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The effects that vermiculture (VC) treatment had on population and community structure of enterococci in domestic biosolids in a residential resort in southeast Queensland were investigated by enumerating and typing enterococci with a biochemical fingerprinting method. Vermiculture beds with a substrate consisting of non-amended biosolids from an activated sludge sewage treatment plant were established. Various treatments (earthworms added and earthworms excluded) beds were sampled on 3 occasions. Enterococci numbers were significantly lower in the earthworm treatments than those without. Of the 300 isolates biochemically fingerprinted, 106 different biochemical phenotypes (BPTs) were identified. The overall mean diversity of enterococci in all beds was high (0.87 ± 0.13; maximum is 1), indicating a diverse enterococci population. The overall mean population similarity (Sp) value amongst beds was quite low (0.16 ± 0.10) also indicating a diverse population. Antibiotic resistance patterns (ARPs) of the 106 BPTs revealed that 83.6% were resistant to rifampicin, 59.6% were resistant to erythromycin, 21.9% were resistant to tetracycline, 7.7% were resistant to ampicillin and 2.9% were resistant to gentamicin and vancomycin. The results indicate that the current VC methods used in the residential resort to create worm castings for potting mixture may not satisfactorily pasteurize the biosolids and significant number of pathogenic microorganisms could be present. There remains a potential health risk to workers and guests and routine monitoring of pathogens is recommended for improved management of stockpiled biosolids.

Objective: To examine the short-term health effects of air pollution on daily mortality in four Australian cities (Brisbane, Melbourne, Perth and Sydney), where more than 50% of Australians reside. Methods: The study used a similar protocol to APHEA2 (Air Pollution and Health: A European Approach) study and derived single-city and pooled estimates. Results: The results derived from the different approaches for the 1996-99 period showed consistent results for different statistical models used. There were significant effects on total mortality, (RR=1.0284 per 1 unit increase in nephelometry [10-4. m-1], RR=1.0011 per 1ppb increase in NO2), and on respiratory mortality (RR=1.0022 per 1ppb increase in O3). No significant differences between cities were found, but the NO2 and particle effects may refer to the same impacts. Meta-analyses carried out for three cities yielded estimates for the increase in the daily total number of deaths of 0.2% (-0.8% to 1.2%) for a 10 μg/m3 increase in PM10 concentration, and 0.9% (-0.7% to 2.5%) for a 10 μg/m3 increase in PM2.5 concentration. Conclusions: Air pollutants in Australian cities have significant effects on mortality.

Urban air pollution levels are associated with increased mortality and cardiorespiratory morbidity. These health effects occur even at exposure levels below those stipulated in current air-quality guidelines, and it is unclear whether a safe threshold exists. Air pollution in Australia and New Zealand comes primarily from motor vehicle emissions, electricity generation from fossil fuels, heavy industry, and home heating using wood and coal. In individual patients a direct link between symptoms and air pollution exposure may be difficult to establish and may not change their clinical management. However, avoiding exposure during periods of peak pollution may be beneficial. Although there is some evidence that urban air pollution in Australia and New Zealand has been decreasing (through reduced car use, improved emission-control technology and use of more energy-efficient devices in the household and in industry), pollution levels are still unsatisfactory. Further reductions may prevent hundreds of cardiorespiratory hospital admissions and deaths each year.