Source-specific Particulate Matter Research Articles

Exposure to source-specific air pollution in residential areas and its association with dementia incidence: a cohort study in Northern Sweden

The aim of this study was to investigate the relationship between source-specific ambient particulate air pollution concentrations and the incidence of dementia. The study encompassed 70,057 participants from the Västerbotten intervention program cohort in Northern Sweden with a median age of 40 years at baseline. High-resolution dispersion models were employed to estimate source-specific particulate matter (PM) concentrations, such as PM10 and PM2.5 from traffic, exhaust, and biomass (mainly wood) burning, at the residential addresses of each participant. Cox regression models, adjusted for potential confounding factors, were used for the assessment. Over 884,847 person-years of follow-up, 409 incident dementia cases, identified through national registers, were observed. The study population’s average exposure to annual mean total PM10 and PM2.5 lag 1–5 years was 9.50 µg/m3 and 5.61 µg/m3, respectively. Increased risks were identified for PM10-Traffic (35% [95% CI 0–82%]) and PM2.5-Exhaust (33% [95% CI − 2 to 79%]) in the second exposure tertile for lag 1–5 years, although no such risks were observed in the third tertile. Interestingly, a negative association was observed between PM2.5-Wood burning and the risk of dementia. In summary, this register-based study did not conclusively establish a strong association between air pollution exposure and the incidence of dementia. While some evidence indicated elevated risks for PM10-Traffic and PM2.5-Exhaust, and conversely, a negative association for PM2.5-Wood burning, no clear exposure–response relationships were evident.

Achieving health-oriented air pollution control requires integrating unequal toxicities of industrial particles

Protecting human health from fine particulate matter (PM) pollution is the ambitious goal of clean air actions, but current control strategies largely ignore the role of source-specific PM toxicity. Here, we proposed health-oriented control strategies by integrating the unequal toxic potencies of the most polluting industrial PMs. Iron and steel industry (ISI)-emitted PM2.5 exhibit about one order of magnitude higher toxic potency than those of cement and power industries. Compared with the current mass-based control strategy (prioritizing implementation of ultralow emission standards in the power sector), the proposed health-oriented control strategy (priority control of the ISI sector) could generate 5.4 times higher reduction in population-weighted toxic potency-adjusted PM2.5 exposure among polluting industries in China. Furthermore, the marginal abatement cost per unit of toxic potency-adjusted mass of ISI-emitted PM2.5 is only a quarter of that of the other two sectors under ultralow emission scenarios. We highlight that a health-oriented air pollution control strategy is urgently required to achieve cost-effective reductions in particulate exposure risks.

Long-term residential exposure to source-specific particulate matter and incidence of diabetes mellitus — A cohort study in northern Sweden

Diabetes mellitus (DM) incidence have been assessed in connection with air pollution exposure in several studies; however, few have investigated associations with source-specific local emissions. This study aims to estimate the risk of DM incidence associated with source-specific air pollution in a Swedish cohort with relatively low exposure. Individuals in the Västerbotten intervention programme cohort were followed until either a DM diagnosis or initiation of treatment with glucose-lowering medication occurred. Dispersion models with high spatial resolution were used to estimate annual mean concentrations of particulate matter (PM) with aerodynamic diameter ≤10 μm (PM10) and ≤2.5 μm (PM2.5) at individual addresses. Hazard ratios were estimated using Cox regression models in relation to moving averages 1–5 years preceding the outcome. During the study period, 1479 incident cases of DM were observed during 261,703 person-years of follow-up. Increased incidence of DM was observed in association with PM10 (4% [95% CI: -54–137%] per 10 μg/m3), PM10-traffic (2% [95% CI: -6–11%] per 1 μg/m3) and PM2.5-exhaust (11% [95% CI: -39–103%] per 1 μg/m3). A negative association was found for both PM2.5 (-18% [95% CI: -99–66%] per 5 μg/m3), but only in the 2nd exposure tertile (-10% [95% CI: -25–9%] compared to the first tertile), and PM2.5-woodburning (-30% [95% CI: -49–4%] per 1 μg/m3). In two-pollutant models including PM2.5-woodburning, there was an 11% [95% CI: -11–38%], 6% [95% CI: -16–34%], 13% [95% CI: -7–36%] and 17% [95% CI: 4–41%] higher risk in the 3rd tertile of PM10, PM2.5, PM10-traffic and PM2.5-exhaust, respectively, compared to the 1st. Although the results lacked in precision they are generally in line with the current evidence detailing particulate matter air pollution from traffic as an environmental risk factor for DM.

Short-term effects of exposure to particulate matter concentrations originating from desert dust on mortality in Athens, Greece

Background & Aim: Evidence on the independent associations of source-specific particulate matter (PM) exposures with health outcomes is limited. Our aim was to investigate the effects of short-term exposure to PM≤ 10μm (PM10) concentrations originating from windblown desert dust and local sources on mortality. Methods: We investigated the effect of exposure to total PM10 concentrations, as well as estimated concentrations originating from desert dust and other sources on total mortality, between the years 2010-2019. We used Poisson regression models to estimate the association between PM10 from different sources, also controlling for possible confounding by season, meteorology, day of the week and holiday effect. Results: During the 10-year study period, 35% of days were affected by desert dust (desert dust PM10> 0μg/m3). An increment of 10μg/m3 in total PM10 concentrations was associated with a 0.52% (lag 0–1, 95% confidence interval (CI): 0.21, 0.83%) increase in natural mortality. When mutually adjusting non-desert and desert dust PM10 concentrations, a 10μg/m3 increase in non-desert was associated with a 0.45% (95% CI: 0.07% to 0.84%) increase in natural mortality. On the other hand, the effect of desert PM10 (lag 0-1 days) concentrations was non-significant (0.59%; 95% CI: -0.53% to 1.72%). Conclusions: Our findings support the hypothesis that daily exposure to traffic-related particles have more toxic effects, compared to ones originating from windblown desert dust, in Athens, Greece leading to increased mortality.

Long-term exposure to source-specific particulate air pollution and mortality

BACKGROUND AND AIM: Many studies have shown associations between particulate matter (PM) air pollution and total and cardiopulmonary morbidity and mortality. However, air pollution is a heterogeneous mixture from various sources, and it is less clear which types and sources that are the most harmful. We analyzed associations between long-term exposure to source-specific PM and total and cardiovascular mortality in population-based cohorts in three Swedish cities. METHODS: Using high-resolution dispersion models of PM from different sources and address registries we assigned annual individual residential mean concentrations to participants in four cohorts in Gothenburg, Stockholm and Umeå for the years 1990-2011. Cause-specific mortality was assigned from death registries. Effects of the last five years of exposure on total natural and cardiovascular mortality was estimated using Cox regression models adjusted for possible confounders, and meta-analyzed including a random effect of cohort. RESULTS:A total number of 7340 natural cause deaths and 2755 cardiovascular cause-specific deaths were observed among 68,679 participants during the study period. For total mortality there were positive associations with road traffic exhaust particles (HR 1.12, 95% CI 1.03-1.21) per 1 µg/m3), and road wear particles (HR 1.02, 95% C 1.01-1.04, per 1 µg/m3), but not with particles from residential heating. Adjustment for road traffic noise, or particles from residential heating, did not substantially affect the results for traffic-related PM. For cardiovascular mortality, there were positive but not statistically significant associations for PM from road traffic, residential heating, or other sources. CONCLUSIONS:Mortality was associated with traffic-related PM, but less with air pollution from residential heating and other sources, in a multi-cohort study at low exposure-levels. KEYWORDS: particulate matter, traffic-related, mixtures, long-term exposures, noise

Air Pollution and Polyclonal Elevation of Serum Free Light Chains: An Assessment of Adaptive Immune Responses in the Prospective Heinz Nixdorf Recall Study

Background:Residential exposure to air pollution (AP) has been shown to activate the immune system (IS). Although innate immune responses to AP have been studied extensively, investigations on the adaptive IS are scarce.Objectives:The aim of this study was to investigate the association between short- to long-term AP exposure and polyclonal free light chains (FLC) produced by plasma cells.Methods:We used repeated data from three examinations (: 2000–2003; : 2006–2008; and : 2011–2015) of the population-based German Heinz Nixdorf Recall cohort of initially 4,814 participants (45–75 y old). Residential exposure to total and source-specific particulate matter (PM) with an aerodynamic diameter of 10 or ( and respectively), nitrogen dioxide (), and particle number concentrations (accumulation mode; ) was estimated using a chemistry transport model with different time windows (1- to 365-d mean ± standard deviation) before blood draw. We applied linear mixed models with a random participant intercept to estimate associations between total, traffic- and industry-related AP exposures and log-transformed FLC, controlling for examination time, sociodemographic and lifestyle variables, estimated glomerular filtration rate and season.Results:Analyzing 9,933 observations from 4,455 participants, we observed generally positive associations between AP exposures and FLC. We observed strongest associations with middle-term exposures, e.g., 3.0% increase in FLC (95% confidence interval: 1.8%, 4.3%) per interquartile range increase in 91-d mean of (). Across the different pollutants, showed strongest associations with FLC, followed by and . Effect estimates for traffic-related exposures were mostly higher compared with total exposures. Although and estimates remained stable upon adjustment for PM, PM estimates decreased considerably upon adjustment for and .Discussion:Our results suggest that middle-term AP exposures in particular might be positively associated with activation of the adaptive IS. Traffic-related PM, , and showed strongest associations. https://doi.org/10.1289/EHP7164

Morphological and elemental characterization of leaf-deposited particulate matter from different source types: a microscopic investigation.

Particulate matter (PM) deposition on urban green enables the collection of particulate pollution from a diversity of contexts, and insight into the physico-chemical profiles of PM is key for identifying main polluting sources. This study reports on the morphological and elemental characterization of PM2-10 deposited on ivy leaves from five different environments (forest, rural, roadside, train, industry) in the region of Antwerp, Belgium. Ca. 40,000 leaf-deposited particles were thoroughly investigated by particle-based analysis using scanning electron microscopy coupled with energy-dispersive X-ray spectroscopy (SEM/EDX) and their physico-chemical characteristics were explored for PM source apportionment purposes. The size distribution of all deposited particles was biased towards small-sized PM, with 32% of the particles smaller than 2.5μm (PM2.5) and median diameters of 2.80-3.09μm. The source type influenced both the particles' size and morphology (aspect ratio and shape), with roadside particles being overall the smallest in size and the most spherical. While forest and rural elemental profiles were associated with natural PM, the industry particles revealed the highest anthropogenic metal input. PM2-10 profiles for roadside and train sites were rather comparable and only distinguishable when evaluating the fine (2-2.5μm) and coarse (2.5-10μm) PM fractions separately, which enabled the identification of a larger contribution of combustion-derived particles (small, circular, Fe-enriched) at the roadside compared to the train. Random forest prediction model classified the source type correctly for 61-85% of the leaf-deposited PM. The still modest classification accuracy denotes the influence of regional background PM and demands for additional fingerprinting techniques to facilitate source apportionment. Nonetheless, the obtained results demonstrate the utility of leaf particle-based analysis to fingerprint and pinpoint source-specific PM, particularly when considering both the composition and size of leaf-deposited particles.

Ambient PM Toxicity Is Correlated with Expression Levels of Specific MicroRNAs.

Uncertainties regarding optimized air pollution control remain as the underlying mechanisms of city-specific ambient particulate matter (PM)-induced health effects are unknown. Here, water-soluble extracts of PMs collected from four global cities via automobile air-conditioning filters were consecutively injected three times by an amount of 1, 2, and 2 mg into the blood circulation of Wistar rats after filtration by a 0.45 μm pore size membrane. Acute health effects, such as immune and inflammatory responses and hemorrhage in alveoli, were observed right after the PM extraction injection. Significant differences between cities in biomarker tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1) levels were detected following the second and third PM injections. Rats' inflammatory responses varied substantially with the injections of city-specific PMs. Repeated PM extract exposure rendered the rats more vulnerable to subsequent challenges, and downregulation of certain microRNAs was observed in rats. Among the studied miRNAs, miR-125b, and miR-21 were most sensitive to the PM exposure, exhibiting a negative dose-response-type relationship with a source-specific PM (oxidative potential) toxicity (r2 = 0.63 and 0.57; p-values < 0.05). The results indicated that city-specific PMs could induce different health effects by selectively regulating different miRNAs, and that certain microRNAs, e.g., miR-125b and miR-21, may be externally mediated to neutralize PM-related health damages.

Long-term exposure to ambient source-specific particulate matter and its components and incidence of cardiovascular events – The Heinz Nixdorf Recall study

BackgroundFew studies have examined the risk of long-term exposure to source-specific airborne pollutants on incidence of cerebrovascular and cardiovascular events. ObjectivesWe aimed to estimate the effect of long-term exposure to source-specific air pollution and particulate matter (PM) components on incidence of stroke, coronary heart disease (CHD), and total cardiovascular events (CVE) in the population-based Heinz Nixdorf Recall study (HNR). MethodsWe used baseline (2000–2003) and 14-year follow-up data of the HNR Study, an ongoing population-based prospective cohort study in Western Germany. Participants’ residential mean exposures to NO2 and total and source-specific PM10, PM2.5, accumulation mode particle number concentration (PNAM), and PM components were modelled using a dispersion and chemical transport model. We used Cox regression to evaluate the effect of pollutants (per 1 μg/m3 increase and per interquartile range – IQR) on risk of stroke and CHD, adjusting for socio-demographic characteristics, lifestyle risk factors and nighttime traffic noise exposure. ResultsIn 4,105 included participants (aged 45–76 at baseline, 52.5% women), we observed 118 cases of first stroke and 373 cases of first CHD during 46,748 person-years under risk. The median survival time within the cohort was 13.3 years. No effect of exposure to ambient air pollution on risk of CHD was observed, but distinct effects were observed for stroke. Ambient traffic-specific PM showed a stronger effect on stroke than industry-specific PM: hazard ratios (95% confidence interval) for total, traffic-specific, and industry-specific PM2.5 were 1.16 (1.02–1.34), 2.53 (1.07–5.97), and 1.27 (1.03–1.56) per 1 μg/m3 increase, respectively. PM components showed no substantially different effects from those of total PM per IQR, but higher associations were observed for NH4 and SO4 per 1 μg/m3. However, the exposure contrast of ammonium and sulfate components was very low. ConclusionTraffic-specific PM exhibited stronger effects than total and industry-specific PM on risk of stroke. Among components, NH4 and SO4 showed higher effects. No effect was observed for PM and CHD.

Prenatal, Early-Life, and Childhood Exposure to Air Pollution and Lung Function: The ALSPAC Cohort.

Rationale: Exposure to air pollution during intrauterine development and through childhood may have lasting effects on respiratory health.Objectives: To investigate lung function at ages 8 and 15 years in relation to air pollution exposures during pregnancy, infancy, and childhood in a UK population-based birth cohort.Methods: Individual exposures to source-specific particulate matter ≤10 μm in aerodynamic diameter (PM10) during each trimester, 0-6 months, 7-12 months (1990-1993), and up to age 15 years (1991-2008) were examined in relation to FEV1% predicted and FVC% predicted at ages 8 (n = 5,276) and 15 (n = 3,446) years using linear regression models adjusted for potential confounders. A profile regression model was used to identify sensitive time periods.Measurements and Main Results: We did not find clear evidence of a sensitive exposure period for PM10 from road traffic. At age 8 years, 1 μg/m3 higher exposure during the first trimester was associated with lower FEV1% predicted (-0.826; 95% confidence interval [CI], -1.357 to -0.296) and FVC% predicted (-0.817; 95% CI, -1.357 to -0.276), but similar associations were seen for exposures for other trimesters, 0-6 months, 7-12 months, and 0-7 years. Associations were stronger among boys, as well as children whose mother had a lower education level or smoked during pregnancy. For PM10 from all sources, the third trimester was associated with lower FVC% predicted (-1.312; 95% CI, -2.100 to -0.525). At age 15 years, no adverse associations with lung function were seen.Conclusions: Exposure to road-traffic PM10 during pregnancy may result in small but significant reductions in lung function at age 8 years.

Associations between Source-Specific Particulate Matter and Respiratory Infections in New York State Adults.

The response of respiratory infections to source-specific particulate matter (PM) is an area of active research. Using source-specific PM2.5 concentrations at six urban sites in New York State, a case-crossover design, and conditional logistic regression, we examined the association between source-specific PM and the rate of hospitalizations and emergency department (ED) visits for influenza or culture-negative pneumonia from 2005 to 2016. There were at most N = 14 764 influenza hospitalizations, N = 57 522 influenza ED visits, N = 274 226 culture-negative pneumonia hospitalizations, and N = 113 997 culture-negative pneumonia ED visits included in our analyses. We separately estimated the rate of respiratory infection associated with increased concentrations of source-specific PM2.5, including secondary sulfate (SS), secondary nitrate (SN), biomass burning (BB), pyrolyzed organic carbon (OP), road dust (RD), residual oil (RO), diesel (DIE), and spark ignition vehicle emissions (GAS). Increased rates of ED visits for influenza were associated with interquartile range increases in concentrations of GAS (excess rate [ER] = 9.2%; 95% CI: 4.3%, 14.3%) and DIE (ER = 3.9%; 95% CI: 1.1%, 6.8%) for lag days 0–3. There were similar associations between BB, SS, OP, and RO, and ED visits or hospitalizations for influenza, but not culture-negative pneumonia hospitalizations or ED visits. Short-term increases in PM2.5 from traffic and other combustion sources appear to be a potential risk factor for increased rates of influenza hospitalizations and ED visits.

Long-term exposure to air pollution components (total and source-specific) and incidence of stroke and cardiac events in the Heinz Nixdorf Recall study

OPS 06: Health effects of source-specific outdoor air pollution, Room 117, Floor 1, August 27, 2019, 10:30 AM - 12:00 PM Background/Aim: Epidemiological studies have established that air pollution (AP) exposure adversely affects cardiovascular health. However, there has been little research on the effects of source-specific (industry and traffic) AP and individual components of particulate pollution. We therefore investigated the association between long-term exposure to components of total and source-specific AP and incidence of stroke and cardiac events (CE). Methods: We used data from the Heinz Nixdorf Recall cohort study (N = 4,814, aged 45–75). We estimated long-term residential AP exposures over the baseline period (2001-2003) using the European Air Pollution Dispersion chemical transport model (EURAD). Exposure was modelled for total NO2, total and source-specific particulate matter (PM) PM10, PM2.5, accumulation mode particle number concentration (PNAM), and PM components (anthropogenic organic compounds, black carbon, elemental carbon, NH4, NO3, SO4). Outcomes were defined as time to first stroke or CE during follow-up (until 2017). We applied Cox proportional hazards model to estimate hazard ratios (HR) per interquartile range increase in exposure to each pollutant/component, controlling for baseline sex, age, socio-economic status, body mass index, smoking, alcohol consumption, physical activity, nutrition, and traffic noise. In the analyzed population without stroke or CE prior to baseline (N = 4,224), a total of 120 strokes and 200 CE were observed during the study period (mean follow-up 12 years). Results: We observed positive associations between AP exposure and incidence of stroke, e.g. for industry-specific PM10 (HR: 1.34, 95% CI: 1.01, 1.78 per 2.22 µg/m3), industry-specific PNAM (HR: 1.28 [1.00, 1.64] per 208 particles/mL), and traffic-specific PNAM (HR: 1.30 [1.01, 1.68] per 138 particles/mL). Point estimates for CE were less consistently elevated. Adjustment for traffic noise did not change the results substantially. Conclusions: Our results support a positive association of long-term residential exposure to source-specific AP and PM components with incidence of stroke.

Is air pollution associated with adaptive immune responses, measured by polyclonal elevation of serum free light chains?-Results from the prospective Heinz Nixdorf Recall Study

OPS 52: Air pollution and respiratory health, Room 110, Floor 1, August 28, 2019, 10:30 AM - 12:00 PM Background/Aim: Residential exposure to particulate matter (PM2.5 and PM10) air pollution (AP) has been shown to activate the immune system (IS). While innate immune responses to AP have been studied extensively, investigations on the adaptive IS are scarce. Objective: To investigate the association between short- to long-term AP exposure and polyclonal free light chains (FLC: κ+λ) produced by plasma cells. Methods: We used repeated data from three examinations (t0: 2000-2003, t1: 2006-2008, t2: 2011-2015) of the Heinz Nixdorf Recall study, a population-based German cohort of initially 4,814 participants (45-75 years). Residential exposure to total and source-specific particulate matter, nitrogen dioxide (NO2) and particle number concentrations (accumulation mode) was estimated using a chemistry transport model with different time windows (28-, 91-, 182-, 270- and 365-day means) before blood draw. We applied linear mixed models with a random participant intercept to estimate associations between air pollution (AP) exposures and log-transformed FLC, controlling for year of enrollment, age, sex, socioeconomic status, lifestyle variables, estimated glomerular filtration rate (eGFR) and season. Results: Analyzing 10,017 observations from 4,207 participants, we mostly observed positive associations between AP exposures and FLC. The strongest associations were observed with 91-day exposures, e.g. 2.9% increase in FLC (95%-Confidence Interval [CI]: 1.6%; 4.1%) per interqurartile range increase in NO2 (14.1 µg/m3). While most AP exposures also showed significant positive effect estimates with an exposure window of 182 days, weaker associations were observed for the other time windows. Across the different pollutants, PM10 and NO2 showed the strongest associations with FLC. Conclusions: Our results suggest that in particular 91-and 182-day mean AP exposures might be positively associated with activation of the adaptive IS.

Inhalation cancer risk estimation of source-specific personal exposure for particulate matter-bound polycyclic aromatic hydrocarbons based on positive matrix factorization.

In previous studies, inhalation cancer risk was estimated using conventional risk assessment method, which was normally based on compound-specific analysis, and cannot provide substantial data for source-specific particulate matter concentrations and pollution control. In the present study, we applied an integrated risk analysis method, which was a synthetic combination of source apportionment receptor model and risk assessment method, to estimate cancer risks associated to individual PAHs coming from specific sources. Personal exposure particulate matter samples referring to an elderly panel were collected in a community of Tianjin, Northern China, in 2009, and 12 PAH compounds were measured using GC-MS. Positive matrix factorization (PMF) was used to extract the potential sources and quantify the source contributions to the PAH mixture. Then, the lung cancer risk of each modeled source was estimated by summing up the cancer risks of all measured PAH species according to the extracted source profile. The final results indicated that the overall cancer risk was 1.12 × 10-5, with the largest contribution from gasoline vehicle emission (44.1%). Unlike other risk estimation studies, this study was successful in combining risk analysis and source apportionment approaches, which allow estimating the potential risk of all source types and provided suitable information to select prior control strategies and mitigate the main air pollution sources that contributing to health risks.

High level of source-specific particulate matter air pollution associated with cardiac arrhythmias

Epidemiological evidence linking source-specific ambient particulate matter with aerodynamic diameter <2.5 μm (PM2.5) and cardiac arrhythmias is limited. In this study, we investigated the impact of source-specific PM2.5 on cardiac arrhythmias in a panel of forty-five healthy adults living in Beijing, China, between 2015 and 2016. Repeated measures of 24-hour electrocardiograms were conducted during clinical visits, and daily counts of four arrhythmia events including supraventricular premature beat (SVPB), atrial tachycardia (AT), premature ventricular contraction (PVC) and ventricular tachycardia (VT) were recorded. One hundred forty-seven constituents in PM2.5 were analyzed for collected particulate samples, in which fifty-six of them above laboratory detection limits were selected for source apportionment analysis using positive matrix factorization. The average contributions of identified five major sources to PM2.5 were 45.9% from secondary nitrate/sulfate, 18.0% from coal combustion, 16.9% from crustal soil, 13.8% from biomass burning, and 5.4% from cooking. Generalized estimating equation models were used to estimate relative risks (RR) of arrhythmias in association with interquartile-range (IQR) increases in PM2.5 constituents and specific sources. Total PM2.5 mass as well as several combustion related constituents were found of significant impacts on increased risks of arrhythmia events. Among the identified sources of PM2.5, coal burning has been found the major source that associated with increased risks of SVPB, PVC and VT with RR of 1.19 [95% confidence intervals (CI): 1.04, 1.36] to 1.64 (95% CI: 1.35, 2.00). PM2.5 from combustion related secondary nitrate/sulfate was also found of significant impact on SVPB and AT, followed by PM2.5 from biomass burning and crustal soil. Our results indicated that PM2.5 from anthropogenic activity related sources were most responsible for increased risks of arrhythmia events. Our findings enhance the understanding of increased risks of arrhythmias from exposure to PM2.5, and provide evidence on source-specific PM control priorities.

Prenatal, Early-Life and Lifetime Exposure to Air Pollution and Childhood Lung Function and Asthma: The Avon Longitudinal Study of Parents and Children (ALSPAC) Cohort Study

Background: Only a few studies have investigated early-life air pollution exposures on childhood lung function and asthma, with inconsistent results. We examined associations of exposure to air pollution during pregnancy, infancy and lifetime periods with lung function and current asthma in the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort.Methods: Forced expiratory volume in 1 second (FEV1) and Forced vital capacity (FVC) were measured at age 8 years and converted into age-height-gender adjusted z-scores. Current asthma was derived from answers to relevant questionnaire items. Exposures to source-specific particulate matter with a diameter&amp;#8804;10µm (PM10) during each trimester, 0-6 months, 7-12 months (1990-1993) through childhood up to age 8 years (1991-2001) were estimated using a dispersion model, accounting for residential mobility. Linear and logistic regression models were fitted to explore the associations, adjusting for gestational age, damp and mould at home, passive smoking exposure, home ownership, maternal education and smoking during pregnancy.Results: 13,963 study children were included in this analysis. At age 8 years, exposure to interquartile (IQR) higher PM10 (0.72µg/m3) from road traffic during the first trimester was associated with lower FEV1 (-0.05, 95%CI:-0.08 to -0.02) and FVC (-0.05, 95%CI:-0.08 to -0.02) z-scores. Similar significant associations were also seen with PM10 in the second and third trimester, 0-6months, 7-12 months and 0-7 years. Associations were stronger among children whose mother had a lower education level or smoked during pregnancy. PM10 from all sources during the third trimester was significantly associated with lower FVC z-scores. Current asthma was not associated with PM10 at any time periods.Conclusion: Preliminary results suggested that exposure to road-traffic PM10 from as early as in the first trimester may result in small but significant reductions in lung function at age 8 years.

Long-term effects of total and source-specific particulate air pollution on incident cardiovascular disease in Gothenburg, Sweden

Background and aimsLong-term exposure to air pollution increases cardiopulmonary morbidity and mortality, but it is not clear which components of air pollution are the most harmful, nor which time window of exposure is most relevant. Further studies at low exposure levels have also been called for. We analyzed two Swedish cohorts to investigate the effects of total and source-specific particulate matter (PM) on incident cardiovascular disease for different time windows of exposure. MethodsTwo cohorts initially recruited to study predictors of cardiovascular disease (the PPS cohort and the GOT-MONICA cohort) were followed from 1990 to 2011. We collected data on residential addresses and assigned each individual yearly total and source-specific PM and Nitrogen Oxides (NOx) exposures based on dispersion models. Using multivariable Cox regression models with time-dependent exposure, we studied the association between three different time windows (lag 0, lag 1–5, and exposure at study start) of residential PM and NOx exposure, and incidence of ischemic heart disease, stroke, heart failure and atrial fibrillation. Results and discussionDuring the study period, there were 2266 new-onset cases of ischemic heart disease, 1391 of stroke, 925 of heart failure and 1712 of atrial fibrillation. The majority of cases were in the PPS cohort, where participants were older. Exposure levels during the study period were moderate (median: 13µg/m3 for PM10 and 9µg/m3 for PM2.5), and similar in both cohorts. Road traffic and residential heating were the largest local sources of PM air pollution, and long distance transportation the largest PM source in total. In the PPS cohort, there were positive associations between PM in the last five years and both ischemic heart disease (HR: 1.24 [95% CI: 0.98–1.59] per 10µg/m3 of PM10, and HR: 1.38 [95% CI: 1.08–1.77] per 5µg/m3 of PM2.5) and heart failure. In the GOT-MONICA cohort, there were positive but generally non-significant associations between PM and stroke (HR: 1.48 [95% CI: 0.88–2.49] per 10µg/m3 of PM10, and HR: 1.50 [95% CI: 0.90–2.51] per 5µg/m3 of PM2.5, in the last five years). Effect estimates were stronger for women, non-smokers, and higher socioeconomic classes. Exposure in the last five years seemed to be more strongly associated with outcomes than other exposure time windows. Associations between source-specific PM air pollution and outcomes were mixed and generally weak. High correlations between the main pollutants limited the use of multi-pollutant models. ConclusionsThe main PM air pollutants were associated with ischemic heart disease and stroke (in women) at the relatively low exposure levels in Gothenburg, Sweden. The associations tended to be stronger for women than for men, for non-smokers than for smokers, and for higher socioeconomic classes than for lower. The associations could not be attributed to a specific PM source or type, and differed somewhat between the two cohorts. The results of this study confirm that further efforts to reduce air pollution exposure should be undertaken in Sweden to reduce the negative health effects in the general population.

Characterization of leaf-level particulate matter for an industrial city using electron microscopy and X-ray microanalysis

This study reports application of monitoring and characterization protocol for particulate matter (PM) deposited on tree leaves, using Quercus ilex as a case study species. The study area is located in the industrial city of Terni in central Italy, with high PM concentrations. Four trees were selected as representative of distinct pollution environments based on their proximity to a steel factory and a street. Wash off from leaves onto cellulose filters were characterized using scanning electron microscopy and energy dispersive X-ray spectroscopy, inferring the associations between particle sizes, chemical composition, and sampling location. Modeling of particle size distributions showed a tri-modal fingerprint, with the three modes centered at 0.6 (factory related), 1.2 (urban background), and 2.6μm (traffic related). Chemical detection identified 23 elements abundant in the PM samples. Principal component analysis recognized iron and copper as source-specific PM markers, attributed mainly to industrial and heavy traffic pollution respectively. Upscaling these results on leaf area basis provided a useful indicator for strategic evaluation of harmful PM pollutants using tree leaves.

Pulmonary inflammatory effects of source-oriented particulate matter from California's San Joaquin Valley

The EPA regulates ambient particulate matter (PM) because substantial associations have been established between PM and health impacts. Presently, regulatory compliance involves broad control of PM emission sources based on mass concentration rather than chemical composition, although PM toxicity is likely to vary depending upon PM physicochemical properties. The overall objective of this study was to help inform source-specific PM emission control regulations. For the first time, source-oriented PM was collected from the atmosphere in Fresno, CA, onto 38 source/size substrates. Mice were exposed via oropharyngeal aspiration to equivalent mass doses [50 μg] of two size fractions: ultrafine (Dp < 0.17 μm) and submicron fine (0.17 < Dp < 1 μm) during summer and winter seasons. At 24 h post-exposure, cellular and biochemical indicators of pulmonary inflammation were evaluated in the bronchoalveolar lavage fluid. Significant inflammatory responses were elicited by vehicle, regional background, and cooking PM sources that were dependent on season and particle size. This is the first study of source-oriented toxicity of atmospheric PM and supports source-specific emissions control strategies.

Differential distributed lag patterns of source-specific particulate matter on respiratory emergency hospitalizations.

While different emission sources and formation processes generate mixtures of particulate matter (PM) with different physicochemical compositions that may differentially affect PM toxicity, evidence of associations between PM sources and respiratory events is scarce. We estimated PM10 sources contributed from 19 chemical constituents by positive matrix factorization, and examined association of short-term sources exposure with emergency respiratory hospitalizations using generalized additive models for single- and distributed lag periods. PM10 contributions from eight sources were identified. Respiratory risks over a consecutive 6-day exposure period were the highest for vehicle exhaust [2.01%; 95% confidence interval (CI): 1.04, 2.99], followed by secondary sulfate (1.59%; 95% CI: 0.82, 2.37). Vehicle exhaust, regional combustion, and secondary nitrate were significantly associated with 0.93%-2.04% increase in respiratory hospitalizations at cumulative lag2-5; significant associations of aged sea salt (1.2%; 95% CI: 0.63, 1.78) and soil/road dust (0.42%; 95% CI: 0.03, 0.82) were at lag0-1. Some effect estimates were no longer significant in two-pollutant models adjusting for PM10; however, a similar temporal pattern of associations remains. Differential lag associations of respiratory hospitalizations with PM10 sources were indicated, which may reflect the different particle size fractions that sources tend to emit. Findings may have potential biological and policy implications.