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1.  Acute effects of winter air pollution on respiratory function in schoolchildren in southern England 
Aim: To investigate the acute health effects of winter outdoor air pollution (nitrogen dioxide (NO2), ozone (O3), sulphur dioxide (SO2), sulphate (SO42-) ,and particles (PM10)) on schoolchildren in an area of southern England where levels of SO2 had been reported to be high.
Methods: A total of 179 children, aged 7–13, from three schools (two urban and one rural location), were included. Peak expiratory flow rate (PEFR) and presence or absence of upper respiratory infections were recorded on 63 school days from 1 November 1996 to 14 February 1997. Air pollution and meteorological data were taken from monitors at each school site. The analysis regressed daily PEFR on pollutant level adjusting for confounders and serial correlation and calculated a weighted pooled estimate of effect overall for each pollutant. In addition, large decrements in PEFR were analysed as a binary outcome. Same day, lag 1, lag 2, and a five day average of pollutant levels were used.
Results: There were no clear effects of any pollutant on mean PEFR. In addition, we analysed large PEFR decrements (a binary outcome), observing consistent negative associations with NO2, SO42-, and PM10, although few lag/pollutant combinations were significant: odds ratios (95% CI) for five day average effect: NO2 24 h average 1.043 (1.000 to 1.089), SO42- 1.090 (0.898 to 1.322), PM10 1.037 (0.992 to 1.084). The observed effects of PM10 (only) were stronger in wheezy children (1.114 (1.057 to 1.174)). There were no consistent negative associations between large decrements and ozone or SO2 .
Conclusions: There is no strong evidence for acute effects of winter outdoor air pollution on mean PEFR overall in this area, but there is evidence for negative effects on large PEFR decrements.
PMCID: PMC1740463  PMID: 12554833
2.  Acute effects of summer air pollution on respiratory function in primary school children in southern England. 
Thorax  1996;51(11):1109-1114.
BACKGROUND: There is growing concern about health effects of air pollution in the UK. Studies in the USA have reported adverse effects on lung function among children but no comparable studies have been published in the UK. This study investigates the relationship between daily changes in ambient air pollution and short term variations in lung function in a panel of school children. METHODS: One hundred and fifty four children aged 7-11 attending a primary school adjacent to a major motorway in Surrey, south-east England, were studied. Bellows spirometry was performed daily on 31 schooldays between 6 June and 21 July 1994. Levels of ozone, nitrogen dioxide, and particulates of less than 10 microns in diameter (PM10) were measured continuously at the school and the pollen count was measured six miles away. Relationships between daily changes in forced expiratory volume in 0.75 seconds (FEV0.75), forced vital capacity (FVC), the FEV0.75/FVC ratio and pollutants were analysed using separate autoregressive models for each child. A weighted average of the resulting slopes was then calculated. RESULTS: There was a significant inverse relationship between daily mean PM10 levels lagged one day and FVC, with a reduction in lung function of 1% (95% CI 0.3% to 2%) across the whole range of PM10 levels (20-150 micrograms/m3). The effect on FEV0.75 was similar (-0.5%) but was not significant when weighted by 1/SE2 (95% CI -1.2% to 0.2%). There was no effect of PM10 levels on the FEV0.75/FVC ratio. No significant association was seen between FEV0.75, FVC, or the FEV0.75/FVC ratio and either ozone or nitrogen dioxide levels. There was no evidence that wheezy children were more affected than healthy children. Pollen levels on the previous day had no effect on lung function and did not change the air pollution results. CONCLUSIONS: There is a very small, but statistically significant, adverse effect of airborne respirable particulate matter, measured as PM10, on lung function in this study group. There is no evidence for an inverse association of lung function with levels of ozone or NO2 measured on the previous day.
PMCID: PMC1090522  PMID: 8958894
3.  Effect of ambient levels of smoke and sulphur dioxide on the health of a national sample of 23 year old subjects in 1981. 
Thorax  1995;50(7):764-768.
BACKGROUND--There is concern that, despite the fall in air pollution levels since the 1950s, there may still be adverse effects at current levels. A study was carried out to investigate the association between air pollution and respiratory symptoms in 23 year old subjects in 1981. METHODS--Data on cough, phlegm, and wheeze were available on 11,552 members of the 1958 national birth cohort. Counties in the UK were ranked by annual average level of black smoke and sulphur dioxide (SO2), and then divided into five groups. The subject's county of residence determined their categorisation of pollution exposure. The association between air pollution exposure and respiratory symptoms was examined by logistic regression, adjusting for social class, sex, and smoking. RESULTS--The ranges of the air pollution groups were 2.0-13.0, 13.1-18.7, 19.6-20.8, 21.0-25.8, and 26.1-55.1 micrograms/m3 for black smoke, and 7.0-36.4, 36.7-42.7, 43.0-50.5, 52.0-59.3, and 60.9-87.7 micrograms/m3 for SO2. The overall prevalences of cough, phlegm, wheezing since age 16, and wheezing in the past year were 13.3%, 10.3%, 9.4%, and 4.4%, respectively. Phlegm symptoms increased with increasing smoke levels with evidence of a plateau. Cough and wheeze were not associated with black smoke; no symptom was associated with SO2. In the subgroup with wheeze at ages 16-23 there was no effect of smoke level on phlegm. CONCLUSIONS--Low ambient levels of black smoke were associated with decreased prevalence of phlegm symptoms in young adults in the UK in 1981. The effect was evident below the current EC guideline of 34-51 micrograms/m3 annual black smoke. In 1991 the annual mean smoke level for each county ranged from 3.4 to 26.5 micrograms/m3, spanning all but the last exposure group used here. This is consistent with the existence of adverse and possibly chronic effects at current levels.
PMCID: PMC474650  PMID: 7570412
4.  Receptor and postreceptor defects contribute to the insulin resistance in noninsulin-dependent diabetes mellitus. 
Journal of Clinical Investigation  1981;68(4):957-969.
We have assessed the mechanisms involved in the pathogenesis of the insulin resistance associated with impaired glucose tolerance and Type II diabetes mellitus by exploring, by means of the euglycemic glucose-clamp technique, the in vivo dose-response relationship between serum insulin and the overall rate of glucose disposal in 14 control subjects; 8 subjects with impaired glucose tolerance, and 23 subjects with Type II diabetes. Each subject had at least three studies performed on separate days at insulin infusion rates of 40, 120, 240, 1,200, or 1,800 mU/M2 per min. In the subjects with impaired glucose tolerance, the dose-response curve was shifted to the right (half-maximally effective insulin level 240 vs. 135 microunits/ml for controls), but the maximal rate of glucose disposal remained normal. In patients with Type II diabetes mellitus, the dose-response curve was also shifted to the right, but in addition, there was a posal. This pattern was seen both in the 13 nonobese and the 10 obese diabetic subjects. Among these patients, an inverse linear relationship exists (r = -0.72) so that the higher the fasting glucose level, the lower the maximal glucose disposal rate. Basal rates of hepatic glucose output were 74 +/- 4, 82 +/- 7, 139 +/- 24, and 125 +/- 16 mg/M2 per min for the control subjects, subjects with impaired glucose tolerance, nonobese Type II diabetic subjects, and obese Type II diabetic subjects, respectively. Higher serum insulin levels were required to suppress hepatic glucose output in the subjects with impaired glucose tolerance and Type II diabetics, compared with controls, but hepatic glucose output could be totally suppressed in each study group. We conclude that the mechanisms of insulin resistance in patients with impaired glucose tolerance and in patients with Type II noninsulin-dependent diabetes are complex, and result from heterogeneous causes. (a) In the patients with the mildest disorders of carbohydrate homeostasis (patients with impaired glucose tolerance) the insulin resistance can be accounted for solely on the basis of decreased insulin receptors. (b) In patients with fasting hyperglycemia, insulin resistance is due to both decreased insulin receptors and postreceptor defect in the glucose mechanisms. (c) As the hyperglycemia worsens, the postreceptor defect in peripheral glucose disposal emerges and progressively increases. And (d) no postreceptor defect was detected in any of the patient groups when insulin's ability to suppress hepatic glucose output was measured.
PMCID: PMC370882  PMID: 7287908

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