This study indicates that airway responsiveness can be present early in life and suggests that a family history of asthma or parental smoking contributes to elevated levels of airway responsiveness at an early age.

The association of environmental factors with atopic disease in children remains poorly understood. The aim of this study was to investigate the relationship between socio-environmental factors and symptoms of asthma and atopy in 6-7-yr-old children assessed as an adjunct to Phase I of the International Study of Asthma and Allergy in Childhood in Perth, Western Australia. Parental questionnaire responses were obtained for 2,193 children (73.6%) in 34 randomly selected primary schools in the Perth metropolitan area. Children born in Australia had a significantly increased risk of current asthma (odds ratio (OR) 237, p = 0.001). Having a mother born in Australia was the only factor independently associated with an increased risk of current hay fever (OR 1.56, p = 0.005). Increasing numbers of people living in the home were significantly associated with a multiplicative decrease in risk of current asthma (OR 0.88, p = 0.03) and eczema (OR 0.82, p = 0.01). Houses made of fibrocement (OR 2.40, p = 0.02) and the presence of mats on less than half of the floor area in the "main bedroom" (relative to wall-to-wall carpet) (OR 3.50, p = 0.003) were associated with an increased risk of current eczema. All reported associations were independent of socioeconomic status (categorized by school), age and sex. This study suggests that household and country-specific environmental factors are associated with asthma, hay fever and eczema risk in 6-7-yr-old schoolchildren, and may have substantially contributed to the increased prevalence of these diseases in Australia.

ObjectiveTo document the results of mutation analysis on 160 individuals with cystic fibrosis and 31 obligate carriers of the cystic fibrosis gene in 191 Western Australian families to facilitate accurate genetic counselling. MethodsWe tested for 17 mutations of the cystic fibrosis gene by either a variation of the polymerase chain reaction amplification refractory mutation system (PCR‐ARMS) or with a series of restriction enzyme cuts and dot blots using chemiluminescent probes. ResultsAt least one of the two intragenic mutations causing cystic fibrosis was identified in 98% of affected individuals and both were detected in 68%. The AF508 deletion occurred in 89.8% of patients: 51% were homozygous for this defect. In carriers, 85% of the mutations were detected with a panel of 16 probes, identifying 17 intragenic defects: the AF508 deletion occurred in 72.4%. Both cystic fibrosis mutations were detected in 68% of cystic fibrosis families. ConclusionsBy analysis with 16 intragenic cystic fibrosis genomic probes, we have documented the frequencies of various mutations in the Western Australian population. These data will be useful in accurate genetic counselling for affected families and carrier screening for the general population.

Haemoptysis in otherwise healthy children is an uncommon event. Two cases of massive haemoptysis, subsequently requiring lobectomy, are discussed. In each case, foreign vegetable matter was identified despite previously normal bronchoscopy and minimal changes on chest radiograph.Haemoptysis in children is usually seen in those with bronchiectasis associated with suppurative lung disease and chronic sputum production, and massive haemoptysis in otherwise healthy children is uncommon. There are few reports of massive haemoptysis in recent paediatric literature and we report two cases in otherwise healthy children, both of whom subsequently required lobectomy. In each case, foreign vegetable matter was identified in the excised lobe. CASE ONEA five-year-old boy presented to the emergency department with mild haemoptysis and cough that had been present for 2 days. Physical examination was normal. A chest radiograph showed minimal change with patchy consolidation in both lower lobes. A provisional diagnosis of bronchitis was made and oral augmentin was administrated as an outpatient.Three days later he represented after coughing approximately 50 mL of fresh blood. On initial examination, the patient was pale, and had respiratory distress, as evidenced by tachypnoea with a rate of 36/minute and mild intercostal recession. Coarse inspiratory crackles were present bilaterally. Oxygen saturation (SaOJ was 89% in room air. A full blood count revealed a haemoglobin of 98 g/L and a platelet count of 268 x 109/L. A coagulation profile was normal. A rigid bronchoscopy was performed within 24 h with no abnormality observed and no blood visible.Three weeks later, he represented with two episodes of haemoptysis of approximate 10 mL, associated with coughing. Bi-basal crackles were noted on physical examination. A repeat chest radiograph showed right lower lobe (RLL) infiltrate consistent with pulmonary haemorrhage or atypical infection. No infective cause was found. A sweat test was normal. A computerised tomography (CT) of the thorax showed a