Peanut allergy in children

Information Section--FdChem. Toxic. Vol. 34, No. 9 Peanut allergy in children A doctor reporting on her experiencesof a single year at a Cambridge allergy clinic has suggested that “the increased incidence of peanut or nut allergy is real and not attributable only to increased awareness and referral”. Between October 1993 and September 1994 62 patients with this type of allergy were seen, including four with life-threatening reactions. Peanuts were the commonest cause of allergy, being reported in 47 patients. At least 16 of those reacting to peanuts were also allergic to other nuts. Although peanut is a pulse, only four of those responding to peanuts also reacted to other pulses. Most of the patients had been sensitizedto peanuts or nuts by the age of 5 yr. Peanuts were responsible for all allergies in children below 1 yr old, but multiple allergies to other nuts increased with age (Ewan, British Medical Journal 1996, 312, 1074). [A commentary on this paper by Hugh Sampson, the Director of the Paediatric Clinical Research Centre, Johns Hopkins University School of Medicine, reports that the conclusions of the UK study are in agreement with data generated within the USA. For infants at increased risk of developing peanut or nut allergy-those from atopic families or from families with other food allergies-he suggests the elimination of all peanut products from the child’s diet for at least the first 3 yr (including from the diet of breast-feeding mothers) (Sampson, ibid. 1996,312, 1050). Chlorpyrifos and birth defects

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body weight/day produced effects on the ovary (Gojmerac et al., Toxicology Letters 1996, 85, 9). Dicofol-reproductive toxicity in kestrels Effects on reproduction (including decreased shell thickness, and both a reduced number of offspring and an increase in their level of testes and ovary abnormality) were seen when kestrels received 5 mg/kg body weight/day by stomach tube of a high-purity sample of dicofol, the active ingredient of Kelthane. Lower doses were not tested. When the second generation was mated with untreated birds, reproductive toxicity was again reported, although there was no effect on shell thickness. The investigators concluded that “the widespread use of pesticidessuch as . . . dicofol may suggesta repetition of DDT-related effects on the environment” (MacLellan et al., Archives of Environmental Contamination and Toxicology 1996, 30, 364). Pesticide mixtures-synergistic, additive?

antagonistic or

An in vitro study using human nerve cells concluded that it was not possible to predict the toxicity of mixed pesticides from their individual toxicities. Evaluation of specific (acetylcholine esteraseactivity) and unspecific (protein synthesis) endpoints demonstrated additivity, synergism, antagonism and a threshold effect, from various combinations of the pesticides azinphos-methyl, benomyl, diazinon, dimethoate and pirimiphos-methyl (Marinovich et al., Toxicology 1996, 108, 201).

Multiple birth defects have been reported in two boys Ethylene glycol ethers-reprotoxicity in workers and two girls born to three US mothers who were exposed during early pregnancy to a pesticide Evidence of adverse effects on reproduction was seen in a study of two US semiconductor manufacturing formulation containing clorpyrifos as its active plants. Potential dermal exposure to ‘ethylene glycol component. Growth was impaired in all four children ethers’ during critical periods was classified as high, and three also had severelearning difficulties. In three of the casesthe mothers’ exposure resulted from use medium, low or none. For the 561 pregnancies in the female employees, the high-exposure group had an of the product in their homes, while the mother of the increased risk of spontaneous abortion (RR 2.8,95% fourth child had been exposed at her workplace for CI 1.4-5.6). An increased risk of subfertility (defined around 3 days during the first 2 wk of pregnancy as taking more than 1 yr of unprotected intercourse (Sherman, Archives of Environmental Health 1996, to conceive) was also seen in this group (odds ratio 51, 5). 4.6, 95% CI 1.613.3). There was a significant dose response for both effects (P for trend = 0.02). Among Flumethrine toxicity in a farmer the 589 pregnancies of wives of male employees, there A 47-yr-old Scottish farmer developed a rash, was some indication of a reduced fertility in the followed by abdominal pain, vomiting, muscle aches high-exposure group (RR 1.7, 95% CI 0.7-4.3) and pain in the joints, requiring hospitalization 1 day (Correa et al., American Journal of Epidemiology after using a sheep dip containing this synthetic 1996, 143, 707). pyrethroid. He failed to wear protective clothing during the dipping process and was exposed for Epichlorohydrin and heart disease around 16 hr over 2 days. No information was A study published in 1990 reported an association available on systemic dose (Box and Lee, Human and between epichlorohydrin exposure at two Shell Experimental Toxicology 1996, 15, 389). chemical plants in the US and an increased risk of death from heart disease. This initial report had Atrazine and ovarian disorders followed the cohort of 863 workers up until 1983. The herbicide atrazine when given in the diet of pigs Data from a further 10 yr of observation (up to 1993 for 19 days of their oestrus cycle at a dose of 2 mg/kg -20% of the men have now died) has failed to find