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M Linet

Publications and source records attributed to M Linet.

29 records · Page 2Linked to original sources

Indirect validation of benzene exposure assessment by association with benzene poisoning.

We present a validation study of a quantitative retrospective exposure assessment method used in a follow-up study of workers exposed to benzene. Assessment of exposure to benzene was carried out in 672 factories in 12 cities in China. Historical exposure data were collected for 3179 unique job titles. The basic unit for exposure assessment was a factory/work unit/job title combination over seven periods between 1949 and 1987. A total of 18,435 exposure estimates was developed, using all available historical information, including 8477 monitoring data. Overall, 38% of the estimates were based on benzene monitoring data. The highest time-weighted average exposures were observed for the rubber industry (30.7 ppm) and for rubber glue applicators (52.6 ppm). Because of its recognized link with benzene exposure, the association between a clinical diagnosis of benzene poisoning and benzene exposure was evaluated to validate the assessment method that we used in the cohort study. Our confidence in the assessment method is supported by the observation of a strong positive trend between benzene poisoning and various measures, especially recent intensity of exposure to benzene.

Benzene↗

An epidemiologic study of early biologic effects of benzene in Chinese workers.

Benzene is a recognized hematotoxin and leukemogen, but its mechanisms of action in humans are still uncertain. To provide insight into these processes, we carried out a cross-sectional study of 44 healthy workers currently exposed to benzene (median 8-hr time-weighted average; 31 ppm), and unexposed controls in Shanghai, China. Here we provide an overview of the study results on peripheral blood cells levels and somatic cell mutation frequency measured by the glycophorin A (GPA) gene loss assay and report on peripheral cytokine levels. All peripheral blood cells levels (i.e., total white blood cells, absolute lymphocyte count, platelets, red blood cells, and hemoglobin) were decreased among exposed workers compared to controls, with the exception of the red blood cell mean corpuscular volume, which was higher among exposed subjects. In contrast, peripheral cytokine levels (interleukin-3, interleukin-6, erythropoietin, granulocyte colony-stimulating factor, tissue necrosis factor-alpha) in a subset of the most highly exposed workers (n = 11) were similar to values in controls (n = 11), suggesting that benzene does not affect these growth factor levels in peripheral blood. The GPA assay measures stem cell or precursor erythroid cell mutations expressed in peripheral red blood cells of MN heterozygous subjects, identifying NN variants, which result from loss of the GPA M allele and duplication of the N allele, and N phi variants, which arise from gene inactivation. The NN (but not N phi) GPA variant cell frequency was elevated in the exposed workers compared with controls (mean +/- SD, 13.9 +/- 8.4 mutants per million cells versus 7.4 +/- 5.2 per million cells, (respectively; p = 0.0002), suggesting that benzene produces gene-duplicating but not gene-inactivating mutations at the GPA locus in bone marrow cells of exposed humans. These findings, combined with ongoing analyses of benzene macromolecular adducts and chromosomal aberrations, will provide an opportunity to comprehensively evaluate a wide range of early biologic effects associated with benzene exposure in humans.

Adult↗

Prenatal and neonatal risk factors for childhood lymphatic leukemia.

BACKGROUND: Because the incidence of childhood acute lymphatic leukemia peaks between 2 and 4 years of age, the risk factors may exert their influence during the prenatal and/or the neonatal periods. Results of previous studies of perinatal risk factors have been contradictory, perhaps because most studies either have been hospital based or have been restricted to limited geographical areas. PURPOSE: A nationwide case-control study was carried out to identify maternal and perinatal risk factors for this disease. METHODS: The case-control study was nested in cohorts defined by all live births in Sweden recorded in the nationwide Medical Birth Register. Since 1973, this register has routinely collected information on all hospital births in regard to maternal demographic data, reproductive history, pregnancy, delivery, and the neonatal period. From the Swedish National Cancer Register, 613 case subjects were identified in successive birth cohorts from 1973 through 1989. Five control subjects per case subject were randomly selected from the pool of children matched by sex and month and year of birth. Conditional logistic regression was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) for potential risk factors and to estimate their effects after adjustment for possible confounders. RESULTS: Risk of childhood lymphatic leukemia at all ages increased with Down's syndrome (OR = 20.0; 95% CI = 4.2-94.2), maternal renal disease (OR = 4.4; 95% CI = 1.6-12.1), use of supplementary oxygen (OR = 2.3; 95% CI = 1.5-3.6), postpartum asphyxia (OR = 1.8; 95% CI = 1.2-2.6), birth weight of more than 4500 g (OR = 1.7; 95% CI = 1.1-2.7), and hypertensive disease during pregnancy (OR = 1.4; 95% CI = 1.0-1.9). Down's syndrome affected risk mostly in children younger than 5 years, whereas other factors affected those children 5 years old or older. Being one of a multiple birth also increased risk among older children (OR = 2.5; 95% CI = 1.0-6.0). Use of supplementary oxygen may act as a causal intermediate (surrogate) for postpartum asphyxia and its causes, as would high birth weight for its causes. CONCLUSIONS: Several maternal and perinatal risk factors were found to be associated with childhood lymphatic leukemia, but they showed age-specific differences. Overall, only a few risk factors were identified, and these accounted for a small proportion of cases. We concluded that most risk factors for childhood lymphatic leukemia remain unidentified in very young children.

Case-Control Studies↗

Cohort study among workers exposed to benzene in China: II. Exposure assessment.

This report describes a retrospective exposure assessment method used in a follow-up mortality study of workers exposed to benzene. The approach quantified historical exposure to benzene in a multi-industry, multicenter cohort, involving 672 factories in 12 cities in China. Historical exposure data were collected to obtain exposure information related to 1,427 work units (departments) and 3,179 unique job titles from benzene-producing or -using factories in which written records and other data sources were evaluated. The basic unit for exposure assessment was a factory/work unit/job title combination which was considered separately during each of seven calendar-year time periods between 1949 and 1987 for a total of 18,435 exposure assignments. Historical information collected to estimate exposure included benzene monitoring data; lists of raw materials and factory products, and the percentage of benzene in each; the total amount and dates of use of benzene or benzene-containing materials; use of engineering controls and personal protective equipment; and other available exposure information. Overall, 38% (ranging from 3% for the earliest periods to 67% for the last period) of the estimates were based primarily on benzene monitoring data. In the absence of job-specific benzene monitoring data for a given calendar period, measurement results or exposure estimates for similar jobs and/or other calendar periods were used in conjunction with other exposure information to derive estimates. Estimated exposure levels are presented by industries and occupations. The highest average exposures during 1949-1987 were observed for the rubber and plastic industry (30.7 ppm), and for rubber glue applicators (52.6 ppm).

Benzene↗

Familial cancers associated with subtypes of leukemia and non-Hodgkin's lymphoma.

To investigate whether a history of hematolymphoproliferative cancers (HLP) and other cancers among a parent or sibling is a risk factor for specific subtypes of leukemia and non-Hodgkin's lymphoma (NHL), data from a population-based case-control study, in Iowa and Minnesota, of 578 leukemia cases, 622 NHL cases and 1245 controls were evaluated. Having at least one sibling with HLP significantly increased the risk for all leukemias combined (odds ratio (OR) = 2.3) and for NHL (OR = 2.7). In particular, chronic lymphocytic leukemia (CLL) was significantly increased among those reporting a sibling with leukemia (OR = 3.0) or lymphoma (OR = 4.3). Elevated risks of small lymphocytic NHL (SML) (OR = 7.3) and diffuse NHL (DIF) (OR = 5.4) were also observed among subjects who had a sibling with lymphoma (primarily Hodgkin's disease). A significantly increased risk of follicular NHL was noted among those with a sibling history of pancreatic cancer (OR = 4.8) and colorectal cancer (OR = 2.7). Parental history of HLP was not associated with any type of leukemia or NHL. A history of stomach cancer among parents was associated with a 2-fold elevation of CLL and DIF compared to controls. Increased risks of CLL and DIF were also linked to breast cancer among sisters and mothers, respectively. Prostate cancer among fathers increased the risk 2-fold for CLL and 3-fold for SML. This study confirms some familial cancer associations previously reported for leukemia and NHL, and provides new information regarding the various subtypes of leukemia and NHL.

Adult↗

Personality and emotional disorder in a community sample of migraine headache sufferers.

To investigate whether individuals who suffer from chronic, severe headaches have more personality abnormalities or emotional disorders than their healthy counterparts, 162 young adults with classical migraine, ascertained by community survey, were compared to matched control subjects without migraine. On the General Health Questionnaire, the prevalence of psychological symptoms among the migraine subjects was 2.5 times the prevalence among the control subjects. The migraine sufferers also had significantly higher scores on the psychoticism (women only), neuroticism, and lie scales of the Eysenck Personality Questionnaire. Frequency of migraine attacks was not related to scores on any of the scales. These results suggest that classical migraine is associated with psychological abnormalities.

Adolescent↗

Matched case-control designs and overmatched analyses.

In a 1:1 matched-pairs case-control study, several pairs may have the same matching criteria. The objective of this paper is to consider various analytic approaches for odds ratio estimation in this situation. One approach is to perform the usual matched-pairs analysis; the alternative is to combine pairs into strata and compute the conditional maximum likelihood or Mantel-Haenszel estimate. Matched-pairs analysis based on theoretic and simulation results may give misleading inferences, although on average it performs nearly as well as the stratified analysis. The occasional poor performance of the matched-pairs analysis results from the possibility of obtaining an extreme number of discordant pairs due to the random pairing within a stratum. It is concluded that the prudent policy is to perform a stratified rather than a paired analysis, even at the expense of additional computation.

Epidemiologic Methods↗

Incidence of aplastic anemia in metropolitan Baltimore: a population-based study.

Incidence rates for aplastic anemia (AA) so far have been unavailable for defined populations in the United States. A study was carried out in the Baltimore Standard Metropolitan Statistical Area (SMSA) to examine the incidence rates for aplastic anemia from 1970 through 1978. Cases of AA (N = 118) were identified through medical records (N = 77) in SMSA hospitals and death certificates (N = 41). All medical charts were reviewed by an oncologist-hematologist for validation purposes. Among whites, average annual age-adjusted incidence rates per million were higher in males (7.1) than in females (5.4), whereas in nonwhites, females had a higher rate (7.3) than males (4.7). None of the sex differences was statistically significant. Age-specific incidence rates were consistently low in young ages, with an exponential increase after age 40. Examination of time trends did not suggest changes in whites, although in blacks, mainly in males, there was a suggestion of a temporal increase. However, rates in blacks were based on small numbers, and trends were not statistically significant. An inconsistent sex differential, as well as the relative stability of rates over time at least in whites, suggests that although sexes may have different types of exposures, occupational exposures and changes in environmental factors over time cannot entirely explain the occurrence of AA in the population. In addition, the age pattern suggests that future studies should examine etiologic agents separately for the younger and the older subjects with AA.

Adolescent↗

Prenatal and neonatal risk factors for childhood myeloid leukemia.

Information about the etiology of childhood myeloid leukemia is limited. A population-based nested case-control study of prenatal and neonatal risk factors for childhood myeloid leukemia was performed with the use of the Swedish National Cancer Register and the Swedish Birth Register. A total of 98 cases of myeloid leukemia were identified in successive birth cohorts from 1973 through 1989. From the Birth Register, five controls were matched to each case. Fourteen of the 98 cases with myeloid leukemia and none of the controls had Down syndrome [odds ratio (OR) = infinity; 95% confidence interval (CI) = 21.0-infinity]. The risk for myeloid leukemia also increased among children who had physiological jaundice (OR = 2.5; 95% CI = 1.2-5.0; children who had been treated with phototherapy (OR = 7.5; 95% CI = 1.8-31.9); or who had been treated in an incubator (OR = 3.5; 95% CI = 1.2-10.2). Excluding cases with Down syndrome, however, decreased these risks, so that their 95% lower confidence interval included the no-effect value. Maternal age < 20 years old (OR = 2.5; 95% CI = 1.1-6.0), hypertension (OR = 2.4; 95% CI = 1.2-5.0), Cesarean section (OR = 2.5; 95% CI = 1.3-4.9), maternal smoking (OR = 2.4; 95% CI = 0.9-6.5), and being one of a multiple birth (OR = 3.6; 95% CI = 1.1-11.3) increased the risk for myeloid leukemia among those without Down syndrome. When the analyses were repeated, by restricting the cases to those with acute myeloid leukemia, the risk associated with young maternal age declined and became nonsignificant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗