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

MALATHION 135
3. HEALTH EFFECTS
Kearns 1997; NRC 1993; Vieira et al. 1996). Whether differences in xenobiotic metabolism make the
child more or less susceptible also depends on whether the relevant enzymes are involved in activation of
the parent compound to its toxic form or in detoxification. There may also be differences in excretion,
particularly in newborns who all have a low glomerular filtration rate and have not developed efficient
tubular secretion and resorption capacities (Altman and Dittmer 1974; NRC 1993; West et al. 1948).
Children and adults may differ in their capacity to repair damage from chemical insults. Children also
have a longer remaining lifetime in which to express damage from chemicals; this potential is particularly
relevant to cancer.
Certain characteristics of the developing human may increase exposure or susceptibility, whereas others
may decrease susceptibility to the same chemical. For example, although infants breathe more air per
kilogram of body weight than adults breathe, this difference might be somewhat counterbalanced by their
alveoli being less developed, which results in a disproportionately smaller surface area for alveolar
absorption (NRC 1993).
No studies were located that specifically addressed effects of exposure to malathion in children. Children
could be exposed to malathion from food and drinking water, but these risks are low and not of concern.
Greater concern exists from postapplication residential exposure to turf treatments, from other home and
garden uses of malathion, and as bystanders from special uses of malathion in public health mosquito
abatement control and the USDA’s (U.S. Department of Agriculture) Boll Weevil Eradication Program.
Because children spend more time outdoors than adults, they may be at a greater risk of exposure to
malathion than nonoccupationally exposed adults by dermal contact with contaminated surfaces or by
hand-mouth activity. Malathion is an organophosphate pesticide, and acute exposure to high amounts
results in typical and easily recognizable signs of poisoning (Aaron and Howland 1998; Abou-Donia
1995; Ecobichon 1994; Taylor 1996). As detailed in Section 3.5.2, Mechanisms of Toxicity, the primary
target of malathion toxicity is the nervous system and secondary ocular, exocrine glands, gastrointestinal,
cardiovascular, and respiratory effects can be observed as a result of the excess acetylcholine at nerve
terminals innervating tissues and organs from these systems. The most common manifestations of
poisoning with organophosphates in general are increased salivation and lacrimation, miosis and blurred
vision, nausea, vomiting, abdominal cramps and diarrhea, excessive bronchial secretions and dyspnea,
bradycardia and low blood pressure, muscle fasciculations, muscle weakness in peripheral and respiratory
muscles, and fatigue and mental confusion. Several reports have described these manifestations in
children following oral poisoning with malathion (Ekin 1971; Healy 1959; Jušić and Milić 1978; Tuthill
1958) and dermal exposure (Parker and Chattin 1955; Ramu et al. 1973), and it does not appear that there