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

MALATHION 159
3. HEALTH EFFECTS
application of malathion in Southern California (Schanker et al. 1992). No delayed hypersensitivity was
seen among these cases. Another study of subjects in Southern California following aerial spraying of
malathion found no significant increases in the number of visits for allergic problems to hospital
emergency departments during the application period compared with the prespray period or the
corresponding period the previous year (Kahn et al. 1992). No information was located regarding
immunological effects in humans following oral exposure to malathion.
Studies in animals suggest that malathion can induce both immune enhancement and immune depression
at noncholinergic dose levels. A number of studies conducted by Rodgers and colleagues showed that
malathion stimulated immune cell function. For example, relatively low (1–2 mg/kg) single oral or
dermal doses of malathion (>99% pure) increased serum histamine levels in rats and mice (Rodgers and
Xiong 1997b). Daily oral dosing for 14 days with 1 mg/kg/day of malathion stimulated macrophage
function in mice (Rodgers and Xiong 1997d). Immunosuppressive effects were reported mostly in
repeated dosing studies. Mice administered malathion in the diet for 3–12 weeks showed alterations in
both humoral immune function and cell mediated immunity (Banerjee et al. 1998). Immune suppression
was also seen in rats and rabbits exposed to malathion for intermediate-duration periods (Banerjee et al.
1998). Cell mediated suppression was also observed in mice administered malathion for 90 days at 1 and
10 mg/kg/day, but cell mediated enhancement was seen at 0.1 mg/kg/day (Rodgers and Xiong 1997c).
Enhancement of antibody production was reported in female mice treated with 0.018 mg/kg/day in a
28-day study (Johnson et al. 2002). The available studies in animals indicate that malathion modulates
immune parameters at relatively low doses, but further research is needed to determine whether these
observed responses place the animals at increased risk when challenged with pathogens. Rodgers and
Ellefson (1992) suggested that malathion-induced mast cell degranulation may be due to inhibition of an
esterase on the cell surface; therefore, further research should explore this possibility. The immune
enhancing properties of malathion may be relevant for people with autoimmune disease as their condition
may aggravate if exposed to malathion. As suggested by Rodgers and Xiong (1997b), it is also possible
that the immune enhancement by malathion may be related to reports of possible contact hypersensitivity
(Milby and Epstein 1964) or skin rashes and irritation after malathion applications for pest control (CDHS
1991; Schanker et al. 1992).
Neurotoxicity. Information in both humans and animals indicates that the nervous system is the main
target of malathion-induced toxicity following acute exposure by any route. This is particularly evident
after exposure to high doses of malathion, as has occurred, for example, in cases of accidental or
intentional ingestion of malathion formulations (Choi et al. 1998; Dive et al. 1994; Jušić and Milić 1978,