Environmental Benzene Exposure Research Articles

The Impact of Environmental Benzene, Toluene, Ethylbenzene, and Xylene Exposure on Blood-Based DNA Methylation Profiles in Pregnant African American Women from Detroit.

African American women in the United States have a high risk of adverse pregnancy outcomes. DNA methylation is a potential mechanism by which exposure to BTEX (benzene, toluene, ethylbenzene, and xylenes) may cause adverse pregnancy outcomes. Data are from the Maternal Stress Study, which recruited African American women in the second trimester of pregnancy from February 2009 to June 2010. DNA methylation was measured in archived DNA from venous blood collected in the second trimester. Trimester-specific exposure to airshed BTEX was estimated using maternal self-reported addresses and geospatial models of ambient air pollution developed as part of the Geospatial Determinants of Health Outcomes Consortium. Among the 64 women with exposure and outcome data available, 46 differentially methylated regions (DMRs) were associated with BTEX exposure (FDR adjusted p-value < 0.05) using a DMR-based epigenome-wide association study approach. Overall, 89% of DMRs consistently exhibited hypomethylation with increasing BTEX exposure. Biological pathway analysis identified 11 enriched pathways, with the top 3 involving gamma-aminobutyric acid receptor signaling, oxytocin in brain signaling, and the gustation pathway. These findings highlight the potential impact of BTEX on DNA methylation in pregnant women.

Framework for Evaluating Potential Causes of Health Risk Factors Using Average Treatment Effect and Uplift Modelling

Acute myeloid leukemia (AML) is a type of blood cancer that affects both adults and children. Benzene exposure has been reported to increase the risk of developing AML in children. The assessment of the potential relationship between environmental benzene exposure and childhood has been documented in the literature using odds ratios and/or risk ratios, with data fitted to unconditional logistic regression. A common feature of the studies involving relationships between environmental risk factors and health outcomes is the lack of proper analysis to evidence causation. Although statistical causal analysis is commonly used to determine causation by evaluating a distribution’s parameters, it is challenging to infer causation in complex systems from single correlation coefficients. Machine learning (ML) approaches, based on causal pattern recognition, can provide an accurate alternative to model counterfactual scenarios. In this work, we propose a framework using average treatment effect (ATE) and Uplift modeling to evidence causation when relating exposure to benzene indoors and outdoors to childhood AML, effectively predicting causation when exposed indoors to this contaminant. An analysis of the assumptions, cross-validation, sample size, and interaction between predictors are also provided, guiding future works looking at the universalization of this approach in predicting health outcomes.

Interaction effects of environmental response gene polymorphisms and benzene exposure on telomere length in shoe-making workers

Benzene is a globally occurring environmental and occupational pollutant that causes leukemia. To better understand telomere length (TL) as a function of benzene toxicity, we recruited 294 shoe-making workers and 102 controls from Wenzhou, China in 2011. Biomarkers of TL, cytokinesis-block micronucleus (MN) frequency, and white blood cells (WBC) were measured. In total, 18 polymorphic sites in environmental response genes, including metabolic and DNA repair genes, were analyzed. Results indicate that benzene exposure led to a longer TL at a threshold of 32 mg/m3-year of cumulative exposure dose (CED). Furthermore, the TL was longer in members of the damaged group, when evaluated for MN frequency (P < 0.001) and reduced WBC (P < 0.001), than in those of the normal group. Workers carrying genotype TT (β = 0.32, P = 0.042) in rs3212986 of ERCC1 and genotype TC (β = 0.24, P = 0.082) in rs1051740 of mEH exon3 were associated with a longer TL as compared to the wild-type group. TA (β = −0.53, P < 0.001) in rs6413432 of CYP2E1 was associated with a shorter TL. Benzene exposure interacted with the TA type in rs6413432 (β = 0.003, 95% CI: 0, 0.006, P = 0.042) and the CC type in rs1051740 (β = 0.007, 95% CI: 0.001, 0.013, P = 0.015) after adjusting for confounding factors. Our results indicate that benzene induces an increase in TL at a threshold of CED ≥32mg/m3-year. Rs1051740, rs3212986, and rs6413432 were found to be involved in benzene-induced telomere growth; in particular, rs1051740 and rs6413432 interacted with the benzene exposure, resulting in an extended TL.

Safe Concentration of Benzene on Workers at Public Gas Stations around Diponegoro University Semarang, Indonesia

Benzene is a liguid aromatic hydrocarbon compound that is clear, colorless, fammable, and volatile. This study aims to determine safe concentration of benzene at public gas stations workers around Diponegoro University Semarang. This is descriptive, observational, and cross sectional study. A total of 28 workers were then taken as sample. Data was taken in form of primary and secondary data, then analyzed manually through calculation of safe concentration of benzene after determination of weight, body surface of experimental animals, body weight body surface area, breathing rate of workers, benzene concentration, Animal Km, Human Km, highest dose of toxin without causing effect, and reference concentration of benzene for workers. The measurement of average concentration of benzene in the air showed a value of 0.82 mg/m' (0.25 ppm). This result is lower than benzene Threshold Limit Value according to Ministry of Manpower Regulation Number 5 of 2018 of 0.5 ppm. In contrast, manual calculation of safe concentration of benzene was 0.01 ppm. In conclusion, average value of benzene concentration is not safe for workers. Efforts to control benzene exposure in work environment are needed to ensure workers health such as use of Personal Protective Eguipment in form of half mask respirators with organic vapor cartridges, consumption of CYP2EI1 enzymes in beef liver and salmon meat, procurement of Golden Phothos or Boston plants, and inspection and regular monitoring of benzene exposure biomarkers in work environment.

Environmental exposure to benzene: evaluation of urinary S-PMA and polymorphism (CYP2E1-1293G&gt;C and NQO1 609C&gt;T) in Campos Elíseos residents, Duque de Caxias, Rio de Janeiro State, Brazil

Benzene is one of the most important substances for assessment, due to its significant use, the environmental contamination resulting from its emission and the effects on human health. It is classified by the International Agency for Research on Cancer (IARC) as a known carcinogen to humans (group 1) and associated with the development of leukemia. In general, the population is exposed to this substance by inhaling contaminated air, which varies according to the location and intensity of its potential sources. The petrochemical industry is one of the most important sources of this compound. The municipality of Duque de Caxias, specifically the Campos Elíseos district, in Rio de Janeiro State, Brazil, houses the Industrial Complex of Campos Elíseos (PICE), a grouping of over 25 industries, which includes the second largest oil refinery in Brazil. Environmental contamination from the PICE has been recognized, but there is a lack of studies concerning its impact on the health of the surrounding population. S-phenylmercapturic acid (S-PMA) concentrations ranging from 0.80 to 8.01μg.g-1 creatinine were observed in the local population, apparently related to hematological changes also observed in exposed population. The quantifiable presence of urinary S-PMA from the benzene metabolism is associated with the fact that 60% of the participants present specific hematological changes, which may be due to the environmental benzene exposure. The allele and genotype frequencies of the CYP2E1 and NQO1 enzymes observed in the study population were similar to those reported in other studies. The presence of the variant allele in the NQO1 genotype may be a risk factor for the observed hematological changes.

The impact of chronic environmental metal and benzene exposure on human urinary metabolome among Chinese children and the elderly population

The health effects of metals and benzene exposure have been extensively investigated; however, information on the impact of chronic environmental metal and benzene exposure on human urinary metabolome is limited. In this study, a total of 566 participants, including 352 elderly and 214 children, were split into the “exposed” and “control” groups. The urine samples of all the participants were collected and stored at − 80 °C until analysis. The urinary levels of 17 metals and S-phenylmercapturic acid (S-PMA) were determined by the ICP–MS and LC–MS/MS methods to comprehensively assess the personal metal and benzene exposure levels, respectively. Then, the individual levels of metal and benzene exposure were correlated to the metabolic consequences of ambient pollutant exposure, which were previously observed in our metabolomics study. As a result, multiple metals, including Cd, Co, Cr, Cu, Fe, Hg, Li, Mo, Ni, Pb, Se, and Zn, exhibited a significant linear dose–dependent association with one or more urinary metabolites, including two amino acids (pyroglutamic acid and 3-methylhistidine), three organic acids (azelaic acid, decenedioic acid, and hydroxytetradecanedioic acid), ten medium-chainacylcarnitines (heptenedioylcarnitine, octenedioylcarnitine, nonenedioylcarnitine, decenedioylglucuronide, 3-hydroxydecanoylcarnitine, dodecanedioylcarnitine, nonanoylcarnitine, decadienylcarnitine, hydroxydodecenoylcarnitine, dodecadienylcarnitine, and dodecenoylcarnitine), and one glucuronide conjugate (decenedioylglucuronide). These observations indicate that the increased environmental metal exposure has caused various oxidative stress-related effects, including the depletion of antioxidants, accelerated muscle proteolysis, elevated activity of UGTs, increased lipid peroxidation, and the disorder of mitochondrial lipid metabolism among exposed children and the elderly. The current study provides new insights into the biological effects induced by metal exposure in the environment.

Safe Concentration of Benzene Exposure in Work Environment at Motor Workshop

Benzene is a colorless liquid that can evaporate rapidly in air and slightly dissolved in water. Exposure of benzene to the body has a very adverse impact on health. The aims of this research were to know benzene risk characteristic or RQ, and safe concentration of benzene exposure in a workshop environment. This research was observational, cross-sectional design with a population of 7 workers of the motor industry in Surabaya. The benzene exposure in the workplace was measured by Gas Chromatography-Flame Ionization Detector (GC-FID). Data analysis was done by using quantitative data. Maximum benzene intake received by workers was 0.1837 mg/kg/day. RQ on average workers more than 1 (&amp;gt; 1), with the highest RQ of 22.673. The highest safe concentration of workers was 3.9 mg/m3 and the lowest safe concentration was 0.4 mg/m3. The concentration of benzene exposure in the motor industry showed was above the threshold limit. According to the regulation of Manpower and Transmigration Ministry No 13 the year 2011, RQ for benzene showed a high-risk impact for workers, the smallest safe concentration for the worker was 0.4 mg/m3.

In Search of the Ultimate Benzene Sensor: The EtQxBox Solution.

In this work we report a comprehensive study leading to the fabrication of a prototype sensor for environmental benzene monitoring. The required high selectivity and ppb-level sensitivity are obtained by coupling a silicon-integrated concentration unit containing the specifically designed EtQxBox cavitand to a miniaturized PID detector. In the resulting stand-alone sensor, the EtQxBox receptor acts at the same time as highly sensitive preconcentrator for BTEX and GC-like separation phase, allowing for the selective desorption of benzene over TEX. The binding energies of the complexes between EtQxBox and BTX are calculated through molecular mechanics calculations. The examination of the corresponding crystal structures confirms the trend determined by computational studies, with the number of C-H···N and CH···π interactions increasing from 6 to 9 along the series from benzene to o-xylene. The analytical performances of EtQxBox are experimentally tested via SPME, using the cavitand as fiber coating for BTEX monitoring in air. The cavitand EFs are noticeably higher than those obtained by using the commercial CAR-DVB-PDMS. The LOD and LOQ are calculated in the ng/m3 range, outperforming the commercial available systems in BTEX adsorption. The desired selective desorption of benzene is achieved by applying a smart temperature program on the EtQxBox mesh, which starts releasing benzene at lower temperatures than TEX, as predicted by the calculated binding energies. The sensor performances are experimentally validated and ppbv level sensitivity toward the carcinogenic target aromatic benzene was demonstrated, as required for environmental benzene exposure monitoring in industrial applications and outdoor environment.

Maternal benzene exposure during pregnancy and risk of childhood acute lymphoblastic leukemia: a meta-analysis of epidemiologic studies.

BackgroundThe prevalence of childhood leukemia is increasing rapidly all over the world. However, studies on maternal benzene exposure during pregnancy and childhood acute lymphoblastic leukemia (ALL) have not been systematically assessed. Therefore, we performed a meta-analysis to investigate the association between maternal solvent, paint, petroleum exposure, and smoking during pregnancy and risk of childhood ALL.MethodsRelevant studies up to September 1st, 2013 were identified by searching the PubMed, EMBASE, Cochrane library and the Web of Science databases. The effects were pooled using either fixed or random effect models based on the heterogeneity of the studies.ResultsTwenty-eight case-control studies and one cohort study were included for analysis, with a total of 16,695 cases and 1,472,786 controls involved. Pooled odds ratio (OR) with 95% confidence interval (CI) for ALL was 1.25 (1.09, 1.45) for solvent, 1.23 (1.02, 1.47) for paint, 1.42 (1.10, 1.84) for petroleum exposure, and 0.99 (0.93, 1.06) for maternal smoking during pregnancy. No publication bias was found in this meta-analysis and consistent results were observed for subgroup and sensitivity analyses.ConclusionsChildhood ALL was associated with maternal solvent, paint, and petroleum exposure during pregnancy. No association was found between ALL and maternal smoking during pregnancy. Avoidance of maternal occupational and environmental benzene exposure during pregnancy could contribute to a decrease in the risk of childhood ALL.

Health consequences of involuntary exposure to benzene following a flaring incident at British Petroleum refinery in Texas City

Environmental exposure to benzene can lead to deleterious effects on many biological systems including blood-forming organs, liver, and kidneys. The authors sought to investigate the health consequences of benzene exposure following a flaring incident that occurred at the British Petroleum (BP) refinery in Texas City, TX. A cohort of subjects who were exposed to a daily sustained release of toxic chemicals including more than 7,711 kg (17,000 lb) of benzene for a total duration of 40 days due to BP's flaring incident. Not applicable to an observational study. Subjects who underwent physical and clinical evaluation between June 2010 and October 2012 were included. Demographic and clinical laboratory data were collected and analyzed. Hematologic data such as white blood cell (WBC) counts, platelet counts, hemoglobin, hematocrit, blood urea nitrogen (BUN), and creatinine levels in the serum were evaluated. In addition, data on alkaline phosphatase (ALP), aspartate amino transferase (AST), and alanine amino transferase (ALT) levels in the serum were examined. Urinary phenol was evaluated as a benzene metabolite. The outcomes were compared between exposed and unexposed patients. A total of 200 subjects (benzene exposed, n = 100 and unexposed, n = 100) were included. Benzene exposed subjects showed significantly higher levels of WBC (×10(3) per μL) count (8.6 ± 5.4 vs 6.5 ± 2.0, p = 0.0003) and platelet (×10(3) per μL) count (291.3 ± 82.7 vs 264.1 ± 74.0, p = 0.0076) compared with the unexposed subjects. ALP (IU/L) was significantly elevated in the benzene exposed subjects compared with the unexposed subjects (121.2 ± 73.7 vs 65.4 ± 23.6, p = 0.000). Similarly, benzene exposed subjects had significantly higher levels of AST (IU/L) compared with unexposed subjects (23.4 ± 11.8 vs 19.5 ± 8.9, p = 0.0089). This retrospective pilot study found that environmental benzene exposure from the BP's flaring incident appears to pose significant health risks including specific alteration of blood cells and liver enzymes, indicating that subjects exposed to benzene may be at a higher risk of developing hepatic or blood related disorders.

Possible sources of urinary benzene among nonoccupationally exposed Japanese subjects

Unmetabolized benzene in urine (U-benzene) is known to be the best marker among the indices for the biological monitoring of occupational and environmental exposure to benzene. In this study, we determined the levels of U-benzene among Japanese university students exposed to benzene nonoccupationally and analyzed the relation between U-benzene levels and the possible factors responsible for environmental benzene exposure. In urinalysis, U-benzene concentration among 124 students was detected in the range from 18 (minimum detection limit) to 249 ng/l. The frequency distribution of U-benzene concentration peaked at 0-19 ng/l. Mean and median values of 40 and 20 ng/l for U-benzene concentration in nonoccupationally exposed subjects were lower than those in a previous study. Stepwise multiple linear regression analysis was performed to assess the potential sources of exposure to environmental benzene by analyzing the relation between U-benzene and personal, behavioral, and environmental factors. The results showed that only smoking habit (P < 0.01) and residential house age (P < 0.05) were independent determinants of U-benzene levels. In addition, U-benzene levels in relation to smoking and house age suggested that these factors could be associated with the synergistic elevation of U-benzene. The present study showed U-benzene levels among non-occupationally exposed Japanese subjects and revealed that the major exposure sources to benzene in the general environment were tobacco smoking and indoor air contamination.

Exposição a hidroquinona e ao fenol sobre a resposta inflamatória pulmonar induzida por bactéria

A gravidade dos efeitos causados pela exposição ambiental e ocupacional ao benzeno determinou o controle de sua utilização. No entanto, mesmo nestas condições, toxicidade ao sistema imune e nervoso tem sido descrita. A toxicidade do benzeno é determinada pelos seus produtos de biotransformação, em que fenol (FE) e hidroquinona (HQ) têm papel relevante na imunotoxicidade. Neste contexto, o presente trabalho mostra que a exposição de ratos Wistar, machos, a doses de 5 ou 10 mg/kg de HQ (via i.p., uma vez ao dia, 13 doses consecutivas, com intervalos de 2 dias a cada 5 doses) provocou reduções acentuadas no influxo de leucócitos polimorfonucleares (PMN) e mononucleares (MN) para o pulmão 24 horas após inalação de Lipopolissacarídeo (LPS) de Salmonella abortus. Diferentemente, a migração de leucócitos em animais expostos ao FE não foi alterada. A exposição a ambos os agentes químicos simultaneamente (dose de 5 mg/kg cada) manteve a redução na migração de MN detectada em animais expostos à HQ e potencializou o efeito inibitório da HQ sobre a migração de leucócitos PMN. Os prejuízos nas migrações de leucócitos não foram decorrentes de modificações no número destas células na circulação. É importante ressaltar que os efeitos foram induzidos por doses dos agentes químicos que não causaram prejuízo à função hepática ou renal, determinados pela atividade das transaminases hepáticas e a concentração de creatinina no soro. Em conjunto, os dados obtidos mostram a exposição a baixas doses de HQ não provoca alterações nos parâmetros empregados como indicadores de toxicidade. No entanto, os efeitos tóxicos são manifestados resposta do organismo ao trauma.

High-Performance Liquid Chromatography Method for Urinary trans, trans-Muconic Acid. Application to Environmental Exposure to Benzene

This report describes a specific and precise high-performance liquid chromatography (HPLC) method for the quantification of trans,trans-muconic acid in human urine. The procedure involved a highly efficient Bond-Elut SAX extraction with 20% acetic acid elution. The HPLC analysis used a sodium acetate/methanol mobile phase with a C18 reverse phase column and UV detection at 265 nm. The recovery, precision, linearity, and limits of detection and quantification of the method were determined. Mean absolute recoveries were between 97% and 115%. The calibration curve showed a correlation coefficient of 0.9955 and the limit of detection was determined to be 10.8 microg/L. The method is suitable for evaluation of occupational and environmental benzene exposure in humans. The study of urinary trans,trans-muconic acid of two populations of children to evaluate environmental benzene exposure is presented.

Monitoring Low Benzene Exposure: Comparative Evaluation of Urinary Biomarkers, Influence of Cigarette Smoking, and Genetic Polymorphisms

Benzene is a human carcinogen and an ubiquitous environmental pollutant. Identification of specific and sensitive biological markers is critical for the definition of exposure to low benzene level and the evaluation of the health risk posed by this exposure. This investigation compared urinary trans,trans-muconic acid (t,t-MA), S-phenylmercapturic acid, and benzene (U-benzene) as biomarkers to assess benzene exposure and evaluated the influence of smoking and the genetic polymorphisms CYP2E1 (RsaI and DraI) and NADPH quinone oxidoreductase-1 on these indices. Gas station attendants, urban policemen, bus drivers, and two groups of controls were studied (415 subjects). Median benzene exposure was 61, 22, 21, 9 and 6 microg/m(3), respectively, with higher levels in workers than in controls. U-benzene, but not t,t-MA and S-phenylmercapturic acid, showed an exposure-related increase. All the biomarkers were strongly influenced by cigarette smoking, with values up to 8-fold higher in smokers compared with nonsmokers. Significant correlations of the biomarkers with each other and with urinary cotinine were found. A possible influence of genetic polymorphism of CYP2E1 (RsaI and/or DraI) on t,t-MA and U-benzene in subjects with a variant allele was found. Multiple linear regression analysis correlated the urinary markers with exposure, smoking status, and CYP2E1 (RsaI; R(2) up to 0.55 for U-benzene). In conclusion, in the range of investigated benzene levels (<478 micro/m(3) or <0.15 ppm), smoking may be regarded as the major source of benzene intake; among the study indices, U-benzene is the marker of choice for biomonitoring low-level occupational and environmental benzene exposure.

A molecular epidemiological approach to health risk assessment of urban air pollution

The ambient air of urban centres is polluted with potentially toxic chemicals mostly arising from the combustion or fuels used for transport. Among these compounds, benzene raises particular concern due to its haematoxicity and leukaemogenic risks. Although limits of benzene in air have been established in the European Union (5 μg/m 3), individual exposure levels—and therefore risk estimates—cannot merely be extrapolated from environmental concentrations. Molecular epidemiology can facilitate health risk assessment by investigating the relationship between exposure to environmental pollutants and quantification of biomarkers that lie on the pathway of carcinogenesis upstream of clinical disease. We review the available for biomarker studies regarding health risks linked to environmental benzene exposure, and make some suggestions for future work.

599 A comparison of environmental benzene exposure in subjects from rural and urban populations using an immunoassay for the specific biomarker S-phenylmercapturic acid (S-PMA)

599 A comparison of environmental benzene exposure in subjects from rural and urban populations using an immunoassay for the specific biomarker S-phenylmercapturic acid (S-PMA)

S -phenylcysteine adduct concentration in serum albumin of countryside residents and factory workers in Estonia

In this communication we present data on S-phenylcysteine (SPC) in human serum albumin in an Estonian cohort. A total of 112 human samples were collected from workers of a benzene processing plant in Kohtla-Järve, Estonia and another 56 samples from nearby countryside residents. Albumin was isolated using a sequential precipitation method designed for low volume plasma samples. The adducted cysteine derivatives were cleaved off from the albumin and subsequently derivatized to phenyl trifluorothioacetate (PTTA) derivatives. Derivatized adducts were subjected to GC/MS analysis utilizing negative chemical ionization and a selected ion monitoring (SIM) technique. The detection limit for the PTTA adduct was 0.2 pmol g−1 albumin and the limit of quantification was 2 pmol g−1 albumin. The method utilized deuterated SPC as an internal standard. The analysis revealed that adduct levels were also high in the population that was not occupationally exposed to benzene. The reason for this is unknown, but may cause problems if not of environmental origin, when one is attempting to monitor low level occupational or environmental benzene exposure.

Trans,trans-Muconic acid excretion in relation to environmental exposure to benzene.

Potential environmental sources of benzene exposure, and intake of foods and beverages susceptible to being preserved with sorbic acid, were investigated in relation to their contribution to the inter-individual variation in background urinary trans,trans-muconic acid ( t,t-MA) excretion among subjects non-occupationally exposed to benzene. We measured urinary t,t-MA excretion in 65 subjects, 34 women and 31 men. A spot sample of morning urine was collected for each subject 10-12 h after they had consumed their last meal. Questionnaire information was collected on diet and possible sources of environmental benzene exposure in the surroundings of the subjects' residences. For each subject, an estimate of the average daily intake of sorbic acid with diet was calculated, based on questionnaire information and laboratory data on samples of local food items. The t,t-MA geometric mean was significantly higher among women (28.7 vs 11.5 microg/g creatinine, P<0.05) and among smokers (37.6 vs 15.6 microg/g creatinine, P<0.05), and increased by years of education among women, but not among men. In the multivariate analysis, smoking was the only significant predictor of elevated t,t-MA excretion. In our study, the average estimated daily sorbic-acid intake with diet was 0.33 ppm (standard deviation: 0.28), and it did not show a correlation with t,t-MA excretion. Urban traffic and residence within 100 m of a fuel station also did not show an association with elevated t,t-MA values. Our study confirms that, among subjects non-occupationally exposed to benzene, smoking contributes significantly to increased background t,t-MA excretion. Further studies should be addressed to confirm our observation of elevated t,t-MA levels among women.

Environmental benzene exposure assessment for parent–child pairs in Rouen, France

There is a lack of data on environmental benzene exposure in children. In this study, we compared personal benzene exposure and inhalation uptake in a group of children to those of their parents. We also compared levels of urinary benzene metabolites, trans,trans-muconic acid (MA) and hydroquinone (HQ), for those two groups, and assessed the correlation between personal benzene exposure and urinary MA and HQ concentrations. The study was performed on 21, 2–3-year-old children and their parents recruited on a voluntary basis among non-smokers from the three largest day-care centers of the town of Rouen in France. Average benzene concentrations were measured over 5 consecutive days with diffusive samplers. The following simultaneous measurements were carried out: personal exposure of the parents, concentrations inside and outside the day care centers, and inside the volunteer's bedrooms. Morning and evening urine samples were collected during the same period. Benzene personal exposure levels were 14.4±7.7 μg/m 3 and 11.09±6.15 μg/m 3 in parents and children, respectively. Benzene inhalation uptake estimates were 2.51±1.23 μg/kg/day in the group of parents and 5.68±3.17 μg/kg/day in the group of children. Detectable levels of MA and HQ were found in 85% and 100% of the samples, respectively. Intra-individual variation of urinary MA and HQ concentrations expressed as a coefficient of variation (CV) ranged from 63 to 232% and from 13 to 144%, respectively. Mean values of MA and HQ (in mg/g creatinine) were 1.6- and 1.8-fold higher in the group of children than in the group of parents ( P=0.008 and P<0.0001, respectively). Significant correlations between metabolites levels and benzene were not found.

Lack of correlation between environmental or biological indicators of benzene exposure at parts per billion levels and micronuclei induction

Despite growing concern for possible carcinogenic effects associated with environmental benzene exposure in the general population, few studies exist at parts per billion (ppb) levels. We investigated the existence of a relationship between airborne/biological measurements of benzene exposure (i.e., personal/area sampling and unmodified urinary benzene/ trans, trans-muconic acid; t,t-MA) and micronuclei induction (cytochalasin B technique) among exposed chemical laboratory workers ( n=47) and traffic wardens ( n=15). Although urinary t,t-MA (106.9±123.17 μg/L urine) correlated ( R 2=0.37) with urinary benzene (0.66±0.99 μg/L urine), neither biological measurement correlated with environmental benzene exposure (14.04±9.71 μg/m 3; 4.39±3.03 ppb), suggesting that, at ppb level (1 ppb=3.2 μg/m 3), airborne benzene constitutes a fraction of the total intake. Traffic wardens and laboratory workers had comparable numbers of micronuclei (4.70±2.63 versus 5.76±3.11; n.s.), similar to levels recorded in the general population. With univariate/multivariate analysis, no association was found between micronuclei induction and air/urinary benzene exposure variables. Notably, among the personal characteristics examined (including age, gender, smoking, drinking, etc.), high body mass index correlated with micronuclei induction while, among females, use of hormonal medication was associated with less micronuclei. Thus the present study provides no evidence that ppb levels of environmental benzene exposure appreciably affect micronuclei incidence (against the background of other relevant factors). However, this should not be taken as an argument against efforts aiming to reduce environmental benzene pollution.