toxicological profile for malathion - Agency for Toxic Substances and ...

MALATHION 140
3. HEALTH EFFECTS
the maximum concentration reported by Kutz et al. (1992), 250 µg/L, was 5 times higher than that found
in the Maryland study, 51 µg/L.
A study of 5 workers and 16 residents exposed to malathion during a spraying operation in Haiti
measured urinary MCA at various times after the operation (Warren et al. 1985). All of the subjects were
tested on Friday after daily spraying during the week and again on Monday after the weekend; eight
residents were tested 1 week later. The residents were not at home during the spraying, but returned
home the Friday after the operation was completed. Urinary MCA levels ranged from 0.9 to 6.8 mg/L
after the spraying week and from 0.047 to 0.13 mg/L after the weekend. Residents showed negligible
levels of MCA when they returned home, but levels increased to 0.084–1.4 mg/L over the weekend. In
eight residents who were tested 1 week after the operation, MCA ranged from negligible to 0.31 mg/L,
suggesting that malathion and/or metabolites may be more persistent in the environment than it had been
previously thought. A study of 19 agricultural workers (mixers and applicators) evaluated dermal
exposure to malathion by monitoring urinary DMTP and DMDTP and also used a fluorescent tracer
technique to monitor exposure (Fenske 1988). Urinary metabolites were monitored for 3 days following
exposure. The results showed that applicators excreted 17% of the applied dose and mixers excreted
23%. Exposure was better correlated with excretion of metabolites for applicators (r=0.91) than for
mixers (r=0.73). A more recent study of date dusters and harvesters in California showed that malathion
metabolites could be detected in the urine as soon as 2–3 hours of work (Krieger and Dinoff 2000). On a
molar basis, DMTP > MCA > DMP > DCA were the most prominent urinary metabolites. Samples of
urine collected on Monday morning during mid-season had low or undetectable levels of MCA and DCA
suggesting that malathion is quickly metabolized and eliminated in the urine.
3.8.2 Biomarkers Used to Characterize Effects Caused by Malathion
Diagnosis of organophosphate poisoning, including malathion, can be made by the presence of
characteristic clinical signs and measurements of serum (plasma) cholinesterase and RBC
acetylcholinesterase activities. Enzyme inhibition, however, is not specific for organophosphates since
exposure to carbamate insecticides also results in cholinesterase inhibition. Nonspecific cholinesterase
(pseudocholinesterase, butyrylcholinesterase) is present in myelin, liver, and plasma, whereas
acetylcholinesterase is present in the central and peripheral nervous systems and in RBC. Plasma
cholinesterase activity can be inhibited by 20–25% without significant physiological consequences
(Abou-Donia 1995). Malathion is a stronger inhibitor of plasma cholinesterase than of RBC acetylcholinesterase
(Maroni et al. 2000). Plasma cholinesterase regenerates at a more rapid rate than RBC