Variations in air pollution exposure within a community may be associated with asthma prevalence. However, studies conducted to date have produced inconsistent results, possibly due to errors in measurement of the exposures.
A standardized asthma survey was administered to children in grades one and eight in Hamilton, Canada, in 1994–95 (N ~1467). Exposure to air pollution was estimated in four ways: (1) distance from roadways; (2) interpolated surfaces for ozone, sulfur dioxide, particulate matter and nitrous oxides from seven to nine governmental monitoring stations; (3) a kriged nitrogen dioxide (NO2) surface based on a network of 100 passive NO2 monitors; and (4) a land use regression (LUR) model derived from the same monitoring network. Logistic regressions were used to test associations between asthma and air pollution, controlling for variables including neighbourhood income, dwelling value, state of housing, a deprivation index and smoking.
There were no significant associations between any of the exposure estimates and asthma in the whole population, but large effects were detected the subgroup of children without hayfever (predominately in girls). The most robust effects were observed for the association of asthma without hayfever and NO2LUR OR = 1.86 (95%CI, 1.59–2.16) in all girls and OR = 2.98 (95%CI, 0.98–9.06) for older girls, over an interquartile range increase and controlling for confounders.
Our findings indicate that traffic-related pollutants, such as NO2, are associated with asthma without overt evidence of other atopic disorders among female children living in a medium-sized Canadian city. The effects were sensitive to the method of exposure estimation. More refined exposure models produced the most robust associations.
In order to address the role that the ambient air pollution mix, comprised of gaseous pollutants and various physical and chemical measures of particulate matter, plays in exacerbating cardiorespiratory disease, daily measures of fine and coarse particulate mass, aerosol chemistry (sulfates and acidity), and gaseous pollution (ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide) were collected in Toronto, Ontario, Canada, in the summers of 1992, 1993, and 1994. These time series were then compared with concurrent data on the number of daily admissions to hospitals for either cardiac diseases (ischemic heart disease, heart failure, and dysthymias) or respiratory diseases (tracheobronchitis, chronic obstructive long disease, asthma, and pneumonia). After adjusting the admission time series for long-term temporal trends, seasonal variations, the effects of short-term epidemics, day of the week effects, and ambient temperature and dew point temperature, positive associations were observed for all ambient air pollutants for both respiratory and cardiac diseases. Ozone was least sensitive to adjustment for the gaseous and particulate pollution measures. However, the association between the health outcomes and carbon monoxide, fine and coarse mass, sulfate levels and aerosol acidity could be explained by adjustment for exposure to gaseous pollutants. Increases in ozone, nitrogen dioxide, and sulfur dioxide equivalent to their interquartile ranges corresponded to an 11% and 13% increase in daily hospitalizations for respiratory and cardiac diseases, respectively. The inclusion of any one of the particulate air pollutants in multiple regression models did not increase these percentages. Particle mass and chemistry could not be identified as an independent risk factor for the exacerbation of cardiorespiratory diseases in this study beyond that attributable to climate and gaseous air pollution. We recommend that effects of particulate matter on health be assessed in conjunction with temporally covarying gaseous air pollutants.
Community levels of air pollution have been associated with variability in mortality rates, but previous studies have inferred exposure to pollutants on a citywide basis. We investigated mortality in relation to neighbourhood levels of income and air pollution in an urban area.
We identified 5228 people in the Hamilton–Burlington area of southern Ontario who had been referred for pulmonary function testing between 1985 and 1999. Nonaccidental deaths that occurred in this group between 1992 and 1999 were ascertained from the Ontario Mortality Registry. Mean household income was estimated by linking the subjects' postal codes with the 1996 census. Mean neighbourhood levels of total suspended particulates and sulfur dioxide were estimated by interpolation from data from a network of sampling stations. We used proportional hazards regression models to compute mortality risk in relation to income and pollutant levels, while adjusting for pulmonary function, body mass index and diagnoses of chronic disease. Household incomes and pollutant levels were each divided into 2 risk categories (low and high) at the median.
Mean pollutant levels tended to be higher in lower-income neighbourhoods. Both income and pollutant levels were associated with mortality differences. Compared with people in the most favourable category (higher incomes and lower particulate levels), those with all other income–particulate combinations had a higher risk of death from nonaccidental causes (lower incomes and higher particulate levels: relative risk [RR] 2.62, 95% confidence interval [CI] 1.67–4.13; lower incomes and lower particulate levels: RR 1.82, 95% CI 1.30–2.55; higher incomes and higher particulate levels: RR 1.33, 95% CI 1.12–1.57). Similar results were observed for sulfur dioxide. The relative risk was lower at older ages.
Mortality rates varied by neighbourhood of residence in this cohort of people whose lung function was tested. Two of the broader determinants of health — income and air pollution levels — were important correlates of mortality in this population.
To estimate long‐term exposure to traffic‐related air pollutants on an individual basis and to assess adverse health effects using a combination of air pollution measurement data, data from geographical information systems (GIS) and questionnaire data.
40 measurement sites in the city of Munich, Germany were selected at which to collect particulate matter with a 50% cut‐off aerodynamic diameter of 2.5 µm (PM2.5) and to measure PM2.5 absorbance and nitrogen dioxide (NO2). A pool of GIS variables (information about street length, household and population density and land use) was collected for the Munich metropolitan area and was used in multiple linear regression models to predict traffic‐related air pollutants. These models were also applied to the birth addresses of two birth cohorts (German Infant Nutritional Intervention Study (GINI) and Influence of Life‐style factors on the development of the Immune System and Allergies in East and West Germany (LISA)) in the Munich metropolitan area. Associations between air pollution concentrations at birth address and 1‐year and 2‐year incidences of respiratory symptoms were analysed.
The following means for the estimated exposures to PM2.5, PM2.5 absorbance and NO2 were obtained: 12.8 μg/m3, 1.7×10−5 m−1 and 35.3 μg/m3, respectively. Adjusted odds ratios (ORs) for wheezing, cough without infection, dry cough at night, bronchial asthma, bronchitis and respiratory infections indicated positive associations with traffic‐related air pollutants. After controlling for individual confounders, significant associations were found between the pollutant PM2.5 and sneezing, runny/stuffed nose during the first year of life (OR 1.16, 95% confidence interval 1.01 to 1.34) Similar effects were observed for the second year of life. These findings are similar to those from our previous analysis that were restricted to a subcohort in Munich city. The extended study also showed significant effects for sneezing, running/stuffed nose. Additionally, significant associations were found between NO2 and dry cough at night (or bronchitis) during the first year of life. The variable “living close to major roads” (<50 m), which was not analysed for the previous inner city cohort with birth addresses in the city of Munich, turned out to increase the risk of wheezing and asthmatic/spastic/obstructive bronchitis.
Effects on asthma and hay fever are subject to confirmation at older ages, when these outcomes can be more validly assessed.
Epidemiologic studies have consistently reported associations between outdoor fine particulate matter (PM2.5) air pollution and adverse health effects. Although Asia bears the majority of the public health burden from air pollution, few epidemiologic studies have been conducted outside of North America and Europe due in part to challenges in population exposure assessment. We assessed the feasibility of two current exposure assessment techniques, land use regression (LUR) modeling and mobile monitoring, and estimated the mortality attributable to air pollution in Ulaanbaatar, Mongolia. We developed LUR models for predicting wintertime spatial patterns of NO2 and SO2 based on 2-week passive Ogawa measurements at 37 locations and freely available geographic predictors. The models explained 74% and 78% of the variance in NO2 and SO2, respectively. Land cover characteristics derived from satellite images were useful predictors of both pollutants. Mobile PM2.5 monitoring with an integrating nephelometer also showed promise, capturing substantial spatial variation in PM2.5 concentrations. The spatial patterns in SO2 and PM, seasonal and diurnal patterns in PM2.5, and high wintertime PM2.5/PM10 ratios were consistent with a major impact from coal and wood combustion in the city’s low-income traditional housing (ger) areas. The annual average concentration of PM2.5 measured at a centrally located government monitoring site was 75 μg/m3 or more than seven times the World Health Organization’s PM2.5 air quality guideline, driven by a wintertime average concentration of 148 μg/m3. PM2.5 concentrations measured in a traditional housing area were higher, with a wintertime mean PM2.5 concentration of 250 μg/m3. We conservatively estimated that 29% (95% CI, 12–43%) of cardiopulmonary deaths and 40% (95% CI, 17–56%) of lung cancer deaths in the city are attributable to outdoor air pollution. These deaths correspond to nearly 10% of the city’s total mortality, with estimates ranging to more than 13% of mortality under less conservative model assumptions. LUR models and mobile monitoring can be successfully implemented in developing country cities, thus cost-effectively improving exposure assessment for epidemiology and risk assessment. Air pollution represents a major threat to public health in Ulaanbaatar, Mongolia, and reducing home heating emissions in traditional housing areas should be the primary focus of air pollution control efforts.
Satellite; Exposure; Nephelometer; Asia; Impact assessment; Coal; Combustion
Epidemiologic studies of air pollution have demonstrated a link between long-term air pollution exposures and mortality. However, many have been limited to city-specific average pollution measures or spatial or land-use regression exposure models in small geographic areas.
Our objective was to develop nationwide models of annual exposure to particulate matter < 10 μm in diameter (PM10) and nitrogen dioxide during 1985–2000.
We used generalized additive models (GAMs) to predict annual levels of the pollutants using smooth spatial surfaces of available monitoring data and geographic information system–derived covariates. Model performance was determined using a cross-validation (CV) procedure with 10% of the data. We also compared the results of these models with a commonly used spatial interpolation, inverse distance weighting.
For PM10, distance to road, elevation, proportion of low-intensity residential, high-intensity residential, and industrial, commercial, or transportation land use within 1 km were all statistically significant predictors of measured PM10 (model R2 = 0.49, CV R2 = 0.55). Distance to road, population density, elevation, land use, and distance to and emissions of the nearest nitrogen oxides–emitting power plant were all statistically significant predictors of measured NO2 (model R2 = 0.88, CV R2 = 0.90). The GAMs performed better overall than the inverse distance models, with higher CV R2 and higher precision.
These models provide reasonably accurate and unbiased estimates of annual exposures for PM10 and NO2. This approach provides the spatial and temporal variability necessary to describe exposure in studies assessing the health effects of chronic air pollution.
GIS; nitrogen dioxide; outdoor air pollution; particulate matter
Study objective: Studies in Europe and North America have reported that living in a disadvantaged neighbourhood is associated with an increased incidence of coronary heart disease. The aim of this study was to test the hypotheses that exposure to traffic and air pollution might account for some of the socioeconomic differences in mortality rates in a city where residents are covered by universal health insurance.
Design: Cohort mortality study. Individual postal codes used to derive: (1) socioeconomic status from census data; (2) mean air pollution levels from interpolation between governmental monitoring stations; (3) proximity to traffic from the geographical information system. Analysis conducted with Cox proportional hazards models.
Setting: Hamilton Census Metropolitan Area, Ontario, Canada, on the western tip of Lake Ontario (population about 480 000).
Participants: 5228 people, aged 40 years or more, identified from register of lung function laboratory at an academic respirology clinic between 1985 and 1999.
Main results: Circulatory disease (cardiovascular and stroke) mortality rates were related to measures of neighbourhood deprivation. Circulatory disease mortality rates were also associated with indices of long term ambient pollution at the subjects' residences (relative risk 1.06, 1.00 to 1.13) and with proximity to traffic (relative risk 1.40, 1.08 to 1.81). Subjects in more deprived neighbourhoods had greater exposure to ambient particulate and gaseous pollutants and to traffic.
Conclusions: At least some of the observed social gradients in circulatory mortality arise from inequalities in environmental exposure to background and traffic air pollutants.
In different weather conditions, constituents and concentrations of pollutants, personal exposure, and biologic responses to air pollution may vary. In this study we assessed the effects of four air pollutants on mortality in both cool and warm seasons in Hong Kong, a subtropical city. Daily counts of mortality, due to all nonaccidental causes, and cardiovascular and respiratory diseases were modeled with daily pollutant concentrations [24-hr means for nitrogen dioxide, sulfur dioxide, and particulate matter < 10 microm in aerodynamic diameter (PM(10)); 8-hr mean for ozone]. using Poisson regression. We controlled for confounding factors by fitting the terms in models, in line with those recommended by the APHEA (Air Pollution and Health: a European Approach) protocol. Exposure-response relationships in warm and cool seasons were examined using generalized additive modeling. During the cool season, for a linear extrapolation of 10th-90th percentiles in the pollutant concentrations of all oxidant pollutants, NO(2), SO(2), and O(3), we found significant effects on all the mortality outcomes under study, with relative risks (RR) of 1.04-1.10 (p < 0.038, except p = 0.079 for SO(2) on respiratory mortality). We observed consistent positive exposure-response relationships during the cool season but not during the warm season. The effects of PM(10) were marginally significant (RR = 1.06; p = 0.054) for respiratory mortality but not for the other outcomes (p > 0.135). In this subtropical city, local air quality objectives should take into account that air pollution has stronger health effects during the cool rather than warm season and that oxidant pollutants are more important indicators of health effects than particulates.
Systemic inflammation may be one of the mechanisms mediating the association between ambient air pollution and cardiovascular morbidity and mortality. Interleukin-6 (IL-6) and fibrinogen are biomarkers of systemic inflammation that are independent risk factors for cardiovascular disease.
We investigated the association between ambient air pollution and systemic inflammation using baseline measurements of IL-6 and fibrinogen from controlled human exposure studies.
In this retrospective analysis we used repeated-measures data in 45 nonsmoking subjects. Hourly and daily moving averages were calculated for ozone, nitrogen dioxide, sulfur dioxide, and particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5). Linear mixed-model regression determined the effects of the pollutants on systemic IL-6 and fibrinogen. Effect modification by season was considered.
We observed a positive association between IL-6 and O3 [0.31 SD per O3 interquartile range (IQR); 95% confidence interval (CI), 0.08–0.54] and between IL-6 and SO2 (0.25 SD per SO2 IQR; 95% CI, 0.06–0.43). We observed the strongest effects using 4-day moving averages. Responses to pollutants varied by season and tended to be higher in the summer, particularly for O3 and PM2.5. Fibrinogen was not associated with pollution.
This study demonstrates a significant association between ambient pollutant levels and baseline levels of systemic IL-6. These findings have potential implications for controlled human exposure studies. Future research should consider whether ambient pollution exposure before chamber exposure modifies IL-6 response.
air pollution; epidemiology; fibrinogen; inflammation; interleukin-6
Health impacts of poor environmental quality have been identified in studies around the world and in Canada. While many of the studies have identified associations between air pollution and mortality or morbidity, few have focused on the role of health care as a potential moderator of impacts. This study assessed the determinants of health care access and utilization in the context of ambient air pollution in Sarnia, Ontario, Canada.
Residents of Sarnia participated in a Community Health Study administered by phone, while several ambient air pollutants including nitrogen dioxide (NO2), sulphur dioxide (SO2) and the volatile organic compounds benzene, toluene, ethylbenzene, mp- and o-xylene (BTEX) were monitored across the city. Land Use Regression models were used to estimate individual exposures to the measured pollutants and logistic regression models were utilized to assess the relative influence of environmental, socioeconomic and health related covariates on general practitioner access and utilization outcomes.
The results show that general practitioner use increased with levels of exposure to nitrogen dioxide (NO2- Odds Ratio [OR]: 1.16, p < 0.05) and sulphur dioxide (SO2- OR: 1.61, p < 0.05). Low household income was a stronger predictor of having no family doctor in areas exposed to high concentrations of NO2 and SO2. Respondents without regular care living in high pollution areas were also more likely to report travelling or waiting for care in excess of 20 minutes (OR: 3.28, p < 0.05) than their low exposure counterparts (OR: 1.11, p > 0.05).
This study provides evidence for inequitable health care access and utilization in Sarnia, with particular relevance to its situation as a sentinel high exposure environment. Levels of exposure to pollution appears to influence utilization of health care services, but poor access to primary health care services additionally burden certain groups in Sarnia, Ontario, Canada.
Several studies have found an effect on mortality of between-city contrasts in long-term exposure to air pollution. The effect of within-city contrasts is still poorly understood.
We studied the association between long-term exposure to traffic-related air pollution and mortality in a Dutch cohort.
We used data from an ongoing cohort study on diet and cancer with 120,852 subjects who were followed from 1987 to 1996. Exposure to black smoke (BS), nitrogen dioxide, sulfur dioxide, and particulate matter ≤mu;M2.5), as well as various exposure variables related to traffic, were estimated at the home address. We conducted Cox analyses in the full cohort adjusting for age, sex, smoking, and area-level socioeconomic status.
Traffic intensity on the nearest road was independently associated with mortality. Relative risks (95% confidence intervals) for a 10-μg/m3 increase in BS concentrations (difference between 5th and 95th percentile) were 1.05 (1.00–1.11) for natural cause, 1.04 (0.95–1.13) for cardiovascular, 1.22 (0.99–1.50) for respiratory, 1.03 (0.88–1.20) for lung cancer, and 1.04 (0.97–1.12) for mortality other than cardiovascular, respiratory, or lung cancer. Results were similar for NO2 and PM2.5, but no associations were found for SO2.
Traffic-related air pollution and several traffic exposure variables were associated with mortality in the full cohort. Relative risks were generally small. Associations between natural-cause and respiratory mortality were statistically significant for NO2 and BS. These results add to the evidence that long-term exposure to ambient air pollution is associated with increased mortality.
air pollution; cohort; mortality; traffic
Fine particulate matter air pollution plus ozone impairs vascular function and raises diastolic blood pressure. We aimed to determine the mechanism and air pollutant responsible. The effects of pollution on heart rate variability, blood pressure, biomarkers, and brachial flow-mediated dilatation were determined in 2 randomized, double-blind, cross-over studies. In Ann Arbor, 50 subjects were exposed to fine particles (150 μg/m3) + ozone (120 ppb) for 2 hours on 3 occasions with pretreatments of an endothelin antagonist (Bosentan 250 mg), anti-oxidant (Vitamin C 2 g), or placebo. In Toronto, 31 subjects were exposed to 4 different conditions (particles + ozone, particles, ozone, and filtered air). In Toronto, diastolic blood pressure significantly increased (2.9 and 3.6 mm Hg) only during particle-containing exposures in association with particulate matter concentration and reductions in heart rate variability. Flow-mediated dilatation significantly decreased (2.0 and 2.9%) only 24 hours after particle-containing exposures in association with particulate matter concentration and increases in blood tumor necrosis factor-alpha. In Ann Arbor, diastolic blood pressure significantly similarly increased during all exposures (2.5 - 4.0 mm Hg), a response not mitigated by pretreatments. Flow-mediated dilatation remained unaltered. Particulate matter, not ozone, was responsible for increasing diastolic blood pressure during air pollution inhalation most plausibly by instigating acute autonomic imbalance. Only particles from urban Toronto additionally impaired endothelial function likely via slower proinflammatory pathways. Our findings demonstrate credible mechanisms whereby fine particulate matter could trigger acute cardiovascular events and that aspects of exposure location may be an important determinant of the health consequences.
hypertension; endothelium; sympathetic nervous system; inflammation; oxidative stress
Study objective: Assess associations between short-term exposure to gaseous pollutants and asthma hospitalisation among boys and girls 6 to12 years of age.
Design: A bi-directional case-crossover analysis was used. Conditional logistic regression models were fitted to the data for boys and girls separately. Exposures averaged over periods ranging from one to seven days were used to assess the effects of gaseous pollutants on asthma hospitalisation. Estimated relative risks for asthma hospitalisation were calculated for an incremental exposure corresponding to the interquartile range in pollutant levels, adjusted for daily weather conditions and concomitant exposure to particulate matter.
Setting: Toronto, Ontario, Canada.
Participants: A total of 7319 asthma hospitalisations for children 6 to 12 years of age (4629 for boys and 2690 for girls) in Toronto between 1981 and 1993.
Main results: A significant acute effect of carbon monoxide on asthma hospitalisation was found in boys, and sulphur dioxide showed significant effects of prolonged exposure in girls. Nitrogen dioxide was positively associated with asthma admissions in both sexes. The lag time for certain gaseous pollutant effects seemed to be shorter in boys (around two to three days for carbon monoxide and nitrogen dioxide), as compared with girls (about six to seven days for sulphur dioxide and nitrogen dioxide). The effects of gaseous pollutants on asthma hospitalisation remained after adjustment of particulate matter. The data showed no association between ozone and asthma hospitalisation in children.
Conclusions: The study showed positive relations between gaseous pollutants (carbon monoxide, sulphur dioxide, and nitrogen dioxide) at comparatively low levels and asthma hospitalisation in children, using bi-directional case-crossover analyses. Though, the effects of certain specific gaseous pollutants were found to vary in boys and girls.
Heart rate variability (HRV), a measure of cardiac autonomic tone, has been associated with cardiovascular morbidity and mortality. Short-term studies have shown that subjects exposed to higher traffic-associated air pollutant levels have lower HRV.
Our objective was to investigate the effect of long-term exposure to nitrogen dioxide on HRV in the Swiss cohort Study on Air Pollution and Lung Diseases in Adults (SAPALDIA).
We recorded 24-hr electrocardiograms in randomly selected SAPALDIA participants ≥ 50 years of age. Other examinations included an interview investigating health status and measurements of blood pressure, body height, and weight. Annual exposure to NO2 at the address of residence was predicted by hybrid models (i.e., a combination of dispersion predictions, land-use, and meteorologic parameters). We estimated the association between NO2 and HRV in multivariable linear regression models. Complete data for analyses were available for 1,408 subjects.
For women, but not for men, each 10-μg/m3 increment in 1-year averaged NO2 level was associated with a decrement of 3% (95% CI, −4 to −1) for the standard deviation of all normal-to-normal RR intervals (SDNN), −6% (95% CI, −11 to −1) for nighttime low frequency (LF), and −5% (95% CI, −9 to 0) for nighttime LF/high-frequency (HF) ratio. We saw no significant effect for 24-hr total power (TP), HF, LF, or LF/HF or for nighttime SDNN, TP, or HF. In subjects with self-reported cardiovascular problems, SDNN decreased by 4% (95% CI, −8 to −1) per 10-μg/m3 increase in NO2.
There is some evidence that long-term exposure to NO2 is associated with cardiac autonomic dysfunction in elderly women and in subjects with cardiovascular disease.
air pollution; autonomic nervous system; cardiovascular diseases; cohort study; heart rate variability; long-term exposure; nitrogen dioxide; sex
Evidence links exposure to ambient air pollution during pregnancy, particularly gaseous pollutants and particulate matter, to an increased risk of adverse reproductive outcomes but the results for birth defects have been inconsistent.
We compared estimated exposure to ambient air pollutants during early pregnancy among mothers of children with oral cleft defects (cases) to that among mothers of controls, adjusting for available risk factors from birth certificates. We obtained ambient air pollutant data from air monitoring sites in New Jersey for carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2), particulate matter less than 10 µm in aerodynamic diameter (PM10) and particulate matter less than 2.5 µm in aerodynamic diameter (PM2.5). We used values from the nearest monitor (within 40 km of the residence at birth) for controls, cleft lip with or without cleft palate (CLP) and cleft palate only (CPO).
Based on logistic regression analyses for each contaminant and all contaminants together, there were no consistent elevated associations between selected air pollutants and cleft malformations. Quartile of CO concentration showed a consistent protective association with CPO (p<.01). For other contaminants, confidence intervals (95%) of the odds ratios for some quartiles excluded one. CLP showed limited evidence of an association with increasing SO2 exposure while CPO showed weak associations with increasing O3 exposure.
There was little consistent evidence associating cleft malformations with maternal exposure to ambient air pollutants. Evaluating particular pollutants or disease subgroups would require more detailed measurement of exposure and classification of cleft defects.
Otitis media is one of the most common infections in young children. Although exposure to environmental tobacco smoke is a known risk factor associated with otitis media, little information is available regarding the potential association with air pollution.
We set out to study the relationship between exposure to traffic-related air pollution and otitis media in two birth cohorts.
Individual estimates of outdoor concentrations of traffic-related air pollutants—nitrogen dioxide, fine particles [particulate matter with aerodynamic diameters ≤ 2.5 μm (PM2.5)], and elemental carbon—were calculated for home addresses of approximately 3,700 and 650 infants from birth cohort studies in the Netherlands and Germany, respectively. Air pollution exposure was analyzed in relation to physician diagnosis of otitis media in the first 2 years of life.
Odds ratios (adjusted for known major risk factors) for otitis media indicated positive associations with traffic-related air pollutants. An increase in 3 μg/m3 PM2.5, 0.5 μg/m3 elemental carbon, and 10 μg/m3 NO2 was associated with odds ratios of 1.13 (95% confidence interval, 1.00–1.27), 1.10 (1.00–1.22), and 1.14 (1.03–1.27) in the Netherlands and 1.24 (0.84–1.83), 1.10 (0.86–1.41), and 1.14 (0.87–1.49) in Germany, respectively.
These findings indicate an association between exposure to traffic-related air pollutants and the incidence of otitis media. Given the ubiquitous nature of air pollution exposure and the importance of otitis media to children’s health, these findings have significant public health implications.
air pollution; cohort studies; infant; otitis media; vehicle emissions
Air pollution influences the development of oral clefts in animals. There are few epidemiologic data on the relation of prenatal air pollution exposure and the risk of oral clefts.
Our goal in this study was to assess the relations between exposure to ambient air pollution and the risk of cleft lip with or without cleft palate (CL/P).
We conducted a population-based case–control study of all 653 cases of CL/P and a random sample of 6,530 control subjects from 721,289 Taiwanese newborns in 2001–2003. We used geographic information systems to form exposure parameters for sulfur dioxide, nitrogen oxides, ozone, carbon monoxide, and particulate matter with an aerodynamic diameter ≤ 10 μm (PM10) during the first 3 months of pregnancy using inverse distance weighting method. We present the effect estimates as odds ratios (ORs) per 10-ppb change for SO2, NOx, and O3, 100-ppb change for CO, and 10-μg/m3 change for PM10.
The risk of CL/P was increased in relation to O3 levels in the first gestational month [adjusted OR = 1.20; 95% confidence interval (CI), 1.02–1.39] and second gestational month (adjusted OR = 1.25; 95% CI, 1.03–1.52) in the range from 16.7 ppb to 45.1 ppb, but was not related to CO, NOx, SO2, or PM10.
The study provides new evidence that exposure to outdoor air O3 during the first and second month of pregnancy may increase the risk of CL/P. Similar levels of O3 are encountered globally by large numbers of pregnant women.
air pollution; cleft lip; ozone; traffic
Study objective: To assess the short term association between air pollution and mortality in different zones of an industrial city. An intra-urban study design is used to test the hypothesis that socioeconomic characteristics modify the acute health effects of ambient air pollution exposure.
Design: The City of Hamilton, Canada, was divided into five zones based on proximity to fixed site air pollution monitors. Within each zone, daily counts of non-trauma mortality and air pollution estimates were combined. Generalised linear models (GLMs) were used to test mortality associations with sulphur dioxide (SO2) and with particulate air pollution measured by the coefficient of haze (CoH).
Main results: Increased mortality was associated with air pollution exposure in a citywide model and in intra-urban zones with lower socioeconomic characteristics. Low educational attainment and high manufacturing employment in the zones significantly and positively modified the acute mortality effects of air pollution exposure.
Discussion: Three possible explanations are proposed for the observed effect modification by education and manufacturing: (1) those in manufacturing receive higher workplace exposures that combine with ambient exposures to produce larger health effects; (2) persons with lower education are less mobile and experience less exposure measurement error, which reduces bias toward the null; or (3) manufacturing and education proxy for many social variables representing material deprivation, and poor material conditions increase susceptibility to health risks from air pollution.
Mild hyperhomocysteinemia is independently associated with an increased risk of cardiovascular disease. Air pollution exposure induces short-term inflammatory changes that may determine hyperhomocysteinemia, particularly in the presence of a preexisting proinflammatory status such as that found in cigarette smokers.
We examined the relation of air pollution levels with fasting and postmethionine-load total homocysteine (tHcy) in 1,213 normal subjects from Lombardia, Italy.
We obtained hourly concentrations of particulate matter < 10 μm in aerodynamic diameter (PM10) and gaseous pollutants (carbon monoxide, nitrogen dioxide, sulfur dioxide, ozone) from 53 monitoring sites covering the study area. We applied generalized additive models to compute standardized regression coefficients controlled for age, sex, body mass index, smoking, alcohol, hormone use, temperature, day of the year, and long-term trends.
The estimated difference in tHcy associated with an interquartile increase in average PM10 concentrations in the 24 hr before the study was nonsignificant [0.4%; 95% confidence interval (CI), −2.4 to 3.3 for fasting; and 1.1%, 95% CI, −1.5 to 3.7 for postmethionine-load tHcy]. In smokers, 24-hr PM10 levels were associated with 6.3% (95% CI, 1.3 to 11.6; p < 0.05) and 4.9% (95% CI, 0.5 to 9.6; p < 0.05) increases in fasting and postmethionine-load tHcy, respectively, but no association was seen in nonsmokers (p-interaction = 0.005 for fasting and 0.039 for postmethionine-load tHcy). Average 24-hr O3 concentrations were associated with significant differences in fasting tHcy (6.7%; 95% CI, 0.9 to 12.8; p < 0.05), but no consistent associations were found when postmethionine-load tHcy and/or 7-day average O3 concentrations were considered.
Air particles may interact with cigarette smoking and increase plasma homocysteine in healthy subjects.
air pollution; cardiovascular risk; generalized additive models; homocysteine; particulate matter; smoking
Background: Air pollution effects on children’s neurodevelopment have recently been suggested to occur most likely through the oxidative stress pathway.
Objective: We aimed to assess whether prenatal exposure to residential air pollution is associated with impaired infant mental development, and whether antioxidant/detoxification factors modulate this association.
Methods: In the Spanish INfancia y Medio Ambiente (INMA; Environment and Childhood) Project, 2,644 pregnant women were recruited during their first trimester. Nitrogen dioxide (NO2) and benzene were measured with passive samplers covering the study areas. Land use regression models were developed for each pollutant to predict average outdoor air pollution levels for the entire pregnancy at each residential address. Maternal diet was obtained at first trimester through a validated food frequency questionnaire. Around 14 months, infant mental development was assessed using Bayley Scales of Infant Development.
Results: Among the 1,889 children included in the analysis, mean exposure during pregnancy was 29.0 μg/m3 for NO2 and 1.5 μg/m3 for benzene. Exposure to NO2 and benzene showed an inverse association with mental development, although not statistically significant, after adjusting for potential confounders [β (95% confidence interval) = –0.95 (–3.90, 1.89) and –1.57 (–3.69, 0.56), respectively, for a doubling of each compound]. Stronger inverse associations were estimated for both pollutants among infants whose mothers reported low intakes of fruits/vegetables during pregnancy [–4.13 (–7.06, –1.21) and –4.37 (–6.89, –1.86) for NO2 and benzene, respectively], with little evidence of associations in the high-intake group (interaction p-values of 0.073 and 0.047). Inverse associations were also stronger in non-breast-fed infants and infants with low maternal vitamin D, but effect estimates and interactions were not significant.
Conclusions: Our findings suggest that prenatal exposure to residential air pollutants may adversely affect infant mental development, but potential effects may be limited to infants whose mothers report low antioxidant intakes.
aromatic hydrocarbons; breast-feeding; child development; cognition; environmental pollution; fruit; intelligence; nitrogen dioxide; vegetables; vitamin D
Although individuals spend the majority of their time indoors, most epidemiological studies estimate personal air pollution exposures based on outdoor levels. This almost certainly results in exposure misclassification as pollutant infiltration varies between homes. However, it is often not possible to collect detailed measures of infiltration for individual homes in large-scale epidemiological studies and thus there is currently a need to develop models that can be used to predict these values. To address this need, we examined infiltration of fine particulate matter (PM2.5) and identified determinants of infiltration for 46 residential homes in Toronto, Canada. Infiltration was estimated using the indoor/outdoor sulphur ratio and information on hypothesized predictors of infiltration were collected using questionnaires and publicly available databases. Multiple linear regression was used to develop the models. Mean infiltration was 0.52 ± 0.21 with no significant difference across heating and non-heating seasons. Predictors of infiltration were air exchange, presence of central air conditioning, and forced air heating. These variables accounted for 38% of the variability in infiltration. Without air exchange, the model accounted for 26% of the variability. Effective modelling of infiltration in individual homes remains difficult, although key variables such as use of central air conditioning show potential as an easily attainable indicator of infiltration.
air exchange; air quality; indoor; infiltration; fine particulate matter; PM2.5; residential; sulphur
Rationale: Ambient air pollution has been associated with heart failure morbidity and mortality. The mechanisms responsible for these associations are unknown but may include the effects of traffic-related pollutants on vascular or autonomic function.
Objectives: We assessed the cross-sectional relation between long-term air pollution, traffic exposures, and important end-organ measures of alterations in cardiac function—left ventricular mass index (LVMI) and ejection fraction—in the Multi-Ethnic Study of Atherosclerosis, a multicenter study of adults without previous clinical cardiovascular disease.
Methods: A total of 3,827 eligible participants (aged 45–84 yr) underwent cardiac magnetic resonance imaging between 2000 and 2002. We estimated air pollution exposures using residential proximity to major roadways and interpolated concentrations of fine particulate matter (less than 2.5 microns in diameter). We examined adjusted associations between these exposures and left ventricular mass and function.
Measurements and Main Results: Relative to participants living more than 150 m from a major roadway, participants living within 50 m of a major roadway showed an adjusted 1.4 g/m2 (95% CI, 0.3–2.5) higher LVMI, a difference in mass corresponding to a 5.6 mm Hg greater systolic blood pressure. Ejection fraction was not associated with proximity to major roadways. Limited variability in estimates of fine particulate matter was observed within cities, and no associations with particulate matter were found for either outcome after adjustment for center.
Conclusions: Living in close proximity to major roadways is associated with higher LVMI, suggesting chronic vascular end-organ damage from a traffic-related environmental exposure. Air pollutants or another component of roadway proximity, such as noise, could be responsible.
epidemiology; particulate matter; hypertrophy; heart failure; magnetic resonance imaging
The relationship between ambient air pollution exposure and mortality of cardiovascular and cerebrovascular diseases in human is controversial, and there is little information about how exposures to ambient air pollution contribution to the mortality of cardiovascular and cerebrovascular diseases among Chinese. The aim of the present study was to examine whether exposure to ambient-air pollution increases the risk for cardiovascular and cerebrovascular disease.
We conducted a retrospective cohort study among humans to examine the association between compound-air pollutants [particulate matter <10 µm in aerodynamic diameter (PM10), sulfur dioxide (SO2) and nitrogen dioxide (NO2)] and mortality in Shenyang, China, using 12 years of data (1998–2009). Also, stratified analysis by sex, age, education, and income was conducted for cardiovascular and cerebrovascular mortality. The results showed that an increase of 10 µg/m3 in a year average concentration of PM10 corresponds to 55% increase in the risk of a death cardiovascular disease (hazard ratio [HR], 1.55; 95% confidence interval [CI], 1.51 to 1.60) and 49% increase in cerebrovascular disease (HR, 1.49; 95% CI, 1.45 to 1.53), respectively. The corresponding figures of adjusted HR (95%CI) for a 10 µg/m3 increase in NO2 was 2.46 (2.31 to 2.63) for cardiovascular mortality and 2.44 (2.27 to 2.62) for cerebrovascular mortality, respectively. The effects of air pollution were more evident in female that in male, and nonsmokers and residents with BMI<18.5 were more vulnerable to outdoor air pollution.
Long-term exposure to ambient air pollution is associated with the death of cardiovascular and cerebrovascular diseases among Chinese populations.
Although acute adverse effects on asthma have been frequently found for the U.S. Environmental Protection Agency's principal criteria air pollutants, there is little epidemiologic information on specific hydrocarbons from toxic emission sources. We conducted a panel study of 22 Hispanic children with asthma who were 10-16 years old and living in a Los Angeles community with high traffic density. Subjects filled out symptom diaries daily for up to 3 months (November 1999 through January 2000). Pollutants included ambient hourly values of ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide and 24-hr values of volatile organic compounds (VOCs), particulate matter with aerodynamic diameter < 10 microm (PM10, and elemental carbon (EC) and organic carbon (OC) PM10 fractions. Asthma symptom severity was regressed on pollutants using generalized estimating equations, and peak expiratory flow (PEF) was regressed on pollutants using mixed models. We found positive associations of symptoms with criteria air pollutants (O3, NO2, SO2, PM10), EC-OC, and VOCs (benzene, ethylbenzene, formaldehyde, acetaldehyde, acetone, 1,3-butadiene, tetrachloroethylene, toluene, m,p-xylene, and o-xylene). Selected adjusted odds ratios for bothersome or more severe asthma symptoms from interquartile range increases in pollutants were, for 1.4 ppb 8-hr NO2, 1.27 [95% confidence interval (CI), 1.05-1.54]; 1.00 ppb benzene, 1.23 (95% CI, 1.02-1.48); 3.16 ppb formaldehyde, 1.37 (95% CI, 1.04-1.80); 37 microg/m3 PM10, 1.45 (95% CI, 1.11-1.90); 2.91 microg/m3 EC, 1.85 (95% CI, 1.11-3.08); and 4.64 microg/m3 OC, 1.88 (95% CI, 1.12-3.17). Two-pollutant models of EC or OC with PM10 showed little change in odds ratios for EC (to 1.83) or OC (to 1.89), but PM10 decreased from 1.45 to 1.0. There were no significant associations with PEF. Findings support the view that air toxins in the pollutant mix from traffic and industrial sources may have adverse effects on asthma in children.
Objective: To investigate the association between ambient concentrations of air pollutants and respiratory and cardiovascular mortalities in Hong Kong.
Methods: Retrospective ecological study. A Poisson regression of concentrations of daily air pollutants on daily mortalities for respiratory and cardiovascular diseases in Hong Kong from 1995 to the end of 1998 was performed using the air pollution and health: the European approach (APHEA) protocol. The effects of time trend, seasonal variations, temperature, and humidity were adjusted. Autocorrelation and overdispersion were corrected. Daily concentrations of nitrogen dioxide (NO2), sulphur dioxide (SO2), ozone (O3), and particulate matter <10 µm in aerodynamic diameter (PM10) were averaged from eight monitoring stations in Hong Kong. Relative risks (RRs) of respiratory and cardiovascular mortalities (per 10 µg/m3 increase in air pollutant concentration) were calculated.
Results: Significant associations were found between mortalities for all respiratory diseases and ischaemic heart diseases (IHD) and the concentrations of all pollutants when analysed singly. The RRs for all respiratory mortalities (for a 10 µg/m3 increase in the concentration of a pollutant) ranged from 1.008 (for PM10) to 1.015 (for SO2) and were higher for chronic obstructive pulmonary diseases (COPD) with all pollutants except SO2, ranging from 1.017 (for PM10) to 1.034 (for O3). RRs for IHD ranged from 1.009 (for O3) to 1.028 (for SO2). In a multipollutant model, O3 and SO2 were significantly associated with all respiratory mortalities, whereas NO2 was associated with mortality from IHD. No interactions were detected between any of the pollutants or with the winter season. A dose-response effect was evident for all air pollutants. Harvesting was not found in the short term.
Conclusions: Mortality risks were detected at current ambient concentrations of air pollutants. The associations with the particulates and some gaseous pollutants when analysed singly were consistent with many reported in temperate countries. PM10 was not associated with respiratory or cardiovascular mortalities in multipollutant analyses.