Respiratory Cancer Mortality Research Articles

Health & Hope Oasis Air Pollution the Silent Killer

Outdoor air pollution is a leading cause of early death, chronic disease, and disability. Motor vehicles are a major contributor to outdoor air pollution, exposing vulnerable population to especially high levels of harmful emissions in urban areas and near major roadways. Fine particles or particulate matter with a diameter of 2.5 micrometers or less (PM 2.5), are among the most harmful vehicle pollutants and are associated with a range of health impacts including cardiovascular and respiratory diseases, lung cancer, and infant mortality. Using gasoline and diesel as transport fuel causes emissions of both greenhouse gases, driving climate change, and of other air pollutants that are dangerous to human health and the natural environment. To prevent destructive climate change and reduce health impacts, the sector needs to move towards fuel that a lower carbon footprint and reduced emissions of sulfur and other conventional pollutants. Low Carbon Technology called Hydrogen on demand or water as fuel (HHO) Technology successfully reduces emission up to 50% and increase fuel efficiency up to 40%. It work equally well with Gasoline and Diesel fuel and recurring cost is almost zero.

Evaluating the Sensitivity of PM2.5-Mortality Associations to the Spatial and Temporal Scale of Exposure Assessment.

The temporal and spatial scales of exposure assessment may influence observed associations between fine particulate air pollution (PM2.5) and mortality, but few studies have systematically examined this question. We followed 2.4 million adults in the 2001 Canadian Census Health and Environment Cohort for nonaccidental and cause-specific mortality between 2001 and 2011. We assigned PM2.5 exposures to residential locations using satellite-based estimates and compared three different temporal moving averages (1, 3, and 8 years) and three spatial scales (1, 5, and 10 km) of exposure assignment. In addition, we examined different spatial scales based on age, employment status, and urban/rural location, and adjustment for O3, NO2, or their combined oxidant capacity (Ox). In general, longer moving averages resulted in stronger associations between PM2.5 and mortality. For nonaccidental mortality, we observed a hazard ratio of 1.11 (95% CI = 1.08, 1.13) for the 1-year moving average compared with 1.23 (95% CI = 1.20, 1.27) for the 8-year moving average. Respiratory and lung cancer mortality were most sensitive to the spatial scale of exposure assessment with stronger associations observed at smaller spatial scales. Adjustment for oxidant gases attenuated associations between PM2.5 and cardiovascular mortality and strengthened associations with lung cancer. Despite these variations, PM2.5 was associated with increased mortality in nearly all of the models examined. These findings support a relationship between outdoor PM2.5 and mortality at low concentrations and highlight the importance of longer-exposure windows, more spatially resolved exposure metrics, and adjustment for oxidant gases in characterizing this relationship.

Incidence and mortality for respiratory cancer and traffic-related air pollution in São Paulo, Brazil

BackgroundMultiple lines of evidence have associated exposure to ambient air pollution with an increased risk of respiratory malignancies. However, there is a dearth of evidence from low-middle income countries, including those within South America, where the social inequalities are more marked. ObjectivesTo quantify the association between exposures to traffic related air pollution and respiratory cancer incidence and mortality within São Paulo, Brazil. Further, we aim to investigate the role of socioeconomic status (SES) upon these outcomes. MethodsCancer incidence between 2002 and 2011 was derived from the population-based cancer registry. Mortality data (between 2002 and 2013) was derived from the Municipal Health Department. A traffic density database and an annual nitrogen dioxide (NO2) land use regression model were used as markers of exposure. Age-adjusted Binomial Negative Regression models were developed, stratifying by SES and gender. ResultsWe observed an increased rate of respiratory cancer incidence and mortality in association with increased traffic density and NO2 concentrations, which was higher among those regions with the lowest SES. For cancer mortality and traffic exposure, those in the most deprived region, had an incidence rate ratio (IRR) of 2.19 (95% CI: 1.70, 2.82) when comparing the highest exposure centile (top 90%) to the lowest (lowest 25%). By contrast, in the least deprived area, the IRR for the same exposure contrast was.1.07 (95% CI: 0.95, 1.20). For NO2 in the most deprived regions, the IRR for cancer mortality in the highest exposed group was 1.44 (95% CI: 1.10, 1.88) while in the least deprived area, the IRR for the highest exposed group was 1.11 (95% CI: 1.01, 1.23). ConclusionsTraffic density and NO2 were associated with an increased rate of respiratory cancer incidence and mortality in São Paulo. Residents from poor regions may suffer more from the impact of traffic air pollution.

The short-term effects of air pollution on respiratory diseases and lung cancer mortality in Hefei: A time-series analysis.

Accumulating evidence has shown the effects of air pollution on respiratory disease and lung cancer mortality, but the evidence is still inconclusive to date. We conducted a time-series analysis, which included 10388 subjects, to assess the short-term effects of air pollution on respiratory disease and lung cancer mortality in Hefei, China, from 2009 to 2015. The mean concentrations of pollutants (PM10, NO2 and SO2) were 106.35, 30.40, and 20.66 μg/m3, respectively, during the study period. An increase of 10 μg/m3 in SO2, NO2, and PM10 was associated with 7.69% (95%CI: 3.41%-12.15%), 4.38% (95%CI: 1.33%-7.53%), and 1.55% (95%CI: 0.80%-2.30%) increase of respiratory diseases mortality, respectively. In contrast, lung cancer mortality was only significantly associated with SO2 level. Subgroup analyses showed that female in respiratory disease patients were more sensitive to air pollution than male. Studies about seasonality of pollutants on respiratory and lung cancer mortality were inconsistent. Further analyses with multiple-pollutant model showed that the effects of pollutants were generally decreased after the other pollutants were adjusted, except the effects of SO2 on lung cancer. These findings demonstrated that air pollution could evidently increase the respiratory disease and lung cancer mortality.

Using long term mortality to determine which perioperative risk factors of mortality following hip and knee replacement may be causal

Observational studies have identified surgical factors that are associated with a reduced risk of mortality after joint replacement. It is not clear whether these are causal or reflect patient selection. Data on the first primary hip (n = 424,156) and knee replacements (n = 469,989) performed for osteoarthritis in the National Joint Registry were analysed. Flexible parametric survival modelling was used to determine if risk factors for mortality in the perioperative period persisted. To explore selection bias, standardised mortality ratios were calculated for all-cause, respiratory and smoking related cancer mortality using population rates. Selection was apparent for hip resurfacing, combined spinal and general anaesthetic and unicondylar knee implants; reduced mortality was observed for many years for both all and other causes of mortality with a waning effect. Mechanical thromboprophylaxis was also suggestive of selection although patients receiving aspirin had sustained reduced mortality, possibly due to to a cardioprotective effect. Posterior approach for hips was ambiguous with a possible causal component. Spinal anaesthesia was suggestive of a causal effect. We are reliant on observational data when it is not feasible to undertake randomised trials. Our approach of looking at long term mortality risks for perioperative interventions provides further insights to differentiate causal interventions from selection. We recommend the use of aspirin chemothromboprophylaxis, the posterior approach and spinal anaesthetic in total hip replacement due to the apparent causal effect on reduced mortality.

Effect of Confounding, Effect Modification, and Exposure Measures on the Association of Long-Term Ozone Exposure and Cause-Specific Mortality

Introduction: Associations between long-term ozone (O3) exposure and cause-specific mortality have been demonstrated, although with varying exposure metrics and confounders.Methods: We assessed the association of warm season (April-September) averages of 1-hour daily maximum O3 and cause-specific mortality for 22.2 million Medicare beneficiaries between 2000-2008. We modeled the national and regional associations between O3 and rate of mortality using age, gender, and race stratified log-linear regression models. We examined confounding by including ecologic and neighborhood-level behavioral covariates and PM2.5 estimated using spatio-temporal models. We also performed sensitivity analyses using exposure assessed as the warm season averages of daily 8-hour maximum and 24-hour average concentrations. We fit a log-linear model with a restricted cubic spline of O3 to estimate the shape of the dose-response relationship between ozone and cause-specific mortality and examined effect modification of these associations by age, gender and race.Results: Our findings show that 1-hour maximum O3 is significantly associated with an increased rate of death for all-cause (1.013 per 10 ppb increase; 95%CI: 1.012, 1.014), respiratory (1.036; 95%CI: 1.032, 1.039), cardiovascular (1.027; 95%CI: 1.025, 1.028) and lung cancer (1.016; 95%CI:1.011, 1.020) mortality, but not for cancer mortality. Associations were generally strongest in the northeast US for all causes as compared to other US regions. Risk ratios were robust to adjustment for ecologic covariates, behavioral covariates and to PM2.5. Results remained significant but were attenuated when 8-hour daily maximum and 24-hour average measures of O3 were used as the exposure measure, although 24-h averaged O3 was associated with decreased all cause and cardiovascular mortality.Conclusions: Long-term exposure to O3 was associated with increased mortality due to all-cause, respiratory, cardiovascular and lung cancer mortality.

Incidence and mortality risk for respiratory tract cancer in the city of São Paulo, Brazil: Bayesian analysis of the association with traffic density

BackgroundThere is evidence that exposure to traffic-related air pollution is related to the incidence of and mortality associated with lung cancer. The aim of this study was to perform a spatial analysis, with a Bayesian approach, to test the hypothesis that high traffic density is associated with increased respiratory tract cancer incidence and mortality risk among individuals over 20 years of age residing in the city of São Paulo, Brazil. MethodsWe employed data from two different databases: the São Paulo Municipal Population-Based Cancer Registry (2002–2011 cancer incidence data); and the Mortality Database of the São Paulo Municipal Health Department (2002–2013 cancer mortality data). The relationships between the number of cases of respiratory tract cancer in each area analyzed and the standardized covariates—traffic density and the Municipal Human Development Index (MHDI)—were evaluated with a Besag–York–Mollié ecological model with relative risks (RRs) estimates. ResultsPer 1-unit standard-deviation increase in traffic density and in the MHDI, the RR for respiratory tract cancer incidence was 1.07 (95% CI: 1.02–1.13) and 1.25 (95% CI: 1.18–1.32), respectively, whereas the RR for mortality was 1.04 (95% CI: 0.99–1.09) and 1.23 (95% CI: 1.16–1.30), respectively. ConclusionOur findings support the hypothesis that residing in areas with high traffic density is associated with increased respiratory tract cancer incidence and mortality risk in the city of São Paulo.

Exposure to environmental tobacco smoke in non - smoking adults in Israel: results of the second Israel biomonitoring survey

BackgroundExposure to environmental tobacco smoke (ETS) increases the risk of heart and respiratory disease, cancer, and premature mortality in non-smoking individuals. Results from the first Israel Biomonitoring Study in 2011 showed that over 60% of non-smoking adults are exposed to ETS. The purpose of the current study was to assess whether policies to restrict smoking in public places have been associated with reductions in exposure to ETS, and to examine predictors of exposure.MethodsWe analyzed urinary cotinine and creatinine concentrations in 194 adult participants in the National Health and Nutrition (RAV MABAT) Survey in 2015–2016. Study participants were interviewed in person on smoking status and exposure to ETS. We calculated creatinine-adjusted and unadjusted urinary cotinine geometric means and medians among smokers and non-smokers. We analyzed associations in univariable analyses, between socio-demographic variables and self – reported exposure, and urinary cotinine concentrations.ResultsThere was no reduction in geometric mean urinary cotinine levels in non-smokers in the current study (1.7 μg/g) compared to that in 2011 (1.6 μg/g). Median cotinine levels among the non – smoking Arab participants were higher in comparison to the Jewish and other participants (2.97 versus 1.56 μg/l, p = 0.035). Participants who reported that they were exposed to ETS at home had significantly higher median levels of creatinine adjusted urinary cotinine than those reporting they were not exposed at home (4.19 μg/g versus 2.9 μg/g, p = 0.0039).ConclusionsDespite additional restrictions on smoking in public places in 2012–2016, over 60% of non-smoking adults in Israel continue to be exposed to ETS. Urinary cotinine levels in non-smokers have not decreased compared to 2011. Results indicate higher exposure to ETS in Arab study participants and those reporting ETS exposure at home. There is an urgent need: (1) to increase enforcement on the ban on smoking in work and public places; (2) for public health educational programs and campaigns about the adverse health effects of ETS; and (3) to develop and disseminate effective interventions to promote smoke free homes. Periodic surveys using objective measures of ETS exposure (cotinine) are an important tool for monitoring progress, or lack thereof, of policies to reduce exposure to tobacco smoke in non-smokers.

Long-Term PM2.5 Exposure and Respiratory, Cancer, and Cardiovascular Mortality in Older US Adults.

The impact of chronic exposure to fine particulate matter (particulate matter with an aerodynamic diameter less than or equal to 2.5 μm (PM2.5)) on respiratory disease and lung cancer mortality is poorly understood. In a cohort of 18.9 million Medicare beneficiaries (4.2 million deaths) living across the conterminous United States between 2000 and 2008, we examined the association between chronic PM2.5 exposure and cause-specific mortality. We evaluated confounding through adjustment for neighborhood behavioral covariates and decomposition of PM2.5 into 2 spatiotemporal scales. We found significantly positive associations of 12-month moving average PM2.5 exposures (per 10-μg/m3 increase) with respiratory, chronic obstructive pulmonary disease, and pneumonia mortality, with risk ratios ranging from 1.10 to 1.24. We also found significant PM2.5-associated elevated risks for cardiovascular and lung cancer mortality. Risk ratios generally increased with longer moving averages; for example, an elevation in 60-month moving average PM2.5 exposures was linked to 1.33 times the lung cancer mortality risk (95% confidence interval: 1.24, 1.40), as compared with 1.13 (95% confidence interval: 1.11, 1.15) for 12-month moving average exposures. Observed associations were robust in multivariable models, although evidence of unmeasured confounding remained. In this large cohort of US elderly, we provide important new evidence that long-term PM2.5 exposure is significantly related to increased mortality from respiratory disease, lung cancer, and cardiovascular disease.

Long term effects of air pollution in Turin, Northern Italy. A population-based cohort study.

Introduction: Air pollution long term effects have been considerably studied in Europe in recent years. Large urban population-based cohorts in Italy are still few. Methods: We studied 655,000 subjects aged 30 or older and resident at least 5 years in the city of Turin, recruited within the Turin Longitudinal Study (a dynamic census cohort) and followed up for mortality (1997-2012) and hospital admissions for selected diseases (2000-2013). Exposure to Nitrogen dioxide (NO2) at the residential address of each cohort member was estimated using Land Use Regression models based on 2010 data, taking into account residential histories. Relative Risks (RR) were estimated with a Poisson model adjusted by age, gender, place of birth, education level, household composition, occupational class, dwelling type (derived by 2001 or 1991 or 1981 census); 2008 census tract income was added to the model at area level. Results are expressed as RR for the highest versus the lowest population weighted quintile of NO2 (>=60 vs <45 µg/m3) Results: All covariates showed coherent effects in the model. The Relative Risk for natural mortality was 1.06 (95% C.I:1.05-1.08.) with a significant linear trend between classes. Significant increase in mortality trend was found also for cardiovascular causes (1.09, 1.07-1.11), ischemic heart diseases (1.07, 1.05-1.08) and cerebrovascular diseases (1.10,1.08-1.13). For respiratory diseases and lung cancer mortality the RR estimates were 1.03 (1.01-1.06) and 1.09 (1.06-1.13), respectively, without a clear trend. We found significant RR for hospital admissions for acute myocardial infarction (considering every first admission in one month span, RR 1.14, 1.09-1.18) and cerebrovascular diseases (1.04, 1.02-1.06). A RR of 1.06 (1.02-1.09) was found for admissions for lung cancer, without a clear trend. Conclusions: This study on a large urban population-based cohort supplies evidence of the adverse health effects of long term exposure to NO2 air pollution.

Respiratory cancer mortality and incidence in an updated cohort of Canadian nickel production workers

ABSTRACTRespiratory cancer mortality and incidence were examined in an updated cohort of >56,000 Canadian nickel mining and refining workers. There was little evidence to suggest increased lung cancer risk in workers who had no experience in high-risk sintering operations that were closed by 1972, apart from that which would be expected from probable increased smoking prevalence relative to the comparison population. There was no substantive evidence of increased laryngeal cancer risk in the cohort, nor was there evidence of increased pharyngeal cancer risk in nonsinter workers. Nasal cancer incidence was elevated in nonsinter workers, but excess risks appeared to be confined to those hired prior to 1960. These findings lead us to tentatively conclude that occupationally-related respiratory risks in workers hired over the past 45 years are either very low or nonexistent.

Impact of large industrial emission sources on mortality and morbidity in Chile: A small-areas study

Chile suffers significant pollution from large industrial emitters associated with the mining, metal processing, paper production, and energy industries. The aim of this research was to determine whether the presence of large industrial facilities (i.e. coal- and oil-fired power plants, pulp and paper mills, mining facilities, and smelters) affects mortality and morbidity rates in Chile. For this, we conducted an ecological study that used Chilean communes as small-area observation units to assess mortality and morbidity. Public databases provided information on large pollution sources relevant to Chile. The large sources studied were oil- and coal-fired power plants, copper smelters, pulp and paper mills, and large mining facilities. Large sources were filtered by first year of production, type of process, and size. Mortality and morbidity data were acquired from public national databases, with morbidity being estimated from hospitalization records. Cause-specific rates were calculated for the main outcomes: cardiovascular, respiratory, cancer; and other more specific health outcomes. The impact of the large pollution sources was estimated using Bayesian models that included spatial correlation, overdispersion, and other covariates. Large and significant increases in health risks (around 20%–100%) were found for communes with power plants and smelters for total, cardiovascular, respiratory, all-cancer, and lung cancer mortality. Higher hospitalization rates for cardiovascular disease, respiratory disease, cancer, and pneumonia (20–100%) were also found for communes with power plants and smelters. The impacts were larger for men than women in terms of both mortality and hospitalizations. The impacts were also larger when the sources were analyzed as continuous (production volume) rather than dichotomous (presence/absence) variables. In conclusion, significantly higher rates of total cardiovascular, respiratory, all-cancer and lung cancer mortality and cardiovascular, respiratory, cancer and pneumonia hospitalizations were observed in communes with power plants and smelters.

Per cent emphysema is associated with respiratory and lung cancer mortality in the general population: a cohort study

BackgroundEmphysema on CT is a risk factor for all-cause mortality in persons with and without airflow obstruction; however, causes of death associated with emphysema remain uncertain, particularly in the general...

Respiratory Cancer and Non-Malignant Respiratory Disease-Related Mortality among Older Construction Workers-Findings from the Health and Retirement Study.

ObjectiveThis study explored the risk of respiratory cancer and non-malignant respiratory disease (NMRD)-related mortality among older construction workers.MethodsAnalyzed data from the 1992–2010 RAND Health and Retirement Study (HRS) and the HRS National Death Index – Cause of Death file. About 25,183 workers aged 50 years and older were examined, including 5,447 decedents and 19,736 survivors, of which 1,460 reported their longest job was in construction. Multinomial logistic regression assessed the differences in mortality between workers’ longest occupations, controlling for confounders.ResultsAfter adjusting for smoking and demographics, construction workers were almost twice as likely to die from respiratory cancer (OR = 1.65; CI: 1.10–2.47) or NMRD (OR = 1.73; CI: 1.16–2.58) compared to white-collar workers.ConclusionsThis study adds to the growing evidence that respiratory cancer and NMRD are frequently associated with construction exposure.

Impact Of Large-Sources On Morbidity And Mortality In Chile: A Small-Areas Analysis

Introduction. Chile has large-industrial emitters associated to mining and metal processing, paper and energy industry. The aim of this research was to determine whether small-area administrative units (municipalities) with these facilities have higher health risks. Methods. Ecological study using municipalities as small-area unit of observation of mortality/morbidity. Information of large-sources relevant for Chile was obtained from public databases. Large-sources studied were oil- and coal-fired power plants, copper smelters, paper mills and large mining facilities. Large-sources were filtered by year of starting production, process type and size. Mortality and morbidity data was acquired from public national databases; morbidity was estimated from hospitalization data. Cause-specific rates were calculated for main outcomes: cardiovascular, respiratory, cancer, among others. Standardized rates were calculated for each municipality using national rates. Impact of large-sources was estimated using Bayesian models (winbugs) including spatial correlation, over dispersion and other covariates. Large-sources were studied as a dichotomous variable (presence/absence) and as a continuous variable (production). Results. 339 municipalities were considered throughout Chile. Large and significant risk increases (around 20% -100%) were found in municipalities with power-plants and smelters for total, cardiovascular, respiratory, all cancer and lung cancer mortality. For hospitalizations, higher rates (20-100%) were also found for municipalities with power-plants and smelters for cardiovascular, respiratory, cancer and pneumonia. Both for mortality and hospitalizations, larger impacts were found for men than for women, and when the sources were analyzed as a continuous rather than as a dichotomous variable. Conclusions. Municipalities with power-plant and smelters presented higher risks of morbidity and mortality for several major outcomes.

Cognitive function and 10 year mortality in an 85 year-old community-dwelling population.

The relationship between mortality and impaired cognitive function has not been thoroughly investigated in a very elderly community-dwelling population, and little is known about the association of disease-specific mortality with Mini-Mental State Examination (MMSE) subscale scores. Here we evaluated these data in Japanese community-dwelling elderly. In 2003, 85 year-olds (n=207) were enrolled; 205 completed the MMSE for cognitive function and were followed-up for 10 years, during which time 120 participants died, 70 survived, and 17 were lost to follow-up. Thirty-eight deaths were due to cardiovascular disease, 22 to senility, 21 to respiratory disease, and 16 to cancer. All-cause mortality decreased by 4.3% with a 1-point increase in the global MMSE score without adjustment, and it decreased by 6.3% with adjustment for both sex and length of education. Cardiovascular mortality decreased by 7.6% and senility mortality decreased by 9.2% with a 1-point increase in the global MMSE score with adjustment for sex and education. No association was found between respiratory diseases or cancer mortality and global MMSE score. All-cause mortality also decreased with increases in MMSE subscale scores for time orientation, place orientation, delayed recall, naming objects, and listening and obeying. Cardiovascular mortality was also associated with the MMSE subscale of naming objects, and senility mortality was associated with the subscales of time orientation and place orientation. Thus, we found that impaired cognitive function determined by global MMSE score and some MMSE subscale scores were independent predictors of all-cause mortality or mortality due to cardiovascular disease or senility in 85 year-olds.

Short-term traffic related exposures and biomarkers of nitro-PAH exposure and oxidative DNA damage.

Exposure to vehicle exhaust has been associated with cardiac and respiratory disease, lung cancer, and greater overall mortality. We investigated whether amino- polycyclic aromatic hydrocarbon (amino-PAH) metabolites of nitro-PAHs could be used as biomarkers of these exposures. Pre- and post-shift urine samples were collected at the beginning and end of a work week from 82 male U.S trucking industry workers. We used repeated-measures analysis to examine associations of total 1- and 2-aminonaphthalene (1 & 2-AN) and 1-aminopyrene (1-AP) urinary concentrations with microenvironment exposures to particulate matter (PM2.5), elemental and organic carbon, and between 1&2-AN and 1-AP with urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG). There was an association between work week mean PM2.5 levels and post-shift 1 & 2-AN, [141.8 pg/ml increase (95% CI:53.3, 230.2) for each IQR increase (5.54 µg/m3) in PM2.5,] but no associations with other exposure measures. There was a statistically significant increase in 8-OHdG concentrations with 1 & 2-AN (2.38 µg/mg creatinine (95%CI: 0.19, 4.58) per 242.85 pg/mg creatinine increase in 1 & 2-AN), and suggestive associations with all other exposure measures. Our findings suggest associations between urinary amino-PAHs with vehicle exhaust related PM2.5 as well as with a biomarker of oxidative DNA damage.

Reconstruction of historical exposures at a Welsh nickel refinery (1953-2000).

Past epidemiological studies of workers in a nickel refinery in Clydach, Wales, have shown evidence of large excess respiratory cancer mortality risks [lung cancer relative risk (RR) ≈ 3; nasal cancer RR ≈ 140] in those employed prior to 1930, with risks dropping dramatically in workers hired subsequently. The pre-1930 risks have generally been attributed to high exposures to mixtures of nickel compounds. More recent studies of this refinery's workers have focused on those first hired in 1953, when many of the operations that presumably gave rise to the high exposures were no longer in operation. While these studies have shown greatly decreased lung cancer risks overall (RR ≈ 1.4), and no substantive evidence of increased nasal cancer risk, the absence of reliable exposure estimates have made it difficult to ascertain whether the increased lung cancer risks are nickel related or due to other factors. This study uses nickel measurements from the 1970s to the present, documentation of process changes, and dust measurements taken around the 1950s to construct an exposure matrix for the recent cohort. It provides evidence of at least 30-fold decreases in levels of nickel exposure from the 1950s to the present, with estimated inhalable nickel concentrations in the 1950s in excess of 5mg Ni m(-3).

Cigarette Taxes and Respiratory Cancers: New Evidence from Panel Co-Integration Analysis

Using a set of state-level longitudinal data from 1954 through 2005, this study investigates the "long-run equilibrium" relationship between cigarette excise taxes and the mortality rates of respiratory cancers in the United States. Statistical tests show that both cigarette excise taxes in real terms and mortality rates from respiratory cancers contain unit roots and are co-integrated. Estimates of co-integrating vectors indicated that a 10 percent increase in real cigarette excise tax rate leads to a 2.5 percent reduction in respiratory cancer mortality rate, implying a decline of 3,922 deaths per year, on a national level in the long run. These effects are statistically significant at the one percent level. Moreover, estimates of co-integrating vectors show that higher cigarette excise tax rates lead to lower mortality rates in most states; however, this relationship does not hold for Alaska, Florida, Hawaii, and Texas.

Mortality Patterns of Army Chemical Corps Veterans Who were Occupationally Exposed to Herbicides in Vietnam

This research examined the risk of disease-related mortality of the Army Chemical Corps (ACC) veterans who handled/sprayed herbicides in Vietnam in comparison with their non-Vietnam veteran peers or U.S. men. Vital status was determined through December 31, 2005. All-cause mortality and cause-specific mortality were compared for individuals who served in Vietnam (n = 2872) versus those who did not (n = 2737). Similar analyses were completed on a subset of the original Vietnam cohort that consisted of individuals who either reported spraying herbicide (n = 662) or not (n = 811). The observed deaths for each of the two base cohorts were also compared with expected deaths for U.S. men. Statistically significant excess mortality was found for ACC Vietnam veterans for chronic obstructive pulmonary disease (adjusted relative risk [ARR], 4.82; 95% confidence interval [95% CI], 1.10-21.18). When examining patterns for veterans in the Vietnam veteran subset, we found nonsignificant elevated ARRs among herbicide sprayers for all-cause, respiratory system disease, and respiratory system cancer mortality. Compared with U.S. men, the Vietnam veteran cohort had significant excess mortality for all-causes (standardized mortality ratio [SMR], 1.13; 95% CI, 1.04-1.23), respiratory system cancer (SMR, 1.35; 95% CI, 1.03-1.73), nonmalignant respiratory system disease (SMR, 1.58; 95% CI, 1.08-2.23), and miscellaneous malignant cancers (SMR, 1.77; 95% CI, 1.03-2.84). The risk of mortality from respiratory disease (malignant or nonmalignant) was significantly greater for ACC Vietnam veterans in comparison with their non-Vietnam veteran peers and U.S. men. Herbicide exposure could be contributing to the patterns observed. Because of the unique nature of their military duties and study limitations, findings may not be generalizeable to Vietnam veterans as a whole.