Adverse Effects Of Air Pollution Research Articles

City-scale assessment of long-term air quality impacts on the respiratory and cardiovascular health.

The impact of the urban environment on human health is a contemporary subject of environmental research. Air pollution is often considered a leading environmental driver. However, a plethora of other factors within the urban exposome may be involved. At the same time, the resolution of spatial data is also an important facet to consider. Generally, systematic tools for accurate health risk assessment in the urban environment are missing or are not implemented. The long-term impact of air quality (PM10, PM2.5, NO2, benzene, and SO2) on respiratory and cardiovascular health was assessed with a log-linear model. We used the most accurate health data in high city scale spatial resolution over the period 2010 to 2018. Selected external exposome parameters were also included in the analysis. Statistically significant associations between air pollution and the health of the urban population were found. The strongest association was between benzene and the incidence of bronchitis in the adult population [RR 1.552 95% CI (1.415-1.704) per 0.5 μg/m3 change in benzene concentration]. A similar relation was observed between NO2 and the same health condition [RR 1.483 95% CI (1.227-1.792) per 8.9 μg/m3 of change in NO2]. Other weaker associations were also found between asthma in children and PMs, NO2, or benzene. Cardiovascular-related hospitalizations in the general population were linked with NO2 [RR 1.218 95% CI (1.119-1.325) per 9.7 μg/m3 change in NO2]. The remaining pollutants were slightly less but still significantly associated with cardiovascular-related hospitalizations. Our findings are mostly highly statistically significant (p ≤ 0.001) and are in line with current literature on the adverse effects of air pollution on the human population. The results highlight the need for continual improvements in air quality. We propose the implementation of this approach as a systematic tool for the investigation of possible health risks over a long period of time. However, further research involving other variables is an essential step toward understanding the complex urban exposome and its implications for human health. An increase in data spatial resolution is especially important in this respect as well as for improving city health risk management.

Attention enhanced hybrid model for spatiotemporal short-term forecasting of particulate matter concentrations

With ever-increasing global air pollution levels, researchers are exploring ways to forecast air pollutant concentrations to prevent the adverse effects of air pollution on humans. Powered by the data obtained from air pollution monitoring stations, we now have a chance to build sophisticated models to estimate the future concentration of various air pollutants. Previous researches show that deep learning models perform a better task of capturing the complex spatiotemporal dynamics from the data as compared to traditional statistical models. In this paper, a hybrid deep learning framework - AGCTCN (Attention based Graph Convolution and Temporal Convolution Network), based on spatial attention, graph convolution and temporal convolution is presented for short-term forecasting of particulate matter (PM) levels. Specifically, quarter-hourly PM10 and PM2.5 data aggregated from 27 ground air pollution monitoring stations in Delhi, India is used for training the AGCTCN model and our model forecasts the concentrations of these pollutants at these stations for a particular horizon in the future. The forecasts generated by our model are compared and contrasted to those generated by other state-of-the-art models like GC-LSTM and ConvLSTM with respect to four widely used evaluation metrics namely RMSE (root mean squared error), MAE (mean absolute error), correlation coefficient, and R2 (coefficient of determination). Our model shows more than 80% improvement over the GC-LSTM model in terms of the R2 metric, performs the best task of estimating the peak PM concentrations and shows variability and correlation close to that of the observed data. A carefully conducted ablation study shows the effectiveness of the individual components of our architecture. The graph convolution layer improves the model accuracy by approximately 34% on average on the PM datasets. Compared to other models, the AGCTCN framework shows the best performance in short-term forecasting of particulate matter concentrations.

Air pollution exposure increases ABCB1 and ASCT1 transporter levels in mouse cortex

Membrane transporters are important for maintaining brain homeostasis by regulating the passage of solutes into, out of, and within the brain. Growing evidence suggests neurotoxic effects of air pollution exposure and its contribution to neurodegenerative disorders, including Alzheimer’s disease (AD), yet limited knowledge is available on the exact cellular impacts of exposure. This study investigates how exposure to ubiquitous solid components of air pollution, ultrafine particles (UFPs), influence brain homeostasis by affecting protein levels of membrane transporters. Membrane transporters were quantified and compared in brain cortical samples of wild-type and the 5xFAD mouse model of AD in response to subacute exposure to inhaled UFPs. The cortical ASCT1 and ABCB1 transporter levels were elevated in wild-type and 5xFAD mice subjected to a 2-week UFP exposure paradigm, suggesting impairment of brain homeostatic mechanisms. This study provides new insight on the molecular mechanisms underlying adverse effects of air pollution on the brain.

Is dietary intake of antioxidant vitamins associated with reduced adverse effects of air pollution on diabetes? Findings from a large cohort study

IntroductionIt remains unknown whether higher dietary intake of antioxidant vitamins could reduce the harmful effects of air pollution on incident diabetes mellitus. MethodsA total of 156,490 participants free of diabetes mellitus in the UK Biobank data were included in this analysis. Antioxidant vitamin intake was measured using a 24-h food intake questionnaire, and results were categorized as sufficient or insufficient according to the British Recommended Nutrient Intake. Exposure to fine particles (PM2.5), thoracic particles (PM10), nitrogen dioxide (NO2), and nitrogen oxide (NOx) was estimated using land use regression models at participants’ residences. Incident diabetes mellitus was identified using health administrative datasets. Cox regression models were used to assess the associations. ResultsA total of 4271 incident diabetes mellitus cases were identified during a median follow-up of 11.7 years. Compared with participants with insufficient intake of antioxidant vitamins, those with sufficient consumption had a weaker association between air pollution (PM2.5, PM10 and NO2) and diabetes mellitus [sufficient vs. insufficient: HR = 1.12 (95 % CI: 0.87, 1.45) vs. 1.69 (95 % CI: 1.42, 2.02) for PM2.5, 1.00 (95 % CI: 0.88, 1.14) vs. 1.21 (95 % CI: 1.10, 1.34) for PM10, and 1.01 (95 % CI: 0.98, 1.04) vs. 1.05 (95 % CI: 1.03, 1.07) for NO2 (all p for comparison < 0.05)]. Among different antioxidant vitamins, we observed stronger effects for vitamin C and E. ConclusionOur study suggests that ambient air pollution is one important risk factor of diabetes mellitus, and sufficient intake of antioxidant vitamins may reduce such adverse effects of air pollution on diabetes mellitus.

Cardiovascular Mortality, Habitual Exercise, and Particulate Matter 2.5 Exposure: A Longitudinal Cohort Study

Habitual exercise may amplify the respiratory uptake of air pollutants in the lung, exacerbating the adverse effects of air pollution. However, it is unclear whether this can reduce the health benefits of habitual exercise (referred to as leisure-time exercise). Thus, the combined effects of habitual exercise and chronic exposure to ambient fine particulate matter 2.5 on cardiovascular mortality were examined among adults in Taiwan. A total of 384,128 adults were recruited between 2001 and 2016 and followed up to May 31, 2019. Participants' vital status was obtained by matching their unique identification numbers with records of cardiovascular death in the National Death Registry of Taiwan. A time-varying Cox regression model was used to analyze the data. Analyses were conducted in 2021. Cardiovascular death risks were inversely associated with habitual exercise and positively associated with chronic exposure to particulate matter 2.5. The beneficial effects of habitual exercise on cardiovascular mortality were not modified by chronic exposure to particulate matter 2.5. Inactive participants with high particulate matter 2.5 exposure exhibited a 123% higher risk of cardiovascular death than high-exercise-group participants exposed to low levels of particulate matter 2.5 (95% CI=89, 163). High level of habitual exercise combined with low exposure level of ambient particulate matter 2.5 is associated with the lowest risk of cardiovascular death. A higher level of habitual exercise is associated with a lower risk of cardiovascular death at all levels of particulate matter 2.5 exposure studied. The results indicate that habitual exercise is a safe health promotion strategy even for people residing in relatively polluted regions.

Association of long-term air pollution exposure with the risk of prediabetes and diabetes: Systematic perspective from inflammatory mechanisms, glucose homeostasis pathway to preventive strategies

BackgroundLimited evidence suggests the association of air pollutants with a series of diabetic cascades including inflammatory pathways, glucose homeostasis disorder, and prediabetes and diabetes. Subclinical strategies for preventing such pollutants-induced effects remain unknown. MethodsWe conducted a cross-sectional study in two typically air-polluted Chinese cities in 2018–2020. One-year average PM1, PM2.5, PM10, SO2, NO2, and O3 were calculated according to participants' residence. GAM multinomial logistic regression was performed to investigate the association of air pollutants with diabetes status. GAM and quantile g-computation were respectively performed to investigate individual and joint effects of air pollutants on glucose homeostasis markers (glucose, insulin, HbA1c, HOMA-IR, HOMA-B and HOMA-S). Complement C3 and hsCRP were analyzed as potential mediators. The ABCS criteria and hemoglobin glycation index (HGI) were examined for their potential in preventive strategy. ResultsLong-term air pollutants exposure was associated with the risk of prediabetes [Prevalence ratio for O3 (PR_O3) = 1.96 (95% CI: 1.24, 3.03)] and diabetes [PR_PM1 = 1.18 (95% CI: 1.05, 1.32); PR_PM2.5 = 1.08 (95% CI: 1.00, 1.16); PR_O3 = 1.35 (95% CI: 1.03, 1.74)]. PM1, PM10, SO2 or O3 exposure was associated with glucose-homeostasis disorder. For example, O3 exposure was associated with increased levels of glucose [7.67% (95% CI: 1.75, 13.92)], insulin [19.98% (95% CI: 4.53, 37.72)], HOMA-IR [34.88% (95% CI: 13.81, 59.84)], and decreased levels of HOMA-S [-25.88% (95% CI: −37.46, −12.16)]. Complement C3 and hsCRP played mediating roles in these relationships with proportion mediated ranging from 6.95% to 60.64%. Participants with HGI ≤ −0.53 were protected from the adverse effects of air pollutants. ConclusionOur study provides comprehensive insights into air pollutant–associated diabetic cascade and suggests subclinical preventive strategies.

Air pollution, cognitive capacity, and borrowing behaviours: evidence from an online peer-to-peer platform

ABSTRACT Borrowing decisions typically involve processing large amounts of financial information. However, it has been understudied whether cognitive capacity factors such as air pollution affect borrowing behaviours. In this paper, we estimate the causal impact of air pollution on borrowing behaviours by using the universe of borrowing application data on an online peer-to-peer platform and a thermal inversion instrument. We find that a 1% increase in air pollution reduces the number of borrowing applications and the total amount requested by 0.05% and 0.31% respectively. The impact is stronger when the borrowing is for more complex and less necessary purposes, and when we examine the areas with lower educational attainment. The results suggest that the adverse effect of air pollution on cognitive capacity prevents people from borrowing.

Physical activity attenuated the associations between ambient air pollutants and metabolic syndrome (MetS): A nationwide study across 28 provinces

The independent associations of air pollution and Physical activity (PA) with metabolic syndrome (MetS) were inconsistent, while the joint associations between PA and air pollution with MetS were still unknown. We aimed to (1) further confirm the independent associations of PA and air pollution; (2) examine whether PA would attenuate the positive associations of air pollutants with MetS. We included 13,418 adults above 45 years old in this study. We defined MetS according to the Joint Interim Societies. The concentration of air pollutants (including fine particulate matter (PM2.5), inhalable particles (PM10), ozone (O3), nitrogen dioxide (NO2), sulfur dioxide (SO2), and carbon monoxide (CO)) were estimated by ground-based measurements and satellite remote sensing products. We assessed the level of PA by metabolic equivalent (MET)-hour/week by summing the MET of all activities. We applied logistic regression models with sampling weight to explore the independent and joint associations of PA and air pollutants on MetS. Interaction plots were conducted to exhibit estimates of air pollutants on MetS as a function of PA. We found that all air pollutants were positively associated with the odds of MetS, while PA showed beneficial associations with MetS. The associations of air pollution on MetS decreased accompanied the increase of PA, while the detrimental effects between air pollutants and MetS did not be reversed by PA. In conclusion, PA may attenuate the associations of air pollutants with MetS, although in polluted areas, suggesting that keeping PA might be an effective way to reduce the adverse effects of air pollution with MetS.

Adverse Effects of Air Pollution on Pulmonary Diseases.

Environmental exposure to air pollution is known to have adverse effects on various organs. Air pollution has greater effects on the pulmonary system as the lungs are directly exposed to contaminants in the air. Here, we review the associations of air pollution with the development, morbidity, and mortality of pulmonary diseases. Short- and long-term exposure to air pollution have been shown to increase mortality risk even at concentrations below the current national guidelines. Ambient air pollution has been shown to be associated with lung cancer. Particularly long-term exposure to particulate matter with a diameter <2.5 μm (PM2.5) has been reported to be associated with lung cancer even at low concentrations. In addition, exposure to air pollution has been shown to increase the incidence risk of chronic obstructive pulmonary disease (COPD) and has been correlated with exacerbation and mortality of COPD. Air pollution has also been linked to exacerbation, mortality, and development of asthma. Exposure to nitrogen dioxide (NO2) has been demonstrated to be related to increased mortality in patients with idiopathic pulmonary fibrosis. Additionally, air pollution increases the incidence of infectious diseases, such as pneumonia, bronchitis, and tuberculosis. Furthermore, emerging evidence supports a link between air pollution and coronavirus disease 2019 transmission, susceptibility, severity and mortality. In conclusion, the stringency of air quality guidelines should be increased and further therapeutic trials are required in patients at high risk of adverse health effects of air pollution.

Systemic inflammation accelerates the adverse effects of air pollution on metabolic syndrome: Findings from the China health and Retirement Longitudinal Study (CHARLS)

Long-term exposure to air pollution and systemic inflammation are associated with increased prevalence of metabolic syndrome (MetS); however, their joint effects in Chinese middle-aged and older adults is unknown. In this cross-sectional study, 11,838 residents aged 45 years and older from the China Health and Retirement Longitudinal Study (CHARLS) Wave 3 in 2015 were included. MetS was diagnosed using the Joint Interim Societies’ definition. C-Reactive Protein (CRP) was assessed to reflect systemic inflammation. Individual exposure to air pollutants (particulate matter with a diameter ≤2.5 μm (PM2.5) or ≤ 10 μm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), and carbon monoxide (CO)) was evaluated using satellite-based spatiotemporal models according to participant residence at county-level. Generalized linear models (GLMs) were applied to examine the association between air pollution and MetS, and the modification effects of CRP between air pollution and MetS were estimated using interaction terms of CRP and air pollutants in the GLM models. The prevalence of MetS was 32.37%. The adjusted odd ratio (OR) of MetS was 1.192 (95% confidence interval (CI): 1.116, 1.272), 1.177 (95% CI: 1.103, 1.255), 1.158 (95% CI: 1.072, 1.252), 1.303 (95% CI: 1.211,1.403), 1.107 (95% CI: 1.046, 1.171) and 1.156 (95% CI:1.083, 1.234), per inter-quartile range increase in PM2.5 (24.04 μg/m3), PM10 (39.00 μg/m3), SO2 (19.05 μg/m3), NO2 (11.28 μg/m3), O3 (9.51 μg/m3) and CO (0.46 mg/m3), respectively. CRP was also associated with increased prevalence of MetS (OR = 1.049, 95% CI: 1.035, 1.064; per 1.90 mg/L increase in CRP). Interaction analysis suggested that high CRP levels enhanced the association between air pollution exposure and MetS. Long-term exposure to air pollution is associated with increased prevalence of MetS, which might be enhanced by systemic inflammation. Given the rapidly aging society and heavy burden of MetS, measures should be taken to improve air quality and reduce systemic inflammation.

The effects of ambient fine particulate matter exposure and physical activity on heart failure: A risk-benefit analysis of a prospective cohort study

BackgroundEvidence supporting the adverse effects of air pollution and the benefits of physical activity (PA) on heart failure (HF) has continued to grow. However, their joint effects remain largely unknown. MethodsOur investigation included a total of 321,672 participants free of HF at baseline from the UK Biobank. Participants were followed up till March 2021. Information on participants' PA levels and additional covariates was collected by questionnaire. The annual fine particulate matter (PM2.5) concentration was estimated using a Land Use Regression (LUR) model. Cox proportional hazards models were used to assess the associations of PA and PM2.5 exposure with incident HF, as well as their interaction on both additive and multiplicative scales. ResultsDuring a median follow-up of 12.0 years, 8212 cases of HF were uncovered. Compared with participants with low PA, the hazard ratios (HRs) were 0.69 (95 % CI: 0.65, 0.73) and 0.61 (95 % CI: 0.58, 0.65) for those with moderate and high PA, respectively. PM2.5 was associated with an elevated risk of incident HF with an HR of 1.11 (95 % CI: 1.08, 1.14) per interquartile range (IQR) increment. The synergistic additive interaction between low PA and high PM2.5 exposure on HF was observed. Compared with participants with high PA and low PM2.5 exposure, those with low PA and high PM2.5 exposure had the highest risk of HF [HR (95 % CI): 1.90 (1.76, 2.06)]. ConclusionsOur findings indicate that PA might still be an appropriate strategy to prevent HF for those living in areas with relatively high air pollution. Individuals with low PA may pay more attention to air pollution.

Air Pollution and Human Health: Investigating the Moderating Effect of the Built Environment

Air pollution seriously threatens human health and even causes mortality. It is necessary to explore effective prevention methods to mitigate the adverse effect of air pollution. Shaping a reasonable built environment has the potential to benefit human health. In this context, this study quantified the built environment, air pollution, and mortality at 1 km × 1 km grid cells. The moderating effect model was used to explore how built environment factors affect the impact of air pollution on cause-specific mortality and the heterogeneity in different areas classified by building density and height. Consequently, we found that greenness played an important role in mitigating the effect of ozone (O3) and nitrogen dioxide (NO2) on mortality. Water area and diversity of land cover can reduce the effect of fine particulate matter (PM2.5) and NO2 on mortality. Additionally, gas stations, edge density (ED), perimeter-area fractal dimension (PAFRAC), and patch density (PD) can reduce the effect of NO2 on mortality. There is heterogeneity in the moderating effect of the built environment for different cause-specific mortality and areas classified by building density and height. This study can provide support for urban planners to mitigate the adverse effect of air pollution from the perspective of the built environment.

Changes in the liver proteome in apoE knockout mice exposed to inhalation of silica nanoparticles indicate mitochondrial damage and impairment of ER stress responses associated with microvesicular steatosis

The adverse effects of air pollution on the cardiovascular system have been well documented. Nonalcoholic fatty liver disease (NAFLD) is an independent risk factor for cardiovascular events. However, the influence of exposure to airborne particles on the development of NAFLD is less recognised. The aim of this study was to investigate the impact of silica nanoparticles (SiNPs) on the development of liver steatosis. We used molecular and proteomic SWATH-MS methods to investigate the changes in the liver proteome of apolipoprotein E-knockout mice (apoE−/− mice) exposed to SiNPs for 4 months in a whole-body exposure chamber. Exposure to SiNPs evoked microvesicular liver steatosis in apoE−/− mice. Quantitative liver proteomics showed significant downregulation of ribosomal proteins and endoplasmic reticulum proteins. Gene expression analysis revealed a reduced level of proteins related to endoplasmic reticulum stress. Treatment with SiNPs decreased mitochondrial membrane potential and increased the production of reactive oxygen species in cultured HepG2 cells. This is the first report that inhalation exposure to SiNPs induces microvesicular steatosis and significant changes in the liver proteome in vivo. Our results highlight the important role of silica and point to the ER stress response and mitochondrial dysfunction as potential mechanisms responsible for the increase in fatty liver by SiNPs.

The impact of air pollution on venture capital: evidence from China.

Utilizing a dataset of VC investment from 2005 to 2018, we investigate the relationship between air pollution and venture capital (VC) investment. We find that startups suffering severe air pollution receive less investment from VCs and experience a lower probability of financing from VCs. Our findings are robust to considering endogeneity concerns and various robustness checks. Moreover, air pollution is detrimental to startup innovation ability and entrepreneurial activities through which air pollution negatively affects VC investment. In response, VCs prefer to co-invest with other VCs to mitigate the adverse effect of air pollution. Our paper sheds new light on the impact of air pollution on the private financial markets.

The impacts of economic level and air pollution on public health at the micro and macro level

China's economic growth is accompanied by air pollution, which has harmed public health. Former scholars have explored the influencing factors of public health from different perspectives with different methods, among which family income and environmental pollution are two important factors. The paper explored the combined effects of economic level and air pollution on public health at the micro and macro level using the multivariate ordered Logit model and panel data regression model. A comparative analysis was also explored between China's eastern and western regions. The results demonstrated that: (1) Both at the micro and macro level, economic level was positively correlated with public health, while air pollution was negatively correlated with it. (2) The improvement of the economic level made public health more susceptible to air pollution at the micro level and at the macro level. (3) The higher the economic level, the lower the effect of economic growth in reducing the adverse effects of air pollution on public health. This paper proposed that sustainable economic growth should be pursued, the emissions of air pollutants should be reduced, regional development should be balanced and the development gap between China's eastern and western regions should be narrowed.

Passage of exogeneous fine particles from the lung into the brain in humans and animals.

There are still significant knowledge gaps in understanding the intrusion and retention of exogeneous particles into the central nervous system (CNS). Here, we uncovered various exogeneous fine particles in human cerebrospinal fluids (CSFs) and identified the ambient environmental or occupational exposure sources of these particles, including commonly found particles (e.g., Fe- and Ca-containing ones) and other compositions that have not been reported previously (such as malayaite and anatase TiO2), by mapping their chemical and structural fingerprints. Furthermore, using mouse and invitro models, we unveiled a possible translocation pathway of various inhaled fine particles from the lung to the brain through blood circulation (via dedicated biodistribution and mechanistic studies). Importantly, with the aid of isotope labeling, we obtained the retention kinetics of inhaled fine particles in mice, indicating a much slower clearance rate of localized exogenous particles from the brain than from other main metabolic organs. Collectively, our results provide a piece of evidence on the intrusion of exogeneous particles into the CNS and support the association between the inhalation of exogenous particles and their transport into the brain tissues. This work thus provides additional insights for the continued investigation of the adverse effects of air pollution on the brain.

Ambient air pollutants relate to hospital admissions for chronic obstructive pulmonary disease in Ganzhou, China.

ABSTRACTOBJECTIVE To evaluate the relationship between ambient air pollutants and chronic obstructive pulmonary disease in relatively low-polluted areas in China.METHODS Atmospheric pollutants levels and meteorological data were obtained from January 2016 to December 2020. The medical database including daily hospital admissions for chronic obstructive pulmonary disease (ICD10: J44) was derived from the First Affiliated Hospital of Gannan Medical University. The generalized additive model was used to analyze the percentage change with 95% confidence interval in daily hospital admissions for chronic obstructive pulmonary disease associated with a 10 µg/m3 increase in atmospheric pollutants levels.RESULTS In total, occurred 4,980 chronic obstructive pulmonary disease hospital admissions (not including emergency department visits) during 2016–2020. The mean concentrations of daily PM2.5, PM10, SO2, NO2, O3, and CO were 37.5 μg/m3, 60.1 μg/m3, 18.7 μg/m3, 23.5 μg/m3, 70.0 μg/m3, and 1.2 mg/m3 in Ganzhou. Each 10 µg/m3 increment of PM2.5, PM10, NO2, and O3 were significantly associated with 2.8% (95%CI: 1.0–4.7), 1.3% (95%CI: 0.3–2.4), 2.8% (95%CI: 0.4–5.4), and 1.5% (95%CI: 0.2–2.7) elevation in daily chronic obstructive pulmonary disease hospital admissions. The estimates of delayed effects of PM2.5, PM10, NO2, and O3 were observed at lag6, lag6, lag8, lag1, respectively. The health effects of particulate pollutants (PM2.5 and PM10) may be independent of other pollutants. The adverse effects of air pollutants were more evident in the warm season (May–Oct) than in the cold season (Nov–Apr).CONCLUSION Our study demonstrated that elevated concentrations of atmospheric pollutant (PM2.5, PM10, NO2, and O3), especially particulate pollutants, can be associated with increased daily count of hospital admissions for chronic obstructive pulmonary disease , which may promote further understanding of the potential hazards of relatively low levels of air pollution on chronic obstructive pulmonary disease and other respiratory disorders.

Traffic-related Air Pollution and Lung Cancer Incidence: The California Multiethnic Cohort Study.

Rationale: Although the contribution of air pollution to lung cancer risk is well characterized, few studies have been conducted in racially, ethnically, and socioeconomically diverse populations. Objectives: To examine the association between traffic-related air pollution and risk of lung cancer in a racially, ethnically, and socioeconomically diverse cohort. Methods: Among 97,288 California participants of the Multiethnic Cohort Study, we used Cox proportional hazards regression to examine associations between time-varying traffic-related air pollutants (gaseous and particulate matter pollutants and regional benzene) and lung cancer risk (n = 2,796 cases; average follow-up = 17 yr), adjusting for demographics, lifetime smoking, occupation, neighborhood socioeconomic status (nSES), and lifestyle factors. Subgroup analyses were conducted for race, ethnicity, nSES, and other factors. Measurements and Main Results: Among all participants, lung cancer risk was positively associated with nitrogen oxide (hazard ratio [HR], 1.15 per 50 ppb; 95% confidence interval [CI], 0.99-1.33), nitrogen dioxide (HR, 1.12 per 20 ppb; 95% CI, 0.95-1.32), fine particulate matter with aerodynamic diameter <2.5 μm (HR, 1.20 per 10 μg/m3; 95% CI, 1.01-1.43), carbon monoxide (HR, 1.29 per 1,000 ppb; 95% CI, 0.99-1.67), and regional benzene (HR, 1.17 per 1 ppb; 95% CI, 1.02-1.34) exposures. These patterns of associations were driven by associations among African American and Latino American groups. There was no formal evidence for heterogeneity of effects by nSES (P heterogeneity > 0.21), although participants residing in low-SES neighborhoods had increased lung cancer risk associated with nitrogen oxides, and no association was observed among those in high-SES neighborhoods. Conclusions: These findings in a large multiethnic population reflect an association between lung cancer and the mixture of traffic-related air pollution and not a particular individual pollutant. They are consistent with the adverse effects of air pollution that have been described in less racially, ethnically, and socioeconomically diverse populations. Our results also suggest an increased risk of lung cancer among those residing in low-SES neighborhoods.

Information entropy tradeoffs for efficient uncertainty reduction in estimates of air pollution mortality

Implementing effective policy to protect human health from the adverse effects of air pollution, such as premature mortality, requires reducing the uncertainty in health outcomes models. Here we present a novel method to reduce mortality uncertainty by increasing the amount of input data of air pollution and health outcomes, and then quantifying tradeoffs associated with the different data gained. We first present a study of long-term mortality from fine particulate matter (PM2.5) based on simulated data, followed by a real-world application of short-term PM2.5-related mortality in an urban area. We employ information yield curves to identify which variables more effectively reduce mortality uncertainty when increasing information. Our methodology can be used to explore how specific pollution scenarios will impact mortality and thus improve decision-making. The proposed framework is general and can be applied to any real case-scenario where knowledge in pollution, demographics, or health outcomes can be augmented through data acquisition or model improvements to generate more robust risk assessments.

Air pollutant dispersion around high-rise buildings due to roof emissions

Air quality in the built environment has a significant impact on public health, particularly in densely populated cities where residents live in closely-packed high-rise buildings. In this case, communicable respiratory diseases are apt to spread through vent pipe emissions on the building roof and facilitate community transmission. This study applied computational fluid dynamics to simulate the dispersion of the pollutants discharged from the roof vent pipes around high-rise buildings. The results show that the dispersion process is dominated by wind-structure interaction, wind incidence angle, air pollutant discharge location, and vent pipe height, and the dispersion is more complex around crucifix-form buildings than cubic ones. When the wind incidence angle reaches around 90°, the air pollutants are entrained in the re-entry of the building, thus impeding the dispersion process. The building areas most adversely affected by air pollutants are located on high floors near the vent pipe. Changing air pollutant discharge location and increasing the height of the vent pipe can significantly reduce the affected area. Where the height of the vent pipe is restricted, parapets at the roof edges are suggested to further reduce the adverse effects of air pollutants. These research findings can help to reduce the risk of airborne contaminants/diseases spreading in current and future built environments.