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Background: The effect of individual pollutants and the period(s) during pregnancy when pollutant levels are likely to have most impact on preterm birth is not clear. We evaluated the effect of prenatal exposure to six common urban air pollutants in the Sydney metropolitan area on preterm birth. Methods: We obtained information on all births in metropolitan Sydney between January 1, 1998 and December 31, 2000. For each birth, exposure to each air pollutant was estimated for the first trimester, the three months preceding birth, the first month after the estimated date of conception and the month prior to delivery. Gestational age was analysed as a categorical variable in logistic regression models. Results: There were 123 840 singleton births in Sydney in 1998-2000 and 4.9% were preterm. Preterm birth was significantly associated with maternal age, maternal smoking, male infant, indigenous status and first pregnancy. Air pollutant levels in the month and three months preceding birth had no significant effect on preterm birth after adjusting for maternal and infant covariates. Ozone levels in the first trimester of pregnancy and spring months of conception and sulphur dioxide were associated with increased risks for preterm births. Nitrogen dioxide was associated with a decreased risk of preterm births. Conclusion: We found more protective than harmful associations between ambient air pollutants and preterm births with most associations non-significant. In view of these inconsistent associations, it is important to interpret the harmful effects with caution. If our results are confirmed by future studies then it will be imperative to reduce Sydney's already low air pollution levels even further. [ABSTRACT FROM AUTHOR]

Background The proportion of asthma in adults that is due to occupational exposures is not known.Aim To examine the contribution of workplace exposures to the development of asthma in adults in New South Wales (NSW) in a cross sectional, population-based study.Methods A randomly selected population of 5331 18- to 49-year olds completed and returned a mailed questionnaire (response rate 37%). In adult-onset asthmatics we examined the association of asthma with reported exposure, within 1 year of asthma onset, to a list of occupations and exposures known to be at risk for occupational asthma (high-risk jobs and exposures).Results Among 910 subjects (18%) with asthma, 383 (7%) subjects reported adult-onset disease. After adjusting for sex, age and smoking, working in any high-risk job or exposure at the time of asthma onset was significantly associated with adult-onset asthma (OR 1.51, 95% CI 1.19–1.92). The population attributable risk (PAR) of adult-onset asthma for either a high-risk job or an exposure was 9.5%. Sudden onset, irritant or reactive airways dysfunction syndrome type exposures were associated with adult-onset asthma (OR 4.65, 95% CI 1.64–13.2). The PAR of adult-onset asthma for these exposures was 0.2%.Conclusion Reported adult onset of asthma is common and occupational exposures may be associated with 9.5% of prevalent cases of adult-onset asthma in NSW. [ABSTRACT FROM AUTHOR]

OBJECTIVES: This study examined the effects of outdoor air pollutants in Sydney, Australia, on daily mortality. METHODS: Time-series analysis was performed on counts of daily mortality and major outdoor air pollutants (particulates, ozone, and nitrogen dioxide) in Sydney (1989 to 1993) with adjustment for seasonal and cyclical factors. Poisson regression was calculated with allowance for overdispersion and autocorrelation. The effects of lagging exposure by 0 to 2 days were assessed with single- and multiple-pollutant models. RESULTS: An increase in daily mean particulate concentration from the 10th to the 90th centile was associated with an increase of 2.63% (95% confidence interval 0.87 to 4.41) in all-cause mortality and 2.68% (0.25 to 5.16) in cardiovascular mortality. An increase in daily maximum 1-hour ozone concentration from the 10th to the 90th centile was associated with an increase of 2.04% (0.37 to 3.73) in all-cause mortality and 2.52% (-0.25 to 5.38) in cardiovascular mortality. An increase in the daily mean nitrogen dioxide concentration from the 10th to the 90th centile was associated with an increase of 7.71% (-0.34 to 16.40) in respiratory mortality. Multiple-pollutant models suggest that the effects of particulates and ozone on all-cause and cardiovascular mortality, and of nitrogen dioxide on respiratory mortality, are independent of the effects of the other pollutants. CONCLUSIONS: Current levels of air pollution in Sydney are associated with daily mortality. [ABSTRACT FROM AUTHOR]

Background: Little research has investigated the health effects of particulate exposure from bushfires (also called wildfires, biomass fires, or vegetation fires), and these exposures are likely to increase, for several reasons. We investigated associations of daily mortality and hospital admissions with bushfire-derived particulates, compared with particulates from urban sources in Sydney, Australia from 1994 through 2002., Methods: On days with the highest particulate matter (PM)10 concentrations, we assumed PM10 was due primarily to bushfires. We calculated the contribution of bushfire PM10 on these days by subtracting the background PM10 concentration estimated from surrounding days. We assumed PM10 on the remaining days was from usual urban sources. We implemented a Poisson model, with a bootstrap-based methodology, to select optimum smoothed covariate functions, and we estimated the effects of bushfire PM10 and urban PM10, lagged up to 3 days., Results: We identified 32 days with extreme PM10 concentrations due to bushfires or vegetation-reduction burns. Although bushfire PM10 was consistently associated with respiratory hospital admissions, we found no consistent associations with cardiovascular admissions or with mortality. A 10 microg/m increase in bushfire PM10 was associated with a 1.24% (95% confidence interval = 0.22% to 2.27%) increase in all respiratory disease admissions (at lag 0), a 3.80% (1.40% to 6.26%) increase in chronic obstructive pulmonary disease admissions (at lag 2), and a 5.02% (1.77% to 8.37%) increase in adult asthma admissions (at lag 0). Urban PM10 was associated with all-cause and cardiovascular mortality, as well as with cardiovascular and respiratory hospital admission, and these associations were not influenced by days with extreme PM10 concentrations., Conclusions: PM10 from bushfires is associated primarily with respiratory morbidity, while PM10 from urban sources is associated with cardiorespiratory mortality and morbidity.

Objectives: To assess the health risks associated with consumption of drinking water with elevated nickel concentration in a NSW country town named Sampleton., Methods: We used enHealth Guidelines (2002) as our risk assessment tool. Laboratory test results for nickel in water samples were compared with the Australian Drinking Water Guidelines 2004 and the World Health Organization's (WHO) Guidelines for Drinking Water Quality 2005., Results: The mean nickel concentration in the drinking water samples tested over a 4-year period (2002-2005) was 0.03 mg/L (95% CI: 0.02-0.04). The average daily consumption of two litres of water by a 70-kg adult provided 0.06 mg (0.03 mg x 2) of nickel, which was only 7% of the lowest observed adverse effect level (LOAEL) based on experiments on nickel-sensitive people in a fasting state., Conclusions: The mean nickel concentration in drinking water appears to have no health risks for the inhabitants of Sampleton.

Health impact assessment is advanced as a formal means to assess the direct and indirect health impacts of urban planning decisions and processes. It is, however, an intrinsically passive policy device. A more comprehensive and practical policy framework or architecture, reminiscent of that devised by Edwin Chadwick and the sanitary reform movement in 19th Century England, will be necessary to reorient the goals and practices of urban planning.