Article

Mortality from Solid Cancers among Workers in Formaldehyde Industries

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Department of Health and Human Services, Bethesda, MD 20892, USA.
American Journal of Epidemiology (Impact Factor: 5.23). 06/2004; 159(12):1117-30. DOI: 10.1093/aje/kwh174
Source: PubMed

ABSTRACT

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.

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    • "Both chronic and acute exposures to formaldehyde have been associated with adverse effects on human health including eye, nose, throat, and skin irritation, allergic contact dermatitis, altered lung functions and immune responses, occupational asthma, and cancer [1] [2]. Based on epidemiological evidence associating formaldehyde exposure with nasopharyngeal cancer and myeloid leukemia [3] [4] [5], formaldehyde was classified as a class I human carcinogen by the International Agency on Cancer Research (IARC) in 2006. However, there exists some controversy Abbreviations: 53BP1, p53 binding protein; ATM, ataxia telangiectasia mutated; ATR, ataxia telangiectasia and Rad3-related; CGRP, calcitonin gene-related peptide; BLM, bloom protein; CHO, Chinese Hamster Ovary; DSB, double-strand break; DPC, DNA-protein crosslink. "
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    ABSTRACT: Formaldehyde is a reactive aldehyde that has been classified as a class I human carcinogen by the International Agency for Cancer Research. There are growing concerns over the possible adverse health effects related to the occupational and environmental human exposures to formaldehyde. Although formaldehyde-induced DNA and protein adducts have been identified, the genomic instability mechanisms and the cellular tolerance pathways associated with formaldehyde exposure are not fully characterized. This study specifically examines the role of a genome stability protein, Bloom (BLM) in limiting formaldehyde-induced cellular and genetic abnormalities. Here, we show that in the absence of BLM protein, formaldehyde-treated cells exhibited increased cellular sensitivity, an immediate cell cycle arrest, and an accumulation of chromosome radial structures. In addition, live-cell imaging experiments demonstrated that formaldehyde-treated cells are dependent on BLM for timely segregation of daughter cells. Both wild-type and BLM-deficient formaldehyde-treated cells showed an accumulation of 53BP1 and γH2AX foci indicative of DNA double-strand breaks (DSBs); however, relative to wild-type cells, the BLM-deficient cells exhibited delayed repair of formaldehyde-induced DSBs. In response to formaldehyde exposure, we observed co-localization of 53BP1 and BLM foci at the DSB repair site, where ATM-dependent accumulation of formaldehyde-induced BLM foci occurred after the recruitment of 53BP1. Together, these findings highlight the significance of functional interactions among ATM, 53BP1, and BLM proteins as responders associated with the repair and tolerance mechanisms induced by formaldehyde. Copyright © 2015. Published by Elsevier B.V.
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    • "Air pollution has been one of the key points of environmental workers both at home and abroad with the development of " person is the core " (Hauptmann, 2004). From the view of human breath exposure, the human living environment can be divided into these three important parts: indoor environment, outdoor atmosphere, and transportation microenvironment. "
    Weng · Jin
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    • "The latter two applications are of great diagnostic value. However, in recent years numerous review articles on the hazardous effects of formalin were published, presenting important evidence-based drawbacks on formalin as a fixative (Beane et al., 2009; Coggon et al., 2003; Hauptmann et al., 2004; Jayalakshmi et al., 2011; 2009; Pinkerton et al., 2004). Formalin has been placed in " group 1 " known carcinogens, along with substances such as asbestos and benzene by the " International Agency for Research on *Correspondence to: Dr. "
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