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BACKGROUND: Cigarette smoking causes accelerated facial wrinkling and predisposes to chronic obstructive pulmonary disease (COPD). However, it has long been recognised that there is a subgroup of susceptible smokers who are at increased risk of developing airflow obstruction. We have tested the hypothesis that there is a common susceptibility for the development of COPD and facial wrinkling in cigarette smokers. METHODS: One hundred and forty nine current and ex-smokers were recruited from a family based study of COPD genetics, 68 (45.6%) of whom fulfilled the definition of COPD. 124 (83.2%) had no or minor facial wrinkling (Daniell /=IV). Generalised estimating equations were used to adjust for familial correlations between related individuals and the potential confounding effects of age and pack years smoked. RESULTS: Forced expiratory volume in 1 second (FEV(1)) was significantly lower in those with wrinkles than in those without (mean difference in FEV(1) % predicted -13.7%, 95% CI -27.5 to 0.0, p = 0.05) and facial wrinkling was associated with a substantially increased risk of COPD (adjusted OR 5.0, 95% CI 1.3 to 18.5, p<0.02). The Daniell score correlated with the extent of emphysema on the CT scan (p<0.05) and facial wrinkling was also associated with a greater risk of more extensive emphysema (adjusted OR 3.0, 95% CI 1.0 to 9.3, p = 0.05). CONCLUSION: Facial wrinkling is associated with COPD in smokers, and both disease processes may share a common susceptibility. Facial wrinkling in smokers may therefore be a biomarker of susceptibility to COPD.

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BACKGROUND: Several antioxidant nutrients have been reported to be inversely associated with asthma. A study was undertaken to assess the independent associations of these nutrients with asthma in adults. METHODS: A nested case-control study was performed in 515 adults with physician diagnosed asthma and 515 matched controls using dietary data obtained from 7 day food diaries. The main outcome measures were physician diagnosed asthma and current symptomatic asthma (diagnosed asthma and self-reported wheeze within the previous 12 months). RESULTS: Cases were similar to controls in age, sex, social class, and daily energy intake but had a lower median intake of fruit (132.1 v 149.1 g/day, p< or =0.05). 51.5% of the population reported zero consumption of citrus fruit; relative to these individuals, people who consumed >46.3 g/day had a reduced risk of diagnosed and symptomatic asthma (OR adjusted for potential confounders 0.59 (95% CI 0.43 to 0.82) and 0.51 (95% CI 0.33 to 0.79), respectively). In nutrient analysis, dietary vitamin C and manganese were inversely and independently associated with symptomatic asthma (adjusted OR per quintile increase 0.88 (95% CI 0.77 to 1.00) for vitamin C and 0.85 (95% CI 0.74 to 0.98) for manganese), but only manganese was independently associated with diagnosed asthma (OR 0.86 (95% CI 0.77 to 0.95)). Adjusted plasma levels of vitamin C were significantly lower in symptomatic cases than in controls (54.3 v 58.2 micromol/l, p = 0.003). CONCLUSIONS: Symptomatic asthma in adults is associated with a low dietary intake of fruit, the antioxidant nutrients vitamin C and manganese, and low plasma vitamin C levels. These findings suggest that diet may be a potentially modifiable risk factor for the development of asthma.

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OBJECTIVE: To assess whether starting to smoke in childhood increases the risk of obstructive airways disease (OAD) in adult life. METHODS: A retrospective cohort analysis was undertaken of 12 504 current and ex-smokers in the EPIC-Norfolk cohort. The main exposure was starting to smoke during childhood (age <16 years). Three definitions of OAD were used: doctor diagnosed asthma, doctor diagnosed bronchitis/emphysema, and "any OAD" (doctor diagnosed asthma or bronchitis/emphysema, or taking medication used in the treatment of OAD). RESULTS: Childhood smokers had significantly more pack years of exposure and poorer lung function than subjects who started to smoke in adulthood (>/=16 years). Compared with starting in adulthood, starting to smoke in childhood was associated with a greater risk of bronchitis/emphysema in female smokers (OR 1.79, 95% CI 1.25 to 2.56) and ex-smokers of both sexes (OR 1.29, 95% CI 1.07 to 1.55 in men and OR 1.40, 95% CI 1.05 to 1.85 in women), and of "any OAD" in female smokers (OR 1.72, 95% CI 1.24 to 2.38) and male and female ex-smokers (OR 1.20, 95% CI 1.03 to 1.40 in men and 1.34, 95% CI 1.07 to 1.57 in women). After adjustment for pack years, childhood smoking was associated with poorer lung function (FEV(1) 92.3% predicted in adult smokers and 89.5% in childhood smokers, p = 0.03) and a greater risk of bronchitis/emphysema (adjusted OR 1.55, 95% CI 1.08 to 2.24) and for "any OAD" (OR 1.54, 95% CI 1.10 to 2.13) in female smokers but not in male and female ex-smokers. CONCLUSION: Starting to smoke in childhood is associated with an increased risk of airways disease because of the extra pack years smoked. In women, childhood smoking is itself an independent risk factor for the development of airways disease.

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Although familial clustering has been described, few studies have quantified the risk of airflow obstruction in siblings of patients with chronic obstructive pulmonary disease (COPD). One hundred fifty-two subjects with airflow obstruction and a low gas transfer factor (but without PiZ alpha(1)-antitrypsin deficiency) were identified and 150 were enrolled in the study. Complete data were obtained from 173 of 221 siblings of these subjects. Forty-four of 126 current or ex-smoking siblings had airflow obstruction (FEV(1)/FVC < 0.7) and 36 also had a FEV(1) < 80% predicted, in keeping with COPD. One hundred eleven current or ex-smoking siblings were matched for age, sex, and smoking history with 419 subjects, without a known family history of COPD, from the European Prospective Investigation of Cancer (EPIC)-Norfolk cohort. The prevalence of COPD was much lower in the EPIC group (9.3%) when compared with the siblings (31.5%; odds ratio, 4.70; 95% confidence interval, 2.63 to 8.41). The odds ratio for COPD in siblings with less than a 30 pack-year smoking history was 5.39 (95% confidence interval, 2.49 to 11.67) when compared with matched control subjects. Taken together these results demonstrate a significant familial risk of airflow obstruction in smoking siblings of patients with severe COPD.

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Environmental cum medical study was conducted in asbestos cement factory. The environment was evaluated for asbestos fiber by the methods recommended by BIS. Total 355 exposed and 312 suitably matched control workers were investigated by spirometer, Wright's peak flow meter and full sized postero-anterior chest radiograph. The levels of asbestos fiber were 2 to 3 times higher than TLV i.e. 2 f/ml in pipe cutting dept., crude fiber grinding inlet count was more than the ACGIH recommended limit i.e. 5 mpccf of air in pipe cutting dept. and silica mill. In the rest of the department, fiber level as well as dust particle count were below prescribed limit. The comparison of mean values of PFT parameters of workers with 16-20 years exposure history with control one was showing statistically significant decline in mean values of FVC only suggesting restrictive type of PFT impairment in this group of workers. But in workers with more than 20 years exposure, the mean values of all the parameters studied were reduced as compared to control one suggesting combined type of PFT impairment. When the mean values of PFT parameters of exposed smokers were compared with exposed non-smokers there was statistically no significant difference. This can be due to marginal contribution of smoking habit in impairment of PFT parameters of exposed smokers. The percentages of workers with parenchymal and pleural changes due to asbestos exposure were nearly two times more in more than 20 years exposure groups as compared to 11-20 years exposure groups. The parenchymal and pleural changes due to asbestos exposure were more common in exposed smokers as compared exposed non-smokers. However the detailed analysis revealed that if smoking contributes to the development of interstitial fibrosis, the contribution is a marginal one in comparison to the effect of asbestos dust exposure.

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The contributions of fragile X syndrome to mental retardation have been underestimated. It is the most common form of familial mental retardation and one of the most common genetic diseases. Its long-term burden upon families and services is considerable.

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Pulmonary function tests (VC, FEV1% and FEF25-75%) were evaluated in 15 to 18 years age workers employed in slate pencil industry exposed to silica dust, in wool carpet industry exposed to wool dust and in diamond cutting and polishing exposed to carbon dust. These values were compared with the values obtained in clinically healthy non-smokers of the same age group. The results revealed significant impairment of VC in diamond workers, and FEF25-75% in slate pencil workers. When the values were observed according to smoking habits in diamond workers, VC, FEV1 and FEF25-75% were all significantly reduced in smokers whereas in non-smokers only VC was lowered significantly. Among slate pencil workers FEF25-75% was significantly reduced in both smokers and non-smokers. Wool dust exposed workers showed reduced values than normal subjects. The detailed results including the prevalence of various pulmonary impairments were presented.

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Alkaline phosphatase (ALP) isoenzyme composition was studied in sera and liver from patients with Indian childhood cirrhosis (ICC). A typical pattern consisting of a fast-moving anodal preliver band with slower moving diffuse liver and placental bands followed by an intestinal band was consistently observed in sera of patients in all stages of ICC and in pregnant mothers of index ICC patients. ICC liver ALP was relatively heat-stable and inhibited by L-phenylalanine and L-leucine. The isoenzyme also had similar immunological determinants to placental ALP and adult intestinal ALP isoenzymes. Total serum ALP isoenzyme and its heat-stable component progressively increased in concentration from early to advanced stages of the disease suggesting that the diseased liver in ICC is the source of the abnormal isoenzyme.

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Fifteen infants recovering from neonatal respiratory disease had arterial blood gases and lung mechanics measured 5 minutes before bolus feeds and at 5, 10, 20, and 30 minutes after feeding to determine physiologic effects of feeding. PaO2 fell significantly from prefeeding values at 5, 10, and 20 minutes after feeds. Mean prefeeding pH and base excess values were significantly different from mean postfeeding values at 5, 10, 20, and 30 minutes, respectively. PaCO2 remained unchanged before and after feeding. Heart rate and systolic and diastolic blood pressure did not change throughout the study. Dynamic lung compliance, respiratory, rate, and tidal volume did not change significantly but there was a trend toward increase in tidal volume. Mean minute volume rose with time as a consequence of the increased tidal volume. Work of breathing remained unchanged at 10 and 20 minutes postfeed and increased slightly at 30 minutes; this was due to a small increase in both elastic and viscous work components at this time.

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A study of adrenocorticosteroids and corticosteroid binding globulins was undertaken in 35 malnourished children with a weight deficit of 10 to 45%. The mean corticosteroid levels 5.9 +/- 3.0 mug% were not significantly different from control values of 6.43 +/- 3.2 mug%. Steroid levels were however low (4.38 +/- 1.8 mug%) in children with marasmic kwashiorkor. The corticosteroid binding globulin was reduced to 11.9 +/- 5.4 mug of cortisol bound in malnourished children with and without edema and was significantly lower than controls. "Free cortisol" levels were significantly raised in the malnourished state. In the presence of acute infection there was a remarkable rise of steroids suggesting that there was no hypofunction of the adrenal cortex. Where the infection was chronic (e.g., pulmonary tuberculosis) the levels were normal suggesting an adaptation to the stress. Early studies of the steroids and corticosteroid binding globulins within 2 to 3 weeks of starting a high protein diet showed that there was a remarkable rise of serum albumin 2.3 +/- 0.4 to 3.3 +/- 0.7 g%, steroids from 5.9 +/- 5.5 to 12.3 +/- 7.4 and corticosteroid binding globulins from 13.0 +/- 4.1 to 20.2 +/- 6.3 mug of cortisol bound per 100 ml. Weight gain was from 0.2 to 1.0 kg. A follow-up of four children for 6 weeks showed that the steroid levels fell to within normal limits. The integrity of the hypothalamohypophyseal adrenal axis was unimpaired in five out of six children studied. In conclusion it appears that marasmic children are well adapted to the stress of malnutrition and the ability of the adrenals to respond to stress is unimpaired.

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