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
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
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.
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 (
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
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.
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
Epidemiological studies of traffic-related air pollution typically estimate exposures at residential locations only; however, if study subjects spend time away from home, exposure measurement error, and therefore bias, may be introduced into epidemiological analyses. For two study areas (Vancouver, British Columbia, and Southern California), we use paired residence- and mobility-based estimates of individual exposure to ambient nitrogen dioxide, and apply error theory to calculate bias for scenarios when mobility is not considered. In Vancouver, the mean bias was 0.84 (range: 0.79-0.89; SD: 0.01), indicating potential bias of an effect estimate toward the null by ~16% when using residence-based exposure estimates. Bias was more strongly negative (mean: 0.70, range: 0.63-0.77, SD: 0.02) when the underlying pollution estimates had higher spatial variation (land-use regression versus monitor interpolation). In Southern California, bias was seen to become more strongly negative with increasing time and distance spent away from home (e.g., 0.99 for 0-2?h spent at least 10?km away, 0.66 for = 10?h spent at least 40?km away). Our results suggest that ignoring daily mobility patterns can contribute to bias toward the null hypothesis in epidemiological studies using individual-level exposure estimates.
Communities impacted by fine-particle air pollution (particles with an aerodynamic diameter less than 2.5 microm; PM(2.5)) from forest fires and residential wood burning require effective, evidence-based exposure-reduction strategies. Public health recommendations during smoke episodes typically include advising community members to remain indoors and the use of air cleaners, yet little information is available on the effectiveness of these measures. Our study attempted to address the following objectives: to measure indoor infiltration factor (F(inf)) of PM(2.5) from forest fires/wood smoke, to determine the effectiveness of high-efficiency particulate air (HEPA) filter air cleaners in reducing indoor PM(2.5), and to analyze the home determinants of F(inf) and air cleaner effectiveness (ACE). We collected indoor/outdoor 1-min PM(2.5) averages and 48-h outdoor PM(2.5) filter samples for 21 winter and 17 summer homes impacted by wood burning and forest fire smoke, respectively, during 2004-2005. A portable HEPA filter air cleaner was operated indoors with the filter removed for one of two sampling days. Particle F(inf) and ACE were calculated for each home using a recursive model. We found mean F(inf)+/-SD was 0.27+/-0.18 and 0.61+/-0.27 in winter (n=19) and summer (n=13), respectively, for days when HEPA filters were not used. Lower F(inf)+/-SD values of 0.10+/-0.08 and 0.19+/-0.20 were found on corresponding days when HEPA filters were in place. Mean+/-SD ACE ([F(inf) without filter-F(inf) with filter]/F(inf) without filter) in winter and summer were 55+/-38% and 65+/-35%, respectively. Number of windows and season predicted F(inf) (P
Land use regression (LUR) is a method for predicting the spatial distribution of traffic-related air pollution. To facilitate risk and exposure assessment, and the design of future monitoring networks and sampling campaigns, we sought to determine the extent to which LUR can be used to predict spatial patterns in air pollution in the absence of dedicated measurements. We evaluate the transferability of one LUR model to two other geographically comparable areas with similar climates and pollution types. The source model, developed in 2003 to estimate ambient nitrogen dioxide (NO(2)) concentrations in Vancouver (BC, Canada) was applied to Victoria (BC, Canada) and Seattle (WA, USA). Model estimates were compared with measurements made with Ogawa passive samplers in both cities. As part of this study, 42 locations were sampled in Victoria for a 2-week period in June 2006. Data obtained for Seattle were collected for a different project at 26 locations in March 2005. We used simple linear regression to evaluate the fit of the source model under three scenarios: (1) using the same variables and coefficients as the source model; (2) using the same variables as the source model, but calculating new coefficients for local calibration; and (3) developing site-specific equations with new variables and coefficients. In Scenario 1, we found that the source model had a better fit in Victoria (R(2)=0.51) than in Seattle (R(2)=0.33). Scenario 2 produced improved R(2)-values in both cities (Victoria=0.58, Seattle=0.65), with further improvement achieved under Scenario 3 (Victoria=0.61, Seattle=0.72). Although it is possible to transfer LUR models between geographically similar cities, success may depend on the between-city consistency of the input data. Modest field sampling campaigns for location-specific model calibration can help to produce transfer models that are equally as predictive as their sources.
There is accumulating evidence that air pollution causes lung cancer. Still, questions remain about exposure misclassification, the components of air pollution responsible, and the histological subtypes of lung cancer that might be produced.
We investigated lung cancer incidence in relation to long-term exposure to three ambient air pollutants and proximity to major roads, using a Canadian population-based case-control study. We compared 2,390 incident, histologically confirmed lung cancer cases with 3,507 population controls in eight Canadian provinces from 1994 to 1997. We developed spatiotemporal models for the whole country to estimate annual residential exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) over a 20-year exposure period. We carried out a subanalysis in urban centers, using exposures derived from fixed-site air pollution monitors, and also examined traffic proximity measures. Hierarchical logistic regression models incorporated a comprehensive set of individual and geographic covariates.
The increase in lung cancer incidence (expressed as fully adjusted odds ratios [ORs]) was 1.29 (95% confidence interval = 0.95-1.76) with a ten-unit increase in PM2.5 (µg/m), 1.11 (1.00-1.24) with a ten-unit increase in NO2 (ppb), and 1.09 (0.85-1.39) with a ten-unit increase in O3 (ppb). The urban monitor-based subanalyses generally supported the national results, with larger associations for NO2 (OR = 1.34; 1.07-1.69) per 10 ppb increase. No dose-response trends were observed, and no clear relationships were found for specific histological cancer subtypes. There was the suggestion of increased risk among those living within 100 m of highways, but not among those living near major roads.
Lung cancer incidence in this Canadian study was increased most strongly with NO2 and PM2.5 exposure. Further investigation is needed into possible effects of O3 on development of lung cancer.
Epidemiologic studies have shown that both air pollution and community noise are associated with cardiovascular disease mortality. Because road traffic is a major contributor to these environmental pollutants in metropolitan areas, it is plausible that the observed associations may be confounded by coexistent pollutants. As part of a large population-based cohort study to address this concern, we used a noise prediction model to assess annual average community noise levels from transportation sources in metropolitan Vancouver, Canada. The modeled annual average noise level was 64 (inter quartile range 60-68) dB(A) for the region. This model was evaluated by comparing modeled annual daytime A-weighted equivalent continuous noise levels (L(day)) with measured 5-min daytime A-weighted equivalent continuous noise levels (L(eq,day,5 min)) at 103 selected roadside sites in the study region. On average, L(day) was 6.2 (95% CI, 6.0-7.9) dB(A) higher than, but highly correlated (r=0.62; 95% CI, 0.48-0.72) with, L(eq,day,5 min). These results suggest that our model-based noise exposure assessment could approximately reflect actual noise exposure in the study region. Overall, modeled noise levels were not strongly correlated with land use regression estimates of traffic-related air pollutants including black carbon, particulate matter with aerodynamic diameter =2.5 µm (PM(2.5)), NO(2) and NO; the highest correlation was with black carbon (r=0.48), whereas the lowest correlation was with PM(2.5) (r=0.18). There was no consistent effect of traffic proximity on the correlations between community noise levels and traffic-related air pollutant concentrations. These results, consistent with previous studies, suggest that it is possible to assess potential adverse cardiovascular effects from long-term exposures to community noise and traffic-related air pollution in prospective epidemiologic studies.
Neighbourhood socioeconomic status (SES) has been associated with numerous chronic diseases, yet little information exists on its association with lung cancer incidence. This outcome presents two key empirical challenges: a long latency period that requires study participants' residential histories and long-term neighbourhood characteristics; and adequate data on many risk factors to test hypothesized mediating pathways between neighbourhood SES and lung cancer incidence. Analysing data on urban participants of a large Canadian population-based lung cancer case-control study, we investigate three issues pertaining to these challenges. First, we examine whether there is an association between long-term neighbourhood SES, derived from 20 years of residential histories and five national censuses, and lung cancer incidence. Second, we determine how this long-term neighbourhood SES association changes when using neighbourhood SES measures based on different latency periods or at time of study entry. Third, we estimate the extent to which long-term neighbourhood SES is mediated by a range of individual-level smoking behaviours, other health behaviours, and environmental and occupational exposures. Results of hierarchical logistic regression models indicate significantly higher odds of lung cancer cases residing in the most compared to the least deprived quintile of the long-term neighbourhood SES index (OR: 1.46; 95% CI: 1.13-1.89) after adjustment for individual SES. This association remained significant (OR: 1.38; 1.01-1.88) after adjusting for smoking behaviour and other known and suspected lung cancer risk factors. Important differences were observed between long-term and study entry neighbourhood SES measures, with the latter attenuating effect estimates by over 50 percent. Smoking behaviour was the strongest partial mediating pathway of the long-term neighbourhood SES effect. This research is the first to examine the effects of long-term neighbourhood SES on lung cancer risk and more research is needed to further identify specific, modifiable pathways by which neighbourhood context may influence lung cancer risk.
Exposure to traffic-related air pollution (TRAP) can adversely impact health but epidemiologic studies are limited in their abilities to assess long-term exposures and incorporate variability in indoor pollutant infiltration.
In order to examine settled house dust levels of hopanes, engine lubricating oil byproducts found in vehicle exhaust, as a novel TRAP exposure measure, dust samples were collected from 171 homes in five Canadian cities and analyzed by gas chromatography-mass spectrometry. To evaluate source contributions, the relative abundance of the highest concentration hopane monomer in house dust was compared to that in outdoor air. Geographic variables related to TRAP emissions and outdoor NO2 concentrations from city-specific TRAP land use regression (LUR) models were calculated at each georeferenced residence location and assessed as predictors of variability in dust hopanes.
Hopanes relative abundance in house dust and ambient air were significantly correlated (Pearson's r=0.48, p
Major forest fires near populated areas during 2003 exacted a huge economic toll on communities in British Columbia. We designed a study to examine associations between PM2.5 and PM10 levels and physician visits in two affected communities.
Measurements of 24-hour averages of particulate matter (PM10 and PM2.5) obtained from the monitoring network of the BC Ministry of Water, Land and Air Protection were used to define weeks where forest fires resulted in increases in ambient PM. Weekly rates of physician visits for respiratory (ICD-9 codes 460-519), cardiovascular (390-459) and mental illnesses (290-319) obtained through the Medical Services Plan of BC, were compared for 2003 and aggregates of the 10 previous years.
Both the Kelowna and Kamloops regions experienced five weeks of elevated 24-hour average PM levels, although maximum levels in Kelowna were greater. In the Kelowna region, increases in physician visits for respiratory diseases of between 46 and 78% above 10-year mean rates were observed for three weeks during the forest fire period. Similar effects were not observed in Kamloops. Effects on visits for cardiovascular diseases or mental disorders were not seen in either community.
Forest fire smoke was associated with an excess of respiratory complaints in Kelowna area residents. The lack of a similar effect in Kamloops is likely due to the population being exposed to lower levels of PM. The absence of apparent cardiovascular health effects may be due to selective effects of forest fire smoke on respiratory tract disease.
As epidemiological studies report associations between ambient air pollution and adverse birth outcomes, it is important to understand determinants of exposures among pregnant women. We measured (48-h, personal exposure) and modeled (using outdoor ambient monitors and a traffic-based land-use regression model) NO, NO(2), fine particle mass and absorbance in 62 non-smoking pregnant women in Vancouver, Canada on 1-3 occasions during pregnancy (total N=127). We developed predictive models for personal measurements using modeled ambient concentrations and individual determinants of exposure. Geometric mean exposures of personal samples were relatively low (GM (GSD) NO=37 ppb (2.0); NO(2)=17 ppb (1.6); 'soot', as filter absorbance=0.8 10(-5) m(-1) (1.5); PM(2.2)=10 microg m(-3) (1.6)). Having a gas stove (vs. electric stove) in the home was associated with exposure increases of 89% (NO), 44% (NO(2)), 20% (absorbance) and 35% (fine PM). Interpolated concentrations from outdoor fixed-site monitors were associated with all personal exposures except NO(2). Land-use regression model estimates of outdoor air pollution were associated with personal NO and NO(2) only. The effects of outdoor air pollution on personal samples were consistent, with and without adjustment for other individual determinants (e.g. gas stove). These findings improve our understanding of sources of exposure to air pollutants among pregnant women and support the use of outdoor concentration estimates as proxies for exposure in epidemiologic studies.