Biological and chemical monitoring of occupational exposure to ethylene oxide

Tates, A.D.; Grummt, Tamara; Törnqvist, Margareta; Farmer, Peter B.; Dam, F.J. van; Mossel, H. van; Schoemaker, H.M.; Osterman-Golkar, Siv; Uebel, Carlos Oscar; Tang, Yuk-Sim; Zwinderman, A. H.; Natarajan, A.T.; Ehrenberg, L.

doi:10.1016/0027-5107(91)90205-3

Cited by 135 publications

(41 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In a recent biomonitoring study of workers exposed to ethylene oxide, a significant increase in the frequencies of HPRT mutants was found (21). Though there was no difference in the frequencies of different classes of mutants induced, a hot spot for mutation at position 617 of the HPRT coding region (amino acid residue 206), which was not present in the control spectrum, was found.…”

Section: Gene Mutationsmentioning

confidence: 93%

“…These cells may represent persistent DNA lesions in long-lived lymphocytes or a sensitive subpopulation. In biomonitoring human populations, consideration of only high-frequency cells appears to be a more sensitive index than consideration of overall SCE values, as demonstrated in a recent study on ethylene oxide-exposed workers (21).…”

Section: Chemically Induced Chromosomal Alterationsmentioning

confidence: 99%

“…Elevated frequencies of SCEs have been found in humans exposed to known genotoxins. A subpopulation of lymphocytes with high frequencies of SCEs (high-frequency cells) has been found in many human population studies (20,21). These cells may represent persistent DNA lesions in long-lived lymphocytes or a sensitive subpopulation.…”

Section: Chemically Induced Chromosomal Alterationsmentioning

confidence: 99%

See 2 more Smart Citations

Mechanisms for induction of mutations and chromosome alterations.

Natarajan

1993

Environ Health Perspect

View full text Add to dashboard Cite

Genotoxic agents induce chromosomal alterations, such as aberrations, micronuclei, and sister chromatid exchanges as well as mutations both in vivo and in vitro. Ionizing radiation and typical radiomimmetic agents such as bleomycin are very efficient inducers of chromosomal aberrations. The type of aberrations induced by these agents are cell-cycle dependent, i.e., chromosome type in pre-replication stages and chromatid type in post-replication stages of the cell cycle. Under optimal DNA repair conditions, DNA double-strand breaks (DSBs) appear to be the most important lesion responsible for the production of aberrations. In human lymphocytes, fast-repairing DSBs lead to exchange-type aberrations. The fact that the dose-response curves for induction of exchange aberrations induced by ionizing radiation are similar in vitro and in vivo allows one to use the yield of induced aberrations to estimate absorbed radiation dose in the case of accidents. In this respect, frequencies of translocations detected by the chromosome painting technique appear to be more sensitive. Mutations do not express immediately after exposure and require an expression time before they can be detected. In humans, it is estimated that for the mutations induced in bone marrow, it takes about 2 months for them to express and to be detected in peripheral blood lymphocytes. Hence, frequency of mutations is of limited value for estimating radiation doses immediately after an accident. This holds true for chemical exposure as well. Most of the lesions induced by chemical mutagens (such as alkylating agents) are converted into aberrations only during the S phase of the cell cycle, and therefore an intervening DNA synthesis following exposure is necessary for the visualization of aberrations. These agents induce mainly the chromatid-type aberrations and are also very efficient in inducing sister chromatid exchanges. Chemical mutagens are more efficient in inducing gene mutations than ionizing radiations. In monitoring human populations, mutations in the hprt locus in peripheral lymphocytes and hemoglobin mutations as well as glycophorin mutations in erythrocytes can be studied. The hprt mutations and glycophorin mutations can arise from single base-pair changes to large deletions, whereas hemoglobin mutations arise from changes in a single codon.

show abstract

Section: Gene Mutationsmentioning

confidence: 93%

Section: Chemically Induced Chromosomal Alterationsmentioning

confidence: 99%

Section: Chemically Induced Chromosomal Alterationsmentioning

confidence: 99%

See 1 more Smart Citation

Mechanisms for induction of mutations and chromosome alterations.

Natarajan

1993

Environ Health Perspect

View full text Add to dashboard Cite

show abstract

“…Although it is not as specific as molecular studies of effects on single genes, the assay monitors the entire genome and proved to be a useful population-monitoring procedure. Exposure to hazardous agents can cause both chromosome breakage and rearrangement (28 (29,30).…”

Section: Methodsmentioning

confidence: 99%

Monitoring of human populations at risk by different cytogenetic end points.

Anwar

1994

Environ Health Perspect

View full text Add to dashboard Cite

Humans are exposed to a large number of environmental genotoxic agents. These can increase the probability that somatic mutation will occur. The use of genotoxicity testing is essential for assessment of potential human toxicity so that hazards can be prevented. Cytogenetic monitoring of human populations exposed to chemicals has proved to be a useful tool for detecting the chemical mutagenic effects. Cytogenetic analysis of human chromosomes in peripheral lymphocytes allows direct detection of mutation in somatic cells. Cytogenetic monitoring of a group of traffic policemen from Cairo, Egypt, was an example of a human population study. The induction of chromosomal damage was studied in a group of 28 traffic policemen with exposure of over 10 years and a control group of 15 policemen trainers. Blood lead level was significantly higher in the traffic policemen (30 ± 8.7) unit compared to the control group (18.2 ± 1.2) unit. The percentage of chromosomal aberrations (7.7 ± 3.1), as well as the mean sister chromatid exchanges (7.5 ± 3.4), were significantly higher among the traffic policemen than in the control group. The percentage of chromosomal aberrations was 2.8 ± 2.1 and the mean sister chromatid exchanges was 4.8 ± 2.9 in the control group. On the other hand, the increase in chromosome damage among the traffic policemen was enhanced further by smoking. studies are discussed. -Environ Health Perspect 102(Suppl 4): 131-134 (1994).

show abstract

“…Furthermore, and P0can in Figure 1D refer not only to tumor localization but also to the influence of age, some two-thirds of the total cancer incidence increment in western populations is expected to occur above age 65, according to Swedish cancer statistics (35). In Figure 4 the resolving power of the most sensitive cytogenetic end point, SCE high-frequency cells (36), is also indicated. This and other genetic biomarkers are generally too insensitive, but they play important roles as early hazard indicators and in the clarification of action mechanisms.…”

Section: Epidemiological Aspectsmentioning

confidence: 99%