Table 1.
Literature Review.
| ID | Variables | Methods/Data Source(s) | Findings |
|---|---|---|---|
| [5] | Fine particulates, including sulfates | Regression, 14–16 year mortality follow-up of 8111 adults in 6 US cities/Prospective cohort study | After adjusting for smoking, mortality strongly associated with air pollution with fine particulates |
| [6] | Race and socioeconomic and gender predictors of early-state non-small cell lung cancer | Regressions/SEER | Higher socioeconomic status helps survival, as does being Caucasian or female. |
| [7] | PM10, SO4, SO2, O3, and NO2 checked for lung cancer | 6,338 nonsmoking, non-Hispanic white SDA residents of California were enrolled in 1977/Adventist Health Study (AHS) | Levels of PM10, SO4, SO2, O3, NO2 far higher for those with lung cancer, especially in males. |
| [8] | PM2.5 and SO2, lung cancer, lung cancer mortality | Cox Proportional hazards model/American cancer society, part of cancer prevention study (CPS-II), ongoing prospective mortality study of 1.2 M adults | PM2.5 and SO2 associated with lung cancer; each 10 microgram/m3 increase associated with 8% increase in lung cancer mortality |
| [9] | Race, gender, SE class, chemicals, not just smoking | Datasets from SEER and NPCR/National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) Program and the Centers for Disease Control and Prevention’s National Program of Cancer Registries (NPCR) | Epidemiologically and biological studies show strong causation between smoking and cellular mutations; racial disparities: Black worst, then white, then other races; lower Socio-Economic class is strongly associated with lung cancer; not gender; race seems to be proxy for Socio-Economic class |
| [10] | carbon dioxide, ozone, cancer, Ozone Mortality, Ozone Hospitalization, Ozone Emergency Room Visits, and Particulate Matter Mortality pollution mortality | Mathematical model/Nasa and EPA and California air resources | A climate-air pollution model showed by cause-and-effect analysis that fossil-fuel CO2 increases U.S. surface ozone, carcinogens, and Coarse Particulate matter, increasing cancer rates |
| [11] | asbestos fibers and ambient Coarse Particulate Matter PM10, PM2.5 and diesel exhaust particles | Chemicals purchased and combined with smoke, passed through filters/experiments | Synergistic effects in the generation of hydroxyl radicals in smoke with environmental asbestos fibers and ambient PM10, PM2.5 and diesel exhaust particles (DEP). The highest synergistic effects were observed with the asbestos fibers, PM2.5 and DEP, producing redox recycling and oxidative action. |
| [12] | Ozone and PM2.5 to predict premature (excess) mortality | Simulations of preindustrial and present-day (2000) concentrations included rural areas/epidemiology literature | Tropospheric O3 and PM2.5 contribute substantially to global premature mortality from lung cancer, which is 14% higher than baseline. |
| [13] | Socioeconomic, Rural-Urban, and Racial Inequalities in US Cancer Mortality: | Stats (regression)/three national data sources: the national mortality database, the decennial census, and the 2009–2010 Area Resource File | Blacks experiencing higher mortality from each cancer than whites within each deprivation group. Socioeconomic gradients in mortality were steeper in non-metropolitan than in metropolitan areas. Mortality disparities may reflect inequalities in smoking and other cancer-risk factors, screening, and treatment. |
| [14] | All of them | Statistics | Intersectionality of all the variables |
| [15] | PM2.5 and O3 | 80,285 AHSMOG-2 participants were followed for an average of 7.5 years; Logistic regression/Adventist Health and Smog Study-2 (AHSMOG-2), a cohort of health-conscious nonsmokers, where 81% have never smoked. | Lung cancer is associated with PM2.5 in never smokers and slightly higher if 1+ hrs./Day outdoors or 5+ years at residence. |
| [16] | Cancer risk index (CRI) Incidence of cancer risk from air toxics | Statistical modelling of San Antonia Texas; racial disparities found/Data for CRI from National Air Toxics Assessment [17] | Cancer risk index is all positively correlated with the ambient diesel coarse particulate matter. Institutional transformations are essential to mitigate the social-ecological divide. |
| [18] | Radon, Lung cancer | Meta-analysis of 8 case-control studies of indoor radon, where n = 200+/Finland (2), USA (2), Sweden (2), China, Canada | Relative risk is 14% greater for those exposed to indoor radon versus the controls |
| [19] | Occupational lung cancer, asbestos, arsenic, chromium, radon, silica, beryllium, nickel, cadmium, diesel exhaust | Review of many studies of workers in the U.S. | Conservative estimates are that relative risk of occupational lung cancer is 1.31 for diesel fumes, 2.0 for asbestos, and 3.69 for arsenic; several million exposed workers in early 1980 s |
| [20] | 24 experts in a working group | Review of many studies: human, occupational, outdoor, indoor, animal. | From many sources, respirable PM10, PM2.5, NO2, SO2, and O3 are frequently and substantially above safe levels. Consistency in studies shows cellular damage, as well as genetic and epigenetic effects. |
| [21] | Demographics, cancer types, cigarette features all lead to mutations and other changes in the genes | Review of smoking: all epidemiologically and biological studies show strong causation, and it parallels the rise and fall of cigarette smoking/Many sources | Prevention important and cessation important because it causes cancer in all demographics. Stopping smoking is the most important cause of lung cancer. |
| [22] | Incidence and survival of Small-Cell Lung Cancer among all lung cancers by Gender and Smoking and Stage of cancer | Analysis of the Surveillance, Epidemiologic, and End Results (SEER) database | Proportion of SCLC has diminished, and survival has increased slightly, attributed to decreasing smoking and increased proportion of low-tar cigarettes |