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Biomedical subjects

Michael Hauptmann

Publications and source records attributed to Michael Hauptmann.

At least 19 recordsLinked to original sources
PubMed2006

Lung cancer risk among US radiologic technologists, 1983-1998.

While exposure to moderate to high-dose ionizing radiation is an established risk factor for lung cancer, the relationship between lung cancer and chronic low dose radiation remains uncertain. We examined lung cancer risk among 71,894 US radiologic technologists who were certified during 1926-1982, responded to a baseline questionnaire (1983-1989), and were free of cancer other than non-melanoma skin cancer at baseline. Study participants were followed until completion of a second questionnaire (1994-1998), death, or August 31, 1998. We identified 287 lung cancer cases: 66 incident cases and 221 decedents. Exposure to radiation was inferred based on work history information provided in the baseline questionnaire. Relative risks (RRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazard models adjusted for age, race/ethnicity and smoking. Smoking-adjusted lung cancer risk was not related to working as a radiologic technologist in early years when radiation exposures were likely highest (RR = 0.9; 95% CI, 0.5-1.8 for year first worked before 1940 compared to year first worked >or=1960), nor was risk related to the year first worked after 1940 or the number of years worked in any decade. While lung cancer risk was increased in radiologic technologists who held patients for X-rays, or who allowed others to take numerous practice X-rays on them, the trend was not statistically significant in either case. Although we adjusted for smoking, the possibility of residual confounding exists. Overall, we find very limited evidence that chronic low-to-moderate dose occupational exposure increased lung cancer risk in the US Radiologic Technologist cohort.

Adult↗
PubMed2006

Relationship between clinical factors and the incidence of toxicity after intra-arterial chemoradiation for head and neck cancer.

BACKGROUND AND PURPOSE: Concomitant chemoradiation is more and more used for advanced head and neck cancer. It improves local control and survival compared to radiotherapy alone, but goes along with serious toxicity. This study was set up to determine the relationship between patient-, tumour- and treatment-related factors and acute/late toxicity after concomitant chemoradiation. PATIENTS AND METHODS: One hundred and twenty-five consecutive patients with newly diagnosed inoperable stage III and IV head and neck cancer were enrolled for intra-arterial chemoradiation. There were 28 women (22%) and 97 men (78%) and the mean age was 55 years (range 30-80). One hundred and nine patients had stage IV disease (87%), 16 patients (13%) had stage III disease. Statistical analyses were performed to identify an association between factors and acute/late toxicity. RESULTS: There were eight treatment-related deaths (6%). Severe acute toxicity (grade 3-4), mainly mucositis and dysphagia as categorized by the RTOG toxicity criteria, was recorded in 51% of the patients. Leucopenia (grade 3-4) occurred in 39% and aspiration pneumonia in 20% of patients. Tracheotomy was necessary in 15 (12%) patients. Neurological complications during treatment occurred in 3 (2%) patients. Severe late toxicity occurred in 34% of the patients. The most important of these were pneumonia (14%), osteoradionecrosis (9%) and swallowing problems with permanent percutaneous gastrostomy (20%). Statistical analysis did show a significant association between site and severe acute mucositis (p = 0.007), site and osteoradionecrosis (p = 0.014) and age and xerostomia (p = 0.004). CONCLUSIONS: Chemoradiation is frequently associated with serious toxicity. Oral cavity tumours and older age are related to acute mucositis/osteoradionecrosis and xerostomia, respectively.

Adult↗
PubMed2006

Thyroid cancer and employment as a radiologic technologist.

The association between chronic occupational ionizing radiation exposure in the medical field and thyroid cancer is not well characterized. Thyroid cancer incidence was ascertained for 2 periods in a cohort of radiologic technologists certified for a minimum 2 years and enumerated in 1983: (i) cases identified prospectively in 73,080 radiologic technologists who were free of thyroid cancer at the baseline survey and completed a second questionnaire a decade later (N = 121), and (ii) cases occurring prior to cohort enumeration among 90,245 technologists who completed the baseline survey and were thyroid cancer free 2 years after certification (N = 148). Survival analyses estimated risks associated with employment as a radiologic technologist, including duration of employment, period of employment, types of procedures and work practices. The only occupational history characteristic associated with prospectively identified thyroid cancer was a history of holding patients for X-ray procedures at least 50 times (HR = 1.47, 95% CI = 1.01-2.15). Total years worked as a radiologic technologist, years performing diagnostic, therapeutic, and nuclear medicine procedures, employment under age 20 and calendar period of first employment were not associated with thyroid cancer risk. Risk of thyroid cancers diagnosed before the baseline questionnaire was inversely associated with decade first employed as a technologist, and was elevated, albeit imprecisely, among those working more than 5 years prior to 1950 (HR = 3.04, 95% CI = 1.01-10.78). These data provide modest evidence of an association between employment as a radiologic technologist and thyroid cancer risk; however, the findings require confirmation with more accurate exposure models.

Adult↗
PubMed2006

Breast cancer incidence in U.S. radiologic technologists.

BACKGROUND: Studies of atomic bomb survivors and medically exposed populations have demonstrated an increased risk of breast cancer associated with acute or protracted, intermediate-dose or high-dose, ionizing radiation; however, the risks associated with low-dose and low-dose-rate (protracted) exposures are less certain. METHODS: The authors evaluated incident breast cancer risks from 1983 to 1998 according to employment characteristics and a 4-level proxy index for cumulative radiation exposure based on 2 mail surveys among 56,436 U.S. female radiologic technologists who were certified from 1925 to 1980, adjusting for established breast cancer risk factors. RESULTS: During follow-up, 1050 new breast cancer diagnoses were ascertained. Compared with radiologic technologists who began working in 1970 or later, adjusted breast cancer risks for those who first worked in the 1960s, 1950s, 1940s, from 1935 to 1939, and before 1935 were 1.0 (95% confidence interval [CI], 0.8-1.2), 1.2 (95% CI, 0.9-1.6), 1.0 (95% CI, 0.7-1.5), 1.8 (95% CI, 1.0-3.2), and 2.9 (95% CI, 1.3-6.2), respectively. The risk rose with the number of years worked before 1940 (P value for trend = .002) and was elevated significantly among those who began working before age 17 years (relative risk, 2.6; 95% CI, 1.3-5.1; 10 women) but was not related to the total years worked in the 1940s or later. Compared with technologists who had a Level 1 (minimal) proxy index for cumulative radiation exposure, breast cancer risks were 1.0 (95% CI, 0.9-1.2), 1.0 (95% CI, 0.7-1.3), and 1.5 (95% CI, 1.0-2.2), respectively, for technologists who had Level 2, Level 3, and Level 4 (highest) exposure. CONCLUSIONS: Breast cancer risk was elevated significantly in female radiologic technologists who experienced daily low-dose radiation exposures over several years that potentially resulted in appreciable cumulative exposure. The increased risk for total years worked before 1940, but not later, was consistent with decreasing occupational radiation exposures, improvements in radiation technology, and more stringent radiation protection standards over time.

Adult↗
PubMed2006

Interventional radiography and mortality risks in U.S. radiologic technologists.

With the exponential increase in minimally invasive fluoroscopically guided interventional radiologic procedures, concern has increased about the health effects on staff and patients of radiation exposure from these procedures. There has been no systematic epidemiologic investigation to quantify serious disease risks or mortality. To quantify all-cause, circulatory system disease and cancer mortality risks in U.S. radiologic technologists who work with interventional radiographic procedures, we evaluated mortality risks in a nationwide cohort of 88,766 U.S. radiologic technologists (77% female) who completed a self-administered questionnaire during 1994-1998 and were followed through 31 December 2003. We obtained information on work experience, types of procedures (including fluoroscopically guided interventional procedures), and protective measures plus medical, family cancer history, lifestyle, and reproductive information. Cox proportional hazards regression models were used to compute relative risks (RRs) with 95% confidence intervals (CIs). Between completion of the questionnaire and the end of follow-up, there were 3,581 deaths, including 1,209 from malignancies and 979 from circulatory system diseases. Compared to radiologic technologists who never or rarely performed or assisted with fluoroscopically guided interventional procedures, all-cause mortality risks were not increased among those working on such procedures daily. Similarly, there was no increased risk of mortality resulting from all circulatory system diseases combined, all cancers combined, or female breast cancer among technologists who daily performed or assisted with fluoroscopically guided interventional procedures. Based on small numbers of deaths (n=151), there were non-significant excesses (40%-70%) in mortality from cerebrovascular disease among technologists ever working with these procedures. The absence of significantly elevated mortality risks in radiologic technologists reporting the highest frequency of interventional radiography procedures must be interpreted cautiously in light of the small number of deaths during the relatively short follow-up. The present study cannot rule out increased risks of cerebrovascular disease, specific cancers, and diseases with low case-fatality rates or a long latency period preceding death.

Adult↗
PubMed2006

Estimating historical radiation doses to a cohort of U.S. radiologic technologists.

Data have been collected and physical and statistical models have been constructed to estimate unknown occupational radiation doses among 90,000 members of the U.S. Radiologic Technologists cohort who responded to a baseline questionnaire during the mid-1980s. Since the availability of radiation dose data differed by calendar period, different models were developed and applied for years worked before 1960, 1960- 1976 and 1977-1984. The dose estimation used available film-badge measurements (approximately 350,000) for individual cohort members, information provided by the technologists on their work history and protection practices, and measurement and other data derived from the literature. The dosimetry model estimates annual and cumulative occupational badge doses (personal dose equivalent) for each technologist for each year worked from 1916 through 1984 as well as absorbed doses to organs and tissues including bone marrow, female breast, thyroid, ovary, testes, lung and skin. Assumptions have been made about critical variables including average energy of X rays, use of protective aprons, position of film badges, and minimum detectable doses. Uncertainty of badge and organ doses was characterized for each year of each technologist's working career. Monte Carlo methods were used to generate estimates of cumulative organ doses for preliminary cancer risk analyses. The models and predictions presented here, while continuing to be modified and improved, represent one of the most comprehensive dose reconstructions undertaken to date for a large cohort of medical radiation workers.

Adolescent↗
PubMed2005

DNA damage among thyroid cancer and multiple cancer cases, controls, and long-lived individuals.

Variation in the detection, signaling, and repair of DNA damage contributes to human cancer risk. To assess capacity to modulate endogenous DNA damage among radiologic technologists who had been diagnosed with breast cancer and another malignancy (breast-other, n=42), early-onset breast cancer (early-onset, age or=75% versus below the median, age-adjusted) was most consistently associated with the highest odds ratios in the breast-other, early-onset, and thyroid cancer groups (with risk increased 10-, 5- or 19-fold, respectively, with wide confidence intervals) and decreased risk among the hyper-normal group. For the other three comet measures, risk of breast-other was elevated approximately three-fold. Risk of early-onset breast cancer was mixed and risk of thyroid cancer ranged from null to a two-fold increase. The hyper-normal group showed decreased odds ratios for tail DNA and OTM, but not CDM. DNA damage, as estimated by all comet measures, was relatively unaffected by survival time, reproductive factors, and prior radiation treatment. We detected a continuum of endogenous DNA damage that was highest among cancer cases, less in controls, and suggestively lowest in hyper-normal individuals. Measuring this DNA damage phenotype may contribute to the identification of susceptible sub-groups. Our observations require replication in a prospective study with a large number of pre-diagnostic samples.

Analysis of Variance↗
PubMed2005

Nonmelanoma skin cancer in relation to ionizing radiation exposure among U.S. radiologic technologists.

Ionizing radiation (IR) is an established cause of nonmelanoma skin cancer, but there is uncertainty about the risk associated with chronic occupational exposure to IR and how it is influenced by ultraviolet radiation (UVR) exposure. We studied 1,355 incident cases with basal cell carcinoma (BCC) and 270 with squamous cell carcinoma (SCC) of the skin in a cohort of 65,304 U.S. white radiologic technologists who responded to the baseline questionnaire survey in 1983-1989 and the follow-up survey in 1994-1998. Cox's proportional-hazards model was used to estimate relative risks of BCC and SCC associated with surrogate measures of occupational exposure to IR and residential UVR exposure during childhood and adulthood, adjusted for potential confounders including pigmentation characteristics. Relative risks of BCC, but not of SCC, were elevated among technologists who first worked during the 1950s (RR = 1.42; 95% CI = 1.12-1.80), 1940s (RR = 2.04; 95% CI = 1.44-2.88) and before 1940 (RR = 2.16; 95% CI = 1.14-4.09), when IR exposures were high, compared to those who first worked after 1960 (p for trend < 0.01). The effect of year first worked on BCC risk was not modified by UVR exposure, but was significantly stronger among individuals with lighter compared to darker eye and hair color (p = 0.013 and 0.027, respectively). This study provides some evidence that chronic occupational exposure to IR at low to moderate levels can increase the risk of BCC, and that this risk may be modified by pigmentation characteristics.

Adult↗
PubMed2005

Particulate air pollution and nonfatal cardiac events. Part I. Air pollution, personal activities, and onset of myocardial infarction in a case-crossover study.

We conducted a prospective case-crossover study to assess the association of particulate air pollution with onset of nonfatal myocardial infarction (MI). Patients who had survived MIs between February 1999 and July 2001 were identified based on the Coronary Event Registry in Augsburg, Southern Germany. The study included 851 MI subjects with known date and time of MI who had survived the first 24 hours and had completed the Registry's standard interview. Of these subjects, 691 provided case and control information for subject-specific MI triggers collected by a diary assessing the 4 days before symptom onset. The exposures of interest were the total number concentration (TNC) of particles as an indicator for ultrafine particles and the mass of particles with an aerodynamic diameter no larger than 2.5 microm (PM2.5). We conducted conditional logistic regression analyses using different control-selection strategies in a case-crossover approach, and Poisson regression analyses of the time-series data.

Activities of Daily Living↗
PubMed2004

Mortality from solid cancers among workers in formaldehyde industries.

In industrial workers, formaldehyde exposure has been associated with cancer of the nasal cavities, nasopharynx, prostate, lung, and pancreas; however, these associations are inconsistent and remain controversial. Animals exposed to formaldehyde show excesses of nasal cancer. In an extended follow-up of a large cohort of formaldehyde-exposed workers, the authors evaluated mortality from solid cancers (1,921 deaths) among 25,619 workers (865,708 person-years) employed in 10 US formaldehyde-producing or -using facilities through 1994. Exposure assessment included quantitative estimates of formaldehyde exposure. Standardized mortality ratios and relative risks were calculated. Compared with that for the US population, mortality from solid cancers was significantly lower than expected among subjects exposed and nonexposed to formaldehyde (standardized mortality ratios = 0.91 and 0.78, respectively). Relative risks for nasopharyngeal cancer (nine deaths) increased with average exposure intensity, cumulative exposure, highest peak exposure, and duration of exposure to formaldehyde (p-trend = 0.066, 0.025, <0.001, and 0.147, respectively). Formaldehyde exposure did not appear to be associated with lung (744 deaths), pancreas (93 deaths), or brain (62 deaths) cancer. Although relative risks for prostate cancer (145 deaths) were elevated for some measures of formaldehyde exposure, the trend was inconsistent. In this cohort of formaldehyde-industry workers, some evidence was found of an exposure-response relation with mortality from nasopharyngeal cancer (based on small numbers) but not for cancers of the pancreas, brain, lung, or prostate.

Adult↗
PubMed2004

Kin-cohort estimates for familial breast cancer risk in relation to variants in DNA base excision repair, BRCA1 interacting and growth factor genes.

BACKGROUND: Subtle functional deficiencies in highly conserved DNA repair or growth regulatory processes resulting from polymorphic variation may increase genetic susceptibility to breast cancer. Polymorphisms in DNA repair genes can impact protein function leading to genomic instability facilitated by growth stimulation and increased cancer risk. Thus, 19 single nucleotide polymorphisms (SNPs) in eight genes involved in base excision repair (XRCC1, APEX, POLD1), BRCA1 protein interaction (BRIP1, ZNF350, BRCA2), and growth regulation (TGFss1, IGFBP3) were evaluated. METHODS: Genomic DNA samples were used in Taqman 5'-nuclease assays for most SNPs. Breast cancer risk to ages 50 and 70 were estimated using the kin-cohort method in which genotypes of relatives are inferred based on the known genotype of the index subject and Mendelian inheritance patterns. Family cancer history data was collected from a series of genotyped breast cancer cases (N = 748) identified within a cohort of female US radiologic technologists. Among 2,430 female first-degree relatives of cases, 190 breast cancers were reported. RESULTS: Genotypes associated with increased risk were: XRCC1 R194W (WW and RW vs. RR, cumulative risk up to age 70, risk ratio (RR) = 2.3; 95% CI 1.3-3.8); XRCC1 R399Q (QQ vs. RR, cumulative risk up to age 70, RR = 1.9; 1.1-3.9); and BRIP1 (or BACH1) P919S (SS vs. PP, cumulative risk up to age 50, RR = 6.9; 1.6-29.3). The risk for those heterozygous for BRCA2 N372H and APEX D148E were significantly lower than risks for homozygotes of either allele, and these were the only two results that remained significant after adjusting for multiple comparisons. No associations with breast cancer were observed for: APEX Q51H; XRCC1 R280H; IGFPB3 -202A>C; TGFss1 L10P, P25R, and T263I; BRCA2 N289H and T1915M; BRIP1 -64A>C; and ZNF350 (or ZBRK1) 1845C>T, L66P, R501S, and S472P. CONCLUSION: Some variants in genes within the base-excision repair pathway (XRCC1) and BRCA1 interacting proteins (BRIP1) may play a role as low penetrance breast cancer risk alleles. Previous association studies of breast cancer and BRCA2 N372H and functional observations for APEX D148E ran counter to our findings of decreased risks. Due to the many comparisons, cautious interpretation and replication of these relationships are warranted.

Aged↗
PubMed2003

Mortality from lymphohematopoietic malignancies among workers in formaldehyde industries.

BACKGROUND: Many U.S. factory workers are exposed to formaldehyde. Although increased risks for leukemia have been found in medical workers and other professionals exposed to formaldehyde, studies in industrial workers, who are thought to have higher exposures, have shown inconsistent associations. We extended follow-up of a cohort of industrial workers to evaluate the association between formaldehyde exposure and lymphohematopoietic cancers. METHODS: The cohort consisted of 25 619 workers (865 708 person-years) employed before January 1, 1966, at one of 10 U.S. industrial plants and followed through December 31, 1994. We analyzed formaldehyde exposure (peak exposure, average exposure intensity, cumulative exposure, and duration of exposure) and mortality from lymphohematopoietic malignancies using standardized mortality ratios and relative risks and 95% confidence intervals (CIs) based on Poisson regression. Statistical tests were two-sided. RESULTS: Among the cohort, there were 178 deaths from lymphohematopoietic malignancies. Relative risks for leukemia (69 deaths), particularly for myeloid leukemia (30 deaths), increased with formaldehyde exposure. Compared with workers exposed to low peak levels of formaldehyde (0.1-1.9 ppm), relative risks for myeloid leukemia were 2.43 (95% CI = 0.81 to 7.25) and 3.46 (95% CI = 1.27 to 9.43) for workers exposed to peak levels of 2.0-3.9 ppm and > or = 4.0 ppm, respectively (P(trend) =.009). Compared with workers exposed to low levels of average exposure intensity of formaldehyde (0.1-0.4 ppm), workers exposed to 0.5-0.9 ppm and > or = 1.0 ppm average intensity had relative risks of 1.15 (95% CI = 0.41 to 3.23) and 2.49 (95% CI = 1.03 to 6.03), respectively (P(trend) =.088). The relative risk for leukemia was not associated with cumulative exposure but was weakly associated with duration of exposure. Relative risks for Hodgkin's disease also increased with formaldehyde exposure. CONCLUSIONS: Exposure to formaldehyde may cause leukemia, particularly myeloid leukemia, in humans. However, results from other investigations are mixed, suggesting caution in drawing definitive conclusions.

Adult↗
PubMed2003

Cancer incidence in the US radiologic technologists health study, 1983-1998.

BACKGROUND: Workers exposed to low doses of radiation can provide information regarding cancer risks that are of public concern. However, characterizing risk at low doses requires large populations and ideally should include a large proportion of women, both of which rarely are available. METHODS: Among 90305 radiologic technologists in the U.S. (77% women) who were followed during 1983-1998, data concerning incident cancer occurrence was obtained from mailed questionnaires and from death records. Standardized incidence ratios (SIRs) were computed using age-specific, gender-specific, race-specific, and calendar year-specific cancer rates from the Surveillance, Epidemiology, and End Results Program. RESULTS: The SIR for all cancers in both genders combined was 1.04 (95% confidence interval [95% CI], 1.00-1.07; n = 3292 technologists). Female technologists had an elevated risk for all solid tumors combined (SIR = 1.06; 95% CI, 1.02-1.10; n = 2168 women) and for breast cancers (SIR = 1.16; 95% CI, 1.09-1.23; n = 970 women), melanoma (SIR = 1.66; 95% CI, 1.43-1.89; n = 181 women), and thyroid cancers (SIR = 1.54; 95% CI, 1.24-1.83; n = 107 women). Male technologists experienced a decreased risk for solid tumors (SIR = 0.92; 95% CI, 0.85-0.98; n = 755 men); however, melanoma (SIR = 1.39; 95% CI, 1.00-1.79; n = 56 men) and thyroid cancers (SIR = 2.23; 95% CI, 1.29-3.59; n = 17 men) were increased. Among both genders, the risks were decreased for buccal cavity/pharyngeal cancers (SIR = 0.73; 95% CI, 0.55-0.90; n = 54 technologists), rectal cancers (SIR = 0.62; 95% CI 0.48-0.76; n = 53 technologists), and lung cancers (SIR = 0.77, 95% CI, 0.70-0.85; n = 307 technologists). CONCLUSIONS: The elevated risk for breast cancer may have been related to occupational radiation exposure. The observed excesses of melanoma and thyroid cancers may reflect, at least in part, earlier detection among medical workers with easy access to health care.

Adult↗
PubMed2003

Risk of melanoma among radiologic technologists in the United States.

Our study examines the risk of melanoma among medical radiation workers in the U.S. Radiologic Technologists (USRT) study. We evaluated 68,588 white radiologic technologists (78.8% female), certified during 1926-1982, who responded to a baseline questionnaire (1983-1989) and were free of cancer other than nonmelanoma skin at that time. Participants were followed through completion of a second questionnaire (1994-1998). We identified 207 cases, 193 subjects who reported first primary melanoma and 14 decedents with melanoma listed as an underlying or contributory cause of death. We examined risks of occupational radiation exposures using work history information on practices, procedures, and protective measures reported on the baseline questionnaire. Based on Cox proportional hazards regression, melanoma was significantly associated with established risk factors, including constitutional characteristics (skin tone, eye and hair color), personal history of nonmelanoma skin cancer, family history of melanoma and indicators of residential sunlight exposure. Melanoma risk was increased among those who first worked before 1950 (RR = 1.8, 95% CI = 0.6-5.5), particularly among those who worked 5 or more years before 1950 (RR = 2.4; 0.7-8.7; p (trend) for years worked before 1950 = 0.03), when radiation exposures were likely highest. Risk was also modestly elevated among technologists who did not customarily use a lead apron or shield when they first began working (RR = 1.4; 0.8-2.5). Clarifying the possible role of exposure to chronic ionizing radiation in melanoma is likely to require nested case-control studies within occupational cohorts, such as this one, which will assess individual radiation doses, and detailed information about sun exposure, sunburn history and skin susceptibility characteristics.

Adult↗
PubMed2003

Mortality from diseases of the circulatory system in radiologic technologists in the United States.

Although increased mortality from diseases of the circulatory system has been observed in patients treated with radiotherapy, the effects of chronic low-dose radiation exposure are not clear. Among 90,284 US radiologic technologists who responded to a mailed questionnaire during 1983-1989, the authors evaluated mortality from circulatory system diseases through 1997 in relation to job history and work procedures as surrogates for radiation exposure. They used Poisson regression models stratified for sex, race, age, and calendar year and adjusted for smoking, body mass index, alcohol intake, marital status, parity, menopausal status, and history of myocardial infarction. A total of 1,107,100 person-years accrued, and 1,070 subjects died from circulatory system diseases. Relative risks for first employment during 1950-1959, 1940-1949, or before 1940, compared with 1960 and later, were 1.01 (95% confidence interval (CI): 0.78, 1.30), 1.14 (95% CI: 0.86, 1.50), and 1.42 (95% CI: 1.04, 1.94), respectively (trend p < 0.001). For the subset of deaths from cerebrovascular disease (n = 174), the respective relative risks were 0.90 (95% CI: 0.45, 1.78), 1.54 (95% CI: 0.74, 3.23), and 2.40 (95% CI: 1.09, 5.31) (trend p = 0.004), and for deaths from ischemic heart disease (n = 633), the relative risks were 0.98 (95% CI: 0.71, 1.35), 1.00 (95% CI: 0.71, 1.42), and 1.22 (95% CI: 0.81, 1.82) (trend p = 0.026). The relative risks for mortality from circulatory system diseases and the subset of cerebrovascular disease increased significantly with the number of years worked before 1950 (trend p = 0.007 and < 0.001, respectively). The data suggest increased mortality from diseases of the circulatory system with occupational radiation exposure before 1950 when radiation doses were likely high.

Adult↗
PubMed2003

Cancer and other causes of mortality among radiologic technologists in the United States.

Data are limited on the role of chronic exposure to low-dose ionizing radiation in the etiology of cancer. In a nationwide cohort of 146,022 U.S. radiologic technologists (73% female), we evaluated mortality risks in relation to work characteristics. Standardized mortality ratios (SMRs) were computed to compare mortality in the total cohort vs. the general population of the United States. Mortality risks were low for all causes (SMR = 0.76) and for all cancers (SMR = 0.82) among the radiologic technologists. We also calculated relative risks (RR) for the 90,305 technologists who responded to a baseline mailed questionnaire, using Poisson regression models, adjusted for known risk factors. Risks were higher for all cancers (RR = 1.28, 95% confidence interval [CI] = 0.93-1.69) and breast cancer (RR = 2.92, 95% CI = 1.22-7.00) among radiologic technologists first employed prior to 1940 compared to those first employed in 1960 or later, and risks declined with more recent calendar year of first employment (p-trend = 0.04 and 0.002, respectively), irrespective of employment duration. Risk for the combined category of acute lymphocytic, acute myeloid and chronic myeloid leukemias was increased among those first employed prior to 1950 (RR = 1.64, 95% CI = 0.42-6.31) compared to those first employed in 1950 or later. Risks rose for breast cancer (p-trend = 0.018) and for acute lymphocytic, acute myeloid and chronic myeloid leukemias (p-trend = 0.05) with increasing duration of employment as a radiologic technologist prior to 1950. The elevated mortality risks for breast cancer and for the combined group of acute lymphocytic, acute myeloid and chronic myeloid leukemias are consistent with a radiation etiology given greater occupational exposures to ionizing radiation prior to 1950 than in more recent times.

Adolescent↗
PubMed2003

Site-specific cancer incidence and mortality after cerebral angiography with radioactive thorotrast.

Few opportunities exist to evaluate the carcinogenic effects of long-term internal exposure to alpha-particle-emitting radionuclides. Patients injected with Thorotrast (thorium-232) during radiographic procedures, beginning in the 1930s, provide one such valuable opportunity. We evaluated site-specific cancer incidence and mortality among an international cohort of 3,042 patients injected during cerebral angiography with either Thorotrast (n = 1,650) or a nonradioactive agent (n = 1,392) and who survived 2 or more years. Standardized incidence ratios (SIR) for Thorotrast and comparison patients (Denmark and Sweden) were estimated and relative risks (RR), adjusted for population, age and sex, were generated with multivariate statistical modeling. For U.S. patients, comparable procedures were used to estimate standardized mortality ratios (SMR) and RR, representing the first evaluation of long-term, site-specific cancer mortality in this group. Compared with nonexposed patients, significantly increased risks in Thorotrast patients were observed for all incident cancers combined (RR = 3.4, 95% CI 2.9-4.1, n = 480, Denmark and Sweden) and for cancer mortality (RR = 4.0, 95% CI 2.5-6.7, n = 114, U.S.). Approximately 335 incident cancers were above expectation, with large excesses seen for cancers of the liver, bile ducts and gallbladder (55% or 185 excess cancers) and leukemias other than CLL (8% or 26 excess cancers). The RR of all incident cancers increased with time since angiography (P < 0.001) and was threefold at 40 or more years; significant excesses (SIR = 4.0) persisted for 50 years. Increasing cumulative dose of radiation was associated with an increasing risk of all incident cancers taken together and with cancers of the liver, gallbladder, and peritoneum and other digestive sites; similar findings were observed for U.S. cancer mortality. A marginally significant dose response was observed for the incidence of pancreas cancer (P = 0.05) but not for lung cancer. Our study confirms the relationship between Thorotrast and increased cancer incidence at sites of Thorotrast deposition and suggests a possible association with pancreas cancer. After injection with >20 ml Thorotrast, the cumulative excess risk of cancer incidence remained elevated for up to 50 years and approached 97%. Caution is needed in interpreting the excess risks observed for site-specific cancers, however, because of the potential bias associated with the selection of cohort participants, noncomparability with respect to the internal or external comparison groups, and confounding by indication. Nonetheless, the substantial risks associated with liver cancer and leukemia indicate that unique and prolonged exposure to alpha-particle-emitting Thorotrast increased carcinogenic risks.

Adult↗