Benzene and Lymphohematopoietic Malignancies in China

Hayes, Richard B.; Yin, Songnian; Rothman, Nathaniel; Dosemeci, Mustafa; Li, Guilan; Travis, Lois T.; Smith, Martyn T.; Linet, Martha S.

doi:10.1080/00984100050166442

Cited by 38 publications

(3 citation statements)

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“…Some of its destructive effects such as chromosomal damage, depression of the immune system [24], [25], [26], progressive degeneration of the bone marrow, and induction of aplastic anemia and leukemia [16] resulted in its classification as a human carcinogen by the International Agency for Research on Cancer [27] and, consequently, in a reduction of its acceptable occupational exposure levels. Its occupational threshold limit value has been lowered to 0.5–1 ppm by many occupational health organizations such as NIOSH and Occupational Safety and Health Administration.…”

Section: Discussionmentioning

confidence: 99%

Urinary Trans, Trans -Muconic Acid is Not a Reliable Biomarker for Low-level Environmental and Occupational Benzene Exposures

Jalai

Ramezani

Ebrahimpour

2017

Safety and Health at Work

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BackgroundBenzene is a known occupational and environmental pollutant. Its urinary metabolite trans, trans-muconic acid (tt-MA) has been introduced by some environmental and occupational health regulatory associations as a biological index for the assessment of benzene exposure; however, recently, doubts have been raised about the specificity of tt-MA for low-level benzene exposures. In the present study, we investigated the association between urinary levels of tt-MA and inhalational exposure to benzene in different exposure groups.MethodsBenzene exposure was assessed by personal air sampling. Collected benzene on charcoal tube was extracted by carbon disulfide and determined by a gas chromatograph (gas chromatography with a flame ionization detector). Urinary tt-MA was extracted by a strong anion-exchange column and determined with high-performance liquid chromatography–UV.ResultsUrinary levels of tt-MA in intensive benzene exposure groups (chemical workers and police officers) were significantly higher than other groups (urban and rural residents), but its levels in the last two groups with significant different exposure levels (mean = 0.081 ppm and 0.019 ppm, respectively) showed no significant difference (mean = 388 μg/g creatinine and 282 μg/g, respectively; p < 0.05). Before work shift, urine samples of workers and police officers showed a high amount of tt-MA and its levels in rural residents’ samples were not zero.ConclusionOur results suggest that tt-MA may not be a reliable biomarker for monitoring low-level (below 0.5 ppm) benzene exposures.

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Section: Discussionmentioning

confidence: 99%

Urinary Trans, Trans -Muconic Acid is Not a Reliable Biomarker for Low-level Environmental and Occupational Benzene Exposures

Jalai

Ramezani

Ebrahimpour

2017

Safety and Health at Work

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“…Benzene metabolites are activated to nucleophilic compounds by myeloperoxidase in the bone marrow causing DNA damage and also may be subsequently reduced by quinone oxidoreductases [101, 102]. Benzene is a confirmed cause of both leukemia and lymphoma [103, 104] and has been linked to the formation of chromosome rearrangements typical of leukemia even in normal healthy, exposed persons as well as hematopoietic defects [105-107]. Other causes of leukemia in adults are chemicals associated with the rubber industry (butadiene, etc.…”

Section: Adult Leukemiasmentioning

confidence: 99%

Perspectives on the causes of childhood leukemia

Wiemels

2012

Chemico-Biological Interactions

220

155

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Acute leukemia is the most common cancer in children but the causes of the disease in the majority of cases are not known. About 80% are precursor-B cell in origin (CD19+, CD10+), and this immunophenotype has increased in incidence over the past several decades in the Western world. Part of this increase may be due to the introduction of new chemical exposures into the child's environment including parental smoking, pesticides, traffic fumes, paint and household chemicals. However, much of the increase in leukemia rates is likely linked to altered patterns of infection during early childhood development, mirroring causal pathways responsible for a similarly increased incidence of other childhood-diagnosed immune-related illnesses including allergy, asthma, and type 1 diabetes. Factors linked to childhood leukemia that are likely surrogates for immune stimulation include exposure to childcare settings, parity status and birth order, vaccination history, and population mixing. In case-control studies, acute lymphoblastic leukemia (ALL) is consistently inversely associated with greater exposure to infections, via daycare and later birth order. New evidence suggests also that children who contract leukemia may harbor a congenital defect in immune responder status, as indicated by lower levels of the immunosuppressive cytokine IL-10 at birth in children who grow up to contract leukemia, as well as higher need for clinical care for infections within the first year of life despite having lower levels of exposure to infections. One manifestation of this phenomenon may be leukemia clusters which tend to appear as a leukemia “outbreak” among populations with low herd immunity to a new infection. Critical answers to the etiology of childhood leukemia will require incorporating new tools into traditional epidemiologic approaches – including the classification of leukemia at a molecular scale, better exposure assessments at all points in a child's life, a comprehensive understanding of genetic risk factors, and an appraisal of the interplay between infectious exposures and the status of immune response in individuals.

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“…Air concentrations of benzene are typically < 0.01 ppm in ambient environments but can exceed 10 ppm in industrial settings where benzene-containing products are used [International Agency for Research on Cancer (IARC) 1989; Wallace 1996]. Workers exposed to benzene have consistently experienced increased risks of hematopoietic disorders and leukemias (Hayes et al 2000; Lan et al 2004; Savitz and Andrews 1997). These toxic effects are thought to result from metabolism of benzene to reactive products (Snyder 2002).…”

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confidence: 99%

Albumin Adducts of Electrophilic Benzene Metabolites in Benzene-Exposed and Control Workers

Lin

Vermeulen

Tsai

et al. 2007

Environ Health Perspect

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BackgroundMetabolism of benzene produces reactive electrophiles, including benzene oxide (BO), 1,4-benzoquinone (1,4-BQ), and 1,2-benzoquinone (1,2-BQ), that are capable of reacting with blood proteins to produce adducts.ObjectivesThe main purpose of this study was to characterize relationships between levels of albumin adducts of these electrophiles in blood and the corresponding benzene exposures in benzene-exposed and control workers, after adjusting for important covariates. Because second blood samples were obtained from a subset of exposed workers, we also desired to estimate within-person and between-person variance components for the three adducts.MethodsWe measured albumin adducts and benzene exposures in 250 benzene-exposed workers (exposure range, 0.26–54.5 ppm) and 140 control workers (exposure range < 0.01–0.53 ppm) from Tianjin, China. Separate multiple linear regression models were fitted to the logged adduct levels for workers exposed to benzene < 1 ppm and ≥ 1 ppm. Mixed-effects models were used to estimate within-person and between-person variance components of adduct levels.ResultsWe observed nonlinear (hockey-stick shaped) exposure–adduct relationships in log-scale, with inflection points between about 0.5 and 5 ppm. These inflection points represent air concentrations at which benzene contributed marginally to background adducts derived from smoking and from dietary and endogenous sources. Adduct levels were significantly affected by the blood-collection medium (serum or plasma containing either heparin or EDTA), smoking, age, and body mass index. When model predictions of adduct levels were plotted versus benzene exposure ≥ 1 ppm, we observed marked downward concavity, particularly for adducts of the benzoquinones. The between-person variance component of adduct levels increased in the order 1,2-BQ < 1,4-BQ < BO, whereas the within-person variance components of the three adducts followed the reverse order.ConclusionsAlthough albumin adducts of BO and the benzoquinones reflect exposures to benzene ≥ 1 ppm, they would not be useful biomarkers of exposure at ambient levels of benzene, which tend to be < 0.01 ppm, or in those working populations where exposures are consistently < 1 ppm. The concavity of exposure–adduct relationships is consistent with saturable metabolism of benzene at air concentrations > 1 ppm. The surprisingly large effect of the blood-collection medium on adduct levels, particularly those of the benzoquinones, should be further investigated.

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Benzene and Lymphohematopoietic Malignancies in China

Cited by 38 publications

References 0 publications

Urinary Trans, Trans -Muconic Acid is Not a Reliable Biomarker for Low-level Environmental and Occupational Benzene Exposures

Urinary Trans, Trans -Muconic Acid is Not a Reliable Biomarker for Low-level Environmental and Occupational Benzene Exposures

Perspectives on the causes of childhood leukemia

Albumin Adducts of Electrophilic Benzene Metabolites in Benzene-Exposed and Control Workers

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