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What is already known about this topic? Benzene is classified as a Class I human carcinogen by the International Agency for Research on Cancer. Long-term exposure to benzene increases the risk of chronic benzene poisoning and leukemia. However, benzene is still widely used in the manufacturing industry. What is added by this report? The scale of enterprises most exposed to benzene was small enterprises, and joint-equity enterprises had the highest number that exceeded the permissible concentration-time weighted average. What are the implications for public health practice? It is still necessary to strengthen the monitoring of benzene concentrations in the manufacturing industry, especially in small enterprises. The occupational exposure limit of benzene should be appropriately reduced.

To discuss the changes in cognitive function and related brain regions in patients with chronic benzene poisoning. Few studies have explored the damage to cognitive function that occurs in benzene toxic encephalopathy. It is important to identify early in the course of disease whether cognitive dysfunction is caused by benzene poisoning so that disease prognosis and appropriate treatment can be determined. We reported on the chronic benzene poisoning of a 41-year-old Han Chinese woman. The patient had graduated from primary school, and she had a cheerful and diligent personality. She had performed painting work for more than five years, and her primary work involved painting swivel chairs. The primary reasons she attended the psychiatric clinic were loss of appetite, she had experienced fatigue for more than 2 months, and she had had memory loss for a month. These symptoms seriously impacted the patient's daily life and ability to work. The patient's husband expressed concern that she could not recognize acquaintances, could not find her way home, and had lost approximately 5 kg per month over two months. We analyzed changes in this chronic benzene poisoning patient's cognitive function with cognitive function assessments and magnetic resonance imaging (MRI). Measurements were taken on presentation to hospital, during the patient's hospitalization, and three months following discharge. Long-term exposure to benzene can damage the central nervous system. However, it is difficult to recognize when cognitive impairment is caused by chronic benzene poisoning, as it rarely presents with a decline in cognitive function as the primary clinical manifestation. Atypical symptoms, such as decreased immune function and gastrointestinal issues, may be the first symptoms to appear, and these atypical symptoms are difficult to detect in the early stages of disease. Regular screening of high-risk groups is required to significantly reduce the incidence of systemic damage caused by benzene poisoning.

Circulating microRNA (miRNA) has attractive interests as a non-invasive biomarker of physiological and pathological conditions. Our study aimed to investigate the potential effects of chronic benzene poisoning (CBP) and benzene exposure on miRNA expression, and identify CBP-related miRNAs.In the discovery stage, we used a microarray assay to detect the miRNA expression profiles among pooled plasma samples from ten CBP patients, ten healthy benzene-exposed individuals and ten non-benzene exposed individuals. Subsequently, we conducted an expanded validation of six candidate miRNAs in 27 CBP patients- low blood counts, 54 healthy benzene-exposed individuals and 54 non-exposed individuals. Moreover, we predicted the biological functions of putative target genes using a Gene Ontology (GO) function enrichment analysis and KEGG pathway analysis.In the discovery stage, compared with non-exposures, 36 and 12 miRNAs demonstrated at least a 1.0-fold differential expression in the CBP patients and the benzene exposures, respectively. And compared with benzene exposures, 58 miRNAs demonstrated at least a 1.0-fold differential expression in the CBP patients. In the expanded validation stage, compared with non-exposures as well as exposures, miR-24-3p and miR-221-3p were significantly up-regulated (1.99- and 2.06-fold for miR-24-3p, 2.19- and 3.93-fold for miR-221-3p, P0.01) while miR-122-5p and miR-638 were significantly down-regulated (-3.45- and -2.60-fold for miR-122-5p, -1.82- and -3.20-fold for miR-638, P0.001) in the CBP patients; compared with non-exposures, the plasma level of miR-638 was significantly up-regulated (1.38-fold, P0.01) while the plasma levels miR-122-5p and miR-221-3p were significantly down-regulated (-0.85- and -1.74-fold, P0.01) in the exposures, which were consistent with the results of microarray analysis.The four indicated plasma miRNAs may be biomarkers of indicating responses to benzene exposure. Further studies are warranted to verify our findings with a large sample and to confirm the underlying mechanisms.

The aim of our study is to seek novel specific biomarkers which could provide clues to the mechanism of chronic benzene poisoning (CBP) and might also be used as specific markers for early detection and diagnosis. In this study, a comparative serological proteome analysis between normal controls and CBP patients at three different levels of poisoning were performed via a 2D-DIGE and MALDI-TOF-MS. As the result a total of 10 proteins were found significantly altered between the normal and the mild, moderate and severe poisoning. The identified differentially expressed proteins were classified according to their molecular functions, biological processes, and protein classes, and three important serum proteins among them, apolipoproteinA-1, alpha-1-antitrypsin and complement C3, were further confirmed by immune turbidimetric analysis for their significant up-regulation in the CBP patients. Our findings suggest that these differential proteins may help elucidate the mechanism of CBP and provide potential biomarkers for diagnosis.

Supplemental Digital Content is available in the text, The study aimed to find novel effect biomarkers for occupational benzene exposure and chronic benzene poisoning (CBP), which might also provide clues to the mechanism of benzene toxicity. We performed a comparative serological proteome analysis between healthy control workers with no benzene exposure, workers with short-term benzene exposure, workers with long-term benzene exposure, and CBP patients using 2D-DIGE and MALDI-TOF-MS. Two of the differentially expressed proteins were then selected to be validated by immune turbidimetric analysis. A total of 10 proteins were found to be significantly altered between different groups. The identified deferentially expressed proteins were classified according to their molecular functions, biological processes, and protein classes. The alteration of 2 important serum proteins among them, apolipoprotein A-I and transthyretin, were further confirmed. Our findings suggest that the identified differential proteins could be used as biomarkers for occupational benzene exposure and CBP, and they may also help elucidate the mechanisms of benzene toxicity.

Workers with chronic benzene poisoning (CBP) sometimes have a white blood cell count (WBC) below 4 x 10(9)/L even after cessation of workplace exposure to benzene for years. In order to explore this phenomenon, 120 workers with CBP were divided into two groups depending on the WBC, the mean diagnostic age of CBP, benzene exposure duration, and body mass index (BMI). The proportion of genotypes of cytochrome P450 2E1 (CYP2E1), glutathione-S-transferase mu-1 (GSTM1), glutathione-S-transferase theta-1 (GSTT1), myeloperoxidase (MPO), and NAD(P)H, quinone oxidoreductase 1 (NQO1) were compared between workers with WBC4 x 10(9)/L and those with WBCor =4 x 10(9)/L. With methods of logistic regression, a risk model was set up to predict the prognosis of CBP workers. The results indicated that the BMI of workers with WBC4 x 10(9)/L was lower than that of workers with WBC ofor =4 x 10(9)/L (21.40 +/- 2.76 versus 23.09 +/- 3.36, P = 0.01), and the logistic regression model suggested there was a 4.5-fold increased risk among workers carrying GSTT1 null genotype (95% CI= 1.13- 17.54) compared with workers with GSTT1 non-null genotype. Our findings suggest that benzene exposure duration, BMI, and GSTT1 genotype may impact prognosis of the CBP workers.

Lifetime exposure to benzene is associated to a variety of blood disorders, and except for the risk of cancer, almost nothing is known concerning health impairment in individuals who are no longer exposed. In Brazil, this exposure is one of the serious problems in workplaces, and many workers have been laid off their jobs due to this intoxication, particularly in the State of Bahia, the largest producer of benzene in Latin America, which is the area of this study. From a larger study to describe health effects and genetic polymorphisms among workers with chronic benzene poisoning (CBP), this previous specific investigation analyzes the association between CBP and the pattern of sub-populations of lymphocytes. The study was performed with a CBP group (n=24) and a control group with other occupational diseases (n=24); both were selected at the Workers Health Study Center in the State of Bahia, Brazil. Clinical and epidemiologic variables were collected from medical records and from a detailed questionnaire. The average age was similar in the two groups (51.1 and 50.7, respectively). Analyzing the mean proportions of the sub-populations of lymphocytes, statistically significant differences were found for T cytotoxic cells (TCD8) (27.9; 19.4; p=0.002) and T helper memory cell (CD4CD45RO) (31.2; 37.0; p=0.015), respectively, for the CBP group and control group. These results should be viewed with caution because of the small sample size, but they strengthen a previous impression that workers exposed to benzene have their immune system impaired, even in the long term, which may contribute to some disorders and carcinogenesis process. These workers must be strictly followed up in a medical surveillance program. Although this problem has been known for a long time, this is the first attempt to study these specific effects in Brazil.

Two patients, one with myeloid metaplasia and the other one with PNH, both due to chronic exposure to benzene are presented. The patient with PNH exhibited also marked monocytosis as a rare hematologic finding of chronic benzene exposure. The etiological relationship between myeloid metaplasia, PNH and chronic benzene exposure is discussed.

Leukocyte alkaline phosphatase (LAP) activity was increased in rats and in workers exposed to benzene. A negative relationship between LAP activity and white blood cell (WBC) level was found. Alkaline phosphatase activity in the bone marrow of benzene-intoxicated rats was also increased. LAP assays are suggested as more sensitive than WBC counts in the diagnosis of chronic benzene poisoning.

In three patients with aplastic anaemia due to chronic benzene poisoning osmotic fragility before and after incubation at 37°C. for 24 hours was performed. Although the results of osmotic fragility before incubation were within normal limits, a mild or moderate increase in osmotic fragility after incubation at 37 C.° for 24 hours was observed in two of them.

Neurological, electromyographical and motor conduction velocity examinations were applied to 6 patients with aplastic anemia and two cases of preleukemia due to chronic exposure to benzene. In addition, sensory conduction velocities were measured in three patients. Neurological abnormalities were found in four out of six pancytopenic individuals. There was a certain relationship between the presence of neurological abnormalities and the period of cessation of the exposure. In the two patients with preleukemia similar neurologic abnormalities were found.

Historically, both bone marrow depression and leukemogenesis have been associated with exposure to benzene in the industrial setting. As early as 1897, Santesson (1) described chronic benzene poisoning in Sweden and, around the time of World War I, Selling (2), at Johns Hopkins, described benzene-induced aplastic anemia in both man and animals. Impaired immunological mechanisms in benzene-treated animals were first reported before World War I (3–8). Prior to the development of modern industrial hygiene, the uncontrolled use of benzene in industry expanded despite the growing appreciation of the dangers of working in an atmosphere laden with this highly volatile solvent.

A retrospective cohort study was conducted in 233 benzene factories and 83 control factories in 12 cities in China. The benzene cohort and the control cohort consisted of 28,460 benzene exposed workers (178,556 person-years in 1972-81) and 28,257 control workers (199,201 person-years). Thirty cases of leukaemia (25 dead and 5 alive) were detected in the former and four cases (all dead) in the latter. The leukaemia mortality rate was 14/100,000 person-years in the benzene cohort and 2/100,000 person-years in the control cohort; the standardized mortality ratio was 5.74 (p less than 0.01 by U test). The average latency of benzene leukaemia was 11.4 years. Most (76.6%) cases of benzene leukaemia were of the acute type. The mortality due to benzene leukaemia was high in organic synthesis plants followed by painting and rubber synthesis industries. The concentration of benzene to which patients with a leukaemia were exposed ranged from 10 to 1000 mg/m3 (mostly from 50 to 500 mg/m3). Of the 25 cases of leukaemia, seven had a history of chronic benzene poisoning before the leukaemia developed.

The distribution of various types of leukemia due to chronic exposure to benzene is described in a series comprising 34 cases. The incidence of leukemia among 31 show-workers was 13.5/100,000. Acute myeloblastic leukemia was the most frequent type, followed by preleukemia, acute erythroleukemia and acute lymphoblastic leukemia. The extreme rarity of chronic myeloid leukemia was a noteworthy finding. The differences and similarities between the distribution of various types of leukemia in different series of patients with chronic exposure to benzene and ionizing radiation are discussed.

Excerpt To the editor: A patient was recently seen in our occupational medicine clinic whose case illustrates a little-known effect of chronic benzene poisoning and emphasizes the continuing need f...

A white man, aged 22, an American, married and father of two children, appeared at the Ohio State University, State Street Dispensary, Dec. 14, 1926, complaining of weakness and shortness of breath. He was told to report to the University Hospital the next day for study and diagnosis, where he was assigned to the general medical service of Dean J. H. J. Upham and to the immediate care of Dr. George I. Nelson, internist. We are indebted to both of these physicians for permission to abstract such parts of the history of the case as are taken from the hospital records made during the patient's six months' stay in the University Hospital. When his history was taken he stated that about August 15 he first noticed a sallowness of the skin. About two months later, weakness, palpitation, dizziness and shortness of breath on exertion appeared. Headaches began about November 13

Serious or measurable damage from exposure to benzene or any gas or vapor, obviously, can be Prevented if the concentration of the contaminant and duration of exposure are so controlled that the amount absorbed is insufficient to produce damage. Unfortunatelyrocedures and information necessary for such control are frequently inadequate or completely lacking. As knowledge and understanding of the phenomena that accompany exposure to a gas or vapor increase, the possibility of more perfect control of the industrial disease hazards also increases. The commonly used procedures for the control of chronic benzene poisoning are examination of the blood, particularly for evidence of anemia and leuko-leukopenia,penia,nation of the amount of benzene in the atmosphere. The Bureau of Mines has recently developed a microco 1 1imetricas many desirable featuresustrial hygiene surveys. Owing to the fact that as little as 0.001 mg. of benzene can be detected, the method is also valuable fore determination