Ambient air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD). However, there is a lack of longitudinal studies to support this assertion.
To investigate the associations of long-term exposure to elevated traffic-related air pollution and woodsmoke pollution with the risk of COPD hospitalization and mortality.
This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents aged 45-85 years who resided in Metropolitan Vancouver, Canada, during the exposure period and did not have known COPD at baseline were included in this study (n = 467,994). Residential exposures to traffic-related air pollutants (black carbon, particulate matter
Center for Environmental and Respiratory Health Research, University of Oulu, P.O. Box 5000, FI-90014 Oulu, Finland; Respiratory Medicine Unit, Department of Medicine, Oulu University Hospital, FI-90029 Oulu, Finland; Medical Research Center Oulu, Oulu, Finland.
The occurrence of cold temperature-related symptoms has not been investigated previously in young adults, although cold weather may provoke severe symptoms leading to activity limitations, and those with pre-existing respiratory conditions may form a susceptible group. We tested the hypothesis that young adults with asthma and allergic rhinitis experience cold-related respiratory symptoms more commonly than young adults in general.
A population-based study of 1623 subjects 20-27 years old was conducted with a questionnaire inquiring about cold weather-related respiratory symptoms, doctor-diagnosed asthma and rhinitis, and lifestyle and environmental exposures.
Current asthma increased the risk of all cold weather-related symptoms (shortness of breath adjusted PR 4.53, 95% confidence interval 2.93-6.99, wheezing 10.70, 5.38-21.29, phlegm production 2.51, 1.37-4.62, cough 3.41, 1.97-5.87 and chest pain 2.53, 0.82-7.79). Allergic rhinitis had additional effect especially on shortness of breath (7.16, 5.30-9.67) and wheezing (13.05, 7.75-22.00), some on phlegm production (3.69, 2.49-5.47), but marginal effect on cough and chest pain.
Our study shows that already in young adulthood those with asthma, and especially those with coexisting allergic rhinitis, experience substantially more cold temperature-related respiratory symptoms than healthy young adults. Hence, young adults with a respiratory disease form a susceptible group that needs special care and guidance for coping with cold weather.
Regular year-round exercise is recommended for patients with coronary artery disease (CAD). However, the combined effects of cold and moderate sustained exercise, both known to increase cardiac workload, on cardiovascular responses are not known. We tested the hypothesis that cardiac workload is increased, and evidence of ischemia would be observed during exercise in the cold in patients with CAD. Sixteen men (59.3?±?7.0 yr, means?±?SD) with stable CAD each underwent 4, 30 min exposures in a randomized order: seated rest and moderate-intensity exercise [walking, 60%-70% of max heart rate (HR)] performed at +22°C and -15°C. Systolic brachial blood pressure (SBP), HR, electrocardiogram (ECG), and skin temperatures were recorded throughout the intervention. Rate pressure product (RPP) and ECG parameters were obtained. The combined effects of cold and submaximal exercise were additive for SBP and RPP and synergistic for HR when compared with rest in a neutral environment. RPP (mmHg·beats/min) was 17% higher during exercise in the cold (18,080?± 3540) compared with neutral (15,490?±?2,940) conditions ( P = 0.001). Only a few ST depressions were detected during exercise but without an effect of ambient temperature. The corrected QT interval increased while exercising in the cold compared with neutral temperature ( P = 0.023). Recovery of postexercise blood pressure was similar regardless of temperature. Whole body exposure to cold during submaximal exercise results in higher cardiac workload compared with a neutral environment. Despite the higher RPP, no signs of myocardial ischemia or abnormal ECG responses were observed. The results of this study are useful for planning year-round exercise-based rehabilitation programs for stable CAD patients.
Residential proximity to road traffic is associated with increased coronary heart disease (CHD) morbidity and mortality. It is unknown, however, whether changes in residential proximity to traffic could alter the risk of CHD mortality.
We used a population-based cohort study with a 5-year exposure period and a 4-year follow-up period to explore the association between changes in residential proximity to road traffic and the risk of CHD mortality. The cohort comprised all residents aged 45-85 years who resided in metropolitan Vancouver during the exposure period and without known CHD at baseline (n = 450,283). Residential proximity to traffic was estimated using a geographic information system. CHD deaths during the follow-up period were identified using provincial death registration database. The data were analyzed using logistic regression.
Compared with the subjects consistently living away from road traffic (>150 m from a highway or >50 m from a major road) during the 9-year study period, those consistently living close to traffic (
Recent evidence suggests that chronic exposure to high levels of ambient particulate matter (PM) is associated with decreased pulmonary function and the development of chronic airflow obstruction. To investigate the possible role of PM-induced abnormalities in the small airways in these functional changes, we examined histologic sections from the lungs of 20 women from Mexico City, a high PM locale. All subjects were lifelong residents of Mexico City, were never-smokers, never had occupational dust exposure, and never used biomass fuel for cooking. Twenty never-smoking, non-dust-exposed subjects from Vancouver, British Columbia, Canada, a low PM region, were used as a control. By light microscopy, abnormal small airways with fibrotic walls and excess muscle, many containing visible dust, were present in the Mexico City lungs. Formal grading analysis confirmed the presence of significantly greater amounts of fibrous tissue and muscle in the walls of the airways in the Mexico City compared with the Vancouver lungs. Electron microscopic particle burden measurements on four cases from Mexico City showed that carbonaceous aggregates of ultrafine particles, aggregates likely to be combustion products, were present in the airway mucosa. We conclude that PM penetrates into and is retained in the walls of small airways, and that, even in nonsmokers, long-term exposure to high levels of ambient particulate pollutants is associated with small airway remodeling. This process may produce chronic airflow obstruction.
Cites: Am J Respir Crit Care Med. 1998 Jul;158(1):289-989655742
Cites: Am J Respir Cell Mol Biol. 2002 Jun;26(6):685-9312034567
Cites: Am J Respir Crit Care Med. 1999 Feb;159(2):373-829927346
Cites: Am J Respir Cell Mol Biol. 1999 May;20(5):1067-7210226078
Cites: Environ Health Perspect. 2000 Aug;108 Suppl 4:713-2310931790
Evidence suggests that air pollution exposure adversely affects pregnancy outcomes. Few studies have examined individual-level intraurban exposure contrasts.
We evaluated the impacts of air pollution on small for gestational age (SGA) birth weight, low full-term birth weight (LBW), and preterm birth using spatiotemporal exposure metrics.
With linked administrative data, we identified 70,249 singleton births (1999-2002) with complete covariate data (sex, ethnicity, parity, birth month and year, income, education) and maternal residential history in Vancouver, British Columbia, Canada. We estimated residential exposures by month of pregnancy using nearest and inverse-distance weighting (IDW) of study area monitors [carbon monoxide, nitrogen dioxide, nitric oxide, ozone, sulfur dioxide, and particulate matter
Cites: Occup Environ Med. 2008 Sep;65(9):579-8618070798
Cites: J Expo Anal Environ Epidemiol. 2005 Mar;15(2):185-20415292906
Sudden cardiac death (SCD) is the leading cause of death. The current paradigm in SCD requires the presence of an abnormal myocardial substrate and an internal or external transient factor that triggers cardiac arrest. Based on prior mechanistic evidence, we hypothesized that an unusually cold weather event (a cold spell) could act as an external factor triggering SCD. We tested potential effect modification of prior diagnoses and select pharmacological agents disrupting pathological pathways between cold exposure and death. The home coordinates of 2572 autopsy-verified cases of ischaemic SCD aged =35 in the Province of Oulu, Finland, were linked to 51 years of home-specific weather data. Based on conditional logistic regression, an increased risk of ischaemic SCD associated with a cold spell preceding death (OR 1.49; 95% CI: 1.06-2.09). Cases without a prior diagnosis of ischaemic heart disease seemed more susceptible to the effects of cold spells (OR 1.70; 95% CI: 1.13-2.56) than cases who had been diagnosed during lifetime (OR 1.14; 95% CI: 0.61-2.10). The use of aspirin, ß-blockers, and/or nitrates, independently and in combinations decreased the risk of ischaemic SCD during cold spells. The findings open up new lines of research in mitigating the adverse health effects of weather.
Cites: Br Med J (Clin Res Ed). 1984 Nov 24;289(6456):1405-8 PMID 6437575
Cites: Am J Hypertens. 2014 May;27(5):656-64 PMID 23964061
Cites: J Am Coll Cardiol. 2006 Jul 18;48(2):287-92 PMID 16843177
Cites: Eur Heart J. 2001 Aug;22(16):1374-450 PMID 11482917
Here we compare PM(2.5) (particles with aerodynamic diameter less than 2.5 microm) mass and filter absorbance measurements with elemental carbon (EC) concentrations measured in parallel at the same site as well as collocated PM(2.5) and PM(10) (particles with aerodynamic diameter less than 10 microm) mass and absorbance measurements. The data were collected within the Traffic-Related Air Pollution on Childhood Asthma (TRAPCA) study in Germany, The Netherlands and Sweden. The study was designed to assess the health impact of spatial contrasts in long-term average concentrations. The measurement sites were distributed between background and traffic locations. Annual EC and PM(2.5) absorbance measurements were at traffic sites on average 43-84% and 26-76% higher, respectively, compared to urban background sites. The contrast for PM(2.5) mass measurements was lower (8-35%). The smaller contrast observed for PM(2.5) mass in comparison with PM(2.5) absorbance and EC documents that PM(2.5) mass underestimates exposure contrasts related to motorized traffic emissions. The correlation between PM(10) and PM(2.5) was high, documenting that most of the spatial variation of PM(10) was because of PM(2.5). The measurement of PM(2.5) absorbance was highly correlated with EC measurements and suggests that absorbance can be used as a simple, inexpensive and non-destructive method to estimate motorized traffic-related particulate air pollution. The EC/absorbance relation differed between countries and site type (background/traffic), supporting the need for site-specific calibrations of the simple absorbance method. While the ratio between PM(2.5) and PM(10) mass ranged from 0.54 to 0.68, the ratio of PM(2.5) absorbance and PM(10) absorbance was 0.96-0.97, indicating that PM(2.5) absorbance captures nearly all of the particle absorbance.
To test the a priori hypothesis that the association between cold spells and ischaemic sudden cardiac death (SCD) is modified by the severity of coronary stenosis.
The home coordinates of 2572 autopsy-verified cases of ischaemic SCD aged =35 in the Province of Oulu, Finland, were linked to 51 years of weather data. Cold spell was statistically defined for each home address as unusually cold weather pertinent to the location and time of year. We estimated the occurrence of cold spells during the hazard period (7 days preceding death) and reference periods (the same calendar days over 51 years) in a case-crossover setting applying conditional logistic regression, controlling for temporal trends and stratifying by severity of coronary stenosis.
The association between cold spells and ischaemic SCD was stronger among patients with 75%-95% stenosis (OR 2.03; 95%?CI 1.31 to 3.17), and weaker to non-existent among patients with
Cites: J Am Coll Cardiol. 2005 Oct 18;46(8):1425-33 PMID 16226165
Cites: Br Med J (Clin Res Ed). 1984 Nov 24;289(6456):1405-8 PMID 6437575
Cites: Am J Hypertens. 2014 May;27(5):656-64 PMID 23964061
The goal was to investigate the epidemiological features of incident bronchiolitis by using a population-based infant cohort.
Outpatient and inpatient health records were used to identify incident bronchiolitis cases among 93,058 singleton infants born in the Georgia Air Basin between 1999 and 2002. Additional health-related databases were linked to provide data on sociodemographic variables, maternal characteristics, and birth outcome measures.
From 1999 to 2002, bronchiolitis accounted for 12,474 incident health care encounters (inpatient or outpatient contacts) during the first year of life (134.2 cases per 1000 person-years). A total of 1588 hospitalized bronchiolitis cases were identified (17.1 cases per 1000 person-years). Adjusted Cox proportional-hazard analyses for both case definitions indicated an increased risk of incident bronchiolitis in the first year of life (follow-up period: 2-12 months) for boys, infants of First Nations status, infants with older siblings, and infants living in neighborhoods with smaller proportions of maternal postsecondary education. The risk also was elevated for infants born to young mothers (
We conducted a population-based study to assess whether work as a nurse during pregnancy increases the risk of low birth weight, preterm delivery, and small-for-gestational-age.
The study population was selected from The Finnish Prenatal Environment and Health Study of 2568 newborns (response 94%) and included 128 (5.0%) newborns of nurses and 559 newborns of office workers (21.8%) as a reference group.
The risk of low birth weight (adjusted odds ratio = 1.02; 95% confidence interval = 0.32-3.22) and preterm delivery (0.81; 0.32-2.05) did not differ between newborns of nurses and office workers, but the risk of small-for-gestational-age was substantially higher among newborns of nurses (1.99; 1.10-3.59). This corresponds to a population attributable fraction of 2.5%.
The results indicate that working as a nurse during pregnancy could reduce fetal growth.
There is increasing recognition of the importance of early environmental exposures in the development of childhood asthma. Outdoor air pollution is a recognized asthma trigger, but it is unclear whether exposure influences incident disease. We investigated the effect of exposure to ambient air pollution in utero and during the first year of life on risk of subsequent asthma diagnosis in a population-based nested case-control study.
We assessed all children born in southwestern British Columbia in 1999 and 2000 (n = 37,401) for incidence of asthma diagnosis up to 34 years of age using outpatient and hospitalization records. Asthma cases were age- and sex-matched to five randomly chosen controls from the eligible cohort. We estimated each individual's exposure to ambient air pollution for the gestational period and first year of life using high-resolution pollution surfaces derived from regulatory monitoring data as well as land use regression models adjusted for temporal variation. We used logistic regression analyses to estimate effects of carbon monoxide, nitric oxide, nitrogen dioxide, particulate matter
This review synthesizes current knowledge of the effects of prenatal and postnatal exposure to environmental tobacco smoke on the respiratory health of children. A Medline database search was conducted for 1966 through October 2000. Limited evidence was found that exposure in pregnancy influences fetal growth, increases the risk of preterm delivery, and predicts the development of asthma and reduced lung function later in life. Both occupational and home environments contribute to the exposure of pregnant women and thus indirectly to adverse effects on children. There is strong and consistent evidence that exposure in childhood causes chronic respiratory symptoms (eg, cough, phlegm, and wheezing) and induces asthma. Limited evidence supports the role of childhood exposure in the poor overall control of established disease. Postnatal exposure is likely to have a small adverse impact on lung function growth. Prenatal and postnatal exposures have an important impact on children's respiratory health. These effects are preventable if pregnant women and children are protected from exposure to environmental tobacco smoke.
The authors assessed the effects of environmental tobacco smoke (ETS) on the development of asthma in adults.
In the Pirkanmaa district of South Finland, all 21- to 63-year-old adults with new cases of asthma diagnosed during a 2.5-year period (n = 521 case patients, out of 441 000 inhabitants) and a random sample of control subjects from the source population (932 control subjects) participated in a population-based incident case-control study.
Risk of asthma was related to workplace ETS exposure (adjusted odds ratio [OR] = 2.16; 95% confidence interval [CI] = 1.26, 3.72) and home exposure (OR = 4.77; 95% CI = 1.29, 17.7) in the past year. Cumulative ETS exposure over a lifetime at work and at home increased the risk.
This study indicates for the first time that both cumulative lifetime and recent ETS exposures increase the risk of adult-onset asthma.
Cites: Am J Epidemiol. 1999 Dec 1;150(11):1223-810588083
Cites: Environ Health Perspect. 1999 Dec;107 Suppl 6:829-3510592138
Cites: Allergy. 2001 Apr;56(4):287-9211284794
Cites: Environ Health Perspect. 2002 May;110(5):543-712003761
Cites: Scand J Work Environ Health. 2002;28 Suppl 2:52-7012058803
Cites: Am J Epidemiol. 1974 May;99(5):325-324825599
BACKGROUND: As part of a multicenter study relating traffic-related air pollution with incidence of asthma in three birth cohort studies (TRAPCA), we used a measurement and modelling procedure to estimate long-term average exposure to traffic-related particulate air pollution in communities throughout the Netherlands; in Munich, Germany; and in Stockholm County, Sweden. METHODS: In each of the three locations, 40-42 measurement sites were selected to represent rural, urban background and urban traffic locations. At each site and fine particles and filter absorbance (a marker for diesel exhaust particles) were measured for four 2-week periods distributed over approximately 1-year periods between February 1999 and July 2000. We used these measurements to calculate annual average concentrations after adjustment for temporal variation. Traffic-related variables (eg, population density and traffic intensity) were collected using Geographic Information Systems and used in regression models predicting annual average concentrations. From these models we estimated ambient air concentrations at the home addresses of the cohort members. RESULTS: Regression models using traffic-related variables explained 73%, 56% and 50% of the variability in annual average fine particle concentrations for the Netherlands, Munich and Stockholm County, respectively. For filter absorbance, the regression models explained 81%, 67% and 66% of the variability in the annual average concentrations. Cross-validation to estimate the model prediction errors indicated root mean squared errors of 1.1-1.6 microg/m for PM(2.5) and 0.22-0.31 *10(-5) m for absorbance.CONCLUSIONS: A substantial fraction of the variability in annual average concentrations for all locations was explained by traffic-related variables. This approach can be used to estimate individual exposures for epidemiologic studies and offers advantages over alternative techniques relying on surrogate variables or traditional approaches that utilize ambient monitoring data alone.
Radiographers process X-ray films using developer and fixer solutions that contain chemicals known to cause or exacerbate asthma. In a study in British Columbia, Canada, radiographers' personal exposures to glutaraldehyde (a constituent of the developer chemistry), acetic acid (a constituent of the fixer chemistry), and sulfur dioxide (a byproduct of sulfites, present in both developer and fixer solutions) were measured. Average full-shift exposures to glutaraldehyde, acetic acid, and sulfur dioxide were 0.0009 mg/m3, 0.09 mg/m3, and 0.08 mg/m3, respectively, all more than one order of magnitude lower than current occupational exposure limits. Local exhaust ventilation of the processing machines and use of silver recovery units lowered exposures, whereas the number of films processed per machine and the time spent near the machines increased exposures. Personnel in clinic facilities had higher exposures than those in hospitals. Private clinics were less likely to have local exhaust ventilation and silver recovery units. Their radiographers spent more time in the processor areas and processed more films per machine. Although exposures were low compared with exposure standards, there are good reasons to continue practices to minimize or eliminate exposures: glutaraldehyde and hydroquinone (present in the developer) are sensitizers; the levels at which health effects occur are not yet clearly established, but appear to be lower than current standards; and health effects resulting from the mixture of chemicals are not understood. Developments in digital imaging technology are making available options that do not involve wet-processing of photographic film and therefore could eliminate the use of developer and fixer chemicals altogether.
Numerous epidemiologic studies report associations between outdoor concentrations of particles and adverse health effects. Because personal exposure to particles is frequently dominated by exposure to nonambient particles (those originating from indoor sources), we present an approach to evaluate the relative impacts of ambient and nonambient exposures.
We developed separate estimates of exposures to ambient and nonambient particles of different size ranges (PM2.5, PM10-2.5 and PM10) based on time-activity data and the use of particle sulfate measurements as a tracer for indoor infiltration of ambient particles. To illustrate the application of these estimates, associations between cardiopulmonary health outcomes and the estimated exposures were compared with associations computed using measurements of personal exposures and outdoor concentrations for a repeated-measures panel study of 16 patients with chronic obstructive pulmonary disease conducted in the summer of 1998 in Vancouver.
Total personal fine particle exposures were dominated by exposures to nonambient particles, which were not correlated with ambient fine particle exposures or ambient concentrations. Although total and nonambient particle exposures were not associated with any of the health outcomes, ambient exposures (and to a lesser extent ambient concentrations) were associated with decreased lung function, decreased systolic blood pressure, increased heart rate, and increased supraventricular ectopic heartbeats. Measures of heart rate variability showed less consistent relationships among the various exposure metrics.
These results demonstrate the usefulness of separating total personal particle exposures into their ambient and nonambient components. The results support previous epidemiologic findings using ambient concentrations by demonstrating an association between health outcomes and ambient (outdoor origin) particle exposures but not with nonambient (indoor origin) particle exposures.
Organic solvents are among the most common exposures in the workplace. Our objective was to elaborate the relationship between prenatal occupational solvent exposure and fetal growth as well as duration of pregnancy, and to quantify the impact of occupational organic solvent exposure.
We conducted a population-based study of 1670 singleton newborns of women who participated in The Finnish Prenatal Environment and Health Study after their delivery (response rate 94%) and who were working during pregnancy (65%). Exposure information was based on questions about exposure to solvents at work before and during pregnancy. The health outcomes, based on information from a questionnaire and the Finnish Medical Birth Registry, were low birth weight (
Despite the recent developments in physically and chemically based analysis of atmospheric particles, no models exist for resolving the spatial variability of pollen concentration at urban scale.
We developed a land use regression (LUR) approach for predicting spatial fine-scale allergenic pollen concentrations in the Helsinki metropolitan area, Finland, and evaluated the performance of the models against available empirical data.
We used grass pollen data monitored at 16 sites in an urban area during the peak pollen season and geospatial environmental data. The main statistical method was generalized linear model (GLM).
GLM-based LURs explained 79% of the spatial variation in the grass pollen data based on all samples, and 47% of the variation when samples from two sites with very high concentrations were excluded. In model evaluation, prediction errors ranged from 6% to 26% of the observed range of grass pollen concentrations. Our findings support the use of geospatial data-based statistical models to predict the spatial variation of allergenic grass pollen concentrations at intra-urban scales. A remote sensing-based vegetation index was the strongest predictor of pollen concentrations for exposure assessments at local scales.
The LUR approach provides new opportunities to estimate the relations between environmental determinants and allergenic pollen concentration in human-modified environments at fine spatial scales. This approach could potentially be applied to estimate retrospectively pollen concentrations to be used for long-term exposure assessments.
Hjort J, Hugg TT, Antikainen H, Rusanen J, Sofiev M, Kukkonen J, Jaakkola MS, Jaakkola JJ. 2016. Fine-scale exposure to allergenic pollen in the urban environment: evaluation of land use regression approach. Environ Health Perspect 124:619-626; http://dx.doi.org/10.1289/ehp.1509761.
Cites: Environ Sci Technol. 2013 Jul 16;47(14):7804-1123763440
Cites: Environ Health Perspect. 2013 Apr;121(4):494-50023322788
Cites: Sci Total Environ. 2014 Jul 1;485-486:435-4024742553
The built environment may influence health in part through the promotion of physical activity and exposure to pollution. To date, no studies have explored interactions between neighborhood walkability and air pollution exposure.
We estimated concentrations of nitric oxide (NO), a marker for direct vehicle emissions), and ozone (O(3)) and a neighborhood walkability score, for 49,702 (89% of total) postal codes in Vancouver, British Columbia, Canada. NO concentrations were estimated from a land-use regression model, O(3) was estimated from ambient monitoring data; walkability was calculated based on geographic attributes such as land-use mix, street connectivity, and residential density.
All three attributes exhibit an urban-rural gradient, with high walkability and NO concentrations, and low O(3) concentrations, near the city center. Lower-income areas tend to have higher NO concentrations and walkability and lower O(3) concentrations. Higher-income areas tend to have lower pollution (NO and O(3)). "Sweet-spot" neighborhoods (low pollution, high walkability) are generally located near but not at the city center and are almost exclusively higher income.
Increased concentration of activities in urban settings yields both health costs and benefits. Our research identifies neighborhoods that do especially well (and especially poorly) for walkability and air pollution exposure. Work is needed to ensure that the poor do not bear an undue burden of urban air pollution and that neighborhoods designed for walking, bicycling, or mass transit do not adversely affect resident's exposure to air pollution. Analyses presented here could be replicated in other cities and tracked over time to better understand interactions among neighborhood walkability, air pollution exposure, and income level.
Cites: JAMA. 2004 Mar 10;291(10):1238-4515010446
Cites: Lancet. 2002 Nov 2;360(9343):1347-6012423980
Cites: Am J Prev Med. 2004 Jul;27(1):67-7615212778
Cites: Am J Prev Med. 2004 Aug;27(2):87-9615261894
Cites: Environ Health Perspect. 2004 Aug;112(11):A600-115289172
Cites: Am J Respir Crit Care Med. 2004 Sep 1;170(5):520-615184208