Introduction



9144001143000ENVIRONMENTAL HEALTH DISPARITIES ASSOCIATED TO AIR STRESSORS IN ALLEGHENY COUNTY, PENNSYLVANIAbyVarun PatelBS – West Chester University of Pennsylvania, 2015BSc – Maharaja Sayajirao University of Baroda, India, 2010Submitted to the Graduate Faculty ofEnvironmental and Occupational HealthGraduate School of Public Health in partial fulfillment of the requirements for the degree ofMaster of Public HealthUniversity of Pittsburgh201900ENVIRONMENTAL HEALTH DISPARITIES ASSOCIATED TO AIR STRESSORS IN ALLEGHENY COUNTY, PENNSYLVANIAbyVarun PatelBS – West Chester University of Pennsylvania, 2015BSc – Maharaja Sayajirao University of Baroda, India, 2010Submitted to the Graduate Faculty ofEnvironmental and Occupational HealthGraduate School of Public Health in partial fulfillment of the requirements for the degree ofMaster of Public HealthUniversity of Pittsburgh2019center57150UNIVERSITY OF PITTSBURGHGRADUATE SCHOOL OF PUBLIC HEALTHThis essay is submittedbyVarun PatelonMay 6, 2019and approved byEssay Advisor:James Peterson, PhDAssociate ProfessorEnvironmental and Occupational HealthGraduate School of Public HealthUniversity of PittsburghEssay Readers:Shaina Stacy, PhD, MPHPost-Doctoral Scholar EpidemiologyGraduate School of Public HealthUniversity of PittsburghJian-Min Yuan, MD, PhDProfessorEpidemiologyGraduate School of Public HealthUniversity of Pittsburgh00UNIVERSITY OF PITTSBURGHGRADUATE SCHOOL OF PUBLIC HEALTHThis essay is submittedbyVarun PatelonMay 6, 2019and approved byEssay Advisor:James Peterson, PhDAssociate ProfessorEnvironmental and Occupational HealthGraduate School of Public HealthUniversity of PittsburghEssay Readers:Shaina Stacy, PhD, MPHPost-Doctoral Scholar EpidemiologyGraduate School of Public HealthUniversity of PittsburghJian-Min Yuan, MD, PhDProfessorEpidemiologyGraduate School of Public HealthUniversity of Pittsburghcenter4648200Copyright ? by Varun Patel201900Copyright ? by Varun Patel2019Jim Peterson, Ph.D.ENVIRONMENTAL HEALTH DISPARITIES ASSOCIATED TO AIR STRESSORS IN ALLEGHENY COUNTY, PENNSYLVANIAVarun Patel, MPHUniversity of Pittsburgh, 2019ABSTRACTAllegheny County, located in southwestern Pennsylvania, has a rich history of industry that includes glass making, steel production, coal-fired power plants, and mining-associated activities such as coke processing. Facilities related to these industries contribute significantly to air pollution, releasing pollutants such as butadiene, formaldehyde, and acetaldehyde into the air. Coke oven emissions are major air stressors in southeast regions of the county. Coke oven emissions are predominantly released from large ovens used in heating coal to produce coke in steel and iron manufacturing facilities. The emissions are complex mixtures of dust, vapors, and gases that typically include carcinogens such as cadmium and arsenic. In addition, traffic-related pollutants including diesel particulate matter also contribute to poor air quality. Spatial associations between cancer incidence and mortality with air pollution are well studied in several cities in the United States and around the world. However, this study is an attempt to examine the association at a smaller scale i.e., census tract level of Allegheny County. For this study, we used United States Census data, the Pennsylvania Cancer Registry, and the Environmental Protection Agency’s (EPA) National Air Toxic Release Assessment (NATA) data for geospatial analysis at the census tract level for Allegheny County. Spatial analysis was used to investigate the association between ambient concentrations of air toxics, lung cancer incidence (N = 6,435) and socioeconomic status (SES) (race/ethnicity and income) in the county from 2010-2015. ArcGIS and QGIS were used to create interactive maps, and GeoDa was used to examine spatial and statistical relationships. We used global and local measures of spatial autocorrelation (Moran’s I) to identify clusters of tracts where lung cancer incidence was significantly higher. We identified a few local “hotspots” of higher cancer incidence. We also found SES positively related to lung cancer incidence as well as ambient levels of certain air toxics. This study revealed associations between lung cancer risk and environmental exposures and identified vulnerable communities where future resources could be allocated to help reduce the disproportionate public health burden.TABLE OF CONTENTSIntroduction……………………………………………………………………………...01Pollutants1,3-Butadiene………………………….………………………………………………...04Acetaldehyde and Formaldehyde……….…………………………………………...…04Benzene………………………………………………………………………….………06Chloroform……………………………………………………………………….….….06Coke Oven Emissions.…………………….…………………………………...………..07Diesel PM………………………………………………………………………………..08Ethylbenzene……………………………………………………………………………09Trichlorethylene……………………………………………………………...................09MATERIALS AND METHODSStudy Population……………………………………..……………………..…………..11Cancer Incidences…………………………………………………………….………...11Environmental Exposure…………………………….…………..……….….…………12Toxic Release Inventory……………………………….…………………….………….13Environmental Justice………………………..……….…………………….………….13Geospatial and Statistical Analysis…………………….……………………………....14RESULTS……………………………………………………………………………………….17CONCLUSION……………………………………………………………………...………….25BIBLIOGRAPHY………………………………………………………………………………27 TOC \o "2-4" \h \z \t "Heading 1,1,Appendix,1,Heading,1" List of tablesTable 1: Distribution of air pollution concentration (?g/m3) in Allegheny County……...……...12Table 2: Descriptive statistics for cancer incidence rates by race, gender, age and SES index…....20Table 3: Association of lung cancer incidence rate adjusted with SES…………………………...21Table 4: Association of exposure to pollutants and lung cancer variables adjusted for SES……...23Table 5: Association of lung cancer and SES, adjusted for Coke Oven Emissions and TCE…......24List of figuresFigure 1: Moran’s I…………………………………………………………….…………………15Figure 2: Toxic Release Sites and EJ Tracts in Allegheny County……………...………………...17Figure 3: Lung Cancer Rates in African Americans in Allegheny County (2010 – 2015)………...18Figure 4: Local Clusters for Each Pollutant………………………………………………….…...19Figure 5: Local Clusters for Total Lung Cancer Incidence Rates……………………………...….20IntroductionCancer is the second leading cause of deaths, which influences a significant public health problem in the United States and across the world. In 2015, the total number of cancer related deaths were 595,930 (22%) out of 2,712,630 deaths and 598,038 (22%) out of 2,744,248 deaths in 2016 in the United States. In 2019, The American Cancer Society estimates 1,762,450 new cancer cases and 606,880 cancer-related deaths in the United States ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.3322/caac.21551","ISSN":"00079235","author":[{"dropping-particle":"","family":"Siegel","given":"Rebecca L.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Miller","given":"Kimberly D.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Jemal","given":"Ahmedin","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"CA: A Cancer Journal for Clinicians","id":"ITEM-1","issue":"1","issued":{"date-parts":[["2019","1","1"]]},"page":"7-34","publisher":"American Cancer Society","title":"Cancer statistics, 2019","type":"article-journal","volume":"69"},"uris":[""]}],"mendeley":{"formattedCitation":"(Siegel, Miller, & Jemal, 2019a)","plainTextFormattedCitation":"(Siegel, Miller, & Jemal, 2019a)","previouslyFormattedCitation":"(Siegel, Miller, & Jemal, 2019a)"},"properties":{"noteIndex":0},"schema":""}(Siegel, Miller, & Jemal, 2019a). Similarly, cancer is also a leading cause of death in Pennsylvania. In 2011, over 77,000 people had a diagnosis of invasive cancer and approximately 28,500 died of cancer ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"Pennsylvania Department of Health","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2015"]]},"title":"The Burden of Cancer in Pennsylvania","type":"article"},"uris":[""]}],"mendeley":{"formattedCitation":"(Pennsylvania Department of Health, 2015)","plainTextFormattedCitation":"(Pennsylvania Department of Health, 2015)","previouslyFormattedCitation":"(Pennsylvania Department of Health, 2015)"},"properties":{"noteIndex":0},"schema":""}(Pennsylvania Department of Health, 2015). A total 79,890 new cases for selected cancers are projected in 2019 in Pennsylvania. ?Beyond new diagnoses each year and the number of lives lost, cancer also inflicts a great financial and emotional burden on cancer patients and their loved ones. The estimated national expenditure for cancer care in 2017 was $147.3 billion in the United States ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"URL":"","accessed":{"date-parts":[["2019","3","23"]]},"author":[{"dropping-particle":"","family":"National Institutes of Health","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2018"]]},"title":"Cancer Statistics","type":"webpage"},"uris":[""]}],"mendeley":{"formattedCitation":"(National Institutes of Health, 2018)","plainTextFormattedCitation":"(National Institutes of Health, 2018)","previouslyFormattedCitation":"(National Institutes of Health, 2018)"},"properties":{"noteIndex":0},"schema":""}(National Institutes of Health, 2018). In 2010, the estimated cancer cost was $7.3 billion in Pennsylvania.Ambient air pollution has various effects on human health including cancer, cardiovascular diseases, and other non-cancerous acute and chronic diseases ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1021/es072042u","ISSN":"0013936X","abstract":"Air toxics are of particular concern in Greater Houston, home to one of the world's largest petrochemical complexes and a quarter ofthe nation's refining capacity. Much of this complex lies along a navigable ship channel that flows 50 miles from east of the central business district through Galveston Bay and into the Gulf of Mexico. Numerous communities, including both poor and affluent neighborhoods, are located in close proximity to the 200 facilities along this channel. Our aim is to examine the spatial distribution of cumulative, air-pollution-related cancer risks in Houston and Harris County, with particular emphasis on identifying ethnic, economic, and social disparities. We employ exposure estimates from NATA-1999 and census data to assess whether the cumulative cancer risks from air toxics in Houston (and Harris County) fall disproportionately on certain ethnicities and on the socially and economically disadvantaged. The cancer risk burden across Harris County census tracts increases with the proportion of residents who are Hispanic and with key indicators of relative social disadvantage. Aggregate disadvantage grows at each higher level of cancer risk. The highest cancer risk in Harris County is concentrated along a corridor flanking the ship channel. These high-risk neighborhoods, however, vary markedly in relative disadvantage, as well as in emission source mix. Much of the risk they face appears to be driven by only a few hazardous air pollutants. Results provide evidence of risk disparities from hazardous air pollution based on ethnicity and social disadvantage. At the highest levels of risk the pattern is more complex, arguing for a neighborhood level of analysis, especially when proximity to high-emissions industries is a substantial contributor to cumulative cancer risk.","author":[{"dropping-particle":"","family":"Linder","given":"Stephen H.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Marko","given":"Dritana","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ken","given":"Sexton","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Environmental Science and Technology","id":"ITEM-1","issue":"12","issued":{"date-parts":[["2008"]]},"page":"4312-4322","title":"Cumulative cancer risk from air pollution in houston: Disparities in risk burden and social disadvantage","type":"article-journal","volume":"42"},"uris":[""]}],"mendeley":{"formattedCitation":"(Linder, Marko, & Ken, 2008)","plainTextFormattedCitation":"(Linder, Marko, & Ken, 2008)","previouslyFormattedCitation":"(Linder, Marko, & Ken, 2008)"},"properties":{"noteIndex":0},"schema":""}(Linder, Marko, & Ken, 2008). More than 30% of cancers may be preventable by lowering ambient air pollution exposure levels, changing lifestyle factors, and with advanced screening technologies to detect cancer at early stages ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"Pennsylvania Department of Health","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2015"]]},"title":"The Burden of Cancer in Pennsylvania","type":"article"},"uris":[""]}],"mendeley":{"formattedCitation":"(Pennsylvania Department of Health, 2015)","plainTextFormattedCitation":"(Pennsylvania Department of Health, 2015)","previouslyFormattedCitation":"(Pennsylvania Department of Health, 2015)"},"properties":{"noteIndex":0},"schema":""}(Pennsylvania Department of Health, 2015). ?Socioeconomic factors such as poverty, inadequate education, lack of health insurance, and location of residence are equally important as biological factors of cancer ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.3322/canjclin.54.2.78","ISSN":"0007-9235","PMID":"15061598","abstract":"This article highlights disparities in cancer incidence, mortality, and survival in relation to race/ethnicity, and census data on poverty in the county or census tract of residence. The incidence and survival data derive from the National Cancer Institute's (NCI) Surveillance, Epidemiology, and End Results (SEER) Program; mortality data are from the National Center for Health Statistics (NCHS); data on the prevalence of major cancer risk factors and cancer screening are from the National Health Interview Survey (NHIS) conducted by NCHS. For all cancer sites combined, residents of poorer counties (those with greater than or equal to 20% of the population below the poverty line) have 13% higher death rates from cancer in men and 3% higher rates in women compared with more affluent counties (less than 10% below the poverty line). Differences in cancer survival account for part of this disparity. Among both men and women, five-year survival for all cancers combined is 10 percentage points lower among persons who live in poorer than in more affluent census tracts. Even when census tract poverty rate is accounted for, however, African American, American Indian/Alaskan Native, and Asian/Pacific Islander men and African American and American Indian/Alaskan Native women have lower five-year survival than non-Hispanic Whites. More detailed analyses of selected cancers show large variations in cancer survival by race and ethnicity. Opportunities to reduce cancer disparities exist in prevention (reductions in tobacco use, physical inactivity, and obesity), early detection (mammography, colorectal screening, Pap tests), treatment, and palliative care.","author":[{"dropping-particle":"","family":"Ward","given":"Elizabeth","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Jemal","given":"Ahmedin","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Cokkinides","given":"Vilma","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Singh","given":"Gopal K.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Cardinez","given":"Cheryll","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ghafoor","given":"Asma","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Thun","given":"Michael","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"CA: a cancer journal for clinicians","id":"ITEM-1","issue":"2","issued":{"date-parts":[["2004","3","1"]]},"page":"78-93","publisher":"American Cancer Society","title":"Cancer disparities by race/ethnicity and socioeconomic status.","type":"article-journal","volume":"54"},"uris":[""]}],"mendeley":{"formattedCitation":"(Ward et al., 2004)","plainTextFormattedCitation":"(Ward et al., 2004)","previouslyFormattedCitation":"(Ward et al., 2004)"},"properties":{"noteIndex":0},"schema":""}(Ward et al., 2004). It is well documented that disadvantaged populations are more likely to have cancer than affluent populations (cite). ?For all cancer sites combined, residents of poorer areas (those with greater than or equal to 20% of the population below the poverty line) have 13% higher death rates from cancer in men and 3% higher rates in women compared with more affluent areas (less than 10% below the poverty line) ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.3322/canjclin.54.2.78","ISSN":"0007-9235","PMID":"15061598","abstract":"This article highlights disparities in cancer incidence, mortality, and survival in relation to race/ethnicity, and census data on poverty in the county or census tract of residence. The incidence and survival data derive from the National Cancer Institute's (NCI) Surveillance, Epidemiology, and End Results (SEER) Program; mortality data are from the National Center for Health Statistics (NCHS); data on the prevalence of major cancer risk factors and cancer screening are from the National Health Interview Survey (NHIS) conducted by NCHS. For all cancer sites combined, residents of poorer counties (those with greater than or equal to 20% of the population below the poverty line) have 13% higher death rates from cancer in men and 3% higher rates in women compared with more affluent counties (less than 10% below the poverty line). Differences in cancer survival account for part of this disparity. Among both men and women, five-year survival for all cancers combined is 10 percentage points lower among persons who live in poorer than in more affluent census tracts. Even when census tract poverty rate is accounted for, however, African American, American Indian/Alaskan Native, and Asian/Pacific Islander men and African American and American Indian/Alaskan Native women have lower five-year survival than non-Hispanic Whites. More detailed analyses of selected cancers show large variations in cancer survival by race and ethnicity. Opportunities to reduce cancer disparities exist in prevention (reductions in tobacco use, physical inactivity, and obesity), early detection (mammography, colorectal screening, Pap tests), treatment, and palliative care.","author":[{"dropping-particle":"","family":"Ward","given":"Elizabeth","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Jemal","given":"Ahmedin","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Cokkinides","given":"Vilma","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Singh","given":"Gopal K.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Cardinez","given":"Cheryll","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ghafoor","given":"Asma","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Thun","given":"Michael","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"CA: a cancer journal for clinicians","id":"ITEM-1","issue":"2","issued":{"date-parts":[["2004","3","1"]]},"page":"78-93","publisher":"American Cancer Society","title":"Cancer disparities by race/ethnicity and socioeconomic status.","type":"article-journal","volume":"54"},"uris":[""]}],"mendeley":{"formattedCitation":"(Ward et al., 2004)","plainTextFormattedCitation":"(Ward et al., 2004)","previouslyFormattedCitation":"(Ward et al., 2004)"},"properties":{"noteIndex":0},"schema":""}(Ward et al., 2004). The association of specific cancer prevalence and cancer mortality varies at individual or area levels. ?The major behavioral determinants of cancer (e.g., smoking, diet, alcohol use, obesity, physical inactivity, reproductive behavior), occupational and environmental exposures, and cancer screening are themselves substantially influenced by individual and area-based socioeconomic factors ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1155/2011/107497","ISSN":"16878558","PMID":"22496688","abstract":"We analyzed socioeconomic, rural-urban, and racial inequalities in US mortality from all cancers, lung, colorectal, prostate, breast, and cervical cancers. A deprivation index and rural-urban continuum were linked to the 2003–2007 county-level mortality data. Mortality rates and risk ratios were calculated for each socioeconomic, rural-urban, and racial group. Weighted linear regression yielded relative impacts of deprivation and rural-urban residence. Those in more deprived groups and rural areas had higher cancer mortality than more affluent and urban residents, with excess risk being marked for lung, colorectal, prostate, and cervical cancers. Deprivation and rural-urban continuum were independently related to cancer mortality, with deprivation showing stronger impacts. Socioeconomic inequalities existed for both whites and blacks, with blacks experiencing higher mortality from each cancer than whites within each deprivation group. Socioeconomic gradients in mortality were steeper in nonmetropolitan than in metropolitan areas. Mortality disparities may reflect inequalities in smoking and other cancer-risk factors, screening, and treatment.","author":[{"dropping-particle":"","family":"Singh","given":"Gopal K.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Williams","given":"Shanita D.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Siahpush","given":"Mohammad","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Mulhollen","given":"Aaron","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Journal of Cancer Epidemiology","id":"ITEM-1","issued":{"date-parts":[["2011"]]},"title":"Socioeconomic, rural-urban, and racial inequalities in US cancer mortality: Part I-All cancers and lung cancer and part II-Colorectal, prostate, breast, and cervical cancers","type":"article-journal","volume":"2011"},"uris":[""]}],"mendeley":{"formattedCitation":"(Singh, Williams, Siahpush, & Mulhollen, 2011)","plainTextFormattedCitation":"(Singh, Williams, Siahpush, & Mulhollen, 2011)","previouslyFormattedCitation":"(Singh, Williams, Siahpush, & Mulhollen, 2011)"},"properties":{"noteIndex":0},"schema":""}(Singh, Williams, Siahpush, & Mulhollen, 2011). Poor families tend to live close to industrial areas because they cannot afford to live in the suburbs. It is also likely that some of these family members are employed at manufacturing facilities. Thus, their exposure is significantly higher than those living far from these facilities. Poor housing also plays a major role in terms of exposure to carcinogens such as asbestoses and heavy metals such as lead ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1093/bmp/ldg023","ISSN":"1471-8391","abstract":"Environmental carcinogens, in a strict sense, include outdoor and indoor air pollutants, as well as soil and drinking water contaminants. An increased risk of mesothelioma has consistently been detected among individuals experiencing residential exposure to asbestos, whereas results for lung cancer are less consistent. At least 14 good-quality studies have investigated lung cancer risk from outdoor air pollution based on measurement of specific agents. Their results tend to show an increased risk in the categories at highest exposure, with relative risks in the range 1.5–2.0, which is not attributable to confounders. Results for other cancers are sparse. A causal association has been established between exposure to environmental tobacco smoke and lung cancer, with a relative risk in the order of 1.2. Radon is another carcinogen present in indoor air which may be responsible for 1% of all lung cancers. In several Asian populations, an increased risk of lung cancer is present in women from indoor pollution from cooking and heating. There is strong evidence of an increased risk of bladder, skin and lung cancers following consumption of water with high arsenic contamination; results for other drinking water contaminants, including chlorination by-products, are inconclusive. A precise quantification of the burden of human cancer attributable to environmental exposure is problematic. However, despite the relatively small relative risks of cancer following exposure to environmental carcinogens, the number of cases that might be caused, assuming a causal relationship, is relatively large, as a result of the high prevalence of exposure.","author":[{"dropping-particle":"","family":"Boffetta","given":"Paolo","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Nyberg","given":"Fredrik","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"British Medical Bulletin","id":"ITEM-1","issue":"1","issued":{"date-parts":[["2003","12","1"]]},"page":"71-94","publisher":"Narnia","title":"Contribution of environmental factors to cancer risk","type":"article-journal","volume":"68"},"uris":[""]}],"mendeley":{"formattedCitation":"(Boffetta & Nyberg, 2003)","plainTextFormattedCitation":"(Boffetta & Nyberg, 2003)","previouslyFormattedCitation":"(Boffetta & Nyberg, 2003)"},"properties":{"noteIndex":0},"schema":""}(Boffetta & Nyberg, 2003). Air pollution is a complex mixture of particulate matter and gaseous compounds. Outdoor air pollution consists of particulate matter (PM), nitrogen oxides (NOx), ozone, sulfur oxides (SOx), diesel exhaust, carbon dioxide (NO2), carbon monoxide (NO) and coke oven emissions. Some pollutants such as acetaldehyde, benzene, butadiene, formaldehyde, and trichloroethylene are present at various levels in the environment. These pollutants predominantly release from refineries, steel manufacturing facilities, power plants, glass manufacturing factories and fuel combustion in automobiles ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1016/j.mrrev.2007.08.003","ISSN":"13835742","abstract":"Combustion emissions account for over half of the fine particle (PM2.5) air pollution and most of the primary particulate organic matter. Human exposure to combustion emissions including the associated airborne fine particles and mutagenic and carcinogenic constituents (e.g., polycyclic aromatic compounds (PAC), nitro-PAC) have been studied in populations in Europe, America, Asia, and increasingly in third-world counties. Bioassay-directed fractionation studies of particulate organic air pollution have identified mutagenic and carcinogenic polycyclic aromatic hydrocarbons (PAH), nitrated PAH, nitro-lactones, and lower molecular weight compounds from cooking. A number of these components are significant sources of human exposure to mutagenic and carcinogenic chemicals that may also cause oxidative and DNA damage that can lead to reproductive and cardiovascular effects. Chemical and physical tracers have been used to apportion outdoor and indoor and personal exposures to airborne particles between various combustion emissions and other sources. These sources include vehicles (e.g., diesel and gasoline vehicles), heating and power sources (e.g., including coal, oil, and biomass), indoor sources (e.g., cooking, heating, and tobacco smoke), as well as secondary organic aerosols and pollutants derived from long-range transport. Biomarkers of exposure, dose and susceptibility have been measured in populations exposed to air pollution combustion emissions. Biomarkers have included metabolic genotype, DNA adducts, PAH metabolites, and urinary mutagenic activity. A number of studies have shown a significant correlation of exposure to PM2.5 with these biomarkers. In addition, stratification by genotype increased this correlation. New multivariate receptor models, recently used to determine the sources of ambient particles, are now being explored in the analysis of human exposure and biomarker data. Human studies of both short- and long-term exposures to combustion emissions and ambient fine particulate air pollution have been associated with measures of genetic damage. Long-term epidemiologic studies have reported an increased risk of all causes of mortality, cardiopulmonary mortality, and lung cancer mortality associated with increasing exposures to air pollution. Adverse reproductive effects (e.g., risk for low birth weight) have also recently been reported in Eastern Europe and North America. Although there is substantial evidence that PAH or substituted PAH ma…","author":[{"dropping-particle":"","family":"Lewtas","given":"Joellen","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Mutation Research - Reviews in Mutation Research","id":"ITEM-1","issue":"1-3","issued":{"date-parts":[["2007"]]},"page":"95-133","title":"Air pollution combustion emissions: Characterization of causative agents and mechanisms associated with cancer, reproductive, and cardiovascular effects","type":"article-journal","volume":"636"},"uris":[""]},{"id":"ITEM-2","itemData":{"DOI":"10.1289/ehp.94102s4187","ISSN":"0091-6765","PMID":"7529702","abstract":"Epidemiological studies on the effect of urban air pollution on lung cancer were surveyed. Overall, the studies from many countries point to a smoking-adjusted risk in urban areas over countryside areas that is higher by a factor of up to 1.5. The extent to which urban air pollution contributes to this excess remains unknown. Studies on diesel-exposed occupational groups show that urban air pollution may have a causative role in lung cancer. Model calculations on unit risk factors of known human carcinogens were carried out to rank carcinogens according to their current ambient air concentrations.","author":[{"dropping-particle":"","family":"Hemminki","given":"K","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Pershagen","given":"G","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Environmental health perspectives","id":"ITEM-2","issue":"Suppl 4","issued":{"date-parts":[["1994","10"]]},"page":"187-92","publisher":"National Institute of Environmental Health Science","title":"Cancer risk of air pollution: epidemiological evidence.","type":"article-journal","volume":"102 Suppl "},"uris":[""]},{"id":"ITEM-3","itemData":{"DOI":"10.1289/ehp.7751","ISSN":"0091-6765","PMID":"16140630","abstract":"We extended our previous analyses of term low birth weight (LBW) and preterm birth to 1994-2000, a period of declining air pollution levels in the South Coast Air Basin. We speculated that the effects we observed previously for carbon monoxide, particulate matter < 10 microm in aerodynamic diameter (PM10), and traffic density were attributable to toxins sorbed to primary exhaust particles. Focusing on CO, PM10, and particulate matter < 2.5 microm in aerodynamic diameter (PM2.5), we examined whether varying residential distances from monitoring stations affected risk estimates, because effect attenuation may result from local pollutant heterogeneity inadequately captured by ambient stations. We geocoded home locations, calculated the distance to the nearest air monitors, estimated exposure levels by pregnancy period, and performed logistic regression analyses for subjects living within 1-4 mi of a station. For women residing within a 1-mi distance, we observed a 27% increase in risk for high (> or = 75th percentile) first-trimester CO exposures and preterm birth and a 36% increase for high third-trimester pregnancy CO exposures and term LBW. For particles, we observed similar size effects during early and late pregnancy for both term LBW and preterm birth. In contrast, smaller or no effects were observed beyond a 1-mi distance of a residence from a station. Associations between CO and PM10 averaged over the whole pregnancy and term LBW were generally smaller than effects for early and late pregnancy. These new results for 1994-2000 generally confirm our previous observations for the period 1989-1993, again linking CO and particle exposures to term LBW and preterm birth. In addition, they confirm our suspicions about having to address local heterogeneity for these pollutants in Los Angeles.","author":[{"dropping-particle":"","family":"Wilhelm","given":"Michelle","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ritz","given":"Beate","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Environmental health perspectives","id":"ITEM-3","issue":"9","issued":{"date-parts":[["2005","9"]]},"page":"1212-21","publisher":"National Institute of Environmental Health Science","title":"Local variations in CO and particulate air pollution and adverse birth outcomes in Los Angeles County, California, USA.","type":"article-journal","volume":"113"},"uris":[""]}],"mendeley":{"formattedCitation":"(Hemminki & Pershagen, 1994; Lewtas, 2007; Wilhelm & Ritz, 2005)","plainTextFormattedCitation":"(Hemminki & Pershagen, 1994; Lewtas, 2007; Wilhelm & Ritz, 2005)","previouslyFormattedCitation":"(Hemminki & Pershagen, 1994; Lewtas, 2007; Wilhelm & Ritz, 2005)"},"properties":{"noteIndex":0},"schema":""}(Hemminki & Pershagen, 1994; Lewtas, 2007; Wilhelm & Ritz, 2005). Three major factors are responsible for many cancers: 1) DNA mutations, which initiate during stem cell replication or are induced by environmental factors, 2) hereditary, and 3) unknown (or a combination of both) factors ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1126/science.1260825","abstract":"Some tissue types give rise to human cancers millions of times more often than other tissue types. Although this has been recognized for more than a century, it has never been explained. Here, we show that the lifetime risk of cancers of many different types is strongly correlated (0.81) with the total number of divisions of the normal self-renewing cells maintaining that tissue's homeostasis. These results suggest that only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to \"bad luck,\" that is, random mutations arising during DNA replication in normal, noncancerous stem cells. This is important not only for understanding the disease but also for designing strategies to limit the mortality it causes. Extreme variation in cancer incidence across different tissues is well known; for example, the lifetime risk of being diagnosed with cancer is 6.9% for lung, 1.08% for thyroid, 0.6% for brain and the rest of the nervous system, 0.003% for pelvic bone and 0.00072% for laryngeal cartilage (1-3). Some of these differences are associated with well-known risk factors such as smoking, alcohol use, ultraviolet light, or human papilloma virus (HPV) (4,5), but this applies only to specific populations exposed to potent mutagens or viruses. And such exposures cannot explain why cancer risk in tissues within the alimentary tract can differ by as much as a factor of 24 [esophagus (0.51%), large intestine (4.82%), small intestine (0.20%), and stomach (0.86%)] (3). Moreover, cancers of the small intestinal epithelium are three times less common than brain tumors (3), even though small intestinal epithelial cells are exposed to much higher levels of environmental mutagens than are cells within the brain, which are protected by the blood-brain barrier. Another well-studied contributor to cancer is inherited genetic variation. However, only 5 to 10% of cancers have a heritable component (6-8), and even when hereditary factors in predisposed individuals can be identified, the way in which these factors contribute to * Corresponding","author":[{"dropping-particle":"","family":"Tomasetti","given":"Cristian","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Vogelstein","given":"Bert","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Science","id":"ITEM-1","issue":"6217","issued":{"date-parts":[["2015"]]},"page":"78-81","title":"Variation in cancer risk among tissues can be explained by the number of stem cell divisions HHS Public Access","type":"article-journal","volume":"347"},"uris":[""]}],"mendeley":{"formattedCitation":"(Tomasetti & Vogelstein, 2015)","plainTextFormattedCitation":"(Tomasetti & Vogelstein, 2015)","previouslyFormattedCitation":"(Tomasetti & Vogelstein, 2015)"},"properties":{"noteIndex":0},"schema":""}(Tomasetti & Vogelstein, 2015). Environmental factors include physical and chemical, behavioral, and social components. Physical and chemical components such as air pollution from various industries, automobile exhaust, water, and food contamination; behavioral components such as smoking, unhealthy diet and lack of exercise; and social components such as poverty, occupation, and lack of education could play a huge role in cancer epidemiology. The aim of this paper is to discuss the environmental risk factors of lung cancer accounting for socioeconomic factors. Ultrafine particles (UFP) of engine exhaust or diesel PM has attracted a great deal of focus because of toxicological associations to morbidity and mortality of chronic diseases including cancer ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1093/aje/kwj343","ISSN":"00029262","abstract":"Pollution from motor vehicles constitutes a major environmental health problem. The present paper describes associations between diesel and gasoline engine emissions and lung cancer, as evidenced in a 1979–1985 population-based case-control study in Montreal, Canada. Cases were 857 male lung cancer patients. Controls were 533 population controls and 1,349 patients with other cancer types. Subjects were interviewed to obtain a detailed lifetime job history and relevant data on potential confounders. Industrial hygienists translated each job description into indices of exposure to several agents, including engine emissions. There was no evidence of excess risks of lung cancer with exposure to gasoline exhaust. For diesel engine emissions, results differed by control group. When cancer controls were considered, there was no excess risk. When population controls were studied, the odds ratios, after adjustments for potential confounders, were 1.2 (95% confidence interval: 0.8, 1.8) for any exposure and 1.6 (95% confidence interval: 0.9, 2.8) for substantial exposure. Confidence intervals between risk estimates derived from the two control groups overlapped considerably. These results provide some limited support for the hypothesis of an excess lung cancer risk due to diesel exhaust but no support for an increase in risk due to gasoline exhaust.","author":[{"dropping-particle":"","family":"Parent","given":"Marie ?lise","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Rousseau","given":"Marie Claude","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Boffetta","given":"Paolo","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Cohen","given":"Aaron","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Siemiatycki","given":"Jack","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"American Journal of Epidemiology","id":"ITEM-1","issue":"1","issued":{"date-parts":[["2007"]]},"page":"53-62","title":"Exposure to diesel and gasoline engine emissions and the risk of lung cancer","type":"article-journal","volume":"165"},"uris":[""]},{"id":"ITEM-2","itemData":{"DOI":"10.1136/oemed-2016-104197","ISSN":"1351-0711","author":[{"dropping-particle":"","family":"Silverman","given":"Debra T","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Occupational and Environmental Medicine","id":"ITEM-2","issue":"4","issued":{"date-parts":[["2017"]]},"page":"233-234","title":"Diesel exhaust causes lung cancer: now what?","type":"article-journal","volume":"74"},"uris":[""]}],"mendeley":{"formattedCitation":"(Parent, Rousseau, Boffetta, Cohen, & Siemiatycki, 2007; Silverman, 2017)","plainTextFormattedCitation":"(Parent, Rousseau, Boffetta, Cohen, & Siemiatycki, 2007; Silverman, 2017)","previouslyFormattedCitation":"(Parent, Rousseau, Boffetta, Cohen, & Siemiatycki, 2007; Silverman, 2017)"},"properties":{"noteIndex":0},"schema":""}(Parent, Rousseau, Boffetta, Cohen, & Siemiatycki, 2007; Silverman, 2017). Pollutants such as particulate matter, diesel and coke oven emissions can generate reactive oxygen species (ROS) that increase risk due to their toxicological mechanism to cause oxidative stress in the body. ?Oxidative stress is typically assessed as elevated levels of oxidized biomolecules, e.g. oxidative DNA damage, which is relevant for carcinogenesis ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1093/carcin/bgh353","ISBN":"26/3/613/2390818","ISSN":"01433334","abstract":"Air pollution, containing high-level of ultrafine particles (UFP) and benzene, is a prominent environmental health problem in many cities of the World. We investigated the level of oxidative DNA damage in mononuclear blood cells (MNBC) by the comet assay as DNA strand breaks (SB) and formamidopyrimidine DNA glycosylase (FPG) sensitive sites in residents from three urban locations in Cotonou, Benin (taxi-moto drivers, subjects living near roads with intense traffic and suburban residents) and rural residents. Exposure was characterized by urinary excretion of S-phenylmercapturic acid (S-PMA), a biomarker of benzene exposure, and by ambient UFP. There were clear stepwise gradients with respect to ambient UFP, S-PMA excretion and oxidative DNA damage with rural subjects < suburban subjects < residents living near highly trafficed roads<taxi-moto drivers. Polymorphisms in glutathione peroxidase (GPX), NAD(P)H:quinone oxidoreductase 1 (NQO1) and glutathione S-transferase (GST) genes were assessed for effect modification. Subjects with GSTT1 null genotype had lower urinary S-PMA excretion than subjects carrying the plus genotype. Urinary S-PMA excretion correlated with SB (R = 0.17) and FPG sites (R = 0.25) in MNBC. The correlation between S-PMA and SB was strongest in subjects with NQO1*1/*2 and *2/*2 genotypes (R = 0.37), and between S-PMA and FPG sensitive sites in subjects with the GSTP1*B/*B genotype (R = 0.39). In conclusion, this study shows that urban air with high levels of benzene and UFP is associated with elevated levels of SB and FPG sites in MNBC, and that NQO1 and GST genes may modulate the effect.","author":[{"dropping-particle":"","family":"Avogbe","given":"Patrice H","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ayi-Fanou","given":"Lucie","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Autrup","given":"Herman","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Loft","given":"Steffen","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Fayomi","given":"Benjamin","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Sanni","given":"Ambaliou","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Vinzents","given":"Peter","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"M?ller","given":"Peter","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Carcinogenesis","id":"ITEM-1","issue":"3","issued":{"date-parts":[["2005"]]},"page":"613-620","title":"Ultrafine particulate matter and high-level benzene urban air pollution in relation to oxidative DNA damage","type":"article-journal","volume":"26"},"uris":[""]}],"mendeley":{"formattedCitation":"(Avogbe et al., 2005)","plainTextFormattedCitation":"(Avogbe et al., 2005)","previouslyFormattedCitation":"(Avogbe et al., 2005)"},"properties":{"noteIndex":0},"schema":""}(Avogbe et al., 2005). It has been reported that toxic effects of ROS on human cells may end in oxidative injury leading to programmed cell death i.e. apoptosis ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"ISBN":"9102572237363","abstract":"Free radicals are common outcome of normal aerobic cellular metabolism. In-built antioxidant system of body plays its decisive role in prevention of any loss due to free radicals. However, imbalanced defense mechanism of antioxi-dants, overproduction or incorporation of free radicals from environment to living system leads to serious penalty leading to neuro-degeneration. Neural cells suffer functional or sensory loss in neurodegenerative diseases. Apart from several other environmental or genetic factors, oxidative stress (OS) leading to free radical attack on neural cells contributes calamitous role to neuro-degeneration. Though, oxygen is imperative for life, imbalanced metabolism and excess reactive oxygen species (ROS) generation end into a range of disorders such as Alzheimer's disease, Parkinson's disease, aging and many other neural disorders. Toxicity of free radicals contributes to proteins and DNA injury, inflammation, tissue damage and subsequent cellular apoptosis. Antioxidants are now being looked upon as persuasive therapeutic against solemn neuronal loss, as they have capability to combat by neutralizing free radicals. Diet is major source of antioxidants, as well as medicinal herbs are catching attention to be commercial source of antioxidants at present. Recognition of upstream and downstream antioxidant therapy to oxidative stress has been proved an effective tool in alteration of any neuronal damage as well as free radical scavenging. Antioxidants have a wide scope to sequester metal ions involved in neuronal plaque formation to prevent oxidative stress. In addition, antioxidant therapy is vital in scavenging free radicals and ROS preventing neuronal degeneration in post-oxidative stress scenario.","author":[{"dropping-particle":"","family":"Uttara","given":"Bayani","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"V","family":"Singh","given":"Ajay","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Zamboni","given":"Paolo","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Mahajan","given":"R T","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Current Neuropharmacology","id":"ITEM-1","issued":{"date-parts":[["2009"]]},"number-of-pages":"65-74","title":"Oxidative Stress and Neurodegenerative Diseases: A Review of Upstream and Downstream Antioxidant Therapeutic Options","type":"report","volume":"7"},"uris":[""]}],"mendeley":{"formattedCitation":"(Uttara, Singh, Zamboni, & Mahajan, 2009)","plainTextFormattedCitation":"(Uttara, Singh, Zamboni, & Mahajan, 2009)","previouslyFormattedCitation":"(Uttara, Singh, Zamboni, & Mahajan, 2009)"},"properties":{"noteIndex":0},"schema":""}(Uttara, Singh, Zamboni, & Mahajan, 2009).The complexity of air pollution often makes it harder to determine one or two pollutants as causative factors for a specific health problem. Prior epidemiological studies at the county level have established an association between air pollution and different kinds of cancers, mainly lung cancer ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"Martien","given":"Philip","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ph","given":"D","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Lau","given":"Virginia","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Tanrikulu","given":"Saffet","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ph","given":"D","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issue":"March","issued":{"date-parts":[["2014"]]},"title":"Identifying Areas with Cumulative Impacts from Air Pollution in the San Francisco Bay Area","type":"article-journal"},"uris":[""]},{"id":"ITEM-2","itemData":{"DOI":"10.1001/jama.287.9.1132","ISSN":"0098-7484","abstract":"ContextAssociations have been found between day-to-day particulate air pollution\nand increased risk of various adverse health outcomes, including cardiopulmonary\nmortality. However, studies of health effects of long-term particulate air\npollution have been less conclusive.ObjectiveTo assess the relationship between long-term exposure to fine particulate\nair pollution and all-cause, lung cancer, and cardiopulmonary mortality.Design, Setting, and ParticipantsVital status and cause of death data were collected by the American\nCancer Society as part of the Cancer Prevention II study, an ongoing prospective\nmortality study, which enrolled approximately 1.2 million adults in 1982.\nParticipants completed a questionnaire detailing individual risk factor data\n(age, sex, race, weight, height, smoking history, education, marital status,\ndiet, alcohol consumption, and occupational exposures). The risk factor data\nfor approximately 500?000 adults were linked with air pollution data\nfor metropolitan areas throughout the United States and combined with vital\nstatus and cause of death data through December 31, 1998.Main Outcome MeasureAll-cause, lung cancer, and cardiopulmonary mortality.ResultsFine particulate and sulfur oxide–related pollution were associated\nwith all-cause, lung cancer, and cardiopulmonary mortality. Each 10-?g/m3 elevation in fine particulate air pollution was associated with approximately\na 4%, 6%, and 8% increased risk of all-cause, cardiopulmonary, and lung cancer\nmortality, respectively. Measures of coarse particle fraction and total suspended\nparticles were not consistently associated with mortality.ConclusionLong-term exposure to combustion-related fine particulate air pollution\nis an important environmental risk factor for cardiopulmonary and lung cancer\nmortality.","author":[{"dropping-particle":"","family":"Pope III","given":"C. Arden","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Burnett","given":"Richard T.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Thun","given":"Michael J.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Calle","given":"Eugenia E.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Krewski","given":"Daniel","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ito","given":"Kazuhiko","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Thurston","given":"George D.","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"JAMA","id":"ITEM-2","issue":"9","issued":{"date-parts":[["2002","3","6"]]},"page":"1132","publisher":"American Medical Association","title":"Lung Cancer, Cardiopulmonary Mortality, and Long-term Exposure to Fine Particulate Air Pollution","type":"article-journal","volume":"287"},"uris":[""]}],"mendeley":{"formattedCitation":"(Martien, Ph, Lau, Tanrikulu, & Ph, 2014; Pope III et al., 2002)","plainTextFormattedCitation":"(Martien, Ph, Lau, Tanrikulu, & Ph, 2014; Pope III et al., 2002)","previouslyFormattedCitation":"(Martien, Ph, Lau, Tanrikulu, & Ph, 2014; Pope III et al., 2002)"},"properties":{"noteIndex":0},"schema":""}(Martien, Ph, Lau, Tanrikulu, & Ph, 2014; Pope III et al., 2002). However, air toxic concentrations vary at spatial levels much smaller than a county. For this epidemiological study, we examined the association of nine pollutants we hypothesize have a spatial relationship with lung cancer prevalence using cancer registry data from 2010 to 2015.Pollutants 1,3-butadiene: The main use of 1,3-butadiene is in manufacturing rubbers and plastics. It is also used in acrylic polymers manufacturing. In addition, automobile exhaust, cigarette smoke and other combustion such as forest fires are major sources of 1,3-butadiene ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"United States Environmental Protection Agency","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2009"]]},"title":"1,3-Butadiene","type":"report"},"uris":[""]}],"mendeley":{"formattedCitation":"(United States Environmental Protection Agency, 2009)","plainTextFormattedCitation":"(United States Environmental Protection Agency, 2009)","previouslyFormattedCitation":"(United States Environmental Protection Agency, 2009)"},"properties":{"noteIndex":0},"schema":""}(United States Environmental Protection Agency, 2009). The International Agency for Research on Cancer (IARC) has identified 1,3-butadiene as a Group 1 carcinogen to humans. Several epidemiological studies have suggested associations of butadiene with leukemia and ?non-Hodgkin lymphoma in workers of rubber and plastic manufacturing ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1097/JOM.0b013e3181c3c663","ISBN":"0b013e3181c3c6","ISSN":"10762752","abstract":"Objective: To evaluate the association between cumulative exposure to 1,3-butadiene (BD) or styrene (STY) and lung cancer among synthetic rubber industry workers. Methods: Internal Cox regression analyses were performed both with and without natural logarithm transformation of exposure variables and both with and without the inclusion of those unexposed to monomers. Results: Among women, analyses using untransformed BD exposure showed no trend. Analyses using natural logarithm-transformed BD exposure indicated a positive trend when the unexposed were included (P 0.05) and an inverse trend when the unexposed were excluded (P 0.05). No exposure-response trends were seen for BD among men or for STY among women or men. Conclusions:These results suggest that the association between BD and lung cancer, seen in some analyses of female employees, is not causal. STY did not appear to be associated with lung cancer.","author":[{"dropping-particle":"","family":"Sathiakumar","given":"Nalini","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Brill","given":"Ilene","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Delzell","given":"Elizabeth","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Journal of Occupational and Environmental Medicine","id":"ITEM-1","issue":"11","issued":{"date-parts":[["2009"]]},"page":"1326-1332","title":"1,3-butadiene, styrene and lung cancer among synthetic rubber industry workers","type":"article-journal","volume":"51"},"uris":[""]}],"mendeley":{"formattedCitation":"(Sathiakumar, Brill, & Delzell, 2009)","plainTextFormattedCitation":"(Sathiakumar, Brill, & Delzell, 2009)","previouslyFormattedCitation":"(Sathiakumar, Brill, & Delzell, 2009)"},"properties":{"noteIndex":0},"schema":""}(Sathiakumar, Brill, & Delzell, 2009) and with lung cancer ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"Sharma","given":"Ravi K.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Stacy","given":"Shaina L.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Xue","given":"Tao","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Talbott","given":"Evelyn O.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Brink","given":"LuAnn L.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Yuan","given":"Jian-Min","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issue":"C","issued":{"date-parts":[["2019"]]},"number-of-pages":"1-33","title":"Neighborhood Disparities in Cancer: A Geospatial Analysis of Socioeconomic and Environmental Factors","type":"report"},"uris":[""]}],"mendeley":{"formattedCitation":"(Sharma et al., 2019)","plainTextFormattedCitation":"(Sharma et al., 2019)","previouslyFormattedCitation":"(Sharma et al., 2019)"},"properties":{"noteIndex":0},"schema":""}(Sharma et al., 2019). Animal studies have identified butadiene ?as a leading factor for early induction and significantly increased incidence of hemangiosarcoma of the heart, malignant lymphomas, alveolar-bronchiolar neoplasms, and squamous cell neoplasms in rats ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"abstract":"Groups of 50 male and 50female B6C3F, mice were exposed 6 hours per day, S days per week, for 60 to 61 weeks to air containing 0, 625, or 1250 parts per million 1,3-butadiene. These concentrations are somewhat below and slightly above the Occupational Safety and Health Administration standard of 1000 parts per million for butadiene. The study was designedfor 104-week exposures but had to be ended early due to cancer-related mortality in both sexes at both exposure concen- trations. There were early induction and significantly increased incidences of hemangiosarcomas of the heart, malignant lymphomas, alveolar-bronchiolar neo- plasms, squamous cell neoplasms of the forestomach in males and females and acinar cell carcinomas of the mammary gland, granulosa cell neoplasms of the ovary, and hepatocellular neoplasms in females. Current workplace standards for exposure to butadiene should be reexamined in view of these findings.","author":[{"dropping-particle":"","family":"Miller","given":"JE Huff; RL Melnick; HA Solleveld; JK Haseman; M Powers; RA","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Science","id":"ITEM-1","issue":"4","issued":{"date-parts":[["1984"]]},"page":"548-549","title":"Carcinogenicity of 1,3-Butadiene in B6C3F1 mice after 60 weeks of inhalation exposure","type":"article-journal","volume":"227"},"uris":[""]}],"mendeley":{"formattedCitation":"(Miller, 1984)","plainTextFormattedCitation":"(Miller, 1984)","previouslyFormattedCitation":"(Miller, 1984)"},"properties":{"noteIndex":0},"schema":""}(Miller, 1984). In the 2005 NATA assessment, the exposure levels of butadiene in Allegheny County recorded were relatively lower (0.09 ppm to 0.20 ppm) than the Occupational Safety and Health Administration’s (OSHA) permissible exposure level (PEL) – 1 ppm and short-term exposure level (STEL) – 5 ppm ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"United States Environmental Protection Agency","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2009"]]},"title":"1,3-Butadiene","type":"report"},"uris":[""]}],"mendeley":{"formattedCitation":"(United States Environmental Protection Agency, 2009)","plainTextFormattedCitation":"(United States Environmental Protection Agency, 2009)","previouslyFormattedCitation":"(United States Environmental Protection Agency, 2009)"},"properties":{"noteIndex":0},"schema":""}(United States Environmental Protection Agency, 2009). Acetaldehyde and Formaldehyde: Acetaldehyde and formaldehyde are the most common aldehydes found in ambient air. The main use of acetaldehyde is as an intermediate in the synthesis of other chemicals. It is used in perfumes, polyester resins, and basic dyes production. Acetaldehyde is also used for preservatives, rubber, and tanning industries ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"United States Environmental Protection Agency","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2016"]]},"title":"Acetaldehyde","type":"report"},"uris":[""]}],"mendeley":{"formattedCitation":"(United States Environmental Protection Agency, 2016a)","plainTextFormattedCitation":"(United States Environmental Protection Agency, 2016a)","previouslyFormattedCitation":"(United States Environmental Protection Agency, 2016a)"},"properties":{"noteIndex":0},"schema":""}(United States Environmental Protection Agency, 2016a). It is a natural product of photo-oxidation and combustion of hydrocarbons in the atmosphere. In a German survey study, nine cancer cases were identified in workers, where the main process was dimerization of acetaldehyde in an aldehyde factory. Formaldehyde is mainly used in many household products and building materials such as pressed-wood products – particleboard, plywood, fiberboard, glues, adhesives, permanent-press fabrics, paper product coatings, and certain insulation materials. Both acetaldehyde and formaldehyde break down rapidly in the air and water and dilute within hours. Similar to acetaldehyde, exposure of formaldehyde was linked with cancer in laboratory animals. Nasal cavity cancers and leukemias are the most common cancers observed in rats after inhaling formaldehyde ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"URL":"","accessed":{"date-parts":[["2019","4","5"]]},"author":[{"dropping-particle":"","family":"American Cancer Society","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2014"]]},"title":"Formaldehyde","type":"webpage"},"uris":[""]}],"mendeley":{"formattedCitation":"(American Cancer Society, 2014)","plainTextFormattedCitation":"(American Cancer Society, 2014)","previouslyFormattedCitation":"(American Cancer Society, 2014)"},"properties":{"noteIndex":0},"schema":""}(American Cancer Society, 2014). There have been adverse effects documented due to formaldehyde exposure from polluted air in countries like China, Egypt, Indonesia, and parts of the United States. Formaldehyde is widely used in hair straightening and other cosmetic products. Hairstylists are highly exposed to formaldehyde from hair products in beauty salons ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1080/01480545.2018.1508215","ISSN":"15256014","abstract":"Hair straitening products are widely used by hairstylists. Many keratin-based hair smoothing products contain formaldehyde. This study aimed to investigate occupational formaldehyde exposure among hairstylists dealing with hair straightening products and the relation between genotoxicity biomarkers and the short-term formaldehyde exposure concentrations and the working years. The study was carried out in Cairo, Egypt on 60 hairstylists use hair straightening products divided into two groups according to the working years. All hairstylists were subjected to micronucleus (MN) frequencies in both epithelial buccal cells (EBC) and peripheral blood lymphocytes (PBL). Fifteen-minute (min) formal-dehyde exposure concentrations were measured at workplace during hair straightening procedure. Fifteen-minute formaldehyde concentrations in both groups exceeded the National Institute for Occupational Safety and Health and the American Conference of Governmental Industrial Hygienist thresholds levels. The MN frequencies in EBC and PBL showed a significant increase in group II in comparison to control and group I, which in turn showed a significant increase in MN frequency in PBL and a nonsignificant increase in the MN frequency in EBC when compared to control. A positive correlation was found between genotoxicity biomarkers and working years. Occupational exposures to hair straightening products in the studied hairstylist were found to expose them to formaldehyde concentrations that exceeded the standard limits. All selected genotoxicity biomarkers showed a significant increase in exposed workers and were positively correlated to the duration of exposure. ARTICLE HISTORY","author":[{"dropping-particle":"","family":"Aglan","given":"Mohamed A","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Mansour","given":"Ghada N","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Drug and Chemical Toxicology","id":"ITEM-1","issued":{"date-parts":[["2018"]]},"title":"Hair straightening products and the risk of occupational formaldehyde exposure in hairstylists","type":"article-newspaper"},"uris":[""]}],"mendeley":{"formattedCitation":"(Aglan & Mansour, 2018)","plainTextFormattedCitation":"(Aglan & Mansour, 2018)","previouslyFormattedCitation":"(Aglan & Mansour, 2018)"},"properties":{"noteIndex":0},"schema":""}(Aglan & Mansour, 2018). Acute toxicity of formaldehyde shows symptoms like ?irritated eyes, tearing, sneezing, coughing, chest congestion, fever, heartburn, lethargy, and loss of appetite. Chronic exposure of formaldehyde may lead to long-term health effects including neurotoxicity, ?pulmonary function damage, ?hematotoxicity, ?reproductive toxicity, and allergic asthma ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1016/j.envint.2009.06.002","ISSN":"18736750","abstract":"Formaldehyde, an economically important chemical, is classified as a human carcinogen that causes nasopharyngeal cancer and probably leukemia. As China is the largest producer and consumer of formaldehyde in the world, the Chinese population is potentially at increased risk for cancer and other associated health effects. In this paper we review formaldehyde production, consumption, exposure, and health effects in China. We collected and analyzed over 200 Chinese and English documents from scientific journals, selected newspapers, government publications, and websites pertaining to formaldehyde and its subsequent health effects. Over the last 20 years, China's formaldehyde industry has experienced unprecedented growth, and now produces and consumes one-third of the world's formaldehyde. More than 65% of the Chinese formaldehyde output is used to produce resins mainly found in wood products - the major source of indoor pollution in China. Although the Chinese government has issued a series of standards to regulate formaldehyde exposure, concentrations in homes, office buildings, workshops, public places, and food often exceed the national standards. In addition, there have been numerous reports of formaldehyde-induced health problems, including poisoning and cancer. The lack of quality epidemiological studies and basic data on exposed populations emphasizes the need for more extensive studies on formaldehyde and its related health effects in China. ? 2009 Elsevier Ltd. All rights reserved.","author":[{"dropping-particle":"","family":"Tang","given":"Xiaojiang","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Bai","given":"Yang","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Duong","given":"Anh","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Smith","given":"Martyn T.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Li","given":"Laiyu","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Zhang","given":"Luoping","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Environment International","id":"ITEM-1","issue":"8","issued":{"date-parts":[["2009"]]},"page":"1210-1224","publisher":"Elsevier Ltd","title":"Formaldehyde in China: Production, consumption, exposure levels, and health effects","type":"article-journal","volume":"35"},"uris":[""]}],"mendeley":{"formattedCitation":"(Tang et al., 2009)","plainTextFormattedCitation":"(Tang et al., 2009)","previouslyFormattedCitation":"(Tang et al., 2009)"},"properties":{"noteIndex":0},"schema":""}(Tang et al., 2009). In a case study, a previously healthy woman was diagnosed with ?pancytopenia – anemia just after moving to another apartment. The formaldehyde concentration in the air was found to be four times higher than the national concentration (0.1 ?g/m3) in the new apartment ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"Huang","given":"Y","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Zou","given":"Z","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Deng","given":"H","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Jiangsu Environ Sci Technol 2007b","id":"ITEM-1","issued":{"date-parts":[["2007"]]},"page":"16-17","title":"An analysis report about peripheral blood anemia induced by excessive formaldehyde in abiding place","type":"article-journal","volume":"20"},"uris":[""]}],"mendeley":{"formattedCitation":"(Huang, Zou, & Deng, 2007)","plainTextFormattedCitation":"(Huang, Zou, & Deng, 2007)","previouslyFormattedCitation":"(Huang, Zou, & Deng, 2007)"},"properties":{"noteIndex":0},"schema":""}(Huang, Zou, & Deng, 2007). Indoor exposure for both acetaldehyde and formaldehyde have a higher magnitude of health effects than the outdoor ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"Samet","given":"Jonathan M","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Marbury","given":"Marian C.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Spengler","given":"John D.","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"The American Review of Respiratory Disease","id":"ITEM-1","issue":"136","issued":{"date-parts":[["1987"]]},"page":"1486-1508","title":"State of Art: Indoor Air Pollution","type":"article-journal"},"uris":[""]},{"id":"ITEM-2","itemData":{"abstract":"The effects of several aldehydes and peroxides on growth and differentiation of normal human bronchial epithelial cells were studied. Cells were exposed to formaldehyde, acetaldehyde, benzoyl peroxide (BPO), or hydrogen peroxide (HPO). The effect of each agent on the following parameters was measured: (a) clonal growth rate; (b) squamous differentiation; (c) DNA dam age; (d) ornithine decarboxylase activity; (e) nucleic acid synthe sis; (f) aryl hydrocarbon hydroxylase activity; and (g) arachidonic acid and choline release. None of the agents were mitogenic, and their effects were assessed at concentrations which reduced growth rate (population doublings per day) to 50% of control. The 50% of control concentrations for the 6-h exposure were found to be 0.065 ITIM BPO, 0.21 HIM formaldehyde, 1.2 mw HPO, and 30 mw acetaldehyde. BPO-exposed cells were smaller than controls (median cell planar area, 620 sq ^m versus 1150 sq tim), and acetaldehyde-exposed cells were larger than con trols (median cell planar area, 3200 sq um). All agents increased the formation of cross-linked envelopes and depressed RNA synthesis more than DNA synthesis. HPO caused DNA single-strand breaks, while formaldehyde and BPO caused detectable amounts of both single-strand breaks and DNA-protein cross links. Other effects included increased arachidonic acid and choline release due to HPO. The similarities and differences of the effects of these aldehydes and peroxides to those caused by tumor promoters are discussed.","author":[{"dropping-particle":"","family":"Salariino","given":"Andrew J","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Willey","given":"James C","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Lechner","given":"John F","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Grafstrom","given":"Roland C","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Laveck","given":"Mo??ra","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Harris5","given":"Curtis C","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"CANCER RESEARCH","id":"ITEM-2","issued":{"date-parts":[["1985"]]},"number-of-pages":"2522-2526","title":"Effects of Formaldehyde, Acetaldehyde, Benzoyl Peroxide, and Hydrogen Peroxide on Cultured Normal Human Bronchial Epithelial Cells","type":"report","volume":"45"},"uris":[""]}],"mendeley":{"formattedCitation":"(Salariino et al., 1985; Samet, Marbury, & Spengler, 1987)","plainTextFormattedCitation":"(Salariino et al., 1985; Samet, Marbury, & Spengler, 1987)","previouslyFormattedCitation":"(Salariino et al., 1985; Samet, Marbury, & Spengler, 1987)"},"properties":{"noteIndex":0},"schema":""}(Salariino et al., 1985; Samet, Marbury, & Spengler, 1987). Benzene: Benzene is a well-studied pollutant in terms of health effects compared to other pollutants. Benzene has been associated with leukemias such as acute non-lymphocytic leukemia (ANLL) and acute myeloid leukemia (AML) in refinery workers. It is used mainly in making plastics, rubber, lubricants, drugs, detergent, and pesticides. About four decades ago, it was predominantly used as an industrial solvent. Nowadays, the main source of benzene is from automobile exhaust as it is a natural component of gasoline. People may get exposed to benzene through emission from industries such as paint and chemical processing factories. Heavily trafficked and surrounding areas of gas stations also have a high level of benzene in the air. Different levels of benzene are present in the ambient air in both urban and rural areas, with urban air typically having higher levels of benzene. ?Myelogenous leukemia, bone marrow depression, and blood cell-related cancers have been linked to high dose exposure of benzene in rodents and humans ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"URL":"","accessed":{"date-parts":[["2019","4","6"]]},"author":[{"dropping-particle":"","family":"American Cancer Society","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2016"]]},"title":"Benzene","type":"webpage"},"uris":[""]},{"id":"ITEM-2","itemData":{"DOI":"10.1093/carcin/bgh353","ISBN":"26/3/613/2390818","ISSN":"01433334","abstract":"Air pollution, containing high-level of ultrafine particles (UFP) and benzene, is a prominent environmental health problem in many cities of the World. We investigated the level of oxidative DNA damage in mononuclear blood cells (MNBC) by the comet assay as DNA strand breaks (SB) and formamidopyrimidine DNA glycosylase (FPG) sensitive sites in residents from three urban locations in Cotonou, Benin (taxi-moto drivers, subjects living near roads with intense traffic and suburban residents) and rural residents. Exposure was characterized by urinary excretion of S-phenylmercapturic acid (S-PMA), a biomarker of benzene exposure, and by ambient UFP. There were clear stepwise gradients with respect to ambient UFP, S-PMA excretion and oxidative DNA damage with rural subjects < suburban subjects < residents living near highly trafficed roads<taxi-moto drivers. Polymorphisms in glutathione peroxidase (GPX), NAD(P)H:quinone oxidoreductase 1 (NQO1) and glutathione S-transferase (GST) genes were assessed for effect modification. Subjects with GSTT1 null genotype had lower urinary S-PMA excretion than subjects carrying the plus genotype. Urinary S-PMA excretion correlated with SB (R = 0.17) and FPG sites (R = 0.25) in MNBC. The correlation between S-PMA and SB was strongest in subjects with NQO1*1/*2 and *2/*2 genotypes (R = 0.37), and between S-PMA and FPG sensitive sites in subjects with the GSTP1*B/*B genotype (R = 0.39). In conclusion, this study shows that urban air with high levels of benzene and UFP is associated with elevated levels of SB and FPG sites in MNBC, and that NQO1 and GST genes may modulate the effect.","author":[{"dropping-particle":"","family":"Avogbe","given":"Patrice H","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ayi-Fanou","given":"Lucie","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Autrup","given":"Herman","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Loft","given":"Steffen","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Fayomi","given":"Benjamin","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Sanni","given":"Ambaliou","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Vinzents","given":"Peter","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"M?ller","given":"Peter","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Carcinogenesis","id":"ITEM-2","issue":"3","issued":{"date-parts":[["2005"]]},"page":"613-620","title":"Ultrafine particulate matter and high-level benzene urban air pollution in relation to oxidative DNA damage","type":"article-journal","volume":"26"},"uris":[""]}],"mendeley":{"formattedCitation":"(American Cancer Society, 2016; Avogbe et al., 2005)","plainTextFormattedCitation":"(American Cancer Society, 2016; Avogbe et al., 2005)","previouslyFormattedCitation":"(American Cancer Society, 2016; Avogbe et al., 2005)"},"properties":{"noteIndex":0},"schema":""}(American Cancer Society, 2016; Avogbe et al., 2005). ROS produced when benzene goes under ?hepatic metabolism, generating hydroquinone, phenol and other compounds with the ability of redox cycling can cause DNA damage. ?The immune-toxic effects of benzene exposure in acute and chronic cases have been reported in both experimental and epidemiologic studies. The published epidemiologic studies, regarding the toxic effects of benzene on immune function, are related to occupational exposure. It is still unclear whether present benzene levels in our environment play any role in the incidence of immunological problems ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1016/j.taap.2014.02.012","ISSN":"10960333","abstract":"Objective: Benzene, as a volatile organic compound, is known as one of the main air pollutants in the environment. The aim of this review is to summarize all available evidences on non-cancerous health effects of benzene providing an overview of possible association of exposure to benzene with human chronic diseases, specially, in those regions of the world where benzene concentration is being poorly monitored. Methodology: A bibliographic search of scientific databases including PubMed, Google Scholar, and Scirus was conducted with key words of \"benzene toxic health effects\", \"environmental volatile organic compounds\", \"diabetes mellitus and environmental pollutants\", \"breast cancer and environmental pollution\", \"prevalence of lung cancer\", and \"diabetes prevalence\". More than 300 peer reviewed papers were examined. Experimental and epidemiologic studies reporting health effects of benzene and volatile organic compounds were included in the study. Results: Epidemiologic and experimental studies suggest that benzene exposure can lead to numerous non-cancerous health effects associated with functional aberration of vital systems in the body like reproductive, immune, nervous, endocrine, cardiovascular, and respiratory. Conclusion: Chronic diseases have become a health burden of global dimension with special emphasis in regions with poor monitoring over contents of benzene in petrochemicals. Benzene is a well known carcinogen of blood and its components, but the concern of benzene exposure is more than carcinogenicity of blood components and should be evaluated in both epidemiologic and experimental studies. Aspect of interactions and mechanism of toxicity in relation to human general health problems especially endocrine disturbances with particular reference to diabetes, breast and lung cancers should be followed up. ? 2014 Elsevier Inc.","author":[{"dropping-particle":"","family":"Bahadar","given":"Haji","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Mostafalou","given":"Sara","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Abdollahi","given":"Mohammad","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Toxicology and Applied Pharmacology","id":"ITEM-1","issue":"2","issued":{"date-parts":[["2014"]]},"page":"83-94","publisher":"Elsevier Inc.","title":"Current understandings and perspectives on non-cancer health effects of benzene: A global concern","type":"article-journal","volume":"276"},"uris":[""]}],"mendeley":{"formattedCitation":"(Bahadar, Mostafalou, & Abdollahi, 2014)","plainTextFormattedCitation":"(Bahadar, Mostafalou, & Abdollahi, 2014)","previouslyFormattedCitation":"(Bahadar, Mostafalou, & Abdollahi, 2014)"},"properties":{"noteIndex":0},"schema":""}(Bahadar, Mostafalou, & Abdollahi, 2014).Chloroform: Chloroform is mainly used to make other chemicals. It releases in the air as a result of its formation in the chlorination of drinking water, wastewater and swimming pools. Chloroform enters the environment from pulp and paper mills, hazardous waste sites, and sanitary landfills emissions ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"United States Environmental Protection Agency","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2000"]]},"title":"Chloroform","type":"report"},"uris":[""]}],"mendeley":{"formattedCitation":"(United States Environmental Protection Agency, 2000)","plainTextFormattedCitation":"(United States Environmental Protection Agency, 2000)","previouslyFormattedCitation":"(United States Environmental Protection Agency, 2000)"},"properties":{"noteIndex":0},"schema":""}(United States Environmental Protection Agency, 2000). In addition, human exposure of chloroform also occurs through drinking water and can absorb through the skin during bath/shower. There is not enough evidence available to link chloroform with carcinogenic effects. However, it can be detected in blood, urine, and body tissues. Most inhalation exposure data gathered from clinical settings, where chloroform was used in anesthesia. Animal studies have shown signs in kidney and liver damage in rats and limited information available on reproductive or developmental effects due to chloroform exposure ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"URL":"","accessed":{"date-parts":[["2019","4","6"]]},"author":[{"dropping-particle":"","family":"Agency for Toxic Substances and Disease Registry (CDC)","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["1997"]]},"title":"Toxicological Profile: Chloroform","type":"webpage"},"uris":[""]}],"mendeley":{"formattedCitation":"(Agency for Toxic Substances and Disease Registry (CDC), 1997)","plainTextFormattedCitation":"(Agency for Toxic Substances and Disease Registry (CDC), 1997)","previouslyFormattedCitation":"(Agency for Toxic Substances and Disease Registry (CDC), 1997)"},"properties":{"noteIndex":0},"schema":""}(Agency for Toxic Substances and Disease Registry (CDC), 1997). Coke Oven Emissions (COE): Coke oven emissions largely release from large ovens used in heating coal to produce coke in steel and iron manufacturing facilities. The emissions are complex mixtures of dust, vapors, and gases that typically include carcinogens such as cadmium, arsenic, 60 other organic compounds and 40 polycyclic aromatic hydrocarbons (PAHs). These PAHs are released from ?various industrial stacks, furnace, basic oxygen furnace, coke oven, electric arc furnace, heavy oil plants, and power plants. ?Several PAHs are known to be mutagenic and carcinogenic toward rodents in the laboratory, and potential carcinogens to humans ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1016/S0304-3894(98)00089-2","ISSN":"03043894","abstract":"The emission of polycyclic aromatic hydrocarbons (PAHs) from various industrial stacks (blast furnace, basic oxygen furnace, coke oven, electric arc furnace, heavy oil plant, power plant and cement plant) in southern Taiwan were investigated. PAH concentrations( μg/N m3) and PAH emission factors (μg/kg feedstock) were determined. In addition to these eight stationary industrial stacks, an industrial waste incinerator, a diesel engine and a gasoline-powered engine were selected and combined for the identification of source indicatory-PAHs in this study. The qualitative contribution of PAHs to the ambient air by various sources was estimated by factor analysis. Combustion of heavy oil produced considerably higher 4, 5 and 6 + 7-ring PAH concentration than other stacks. In addition, the HMW (higher molecular weight) PAH concentrations were significantly higher for the coke oven, the electric arc furnace and heavy oil combustion. Measured total-PAHs emission factors of eight stationary sources were between 77.0 and 3970 μg/kg feedstock, while BaP (the most carcinogenic PAH) emission factors were between 1.87 and 15.5 μg/kg feedstock. Among these eight emission sources, the heavy oil plant had both the highest total-PAH and the highest BaP emission factor. Indicatory PAHs of the cement plant were AcPy, Acp and Ant, which are all 3-ringed PAHs. However, the indicatory PAHs of the industrial waste incinerator were IND and CHR. For mobile sources (diesel- and gasoline-powered vehicles), the indicatory PAHs were mainly lower molecular weight PAHs (AcPy, FL and Flu). By using factor analysis, the cursorily qualitative analysis of PAH emission was found to be practicable.","author":[{"dropping-particle":"","family":"Yang","given":"Hsi Hsien","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Lee","given":"Wen Jhy","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Chen","given":"Shui Jen","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Lai","given":"Soon Onn","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Journal of Hazardous Materials","id":"ITEM-1","issue":"2","issued":{"date-parts":[["1998"]]},"page":"159-174","title":"PAH emission from various industrial stacks","type":"article-journal","volume":"60"},"uris":[""]}],"mendeley":{"formattedCitation":"(Yang, Lee, Chen, & Lai, 1998)","plainTextFormattedCitation":"(Yang, Lee, Chen, & Lai, 1998)","previouslyFormattedCitation":"(Yang, Lee, Chen, & Lai, 1998)"},"properties":{"noteIndex":0},"schema":""}(Yang, Lee, Chen, & Lai, 1998). There is epidemiologic evidence available suggesting that COE rich in polycyclic aromatic hydrocarbons can cause lung cancer in humans ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"ISSN":"00916765","abstract":"In the 1950s evidence of an ongoing epidemic of lung cancer in the United States and Western Europe led researchers to examine the role of outdoor air pollution, which was considered by some to be a likely cause. Although epidemiologic research quickly identified the central role of cigarette smoking in this epidemic, and despite progress in reducing outdoor air pollution in Western industrialized countries, concerns that ambient air pollution is causing lung cancer have persisted to the present day. This concern is based on the fact that known carcinogens continue to be released into outdoor air from industrial sources, power plants, and motor vehicles, and on a body of epidemiologic research that provides some evidence for an association between outdoor air pollution and lung cancer. This article reviews the epidemiologic evidence for this association and discusses the limitations of current studies for estimating the lung cancer risk in the general population. It also identifies research needs and suggests possible approaches to addressing outstanding questions.","author":[{"dropping-particle":"","family":"Cohen","given":"Aaron J","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Environmental Health","id":"ITEM-1","issue":"September 1999","issued":{"date-parts":[["2000"]]},"page":"743-750","title":"Outdoor Air Pollution and Lung Cancer Exposures to Carcinogens in Outdoor Air","type":"article-journal","volume":"108"},"uris":[""]},{"id":"ITEM-2","itemData":{"ISSN":"00916765","abstract":"The usefulness of data from various sources for a cancer risk estimation of urban air pollution is discussed. Considering the irreversibility of initiations, a multiplicative model is preferred for solid tumors. As has been concluded for exposure to ionizing radiation, the multiplicative model, in comparison with the additive model, predicts a relatively larger number of cases at high ages, with enhanced underestimation of risks by short follow-up times in disease-epidemiological studies. For related reasons, the extrapolation of risk from animal tests on the basis of daily absorbed dose per kilogram body weight or per square meter surface area without considering differences in life span may lead to an underestimation, and agreements with epidemiologically determined values may be fortuitous. Considering these possibilities, the most likely lifetime risks of cancer death at the average exposure levels in Sweden were estimated for certain pollution fractions or indicator compounds in urban air. The risks amount to approximately 50 deaths per 100,000 for inhaled particulate organic material (POM), with a contribution from ingested POM about three times larger, and alkenes, and butadiene cause 20 deaths, respectively, per 100,000 individuals. Also, benzene and formaldehyde are expected to be associated with considerable risk increments. Comparative potency methods were applied for POM and alkenes. Due to incompleteness of the list of compounds considered and the uncertainties of the above estimates, the total risk calculation from urban air has not been attempted here.","author":[{"dropping-particle":"","family":"Tornqvist","given":"Margareta","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ehrenberg","given":"L","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Environmental Health Perspectives","id":"ITEM-2","issue":"SUPPL. 4","issued":{"date-parts":[["1994"]]},"page":"173-182","title":"On cancer risk estimation of urban air pollution","type":"paper-conference","volume":"102"},"uris":[""]}],"mendeley":{"formattedCitation":"(Cohen, 2000; Tornqvist & Ehrenberg, 1994)","plainTextFormattedCitation":"(Cohen, 2000; Tornqvist & Ehrenberg, 1994)","previouslyFormattedCitation":"(Cohen, 2000; Tornqvist & Ehrenberg, 1994)"},"properties":{"noteIndex":0},"schema":""}(Cohen, 2000; Tornqvist & Ehrenberg, 1994). Similar to benzene, most COE studies have been conducted on occupational cohorts – steelworkers. COE was linked to employment in coke production and cancer of the skin, urinary bladder, and respiratory tract before 1950. Thereafter, numerous studies conducted in different countries linked exposure to COE with lung cancer. Other studies have reported an increased number of hematopoietic and renal cancers in coke workers in the United States ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"National Toxicology Program (NIH)","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2016"]]},"title":"Report on Carcinogens, Fourteenth Edition Coke-Oven Emissions","type":"report"},"uris":[""]}],"mendeley":{"formattedCitation":"(National Toxicology Program (NIH), 2016)","plainTextFormattedCitation":"(National Toxicology Program (NIH), 2016)","previouslyFormattedCitation":"(National Toxicology Program (NIH), 2016)"},"properties":{"noteIndex":0},"schema":""}(National Toxicology Program (NIH), 2016). IARC Monographs has evaluated COE as a causative factor for lung cancer in 1984; since then, no new studies have been published. Diesel PM: Air pollution, containing a high level of UFP (2.5 – 10 ?m) is a leading public and environmental health issue in many cities around the world. Motorized traffic is the major source of particulate matter, especially diesel particulates. Diesel PM releases from heavy-duty vehicles such as buses and trucks. In cities like Pittsburgh, where the public transportation is heavily depended on diesel engine buses, the exposure from bus exhaust is higher for people who are living in the city and close to the busy busways. Several studies have suggested an association exists between living close to heavily trafficked roadways and adverse health effects in the respiratory system ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"abstract":"To assess exposure to air pollution from traffic of children attending schools near motorways, traffic related air pollution (PM2:5;NO2 andbenzene) was measuredin and outside 24 schools locatedwithin 400 m of motorways in the Netherlands. Reflectance ofPM2:5 filters was measuredas a proxy for elemental carbon (EC). The relationship between this proxy and measurements of EC was studied in a sub-sample and a high correlation was established. In both indoor andoutdoor air, concentrations of PM2:5 and‘‘soot’’ significantly increasedwith increasing truck traffic density and significantly decreased with increasing distance. Indoor NO2 concentrations significantly increasedwith increasing car traffic. The percentage of time that the school was downwind of the motorway during the measurements was significantly associatedwith ‘‘soot’’ andNO2, but not with PM2:5 andbenzene. Estimatedyearly averaged concentrations, calculated after standardising for differences in the background concentrations during the measurements, showed an about 2.5 fold range in ‘‘soot’’, benzene (indoors and outdoors) and NO2 (indoors) concentrations. For PM2:5 (indoors and outdoors) and NO2 outdoors the range was smaller (1.4–1.7). Standardised concentrations were highly correlatedwith the results of two other approaches that were usedto order the exposures at the schools. This study has shown that concentrations of air pollutants in and outside schools near motorways are significantly associated with distance, traffic density and composition, and percentage of time downwind. These variables can therefore be usedto assess exposure to traffic relatedair pollution of subjects living near motorways. Furthermore, the yearly averagedconcentrations of PM2:5, ‘‘soot’’, NO2 andbenzene can be usedas a more direct measure of long-term exposure in epidemiological studies of the children attending the 24 schools.","author":[{"dropping-particle":"","family":"Janssen","given":"Nicole A H","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"Van","family":"Vliet","given":"Patricia H N","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Harssema","given":"Hendrik","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Brunekreef","given":"Bert","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Atmospheric Environment","id":"ITEM-1","issue":"2","issued":{"date-parts":[["2001"]]},"page":"3875-3884","title":"Assessment of exposure to traffic relatedair pollution of children attending schools near motorways","type":"article-journal","volume":"35"},"uris":[""]}],"mendeley":{"formattedCitation":"(Janssen, Vliet, Harssema, & Brunekreef, 2001)","plainTextFormattedCitation":"(Janssen, Vliet, Harssema, & Brunekreef, 2001)","previouslyFormattedCitation":"(Janssen, Vliet, Harssema, & Brunekreef, 2001)"},"properties":{"noteIndex":0},"schema":""}(Janssen, Vliet, Harssema, & Brunekreef, 2001). Diesel PM includes a combination of arsenic, benzene, formaldehyde, and nickel. Thus, it can potentially contribute to mutations that can lead to cancer. Particulate matter can penetrate into respiratory airways and ?deposit in the respiratory bronchioles and alveoli. ?The most important factors present are transition metals with redox properties, persistent free radicals, redox-cycling of quinones, polycyclic aromatic hydrocarbons (PAHs) and volatile organic compounds (VOCs) which may be metabolically activated to ROS that can react to form bulky adducts or strand breaks on cellular DNA. The association of oxidative stress and ?incidence of malignant respiratory diseases due to inflammation, activation of transcriptional factors and DNA damage are well studied in cellular biology ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.3390/ijerph10093886","ISBN":"3021072747","ISSN":"16617827","abstract":"Reactive oxygen or nitrogen species (ROS, RNS) and oxidative stress in the respiratory system increase the production of mediators of pulmonary inflammation and initiate or promote mechanisms of carcinogenesis. The lungs are exposed daily to oxidants generated either endogenously or exogenously (air pollutants, cigarette smoke, etc.). Cells in aerobic organisms are protected against oxidative damage by enzymatic and non-enzymatic antioxidant systems. Recent epidemiologic investigations have shown associations between increased incidence of respiratory diseases and lung cancer from exposure to low levels of various forms of respirable fibers and particulate matter (PM), at occupational or urban air polluting environments. Lung cancer increases substantially for tobacco smokers due to the synergistic effects in the generation of ROS, leading to oxidative stress and inflammation with high DNA damage potential. Physical and chemical characteristics of particles (size, transition metal content, speciation, stable free radicals, etc.) play an important role in oxidative stress. In turn, oxidative stress initiates the synthesis of mediators of pulmonary inflammation in lung epithelial cells and initiation of carcinogenic mechanisms. Inhalable quartz, metal powders, mineral asbestos fibers, ozone, soot from gasoline and diesel engines, tobacco smoke and PM from ambient air pollution (PM?? and PM?.?) are involved in various oxidative stress mechanisms. Pulmonary cancer initiation and promotion has been linked to a series of biochemical pathways of oxidative stress, DNA oxidative damage, macrophage stimulation, telomere shortening, modulation of gene expression and activation of transcription factors with important role in carcinogenesis. In this review we are presenting the role of ROS and oxidative stress in the production of mediators of pulmonary inflammation and mechanisms of carcinogenesis.","author":[{"dropping-particle":"","family":"Valavanidis","given":"Athanasios","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Vlachogianni","given":"Thomais","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Fiotakis","given":"Konstantinos","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Loridas","given":"Spyridon","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"International Journal of Environmental Research and Public Health","id":"ITEM-1","issue":"9","issued":{"date-parts":[["2013"]]},"page":"3886-3907","title":"Pulmonary oxidative stress, inflammation and cancer: Respirable particulate matter, fibrous dusts and ozone as major causes of lung carcinogenesis through reactive oxygen species mechanisms","type":"article-journal","volume":"10"},"uris":[""]}],"mendeley":{"formattedCitation":"(Valavanidis, Vlachogianni, Fiotakis, & Loridas, 2013)","plainTextFormattedCitation":"(Valavanidis, Vlachogianni, Fiotakis, & Loridas, 2013)","previouslyFormattedCitation":"(Valavanidis, Vlachogianni, Fiotakis, & Loridas, 2013)"},"properties":{"noteIndex":0},"schema":""}(Valavanidis, Vlachogianni, Fiotakis, & Loridas, 2013). According to the California Environmental Protection Agency (CAEPA), long term exposure of diesel PM has the highest cancer risk compared to any other pollutants present in the air ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"Office of Environmental Health Hazard Assessment","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2001"]]},"title":"Health Effects of Diesel Exhaust","type":"report"},"uris":[""]}],"mendeley":{"formattedCitation":"(Office of Environmental Health Hazard Assessment, 2001)","plainTextFormattedCitation":"(Office of Environmental Health Hazard Assessment, 2001)","previouslyFormattedCitation":"(Office of Environmental Health Hazard Assessment, 2001)"},"properties":{"noteIndex":0},"schema":""}(Office of Environmental Health Hazard Assessment, 2001). An Eastern European study examined reproductive effects due to PM exposure and found elevations of reproductive effects in male (lower sperm count) and females (lower birthweight and embryo toxicity) who were living in industrial areas. They also suggested a link between exposure of particulate matter and ?intrauterine growth retardation (IUGR) or fetal growth retardation leading to low birth weights ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1016/j.mrrev.2007.08.003","ISSN":"13835742","abstract":"Combustion emissions account for over half of the fine particle (PM2.5) air pollution and most of the primary particulate organic matter. Human exposure to combustion emissions including the associated airborne fine particles and mutagenic and carcinogenic constituents (e.g., polycyclic aromatic compounds (PAC), nitro-PAC) have been studied in populations in Europe, America, Asia, and increasingly in third-world counties. Bioassay-directed fractionation studies of particulate organic air pollution have identified mutagenic and carcinogenic polycyclic aromatic hydrocarbons (PAH), nitrated PAH, nitro-lactones, and lower molecular weight compounds from cooking. A number of these components are significant sources of human exposure to mutagenic and carcinogenic chemicals that may also cause oxidative and DNA damage that can lead to reproductive and cardiovascular effects. Chemical and physical tracers have been used to apportion outdoor and indoor and personal exposures to airborne particles between various combustion emissions and other sources. These sources include vehicles (e.g., diesel and gasoline vehicles), heating and power sources (e.g., including coal, oil, and biomass), indoor sources (e.g., cooking, heating, and tobacco smoke), as well as secondary organic aerosols and pollutants derived from long-range transport. Biomarkers of exposure, dose and susceptibility have been measured in populations exposed to air pollution combustion emissions. Biomarkers have included metabolic genotype, DNA adducts, PAH metabolites, and urinary mutagenic activity. A number of studies have shown a significant correlation of exposure to PM2.5 with these biomarkers. In addition, stratification by genotype increased this correlation. New multivariate receptor models, recently used to determine the sources of ambient particles, are now being explored in the analysis of human exposure and biomarker data. Human studies of both short- and long-term exposures to combustion emissions and ambient fine particulate air pollution have been associated with measures of genetic damage. Long-term epidemiologic studies have reported an increased risk of all causes of mortality, cardiopulmonary mortality, and lung cancer mortality associated with increasing exposures to air pollution. Adverse reproductive effects (e.g., risk for low birth weight) have also recently been reported in Eastern Europe and North America. Although there is substantial evidence that PAH or substituted PAH ma…","author":[{"dropping-particle":"","family":"Lewtas","given":"Joellen","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Mutation Research - Reviews in Mutation Research","id":"ITEM-1","issue":"1-3","issued":{"date-parts":[["2007"]]},"page":"95-133","title":"Air pollution combustion emissions: Characterization of causative agents and mechanisms associated with cancer, reproductive, and cardiovascular effects","type":"article-journal","volume":"636"},"uris":[""]}],"mendeley":{"formattedCitation":"(Lewtas, 2007)","plainTextFormattedCitation":"(Lewtas, 2007)","previouslyFormattedCitation":"(Lewtas, 2007)"},"properties":{"noteIndex":0},"schema":""}(Lewtas, 2007). Another case-control study found that risk of low birth weight ?increased with exposure to ambient air pollution related to the petroleum combustion products emitted from vehicles in Southern California ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1016/j.mrrev.2007.08.003","ISSN":"13835742","abstract":"Combustion emissions account for over half of the fine particle (PM2.5) air pollution and most of the primary particulate organic matter. Human exposure to combustion emissions including the associated airborne fine particles and mutagenic and carcinogenic constituents (e.g., polycyclic aromatic compounds (PAC), nitro-PAC) have been studied in populations in Europe, America, Asia, and increasingly in third-world counties. Bioassay-directed fractionation studies of particulate organic air pollution have identified mutagenic and carcinogenic polycyclic aromatic hydrocarbons (PAH), nitrated PAH, nitro-lactones, and lower molecular weight compounds from cooking. A number of these components are significant sources of human exposure to mutagenic and carcinogenic chemicals that may also cause oxidative and DNA damage that can lead to reproductive and cardiovascular effects. Chemical and physical tracers have been used to apportion outdoor and indoor and personal exposures to airborne particles between various combustion emissions and other sources. These sources include vehicles (e.g., diesel and gasoline vehicles), heating and power sources (e.g., including coal, oil, and biomass), indoor sources (e.g., cooking, heating, and tobacco smoke), as well as secondary organic aerosols and pollutants derived from long-range transport. Biomarkers of exposure, dose and susceptibility have been measured in populations exposed to air pollution combustion emissions. Biomarkers have included metabolic genotype, DNA adducts, PAH metabolites, and urinary mutagenic activity. A number of studies have shown a significant correlation of exposure to PM2.5 with these biomarkers. In addition, stratification by genotype increased this correlation. New multivariate receptor models, recently used to determine the sources of ambient particles, are now being explored in the analysis of human exposure and biomarker data. Human studies of both short- and long-term exposures to combustion emissions and ambient fine particulate air pollution have been associated with measures of genetic damage. Long-term epidemiologic studies have reported an increased risk of all causes of mortality, cardiopulmonary mortality, and lung cancer mortality associated with increasing exposures to air pollution. Adverse reproductive effects (e.g., risk for low birth weight) have also recently been reported in Eastern Europe and North America. Although there is substantial evidence that PAH or substituted PAH ma…","author":[{"dropping-particle":"","family":"Lewtas","given":"Joellen","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Mutation Research - Reviews in Mutation Research","id":"ITEM-1","issue":"1-3","issued":{"date-parts":[["2007"]]},"page":"95-133","title":"Air pollution combustion emissions: Characterization of causative agents and mechanisms associated with cancer, reproductive, and cardiovascular effects","type":"article-journal","volume":"636"},"uris":[""]}],"mendeley":{"formattedCitation":"(Lewtas, 2007)","plainTextFormattedCitation":"(Lewtas, 2007)","previouslyFormattedCitation":"(Lewtas, 2007)"},"properties":{"noteIndex":0},"schema":""}(Lewtas, 2007).Ethylbenzene: Ethylbenzene, naturally found in oil, is predominantly used in making styrene in the United States. It is also used in fuels and solvents such as paints, carpet glues, gasoline, paint, and automotive products. Ethylbenzene is present in low levels in rural areas and slightly higher in urban areas, especially close to tunnels and gas stations. Cigarette smoke also has been identified as a source of exposure to this chemical. People who are living near manufacturing facilities, petroleum refineries, and hazardous waste disposal sites and those working or residing in high traffic areas may potentially be exposed to ethylbenzene ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.3390/ijerph14101243","ISSN":"1660-4601","abstract":"The environmental burden of disease is the mortality and morbidity attributable to exposures of air pollution and other stressors. The inequality metrics used in cumulative impact and environmental justice studies can be incorporated into environmental burden studies to better understand the health disparities of ambient air pollutant exposures. This study examines the diseases and health disparities attributable to air pollutants for the Detroit urban area. We apportion this burden to various groups of emission sources and pollutants, and show how the burden is distributed among demographic and socioeconomic subgroups. The analysis uses spatially-resolved estimates of exposures, baseline health rates, age-stratified populations, and demographic characteristics that serve as proxies for increased vulnerability, e.g., race/ethnicity and income. Based on current levels, exposures to fine particulate matter (PM2.5), ozone (O3), sulfur dioxide (SO2), and nitrogen dioxide (NO2) are responsible for more than 10,000 disability-adjusted life years (DALYs) per year, causing an annual monetized health impact of $6.5 billion. This burden is mainly driven by PM2.5 and O3 exposures, which cause 660 premature deaths each year among the 945,000 individuals in the study area. NO2 exposures, largely from traffic, are important for respiratory outcomes among older adults and children with asthma, e.g., 46% of air-pollution related asthma hospitalizations are due to NO2 exposures. Based on quantitative inequality metrics, the greatest inequality of health burdens results from industrial and traffic emissions. These metrics also show disproportionate burdens among Hispanic/Latino populations due to industrial emissions, and among low income populations due to traffic emissions. Attributable health burdens are a function of exposures, susceptibility and vulnerability (e.g., baseline incidence rates), and population density. Because of these dependencies, inequality metrics should be calculated using the attributable health burden when feasible to avoid potentially underestimating inequality. Quantitative health impact and inequality analyses can inform health and environmental justice evaluations, providing important information to decision makers for prioritizing strategies to address exposures at the local level.","author":[{"dropping-particle":"","family":"Martenies","given":"Sheena E.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Milando","given":"Chad W.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Williams","given":"Guy O.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Batterman","given":"Stuart A.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Martenies","given":"Sheena E.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Milando","given":"Chad W.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Williams","given":"Guy O.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Batterman","given":"Stuart A.","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"International Journal of Environmental Research and Public Health","id":"ITEM-1","issue":"10","issued":{"date-parts":[["2017","10","19"]]},"page":"1243","publisher":"Multidisciplinary Digital Publishing Institute","title":"Disease and Health Inequalities Attributable to Air Pollutant Exposure in Detroit, Michigan","type":"article-journal","volume":"14"},"uris":[""]}],"mendeley":{"formattedCitation":"(Martenies et al., 2017)","plainTextFormattedCitation":"(Martenies et al., 2017)"},"properties":{"noteIndex":0},"schema":""}(Martenies et al., 2017). Very limited data are available on ethylbenzene’s toxicity and/or carcinogenicity in humans. However, several studies have suggested systematic effects of ethylbenzene in animals. Acute and intermediate exposure was associated with respiratory irritation, changes to the liver (increased organ weights and induction of microsomal enzymes), and effects on the hematological system (decreased platelets and increased leukocyte counts). Chronic exposure is associated with adverse effects to the liver (necrosis and hypertrophy), kidney (nephropathy and hyperplasia), and endocrine system (thyroid and pituitary hyperplasia) in animals ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"URL":"","accessed":{"date-parts":[["2019","4","7"]]},"author":[{"dropping-particle":"","family":"Agency for Toxic Substances and Disease Registry (CDC)","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2010"]]},"title":"Toxicological Profile: Ethylbenzene","type":"webpage"},"uris":[""]}],"mendeley":{"formattedCitation":"(Agency for Toxic Substances and Disease Registry (CDC), 2010)","plainTextFormattedCitation":"(Agency for Toxic Substances and Disease Registry (CDC), 2010)","previouslyFormattedCitation":"(Agency for Toxic Substances and Disease Registry (CDC), 2010)"},"properties":{"noteIndex":0},"schema":""}(Agency for Toxic Substances and Disease Registry (CDC), 2010). There is not enough evidence to associate ethylbenzene with reproductive effects ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"United States Environmental Protection Agency","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2016"]]},"title":"Ethylbenzene","type":"report"},"uris":[""]}],"mendeley":{"formattedCitation":"(United States Environmental Protection Agency, 2016b)","plainTextFormattedCitation":"(United States Environmental Protection Agency, 2016b)","previouslyFormattedCitation":"(United States Environmental Protection Agency, 2016b)"},"properties":{"noteIndex":0},"schema":""}(United States Environmental Protection Agency, 2016b). Trichloroethylene (TCE): Trichloroethylene is a colorless and toxic volatile organic (VOC) compound. The primary use of TCE is as a solvent to make refrigerant chemicals. It is also used as metal degreasing and dry cleaning agent ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"abstract":"Fact sheet on Trichloroethylene (TCE).","author":[{"dropping-particle":"","family":"United States Environmental Protection Agency","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2017"]]},"title":"Risk Management for Trichloroethylene (TCE)","type":"article-journal"},"uris":[""]}],"mendeley":{"formattedCitation":"(United States Environmental Protection Agency, 2017)","plainTextFormattedCitation":"(United States Environmental Protection Agency, 2017)","previouslyFormattedCitation":"(United States Environmental Protection Agency, 2017)"},"properties":{"noteIndex":0},"schema":""}(United States Environmental Protection Agency, 2017). TCE enters the environment from manufacturing and processing facilities. It breaks down slowly in the air, thus, remains in the air for a long period of time. People are exposed to TCE by inhaling, as well as through drinking contaminated water. The levels of TCE in ambient air have been declining recently. Based on numerous human studies showing a causal association between exposure to TCE and increased lung cancer risk, as well as similar findings in animals, TCE has been upgraded to known to be a human carcinogen ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"Agency for Toxic Substances and Disease Registry (CDC)","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2016"]]},"title":"National Toxicology Program Trichloroethylene (TCE) Exposure","type":"report"},"uris":[""]}],"mendeley":{"formattedCitation":"(Agency for Toxic Substances and Disease Registry (CDC), 2016)","plainTextFormattedCitation":"(Agency for Toxic Substances and Disease Registry (CDC), 2016)","previouslyFormattedCitation":"(Agency for Toxic Substances and Disease Registry (CDC), 2016)"},"properties":{"noteIndex":0},"schema":""}(Agency for Toxic Substances and Disease Registry (CDC), 2016). Several human studies have associated TCE with kidney cancer and non-Hodgkin lymphoma. An animal study has suggested plausible evidence for the development of the morphological lesion and biochemical changes in the mouse lung after exposure to trichloroethylene ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1016/0009-2797(92)90042-J","ISSN":"00092797","abstract":"Female CD-1 mice exposed to trichloroethylene (6 h/day) at concentrations from 20-2000 ppm developed a highly specific lung lesion after a single exposure, characterised by vacuolation of the Clara cells, the number of cells affected increasing with increasing dose level. At the highest dose levels pyknosis of the Clara cells was apparent. After 5 days of repeated exposures the lesion had resolved but exposure of mice following a 2-day break resulted in recurrence of the lesion. The changes in mouse lung Clara cells were accompanied by a marked loss of cytochrome P-450 activities. No morphological changes were seen in the lungs of rats exposed to either 500 or 1000 ppm trichloroethylene. Isolated mouse lung Clara cells were shown to metabolize trichloroethylene to chloral, trichloroethanol and trichloroacetic acid. Chloral was the major metabolite. Trichloroethanol glucuronide was not detected. In comparative experiments using mouse hepatocytes the major metabolites were trichloroethanol and its glucuronide conjugate. The activity of UDP-glucuronosyltransferase was compared in mouse lung Clara cells and hepatocytes using two phenolic substrates and trichloroethanol. Hepatocytes readily formed glucuronides from all three substrates whereas Clara cells were only active with the two phenolic substrates. The three major metabolites of trichloroethylene, chloral, trichloroethanol and trichloroacetic acid were each dosed to mice and of these metabolites, only chloral had an effect on mouse lung causing a lesion (Clara cell) identical to that seen with trichloroethylene. It is proposed that the failure of Clara cells to conjugate trichloroethanol leads to an accumulation of chloral which results in cytotoxicity. The known genotoxicity of chloral suggests that this lesion may be related to the development of lung tumours in mice exposed to trichloroethylene by inhalation. ? 1992.","author":[{"dropping-particle":"","family":"Odum","given":"J.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Foster","given":"J. R.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Green","given":"T.","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Chemico-Biological Interactions","id":"ITEM-1","issue":"2","issued":{"date-parts":[["1992"]]},"page":"135-153","title":"A mechanism for the development of Clara cell lesions in the mouse lung after exposure to trichloroethylene","type":"article-journal","volume":"83"},"uris":[""]}],"mendeley":{"formattedCitation":"(Odum, Foster, & Green, 1992)","plainTextFormattedCitation":"(Odum, Foster, & Green, 1992)","previouslyFormattedCitation":"(Odum, Foster, & Green, 1992)"},"properties":{"noteIndex":0},"schema":""}(Odum, Foster, & Green, 1992). A systematic review study was conducted to identify the evidence of an association between TCE exposure and kidney cancer, non-Hodgkin lymphoma and liver cancers. After reviewing twenty-four studies they conclude that (occupational) exposure of TCE increases kidney cancer 2-fold. The objective of this study is to conduct geospatial and statistical analysis to examine associations between environmental exposures (to the agents listed above) and risk of lung cancer at a small geographic level, i.e. the census tract. For this study, we mapped disparities in lung cancer for each census tract and focused only on ambient exposure levels of air toxics.Materials and Methods Study Population: Allegheny County is our study population for this study. The county consists of 416 census tracts; the maps were created based on 2000 American Community Survey (ACS) census data for total population, population by gender, race and age groups. We also derived socioeconomic status (SES) data for poverty and educational attainment from ACS. The SES variable was based on total percentage of poverty by census tract. Similarly, the percentage of the population who at least have a high school education. We excluded the population under 40 years of age from this study, considering the lifetime risk of diagnosing with cancer increases after 40 years of age in both men and women ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1016/j.amepre.2013.10.029","ISSN":"07493797","abstract":"This article challenges the idea that cancer cannot be prevented among older adults by examining different aspects of the relationship between age and cancer. Although the sequential patterns of aging cannot be changed, several age-related factors that contribute to disease risk can be. For most adults, age is coincidentally associated with preventable chronic conditions, avoidable exposures, and modifiable risk behaviors that are causally associated with cancer. Midlife is a period of life when the prevalence of multiple cancer risk factors is high and incidence rates begin to increase for many types of cancer. However, current evidence suggests that for most adults, cancer does not have to be an inevitable consequence of growing older. Interventions that support healthy environments, help people manage chronic conditions, and promote healthy behaviors may help people make a healthier transition from midlife to older age and reduce the likelihood of developing cancer. Because the number of adults reaching older ages is increasing rapidly, the number of new cancer cases will also increase if current incidence rates remain unchanged. Thus, the need to translate the available research into practice to promote cancer prevention, especially for adults at midlife, has never been greater. ? 2014 American Journal of Preventive Medicine .","author":[{"dropping-particle":"","family":"White","given":"Mary C","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Holman","given":"Dawn M","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Boehm","given":"Jennifer E","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Peipins","given":"Lucy A","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Grossman","given":"Melissa","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Jane Henley","given":"S.","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"American Journal of Preventive Medicine","id":"ITEM-1","issue":"3 SUPPL. 1","issued":{"date-parts":[["2014"]]},"title":"Age and cancer risk: A potentially modifiable relationship","type":"article-journal","volume":"46"},"uris":[""]}],"mendeley":{"formattedCitation":"(White et al., 2014)","plainTextFormattedCitation":"(White et al., 2014)","previouslyFormattedCitation":"(White et al., 2014)"},"properties":{"noteIndex":0},"schema":""}(White et al., 2014). We only accounted for African American and Whites population in the study. Cancer Incidence: For this study, we collected lung cancer (N = 6,348) data from the Pennsylvania Cancer Registry (PCR) from 2010 to 2015 for Allegheny County. Information for each cancer case was available including, ?International Classification of Diseases for Oncology (ICD-O-3) codes for primary sites, patient ID, race, sex, diagnosed date, last contacted and geographic coordinates. Recurring cancer incidence accounted only once by patient ID when patients were diagnosed for the first time, duplicate records were excluded. ?If a patient developed a second primary cancer, he or she was counted only once for total cancer and once for each specific cancer. ?Age-adjusted incidence rates expressed per 1,000 population were computed using the 2000 US standard population.Environmental Exposure: We obtained ambient air pollution concentration levels for the nine pollutants described in the introduction – 1,3-butadiene, acetaldehyde, benzene, chloroform, COE, diesel PM, ethylbenzene, formaldehyde, and TCE, from EPA’s 2005 NATA program. NATA is a wide-ranging assessment of different pollutants in the United States, which estimates ambient air concentration at county and census tract level. About 180 different kinds of pollutants (plus diesel PM) are included in the 2005 NATA assessment ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"URL":"","abstract":"NATA is an ongoing thorough evaluation of air toxics in the U.S. Intended as a screening tool, it helps air agencies learn which pollutants, emission sources and places they may wish to study further to better understand possible public health risks.","accessed":{"date-parts":[["2019","4","8"]]},"author":[{"dropping-particle":"","family":"United States Environmental Protection Agency","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2018"]]},"title":"National Air Toxics Assessment","type":"webpage"},"uris":[""]}],"mendeley":{"formattedCitation":"(United States Environmental Protection Agency, 2018)","plainTextFormattedCitation":"(United States Environmental Protection Agency, 2018)","previouslyFormattedCitation":"(United States Environmental Protection Agency, 2018)"},"properties":{"noteIndex":0},"schema":""}(United States Environmental Protection Agency, 2018). These nine pollutants were selected for this study for two reasons; first, literatures have suggested direct or indirect links to lung cancer risk and second, their exposure level variability was much larger than other pollutants (Table 1). Although, benzene and ethylbenzene are possible carcinogenic to humans, there have not been enough studies conducted to link them with lung cancer.Table 1: Distribution of air pollution concentration (?g/m3) in Allegheny County aMeanMedianS.D.bRange1,3-Butadiene 0.1100.1060.0140.093 – 0.195Acetaldehyde1.7341.7160.1321.456 – 2.167Benzene1.3561.2960.3200.916 – 3.789Chloroform0.1070.1020.0230.071 – 0.364Coke Oven Emission0.0180.0120.0230.004 – 0.257Diesel PM0.7980.6420.6950.184 – 8.298Ethylbenzene0.2080.1880.1070.058 – 0.939Formaldehyde1.7711.7410.2211.333 – 2.728Trichloroethylene0.2600.2480.0450.203 – 0.494a Total 416 census tractsb Standard DeviationData Derived from EPA 2005 NATA ProgramToxic Release Inventory (TRI): Almost all the pollutants described above are released from TRI sites in Allegheny County (except diesel PM). EPA developed a TRI program to track the management of certain chemicals that may pose a threat to human health and the environment. Manufacturing and processing facilities are required to report annually the quantity of chemical released (into air, water or landfill) to the environment and/or managed through recycling, energy recovery, and treatment ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"URL":"","abstract":"An overview of the Toxics Release Inventory (TRI) Program, which tracks industrial management of certain toxic chemicals and makes the information publicly available to support informed decision-making.","accessed":{"date-parts":[["2019","4","7"]]},"author":[{"dropping-particle":"","family":"United States Environmental Protection Agency","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2019"]]},"title":"Toxics Release Inventory (TRI) Program","type":"webpage"},"uris":[""]}],"mendeley":{"formattedCitation":"(United States Environmental Protection Agency, 2019b)","plainTextFormattedCitation":"(United States Environmental Protection Agency, 2019b)","previouslyFormattedCitation":"(United States Environmental Protection Agency, 2019b)"},"properties":{"noteIndex":0},"schema":""}(United States Environmental Protection Agency, 2019b). A total of 67 TRI sites are located in Allegheny County, including coke processing, steel works, paper mills, glass making, power plants, landfill sites, and wastewater treatment facilities. In order to create maps of TRI sites, we retrieved publicly available shapefiles from The Western Pennsylvania Regional Data Center ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"URL":"","accessed":{"date-parts":[["2019","4","7"]]},"author":[{"dropping-particle":"","family":"Western Pennsylvania Regional Data Center","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2019"]]},"title":"The Region's Open Data at Your Fingertips","type":"webpage"},"uris":[""]}],"mendeley":{"formattedCitation":"(Western Pennsylvania Regional Data Center, 2019)","plainTextFormattedCitation":"(Western Pennsylvania Regional Data Center, 2019)","previouslyFormattedCitation":"(Western Pennsylvania Regional Data Center, 2019)"},"properties":{"noteIndex":0},"schema":""}(Western Pennsylvania Regional Data Center, 2019).Environmental Justice (EJ) Areas: Environmental justice movement started in the early 1980s. This social movement focused on the fair distribution of environmental resources and burden in communities. The EPA defines EJ as: “Environmental justice is the fair treatment and meaningful involvement of all people regardless of race, color, national origin, or income, with respect to the development, implementation, and enforcement of environmental laws, regulations, and policies. This goal will be achieved when everyone enjoys the same degree of protection from environmental and health hazards, and equal access to the decision-making process to have a healthy environment in which to live, learn, and work.” ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"abstract":"This site provides EJ policy, information resources, compliance and enforcement data tools and community outreach activities. Additional topics are grants and program info documents, federal advisory committee and interagency working group activities.","author":[{"dropping-particle":"","family":"United States Environmental Protection Agency","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2019"]]},"title":"Environmental Justice","type":"article-journal"},"uris":[""]}],"mendeley":{"formattedCitation":"(United States Environmental Protection Agency, 2019a)","plainTextFormattedCitation":"(United States Environmental Protection Agency, 2019a)","previouslyFormattedCitation":"(United States Environmental Protection Agency, 2019a)"},"properties":{"noteIndex":0},"schema":""}(United States Environmental Protection Agency, 2019a). Pennsylvania Department of Environmental Protection (PA DEP) defined EJ tracts as any census tract where 30% or more population is a minority (identified as non-white) and at least 20% of the population lives below poverty level ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"URL":"","accessed":{"date-parts":[["2019","4","7"]]},"author":[{"dropping-particle":"","family":"Pennsylvania Department of Health","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2019"]]},"title":"PA Environmental Justice Areas","type":"webpage"},"uris":[""]}],"mendeley":{"formattedCitation":"(Pennsylvania Department of Health, 2019)","plainTextFormattedCitation":"(Pennsylvania Department of Health, 2019)","previouslyFormattedCitation":"(Pennsylvania Department of Health, 2019)"},"properties":{"noteIndex":0},"schema":""}(Pennsylvania Department of Health, 2019). To examine the locations of TRI sites in proximity of EJ areas – census tracts, we downloaded the shapefiles for EJ tracts from Western Pennsylvania Regional Data Center ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"URL":"","accessed":{"date-parts":[["2019","4","7"]]},"author":[{"dropping-particle":"","family":"Western Pennsylvania Regional Data Center","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2016"]]},"title":"Allegheny County Environmental Justice Areas - Datasets","type":"webpage"},"uris":[""]}],"mendeley":{"formattedCitation":"(Western Pennsylvania Regional Data Center, 2016)","plainTextFormattedCitation":"(Western Pennsylvania Regional Data Center, 2016)","previouslyFormattedCitation":"(Western Pennsylvania Regional Data Center, 2016)"},"properties":{"noteIndex":0},"schema":""}(Western Pennsylvania Regional Data Center, 2016). We briefly examined the impact of air pollution for the EJ tracts because environmental exposure is higher in the communities with lower SES, and minorities have a higher health-related burden. Often times, they are not informed regarding environmental hazard present in their communities ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"ISBN":"4126247335","author":[{"dropping-particle":"","family":"Fabisiak","given":"James","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Jackson","given":"Erica","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Brink","given":"LuAnn","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Presto","given":"Albert","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2018"]]},"title":"Environmental Health Perspectives A Risk-based Model to Assess Environmental Justice and Coronary Heart Disease Burden from Traffic-related Air Pollutants","type":"report"},"uris":[""]}],"mendeley":{"formattedCitation":"(Fabisiak, Jackson, Brink, & Presto, 2018)","plainTextFormattedCitation":"(Fabisiak, Jackson, Brink, & Presto, 2018)","previouslyFormattedCitation":"(Fabisiak, Jackson, Brink, & Presto, 2018)"},"properties":{"noteIndex":0},"schema":""}(Fabisiak, Jackson, Brink, & Presto, 2018). Geospatial and Statistical Analysis: For this study, we utilized GeoDa software to conduct exploratory spatial data analysis. Spatial autocorrelation for the variables was explored using the global (test for clustering) and local (test for the cluster) Moran’s I statistics. The term “global” refers to testing for spatial autocorrelation for the entire study area at once and deriving a single value indicating whether spatial autocorrelation exists and if so, then at what strength. “Local” refers to testing for spatial autocorrelation with neighbors ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1186/1476-072X-11-19","abstract":"Background: Lithium as a substance occurring naturally in food and drinking water may exert positive effects on mental health. In therapeutic doses, which are more than 100 times higher than natural daily intakes, lithium has been proven to be a mood-stabilizer and suicide preventive. This study examined whether natural lithium content in drinking water is regionally associated with lower suicide rates. Methods: Previous statistical approaches were challenged by global and local spatial regression models taking spatial autocorrelation as well as non-stationarity into account. A Geographically Weighted Regression model was applied with significant independent variables as indicated by a spatial autoregressive model. Results: The association between lithium levels in drinking water and suicide mortality can be confirmed by the global spatial regression model. In addition, the local spatial regression model showed that the association was mainly driven by the eastern parts of Austria.","author":[{"dropping-particle":"","family":"Helbich","given":"Marco","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Leitner","given":"Michael","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Kapusta","given":"Nestor D","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"International Journal of Health Geographics","id":"ITEM-1","issued":{"date-parts":[["2012"]]},"number-of-pages":"1","title":"Geospatial examination of lithium in drinking water and suicide mortality","type":"report","volume":"11"},"uris":[""]}],"mendeley":{"formattedCitation":"(Helbich, Leitner, & Kapusta, 2012)","plainTextFormattedCitation":"(Helbich, Leitner, & Kapusta, 2012)","previouslyFormattedCitation":"(Helbich, Leitner, & Kapusta, 2012)"},"properties":{"noteIndex":0},"schema":""}(Helbich, Leitner, & Kapusta, 2012). Census tracts which share common boundaries are called “neighbors”. Consequently, we used Moran’s I to evaluate the correlation among neighboring tracts and categorized spatial clustering strengths and levels. The values of Moran’s I may range from -1 to +1. Moran’s I = -1 indicates the lack of spatial correlation, in other words, variables are not clustered (Figure 1-A). Moran’s I = +1 when clusters are present (Figure 1-B), and Moran’s I = 0 represents perfect randomness (Figure 1-C) ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1111/j.0016-7363.2005.00671.x","ISSN":"0016-7363","author":[{"dropping-particle":"","family":"Anselin","given":"Luc","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Syabri","given":"Ibnu","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Kho","given":"Youngihn","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Geographical Analysis","id":"ITEM-1","issue":"1","issued":{"date-parts":[["2006","1","1"]]},"page":"5-22","publisher":"John Wiley & Sons, Ltd (10.1111)","title":"GeoDa: An Introduction to Spatial Data Analysis","type":"article-journal","volume":"38"},"uris":[""]},{"id":"ITEM-2","itemData":{"author":[{"dropping-particle":"","family":"Sharma","given":"Ravi K.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Stacy","given":"Shaina L.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Xue","given":"Tao","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Talbott","given":"Evelyn O.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Brink","given":"LuAnn L.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Yuan","given":"Jian-Min","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-2","issue":"C","issued":{"date-parts":[["2019"]]},"number-of-pages":"1-33","title":"Neighborhood Disparities in Cancer: A Geospatial Analysis of Socioeconomic and Environmental Factors","type":"report"},"uris":[""]}],"mendeley":{"formattedCitation":"(Anselin, Syabri, & Kho, 2006; Sharma et al., 2019)","plainTextFormattedCitation":"(Anselin, Syabri, & Kho, 2006; Sharma et al., 2019)","previouslyFormattedCitation":"(Anselin, Syabri, & Kho, 2006; Sharma et al., 2019)"},"properties":{"noteIndex":0},"schema":""}(Anselin, Syabri, & Kho, 2006; Sharma et al., 2019). We recalculated the Moran’s I by 999 permutations. The approach assesses the sensitivity of the results due to multiple comparisons ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1111/j.0016-7363.2005.00671.x","ISSN":"0016-7363","author":[{"dropping-particle":"","family":"Anselin","given":"Luc","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Syabri","given":"Ibnu","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Kho","given":"Youngihn","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Geographical Analysis","id":"ITEM-1","issue":"1","issued":{"date-parts":[["2006","1","1"]]},"page":"5-22","publisher":"John Wiley & Sons, Ltd (10.1111)","title":"GeoDa: An Introduction to Spatial Data Analysis","type":"article-journal","volume":"38"},"uris":[""]}],"mendeley":{"formattedCitation":"(Anselin et al., 2006)","plainTextFormattedCitation":"(Anselin et al., 2006)","previouslyFormattedCitation":"(Anselin et al., 2006)"},"properties":{"noteIndex":0},"schema":""}(Anselin et al., 2006). Global Moran’s I is important to examine the strengths of clustering; however, it does not provide any information about cluster locations. It also does not provide any information on what type of spatial correlation exists between clusters, for example, the correlation between higher values or lower values. In that case, local indicators of spatial association (LISA) specifies the measure of association for each spatial unit – census tract and provides information about types of spatial correlation (?clustering of similar values around that observation) ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"Anselin","given":"Luc","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Geographical Analysis","id":"ITEM-1","issued":{"date-parts":[["1995"]]},"page":"1-25","publisher":"Ohio State University Press","title":"Local indicators of spatial organization -LISA","type":"chapter"},"uris":[""]}],"mendeley":{"formattedCitation":"(Anselin, 1995)","plainTextFormattedCitation":"(Anselin, 1995)","previouslyFormattedCitation":"(Anselin, 1995)"},"properties":{"noteIndex":0},"schema":""}(Anselin, 1995). We created LISA cluster maps for all pollutants and cancer rate to ?classify the locations by type of association. ? High positive values refer to “hot spots” and high negative values to “cold spots”. As such, “hot spots” can be described as areas where tracts with high levels are surrounded by other tracts with high levels. In contrast, “cold spots” are clusters with low-level tracts surrounded by other low-level tracts. In addition to LISA maps, the standard output of a LISA analysis includes a Moran scatter plot depicting the distribution of the local statistic.368595361594(B)00(B)95692975771(A)00(A) INCLUDEPICTURE "" \* MERGEFORMATINET INCLUDEPICTURE "" \* MERGEFORMATINET 232498682918(C)00(C)390525012700Moran’s I = +100Moran’s I = +170485041275Moran’s I = -100Moran’s I = -1 INCLUDEPICTURE "" \* MERGEFORMATINET 2295525100330Moran’s I = 000Moran’s I = 0Figure 1: Moran’s ICancer rate variables were classified in the following classes: race (African Americans and Whites), gender (Males and Females), combination of race and gender (White Males, White Females, African American Males and African American Females) and age groups (40-49, 50-59, 60-69, 70-79, and 80 and over years). SPSS and GeoDa were utilized to performed simple linear regression to examine the association between lung cancer rates, the concentration of pollutants and SES by census tract. Since the sample size was smaller for some tracts, the data was not normally distributed within the county. Consequently, the log transformation was performed for cancer rate variables.ResultsOut of a total 67 TRI site, 30 sites (45%) were located in EJ tracts, and 16 (24%) located close proximity to EJ areas (Figure 2). Almost half of the TRI sites were also located close to Pittsburgh’s three major rivers – Allegheny, Monongahela and Ohio rivers. Recently an environmental group reported about 40% of industrial facilities in Allegheny County have exceeded their pollution limit at least once in 2017 () ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"author":[{"dropping-particle":"","family":"Lancianese","given":"Adelina","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2018","3","28"]]},"title":"New Report Finds Industrial Pollution Flowing Illegally into PA Rivers - The Allegheny Front","type":"article-newspaper"},"uris":[""]}],"mendeley":{"formattedCitation":"(Lancianese, 2018)","plainTextFormattedCitation":"(Lancianese, 2018)","previouslyFormattedCitation":"(Lancianese, 2018)"},"properties":{"noteIndex":0},"schema":""}(Lancianese, 2018). Figure 2: Toxic Release Sites and EJ Tracts in Allegheny CountyTo analyze the impact of lung cancer in the African American population, a map was created to demonstrate cases of lung cancer by census tract (Figure 3). About 83% of African American lung cancer cases were located in EJ areas. EJ tracts represent both percentages of poverty and minority. Figure 3 suggests that there is higher incidence of lung cancer in poor areas with higher minorities.Figure 3: Lung Cancer Rates in African Americans in Allegheny County (2010 – 2015)The most impacted areas with air pollution are in the city limits of Pittsburgh. However, the areas with high coke oven emissions are clustered significantly higher in the southeast side of Allegheny County, which indicates the lower air quality due to coke works facilities (Figure 4). The higher exposure for all pollutants showed spatial clustering in the city of Pittsburgh neighborhoods, with Moran’s I ranging from 0.20 to 0.74. Diesel PM, formaldehyde and acetaldehyde are clustered in the trafficked areas in Downtown. In addition, the impacted areas are relatively less affluent than the less impacted areas. Similarly, the total lung cancer incidence rates significantly clustered (Moran’s I = 0.66) in the same areas where air pollution is relatively higher (Figure 5). A total 6,348 lung cancer cases were observed in Allegheny County from 2010 – 2015. There were large variations in the rates of cancer cases. The mean of the total lung cancer incidence rate is 10.74 cases per 1,000 population. The variability was much larger in African American males and females. The increased cancer incidence rate was observed with increments of age (Table 2). (A) 1,3-Butadiene(B) Acetaldehyde(C) BenzeneMoran’s I = 0.70Moran’s I = 0.74Moran’s I = 0.65(D) Chloroform(E) COE(F) Diesel PMMoran’s I = 0.49Moran’s I = 0.74Moran’s I = 0.20(G) Ethylbenzene(H) Formaldehyde(I) TCEMoran’s I = 0.65Moran’s I = 0.69Moran’s I = 0.63Figure 4: Local Clusters for Each PollutantMoran’s I = 0.66Figure 5: Local Clusters for Total Lung Cancer Incidence RatesTable 2: Descriptive statistics for cancer incidence rates by race, gender, age and SESa indexCancer Rate per 1,000MeanMedianS.D.bRangeTotal 10.749.696.110.00 – 75.00Race White11.019.5810.200.00 – 125.00 African American16.370.0038.770.00 – 333.33Gender Male11.7010.597.240.00 – 68.49 Female10.099.098.510.00 – 125.00Race and Gender White Male11.649.8012.460.00 – 142.86 White Female10.418.6313.620.00 – 200.00 African American Male18.090.0063.360.00 – 1000.00 African American Female18.300.0075.290.00 – 1000.00Age 40 – 49 Years0.940.001.900.00 – 17.24 50 – 59 Years7.255.238.850.00 – 111.11 60 – 69 Years17.4514.4114.690.00 – 142.68 70 – 79 Years19.5617.2715.310.00 – 172.41 80 and Over Years28.0821.8534.210.00 – 545.45Table 2 continuedSES % African American16.193.5026.370.00 – 98.00 % Family Below Poverty12.986.1050.160.00 – 100.00 % Individuals Below Poverty13.819.1013.510.00 – 100.00 % At Least High School 84.7586.209.0827.90 – 100.00a Socioeconomic Statusb Standard DeviationThe aggregate lung cancer rates were strongly associated with coke over emissions (p = < 0.001) and TCE (p = 0.002) among all pollutants (Table 3). Table 3: Association of lung cancer incidence rate adjusted with SES.Coefficient ()Standard Errorp-value1,3- Butadiene-21.33645.7410.641Acetaldehyde10.6408.3210.202Benzene-3.8242.5630.136Chloroform-10.7097.9690.180Coke Oven Emission20.9145.811<0.001Diesel PM0.0980.4110.813Ethylbenzene14.1939.2910.127Formaldehyde-7.0036.1330.254TCEa4.2204.6670.002a Trichloroethylene After log transformation (to achieve normality), linear regression revealed the relationship between lung cancer rates and exposure of coke oven emissions, and trichloroethylene by race, gender and age groups. TCE exposure was significantly associated with total lung cancer incidence rates (Table 4). SES, including the percentage of families below the poverty level and percentage of the population with at least high school education, were adjusted for in the analysis. Lung cancer in women seemed to be more strongly associated with coke oven emissions and TCE exposure than men (Table 4). After adjusting for coke oven emissions and TCE, we found a statistically significant, positive relationship with percent families below poverty (p-value = <0.001) and negative relationship with educational attainment (p-value = <0.001). Population with less than high school education is at higher risk for lung cancer (Table 5).Table 4: Association of exposure of pollutants and lung cancer variables adjusted for SESaCoke Oven EmissionsbTrichloroethylenebStandardized Incidence RatesCoefficient ()tp-valueCoefficient ()tp-valueTotal 0.1051.8890.0600.2592.9720.003Race White0.0280.5050.6140.2863.3050.001 African American0.0670.8490.3970.0230.1950.846Gender Male0.0520.9390.3480.0520.9390.348 Female0.1031.7600.0790.2592.8840.004Race and Gender White Male0.0240.4130.6800.1691.8910.059 White Female0.0410.6870.4930.2682.9010.004 African American Male0.0800.9360.3510.0150.1110.912 African American Female0.0140.1580.874-0.091-0.7020.484Age 40 – 49 Years0.1261.3100.1930.2852.0120.047 50 – 59 Years0.1202.0770.0390.0050.0540.957 60 – 69 Years0.0941.5860.1140.2102.3250.021 70 – 79 Years-0.188-3.1790.0020.0860.9610.337 80 and Over Years-0.069-1.1310.2590.1101.1650.245a Socioeconomic Statusb explanatory variablesTable 5: Association of lung cancer and SESa, adjusted with Coke Oven Emissions and TCEa.Coefficient ()tp-valueBelow Poverty - Families0.1838.234<0.001Educational Attainment – At Least High School Education-0.219-3.644<0.001a Socioeconomic Statusb Trichloroethylene ConclusionOver the past decade, there has been increasing awareness of cancer disparities in the United States. The federal government has initiated several programs to reduce the disparities such as ?CDC’s Racial and Ethnic Approaches to Community Health (REACH) and ?National Center on Minority Health and Health Disparities to lead and coordinate scientific efforts to improve the health of minorities and medically underserved people ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.3322/canjclin.54.2.78","ISSN":"0007-9235","PMID":"15061598","abstract":"This article highlights disparities in cancer incidence, mortality, and survival in relation to race/ethnicity, and census data on poverty in the county or census tract of residence. The incidence and survival data derive from the National Cancer Institute's (NCI) Surveillance, Epidemiology, and End Results (SEER) Program; mortality data are from the National Center for Health Statistics (NCHS); data on the prevalence of major cancer risk factors and cancer screening are from the National Health Interview Survey (NHIS) conducted by NCHS. For all cancer sites combined, residents of poorer counties (those with greater than or equal to 20% of the population below the poverty line) have 13% higher death rates from cancer in men and 3% higher rates in women compared with more affluent counties (less than 10% below the poverty line). Differences in cancer survival account for part of this disparity. Among both men and women, five-year survival for all cancers combined is 10 percentage points lower among persons who live in poorer than in more affluent census tracts. Even when census tract poverty rate is accounted for, however, African American, American Indian/Alaskan Native, and Asian/Pacific Islander men and African American and American Indian/Alaskan Native women have lower five-year survival than non-Hispanic Whites. More detailed analyses of selected cancers show large variations in cancer survival by race and ethnicity. Opportunities to reduce cancer disparities exist in prevention (reductions in tobacco use, physical inactivity, and obesity), early detection (mammography, colorectal screening, Pap tests), treatment, and palliative care.","author":[{"dropping-particle":"","family":"Ward","given":"Elizabeth","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Jemal","given":"Ahmedin","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Cokkinides","given":"Vilma","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Singh","given":"Gopal K.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Cardinez","given":"Cheryll","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ghafoor","given":"Asma","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Thun","given":"Michael","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"CA: a cancer journal for clinicians","id":"ITEM-1","issue":"2","issued":{"date-parts":[["2004","3","1"]]},"page":"78-93","publisher":"American Cancer Society","title":"Cancer disparities by race/ethnicity and socioeconomic status.","type":"article-journal","volume":"54"},"uris":[""]}],"mendeley":{"formattedCitation":"(Ward et al., 2004)","plainTextFormattedCitation":"(Ward et al., 2004)","previouslyFormattedCitation":"(Ward et al., 2004)"},"properties":{"noteIndex":0},"schema":""}(Ward et al., 2004). Despite incredible efforts, knowledge is still limited for cancer prevention in vulnerable communities. This study attempted to identify the disadvantaged areas that are impacted the most from air pollution. This study utilized available cancer incidence data and exposure levels in Allegheny County to describe risk factors by specific areas. Nine pollutants were examined against lung cancer rates; trichloroethylene and coke oven emission were found to be the most associated with lung cancer. As described in the introduction, both pollutants emit in the environment from automobile exhaust and coke processing facilities. Further epidemiological studies will need to be undertaken to direct link these pollutants to lung cancer. However, occupational cohort studies have provided substantial evidence to assert trichloroethylene and coke oven emission as carcinogens ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.1001/jama.287.9.1132","ISSN":"0098-7484","abstract":"ContextAssociations have been found between day-to-day particulate air pollution\nand increased risk of various adverse health outcomes, including cardiopulmonary\nmortality. However, studies of health effects of long-term particulate air\npollution have been less conclusive.ObjectiveTo assess the relationship between long-term exposure to fine particulate\nair pollution and all-cause, lung cancer, and cardiopulmonary mortality.Design, Setting, and ParticipantsVital status and cause of death data were collected by the American\nCancer Society as part of the Cancer Prevention II study, an ongoing prospective\nmortality study, which enrolled approximately 1.2 million adults in 1982.\nParticipants completed a questionnaire detailing individual risk factor data\n(age, sex, race, weight, height, smoking history, education, marital status,\ndiet, alcohol consumption, and occupational exposures). The risk factor data\nfor approximately 500?000 adults were linked with air pollution data\nfor metropolitan areas throughout the United States and combined with vital\nstatus and cause of death data through December 31, 1998.Main Outcome MeasureAll-cause, lung cancer, and cardiopulmonary mortality.ResultsFine particulate and sulfur oxide–related pollution were associated\nwith all-cause, lung cancer, and cardiopulmonary mortality. Each 10-?g/m3 elevation in fine particulate air pollution was associated with approximately\na 4%, 6%, and 8% increased risk of all-cause, cardiopulmonary, and lung cancer\nmortality, respectively. Measures of coarse particle fraction and total suspended\nparticles were not consistently associated with mortality.ConclusionLong-term exposure to combustion-related fine particulate air pollution\nis an important environmental risk factor for cardiopulmonary and lung cancer\nmortality.","author":[{"dropping-particle":"","family":"Pope III","given":"C. Arden","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Burnett","given":"Richard T.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Thun","given":"Michael J.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Calle","given":"Eugenia E.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Krewski","given":"Daniel","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ito","given":"Kazuhiko","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Thurston","given":"George D.","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"JAMA","id":"ITEM-1","issue":"9","issued":{"date-parts":[["2002","3","6"]]},"page":"1132","publisher":"American Medical Association","title":"Lung Cancer, Cardiopulmonary Mortality, and Long-term Exposure to Fine Particulate Air Pollution","type":"article-journal","volume":"287"},"uris":[""]},{"id":"ITEM-2","itemData":{"ISSN":"00916765","abstract":"The OSHA standard for coke oven emissions, which went into effect in January 1977, sets a permissible exposure limit to coke oven emissions of 150 jig/m3 benzene-soluble fraction of total particulate matter (BSFTPM). Review of the epidemiologic evidence for the standard indicates an excess relative risk for lung cancer as high as 16-fold in topside coke oven workers with 15 years of exposure or more. There is also evidence for a consistent dose-response relationship in lung cancer mortality when duration and loca-tion of employment at the coke ovens are considered. Dose-response models fitted to these same data indicate that, while excess risks may still occur under the OSHA standard, the predicted levels of increased relative risk would be about 30-50% if a linear dose-response model is assumed and 3-7% if a quadratic model is assumed. Lung cancer mortality data for other steelworkers suggest the predicted excess risk has probably been somewhat overestimated, but lack of information on important confounding factors limits further dose-response analysis.","author":[{"dropping-particle":"","family":"Redmond","given":"Carol K","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"Environmental Health Perspectives","id":"ITEM-2","issued":{"date-parts":[["1983"]]},"page":"67-73","title":"Cancer mortality among coke oven workers","type":"article-journal","volume":"VOL. 52"},"uris":[""]},{"id":"ITEM-3","itemData":{"DOI":"10.3390/ijerph8114238","ISSN":"16604601","abstract":"We conducted a meta-analysis focusing on studies with high potential for trichloroethylene (TCE) exposure to provide quantitative evaluations of the evidence for associations between TCE exposure and kidney, liver, and non-Hodgkin lymphoma (NHL) cancers. A systematic review documenting essential design features, exposure assessment approaches, statistical analyses, and potential sources of confounding and bias identified twenty-four cohort and case-control studies on TCE and the three cancers of interest with high potential for exposure, including five recently published case-control studies of kidney cancer or NHL. Fixed- and random-effects models were fitted to the data on overall exposure and on the highest exposure group. Sensitivity analyses examined the influence of individual studies and of alternative risk estimate selections. For overall TCE exposure and kidney cancer, the summary relative risk (RRm) estimate from the random effects model was 1.27 (95% CI: 1.13, 1.43), with a higher RRm for the highest exposure groups (1.58, 95% CI: 1.28, 1.96). The RRm estimates were not overly sensitive to alternative risk estimate selections or to removal of an individual study. There was no apparent heterogeneity or publication bias. For NHL, RRm estimates for overall exposure and for the highest exposure group, respectively, were 1.23 (95% CI: 1.07, 1.42) and 1.43 (95% CI: 1.13, 1.82) and, for liver cancer, 1.29 (95% CI: 1.07, 1.56) and 1.28 (95% CI: 0.93, 1.77). Our findings provide strong support for a causal association between TCE exposure and kidney cancer. The support is strong but less robust for NHL, where issues of study heterogeneity, potential publication bias, and weaker exposure-response results contribute uncertainty, and more limited for liver cancer, where only cohort studies with small numbers of cases were available.","author":[{"dropping-particle":"","family":"Scott","given":"Cheryl Siegel","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Jinot","given":"Jennifer","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"International Journal of Environmental Research and Public Health","id":"ITEM-3","issue":"11","issued":{"date-parts":[["2011"]]},"page":"4238-4272","title":"Trichloroethylene and cancer: Systematic and quantitative review of epidemiologic evidence for identifying hazards","type":"article-journal","volume":"8"},"uris":[""]}],"mendeley":{"formattedCitation":"(Pope III et al., 2002; Redmond, 1983; Scott & Jinot, 2011)","plainTextFormattedCitation":"(Pope III et al., 2002; Redmond, 1983; Scott & Jinot, 2011)","previouslyFormattedCitation":"(Pope III et al., 2002; Redmond, 1983; Scott & Jinot, 2011)"},"properties":{"noteIndex":0},"schema":""}(Pope III et al., 2002; Redmond, 1983; Scott & Jinot, 2011). This study also attempted to visualize exploratory spatial data on maps. Informative maps can provide comprehensive information to policymakers, researchers, and public health professionals in reducing air pollution and cancer prevention efforts. This study’s results are also consistent with the previous studies that predicated probability of lung cancer increases with age ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"DOI":"10.3322/CA.2007.0010","ISSN":"0007-9235","author":[{"dropping-particle":"","family":"Jemal","given":"A.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Siegel","given":"R.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Ward","given":"E.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Hao","given":"Y.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Xu","given":"J.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Murray","given":"T.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Thun","given":"M. J.","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"CA: A Cancer Journal for Clinicians","id":"ITEM-1","issue":"2","issued":{"date-parts":[["2008","1","28"]]},"page":"71-96","publisher":"American Cancer Society","title":"Cancer Statistics, 2008","type":"article-journal","volume":"58"},"uris":[""]},{"id":"ITEM-2","itemData":{"DOI":"10.3322/caac.21551","ISSN":"00079235","author":[{"dropping-particle":"","family":"Siegel","given":"Rebecca L.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Miller","given":"Kimberly D.","non-dropping-particle":"","parse-names":false,"suffix":""},{"dropping-particle":"","family":"Jemal","given":"Ahmedin","non-dropping-particle":"","parse-names":false,"suffix":""}],"container-title":"CA: A Cancer Journal for Clinicians","id":"ITEM-2","issue":"1","issued":{"date-parts":[["2019","1"]]},"page":"7-34","title":"Cancer statistics, 2019","type":"article-journal","volume":"69"},"uris":[""]}],"mendeley":{"formattedCitation":"(Jemal et al., 2008; Siegel, Miller, & Jemal, 2019b)","plainTextFormattedCitation":"(Jemal et al., 2008; Siegel, Miller, & Jemal, 2019b)","previouslyFormattedCitation":"(Jemal et al., 2008; Siegel, Miller, & Jemal, 2019b)"},"properties":{"noteIndex":0},"schema":""}(Jemal et al., 2008; Siegel, Miller, & Jemal, 2019b). About 80% to 90% of lung cancer deaths are linked to the consumption of tobacco products and cigarette smoking ADDIN CSL_CITATION {"citationItems":[{"id":"ITEM-1","itemData":{"URL":"","accessed":{"date-parts":[["2019","4","12"]]},"author":[{"dropping-particle":"","family":"Centers for Disease Control and Prevention","given":"","non-dropping-particle":"","parse-names":false,"suffix":""}],"id":"ITEM-1","issued":{"date-parts":[["2018"]]},"title":"What Are the Risk Factors for Lung Cancer?","type":"webpage"},"uris":[""]}],"mendeley":{"formattedCitation":"(Centers for Disease Control and Prevention, 2018)","plainTextFormattedCitation":"(Centers for Disease Control and Prevention, 2018)","previouslyFormattedCitation":"(Centers for Disease Control and Prevention, 2018)"},"properties":{"noteIndex":0},"schema":""}(Centers for Disease Control and Prevention, 2018). This study did not include variables such as smoking, occupation or other behavioral factors such as diet that may play a contributing role in lung cancer prevalence. Thus, this study may not be sufficient to affirm coke oven emission and TCE as sole contributors to lung cancer. Major limitations of this study are, the exposure was determined based on EPA’s modeled estimation; therefore, we assign exposure at a group level (census tract) but not individually. Indoor exposure for certain pollutants may be higher for some populations, such as those who rely on woodfire heat, are exposed to secondhand smoking, etc., which was not accounted in this study. Also, the migration to immigration ratio was ignored to maintain simplicity in the study. Seven pollutants in this study which were not found associated with lung cancer may suggest that their ambient presence may not pose any significant cancer risk. However, it is worth reevaluating the animal studies to identify exposure magnitude of these agents to humans by better modeling. Future research could be done to study other cancer incidences as well as cancer mortality. The geospatial analysis could be done for other cancers to examine the spatial relationship between exposure and impact on health in vulnerable communities. bibliographyADDIN Mendeley Bibliography CSL_BIBLIOGRAPHY Agency for Toxic Substances and Disease Registry (CDC). (1997). Toxicological Profile: Chloroform. Retrieved April 6, 2019, from for Toxic Substances and Disease Registry (CDC). (2010). Toxicological Profile: Ethylbenzene. Retrieved April 7, 2019, from for Toxic Substances and Disease Registry (CDC). (2016). National Toxicology Program Trichloroethylene (TCE) Exposure. Retrieved from , M. A., & Mansour, G. N. (2018). Hair straightening products and the risk of occupational formaldehyde exposure in hairstylists. Drug and Chemical Toxicology. Cancer Society. 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