In this paper, we related daily fluctuations in cardiac and respiratory hospital admissions for people < 65-years old and 65+ to daily variations in ambient levels of particulates and gaseous air pollutants in London, Ontario using data from 1995–2000.
The findings show that CO and COH contribute significantly to cardiovascular hospitalization. These results are quite consistent with previous findings in the literature. Using daily 1-h maximum concentration of CO data from 1981–1991, Burnett et al.
] found positive associations with congestive heart failure hospitalization among the elderly in London, Ontario. In London, UK, Atkinson et al.
] found a positive association between CO and emergency admission for cardiovascular disease. Lin et al.
] also found an association between CO and ischaemic cardiac diseases in São Paulo, Brazil albeit for ages 45 to 80 years. Furthermore, Morris et al.
] found that among the gaseous pollutants, CO was the only consistent pollutant for congestive heart failure admissions in seven large American cities. Similarly, Schwartz and Morris [31
] found that CO and PM10
were significant predictors of ischaemic heart disease hospitalizations in Detroit, Michigan using a two-pollutant model.
Our results also showed COH to be a significant predictor of cardiac admissions of people < 65 years of age in the single pollutant model. This is in agreement with recent results of Goldberg et al.
] who found positive association between daily mortality for congestive heart failure and COH in Montreal, Quebec. The associations between cardiovascular diseases and some of the measures of NO2
were positive although not significant in this analysis.
While epidemiological findings linking air pollution to heart disease maybe consistent, the issue of biological plausibility remains uncertain since the underlying mechanisms of an acute heart effect of air pollution are still unknown [32
]. Physiopathological pathways have been proposed for the relationship between particulate air pollution and cardiovascular health [33
]. One of the major hypotheses is that particles induce activation of some mediators/indicators of alterations in blood coagulability [35
]. Another mechanism that has been examined relates to cardiac autonomic control, such as heart rate and various indices of its variability [36
]. Recently, Pope et al.
] hypothesized that the link between fine particulates to cardiovascular mortality is via mechanisms that likely include pulmonary and systematic inflammation, accelerated atherosclerosis and altered cardiac autonomic function.
The significant association between PM10
and asthma admissions among the elderly in the city of London is consistent with those of Luginaah et al.
] who found a significant increase in daily asthma admissions among the elderly women in Windsor, Ontario with elevated levels of PM10
. Schwartz [5
] also found PM10
to be significantly associated with respiratory hospital admissions for elderly women in Spokane, Washington. Epidemiological studies [37
] have demonstrated that acute increase in PM10
results in a greater use of asthma medication, more consultations of GPs and increased hospital admissions for asthma. However, the role of PM10
in raising the chances of initial sensitization and induction of disease has not been proved [40
Our analysis showed a 2–3% increase in respiratory admissions among the elderly for ozone but it is not statistically significant. Yang et al.
] found a positive association between O3
and respiratory hospital admission among the elderly in Vancouver. In the 16 cities study across Canada, Burnett et al.
] using data from 1981 to 1991, found positive associations between ozone and admission to hospital for respiratory diseases. However, Atkinson et al.
] working in London, UK, did not find any association between O3
and respiratory diseases.
Although the risks of health effects due to air pollution observed in these analyses are generally low, the implications for public health are important. Despite improvements in ambient air quality as a result of tighter regulations in the past few years [20
], the event of 9/11 has brought with it renewed concerns about the effects of air pollution in Southwestern Ontario. The increasing delays resulting in long lines of trucks at the border crossing points, and the idling trucks spewing toxic pollutants from their archaic exhaust systems into the air is of grave concern. With London located downwind of Windsor and Detroit area, (which together is a major source of industrial pollutants), the combined effect of these factors is that the conditions here may deteriorate. Increasing concerns about poor environmental quality in this region resulted in joint Canada and US border air strategy aimed at mapping the Southwestern Ontario air shed, and exploring its health impacts [42
]. The plausible next step is to conduct more frequent air quality studies to continue to monitor any changes in hospitalizations due to ambient air pollution that may be taking place in London and the entire region.