An expanded cohort study of cancer among benzene-exposed workers in China. Benzene Study Group.

Yin, Shu; Hayes, Richard B.; Linet, Martha S.; Li, G L; Dosemeci, Mustafa; Travis, Lois B.; Zhang, Z N; Li, D G; Chow, WH; Wacholder, Sholom; Blot, William J.

doi:10.1289/ehp.961041339

Cited by 58 publications

(40 citation statements)

References 19 publications

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“…A follow-up survey of 28,460 benzene-exposed and 28,257 unexposed workers from 1972 through 1981 found an increased risk of mortality due to leukemia [standardized mortality ratio (SMR) = 5.7] (123). In 1987, the U.S. National Cancer Institute (NCI) began collaborating with the CAPM team to identify all incident cases of hematologic neoplasms and related disorders in an expanded study cohort of 74,828 benzene-exposed and 35,805 unexposed workers employed from 1972 through 1987 in 12 cities in China (37, 122). The study confirmed increased risks of acute myeloid leukemia (AML) and other malignant and non-malignant hematopoietic disorders associated with benzene exposure and found evidence for hematopoietic cancer risks at levels substantially lower than had previously been established.…”

Section: Traditional Epidemiological Studies Of the Carcinogenic Effementioning

confidence: 99%

Advances in Understanding Benzene Health Effects and Susceptibility

Smith

2010

Annu. Rev. Public Health

332

247

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Benzene is a ubiquitous chemical in our environment that causes acute leukemia and probably other hematological cancers. Evidence for an association with childhood leukemia is growing. Exposure to benzene can lead to multiple alterations that contribute to the leukemogenic process, indicating a multimodal mechanism of action. Research is needed to elucidate the different roles of multiple metabolites in benzene toxicity and the pathways that lead to their formation. Studies to date have identified a number of polymorphisms in candidate genes that confer susceptibility to benzene hematotoxicity. However, a genome-wide study is needed to truly assess the role of genetic variation in susceptibility. Benzene affects the blood-forming system at low levels of occupational exposure, and there is no evidence of a threshold. There is probably no safe level of exposure to benzene, and all exposures constitute some risk in a linear, if not supralinear, and additive fashion.

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Section: Traditional Epidemiological Studies Of the Carcinogenic Effementioning

confidence: 99%

Advances in Understanding Benzene Health Effects and Susceptibility

Smith

2010

Annu. Rev. Public Health

332

247

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“…In reviewing the literature, however, there are no in vivo studies related to the effects of benzene exposure on lung cell apoptosis. Yet animal studies have shown that the lung is a target organ of benzene tumorigenicity, while human subjects exhibit increased risks for adenocarcinoma and squamous cell carcinoma of the lung when occupationally exposed to benzene (Aksoy, 1989;Yin et al, 1989Yin et al, , 1996aHayes et al, 1996) as well as to cigarette smoke (Darrall et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

The effects of benzene exposure on apoptosis in epithelial lung cells: Localization by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and the immunocytochemical localization of apoptosis-related gene products

Weaver¹,

Liu²,

Lü³

et al. 2006

Cell Biol Toxicol

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Although benzene, a well-known human carcinogen, has been shown to induce apoptosis in vitro, no studies have been carried out to confirm and characterize its role in activating apoptosis in vivo. The present study investigated the effects of benzene inhalation on the epithelial cells lining the respiratory tract including bronchioles, terminal bronchioles, respiratory bronchioles and alveoli of male Sprague-Dawley rats. Inhalation of benzene 300 ppm for 7 days induced apoptotic changes in the parenchymal components in the lung that significantly exceeded the events of programmed cell death in normal control tissues. Apoptosis was confirmed by the electrophoretic analysis of internucleosomal DNA fragmentation of benzene-exposed lung tissues, which exhibited 180-200 bp laddering subunits indicative of genomic DNA degradation. Furthermore, semi-quantitative analysis of intracellular localization of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling TUNEL) showed a significant (p < 0.001) increase in the apoptotic index calculated for bronchiolar 73.5%, terminal bronchiolar (65%), and respiratory bronchiolar 60.8% segmental epithelial components as well as alveolar (55%) epithelia. Analysis of immunohistochemical expression of apoptosis-related gene products also supported the hypothesis that benzene can induce apoptosis in chemosensitive target cells in the lung parenchyma. Quantitative immunhistochemistry showed a statistically significant increase p < 0.001 in the immunoreactive staining index for cytochrome c, Apaf-1 (apoptosis activating factor-1), DNA fragmentation factor, and representative cysteine proteases including caspase-1, caspase-2L, caspase-8 and caspase-9. Thus this is the first study of the respiratory system that demonstrates that benzene inhalation induces lung cell apoptosis as confirmed by DNA electrophoresis, in situ nick end labeling, and the upregulation of apoptosis-related gene products that facilitate caspase-cleaved enzymes which lead to cell degradation via programmed cell death. These responses may represent an important defense mechanism within the parenchymal cells of the respiratory system that reduce mutational hazard and the potential carcinogenic effects of benzene-initiated pathogenesis.

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“…Better integration of these disciplines will lead to stronger study designs, for example, by reducing the common occurrence of occupational cohorts that include women but fail to report data for breast cancer even though they are studying exposures to chemicals that cause mammary gland tumors. [6][7][8][9] Second, we seek to strengthen the practice of toxicology, including animal testing and risk assessment, as a tool for breast cancer prevention. Focusing on the mammary tumor endpoint may identify ways to strengthen chemical screening and testing, and improve interpretation of data from these tests in order to maximize the relevance to human breast cancer.…”

mentioning

confidence: 99%

Chemicals causing mammary gland tumors in animals signal new directions for epidemiology, chemicals testing, and risk assessment for breast cancer prevention

Rudel

Attfield

Schifano

et al. 2007

Cancer

184

191

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Identifying chemical carcinogens in animal studies is currently the primary means of anticipating cancer effects in humans. Animal studies to evaluate potential chemical carcinogenicity are particularly important for breast cancer because environmental and occupational epidemiologic research is sparse.Chemicals that increased mammary gland tumors in animal studies were compiled from the International Agency for Research on Cancer (IARC), the U.S. National Toxicology Program (NTP), and other sources. Summary assessments of the carcinogenic potential for each chemical and potentially exposed populations were also compiled. In all, 216 chemicals were identified that have been associated with increases in mammary gland tumors in at least 1 study. These include industrial chemicals, chlorinated solvents, products of combustion, pesticides, dyes, radiation, drinking water disinfection byproducts, pharmaceuticals and hormones, natural products, and research chemicals. Twenty-nine are produced in the U.S. at >1 million pounds/year; 35 are air pollutants, 25 have involved occupational exposures to >5000 women, and 73 have been present in consumer products or as contaminants of food. Thus, exposure is widespread. Nearly all of the chemicals were mutagenic and most caused tumors in multiple organs and species; these characteristics are generally believed to indicate likely carcinogenicity in humans. To our knowledge, this is the most comprehensive list developed of animal mammary gland carcinogens and, along with associated data, is publicly available at URL: www.silentspring.org/sciencereview and at URL: www.komen. org/environment. Valuable information from cancer bioassays is not well utilized in risk assessment and regulatory processes, suggesting a need to strengthen chemicals testing and risk assessment as tools for breast cancer prevention.

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An expanded cohort study of cancer among benzene-exposed workers in China. Benzene Study Group.

Cited by 58 publications

References 19 publications

Advances in Understanding Benzene Health Effects and Susceptibility

Advances in Understanding Benzene Health Effects and Susceptibility

The effects of benzene exposure on apoptosis in epithelial lung cells: Localization by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and the immunocytochemical localization of apoptosis-related gene products

Chemicals causing mammary gland tumors in animals signal new directions for epidemiology, chemicals testing, and risk assessment for breast cancer prevention

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