Asthma is common in childhood and, while many causes for its occurrence and increasing prevalence are known, much remains unanswered in terms of causes. In adults, 10-15% of newly diagnosed asthma is due to an occupational exposure to either low (e.g. isocyanates) or high (e.g. proteins in animal urine) molecular weight asthmagens. Lung disease in the spouses and children of workers exposed to asbestos at work is accepted and recognized. There is a report of children being sensitized to occupational sensitizers, to which their parents have been exposed at work, there is also a report of a child exposed to occupational sensitizers in the workplace developing 'occupational' asthma. In addition there are reports of asthma related to spousal occupation. The magnitude of this potential problem has not been investigated.

We wish to test the hypothesis that children are more likely to develop asthma if their parents work in occupations known to be associated with a risk of occupational asthma because parents may bring asthmagens home on their clothing, resulting in their children being exposed. In addition, we will take the opportunity to determine whether the partner of a worker exposed to occupational sensitizers is more likely to develop asthma. The hypothesis will concentrate on high molecular weight causes although potential exposure to low molecular weight agents will be analysed.

We will use existing data from the ALSPAC cohort of children to relate childhood wheezing, diagnosed asthma, and rhinitis, to parental occupation. In addition, parental occupation will also be related to objective parameters such as ventilatory function and bronchial responsiveness in later childhood (8 1/2 years) to determine if early life and/or cumulative exposure to parents in high-risk occupations are associated with physiological changes. Maternal wheeze, diagnosed asthma, and rhinitis will also be related to her partner's occupation.

Data on occupation have been obtained for both mother and father prospectively and will be coded using the CASCOT system developed by the University of Warwick. Parental occupations will be classified according to recognized associations with occupational asthma. We will also explore whether there is any relationship between the timing of childhood exposure to potential parental occupational asthmagens at 21 months of age and the likelihood of developing asthma. Risk modification by atopy and environmental tobacco smoke exposure will be investigated. The dataset will also provide the opportunity to consider parental self reported asthma or rhinitis in relation to occupation, adding to the limited population data in this area. Finally we will be able to assess the level of agreement between maternal and direct report of spouse's occupation and compare these with the codes generated by automatic and semi-automatic coding software (i.e. SOC 1990 and SOC 2000 codes from CASCOT).

If occupation is shown to increase the risk of asthma in children and partners, help and advice will need to be given to workers in at risk occupations to reduce carriage of asthmagens home on their clothes, in order to reduce the risk of their children and partner developing 'bystander occupational' asthma.