROUND: Chronic respiratory symptoms involving bronchitis, cough and phlegm in children are underappreciated but pose a significant public health burden. Efforts for prevention and management could be supported by an understanding of the relative importance of determinants, including environmental exposures. Thus, we aim to develop a prediction model for bronchitic symptoms. METHODS: Schoolchildren from the population-based southern California Children's Health Study were visited annually from 2003 to 2012. Bronchitic symptoms over the prior 12 months were assessed by questionnaire. A gradient boosting model was fit using groups of risk factors (including traffic/air pollution exposures) for all children and by asthma status. Training data consisted of one observation per participant in a random study year (for 50% of participants). Validation data consisted of: (1) a random (later) year in the same participants (within-participant); (2) a random year in participants excluded from the training data (across-participant). RESULTS: At baseline, 13.2% of children had asthma and 18.1% reported bronchitic symptoms. Models performed similarly within- and across-participant. Previous year symptoms/medication use provided much of the predictive ability (across-participant area under the receiver operating characteristic curve (AUC): 0.76 vs 0.78 for all risk factors, in all participants). Traffic/air pollution exposures added modestly to prediction as did body mass index percentile, age and parent stress. CONCLUSIONS: Regardless of asthma status, previous symptoms were the most important predictors of current symptoms. Traffic/air pollution variables contribute modest predictive information, but impact large populations. Methods proposed here could be generalized to personalized exacerbation predictions in future longitudinal studies to support targeted prevention efforts.

An integrated Bayesian model for estimating the long-term health effects of air pollution by fusing modelled and measured pollution data: A case study of nitrogen dioxide concentrations in Scotland.

The long-term health effects of air pollution can be estimated using a spatio-temporal ecological study, where the disease data are counts of hospital admissions from populations in small areal units at yearly intervals. Spatially representative pollution concentrations for each areal unit are typically estimated by applying Kriging to data from a sparse monitoring network, or by computing averages over grid level concentrations from an atmospheric dispersion model. We propose a novel fusion model for estimating spatially aggregated pollution concentrations using both the modelled and monitored data, and relate these concentrations to respiratory disease in a new study in Scotland between 2007 and 2011.

DNA damage in buccal mucosa cells of pre-school children exposed to high levels of urban air pollutants.

Air pollution has been recognized as a human carcinogen. Children living in urban areas are a high-risk group, because genetic damage occurring early in life is considered able to increase the risk of carcinogenesis in adulthood. This study aimed to investigate micronuclei (MN) frequency, as a biomarker of DNA damage, in exfoliated buccal cells of pre-school children living in a town with high levels of air pollution. A sample of healthy 3-6-year-old children living in Brescia, Northern Italy, was investigated. A sample of the children's buccal mucosa cells was collected during the winter months in 2012 and 2013. DNA damage was investigated using the MN test. Children's exposure to urban air pollution was evaluated by means of a questionnaire filled in by their parents that included items on various possible sources of indoor and outdoor pollution, and the concentration of fine particulate matter (PM10, PM2.5) and NO2 in the 1-3 weeks preceding biological sample collection. 181 children (mean age ± SD: 4.3 ± 0.9 years) were investigated. The mean ± SD MN frequency was 0.29 ± 0.13%. A weak, though statistically significant, association of MN with concentration of air pollutants (PM10, PM2.5 and NO2) was found, whereas no association was apparent between MN frequency and the indoor and outdoor exposure variables investigated via the questionnaire. This study showed a high MN frequency in children living in a town with heavy air pollution in winter, higher than usually found among children living in areas with low or medium-high levels of air pollution.

[Case of dyspnea due to toilet cleaner containing nitric acid for household use].

A 40-year-old male tried to clean a urinal at his home storing 900 mL of a toilet cleaner containing 9.8% nitric acid to remove calcium deposit, and clean the toilet floor for twenty minutes. Immediately after using the cleaner, he experienced eye irritation. He washed out the toilet cleaner. However, he thereafter experienced dyspnea, a compressive sensation in his chest, and chest and back pain about 40 minutes after the cleaning the toilet. He monitored his symptoms overnight and found them to gradually improve. However, the symptoms still remained the next morning and therefore he came to our department on foot. He had no particular past or family history. On arrival, his physiological findings and chest computed tomography scan were negative for any abnormalities. His arterial blood gas analysis revealed a mild abnormality of oxygenation. Observation without any drugs revealed that a complete remission of his symptoms occurred after approximately 4 weeks. Based on the results of the experiments, contact with the mucosal membrane and nitric acid gas produced by any accidentally coexisting metals or contact with moisture, including nitric acid produced by a reaction between CaCO3 and cleaner, may have been the mechanism of occurrence for the symptoms observed in this case. This is the first reported case of nitric acid poisoning due to the use of a toilet cleanser intended for household use.

Ice hockey lung - a case of mass nitrogen dioxide poisoning in the Czech Republic.

Nitrogen dioxide (NO2) is a toxic gas, a product of combustion in malfunctioning ice-resurfacing machines. NO2 poisoning is rare but potentially lethal. The authors report a case of mass NO2 poisoning involving 15 amateur ice hockey players in the Czech Republic. All players were treated in the Department of Respiratory Diseases at Brno University Hospital in November 2010 - three as inpatients because they developed pneumonitis. All patients were followed-up until November 2011. Complete recovery in all but one patient was achieved by December 2010. None of the 15 patients developed asthma-like disease or chronic cough. Corticosteroids appeared to be useful in treatment. Electric-powered ice-resurfacing machines are preferable in indoor ice skating arenas.

Exposure to nitrogen dioxide in an indoor ice arena - New Hampshire, 2011.

In January 2011, the New Hampshire Department of Health and Human Services (NHDHHS) investigated acute respiratory symptoms in a group of ice hockey players. The symptoms, which included cough, shortness of breath, hemoptysis, and chest pain or tightness, were consistent with exposure to nitrogen dioxide gas (NO), a byproduct of combustion. Environmental and epidemiologic investigations were begun to determine the source of the exposure and identify potentially exposed persons. This report summarizes the results of those investigations, which implicated a local indoor ice arena that had hosted two hockey practice sessions during a 24-hour period when the arena ventilation system was not functioning. A total of 43 exposed persons were interviewed, of whom 31 (72.1%) reported symptoms consistent with NO exposure. The highest attack rate was among the hockey players (87.9%). After repair of the ventilation system, no additional cases were identified. To prevent similar episodes, ice arena operators should ensure ventilation systems and alarms are operating properly and that levels of NO and carbon monoxide (CO) are monitored continuously for early detection of increased gas levels.

Residential proximity to heavy traffic and birth weight in Shizuoka, Japan.

An association between exposure to traffic-related air pollution and reduced birth weight has been suggested. However, previous studies have failed to adjust for maternal size, which is an indicator of individual genetic growth potential. Therefore, we evaluated the association of air pollution with birth weight, term low birth weight (term-LBW), and small for gestational age (SGA), with adjustment for maternal size. Individual data were extracted from a database that is maintained by a maternal and perinatal care center in Shizuoka, Japan. We identified liveborn singleton births (n=14,204). Using geocoded residential information, each birth was assigned a number of traffic-based exposure indicators: distance to a major road; distance-weighted traffic density; and estimated concentration of nitrogen dioxide by land use regression. The multivariate adjusted odds ratios and their 95% confidence intervals (CIs) for the associations between exposure indicators and outcomes were then estimated using logistic regression models. Overall, exposure indicators of air pollution showed no clear pattern of association. Although there are many limitations, we did not find clear associations between birth-weight-related outcomes and the three markers of traffic-related air pollution.

Acute effects of air pollution on pediatric asthma exacerbation: evidence of association and effect modification.

We investigated the short-term effects of particulate matter with aerodynamic diameter <10 µg/m(3) (PM(10)), sulfur dioxide (SO(2)), nitrogen dioxide (NO(2)) and ozone (O(3)) on pediatric asthma emergency admissions in Athens, Greece over the period 2001-2004. We explored effect modification patterns by season, sex, age and by the presence of desert dust transported mainly from the Sahara area. We used daily time-series data provided by the children's hospitals and the fixed monitoring stations. The associations were investigated using Poisson regression models controlling for seasonality, weather, influenza episodes, day of the week and holiday effects. A 10 µg/m(3) increase in PM(10) was associated with a 2.54% increase (95% confidence interval (CI): 0.06%, 5.08%) in the number of pediatric asthma hospital admissions, while the same increase in SO(2) was associated with a 5.98% (95% CI: 0.88%, 11.33%) increase. O(3) was associated with a statistically significant increase in asthma admissions among older children in the summer. Our findings provide limited evidence of an association between NO(2) exposure and asthma exacerbation. Statistically significant PM(10) effects were higher during winter and during desert dust days, while SO(2) effects occurred mainly during spring. Our study confirms previously reported PM(10) effects on emergency hospital admissions for pediatric asthma and further provides evidence of stronger effects during desert dust days. We additionally report severe effects of SO(2), even at today's low concentration levels.

Ambient air pollution and congenital heart disease: a register-based study.

Maternal exposure to ambient air pollution has increasingly been linked to adverse pregnancy outcomes. The evidence linking this exposure to congenital anomalies is still limited and controversial. This case-control study investigated the association between maternal exposure to ambient particulate matter with aerodynamic diameter less than 10 µm (PM(10)), sulfur dioxide (SO(2)), nitrogen dioxide, nitric oxide (NO), ozone (O(3)), and carbon monoxide (CO) and the occurrence of congenital heart disease in the population of Northeast England (1993-2003). Each case and control was assigned weekly average (weeks 3-8 of pregnancy) of pollutant levels measured by the closest monitor to the mother's residential postcode. Using exposure as both continuous and categorical variables, logistic regression models were constructed to quantify the adjusted odds ratios of exposure to air pollutants and the occurrence of each outcome group. We found exposure to CO and NO to be associated with ventricular septal defect and cardiac septa malformations. CO was also associated with congenital pulmonary valve stenosis and NO with pooled cases of congenital heart disease and tetralogy of Fallot. Findings for SO(2), O(3) and PM(10) were less consistent.

The risk of dying on days of higher air pollution among the socially disadvantaged elderly.

RATIONALE: The estimated mortality rate associated with ambient air pollution based on general population studies may not be applicable to certain subgroups. OBJECTIVE: The objective of the present study was to determine the influence of age, education, employment status and income on the risk of mortality associated with ambient air pollution. METHODS: Daily time-series analyses tested the association between daily air pollution and daily mortality in seven Chilean urban centers during the period January 1997-December 2007. Results were adjusted for long-term trends, day-of-the week and humidex. RESULTS: Interquartile increases in particulate matter (PM(10) and PM(2.5)), sulphur dioxide, nitrogen dioxide, carbon monoxide, and elemental and organic carbon were associated with a 4-7% increase in mortality among those who did not complete primary school (p<0.05) vs. 0.5-1.5% among university graduates (p>0.05). Among those at least 85 years of age respective estimates were 2-7%. However, among the elderly who did not complete primary school, respective estimates were 11-19% (p<0.05). The degree of effect modification was less for income and employment status than education, and sex did not modify the results. CONCLUSION: The socially disadvantaged, especially if elderly appear to be especially susceptible to dying on days of higher air pollution. Concentrations deemed acceptable for the general population would not appear to protect this susceptible subgroup.

Gaseous air pollution and emergency hospital visits for hypertension in Beijing, China: a time-stratified case-crossover study.

BACKGROUND: A number of epidemiological studies have been conducted to research the adverse effects of air pollution on mortality and morbidity. Hypertension is the most important risk factor for cardiovascular mortality. However, few previous studies have examined the relationship between gaseous air pollution and morbidity for hypertension. METHODS: Daily data on emergency hospital visits (EHVs) for hypertension were collected from the Peking University Third Hospital. Daily data on gaseous air pollutants (sulfur dioxide (SO2) and nitrogen dioxide (NO2)) and particulate matter less than 10 µm in aerodynamic diameter (PM10) were collected from the Beijing Municipal Environmental Monitoring Center. A time-stratified case-crossover design was conducted to evaluate the relationship between urban gaseous air pollution and EHVs for hypertension. Temperature and relative humidity were controlled for. RESULTS: In the single air pollutant models, a 10 µg/m3 increase in SO2 and NO2 were significantly associated with EHVs for hypertension. The odds ratios (ORs) were 1.037 (95% confidence interval (CI): 1.004-1.071) for SO2 at lag 0 day, and 1.101 (95% CI: 1.038-1.168) for NO2 at lag 3 day. After controlling for PM10, the ORs associated with SO2 and NO2 were 1.025 (95% CI: 0.987-1.065) and 1.114 (95% CI: 1.037-1.195), respectively. CONCLUSION: Elevated urban gaseous air pollution was associated with increased EHVs for hypertension in Beijing, China.

Children's asthma hospitalizations and relative risk due to nitrogen dioxide (NO2): effect modification by race, ethnicity, and insurance status.

BACKGROUND: This study explores the role of race, ethnicity, and insurance status in modifying the effects of air pollution on children's asthma hospitalizations in Phoenix, Arizona (US) between 2001 and 2003. While controlling for weather, interactions between nitrous dioxide (NO(2)) and race, ethnicity, and insurance status are used to predict relative risk for subgroups of children. METHODS: The generalized logit regression model for nominal categorical data within a multinomial likelihood framework was used. This model is specifically suited to small counts and the reporting of 95% confidence intervals for the odds ratio of hospital admission for one group as compared to another. The odds ratio is known to approximate relative risk for rare events. RESULTS: Several significant findings were found for race, ethnicity, and insurance status as modulators for the effect of NO(2) on children's risk for asthma hospitalization: (1) children without insurance have 1.4 (95% CI: 1.1-1.8) times higher risk of asthma admissions than those with private insurance at exceedances of 0.02 parts per million (ppm) of NO(2) above the seasonal mean; the same finding holds for children without insurance as compared to those with Medicaid; (2) black children have 2.1 (95% CI: 1.3-3.3) times higher risk of hospitalization than Hispanic children at seasonal mean NO(2) levels, but this disproportionate risk shrinks to 1.7 with exceedances of 0.02 ppm of NO(2) above the seasonal mean. Specific to finding (1) among those children without health insurance, Hispanic children have 2.1 (95% CI: 1.1-3.8) times higher risk of hospitalization than white children. Among all Hispanic children, those without health insurance have 1.9 (95% CI: 1.3-3.0) times greater risk than those with private insurance; the same finding holds for Hispanic children without insurance as compared to Hispanic children with Medicaid. Specific to finding (2), among children with private insurance, the disproportionate risk of black children as compared to Hispanic children is magnified by a factor of 1.3 (95% CI: 1.0-1.8) for exceedances of 0.02 ppm of NO(2) above the seasonal mean. CONCLUSIONS: Although we cannot confirm a cause-effect relationship, this analysis suggests that increasing insurance enrollment for all children, and specifically Hispanic children, may reduce their disproportionate risk from exceedances of air pollution. There are few black children in Phoenix, so further studies are needed to investigate the increasing risk of black children with private insurance as compared to Hispanics at exceedances of NO(2).

Temperature-dependent association between mortality rate and carbon monoxide level in a subtropical city: Kaohsiung, Taiwan.

The objective of this study was to explore the combined effect of temperature and air pollutant levels on daily non-accidental deaths and cardiovascular causes of mortality. In this study, associations were assessed by means of time-series analyses over the period 1995-1999 for Kaohsiung, Taiwan's largest industrial city, which has a subtropical climate. Ambient exposures to various air pollutants, including carbon monoxide (CO), sulfur dioxide (SO(2)), ozone (O(3)), nitrogen dioxide (NO(2)), and particulate matter (PM(10)), were estimated from the arithmetic means of all daily measurements taken by an air quality monitoring station nearest to the residential district. Generalized additive models with non-parametric spline were used to identify associations between daily mortality and air pollutants as well as the air pollutant-temperature interaction correlation. Our findings indicate that CO is associated with increased risks of non-accidental and cardiovascular mortality. For a 0.2 ppm increase in CO, the increased relative daily risk of non-accidental death is at least 4% on the same day, when the mean temperature is above 24.8 degrees C, while the increased relative risk of mortality due to cardiovascular diseases is 7% two days later at 19.7 degrees C. The study also suggests a statistically significant interaction between CO concentration and daily mean temperature, with non-accidental mortality increasing with a warm outdoor temperature and the effect of CO on cardiovascular mortality being modified by a cold climate. Further reduction of CO pollution is thus deemed crucial for the benefit of public health.

A comparison of self reported air pollution problems and GIS-modeled levels of air pollution in people with and without chronic diseases.

OBJECTIVE: To explore various contributors to people's reporting of self reported air pollution problems in area of living, including GIS-modeled air pollution, and to investigate whether those with respiratory or other chronic diseases tend to over-report air pollution problems, compared to healthy people. METHODS: Cross-sectional data from the Oslo Health Study (2000-2001) were linked with GIS-modeled air pollution data from the Norwegian Institute of Air Research. Multivariate regression analyses were performed. 14 294 persons aged 30, 40, 45, 60 or 75 years old with complete information on modeled and self reported air pollution were included. RESULTS: People who reported air pollution problems were exposed to significantly higher GIS-modeled air pollution levels than those who did not report such problems. People with chronic disease, reported significantly more air pollution problems after adjustment for modeled levels of nitrogen dioxides, socio-demographic variables, smoking, depression, dwelling conditions and an area deprivation index, even if they had a non-respiratory disease. No diseases, however, were significantly associated with levels of nitrogen dioxides. CONCLUSION: Self reported air pollution problems in area of living are strongly associated with increased levels of GIS-modeled air pollution. Over and above this, those who report to have a chronic disease tend to report more air pollution problems in area of living, despite no significant difference in air pollution exposure compared to healthy people, and no associations between these diseases and NO2. Studies on the association between self reported air pollution problems and health should be aware of the possibility that disease itself may influence the reporting of air pollution.

Nitrogen dioxide (silo gas) poisoning in dairy cattle.

Toxic silo gases are a potential danger to livestock housed in close proximity to roughage silos. These gases, such as nitrogen dioxide (NO2), may be produced during the early stages of (maize and grass) silage making. In humans, inhalation of these gases causes a condition known as 'Silo Filler's Disease' (SFD), which is a recognized occupational hazard for workers in upright forage silos in many countries. NO2 accumulates on top of silage, is inhaled by workers, and reacts with water on the airway surfaces to form nitrous acid, which damages the lung and causes pulmonary oedema, bronchiolitis, and death in severe cases. On a dairy farm, a cloud of reddish-brown NO2 gas (which is heavier than air) was noticed to escape from underneath the plastic sheet of a horizontal maize bunker and to enter a cubicle house for dairy cows 1 day after ensiling. Eleven cows became dyspnoeic, 3 of which subsequently died. A combination of weather conditions, an insufficient sand load on the maize bunker, the utilization of a lactobacillus starter culture, and the close proximity of the silo to the cubicle house may have caused the incident.

Inhalational lung injury due to nitrogen dioxide: high-resolution computed tomography findings in 3 patients.

Chest radiographic and high-resolution computed tomography findings of 3 patients with inhalational lung injury due to nitrogen dioxide were reported. Chest radiographs showed ill-defined round opacities which tended to coalesce in both lung with inner lung predominance. High-resolution computed tomography showed ground-glass attenuation and ill-defined centrilobular nodules distributed predominantly in the inner and middle lung zones. One patient showed progression of opacities, which corresponded to the findings of acute respiratory distress syndrome.

Air pollution and hospital admissions for cardiovascular disease in Taipei, Taiwan.

This study was undertaken to determine whether there is an association between air pollutants levels and hospital admissions for cardiovascular diseases (CVD) in Taipei, Taiwan. Hospital admissions for CVD and ambient air pollution data for Taipei were obtained for the period 1997-2001. The relative risk of hospital admission was estimated using a case-crossover approach, controlling for weather variables, day of the week, seasonality, and long-term time trends. For the one-pollutant models, on warm days (>or=20 degrees C) statistically significant positive associations were found between levels of particulate matter <10-microm aerodynamic diameter (PM10), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3). On cool days (<20 degrees C), all pollutants except O3 and SO2 were significantly associated with CVD admissions. For the two-pollutant models, CO, NO2, and O3 were significant in combination with each of the other four pollutants on warm days. On cool days, PM10 remained statistically significant in all the two-pollutant models. This study provides evidence that higher levels of ambient pollutants increase the risk of hospital admissions for CVD.

Association of FEV1 in asthmatic children with personal and microenvironmental exposure to airborne particulate matter.

Exposure to particulate matter (PM) air pollution has been shown to exacerbate children's asthma, but the exposure sources and temporal characteristics are still under study. Children's exposure to PM is likely to involve both combustion-related ambient PM and PM related to a child's activity in various indoor and outdoor microenvironments. Among 19 children with asthma, 9-17 years of age, we examined the relationship of temporal changes in percent predicted forced expiratory volume in 1 sec (FEV1) to personal continuous PM exposure and to 24-hr average gravimetric PM mass measured at home and central sites. Subjects were followed for 2 weeks during either the fall of 1999 or the spring of 2000, in a southern California region affected by transported air pollution. FEV(subscript)1(/subscript) was measured by subjects in the morning, afternoon, and evening. Exposure measurements included continuous PM using a passive nephelometer carried by subjects; indoor, outdoor home, and central-site 24-hr gravimetric PM2.5 (PM of aerodynamic diameter < 2.5 microm) and PM10; and central-site hourly PM10, nitrogen dioxide, and ozone. Data were analyzed with linear mixed models controlling for within-subject autocorrelation, FEV1 maneuver time, and exposure period. We found inverse associations of FEV1 with increasing PM exposure during the 24 hr before the FEV1 maneuver and with increasing multiday PM averages. Deficits in percent predicted FEV1 (95% confidence interval) for given PM interquartile ranges measured during the preceding 24-hr were as follows: 128 microg/m3 1-hr maximum personal PM, -6.0% (-10.5 to -1.4); 30 microg/m3 24-hr average personal PM, -5.9% (-10.8 to -1.0); 6.7 microg/m3 indoor home PM2.5, -1.6% (-2.8 to -0.4); 16 microg/m3 indoor home PM10, -2.1% (-3.7 to -0.4); 7.1 microg/m3 outdoor home PM2.5, -1.1% (-2.4 to 0.1); and 7.5 microg/m3 central-site PM2.5, -0.7% (-1.9 to 0.4). Stronger associations were found for multiday moving averages of PM for both personal and stationary-site PM. Stronger associations with personal PM were found in boys allergic to indoor allergens. FEV1 was weakly associated with NO2 but not with O3. Results suggest mixed respiratory effects of PM in asthmatic children from both ambient background exposures and personal exposures in various microenvironments.

Indoor exposures and acute respiratory effects in two general population samples from a rural and an urban area in Italy.

A study of indoor air exposures and acute respiratory effects in adults was conducted in the Po Delta (rural) and Pisa (urban) areas of Italy. Indoor exposures were monitored for nitrogen dioxide (NO(2)) and particulate matter <2.5 microm (PM(2.5)) for 1 week during the winter or summer in a total of 421 houses (2/3 in Pisa). Information on house characteristics, subjects' daily activity pattern and presence of acute respiratory symptoms was collected by a standardized questionnaire. Peak expiratory flow (PEF) maneuvers were performed by adult subjects four times daily; maximum amplitude and diurnal variation were taken into account. Indices of NO(2) and PM(2.5) exposures were computed as the product of weekly mean pollutant concentration by the time of daily exposure. Mean levels of pollutants were significantly higher in winter than in summer, regardless of the area. The relationship between exposure indices and acute respiratory symptoms was investigated only in winter. In spite of a slightly lower indoor level in the urban than in the rural area in winter (NO(2): 15 vs. 22 ppb; PM(2.5): 67 vs. 76 microg/m(3)), prevalence rates of acute respiratory symptoms were significantly higher in the urban than in the rural area. Acute respiratory illnesses with fever were significantly associated with indices of NO(2) (odds ratio (OR)=1.66; 95% CI=1.08-2.57) and PM(2.5) exposures (OR=1.62; 95% CI=1.04-2.51), while bronchitic/asthmatic symptoms were associated only with PM(2.5) (OR=1.39; 95% CI=1.17-1.66). PEF variability was positively related only to PM(2.5) exposure index (OR=1.38; 95% CI=1.24-1.54, for maximum amplitude; OR=1.37; 95% CI=1.23-1.53, for diurnal variation). In conclusion, indoor pollution exposures were associated with the presence of acute respiratory symptoms and mild lung function impairment in a rural and an urban area of Northern-Central Italy.