Empirical approaches for the investigation of toxicant-induced loss of tolerance.

It has been hypothesized that sensitivity to low-level chemical exposures develops in two steps: initiation by an acute or chronic chemical exposure, followed by triggering of symptoms by low levels of previously tolerated chemical inhalants, foods, or drugs. The Working Group on Toxicant-induced Loss of Tolerance has formulated a series of research questions to test this hypothesis: Do some individuals experience sensitivity to chemicals at levels of exposure unexplained by classical toxicological thresholds and dose-response relationships, and outside normally expected variation in the population? Do chemically sensitive subjects exhibit masking that may interfere with the reproducibility of their responses to chemical challenges? Does chemical sensitivity develop because of acute, intermittent, or continuous exposure to certain substances? If so, what substances are most likely to initiate this process? An experimental approach for testing directly the relationship between patients' reported symptoms and specific exposures was outlined in response to the first question, which was felt to be a key question. Double-blind, placebo-controlled challenges performed in an environmentally controlled hospital facility (environmental medical unit) coupled with rigorous documentation of both objective and subjective responses are necessary to answer this question and to help elucidate the nature and origins of chemical sensitivity

The factors associated with food fussiness in Irish school-aged children

Objective: To establish the factors that determine food fussiness, to explore if child age determines the extent to which these factors influence food fussiness and to identify whether parental neophobia is an independent determinant of food fussiness. Design: Cross-sectional data from the National Children’s Food Survey (2003–2004). The Children’s Eating Behaviour Questionnaire (CEBQ) assessed eating behaviours in children. The Food Neophobia Scale (FNS) assessed parental food neophobia. Young children were classified as 5–8 years old with older children classified as 9–12 years old. Setting: Republic of Ireland. Participants: Nationally representative sample of Irish children aged 5–12 years (n 594). Results: Parents identifying child’s food preferences as a barrier to providing their child with a healthy diet was significantly associated with increased food fussiness in younger (P<0·001) and older children (P<0·001). Higher levels of parental neophobia were significantly associated with an increase in food fussiness in younger (P<0·05) and older (P<0·001) children. Food advertising as a barrier to providing a healthy diet was inversely associated with food fussiness in younger children (P<0·05). In older children, there was a significant inverse association between child’s BMI and food fussiness (P<0·05), but not to the extent that a difference in weight status was noted. Family mealtimes in older children were associated with significantly lower levels of food fussiness (P<0·05). Conclusions: Findings from the present study identify that a child’s age does determine the extent to which certain factors influence food fussiness and that parental neophobia is an independent determinant of food fussiness