Changes in risk factors for preterm birth in Western Australia 1984-2006.

OBJECTIVE: To characterise changing risk factors of preterm birth in Western Australia between 1984 and 2006. DESIGN: Population-based study. SETTING: Western Australia. POPULATION: All non-Aboriginal women giving birth to live singleton infants between 1984 and 2006. METHODS: Multinomial, multivariable regression models were used to assess antecedent profiles by preterm status and labour onset types (spontaneous, medically indicated, prelabour rupture of membranes [PROM]). Population attributable fraction (PAF) estimates characterized the contribution of individual antecedents as well as the overall contribution of two antecedent groups: pre-existing medical conditions (including previous obstetric history) and pregnancy complications. MAIN OUTCOME MEASURE: Antecedent relationships with preterm birth, stratified by labour onset type. RESULTS: Marked increases in maternal age and primiparous births were observed. A four-fold increase in the rates of pre-existing medical complications over time was observed. Rates of pregnancy complications remained stable. Multinomial regression showed differences in antecedent profiles across labour onset types. PAF estimates indicated that 50% of medically indicated preterm deliveries could be eliminated after removing six antecedents from the population; estimates for PROM and spontaneous preterm reduction were between 10 and 20%. Variables pertaining to previous and current obstetric complications (previous preterm birth, previous caesarean section, pre-eclampsia and antepartum haemorrhage) were the most influential predictors of preterm birth and adverse labour onset (PROM and medically indicated). CONCLUSIONS: Preterm antecedent profiles have changed markedly over the 23 years studied. Some changes may be attributable to true change, others to advances in surveillance and detection. Still others may signify change in clinical practice.

Exposure-response analysis and risk assessment for silica and silicosis mortality in a pooled analysis of six cohorts.

AIMS: To study the relation between exposure to crystalline silica and silicosis mortality. Although mortality is an important endpoint for regulators, there have been no exposure-response studies for silicosis mortality, because of the relative rareness of silicosis as an underlying cause of death, and the limited availability of quantitative exposure estimates. METHODS: Data from six occupational cohorts were pooled with good retrospective exposure data in which 170 deaths from silicosis were reported. Standard life table analyses, nested case-control analyses, and risk assessment were performed. RESULTS: The rate of silicosis mortality in the combined data was 28/100 000 py, increasing in nearly monotonic fashion from 4.7/100 000 for exposure of 0-0.99 mg/m(3)-years to 233/100 000 for exposure of >28.1 mg/m(3)-years. The estimated risk of death up to age 65 from silicosis after 45 years of exposure at 0.1 mg/m(3) silica (the current standard in many countries) was 13 per 1000, while the estimated risk at an exposure of 0.05 mg/m(3) was 6 per 1000. Both of these risks are above the risk of 1 per 1000 typically deemed acceptable by the US OSHA. CONCLUSION: The findings from this pooled analysis add further support to the need to control silica exposure and to lower the occupational standards. Our estimates of lifetime silicosis mortality risk are probably underestimates as, in addition to exposure misclassification, our study might have suffered from outcome misclassification in that silicosis deaths might have been coded to other related causes, such as tuberculosis or chronic obstructive pulmonary disease.

Pooled exposure-response analyses and risk assessment for lung cancer in 10 cohorts of silica-exposed workers: an IARC multicentre study.

OBJECTIVES: Silica is one of the most common occupational exposures worldwide. In 1997 the International Agency for Research on Cancer (IARC) classified inhaled crystalline silica as a human carcinogen (group 1), but acknowledged limitations in the epidemiologic data, including inconsistencies across studies and the lack of extensive exposure-response data. We have conducted a pooled exposure-response analysis of 10 silica-exposed cohorts to investigate lung cancer. METHODS: The pooled cohort included 65,980 workers (44,160 miners, 21,820 nominees), and 1,072 lung cancer deaths (663 miners, 409 nonminers). Follow-up has been extended for five of these cohorts beyond published data. Quantitative exposure estimates by job and calendar time were adopted, modified, or developed to permit common analyses by respirable silica (mg/m3) across cohorts. RESULTS: The log of cumulative exposure, with a 15-year lag, was a strong predictor of lung cancer (p = 0.0001), with consistency across studies (test for heterogeneity, p = 0.34). Results for the log of cumulative exposure were consistent between underground mines and other facilities. Categorical analyses by quintile of cumulative exposure resulted in a monotonic trend with odds ratios of 1.0. 1.0, 1.3, 1.5, 1.6. Analyses using a spline curve also showed a monotonic increase in risk with increasing exposure. The estimated excess lifetime risk (through age 75) of lung cancer for a worker exposed from age 20 to 65 at 0.1 mg/m3 respirable crystalline silica (the permissible level in many countries) was 1.1-1.7%, above background risks of 3-6%. CONCLUSIONS: Our results support the decision by the IARC to classify inhaled silica in occupational settings as a carcinogen, and suggest that the current exposure limits in many countries may be inadequate. These data represent the first quantitative exposure-response analysis and risk assessment for silica using data from multiple studies.

A comparison of blood pressure measurements obtained with the Dinamap 845XT, the standard mercury sphygmomanometer and the London School of Hygiene device.

Blood pressure measurements obtained with the Dinamap 845XT Vital Signs monitor were compared with measurements obtained with a standard mercury sphygmomanometer and a London School of Hygiene mercury sphygmomanometer in a group of 31 normotensive and hypertensive subjects. The experimental design allowed reading to be taken with all 3 devices at approximately the same time. 12 sets of readings were obtained with each device in each subject. Although inter-device differences estimated from analysis of variance were small (less than 2 mmHg after allowing for calibration differences) differences between measurements taken simultaneously with the 3 devices were often substantial. Agreement between the two mercury sphygmomanometers was better than that between either sphygmomanometer and the Dinamap. This may be a reflection of fundamental differences between auscultatory and oscillometric measurements. Differences between devices were unrelated to blood pressure level. The observed variability within subjects was similar with each device.

Plasma catecholamines following exercise in hypertensives treated with pindolol: comparison with placebo and metoprolol.

This study re-examines the proposal that beta-adrenoceptor blockers with intrinsic sympathomimetic activity decrease plasma noradrenaline levels. Thirteen patients (aged 29-65 years) with uncomplicated essential hypertension were randomly allocated to a three period, double-blind cross-over trial. The treatment periods, each of 3 weeks duration, were composed of placebo, pindolol (5 mg twice daily) and metoprolol (100 mg twice daily), dispensed in identical capsules. At the end of each treatment period, patients were exercised on a bicycle ergometer to a predetermined workload. Blood pressure and heart rate were measured before, immediately on completion of exercise and after 10 min post-exercise rest. Blood samples for plasma noradrenaline and adrenaline determination were also collected at these times. Blood pressures were similar during treatment with pindolol and metoprolol. As expected, heart rate was consistently lower during metoprolol treatment. Basal, pre-exercise plasma noradrenaline and adrenaline were similar at the end of each treatment period. However, the increase following exercise was significantly greater during metoprolol treatment. The post-exercise increase during pindolol treatment was indistinguishable from that in the placebo period. These findings, in a randomised placebo-controlled study, therefore demonstrate that pindolol does not influence basal or exercise-stimulated plasma noradrenaline and adrenaline concentrations. This is best explained by a lack of effect of pindolol on the plasma clearance of catecholamines, which is impaired by beta-adrenoceptor blockers devoid of intrinsic sympathomimetic activity.

Blood pressure and catecholamines following exercise during selective beta-blockade in hypertension.

This study examines and compares the hemodynamic and sympathoadrenal response to bicycle exercise in hypertensive subjects during two weeks' treatment with a cardio-selective (metoprolol) and nonselective (propranolol) beta-blocker. The increase in plasma norepinephrine and epinephrine concentration following exercise was augmented to a similar degree with each beta-blocker. Pre-exercise blood pressure and heart rate were similar for the two drugs. However immediately after exercise and particularly after resting for 20 min post exercise, diastolic blood pressure was lower during metoprolol treatment. Systolic blood pressure was also lower 20 min post exercise during metoprolol treatment. These observations indicate that cardio-selective beta-blockers offer advantages in blood pressure control during exercise through intact vascular beta 2-adrenoceptors opposing sympathetically mediated vasoconstriction.