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Objectives: To examine the risk of a subsequent pulmonary or extra-pulmonary cancer diagnosis following a first-time hospital-based diagnosis of pneumonia., Design: Population-based cohort study using Danish medical registries., Setting: All hospitals in Denmark., Subjects: A total of 342,609 patients with a first-time hospital-based (inpatient, emergency room or outpatient clinic) diagnosis of pneumonia between 1995 and 2011., Main Outcome Measures: We quantified the excess risk of various cancers amongst pneumonia patients compared to the expected risk in the general population, using relative [standardised incidence ratios (SIRs)] and absolute risk calculations. Follow-up started 1 month after a hospital-based diagnosis of pneumonia and ended on 31 December 2011., Results: A total of 28,496 cancers were observed, compared with 21,625 expected, amongst 342,609 pneumonia patients followed for a median of 4.2 years. The absolute risk of a cancer diagnosis 1 to <6 months following a pneumonia diagnosis was 1.4%, with a corresponding SIR of 2.48 [95% confidence interval (CI) 2.41-2.55]. This was mainly due to an increased risk of lung cancer (eightfold) and haematological cancers (fourfold). The SIR for any cancer remained increased at 1.35 (95% CI 1.30-1.40) during 6-12 months of follow-up, and 1.20 (95% CI 1.18-1.22) during 1-5 years of follow-up. Beyond 5 years, an increased risk was maintained for lung, oesophageal, liver and bladder cancers, squamous cell carcinoma of the skin, lymphoma and multiple myeloma., Conclusions: A hospital-based pneumonia diagnosis was associated with an increased risk of a cancer diagnosis, especially in the ensuing months, but the absolute risk was small., (© 2014 The Association for the Publication of the Journal of Internal Medicine.)

A historical cohort study was conducted to evaluate cancer incidence among chemical workers with occupational and environmental exposure to alachlor, the active ingredient in a family of pre-emergent acetanilide herbicides. The study followed 943 workers with at least 1 year of cumulative employment at the Monsanto plant in Muscatine, Iowa, from startup of the alachlor manufacturing process in March 1968 through December 1990. Approximately 96% of all workers were successfully traced to determine their last known residence and cancer status. Eighteen workers were diagnosed with cancer during the follow-up period, based on pathology information from the statewide cancer registry maintained by the State Health Registry of Iowa. The standardized incidence ratio for all cancers was 1.5 (95% CI 0.9-2.4) for all workers exposed to alachlor, which was due primarily to elevated rates for colorectal cancer and chronic myeloid leukemia. Workers with 5 or more years in estimated high alachlor exposure jobs had elevated rates of colorectal cancer (3 cases, SIR = 5.2, 95% CI 1.1-15.1). Interpretation of the study results is limited by the small size of the study population, minimal length of follow-up, and current information concerning alachlor metabolism in primates and humans. Nonetheless, the findings suggest the need for continued evaluation of this and other alachlor-exposed cohorts.

Population-based data from the Texas Cancer Registry were used to describe the incidence of cancer in 1990 among Texas residents younger than 20 years. A total of 788 primary malignant neoplasms were diagnosed. Higher incidence of all cancers was observed among Texas Anglo children compared with Hispanics or African-Americans, and lower rates of central nervous system (CNS) neoplasms were seen among Hispanics. Compared with national data, significantly fewer cases of all cancers combined, non-Hodgkin's lymphoma, neuroblastoma, and CNS neoplasms were seen in Texas Hispanics. The overall incidence of leukemia and acute nonlymphocytic leukemia (ANLL) was highest in Hispanics compared with other Texas children, and a three-fold statistically significant excess of ANLL was evident in Hispanic females compared with national whites. In summary, the incidence of cancer in Texas Hispanic children and adolescents differs from that seen in other racial and ethnic groups. Incidence data for Texas provide additional insight into the descriptive nature of childhood and adolescent cancers.

Exposure to perchloroethylene (PCE) occurs in a number of occupational settings in which organic solvents are used, and, in particular, is widely prevalent in the dry-cleaning industry. This review summarizes the results of studies of the occurrence of the individual types of cancer in dry cleaners. Two of those cancers of greatest a priori concern (because of results in PCE-exposed experimental animals)--liver cancer and leukemia--have not occurred with increased frequency among persons employed in the dry-cleaning industry. Rates were elevated by about a factor of two for esophageal and bladder cancers, but not increased clearly for any other site. The excess mortality from esophageal cancer was well beyond the limits of chance, based on a total of 23 deaths that occurred in the two principal cohort-studies of dry cleaners. There was some indication of a particularly high risk associated with prolonged employment and a long interval since first employment. However, the possible confounding effect of the combination of cigarette smoking and heavy alcohol consumption, a very strong risk factor for the development of esophageal cancer, could be taken into account only partially in these studies. With regard to bladder cancer, the limited data available suggest that the observed increased risk could be due to exposure to other solvents than PCE used in dry cleaning. The potential influence of occupational exposure to PCE on the occurrence of esophageal and bladder cancer needs continued examination in further follow-up of existing cohorts of dry cleaners, the assembly of additional cohorts, and in large case-control studies that ascertain occupational exposures in some detail.

In order to determine if exposure to carcinogens in fire smoke increases the risk of cancer, we examined the incidence of cancer in a cohort of 2,447 male firefighters in Seattle and Tacoma, (Washington, USA). The study population was followed for 16 years (1974-89) and the incidence of cancer, ascertained using a population-based tumor registry, was compared with local rates and with the incidence among 1,878 policemen from the same cities. The risk of cancer among firefighters was found to be similar to both the police and the general male population for most common sites. An elevated risk of prostate cancer was observed relative to the general population (standardized incidence ratio [SIR] = 1.4, 95 percent confidence interval [CI] = 1.1-1.7) but was less elevated compared with rates in policemen (incidence density ratio [IDR] = 1.1, CI = 0.7-1.8) and was not related to duration of exposure. The risk of colon cancer, although only slightly elevated relative to the general population (SIR = 1.1, CI = 0.7-1.6) and the police (IDR = 1.3, CI = 0.6-3.0), appeared to increase with duration of employment. Although the relationship between firefighting and colon cancer is consistent with some previous studies, it is based on small numbers and may be due to chance. While this study did not find strong evidence for an excess risk of cancer, the presence of carcinogens in the firefighting environment warrants periodic re-evaluation of cancer incidence in this population and the continued use of protective equipment.

In registry-based population studies on marital status in relation to cancer, incidence rates sometimes have been calculated using marital status-specific populations that have been estimated by interpolation and extrapolation from census data as a denominator. Alternatively, other cancers from the same registry have been used to estimate the proportion of the population in each marital-status category in the calculation of the relative risk (RR) of a given cancer. Using cancer registry data from four United States populations for the years 1979-87, we compared the relative incidence estimated using each of the two methods. For selected cancers diagnosed during 1979-81, the age-adjusted risks of never-married Black persons were 1.5 to 2.2 times those of married persons when the population size was estimated from census data. The corresponding RRs were 0.7 to 1.1 when the 'control' cancers were used. Among Whites, the differences between the two methods were about 20 to 30 percent. For both races, the difference between the methods was greater still for the years for which we relied on extrapolation to estimate the population (1981-87). The differences between the risk estimates from the two methods may be related to underenumeration in the census, inconsistent definitions of marital status between cancer registries and the census, errors in the extrapolation of the population, and/or the possible association of the incidence of 'control' cancers with marital status. In the US, while each method has some potential for bias, we believe that the likelihood of bias is relatively greater using the census-based method.

Studies of cancer incidences among occupational cohorts are rarely performed in the United States because of incomplete registration and a limited time period available for follow-up. This study used data from concurrent studies of cancer mortality and incidence among a cohort of 4,528 fire fighters and police officers employed by the cities of Seattle and Tacoma, Washington, between 1944 and 1979 to examine the relative advantages of tumor registry and death certificate information. As expected, an increased ability to study relatively common cancers with low fatality rates was demonstrated using incidence data. The most dramatic example was seen for bladder cancer. Twenty-four bladder cancers had been diagnosed among the study cohort between 1974 and 1989, whereas only two deaths were attributed to this malignancy. The standardized incidence ratio for bladder cancer was 1.05 (95% confidence interval 0.67-1.55), whereas the corresponding standardized mortality ratio was 0.46 (95% confidence interval 0.05-1.65). The observed relative risk estimates for rapidly fatal cancers were similar using the two sources of information, and no increase in precision was observed. Of 142 persons in the registry area who died of cancer during the study period, 20 (14%) had a different site listed on the death certificate than was identified by the registry. Approximately 7% of the potential person-years of follow-up were lost due to migration out of the registry area; loss to follow-up was greater among older and short-term workers, but did not exceed 13% of the person-years. Population-based tumor registries can be a useful resource in the investigation of occupational cancer in the United States, especially for the study of cancers with high survival rates.

To an increasing extent, case-control studies are being undertaken to determine if use of early detection procedures is associated with reduced mortality from cancer. The authors recommend that in such studies the analysis focus on screening activity in cases that occurs during an interval prior to diagnosis in which the cancer is believed to be detectable and still curable and to a corresponding time period in controls. This approach places a heavy burden on the investigator to estimate accurately the period during which the tumor ought to be detectable using the test in question and to sort out reliably tests done in response to signs or symptoms of the cancer from screening tests per se. Nonetheless, the authors feel that it offers the greatest ability to discern a true benefit of screening, while minimizing the numerous potential biases that can be present in this type of study.

Background: There is considerable interindividual variation in the activity of enzymes which metabolize polycyclic aromatic hydrocarbon constituents of tobacco smoke. Low activity of enzymes which detoxify carcinogenic polycyclic aromatic hydrocarbon metabolites may be associated with increased susceptibility to cancers etiologically related to cigarette smoking., Purpose: We conducted a population-based, case-control study to determine whether patients with cancers related to smoking had lower activity of detoxifying isoenzymes of glutathione S-transferase (GST) and epoxide hydrolase (EH) than control subjects., Methods: Enzyme activities were measured in leukocytes from 113 King County (Washington) residents diagnosed during 1987 with one of three smoking-related cancers (lung, oropharynx/oral cavity, or bladder), 50 King County residents with cancers believed unrelated to smoking (prostate cancer or non-Hodgkin's lymphoma), and 120 persons selected at random from the King County population. Enzyme activity measurements were made for leukocyte cytosolic GST toward transstilbene oxide (TSO), 1-chloro-2,4-dinitrobenzene, and benzo[a]pyrene-4,5-oxide (BaPO), and for microsomal EH toward BaPO., Results: Overall, the distribution of activity levels of GST toward TSO and BaPO did not differ in case patients with smoking-related cancer compared with control subjects. The activities of GST toward 1-chloro-2,4-dinitrobenzene and of EH toward BaPO were somewhat lower on average in case patients with smoking-related cancers than in control subjects, but these differences were well within the limits of chance. Among the heaviest smokers, there were proportionately fewer patients with smoking-related cancers than control subjects with intermediate or high GST activity toward TSO (odds ratio = 0.6), but this difference was also plausibly due to chance (95% confidence interval = 0.3-1.1)., Conclusions: While the findings of this study are compatible with a moderate protective effect of high or intermediate enzyme activity among persons heavily exposed to tobacco, as suggested by an earlier report, the data are by no means conclusive.

A retrospective cohort mortality study of 1,008 male oil refinery workers who ever worked on the lubricating-dewaxing process of the lube oil department and who have been followed for a period of 43 years is presented. These workers were exposed to a number of solvents, primarily methyl ethyl ketone [(MEK) CAS: 78-93-3] and toluene (CAS: 108-88-3), but at levels far below the current Occupational Safety and Health Administration's standard. The standardized mortality ratio (SMR) for all causes (0.70) and the SMR for cancer (0.86) are much lower than unity when they are compared to the mortality experience of the U.S. population. Also observed in this study were 8 prostate cancer deaths (4.4 expected) with an SMR of 1.82, which was not statistically significant (P = .16). Seven of these 8 prostate cancer deaths occurred among nonwhite males, who showed an SMR of 2.47 (P = 0.53). However, only 1 prostate cancer death was seen among workers specifically assigned to the MEK units. The remaining deaths occurred among maintenance workers who had lube oil department-wide assignments. This cancer risk increased with increasing duration of employment in the lube oil department. A latency of 20 years or more was also observed for these prostate cancer deaths. In this study the processing of lubricating oils was found to be at least as important as the MEK solvents, and department-wide maintenance workers were as much at risk as the MEK unit workers. In view of this finding and findings obtained by others, it seems prudent to continue to study lubricating-dewaxing process workers, including the medical monitoring of all such workers for prostate cancer.

A nested case-control study was conducted to assess the relation between serum levels of selenium and retinol and the subsequent risk of cancer. During the years 1972-1984, in northwest Washington State, 156 cases of cancer were identified among members of two employee cohorts from whom specimens had been previously obtained and stored. Two hundred eighty-seven controls were selected from these cohorts and matched to cases on the basis of employer, age, sex, race, and date of blood draw. Selenium and retinol levels were measured by neutron activation and high pressure liquid chromatography, respectively. Information on known cancer risk factors was collected by telephone interviews of subjects and next of kin. Levels of selenium and retinol were unassociated with the incidence of cancer of all sites combined, both overall and within subgroups defined by age, sex, levels of the other micronutrient, time between blood draw and diagnosis, smoking status, and family history of cancer. These findings suggest that neither serum levels of selenium nor those of retinol have an appreciable effect on the risk of cancer.

The relationship of weight at birth to the occurrence of childhood cancer was studied with emphasis on the influence of age at diagnosis. Birth certificates for 681 children with cancer born in Washington State were linked with cancer registry data. Among children diagnosed with cancer during the first several years of life, there was an increased proportion with a high birth weight (greater than 4,000 g). The relationship was strongest for children under 2 years of age; about twice as many of them had high birth weights. However, the relationship was not present at all in those whose cancer was diagnosed at age 4 or older. This excess risk in young children associated with high birth weight was distributed among several types of cancer, including the two most common ones (leukemia and neuroblastoma).

A nested, matched case-control study was conducted to assess the relationship between serum levels of copper and the subsequent risk of cancer. One hundred thirty-three cases of cancer were identified during 1974-1984 among 5000 members of a northwest Washington State employee cohort from whom serum specimens had been previously obtained and stored. Two hundred forty-one controls were selected at random from the cohort and were matched to the cases on the basis of age, sex, race, and date of blood draw. Serum copper levels were measured by atomic absorption spectrometry. Risk of a subsequent diagnosis of cancer was positively associated with serum copper levels, but only among those cases diagnosed within 4 years of the time the serum specimens were collected. Among cases diagnosed more than 4 years after specimen collection, there was no consistent association between serum copper levels and risk. Adjustment for age, sex, race, occupational status, cigarette smoking, family history of cancer, alcohol consumption, and, among females, use of exogenous hormones had no appreciable effect on these relationships. The findings suggest that the presence of cancer may increase serum copper levels several years prior to its diagnosis. They are less supportive of the hypothesis that serum copper levels affect cancer risk.