Cancer Mortality Ratios Research Articles

Relationship between cancer mortality/incidence and ambient ultraviolet B irradiance in China

Studies finding an inverse correlation of ambient solar irradiance with cancer mortality were the first to suggest that sun exposure and probably, therefore, vitamin D might protect against some cancers. Such correlation has been shown in Asian populations in some studies. We analyzed the correlation between mortality and incidence from a number of cancers and ambient solar ultraviolet (UV) B irradiance in China. Cancer mortality data were obtained from the Second National Death Survey conducted in a sample of 263 counties in China from 1990 to 1992. National cancer registration data 1998-2002 in China were used for estimation of cancer incidence. Satellite measurements of cloud-adjusted ambient UVB intensity at 305nm were obtained from a NASA database and GIS methods used to estimate the average daily irradiance for the 263 counties in 1990. We estimated cancer mortality rate ratios per 10 mW/(nmm(2)) change in UVB by fitting a negative binomial regression model with mortality as the response variable and UVB as the independent variable, adjusted for sex, age, and urban or rural area. Mortality rates for all cancers and cancers of the esophagus, stomach, colon and rectum, liver, lung, breast, and bladder were inversely correlated with ambient UVB. This correlation was present in men and women and rural residents for all these cancers but not urban residents for cancers of the esophagus, colon and rectum and liver. Lung cancer mortality showed the strongest inverse correlation with an estimated 12% fall per 10 mW/(nmm(2)) increase in UVB irradiance even if adjusted for smoking. Only incidence rates for cancers of the esophagus, stomach, colon and rectum and cervix were inversely correlated with ambient UVB. Mortality and incidence from nasopharyngeal cancer increased with increasing UVB [respectively 27 and 12% per mW/(nmm(2))]. Mortality from cancer of the cervix also increased, but to a lesser extent and mortality from leukemia was not consistently correlated with UVB irradiance. Mortality from all cancers together and most major cancers in China was inversely associated with solar UVB. These associations were similar to those observed in a number of populations of European origin. Incidence of some cancer types had the same correlation with UVB. They suggest the possibility that vitamin D may reduce the incidence or improve the outcome of cancer in Chinese people.

Prise en charge de l’insécurité alimentaire des enfants pauvres en France

The major decrease in exposure to secondhand smoke (SHS) in public places in recent decades could have contributed to the decline in smoking-related cancer mortality observed in the US population.Prospective study among 11,856 non-smoking adults aged ≥40 years who participated in NHANES 1988–1994 or 1999–2004 and were followed for mortality through 2006. We estimated the amount of change in cancer mortality over time attributed to the intermediate pathway of changes in SHS exposure in public places, after adjustment for risk factors and SHS exposure at home.The adjusted smoking-related cancer mortality rate ratios (95% CI) for a two-fold increase in serum cotinine and a 1-hour increase in occupational SHS exposure time were 1.10 (1.03, 1.17) and 1.14 (1.06, 1.24) for all-cancer, and 1.13 (1.03, 1.24) and 1.14 (1.02, 1.26) for smoking-related cancer, respectively. The absolute reduction in mortality comparing 1999–2004 to 1988–1994 was 75.8 (−25.5, 177.0) and 77.0 (2.6, 151.4) deaths/100,000 person-years, for all-cancer and smoking-related cancer, respectively. Among these avoided all-cancer deaths, 45.8 (2.8, 89.5) and 18.1 (−1.2, 39.6)/100,000 person-year were attributable to changes in serum cotinine concentrations and occupational SHS exposure time, respectively. The corresponding numbers of smoking-related cancer avoided deaths were 36.4 (0.7, 72.8) and 9.9 (−3.8, 24.9)/100,000 person-year.Declines in SHS exposure were associated with reductions in all-cancer and smoking-related cancer mortality, supporting that smoking bans in public places may have reduced cancer mortality among non-smoking adults.

Relationship between serum levels of insulin-like growth factors and subsequent risk of cancer mortality: Findings from a nested case–control study within the Japan Collaborative Cohort Study

Background: We investigated the association between serum levels of IGF-I, IGF-II, and IGFBP-3 and the subsequent risk of cancer mortality. Methods: Our case–control study examined samples from 914 cancer deaths and their 2739 matched controls within the Japan Collaborative Cohort Study. Blood samples were obtained at the baseline and stored at −80 °C until analysis for IGF-I, IGF-II, and IGFBP-3 levels. The conditional logistic model was used to estimate odds ratios (ORs) for cancer mortality associated with these serum levels. Results: The adjusted ORs for IGF-I quartiles ranged from 0.81 to 0.96 but were not significant. The adjusted ORs and 95% confidence interval (CI) for the second, third, and fourth IGF-II quartiles were 0.64 (95% CI: 0.52–0.79), 0.71 (95% CI: 0.58–0.88), and 0.73 (95% CI: 0.59–0.91), respectively, while those for the respective IGFBP-3 quartiles were 0.77 (95% CI: 0.63–0.96), 0.75 (95% CI: 0.60–0.94), and 0.71 (95% CI: 0.56–0.90). In the model of IGF-I, and IGF-II additionally adjusted for IGFBP-3, the associations of high IGFs levels were similar as observed in the above models, while the association of IGFBP-3 shifted into non-significance after adjusting for IGF-II. Conclusion: An increased level of IGF-II was significantly associated with decreased risk of cancer mortality, whereas the association between IGF-I and all cancer mortality was not significant. The inverse association of IGFBP-3 level with all cancer mortality was affected when adjusting for IGF-II levels, shifting from significant to non-significant. Confirmation of these results from further cohort studies may aid in identifying the potential association between these molecules and the risk of cancer among the general Japanese population.

Unusual Cancer Excess After Neonatal Arsenic Exposure From Contaminated Milk Powder

Chronic exposure to inorganic arsenic via inhalation or drinking water ingestion has been convincingly linked to cancer of the lung, skin, and urinary bladder (1). This conclusion mainly relies on long-term exposures, and little is known about the consequences of developmental exposures. During the summer of 1955, mass arsenic poisoning of bottle-fed infants occurred in the western part of Japan because of contaminated milk powder (2). Although the milk powder was distributed countrywide, Okayama was the most severely affected prefecture, with a consumption of at least 33 500 one-pound cans of milk powder (3). Although Okayama represents less than 2% of the Japanese population, the 2000 infants who were poisoned or died in Okayama represent 17% of the total number of affected children (3). The dose of poisoned milk powder needed to cause clinical poisoning in an infant corresponds to five cans (2), and the number of possible acute poisonings in Okayama could, therefore, have been three times the official estimate. We examined the cancer mortality in Okayama by abstracting data for 5-year age and calendar periods from official vital statistics during the period of 1970–2006. We compared the cancer mortality in the 5-year birth cohort that included the subjects born before milk poisoning (exposed group) with a similar cohort born after the milk poisoning (control group). Because the size of a 5-year birth cohort in Okayama is approximately 150 000, the number of clinically poisoned subjects may represent at least 4% of the cohort. After adjustment for the mortality for the country as a whole, we compared the cancer mortality in the exposed cohort with the next (younger) 5-year birth cohort within the same 5-year calendar period and with the same 5-year age group during the subsequent 5-year calendar period. Mortality ratios and their confidence intervals were calculated for total cancer and individual sites. Both comparisons showed that the mortality from total cancers and lung cancer were not elevated in the exposed cohort, but both skin cancer (including melanoma) and liver cancer were increased (Table 1). Unexpectedly, mortality ratios of pancreatic cancers (all age groups) and leukemia (ages 30–39 years) were elevated in both comparisons. Although little attention has been paid to the pancreas as a possible target of arsenic exposure, arsenic has been reported to induce type 2 diabetes mellitus (4), which may be a risk factor for pancreatic cancer (5). The association with leukemia is consistent with a previous environmental study (6), and the observed narrow latency interval is similar to observations in regard to leukemogenic chemicals (7). Table 1 Numbers of deaths and mortality ratios (MRs, with 95% confidence intervals [CIs]) for total cancer and individual sites for the exposed birth cohort from Okayama prefecture, Japan* Serious dilution is present in these ecological data on survivors of the poisoning incident, but our findings suggest that pancreatic cancer and leukemia could be linked to high-level exposures to inorganic arsenic during infancy. This observation therefore extends previous findings of increased rates for skin, lung, liver, and urinary tract cancer in populations with long-term arsenic exposures at lower levels.

Abstract B142: The risk level of liver cancer cases among smokers in developing countries

Abstract Introduction: Tobacco use is a rising concern for the developing world. It causes about 5million deaths yearly and is projected to cause 10 million deaths yearly by 2025 with 80% of these deaths from the developing countries if current trends continue. Tobacco is also a majo risk factor for all kinds of cancer including Liver cancer. Goal: To help determine whether the risk of liver cancer from smoking was less or greater than other forms of cancers caused by tobacco. Methods: In this study, we ascertained retrospectively the smoking habits of 24,000 adults who had died from liver cancer (cases) in 10 Chines cities, 7 Indian Cities and 5 Nigerian Cities. These areas were choosen for reasons of high population. Smokers from these three countries constitute 40% of smokers worldwide. Calculations of the smoker risk ratios (RR) for liver cancer mortality were standardised for age and locality. We used Cox proportional hazard regression models to adjust for confounding variables. We conducted analyses on the entire study population, among male and females who had smoked for at least 20 years separately for each country. Results: Among adult men (aged 35+) there was a 36% excess risk of death from liver cancer (smoker standardised risk ratio [RR] =1.36, with 95% confidence interval [Cl] 1.29–1.43, 2p<0.00001; attributable fraction 18%). In the general male population, this indicates absolute risks of death from liver cancer before age 70 of about 4% in smokers (in the absence of other causes). The RR was approximately independent of age, was similar in urban and rural areas, was not significantly related to the age when smoking started but was significantly (p<0.001) greater for cigarette smokers than for smokers of other forms of tobacco. Among men who smoked only cigarettes, the RR was significantly (p<0.001 for trend) related to daily consumption, with a greater hazard among those who smoked 20/day (RR 1.50, 95% CI 1.39–1.62) than among those who smoked fewer (mean 10/day: RR=1.32, 95% Cl 1.23–1.41). Smoking was also associated with a significant excess of liver cancer death in women (RR 1.17, 95% CI 1.06–1.29, 2p=0.003; attributable fraction 3%), but fewer women (17%) than men (62%) were smokers, and their cigarette consumption per smoker was lower. Among women who smoked only cigarettes, there was a significantly greater hazard among those who smoked at least 20/day (mean 22/day: RR=1.45, 95% Cl 1.18–1.79) than among those who smoked fewer (mean 8/day: RR=1.09, 95% Cl 0.94–1.25). Conclusion: This study goes to show that even though liver cancer from tobacco use kills about 200,000 people yearly in these three developing countries, the deaths from lung cancer (1.5 million yearly worldwide) is still higher than liver cancer deaths. Citation Information: Cancer Prev Res 2010;3(1 Suppl):B142.

Socioeconomic inequalities in cancer incidence and mortality—a spatial analysis in Bremen, Germany

Several international studies have already investigated the influence of socioeconomic factors on the risk of cancer. For Germany, however, the data are still insufficient. We examined the effects of social differences on cancer incidence and mortality on the population of Bremen, a town in northwest Germany. Data were obtained from the Bremen Cancer Registry, a population-based registry. The database comprised 27,430 incident cases, newly diagnosed between 2000 and 2006. The allocation of social class for each patient was based on the home address at the time of diagnosis, which led to the corresponding town district, which again could be linked to the “Bremen discrimination index.” Based on this index, cases were allocated to five categories, for which we compared standardized incidence ratios (SIR) and mortality ratios (SMR) for different cancers: prostate, breast, lung, colorectal, bladder, uterine, ovarian, cervical, malignant melanoma of the skin, non-melanoma skin cancer and all cancer sites summarized. The influence of social status was observed for different cancer sites. An inverse association was ascertained for all cancer sites (only men) and for tumors of the oral cavity and pharynx, and for lung, cervical and bladder cancers. A positive correlation was observed for female breast cancer, malignant melanoma, non-melanoma skin tumors and prostate cancer. In spite of the methodical restrictions, our analyses suggest an association between social factors and cancer incidence and mortality. The results are in agreement with international studies. Many of the observed social class differences could probably be explained by known risk factors, such as smoking, alcohol consumption, diet and physical activity.

LUNG, LIVER AND BONE CANCER MORTALITY AFTER PLUTONIUM EXPOSURE IN BEAGLE DOGS AND NUCLEAR WORKERS

The Mayak Production Association (MPA) worker registry has shown evidence of plutonium-induced health effects. Workers were potentially exposed to plutonium nitrate [(239)Pu(NO(3))(4)] and plutonium dioxide ((239)PuO(2)). Studies of plutonium-induced health effects in animal models can complement human studies by providing more specific data than is possible in human observational studies. Lung, liver, and bone cancer mortality rate ratios in the MPA worker cohort were compared to those seen in beagle dogs, and models of the excess relative risk of lung, liver, and bone cancer mortality from the MPA worker cohort were applied to data from life-span studies of beagle dogs. The lung cancer mortality rate ratios in beagle dogs are similar to those seen in the MPA worker cohort. At cumulative doses less than 3 Gy, the liver cancer mortality rate ratios in the MPA worker cohort are statistically similar to those in beagle dogs. Bone cancer mortality only occurred in MPA workers with doses over 10 Gy. In dogs given (239)Pu, the adjusted excess relative risk of lung cancer mortality per Gy was 1.32 (95% CI 0.56-3.22). The liver cancer mortality adjusted excess relative risk per Gy was 55.3 (95% CI 23.0-133.1). The adjusted excess relative risk of bone cancer mortality per Gy(2) was 1,482 (95% CI 566.0-5686). Models of lung cancer mortality based on MPA worker data with additional covariates adequately described the beagle dog data, while the liver and bone cancer models were less successful.

The Influence of Radon Exposures on Lung Cancer Mortality in German Uranium Miners, 1946–2003

Extensive uranium extraction took place from 1946 until 1990 at the former Wismut mining company in East Germany. A total of 58,987 male former employees of this company form the largest single uranium miners cohort that has been followed up for causes of mortality occurring from the beginning of 1946 to the end of 2003. The purpose of this study was to investigate and evaluate different forms of models for the radon exposure-related lung cancer mortality risk based on 3,016 lung cancer deaths and 2 million person years. Other exposure covariables such as occupational exposure to external gamma radiation, long-lived radionuclides, arsenic, fine dust and silica dust are available. The standardized mortality ratio for lung cancer is 2.03 (95% CI: 1.96; 2.10). The simple cohort excess relative risk (ERR/WLM) for lung cancer is estimated as 0.0019 (95% CI: 0.0016; 0.0022). The BEIR VI model produced risks similar to those obtained with a selected mathematically continuous ERR model for lung cancer. The continuous model is linear in radon exposure with exponential effect modifiers that depend on the whole range of age at median exposure, time since median exposure, and radon exposure rate. In this model the central estimate of ERR/WLM is 0.0054 (95% CI: 0.0040; 0.0068) for an age at median exposure of 30 years, a time since median exposure of 20 years, and a mean exposure rate of 3 WL. The ERR decreases by 5% for each unit of exposure-rate increase. The ERR decreases by 28% with each decade increase in age at median exposure and also decreases by 51% with each decade increase in time since median exposure. The method of determination of radon exposure (i.e., whether the exposures were estimated or measured) did not play an important role in the determination of the ERR. The other exposure covariables were found to have only minor confounding influences on the ERR/WLM for the finally selected continuous model when included in an additive way.

282 Ten-year risk of cancer mortality according to lipid levels and use of lipid-lowering drugs in the French general population

Purpose The beneficial effect of lipid-lowering drugs on cardiovascular mortality is well established, but long term safety data remain scarce. The aim of this study was to assess 10-year risk of cancer mortality according to blood lipid levels and lipid-lowering drug exposure, in the French general population. Methods Our analysis was based on the Third French MONICA Cross-sectional survey on cardiovascular risk factors (1995-1996). Participants aged 35-64 years were randomly recruited from French polling lists. Subjects with a history of cancer at baseline were excluded from the analysis. Vital status and cause of mortality were obtained 10 years after inclusion. Results There were 3262 participants and 177 deaths were recorded (78 due to cancer). The sample was mainly composed of subjects in primary cardiovascular prevention (96%) and comprised 64% of normolipidemic, 25% of untreated dyslipidemic (total cholesterol ≥ 6.5 mmol/L or triglycerides ≥ 3.5 mmol/L) and 11% of dyslipidemic subjects treated with a lipid-lowering drug (4% statin, 6% fibrate). After adjustment for centre, age, smoking, gamma-glutamyl transpeptidase and mean corpuscular volume, which were all significantly associated with cancer mortality, the hazard ratio (HR) for cancer mortality in subjects with non HDL-cholesterol Conclusion In this cohort mainly composed of primary prevention subjects, low HDL- and low non HDL-cholesterol levels were associated with increased cancer mortality, whereas risk of cancer death was reduced in users of lipid-lowering drugs. This suggests that the impact of low cholesterol on cancer risk may be different in subjects with spontaneously low levels and in those for whom cholesterol is lowered by lipid-lowering drugs.

Kidney Cancer Mortality

Arsenic in drinking water is associated with kidney cancer. Beginning in 1958, a region of Chile experienced a rapid onset of high arsenic exposure in drinking water, followed by sharp declines when water treatment plants were installed in 1971. For the years 1950-1970, we obtained mortality data from death certificates for an exposed region and an unexposed region in Chile. We obtained computerized mortality data for all of Chile for 1971-2000. Kidney cancer risks for the exposed region compared with the unexposed started to increase about 10 years after high arsenic exposures began in 1958. The peak kidney cancer mortality rate ratio (RR) was 3.4 (95% confidence interval = 2.2-5.1) for men in 1981-1985, with subsequent declines to 1.6 (1.2-2.1) by 1996-2000. Mortality RRs among women were 2.9 (1.8-4.7) in 1981-1985 but remained high longer than for men, increasing further to a RR of 4.4 (3.0-6.4) in 1991-1995. Early-life exposure resulted in an increased RR of 7.1 (3.1-14) for young adults aged 30-39 years, born just before or during the high exposure period. This study shows a latency pattern of increased mortality from kidney cancer, continuing for at least 25 years after the high exposures began to decline. Early life exposure resulted in markedly higher kidney cancer mortality in young adults.

Metformin Associated With Lower Cancer Mortality in Type 2 Diabetes

OBJECTIVESeveral studies have suggested an association between specific diabetes treatment and cancer mortality. We studied the association between metformin use and cancer mortality in a prospectively followed cohort.RESEARCH DESIGN AND METHODSIn 1998 and 1999, 1,353 patients with type 2 diabetes were enrolled in the Zwolle Outpatient Diabetes project Integrating Available Care (ZODIAC) study in the Netherlands. Vital status was assessed in January 2009. Cancer mortality rate was evaluated using standardized mortality ratios (SMRs), and the association between metformin use and cancer mortality was evaluated with a Cox proportional hazards model, taking possible confounders into account.RESULTSMedian follow-up time was 9.6 years, average age at baseline was 68 years, and average A1C was 7.5%. Of the patients, 570 died, of which 122 died of malignancies. The SMR for cancer mortality was 1.47 (95% CI 1.22–1.76). In patients taking metformin compared with patients not taking metformin at baseline, the adjusted hazard ratio (HR) for cancer mortality was 0.43 (95% CI 0.23–0.80), and the HR with every increase of 1 g of metformin was 0.58 (95% CI 0.36–0.93).CONCLUSIONSIn general, patients with type 2 diabetes are at increased risk for cancer mortality. In our group, metformin use was associated with lower cancer mortality compared with nonuse of metformin. Although the design cannot provide a conclusion about causality, our results suggest a protective effect of metformin on cancer mortality.

Cardiac disease and second lung cancer after radiotherapy for breast cancer

Radiotherapy (RT) is an important tool in the multidisciplinary management of breast cancer. The Early Breast Cancer Trialists’ Collaborative Group (EBCTCG) meta-analysis of randomised clinical trials demonstrated that the addition of RT to breast cancer therapy resulted in a significant reduction in the risk of local breast cancer recurrence, leading to a reduction in the risk of mortality. For every four local recurrences avoided by RT in years 1–5, about one death from breast cancer was avoided by year 15 [1]. However, when targeting the breast/chest wall with RT, some radiation is also delivered to the underlying normal tissues (e.g. heart and lung), and RT has been associated with an increased risk of late onset cardiotoxicity and second malignancies. In the EBCTCG analysis there was a significant excess of fatal heart disease (rate ratio 1.27, standard error (SE) 0.07, P = 0.0001) among irradiated women. Similarly, an excess incidence of second lung cancer (rate ratio 1.61, SE 0.18, P = 0.0007) and lung cancer deaths (rate ratio 1.78, SE 0.22, P = 0.0004) was found for irradiated patients. These long term side effects tend to offset the beneficial effect of RT. For example, in the meta-analysis, overall survival remained significantly improved for women given breast conserving surgery and for women with node-positive disease treated with mastectomy and axillary clearance, but for women with node-negative disease treated with mastectomy and axillary clearance, the beneficial effect of RT on breast cancer survival was very small and the toxic side effects outweighed it. The amount of incidental radiation delivered to the underlying heart is greater with left-sided versus right-sided RT. Similarly, the amount of incidental lung irradiation will generally be greater for the ipsilateral versus contralateral lung. These differences in exposure have been used to evaluate the risk of cardiac disease and second lung cancer associated with RT. Among women diagnosed with breast cancer during 1973–1982 in US SEER cancer registries, an excess cardiac mortality (ratio of 1.42 (1.11−1.82)) for left-side irradiated patients, and excess lung cancer mortality (ratio of 2.00 (1.00–4.00)) for ipsilateral lung cancer at 10–14 years after RT was found [2]. These excess risks increased significantly and progressively with time since RT: cardiac mortality 1.58 (1.29–1.95) and ipsilateral lung cancer mortality 2.71 (1.65–4.48) at 15 years or more after RT. The risk of late radiation-associated sequelae with modern cancer treatment is uncertain, because older radiotherapy regimens resulted in larger cardiac dosevolume distributions to organs at risk than what is common with modern radiation techniques [3,4]. Nearly all of the above mentioned studies analysed data from an era before the routine use of threedimensional (3-D) simulation and planning, which allows for more accurate delineation of irradiated heart and lung volumes. Coincident with improvements in RT techniques, there have been observations of decreased incidence of radiation-associated sequelae over time [2,5]. Current research in this area is attempting to define more precisely the risk of radiation-associated sequelae and to deliver RT with improved sparing of organs at risk. A case-control study in Sweden and Denmark, Radiation-Associated Cardiovascular Events (RACE), is estimating irradiated cardiac volumes and correlating estimated cardiac dose with clinical events in an attempt to characterise the cardiac dose-response relationship [6]. Similarly, estimates of the mean ipsilateral lung RT dose have allowed for assessment of second lung cancer risk by RT dose. Two separate studies have reported an estimated increase in the relative risk for second lung cancer of approximately 0.1−0.2 per Gy (mean ipsilateral lung radiation dose) at 10 or more years after RT [7,8]. Other cancer treatment factors may also potentially increase the risk of late sequelae. Chemotherapeutic agents have changed over time, and newer agents such as anthracycline chemotherapy (doxorubicin and epirubicin) and immunotherapy (trastuzumab), which are themselves cardiotoxic, are increasingly being

Cancer mortality in kidney transplantation.

Immunosuppression is associated with an increased risk of cancer in kidney transplant recipients compared to the general population. It is less clear whether standardized cancer mortality ratios (SMRs) are also increased. This study's hypothesis is that SMRs are not increased because of competing risks of death. During the median follow-up of 5.05 years (Q1-Q3: 2.36-8.62), there were 1937 cancer deaths and 36 619 noncancer deaths among 164 078 first kidney-only transplant recipients captured in the United States Renal Data System between January 1990 and December 2004. The observed cancer death rate was 206 per 100 000 patient-years compared to an expected rate of 215 per 100,000 patient-years in the general population. The overall age- and sex-adjusted SMR was only 0.96 (95% CI 0.92-1.00). However, patients <50 years had SMRs significantly greater than unity while patients >60 had SMRs lower than unity. Up to 25% of cancer-related deaths occurred after allograft failure. These findings challenge the notion that cancer is a major cause of premature death in all kidney transplant recipients and has implications for design of cancer prevention strategies in kidney transplant recipients.

Socioeconomic status and prostate cancer incidence and mortality rates among the diverse population of California

BackgroundThe racial/ethnic disparities in prostate cancer rates are well documented, with the highest incidence and mortality rates observed among African-Americans followed by non-Hispanic Whites, Hispanics, and Asian/Pacific Islanders. Whether socioeconomic status (SES) can account for these differences in risk has been investigated in previous studies, but with conflicting results. Furthermore, previous studies have focused primarily on the differences between African-Americans and non-Hispanic Whites, and little is known for Hispanics and Asian/Pacific Islanders.ObjectiveTo further investigate the relationship between SES and prostate cancer among African-Americans, non-Hispanic Whites, Hispanics, and Asian/Pacific Islanders, we conducted a large population-based cross-sectional study of 98,484 incident prostate cancer cases and 8,997 prostate cancer deaths from California.MethodsData were abstracted from the California Cancer Registry, a population-based surveillance, epidemiology, and end results (SEER) registry. Each prostate cancer case and death was assigned a multidimensional neighborhood-SES index using the 2000 US Census data. SES quintile-specific prostate cancer incidence and mortality rates and rate ratios were estimated using SEER*Stat for each race/ethnicity categorized into 10-year age groups.ResultsFor prostate cancer incidence, we observed higher levels of SES to be significantly associated with increased risk of disease [SES Q1 vs. Q5: relative risk (RR) = 1.28; 95% confidence interval (CI): 1.25–1.30]. Among younger men (45–64 years), African-Americans had the highest incidence rates followed by non-Hispanic Whites, Hispanics, and Asian/Pacific Islanders for all SES levels. Yet, among older men (75–84 years) Hispanics, following African-Americans, displayed the second highest incidence rates of prostate cancer. For prostate cancer deaths, higher levels of SES were associated with lower mortality rates of prostate cancer deaths (SES Q1 vs. Q5: RR = 0.88; 95% CI: 0.92–0.94). African-Americans had a twofold to fivefold increased risk of prostate cancer deaths in comparison to non-Hispanic Whites across all levels of SES.ConclusionsOur findings suggest that SES alone cannot account for the greater burden of prostate cancer among African-American men. In addition, incidence and mortality rates of prostate cancer display different age and racial/ethnic patterns across gradients of SES.Electronic supplementary materialThe online version of this article (doi:10.1007/s10552-009-9369-0) contains supplementary material, which is available to authorized users.

An Ecological Study of Lung Cancer Mortality and Severe Air Pollution in the 1960s in an Industrial City in Japan

This study aimed at assessing the association between exposure to severe air pollution in the past and the subsequent transition in lung cancer mortality among persons who lived in an industrial city. Vital statistics from 1983 to 2006 and the data on air pollution measurements from 1960 to 1990 in Amagasaki City, Japan, were used. Pearson correlation coefficients were calculated between the standardized mortality ratios (SMRs) for lung cancer and the air pollution levels in 6 wards of Amagasaki City. The associations between changes in air pollution levels and the annual SMRs were also evaluated in the light of a potential latency period. The levels of air pollution were extremely high in the 1960s, and they decreased since 1970. The SMRs for lung cancer in 1989-1993 among females for 6 wards were significantly associated with the amounts of both sulfur oxides and dust fall in the past for each ward. The positive associations were observed between the annual SMRs among females and the amounts of both pollutants when the lag time of 20-30 years was taken into account. These results suggest that severe air pollution in the 1960s in an industrial city affected the subsequent increase in lung cancer mortality.

A prospective study of cardiorespiratory fitness and breast cancer mortality.

Physical activity may protect against breast cancer. Few prospective studies have evaluated breast cancer mortality in relation to cardiorespiratory fitness (CRF), an objective marker of physiologic response to physical activity habits. We examined the association between CRF and risk of death from breast cancer in the Aerobics Center Longitudinal Study. Women (N = 14,811), aged 20 to 83 yr with no prior breast cancer history, received a preventive medical examination at the Cooper Clinic in Dallas, Texas, between 1970 and 2001. Mortality surveillance was completed through December 31, 2003. CRF was quantified as maximal treadmill exercise test duration and was categorized for analysis as low (lowest 20% of exercise duration), moderate (middle 40%), and high (upper 40%). At baseline, all participants were able to complete the exercise test to at least 85% of their age-predicted maximal heart rate. A total of 68 breast cancer deaths occurred during follow-up (mean = 16 yr). Age-adjusted breast cancer mortality rates per 10,000 woman-years were 4.4, 3.2, and 1.8 for low, moderate, and high CRF groups, respectively (trend P = 0.008). After further controlling for body mass index, smoking, drinking, chronic conditions, abnormal exercise ECG responses, family history of breast cancer, oral contraceptive use, and estrogen use, hazard ratios (95% CI) for breast cancer mortality across incremental CRF categories were 1.00 (referent), 0.67 (0.35-1.26), and 0.45 (0.22-0.95) (trend P = 0.04). These results indicate that CRF is associated with a reduced risk of dying from breast cancer in women.

Increased lung cancer risks are similar whether arsenic is ingested or inhaled.

In 1980, the International Agency for Research on Cancer (IARC) determined there was sufficient evidence to support that inorganic arsenic was a human lung carcinogen based on studies involving exposure through inhalation. In 2004, IARC listed arsenic in drinking water as a cause of lung cancer, making arsenic the first substance established to cause human cancer through two unrelated pathways of exposure. It may initially seem counterintuitive that arsenic in drinking water would cause human lung cancer, and even if it did, one might expect risks to be orders of magnitude lower than those from direct inhalation into the lungs. In this paper, we consider lung cancer dose-response relationships for inhalation and ingestion of arsenic by focusing on two key studies, a cohort mortality study in the United States involving Tacoma smelter workers inhaling arsenic, and a lung cancer case-control study involving ingestion of arsenic in drinking water in northern Chile. When exposure was assessed based on the absorbed dose identified by concentrations of arsenic in urine, there was very little difference in the dose-response findings for lung cancer relative risks between inhalation and ingestion. The lung cancer mortality rate ratio estimate was 8.0 (95% CI 3.2-16.5, P<0.001) for an average urine concentration of 1179 microg/l after inhalation, and the odds ratio estimate of the lung cancer incidence rate ratio was 7.1 (95% CI 3.4-14.8, P<0.001) for an estimated average urine concentration of 825 microg/l following ingestion. The slopes of the linear dose-response relationships between excess relative risk (RR-1) for lung cancer and urinary arsenic concentration were similar for the two routes of exposure. We conclude that lung cancer risks probably depend on absorbed dose, and not on whether inorganic arsenic is ingested or inhaled.

Radon Exposure and Mortality Among White and American Indian Uranium Miners: An Update of the Colorado Plateau Cohort

Studies of uranium miners on the US Colorado Plateau have identified associations between exposure to radon progeny and risk of lung cancer. This study added 15 years of mortality follow-up for the 4,137 miners (primarily white or American Indian) in the Colorado Plateau cohort. The cohort experienced 209 new lung cancer deaths. For white miners, the standardized mortality ratio for lung cancer compared with the regional population was 3.99 (95% confidence interval: 3.43, 4.62) for the period 1991-2005. For American Indian miners, the lung cancer standardized mortality ratio was 3.27 (95% confidence interval: 2.19, 4.73). These standardized mortality ratios have not declined substantially since the 1980s. Internally standardized rate ratios by radon exposure category over the entire follow-up period are similar to those based on earlier follow-up, although estimates within smoking categories demonstrated improved precision. The apparent interaction between radon and smoking in causing lung cancer remains submultiplicative but greater than additive. Mortality rates from silicosis remain highly elevated in the cohort. Elevated mortality rates were observed from interstitial pulmonary fibrosis, multiple myeloma, and non-Hodgkin lymphoma. Significant trends were observed with increased radon exposure in silicosis and pulmonary fibrosis mortality and in the incidence of diabetes-related end-stage renal disease among white miners.

Oesophageal-cancer-derived death in the population of Belgrade in a period 1989-2006

Oesophageal cancer is the sixth most common cause of death from all malignant tumors in the world (fifth in men, eighth in women). This cancer was estimated to account for about 529 000 new cases and about 442 000 deaths in the year 2007. In the year 2002 the highest standardized mortality rates (per 100 000 habitants) of oesophageal carcinoma were noticed in the East Asia (men/women: 18.8/7.7) and East Africa (18.6/7.8), while the lowest were noticed in the Middle Africa (1.4/0.2) and West Africa (1.3/0.5). The aim of this descriptive epidemiologic study was to analyze epidemiologic situation of oesophageal cancer in Belgrade population during the period 1989-2006, using mortality data. Mortality data were collected from the City Organization for Statistics. In data analysis we used mortality rates which were standardized directly using those of the world population as the standard, and proportions. A denominator for mortality rates was calculated using the Belgrade population which was an average of the two latest register years (1991 and 2002). In order to analyze trend mortality from oesophageal cancer we used linear trend. In Belgrade deaths from oesophageal cancer accounted for about 5.2% of all malignant tumors of intestinal system in male population, and 2.4% in female population. This cancer is, according to standardized mortality rates (per 100 000 habitants), on the fifth place in Belgrade population behind colorectal, stomach, pancreatic, liver and cholecystic cancer. During the period 1989-2006 in Belgrade 44 persons died from oesophageal carcinoma on the average each year, mainly men (75%), and the rest were women (25%). In male population during the same period we noticed a significant increase in trend mortality (y = 1.61 + 0.06x, p = 0.001), while in female population the increase of mortality was not significant. The male/female oesophageal cancer mortality ratio was 3:1. Mortality rates for oesophageal cancer rise with age in both sexes and they are highest in the age group of 70 and more years. Significant increase in mortality from oesophageal cancer was noticed in age groups 20-29 and over 70 in male population, and age group 40-49 in female population. Increasing trend in oesophageal mortality suggests the necessity for improving measures of primary prevention including education about risk factors for this carcinoma (smoking, alcohol consumption, hot food and drinks), early diagnosis, and treatment.

Does Arsenic Exposure Increase the Risk for Prostate Cancer?

Arsenic has been well documented as the major risk factor for blackfoot disease (BFD), a unique peripheral vascular disease that was endemic to the southwestern coast of Taiwan, where residents consumed artesian well water containing high levels of arsenic for more than 50 yr. Chronic arsenic exposure was also reported to be associated with mortality attributed to prostate cancer in a dose-response relationship. A tap-water supply system was implemented in the early 1960s in the BFD-endemic areas in Taiwan. Artesian well water was no longer used for drinking and cooking after the mid-1970s. The objective of this study was to determine whether prostate cancer mortality decreased after the improvement of drinking-water supply system through elimination of arsenic ingestion from artesian well water. Standardized mortality ratios (SMRs) for prostate cancer were calculated for the BFD-endemic area for the years 1971–2006. Results showed that mortality attributed to prostate cancer declined gradually after the improvement of drinking-water supply system. Based on the reversibility criterion, the association between arsenic exposure and development of prostate cancer is likely to be causal.