Carcinogenicity of quinoline, styrene, and styrene-7,8-oxide

Kogevinas, Manolis; Gwinn, William M.; Kriebel, David; Phillips, David H.; Sim, Malcolm Ross; Bertke, Stephen; Calaf, Gloria M.; Colosio, Claudio; Fritz, Jason M.; Fukushima, Shoji; Hemminki, Kari; Jensen, Allan Astrup; Kolstad, Henrik Albert; Mráz, Jaroslav; Nesnow, Stephen; Nylander‐French, Leena A.; Parent, Marie‐Élise; Sandy, Martha S.; Smith‐Roe, Stephanie L.; Stoner, Gary D.; Suzuki, Takayoshi; Teixeira, João Paulo; Vodička, Pavel; Tornero‐Velez, Rogelio; Guyton, Kathryn Z.; Grosse, Yann; Ghissassi, Fatiha El; Bouvard, Véronique; Benbrahim‐Tallaa, Lamia; Guha, Neela; Vilahur, Nadia; Driscoll, Tim; Hall, Amy Laura; Middleton, Daniel; Jaillet, Corentin; Mattock, Heidi; Straif, Kurt

doi:10.1016/s1470-2045(18)30316-4

Cited by 29 publications

(9 citation statements)

References 13 publications

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“…IARC () has characterized BD as carcinogenic to humans based on limited epidemiologic evidence for a causal association with NHL, multiple myeloma, and chronic lymphocytic leukemia. More recently, IARC characterized styrene as probably carcinogenic to humans based on limited evidence from epidemiologic studies of LHMs and myeloid leukemia, as well as sinonasal adenocarcinoma (Kogevinas et al., ). An IUR of 3 × 10 −5 per μg/m 3 was derived for butadiene, in part based on these epidemiologic studies; however, an IUR was not derived for styrene (Supporting Information Table ).…”

Section: Case Studiesmentioning

confidence: 99%

Peak Exposures in Epidemiologic Studies and Cancer Risks: Considerations for Regulatory Risk Assessment

Checkoway

Lees

Dell³

et al. 2019

Risk Analysis

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We review approaches for characterizing “peak” exposures in epidemiologic studies and methods for incorporating peak exposure metrics in dose–response assessments that contribute to risk assessment. The focus was on potential etiologic relations between environmental chemical exposures and cancer risks. We searched the epidemiologic literature on environmental chemicals classified as carcinogens in which cancer risks were described in relation to “peak” exposures. These articles were evaluated to identify some of the challenges associated with defining and describing cancer risks in relation to peak exposures. We found that definitions of peak exposure varied considerably across studies. Of nine chemical agents included in our review of peak exposure, six had epidemiologic data used by the U.S. Environmental Protection Agency (US EPA) in dose–response assessments to derive inhalation unit risk values. These were benzene, formaldehyde, styrene, trichloroethylene, acrylonitrile, and ethylene oxide. All derived unit risks relied on cumulative exposure for dose–response estimation and none, to our knowledge, considered peak exposure metrics. This is not surprising, given the historical linear no‐threshold default model (generally based on cumulative exposure) used in regulatory risk assessments. With newly proposed US EPA rule language, fuller consideration of alternative exposure and dose–response metrics will be supported. “Peak” exposure has not been consistently defined and rarely has been evaluated in epidemiologic studies of cancer risks. We recommend developing uniform definitions of “peak” exposure to facilitate fuller evaluation of dose response for environmental chemicals and cancer risks, especially where mechanistic understanding indicates that the dose response is unlikely linear and that short‐term high‐intensity exposures increase risk.

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Section: Case Studiesmentioning

confidence: 99%

Peak Exposures in Epidemiologic Studies and Cancer Risks: Considerations for Regulatory Risk Assessment

Checkoway

Lees

Dell³

et al. 2019

Risk Analysis

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“…Volatile organic compounds (VOCs) are defined, according to the European Union [1], as any organic compound having an initial boiling point less than or equal to 250 • C measured at a standard atmospheric pressure. Some VOCs are toxic to humans and some of them have also been classified as carcinogenic to humans by the International Agency for Research on Cancer (IARC), including 1,3-butadiene and benzene (known carcinogenic, group 1) [2,3], acrylamide and styrene (probable carcinogenic, group 2A) [4,5], propylene oxide and acrylonitrile (possible carcinogenic, group 2B) [4,6]. Moreover, chronic exposure to VOCs is associated with respiratory, neurological, reproductive, and developmental effects [7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Urinary Mercapturic Acids to Assess Exposure to Benzene and Other Volatile Organic Compounds in Coke Oven Workers

Frigerio

Campo

Mercadante

et al. 2020

IJERPH

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Coke production was classified as carcinogenic to humans by the International Agency for Research on Cancer. Besides polycyclic aromatic hydrocarbons, coke oven workers may be exposed to benzene and other volatile organic compounds (VOCs). The aim of this study was to assess the exposure to several VOCs in 49 coke oven workers and 49 individuals living in the same area by determining urinary mercapturic acids. Active tobacco smoking was an exclusion criterion for both groups. Mercapturic acids were investigated by a validated isotopic dilution LC-MS/MS method. Linear models were built to correct for different confounding variables. Urinary levels of N-acetyl-S-phenyl-L-cysteine (SPMA) (metabolite of benzene), N-acetyl-S-(2-hydroxy-1/2-phenylethyl)-L-cysteine (PHEMA) (metabolite of styrene), N-acetyl-S-(2-cyanoethyl)-L-cysteine (CEMA) (metabolite of acrylonitrile), N-acetyl-S-[1-(hydroxymethyl)-2-propen-1-yl)-L-cysteine and N-acetyl-S-(2-hydroxy-3-buten-1-yl)-L-cysteine (MHBMA) (metabolites of 1,3-butadiene) were 2–10 fold higher in workers than in controls (p < 0.05). For SPMA, in particular, median levels were 0.02 and 0.31 µg/g creatinine in workers and controls, respectively. Among workers, coke makers were more exposed to PHEMA and SPMA than foremen and engine operators. The comparison with biological limit values shows that the exposure of workers was within 20% of the limit values for all biomarkers, moreover three subjects exceeded the restrictive occupational limit value recently proposed by the European Chemicals Agency (ECHA) for SPMA.

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“…Noise is the most frequent cause of irreversible sensorineural hearing loss in the workplace. Styrene and other simple aromatic chemicals such as toluene, ethylbenzene, and xylenes have been linked to hearing loss in the workplace, particularly in conjunction with exposure to noise (Fechter 1999;Hormozi et al 2017;Johnson 2007;Johnson et al 2006;Lawton, Hoffmann, and Triebig 2006;Metwally et al 2012;Morata et al 2011;Sisto et al 2016Sisto et al , 2013Śliwińska-Kowalska et al 2005;Tognola et al 2015;Triebig, Bruckner, and Seeber 2009;Triebig et al 2001). The evidence base is reasonably robust for this effect, and supported by a number of high-quality toxicological and mechanistic animal studies (Campo et al 1999(Campo et al , 2001(Campo et al , 2003(Campo et al , 2011(Campo et al , 2014Chen et al 2007;Chen, Tanaka, and Henderson 2008;Chen and Henderson 2009;Loquet, Campo, and Lataye 1999;Fetoni et al 2016;Gagnaire and Langlais 2005;Gagnaire et al 2006;Lataye, Campo, and Loquet 2000;Lataye et al 2001Lataye et al , 2003Lataye et al , 2004Mäkitie et al 2002;Pouyatos et al 2004;Pouyatos, Campo, and Lataye 2005;Venet et al 2015;Wang et al 2...…”

Section: Non-cancer Health Effectsmentioning

confidence: 99%

Evaluation of potential health effects associated with occupational and environmental exposure to styrene – an update

Banton

Bus

Collins

et al. 2019

Journal of Toxicology and Environmental Health, Part B

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The potential chronic health risks of occupational and environmental exposure to styrene were evaluated to update health hazard and exposure information developed since the Harvard Center for Risk Analysis risk assessment for styrene was performed in 2002. The updated hazard assessment of styrene's health effects indicates human cancers and ototoxicity remain potential concerns. However, mechanistic research on mouse lung tumors demonstrates these tumors are mouse-specific and of low relevance to human cancer risk. The updated toxicity database supports toxicity reference levels of 20 ppm (equates to 400 mg urinary metabolites mandelic acid + phenylglyoxylic acid/g creatinine) for worker inhalation exposure and 3.7 ppm and 2.5 mg/kg bw/day, respectively, for general population inhalation and oral exposure. No cancer risk value estimates are proposed given the established lack of relevance of mouse lung tumors and inconsistent epidemiology evidence. The updated exposure assessment supports inhalation and ingestion routes as important. The updated risk assessment found estimated risks within acceptable ranges for all age groups of the general population and workers with occupational exposures in non-fiber-reinforced polymer composites industries and fiber-reinforced polymer composites (FRP) workers using closedmold operations or open-mold operations with respiratory protection. Only FRP workers using open-mold operations not using respiratory protection have risk exceedances for styrene and should be considered for risk management measures. In addition, given the reported interaction of styrene exposure with noise, noise reduction to sustain levels below 85 dB(A) needs be in place.

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Carcinogenicity of quinoline, styrene, and styrene-7,8-oxide

Cited by 29 publications

References 13 publications

Peak Exposures in Epidemiologic Studies and Cancer Risks: Considerations for Regulatory Risk Assessment

Peak Exposures in Epidemiologic Studies and Cancer Risks: Considerations for Regulatory Risk Assessment

Urinary Mercapturic Acids to Assess Exposure to Benzene and Other Volatile Organic Compounds in Coke Oven Workers

Evaluation of potential health effects associated with occupational and environmental exposure to styrene – an update

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