This article briefly reviews evidence of health effects associated with exposure to particulate matter (PM) air pollution from five common outdoor emission sources: traffic, coal-fired power stations, diesel exhaust, domestic wood combustion heaters, and crustal dust. The principal purpose of this review is to compare the evidence of health effects associated with these different sources with a view to answering the question: Is exposure to PM from some emission sources associated with worse health outcomes than exposure to PM from other sources? Answering this question will help inform development of air pollution regulations and environmental policy that maximises health benefits. Understanding the health effects of exposure to components of PM and source-specific PM are active fields of investigation. However, the different methods that have been used in epidemiological studies, along with the differences in populations, emission sources, and ambient air pollution mixtures between studies, make the comparison of results between studies problematic. While there is some evidence that PM from traffic and coal-fired power station emissions may elicit greater health effects compared to PM from other sources, overall the evidence to date does not indicate a clear ‘hierarchy’ of harmfulness for PM from different emission sources. Further investigations of the health effects of source-specific PM with more advanced approaches to exposure modeling, measurement, and statistics, are required before changing the current public health protection approach of minimising exposure to total PM mass.

Background There is inconclusive evidence from observational studies that disinfection by-products (DBPs) in drinking water are associated with colorectal cancer. Methods A literature search, without language or time limits, was performed to identify relevant case–control and cohort studies. Separate risk estimates for colon and rectal cancer were extracted from studies meeting the inclusion criteria. Relative risks (RRs) or odds ratios (ORs) comparing the highest exposure category with the lowest were pooled using random effects methods. Results A total of 13 studies (3 cohort and 10 case–control) were analysed. For colon cancer, the pooled RR estimates were 1.11 [95% confidence interval (CI): 0.73–1.70] for cohort studies, 1.33 (95% CI: 1.12–1.57) for case–control studies and 1.27 (95% CI: 1.08–1.50) combining both study types. For rectal cancer, the corresponding RR estimates were 0.88 (0.57–1.35), 1.40 (1.15–1.70) and 1.30 (1.06–1.59). Sensitivity analysis showed these results were not importantly influenced by any single study. Publication bias was not evident for the colon cancer analysis but may have been a minor issue for the rectal cancer analysis. The results for rectal cancer may have been influenced by the quality of the studies. Conclusions The study findings provide limited evidence of a positive association between colorectal cancer and exposure to DBPs in drinking water. The small number of studies and limitations in study quality prevent causal inference.

Epidemiological studies show that long-term exposure to ambient air pollution reduces life expectancy. Most studies have been in environments with relatively high concentrations such as North America, Europe and Asia. Associations at the lower end of the concentration-response function are not well defined. We assessed associations between all-cause mortality and exposure to annual average particulate matter <2.5 μm (PM2.5) and nitrogen dioxide (NO2) in Sydney, Australia, where concentrations are relatively low. The '45 and Up Study' comprises a prospective longitudinal cohort from the state of New South Wales, Australia with 266,969 participants linked to death registry data. We analyzed data for the participants who resided in Sydney at baseline questionnaire (n = 75,268). Exposures to long-term pollution were estimated using annual averages from a chemical transport model (PM2.5), and a satellite-based land-use regression model (NO2). Socio-demographic information was extracted from the baseline questionnaire. Cox proportional hazard models were applied to estimate associations, while adjusting for covariates. In our cohort mean annual PM2.5 was 4.5 μg/m3 and mean NO2 was 17.8 μg/m3. The mortality rate was 4.4% over the 7 years of follow up. Models that adjusted for individual-level and area-level risk factors resulted in a detrimental non statistically significant hazard ratio (HR) of 1.05 (95% CI: 0.98-1.12) per 1 μg/m3 increase in PM2.5, and 1.03 (95% CI: 0.98-1.07) per 5 μg/m3 increase in NO2. We found evidence that low-level air pollution exposure was associated with increased risk of mortality in this cohort of adults aged 45 years and over, even at the relatively low concentrations seen in Sydney. However, a clear determination of the association with mortality is difficult because the results were sensitive to some covariates. Our findings are supportive of emerging evidence that exposure to low levels of air pollution reduces life expectancy.

Short- and long-term spatiotemporal variation in exposure to air pollution is associated with respiratory morbidity in areas with moderate-to-high level of air pollution, but very few studies have examined whether these associations also exist in areas with low level exposure. We assessed the association between spatial variation in long-term exposure to PM2.5 and NO2 and hospitalisation for all respiratory diseases, asthma, chronic obstructive pulmonary disease (COPD), and pneumonia, in older adults residing in Sydney, Australia, a city with low-level concentrations. We recorded data on hospitalisations for 100,084 participants, who were aged >45 years at entry in 2006-2009 until June 2014. Annual NO2 and PM2.5 concentrations were estimated for the participants' residential addresses and Cox proportional hazards regression was used to model the association between exposure to air pollutants and first episode of hospitalisation, controlling for personal and area level covariates. We further investigated the shape of the exposure-response association and potential effect modification by age, sex, education level, smoking status, and BMI. NO2 and PM2.5 annual mean exposure estimates were 17.5 μg·m-3 and 4.5 μg·m-3 respectively. NO2 and PM2.5 was positively, although not significantly, associated with asthma. The adjusted hazard ratio for a 1 μg·m-3 increase in PM2.5 was 1.08, 95% confidence interval 0.89-1.30. The adjusted hazard ratio for a 5 μg·m-3 increase in NO2 was 1.03, 95% confidence interval 0.88-1.19. We found no positive statistically significant associations with hospitalisation for all respiratory diseases, and pneumonia while negative associations were observed with COPD. We found weak positive associations of exposure to air pollution with hospitalisation for asthma while there was no evidence of an association for all respiratory diseases.