A Chronic Reference Value for 1,3-Butadiene Based on an Updated Noncancer Toxicity Assessment

Grant, Roberta L.; Haney, Joseph T.; Curry, Angela L.; Honeycutt, Michael

doi:10.1080/10937404.2010.499735

Cited by 8 publications

(4 citation statements)

References 37 publications

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“…Although BD undergoes rapid destruction in the atmosphere, it is remains present at very low concentrations (0.1-1.0 parts per billion) in urban and suburban areas [122]. This is likely related to the fact that these chemicals have also XENOBIOTIC EFFECTS ON OVARIAN PREANTRAL FOLLICLES been reported in cigarette smoke, automobile exhaust, and biomass burning [123][124][125]. Compounds known to contain epoxide moieties (or which are capable of bioactivation by epoxidation) have been shown to affect reproductive function in laboratory animals.…”

Section: Occupational Chemicalsmentioning

confidence: 99%

Xenobiotic Effects on Ovarian Preantral Follicles1

Mark-Kappeler

Hoyer

Devine

2011

Biology of Reproduction

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Women are born with a finite population of ovarian follicles, which are slowly depleted during their reproductive years until reproductive failure (menopause) occurs. The rate of loss of primordial follicles is determined by genetic and environmental influences, but certain toxic exposures can accelerate this process. Ionizing radiation reduces preantral follicle numbers in rodents and humans in a dose-dependent manner. Cigarette smoking is linked to menopause occurring 1-4 yr earlier than with nonsmokers, and components of smoke, polycyclic aromatic hydrocarbons, can cause follicle depletion in rodents or in ovaries in vitro. Chemotherapeutic agents, such as alkylating drugs and cisplatin, also cause loss of preantral ovarian follicles. Effects depend on dose, type, and reactivity of the drug, and the age of the individual. Evidence suggests DNA damage may underlie follicle loss induced by one common alkylating drug, cyclophosphamide. Occupational exposures have also been linked to ovarian damage. In an industrial setting, 2-bromopropane caused infertility in men and women, and it can induce ovarian follicle depletion in rats. Solvents, such as butadiene, 4-vinylcyclohexene, and their diepoxides, can also cause specific preantral follicle depletion. The mechanism(s) underlying effects of the latter compound may involve alterations in apoptosis, survival factors such as KIT/Kit Ligand, and/or the cellular signaling that maintains primordial follicle dormancy. Estrogenic endocrine disruptors may alter follicle formation/development and impair fertility or normal development of offspring. Thus, specific exposures are known or suspected of detrimentally impacting preantral ovarian follicles, leading to early ovarian failure.

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Section: Occupational Chemicalsmentioning

confidence: 99%

Xenobiotic Effects on Ovarian Preantral Follicles1

Mark-Kappeler

Hoyer

Devine

2011

Biology of Reproduction

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“…TCEQ conducts chemical-specific toxicity assessments for all permitted chemicals to assess safe levels in air. A similar analytical approach used for DEA was used for hazard identification and dose–response assessment to derive acute and chronic ReVs for 1,3-butadiene (Grant et al, 2010 ), ethylene (Erranguntla & Grant, 2015 ), hexamethylenediamine (Myers & Grant, 2015 ) as well as numerous other chemicals (Final Development Support Documents at http://www.tceq.state.tx.us/toxicology/dsd/final.html ).…”

Section: Discussionmentioning

confidence: 99%

Assessment of chronic inhalation non-cancer toxicity for diethylamine

Grant

Taiwo

McCant

2015

Inhalation Toxicology

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A non-cancer inhalation chronic toxicity assessment for diethylamine (DEA, CAS number 109-89-7) was conducted by the Texas Commission on Environmental Quality. A chronic Reference Value (ReV) was determined based on a high-quality study conducted in mice and rats by the National Toxicology Program. Chronic inhalation ReVs are health-based exposure concentrations used in assessing health risks of long-term (i.e. lifetime) chemical exposure. DEA is used industrially as an organic intermediate to produce corrosion inhibitors, and is widely used in rubber, pharmaceuticals, resins, pesticides, insect repellants, dye processing and as a polymerization inhibitor. Although systemic effects have been noted at higher concentrations, DEA acts primarily as a respiratory irritant with effects occurring in the upper respiratory tract. Rats were exposed to 0, 31, 62.5 and 125 ppm DEA and mice to 0, 16, 31 and 62.5 ppm DEA for 6 h/day, 5 days/week for 105 weeks. Mice were slightly more sensitive than rats. The critical effect identified in mice was hyperostosis in the turbinates although DEA caused a number of other non-neoplatic lesions. Dose–response data were suitable to benchmark concentration (BMC) modeling. The human equivalent point of departure (PODHEC) was calculated from the 95% lower limit of the BMC(10) using default duration and animal-to-human dosimetric adjustments. Total uncertainty factors of 90 were applied to the PODHEC to account for variation in sensitivity within the human population, toxicodynamic differences between mice and humans, and database uncertainty. The chronic ReV for DEA is 11 ppb (33 µg/m3).

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“…As a result of varying ways to account for species differences, various reports by agencies, authorizations and publications have been published (Anderson et al , 1998; ATSDR, 1992, 2012; CEPA, 2000; ECB, 2002; EPA, 2002b; Grant et al , 2010; Hackett et al , 1987; Hazelton-Laboratories-Europe, 1981; IARC, 2008; IRIS, 2013; Kirman and Grant, 2012; Kirman et al , 2010; NTP, 1984, 1993; Stayner et al , 2000). For the present purpose, studies were selected from reports from Health Canada (CEPA, 2000), the European Union (ECB, 2002), the Dutch government (Hernández et al , 2011), and the U.S. Environmental Protection Agency (U.S. EPA) (IRIS, 2013).…”

Section: Methodsmentioning

confidence: 99%

Tobacco Smoke–Related Health Effects Induced by 1,3-Butadiene and Strategies for Risk Reduction

Soeteman‐Hernández¹,

Bos

Talhout³

2013

Toxicological Sciences

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1,3-Butadiene (BD) is a smoke component selected by the World Health Organization (WHO) study group on Tobacco Product Regulation (TobReg) for mandated lowering. We examined the tobacco smoke–related health effects induced by BD and possible health impacts of risk reduction strategies. BD levels in mainstream smoke (MSS) from international and Canadian cigarettes and environmental tobacco smoke (ETS) were derived from scientific journals and international government reports. Dose-response analyses from toxicity studies from government reports were evaluated and the most sensitive cancer and noncancer endpoints were selected. The risks were evaluated by taking the ratio (margin of exposure, MOE) from the most sensitive toxicity endpoint and appropriate exposure estimates for BD in MSS and ETS. BD is a good choice for lowering given that MSS and ETS were at levels for cancer (leukemia) and noncancer (ovarian atrophy) risks, and the risks can be significantly lowered when lowering the BD concentrations in smoke. Several risk reduction strategies were analyzed including a maximum level of 125% of the median BD value per milligram nicotine obtained from international brands as recommended by the WHO TobReg, tobacco substitute sheets, dual and triple carbon filters, and polymer-derived carbon. The use of tobacco substitute sheet with a polymer-derived carbon filter resulted in the most significant change in risk for cancer and noncancer effects. Our results demonstrate that MOE analysis might be a practical way to assess the impact of risk reduction strategies on human health in the future.

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A Chronic Reference Value for 1,3-Butadiene Based on an Updated Noncancer Toxicity Assessment

Cited by 8 publications

References 37 publications

Xenobiotic Effects on Ovarian Preantral Follicles1

Xenobiotic Effects on Ovarian Preantral Follicles1

Assessment of chronic inhalation non-cancer toxicity for diethylamine

Tobacco Smoke–Related Health Effects Induced by 1,3-Butadiene and Strategies for Risk Reduction

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