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Long-term exposure to ambient ultrafine particles and respiratory disease incidence in in Toronto, Canada: a cohort study.

ABSTRACT: Little is known about the long-term health effects of ambient ultrafine particles (<0.1 ?m) (UFPs) including their association with respiratory disease incidence. In this study, we examined the relationship between long-term exposure to ambient UFPs and the incidence of lung cancer, adult-onset asthma, and chronic obstructive pulmonary disease (COPD).Our study cohort included approximately 1.1 million adults who resided in Toronto, Canada and who were followed for disease incidence between 1996 and 2012. UFP exposures were assigned to residential locations using a land use regression model. Random-effect Cox proportional hazard models were used to estimate hazard ratios (HRs) describing the association between ambient UFPs and respiratory disease incidence adjusting for ambient fine particulate air pollution (PM2.5), NO2, and other individual/neighbourhood-level covariates.In total, 74,543 incident cases of COPD, 87,141 cases of asthma, and 12,908 cases of lung cancer were observed during follow-up period. In single pollutant models, each interquartile increase in ambient UFPs was associated with incident COPD (HR = 1.06, 95% CI: 1.05, 1.09) but not asthma (HR = 1.00, 95% CI: 1.00, 1.01) or lung cancer (HR = 1.00, 95% CI: 0.97, 1.03). Additional adjustment for NO2 attenuated the association between UFPs and COPD and the HR was no longer elevated (HR = 1.01, 95% CI: 0.98, 1.03). PM2.5 and NO2 were each associated with increased incidence of all three outcomes but risk estimates for lung cancer were sensitive to indirect adjustment for smoking and body mass index.In general, we did not observe clear evidence of positive associations between long-term exposure to ambient UFPs and respiratory disease incidence independent of other air pollutants. Further replication is required as few studies have evaluated these relationships.

SUBMITTER: Weichenthal S

PROVIDER: S-EPMC5477122 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature

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Long-term exposure to ambient ultrafine particles and respiratory disease incidence in in Toronto, Canada: a cohort study.

Weichenthal Scott S Bai Li L Hatzopoulou Marianne M Van Ryswyk Keith K Kwong Jeffrey C JC Jerrett Michael M van Donkelaar Aaron A Martin Randall V RV Burnett Richard T RT Lu Hong H Chen Hong H

Environmental health : a global access science source 20170619 1

<h4>Background</h4>Little is known about the long-term health effects of ambient ultrafine particles (<0.1 μm) (UFPs) including their association with respiratory disease incidence. In this study, we examined the relationship between long-term exposure to ambient UFPs and the incidence of lung cancer, adult-onset asthma, and chronic obstructive pulmonary disease (COPD).<h4>Methods</h4>Our study cohort included approximately 1.1 million adults who resided in Toronto, Canada and who were followed ...[more]

PMID: 28629362

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Project description:BackgroundThere is growing evidence that exposure to ultrafine particles (UFP; particles smaller than [Formula: see text]) may play an underexplored role in the etiology of several illnesses, including cardiovascular disease (CVD).ObjectivesWe aimed o investigate the relationship between long-term exposure to ambient UFP and incident cardiovascular and cerebrovascular disease (CVA). As a secondary objective, we sought to compare effect estimates for UFP with those derived for other air pollutants, including estimates from two-pollutant models.MethodsUsing a prospective cohort of 33,831 Dutch residents, we studied the association between long-term exposure to UFP (predicted via land use regression) and incident disease using Cox proportional hazard models. Hazard ratios (HR) for UFP were compared to HRs for more routinely monitored air pollutants, including particulate matter with aerodynamic diameter [Formula: see text] ([Formula: see text]), PM with aerodynamic diameter [Formula: see text] ([Formula: see text]), and [Formula: see text].ResultsLong-term UFP exposure was associated with an increased risk for all incident CVD [[Formula: see text] per [Formula: see text]; 95% confidence interval (CI): 1.03, 1.34], myocardial infarction (MI) ([Formula: see text]; 95% CI: 1.00, 1.79), and heart failure ([Formula: see text]; 95% CI: 1.17, 2.66). Positive associations were also estimated for [Formula: see text] ([Formula: see text]; 95% CI: 1.01, 1.48 per [Formula: see text]) and coarse PM ([Formula: see text]; HR for all [Formula: see text]; 95% CI: 1.01, 1.45 per [Formula: see text]). CVD was not positively associated with [Formula: see text] (HR for all [Formula: see text]; 95% CI: 0.75, 1.28 per [Formula: see text]). HRs for UFP and CVAs were positive, but not significant. In two-pollutant models ([Formula: see text] and [Formula: see text]), positive associations tended to remain for UFP, while HRs for [Formula: see text] and [Formula: see text] generally attenuated towards the null.ConclusionsThese findings strengthen the evidence that UFP exposure plays an important role in cardiovascular health and that risks of ambient air pollution may have been underestimated based on conventional air pollution metrics. https://doi.org/10.1289/EHP3047.

Project description:Particulate matter and volatile organic compounds, including total hydrocarbons (THCs), are major ambient air pollutants. Primary nonmethane hydrocarbons (NMHCs) originate from vehicle emissions. The association between air pollution and urinary bladder cancer (UBC) is debatable. We investigated whether long-term exposure to ambient hydrocarbons increases UBC risk among people aged ≥ 20 years in Taiwan. Linkage dataset research with longitudinal design was conducted among 589,135 initially cancer-free individuals during 2000-2013; 12 airborne pollutants were identified. Several Cox models considering potential confounders were employed. The study outcomes were invasive or in situ UBC incidence over time. The targeted pollutant concentration was divided into three tertiles: T1/T2/T3. The mean age of individuals at risk was 42.5 (SD 15.7), and 50.5% of the individuals were men. The mean daily average over 10 years of airborne THC concentration was 2.25 ppm (SD 0.13), and NMHC was 0.29 ppm (SD 0.09). Both pollutants show long-term monotonic downward trend over time using the Mann-Kendall test. There was a dose-dependent increase in UBC at follow-up. UBC incidence per 100,000 enrollees according to T1/T2/T3 exposure to THC was 60.9, 221.2, and 651.8, respectively; it was 170.0/349.5/426.7 per 100,000 enrollees, corresponding to T1/T2/T3 exposure to NMHC, respectively. Without controlling for confounding air pollutants, the adjusted hazard ratio (adj.HR) was 1.83 (95% CI 1.75-1.91) per 0.13-ppm increase in THC; after controlling for PM2.5, adj.HR was even higher at 2.09 (95% CI 1.99-2.19). The adj.HR was 1.37 (95% CI 1.32-1.43) per 0.09-ppm increase in ambient NMHC concentration. After controlling for SO2 and CH4, the adj.HR was 1.10 (95% CI 1.06-1.15). Sensitivity analyses showed that UBC development risk was not sex-specific or influenced by diabetes status. Long-term exposure to THC and NMHC may be a risk factor for UBC development. Acknowledging pollutant sources can inform risk management strategies.

Project description:BACKGROUND:Long-term exposure to fine particulate matter has been linked to cardiovascular disease and systemic inflammatory responses; however, evidence is limited regarding the effects of long-term exposure to ultrafine particulate matter (UFP, <100nm). We used a cross-sectional study design to examine the association of long-term exposure to near-highway UFP with measures of systemic inflammation and coagulation. METHODS:We analyzed blood samples from 408 individuals aged 40-91years living in three near-highway and three urban background areas in and near Boston, Massachusetts. We conducted mobile monitoring of particle number concentration (PNC) in each area, and used the data to develop and validate highly resolved spatiotemporal (hourly, 20m) PNC regression models. These models were linked with participant time-activity data to determine individual time-activity adjusted (TAA) annual average PNC exposures. Multivariable regression modeling and stratification were used to assess the association between TAA-PNC and single peripheral blood measures of high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), tumor-necrosis factor alpha receptor II (TNFRII) and fibrinogen. RESULTS:After adjusting for age, sex, education, body mass index, smoking and race/ethnicity, an interquartile-range (10,000particles/cm(3)) increase in TAA-PNC had a positive non-significant association with a 14.0% (95% CI: -4.6%, 36.2%) positive difference in hsCRP, an 8.9% (95% CI: -0.4%, 10.9%) positive difference in IL-6, and a 5.1% (95% CI: -0.4%, 10.9%) positive difference in TNFRII. Stratification by race/ethnicity revealed that TAA-PNC had larger effect estimates for all three inflammatory markers and was significantly associated with hsCRP and TNFRII in white non-Hispanic, but not East Asian participants. Fibrinogen had a negative non-significant association with TAA-PNC. CONCLUSIONS:Our findings suggest an association between annual average near-highway TAA-PNC and subclinical inflammatory markers of CVD risk.

Project description:ImportanceFew studies have investigated the association of long-term ambient ozone exposures with respiratory morbidity among individuals with a heavy smoking history.ObjectiveTo investigate the association of historical ozone exposure with risk of chronic obstructive pulmonary disease (COPD), computed tomography (CT) scan measures of respiratory disease, patient-reported outcomes, disease severity, and exacerbations in smokers with or at risk for COPD.Design, setting, and participantsThis multicenter cross-sectional study, conducted from November 1, 2010, to July 31, 2018, obtained data from the Air Pollution Study, an ancillary study of SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study). Data analyzed were from participants enrolled at 7 (New York City, New York; Baltimore, Maryland; Los Angeles, California; Ann Arbor, Michigan; San Francisco, California; Salt Lake City, Utah; and Winston-Salem, North Carolina) of the 12 SPIROMICS clinical sites. Included participants had historical ozone exposure data (n = 1874), were either current or former smokers (≥20 pack-years), were with or without COPD, and were aged 40 to 80 years at baseline. Healthy persons with a smoking history of 1 or more pack-years were excluded from the present analysis.ExposuresThe 10-year mean historical ambient ozone concentration at participants' residences estimated by cohort-specific spatiotemporal modeling.Main outcomes and measuresSpirometry-confirmed COPD, chronic bronchitis diagnosis, CT scan measures (emphysema, air trapping, and airway wall thickness), 6-minute walk test, modified Medical Research Council (mMRC) Dyspnea Scale, COPD Assessment Test (CAT), St. George's Respiratory Questionnaire (SGRQ), postbronchodilator forced expiratory volume in the first second of expiration (FEV1) % predicted, and self-report of exacerbations in the 12 months before SPIROMICS enrollment, adjusted for demographics, smoking, and job exposure.ResultsA total of 1874 SPIROMICS participants were analyzed (mean [SD] age, 64.5 [8.8] years; 1479 [78.9%] white; and 1013 [54.1%] male). In adjusted analysis, a 5-ppb (parts per billion) increase in ozone concentration was associated with a greater percentage of emphysema (β = 0.94; 95% CI, 0.25-1.64; P = .007) and percentage of air trapping (β = 1.60; 95% CI, 0.16-3.04; P = .03); worse scores for the mMRC Dyspnea Scale (β = 0.10; 95% CI, 0.03-0.17; P = .008), CAT (β = 0.65; 95% CI, 0.05-1.26; P = .04), and SGRQ (β = 1.47; 95% CI, 0.01-2.93; P = .048); lower FEV1% predicted value (β = -2.50; 95% CI, -4.42 to -0.59; P = .01); and higher odds of any exacerbation (odds ratio [OR], 1.37; 95% CI, 1.12-1.66; P = .002) and severe exacerbation (OR, 1.37; 95% CI, 1.07-1.76; P = .01). No association was found between historical ozone exposure and chronic bronchitis, COPD, airway wall thickness, or 6-minute walk test result.Conclusions and relevanceThis study found that long-term historical ozone exposure was associated with reduced lung function, greater emphysema and air trapping on CT scan, worse patient-reported outcomes, and increased respiratory exacerbations for individuals with a history of heavy smoking. The association between ozone exposure and adverse respiratory outcomes suggests the need for continued reevaluation of ambient pollution standards that are designed to protect the most vulnerable members of the US population.

Project description:BACKGROUND:Few longitudinal studies have examined the association between ultrafine particulate matter (UFP, particles <?0.1 ?m aerodynamic diameter) exposure and cardiovascular disease (CVD) risk factors. We used data from 791 adults participating in the longitudinal Boston Puerto Rican Health Study (Massachusetts, USA) between 2004 and 2015 to assess whether UFP exposure was associated with blood pressure and high sensitivity C-reactive protein (hsCRP, a biomarker of systemic inflammation). METHODS:Residential annual average UFP exposure (measured as particle number concentration, PNC) was assigned using a model accounting for spatial and temporal trends. We also adjusted PNC values for participants' inhalation rate to obtain the particle inhalation rate (PIR) as a secondary exposure measure. Multilevel linear models with a random intercept for each participant were used to examine the association of UFP with blood pressure and hsCRP. RESULTS:Overall, in adjusted models, an inter-quartile range increase in PNC was associated with increased hsCRP (??=?6.8; 95% CI?=?-?0.3, 14.0%) but not with increased systolic blood pressure (??=?0.96; 95% CI?=?-?0.33, 2.25 mmHg), pulse pressure (??=?0.70; 95% CI?=?-?0.27, 1.67 mmHg), or diastolic blood pressure (??=?0.55; 95% CI?=?-?0.20, 1.30 mmHg). There were generally stronger positive associations among women and never smokers. Among men, there were inverse associations of PNC with systolic blood pressure and pulse pressure. In contrast to the primary findings, an inter-quartile range increase in the PIR was positively associated with systolic blood pressure (??=?1.03; 95% CI?=?0.00, 2.06 mmHg) and diastolic blood pressure (??=?1.01; 95% CI?=?0.36, 1.66 mmHg), but not with pulse pressure or hsCRP. CONCLUSIONS:We observed that exposure to PNC was associated with increases in measures of CVD risk markers, especially among certain sub-populations. The exploratory PIR exposure metric should be further developed.

Dataset Information

Long-term exposure to ambient ultrafine particles and respiratory disease incidence in in Toronto, Canada: a cohort study.

Publications

Long-term exposure to ambient ultrafine particles and respiratory disease incidence in in Toronto, Canada: a cohort study.

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