Clastogenic activity in urine of workers occupationally exposed to pesticides

doi:10.1016/0165-1218(90)90022-T

Mutation Research/Genetic Toxicology

Volume 241, Issue 3, July 1990, Pages 251-259

https://doi.org/10.1016/0165-1218(90)90022-T Get rights and content

Abstract

Genotoxicity in the urine of orchardists occupationally exposed to pesticides was investigated. Urine samples were obtained during pre-spraying and spraying periods from 22 non-smoking orchardists who spray large amounts of pesticides during the fruit growing season. For comparison purposes, urine was collected from 11 non-smoking personnel at an agricultural research station located near the application site and from 21 non-smoking individuals (reference controls) in a non-agricultural area. Organic material was isolated from urine by preparative reversed-phase high-pressure liquid chromatography, and assayed for clastogenic activity using Chinese hamster ovary cells. Urine samples collected during the pre-spraying period showed no significant differences in clastogenic activity compared to that found for the reference control group. However, clastogenic activity of urine specimens collected during the spraying period was significantly elevated (p < 0.001) for the highly-exposed orchardists, but not for the research station personnel. Clastogenicity of orchardists' urine was observed within 8 h of pesticide application.

References (55)

H.U. Aeschbacher et al.
Non-mutagenicity of urine from coffee drinkers compared with that from cigarette smokers
Mutation Res.
(1981)
R. Baker et al.
Detection of mutagenic activity in human urine following fried pork or bacon meals
Cancer Lett.
(1982)
B. Beek et al.
Induction of sister-chromatid exchanges, cell-cycle delay and chromosomal aberrations by human urine concentrates
Mutation Res.
(1982)
R.P. Bos et al.
Excretion of mutagens in human urine after passive smoking
Cancer Lett.
(1983)
B.A. Bridges
The mutagenicity of captan and related fungicides
Mutation Res.
(1975)
A. Carere et al.
Microbiological mutagenicity studies of pesticides in vitro
Mutation Res.
(1978)
R. de Cassia Stocco et al.
Cytogenetic study of workers exposed to methyl-parathion
Mutation Res.
(1982)
V. Drevenkar et al.
The rate of urinary excretion of phosalone residues in occupationally exposed persons
Sci. Total Environ.
(1979)
F.N. Dulout et al.
Sister-chromatid exchanges and chromosomal aberrations in a population exposed to pesticides
Mutation Res.
(1985)
B.P. Dunn et al.
Clastogenic agents in the urine of coffee drinkers and cigarette smokers
Mutation Res.
(1985)

K. Falck et al.

Mutagenicity in urine of workers in the rubber industry

Mutation Res.

(1980)

A. Kappas et al.

Benomyl — a novel type of base analogue mutagen?

Mutation Res.

(1976)

D. Kriebel et al.

Detection of occupational exposure to genotoxic agents with a urinary mutagen assay

Mutation Res.

(1983)

A. Matsuoka et al.

Chromosomal aberration tests on 29 chemicals combined with S9 mix in vitro

Mutation Res.

(1979)

M. Moriya et al.

Further mutagenicity on pesticides in bacterial reversion assay systems

Mutation Res.

(1983)

J.M. Parry

Induction of gene conversion in yeast by herbicide preparation

Mutation Res.

(1973)

R.M. Putzrath et al.

Analysis of mutagenic activity in cigarette smoker's urine by high performance liquid chromatography

Mutation Res.

(1981)

M.N. Rabello et al.

Cytogenetic study on individuals occupationally exposed to DDT

Mutation Res.

(1975)

M.D. Reuber

Carcinogenicity of dimethoate

Environ. Res.

(1984)

J. Sousa et al.

Detection of mutagenic activity in human urine following a fried beef meal

Mutation Res.

(1985)

H.F. Stich et al.

Mutagenicity of fecal extracts from carnivorous and herbivorous animals

Mutation Res.

(1980)

H.F. Stich et al.

The action of transition metals on the genotoxicity of simple phenols, phenolic acids and cinnamic acids

Cancer Lett.

(1981)

L.A. Wheeler et al.

Mutagenicity of urine from psoriatic patients undergoing treatment with coal tar and ultraviolet light

J. Invest. Dermatol.

(1981)

J. Yoder et al.

Lymphocyte chromosome analysis of agricultural workers during extensive occupational exposure to pesticides

Mutation Res.

(1973)

M.T. Alam et al.

Chromosomal anomalies induced by the organic phosphate pesticide guthion in Chinese hamster cells

Chromosoma

(1974)

O. Axelson et al.

Herbicide exposure, mortality and tumor incidence

E. Barthel

Increased risk of lung cancer in pesticide-exposed male agricultural workers

J. Toxicol. Environ. Health

(1981)

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^∗: Present address: Division of Infectious Diseases, Department of Medicine, The University of British Columbia, 2733 Heather Street, Vancouver, B.C. V6Z 1M9 (Canada).

^∗∗: Present address: Microbiological Associates Inc., 9900 Blackwell Road, Rockville, MD 20850 (U.S.A.).

View full text

Clastogenic activity in urine of workers occupationally exposed to pesticides

Abstract

Mutation Res.

Cancer Lett.

Mutation Res.

Cancer Lett.

Mutation Res.

Mutation Res.

Mutation Res.

Sci. Total Environ.

Mutation Res.

Mutation Res.

Mutation Res.

Mutation Res.

Mutation Res.

Mutation Res.

Mutation Res.

Mutation Res.

Mutation Res.

Mutation Res.

Environ. Res.

Mutation Res.

Mutation Res.

Cancer Lett.

J. Invest. Dermatol.

Mutation Res.

Chromosomal anomalies induced by the organic phosphate pesticide guthion in Chinese hamster cells

Chromosoma

Herbicide exposure, mortality and tumor incidence

Increased risk of lung cancer in pesticide-exposed male agricultural workers

J. Toxicol. Environ. Health