Cancer incidence among semiconductor and electronic storage device workers.

AIMS: To evaluate cancer incidence among workers at two facilities in the USA that made semiconductors and electronic storage devices. METHODS: 89 054 men and women employed by International Business Machines (IBM) were included in the study. We compared employees' incidence rates with general population rates and examined incidence patterns by facility, duration of employment, time since first employment, manufacturing era, potential for exposure to workplace environments other than offices and work activity. RESULTS: For employees at the semiconductor manufacturing facility, the standardised incidence ratio (SIR) for all cancers combined was 81 (1541 observed cases, 95% confidence interval (CI) 77 to 85) and for those at the storage device manufacturing facility the SIR was 87 (1319 observed cases, 95% CI 82 to 92). The subgroups of employees with > or =15 years since hiring and > or =5 years worked had 6-16% fewer total incidents than expected. SIRs were increased for several cancers in certain employee subgroups, but analyses of incidence patterns by potential exposure and by years spent and time since starting in specific work activities did not clearly indicate that the excesses were due to occupational exposure. CONCLUSIONS: This study did not provide strong or consistent evidence of causal associations with employment factors. Data on employees with long potential induction time and many years worked were limited. Further follow-up will allow a more informative analysis of cancer incidence that might be plausibly related to workplace exposures in the cohort.

Birth weight, maternal weight and childhood leukaemia.

There is mounting evidence that childhood leukaemia is associated with high birth weight, but few studies have examined the relationship between leukaemia and other perinatal factors that influence birth weight, such as maternal weight or gestational weight gain. This case-cohort study included 916 acute lymphocytic leukaemia (ALL) and 154 acute myeloid leukaemia (AML) cases diagnosed prior to age 10 years between 1985 and 2001 and born in New York State excluding New York City between 1978 and 2001. Controls (n=9686) were selected from the birth cohorts for the same years. Moderate increased risk of both ALL and AML was associated with birth weight 3500 g or more. For ALL, however, there was evidence of effect modification with birth weight and maternal prepregnancy weight. High birth weight was associated with ALL only when the mother was not overweight while heavier maternal weight was associated with ALL only when the infant was not high birth weight. Increased pregnancy-related weight gain was associated with ALL. For AML, birth weight under 3000 g and higher prepregnancy weight were both associated with increased risk. These findings suggest childhood leukaemia may be related to factors influencing abnormal fetal growth patterns.

Cancer incidence in New York State acquired immunodeficiency syndrome patients.

To identify cancers that occur at higher rates in acquired immunodeficiency syndrome (AIDS) patients, the cancer experience of New York State (NYS) AIDS patients aged 15-69 years who were diagnosed between 1981 and 1994 was compared with that of the NYS general population. Sex and HIV risk group-specific standardized incidence ratios (SIRs), post-AIDS relative risks, and trends of relative risks were calculated to determine cancer risk. Among non-AIDS-related cancers, elevated SIRs were found for Hodgkin's disease (male, 8.0; female, 6.4; heterosexually infected males, 31.3); cancer of the rectum, rectosigmoid, and anus (male, 3.3; female, 3.0); trachea, bronchus, and lung (male, 3.3; female, 7.5); and brain and central nervous system (male, 3.1; female, 3.4; heterosexually infected females, 23.8) cancers. Moreover, significant trends of increasing relative risks from the pre-AIDS to the post-AIDS period were found for cancers of the rectum, rectosigmoid, and anus; trachea, bronchus, and lung; skin; and connective tissues (all sites, p < 0.05) among males. For AIDS-related cancers in women, invasive cervical cancer had an overall SIR of 9.1 (95% confidence interval: 6.9, 10.8) and a post-AIDS relative risk of 6.5 (95% confidence interval: 4.1, 9.7). This population-based registry linkage analysis evaluates cancer risk in AIDS patients by sex and risk factors and adds evidence that HIV-associated immunosuppression increases the risks of specific types of cancer.

Relationship of leukemia risk to radiation dose following cancer of the uterine corpus.

BACKGROUND: Radiotherapy has been linked infrequently to secondary leukemia despite extensive exposure of the active bone marrow to ionizing radiation. Few studies include substantial numbers of elderly patients. PURPOSE: We evaluated women with cancer of the uterine corpus, the majority of whom were treated at older ages, to gain additional information on cancer risk following partial-body radiotherapy and to examine differences in risk between external-beam therapy and brachytherapy. METHODS: A cohort of 110,000 women with invasive cancer of the uterine corpus who survived at least 1 year following their initial cancer was assembled from nine population-based cancer registries. Cancer diagnoses occurred from 1935 through 1985, and most patients were diagnosed during the 1960s and 1970s. Radiation doses were computed to 17 sections of the active bone marrow for 218 women who developed leukemia and for 775 matched control subjects. RESULTS: Radiotherapy did not increase the risk of chronic lymphocytic leukemia (CLL) (relative risk [RR] = 0.90; 95% confidence interval [CI] = 0.4-1.9). However, for all leukemias except CLL, a significant risk was identified (RR = 1.92; 95% CI = 1.3-2.9). Overall, the pattern of risk in relation to dose was erratic and was most consistent with a constant increased risk across the entire dose range. The risk following continuous exposures from brachytherapy at comparatively low doses and low dose rates (RR = 1.80; 95% CI = 1.1-2.8; mean dose = 1.72 Gy) was similar to that after fractionated exposures at much higher doses and higher dose rates from external-beam treatment (RR = 2.29; 95% CI = 1.4-3.7; mean dose = 9.88 Gy), indicating a large difference in the estimated risk per unit dose. Risk did not vary by age at first exposure; increased risks were apparent for irradiated patients aged 65 years or older (RR = 1.77; 95% CI = 0.9-3.5). CONCLUSION: The leukemia risk associated with partial-body radiotherapy for uterine corpus cancer was small; about 14 excess leukemia cases were due to radiation per 10,000 women followed for 10 years. Women aged 65 years or older had a radiation risk comparable with that found in younger women. The relationship of leukemia risk to radiation dose was found to be complex due to the competing processes of cell killing, transformation, and repair. At very high doses delivered at high rates, destruction of cells likely dominates, and the risk per unit dose is low. In the low dose range, where dose was protracted and delivered at relatively low dose rates, the leukemia risk appears lower than that projected from risk estimates derived from the instantaneous whole-body exposures of atomic bomb survivors.

Patterns of invasive melanoma in the Connecticut Tumor Registry. Is the long-term increase real?

The decades-long increase in incidence rates for melanoma has been ascribed to artifactual changes in case ascertainment rather than to true changes in disease risk. In this study, population-based incidence data for invasive cutaneous malignant melanoma from the Connecticut Tumor Registry were categorized into seven age groups and four time periods to examine the pattern of change over four decades. Analyses of age, period, and cohort variables focused on the curvature components, which are estimable functions. Statistical modeling demonstrated the following: (1) incidence rates have increased by birth cohort in both sexes with no requirement for a period variable, regardless of whether data are examined by 10-year, 5-year, or 1-year intervals of diagnosis; (2) this pattern in incidence rates differed from the patterns of change in the two indices of case ascertainment, the proportion of cases confirmed microscopically and the proportion of cases in localized stage, both of which exhibited changes by period of diagnosis rather than by birth cohort; and (3) adjustment for these two indices caused a downward bend in the cohort curve for females but not for males. The results suggested that much of the observed increase for this tumor was real.

Trends in the incidence of childhood and adolescent cancer in Connecticut, 1935-1979.

Trends in the incidence of childhood cancer in Connecticut are reported and analyzed for the period 1935-1979 by 5-year age groups (0-4, 5-9, 10-14, 15-19 years), using a log linear model method. A threefold increase (P less than .001) in the incidence of ALL in males 0-4 years of age was observed, with significant increases of smaller magnitude seen in males aged 5-9 and 15-19 and females aged 0-4 and 5-9. The incidence of central nervous system cancers also increased in several age groups for both sexes with the largest increase seen in males 0-4 years old. Significant increases in incidence of large magnitude were also observed for Hodgkin's disease, in males aged 15-19 years and females aged 10-19 years, for neuroblastoma in both sexes at ages 0-4 years, and for testis and ovarian cancer at ages 15-19 years. This study of trends in incidence of childhood cancers by 5-year age groups has revealed significant changes, which would not have been as apparent if broader age groups had been used. These results provide relevant data for investigating the etiology of cancer during infancy, childhood, and adolescence. Trends in Connecticut are compared with findings from other registries in the United States and other countries.

Time and age trends for sinonasal cancer in Connecticut incidence and US mortality rates.

Population-based rates for sinonasal cancer are examined in US mortality data among whites and in Connecticut incidence data. The observed rates are fitted to a log-linear model in order to examine the effect of each of the three variables, age, period and cohort, simultaneously for each sex. For Connecticut incidence, there is little evidence of either an increase or decrease from 1865 to 1955 birth cohorts. For the US mortality rates, from the 1875 to 1950 birth cohorts, there is a decline by more than twofold in men and more than threefold in women. Monitoring of those trends is discussed with respect to increases in exposure to cigarette smoking and formaldehyde. Regarding the age distribution, both incidence and mortality data are consistent: men show a linear increase of the log (rate) with log (age) in a fashion characteristic of other epithelial nongynecologic malignancies; for women, in contrast, there is a downward curvature around age 50 followed by an upward curvature in the 55 to 70 age range. The rate in most postmenopausal age groups is 20% to 67% of the rate expected on the basis of a linear increase of the log (rate) with log (age). The age patterns in women are similar to "Clemmesen's hook" observed for female breast cancer. There is evidence that the pattern in female subjects differs significantly from that for male subjects. The female age pattern requires confirmation in other populations. An etiologic role for sex hormones is hypothesized in view of that age distribution and in view of physiologic and laboratory observations.

Risk for cutaneous melanoma in recent Connecticut birth cohorts.

Mortality trends suggest that increases in Connecticut incidence for cutaneous melanoma (CM) equal or under estimate increases for the entire country. One-sixth of CM in Connecticut occurs under age 35. In the 1955 birth cohort, modeled incidence rates per 100,000 age-adjusted to the 1960 US population are 38.2 in males and 28.9 in females. These estimated rates for CM rival those for colon cancer (now the third most common malignancy in the United States) and have special implications for young adults.

Time period compared to birth cohort in Connecticut incidence rates for twenty-five malignant neoplasms.

Out of necessity and convenience many reports on population-based rates for cancer are limited to analyses by time period of diagnosis, and just how often cohort effects are important in cancer data has not been fully explored. To address this question, Connecticut cancer incidence rates for the years 1940-79 were fitted to the model: Log (incidence rate) = constant + age effect + period effect + birth cohort effect + error term. Data for each cancer site and sex were categorized into 10-year intervals by time period and age group. Significance testing for the curvilinear effects (which are estimable functions) of age (A), period (P), and cohort (C) in the 44 data sets led to no clear choice of model for three data sets; an APC model for 20, an AP model for 7, and an AC model for 14. These choices were corroborated by the RA2 index. Limitations in the interpretation of the results were enumerated. Presentation of population-based cancer rates by implicitly assuming an AP model is valuable (e.g., for studying age distribution in different regions or for age-adjustment in examining international variation or time trends). However, the assumption of an AP model may often be incorrect, as was shown to be the case for most of these 44 data sets. The implications for monitoring trends and generating etiologic hypotheses were discussed in light of the results for cutaneous malignant melanoma and cancers of the cervix, breast, ovary, lung, and bladder.

Secular and age distribution of scrotal cancer in Connecticut and a review of United States literature.

In contrast with the expectations of the authors and with reports suggesting a decline in risk for scrotal cancer, Connecticut Tumor Registry data neither showed detectable decrease in risk over the 45-year-period for all 95 scrotal malignancies nor for the 71 epithelial cancers. The age distribution of scrotal cancer in Connecticut was similar to that of the more common tumors thought to be caused by exogenous agents. The risk increased up to age 75 in a geometric fashion, followed by a plateau and decline in risk among the very elderly. United States literature on scrotal cancer points to a change in occupational risks; this literature and recent occupational data from Connecticut suggest that metalworking may have been associated with a high proportion of cases in recent decades. Evidence is lacking that scrotal cancer and its most recent marker of carcinogenic risk have been fully eliminated.