Long-term exposure to several constituents and sources of PM2.5 is associated with incidence of upper aerodigestive tract cancers but not gastric cancer: Results from the large pooled European cohort of the ELAPSE project.

It is unclear whether cancers of the upper aerodigestive tract (UADT) and gastric cancer are related to air pollution, due to few studies with inconsistent results. The effects of particulate matter (PM) may vary across locations due to different source contributions and related PM compositions, and it is not clear which PM constituents/sources are most relevant from a consideration of overall mass concentration alone. We therefore investigated the association of UADT and gastric cancers with PM2.5 elemental constituents and sources components indicative of different sources within a large multicentre population based epidemiological study. Cohorts with at least 10 cases per cohort led to ten and eight cohorts from five countries contributing to UADT- and gastric cancer analysis, respectively. Outcome ascertainment was based on cancer registry data or data of comparable quality. We assigned home address exposure to eight elemental constituents (Cu, Fe, K, Ni, S, Si, V and Zn) estimated from Europe-wide exposure models, and five source components identified by absolute principal component analysis (APCA). Cox regression models were run with age as time scale, stratified for sex and cohort and adjusted for relevant individual and neighbourhood level confounders. We observed 1139 UADT and 872 gastric cancer cases during a mean follow-up of 18.3 and 18.5 years, respectively. UADT cancer incidence was associated with all constituents except K in single element analyses. After adjustment for NO2, only Ni and V remained associated with UADT. Residual oil combustion and traffic source components were associated with UADT cancer persisting in the multiple source model. No associations were found for any of the elements or source components and gastric cancer incidence. Our results indicate an association of several PM constituents indicative of different sources with UADT but not gastric cancer incidence with the most robust evidence for traffic and residual oil combustion.

Life Expectancy and Built Environments in the U.S.: A Multilevel Analysis.

INTRODUCTION: The purpose of this study is to examine the associations between built environments and life expectancy across a gradient of urbanicity in the U.S. METHODS: Census tract‒level estimates of life expectancy between 2010 and 2015, except for Maine and Wisconsin, from the U.S. Small-Area Life Expectancy Estimates Project were analyzed in 2022. Tract-level measures of the built environment included: food, alcohol, and tobacco outlets; walkability; park and green space; housing characteristics; and air pollution. Multilevel linear models for each of the 4 urbanicity types were fitted to evaluate the associations, adjusting for population and social characteristics. RESULTS: Old housing (built before 1979) and air pollution were important built environment predictors of life expectancy disparities across all gradients of urbanicity. Convenience stores were negatively associated with life expectancy in all urbanicity types. Healthy food options were a positive predictor of life expectancy only in high-density urban areas. Park accessibility was associated with increased life expectancy in all areas, except rural areas. Green space in neighborhoods was positively associated with life expectancy in urban areas but showed an opposite association in rural areas. CONCLUSIONS: After adjusting for key social characteristics, several built environment characteristics were salient risk factors for decreased life expectancy in the U.S., with some measures showing differential effects by urbanicity. Planning and policy efforts should be tailored to local contexts.

Portable air cleaner use and biomarkers of inflammation: A systematic review and meta-analysis.

Fine particulate matter air pollution (PM2.5) is a major contributor to cardiovascular morbidity and mortality, potentially via increased inflammation. PM2.5 exposure increases inflammatory biomarkers linked to cardiovascular disease, including CRP, IL-6 and TNFα. Portable air cleaners (PACs) reduce individual PM2.5 exposure but evidence is limited regarding whether PACs also reduce inflammatory biomarkers. We performed a systematic review and meta-analysis of trials evaluating the use of PACs to reduce PM2.5 exposure and inflammatory biomarker concentrations. We identified English-language articles of randomized sham-controlled trials evaluating high efficiency particulate air filters in non-smoking, residential settings measuring serum CRP, IL-6 and TNFα before and after active versus sham filtration, and performed meta-analysis on the extracted modeled percent change in biomarker concentration across studies. Of 487 articles identified, we analyzed 14 studies enrolling 778 participants that met inclusion criteria. These studies showed PACs reduced PM2.5 by 61.5 % on average. Of the 14 included studies, 10 reported CRP concentrations in 570 participants; these showed active PAC use was associated with 7 % lower CRP (95 % CI: -14 % to 0.0 %, p = 0.05). Nine studies of IL-6, with 379 participants, showed active PAC use was associated with 13 % lower IL-6 (95 % CI: [-23 %, -3 %], p = 0.009). Six studies, with 269 participants, reported TNF-α and demonstrated no statistical evidence of difference between active and sham PAC use. Portable air cleaners that reduce PM2.5 exposure can decrease concentrations of inflammatory biomarkers associated with cardiovascular disease. Additional studies are needed to evaluate clinical outcomes and other biomarkers.

Evaluation of a commercial database to estimate residence histories in the los angeles ultrafines study.

BACKGROUND: Commercial databases can be used to identify participant addresses over time, but their quality and impact on environmental exposure assessment is uncertain. OBJECTIVE: To evaluate the performance of a commercial database to find residences and estimate environmental exposures for study participants. METHODS: We searched LexisNexis® for participant addresses in the Los Angeles Ultrafines Study, a prospective cohort of men and women aged 50-71 years. At enrollment (1995-1996) and follow-up (2004-2005), we evaluated attainment (address found for the corresponding time period) and match rates to survey addresses by participant characteristics. We compared geographically-referenced predictors and estimates of ultrafine particulate matter (UFP) exposure from a land use regression model using LexisNexis and survey addresses at enrollment. RESULTS: LexisNexis identified an address for 69% of participants at enrollment (N = 50,320) and 95% of participants at follow-up (N = 24,432). Attainment rate at enrollment modestly differed (≥5%) by age, smoking status, education, and residential mobility between surveys. The match rate at both survey periods was high (82-86%) and similar across characteristics. When using LexisNexis versus survey addresses, correlations were high for continuous values of UFP exposure and its predictors (rho = 0.86-0.92). SIGNIFICANCE: Time period and population characteristics influenced the attainment of addresses from a commercial database, but accuracy and subsequent estimation of specific air pollution exposures were high in our older study population.

Use of continuous sample translation to reduce radiation damage for XPCS studies of protein diffusion.

An experimental setup to measure X-ray photon correlation spectroscopy during continuous sample translation is presented and its effectiveness as a means to avoid sample damage in dynamics studies of protein diffusion is evaluated. X-ray damage from focused coherent synchrotron radiation remains below tolerable levels as long as the sample is translated through the beam sufficiently quickly. Here it is shown that it is possible to separate sample dynamics from the effects associated with the transit of the sample through the beam. By varying the sample translation rate, the damage threshold level, Dthresh = 1.8 kGy, for when beam damage begins to modify the dynamics under the conditions used, is also determined. Signal-to-noise ratios, Rsn ≥ 20, are obtained down to the shortest delay times of 20 µs. The applicability of this method of data collection to the next generation of multi-bend achromat synchrotron sources is discussed and it is shown that sub-microsecond dynamics should be obtainable on protein samples.

Application of data science methods to identify school and home risk factors for asthma and allergy-related symptoms among children in New York.

OBJECTIVES: Few studies have comprehensively assessed multiple environmental exposures affecting children's health. This study applied machine-learning methods to evaluate how indoor environmental conditions at home and school contribute to asthma and allergy-related symptoms. METHODS: We randomly selected 10 public schools representing different socioeconomic statuses in New York State (2017-2019) and distributed questionnaires to students to collect health status and home-and school-environmental exposures. Indoor air quality was measured at school, and ambient particle exposures (PM2.5 and components) were measured using real-time personal monitors for 48 h. We used random forest model to identify the most important risk factors for asthma and allergy-related symptoms, and decision tree for visualizing the inter-relationships among the multiple risk factors with the health outcomes. RESULTS: The top contributing factors identified for asthma were family rhinitis history (relative importance: 10.40%), plant pollen trigger (5.48%); bedroom carpet (3.58%); environmental tobacco smoke (ETS) trigger symptom (2.98%); and ETS exposure (2.56%). For allergy-related symptoms, plant pollen trigger (10.88%), higher paternal education (7.33%), bedroom carpet (5.28%), family rhinitis history (4.78%), and higher maternal education (4.25%) were the strongest contributing factors. Conversely, primary heating with hot water radiator was negatively (-6.86%) associated with asthma symptoms. Younger children (<9 years old) with family history of rhinitis and carpeting in the bedroom were the prominent combined risk factors for asthma. Children jointly exposed to pollen, solvents, and carpeting in their home tended to have greater risks of allergy-related symptoms, even without family history of rhinitis. CONCLUSION: Family rhinitis history, bedroom carpet, and pollen triggers were the most important risk factors for both asthma and allergy-related symptoms. Our new findings included that hot-water radiator was related to reduced asthma symptoms, and the combination of young age, rhinitis history, and bedroom carpeting was related to increased asthma symptoms. Further studies are needed to confirm our findings.

Outdoor air pollution and cancer: An overview of the current evidence and public health recommendations.

Outdoor air pollution is a major contributor to the burden of disease worldwide. Most of the global population resides in places where air pollution levels, because of emissions from industry, power generation, transportation, and domestic burning, considerably exceed the World Health Organization's health-based air-quality guidelines. Outdoor air pollution poses an urgent worldwide public health challenge because it is ubiquitous and has numerous serious adverse human health effects, including cancer. Currently, there is substantial evidence from studies of humans and experimental animals as well as mechanistic evidence to support a causal link between outdoor (ambient) air pollution, and especially particulate matter (PM) in outdoor air, with lung cancer incidence and mortality. It is estimated that hundreds of thousands of lung cancer deaths annually worldwide are attributable to PM air pollution. Epidemiological evidence on outdoor air pollution and the risk of other types of cancer, such as bladder cancer or breast cancer, is more limited. Outdoor air pollution may also be associated with poorer cancer survival, although further research is needed. This report presents an overview of outdoor air pollutants, sources, and global levels, as well as a description of epidemiological evidence linking outdoor air pollution with cancer incidence and mortality. Biological mechanisms of air pollution-derived carcinogenesis are also described. This report concludes by summarizing public health/policy recommendations, including multilevel interventions aimed at individual, community, and regional scales. Specific roles for medical and health care communities with regard to prevention and advocacy and recommendations for further research are also described.

Exposure to air pollution is associated with adverse cardiopulmonary health effects in international travellers.

BACKGROUND: With the number of annual global travellers reaching 1.2 billion, many individuals encounter greater levels of air pollution when they travel abroad to megacities around the world. This study's objective was to determine if visits to cities abroad with greater levels of air pollution adversely impact cardiopulmonary health. METHODS: A total of 34 non-smoking healthy adult participants who travelled abroad to selected cities from the New York City (NYC) metropolitan area were pre-trained to measure lung function, blood pressure and heart rate (HR)/HR variability (HRV) and record symptoms before, during and after travelling abroad. Outdoor particulate matter (PM)2.5 concentrations were obtained from central monitors in each city. Associations between PM exposure concentrations and cardiopulmonary health endpoints were analysed using a mixed effects statistical design. RESULTS: East and South Asian cities had significantly higher PM2.5 concentrations compared with pre-travel NYC PM2.5 levels, with maximum concentrations reaching 503 µg/m3. PM exposure-related associations for lung function were statistically significant and strongest between evening Forced Expiratory Volume in the first second (FEV1) and same-day morning PM2.5 concentrations; a 10-µg/m3 increase in outdoor PM2.5 was associated with a mean decrease of 7 mL. Travel to a highly polluted city (PM2.5 > 100 µg/m3) was associated with a 209-ml reduction in evening FEV1 compared with a low polluted city (PM2.5 < 35 µg/m3). In general, participants who travelled to East and South Asian cities experienced increased respiratory symptoms/scores and changes in HR and HRV. CONCLUSIONS: Exposure to increased levels of PM2.5 in cities abroad caused small but statistically significant acute changes in cardiopulmonary function and respiratory symptoms in healthy young adults. These data suggest that travel-related exposure to increased PM2.5 adversely impacts cardiopulmonary health, which may be particularly important for travellers with pre-existing respiratory or cardiac disease.

Water Pipe (Hookah) Smoking and Cardiovascular Disease Risk: A Scientific Statement From the American Heart Association.

Tobacco smoking with a water pipe or hookah is increasing globally. There are millions of water pipe tobacco smokers worldwide, and in the United States, water pipe use is more common among youth and young adults than among adults. The spread of water pipe tobacco smoking has been abetted by the marketing of flavored tobacco, a social media environment that promotes water pipe smoking, and misperceptions about the addictive potential and potential adverse health effects of this form of tobacco use. There is growing evidence that water pipe tobacco smoking affects heart rate, blood pressure regulation, baroreflex sensitivity, tissue oxygenation, and vascular function over the short term. Long-term water pipe use is associated with increased risk of coronary artery disease. Several harmful or potentially harmful substances present in cigarette smoke are also present in water pipe smoke, often at levels exceeding those found in cigarette smoke. Water pipe tobacco smokers have a higher risk of initiation of cigarette smoking than never smokers. Future studies that focus on the long-term adverse health effects of intermittent water pipe tobacco use are critical to strengthen the evidence base and to inform the regulation of water pipe products and use. The objectives of this statement are to describe the design and operation of water pipes and their use patterns, to identify harmful and potentially harmful constituents in water pipe smoke, to document the cardiovascular risks of water pipe use, to review current approaches to water pipe smoking cessation, and to offer guidance to healthcare providers for the identification and treatment of individuals who smoke tobacco using water pipes.

Air Pollution and Noncommunicable Diseases: A Review by the Forum of International Respiratory Societies' Environmental Committee, Part 2: Air Pollution and Organ Systems.

Although air pollution is well known to be harmful to the lung and airways, it can also damage most other organ systems of the body. It is estimated that about 500,000 lung cancer deaths and 1.6 million COPD deaths can be attributed to air pollution, but air pollution may also account for 19% of all cardiovascular deaths and 21% of all stroke deaths. Air pollution has been linked to other malignancies, such as bladder cancer and childhood leukemia. Lung development in childhood is stymied with exposure to air pollutants, and poor lung development in children predicts lung impairment in adults. Air pollution is associated with reduced cognitive function and increased risk of dementia. Particulate matter in the air (particulate matter with an aerodynamic diameter < 2.5 µm) is associated with delayed psychomotor development and lower child intelligence. Studies link air pollution with diabetes mellitus prevalence, morbidity, and mortality. Pollution affects the immune system and is associated with allergic rhinitis, allergic sensitization, and autoimmunity. It is also associated with osteoporosis and bone fractures, conjunctivitis, dry eye disease, blepharitis, inflammatory bowel disease, increased intravascular coagulation, and decreased glomerular filtration rate. Atopic and urticarial skin disease, acne, and skin aging are linked to air pollution. Air pollution is controllable and, therefore, many of these adverse health effects can be prevented.

Global estimates of mortality associated with long-term exposure to outdoor fine particulate matter.

Exposure to ambient fine particulate matter (PM2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries-the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5-10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9-8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3-4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.

Comparing the Health Effects of Ambient Particulate Matter Estimated Using Ground-Based versus Remote Sensing Exposure Estimates.

BACKGROUND: Remote sensing (RS) is increasingly used for exposure assessment in epidemiological and burden of disease studies, including those investigating whether chronic exposure to ambient fine particulate matter (PM2.5) is associated with mortality. OBJECTIVES: We compared relative risk estimates of mortality from diseases of the circulatory system for PM2.5 modeled from RS with that for PM2.5 modeled using ground-level information. METHODS: We geocoded the baseline residence of 668,629 American Cancer Society Cancer Prevention Study II (CPS-II) cohort participants followed from 1982 to 2004 and assigned PM2.5 levels to all participants using seven different exposure models. Most of the exposure models were averaged for the years 2002-2004, and one RS estimate was for a longer, contemporaneous period. We used Cox proportional hazards regression to estimate relative risks (RRs) for the association of PM2.5 with circulatory mortality and ischemic heart disease. RESULTS: Estimates of mortality risk differed among exposure models. The smallest relative risk was observed for the RS estimates that excluded ground-based monitors for circulatory deaths [RR = 1.02, 95% confidence interval (CI): 1.00, 1.04 per 10 µg/m3 increment in PM2.5]. The largest relative risk was observed for the land-use regression model that included traffic information (RR = 1.14, 95% CI: 1.11, 1.17 per 10 µg/m3 increment in PM2.5). CONCLUSIONS: We found significant associations between PM2.5 and mortality in every model; however, relative risks estimated from exposure models using ground-based information were generally larger than those estimated using RS alone.

Perception and reality of particulate matter exposure in New York City taxi drivers.

Exposure to fine particulate matter (PM2.5) and black carbon (BC) have been linked to negative health risks, but exposure among professional taxi drivers is understudied. This pilot study measured drivers' knowledge, attitudes, and beliefs (KAB) about air pollution compared with direct measures of exposures. Roadside and in-vehicle levels of PM2.5 and BC were continuously measured over a single shift on each subject, and exposures compared with central site monitoring. One hundred drivers completed an air pollution KAB questionnaire, and seven taxicabs participated in preliminary in-cab air sampling. Taxicab PM2.5 and BC concentrations were elevated compared with nearby central monitoring. Average PM2.5 concentrations per 15-min interval were 4-49 µg/m3. BC levels were also elevated; reaching>10 µg/m3. Fifty-six of the 100 drivers surveyed believed they were more exposed than non-drivers; 81 believed air pollution causes health problems. Air pollution exposures recorded suggest that driver exposures would likely exceed EPA recommendations if experienced for 24 h. Surveys indicated that driver awareness of this was limited. Future studies should focus on reducing exposures and increasing awareness among taxi drivers.

Ambient Particulate Matter Air Pollution Exposure and Mortality in the NIH-AARP Diet and Health Cohort.

BACKGROUND: Outdoor fine particulate matter (≤ 2.5 µm; PM2.5) has been identified as a global health threat, but the number of large U.S. prospective cohort studies with individual participant data remains limited, especially at lower recent exposures. OBJECTIVES: We aimed to test the relationship between long-term exposure PM2.5 and death risk from all nonaccidental causes, cardiovascular (CVD), and respiratory diseases in 517,041 men and women enrolled in the National Institutes of Health-AARP cohort. METHODS: Individual participant data were linked with residence PM2.5 exposure estimates across the continental United States for a 2000-2009 follow-up period when matching census tract-level PM2.5 exposure data were available. Participants enrolled ranged from 50 to 71 years of age, residing in six U.S. states and two cities. Cox proportional hazard models yielded hazard ratio (HR) estimates per 10 µg/m3 of PM2.5 exposure. RESULTS: PM2.5 exposure was significantly associated with total mortality (HR = 1.03; 95% CI: 1.00, 1.05) and CVD mortality (HR = 1.10; 95% CI: 1.05, 1.15), but the association with respiratory mortality was not statistically significant (HR = 1.05; 95% CI: 0.98, 1.13). A significant association was found with respiratory mortality only among never smokers (HR = 1.27; 95% CI: 1.03, 1.56). Associations with 10-µg/m3 PM2.5 exposures in yearly participant residential annual mean, or in metropolitan area-wide mean, were consistent with baseline exposure model results. Associations with PM2.5 were similar when adjusted for ozone exposures. Analyses of California residents alone also yielded statistically significant PM2.5 mortality HRs for total and CVD mortality. CONCLUSIONS: Long-term exposure to PM2.5 air pollution was associated with an increased risk of total and CVD mortality, providing an independent test of the PM2.5-mortality relationship in a new large U.S. prospective cohort experiencing lower post-2000 PM2.5 exposure levels. CITATION: Thurston GD, Ahn J, Cromar KR, Shao Y, Reynolds HR, Jerrett M, Lim CC, Shanley R, Park Y, Hayes RB. 2016. Ambient particulate matter air pollution exposure and mortality in the NIH-AARP Diet and Health cohort. Environ Health Perspect 124:484-490; http://dx.doi.org/10.1289/ehp.1509676.

Ischemic Heart Disease Mortality and Long-Term Exposure to Source-Related Components of U.S. Fine Particle Air Pollution.

BACKGROUND: Fine particulate matter (PM2.5) air pollution exposure has been identified as a global health threat. However, the types and sources of particles most responsible are not yet known. OBJECTIVES: We sought to identify the causal characteristics and sources of air pollution underlying past associations between long-term PM2.5 exposure and ischemic heart disease (IHD) mortality, as established in the American Cancer Society's Cancer Prevention Study-II cohort. METHODS: Individual risk factor data were evaluated for 445,860 adults in 100 U.S. metropolitan areas followed from 1982 through 2004 for vital status and cause of death. Using Cox proportional hazard models, we estimated IHD mortality hazard ratios (HRs) for PM2.5, trace constituents, and pollution source-associated PM2.5, as derived from air monitoring at central stations throughout the nation during 2000-2005. RESULTS: Associations with IHD mortality varied by PM2.5 mass constituent and source. A coal combustion PM2.5 IHD HR = 1.05 (95% CI: 1.02, 1.08) per microgram/cubic meter, versus an IHD HR = 1.01 (95% CI: 1.00, 1.02) per microgram/cubic meter PM2.5 mass, indicated a risk roughly five times higher for coal combustion PM2.5 than for PM2.5 mass in general, on a per microgram/cubic meter PM2.5 basis. Diesel traffic-related elemental carbon (EC) soot was also associated with IHD mortality (HR = 1.03; 95% CI: 1.00, 1.06 per 0.26-µg/m3 EC increase). However, PM2.5 from both wind-blown soil and biomass combustion was not associated with IHD mortality. CONCLUSIONS: Long-term PM2.5 exposures from fossil fuel combustion, especially coal burning but also from diesel traffic, were associated with increases in IHD mortality in this nationwide population. Results suggest that PM2.5-mortality associations can vary greatly by source, and that the largest IHD health benefits per microgram/cubic meter from PM2.5 air pollution control may be achieved via reductions of fossil fuel combustion exposures, especially from coal-burning sources. CITATION: Thurston GD, Burnett RT, Turner MC, Shi Y, Krewski D, Lall R, Ito K, Jerrett M, Gapstur SM, Diver WR, Pope CA III. 2016. Ischemic heart disease mortality and long-term exposure to source-related components of U.S. fine particle air pollution. Environ Health Perspect 124:785-794; http://dx.doi.org/10.1289/ehp.1509777.

Repeated measures of inflammation, blood pressure, and heart rate variability associated with traffic exposures in healthy adults.

BACKGROUND: Previous human exposure studies of traffic-related air pollutants have demonstrated adverse health effects in human populations by comparing areas of high and low traffic, but few studies have utilized microenvironmental monitoring of pollutants at multiple traffic locations while looking at a vast array of health endpoints in the same population. We evaluated inflammatory markers, heart rate variability (HRV), blood pressure, exhaled nitric oxide, and lung function in healthy participants after exposures to varying mixtures of traffic pollutants. METHODS: A repeated-measures, crossover study design was used in which 23 healthy, non-smoking adults had clinical cardiopulmonary and systemic inflammatory measurements taken prior to, immediately after, and 24 hours after intermittent walking for two hours in the summer months along three diverse roadways having unique emission characteristics. Measurements of PM2.5, PM10, black carbon (BC), elemental carbon (EC), and organic carbon (OC) were collected. Mixed effect models were used to assess changes in health effects associated with these specific pollutant classes. RESULTS: Minimal associations were observed with lung function measurements and the pollutants measured. Small decreases in BP measurements and rMSSD, and increases in IL-1ß and the low frequency to high frequency ratio measured in HRV, were observed with increasing concentrations of PM2.5 EC. CONCLUSIONS: Small, acute changes in cardiovascular and inflammation-related effects of microenvironmental exposures to traffic-related air pollution were observed in a group of healthy young adults. The associations were most profound with the diesel-source EC.

The Global Burden of Cancer 2013.

IMPORTANCE: Cancer is among the leading causes of death worldwide. Current estimates of cancer burden in individual countries and regions are necessary to inform local cancer control strategies. OBJECTIVE: To estimate mortality, incidence, years lived with disability (YLDs), years of life lost (YLLs), and disability-adjusted life-years (DALYs) for 28 cancers in 188 countries by sex from 1990 to 2013. EVIDENCE REVIEW: The general methodology of the Global Burden of Disease (GBD) 2013 study was used. Cancer registries were the source for cancer incidence data as well as mortality incidence (MI) ratios. Sources for cause of death data include vital registration system data, verbal autopsy studies, and other sources. The MI ratios were used to transform incidence data to mortality estimates and cause of death estimates to incidence estimates. Cancer prevalence was estimated using MI ratios as surrogates for survival data; YLDs were calculated by multiplying prevalence estimates with disability weights, which were derived from population-based surveys; YLLs were computed by multiplying the number of estimated cancer deaths at each age with a reference life expectancy; and DALYs were calculated as the sum of YLDs and YLLs. FINDINGS: In 2013 there were 14.9 million incident cancer cases, 8.2 million deaths, and 196.3 million DALYs. Prostate cancer was the leading cause for cancer incidence (1.4 million) for men and breast cancer for women (1.8 million). Tracheal, bronchus, and lung (TBL) cancer was the leading cause for cancer death in men and women, with 1.6 million deaths. For men, TBL cancer was the leading cause of DALYs (24.9 million). For women, breast cancer was the leading cause of DALYs (13.1 million). Age-standardized incidence rates (ASIRs) per 100 000 and age-standardized death rates (ASDRs) per 100 000 for both sexes in 2013 were higher in developing vs developed countries for stomach cancer (ASIR, 17 vs 14; ASDR, 15 vs 11), liver cancer (ASIR, 15 vs 7; ASDR, 16 vs 7), esophageal cancer (ASIR, 9 vs 4; ASDR, 9 vs 4), cervical cancer (ASIR, 8 vs 5; ASDR, 4 vs 2), lip and oral cavity cancer (ASIR, 7 vs 6; ASDR, 2 vs 2), and nasopharyngeal cancer (ASIR, 1.5 vs 0.4; ASDR, 1.2 vs 0.3). Between 1990 and 2013, ASIRs for all cancers combined (except nonmelanoma skin cancer and Kaposi sarcoma) increased by more than 10% in 113 countries and decreased by more than 10% in 12 of 188 countries. CONCLUSIONS AND RELEVANCE: Cancer poses a major threat to public health worldwide, and incidence rates have increased in most countries since 1990. The trend is a particular threat to developing nations with health systems that are ill-equipped to deal with complex and expensive cancer treatments. The annual update on the Global Burden of Cancer will provide all stakeholders with timely estimates to guide policy efforts in cancer prevention, screening, treatment, and palliation.

Ambient particulate matter air pollution and cardiopulmonary diseases.

Population exposures to ambient outdoor particulate matter (PM) air pollution have been assessed to represent a major burden on global health. Ambient PM is a diverse class of air pollution, with characteristics and health implications that can vary depending on a host of factors, including a particle's original source of emission or formation. The penetration of inhaled particles into the thorax is dependent on their deposition in the upper respiratory tract during inspiration, which varies with particle size, flow rate and tidal volume, and in vivo airway dimensions. All of these factors can be quite variable from person to person, depending on age, transient illness, cigarette smoke and other short-term toxicant exposures that cause transient bronchoconstriction, and occupational history associated with loss of lung function or cumulative injury. The adverse effects of inhaled PM can result from both short-term (acute) and long-term (chronic) exposures to PM, and can range from relatively minor, such as increased symptoms, to very severe effects, including increased risk of premature mortality and decreased life expectancy from long-term exposure. Control of the most toxic PM components can therefore provide major health benefits, and can help guide the selection of the most human health optimal air quality control and climate change mitigation policy measures. As such, a continued improvement in our understanding of the nature and types of PM that are most dangerous to health, and the mechanism(s) of their respective health effects, is an important public health goal.

Black carbon and particulate matter (PM2.5) concentrations in New York City's subway stations.

The New York City (NYC) subway is the main mode of transport for over 5 million passengers on an average weekday. Therefore, airborne pollutants in the subway stations could have a significant impact on commuters and subway workers. This study looked at black carbon (BC) and particulate matter (PM2.5) concentrations in selected subway stations in Manhattan. BC and PM2.5 levels were measured in real time using a Micro-Aethalometer and a PDR-1500 DataRAM, respectively. Simultaneous samples were also collected on quartz filters for organic and elemental carbon (OC/EC) analysis and on Teflon filters for gravimetric and trace element analysis. In the underground subway stations, mean real time BC concentrations ranged from 5 to 23 µg/m(3), with 1 min average peaks >100 µg/m(3), while real time PM2.5 levels ranged from 35 to 200 µg/m(3). Mean EC levels ranged from 9 to 12.5 µg/m(3). At street level on the same days, the mean BC and PM2.5 concentrations were below 3 and 10 µg/m(3), respectively. This study shows that both BC soot and PM levels in NYC's subways are considerably higher than ambient urban street levels and that further monitoring and investigation of BC and PM subway exposures are warranted.

Spatial analysis of air pollution and mortality in California.

RATIONALE: Although substantial scientific evidence suggests that chronic exposure to ambient air pollution contributes to premature mortality, uncertainties exist in the size and consistency of this association. Uncertainty may arise from inaccurate exposure assessment. OBJECTIVES: To assess the associations of three types of air pollutants (fine particulate matter, ozone [O3], and nitrogen dioxide [NO2]) with the risk of mortality in a large cohort of California adults using individualized exposure assessments. METHODS: For fine particulate matter and NO2, we used land use regression models to derive predicted individualized exposure at the home address. For O3, we estimated exposure with an inverse distance weighting interpolation. Standard and multilevel Cox survival models were used to assess the association between air pollution and mortality. MEASUREMENTS AND MAIN RESULTS: Data for 73,711 subjects who resided in California were abstracted from the American Cancer Society Cancer Prevention II Study cohort, with baseline ascertainment of individual characteristics in 1982 and follow-up of vital status through to 2000. Exposure data were derived from government monitors. Exposure to fine particulate matter, O3, and NO2 was positively associated with ischemic heart disease mortality. NO2 (a marker for traffic pollution) and fine particulate matter were also associated with mortality from all causes combined. Only NO2 had significant positive association with lung cancer mortality. CONCLUSIONS: Using the first individualized exposure assignments in this important cohort, we found positive associations of fine particulate matter, O3, and NO2 with mortality. The positive associations of NO2 suggest that traffic pollution relates to premature death.