Several species of wild birds can act as biological or mechanical carriers of human pathogens as well as of vectors of infectious agents (Olsen et al., 1995; Klich et al., 1996; Gylfe etal.,2000; Friend et al., 2001; Pereira et al., 2001; Broman et al., 2002; Moore et al., 2002; Niskanen et al., 2003; Rappole and Hubalek, 2003; Reed et al., 2003; Fallacara et al., 2004; Hubalek, 2004; Krauss et al., 2004). Many of these birds are migratory species that seasonally fly long distances through different continents (de Graaf and Rappole, 1995; Webster et al., 2002b). Climate change has been implicated in changes in the migratory and reproductive phenology (advancement in breeding and migration dates) of several bird species, their abundance and population dynamics, as well as a northward expansion of their geographical range in Europe (Sillett et al., 2000; Barbraud and Weimerskirch, 2001; Parmesan and Yohe, 2003; Brommer, 2004; Visser et al., 2004; Both and Visser, 2005). Two possible consequences of these phenological changes in birds to the dispersion of pathogens and their vectors are:
1. shifts in the geographical distribution of the vectors and pathogens due to altered distributions or changed migratory patterns of bird populations;
2. changes in the life cycles of bird-associated pathogens due to the mistiming between bird breeding and the breeding of vectors, such as mosquitoes. One example is the transmission of St. Louis encephalitis virus, which depends on meteorological triggers (e.g., precipitation) to bring the pathogen, vector and host (nestlings) cycles into synchrony, allowing an overlap that initiates and facilitates the cycling necessary for virus amplification between mosquitoes and wild birds (Day, 2001).
spatial (Hales et al., 2002), temporal (Hales et al., 1999; Corwin et al., 2001; Gagnon et al., 2001) or spatiotemporal patterns of dengue and climate (Hales et al., 1999; Corwin et al., 2001; Gagnon et al., 2001; Cazelles et al., 2005). However, these reported associations are not entirely consistent, possibly reflecting the complexity of climatic effects on transmission, and/or the presence of competing factors (Cummings, 2004). While high rainfall or high temperature can lead to an increase in transmission, studies have shown that drought can also be a cause if household water storage increases the number of suitable mosquito breeding sites (Pontes et al., 2000; Depradine and Lovell, 2004; Guang et al., 2005).
Climate-based (temperature, rainfall, cloud cover) density maps of the main dengue vector Stegomyia (previously called
Aedes) aegypti are a good match with the observed disease distribution (Hopp and Foley, 2003). The model of vector abundance has good agreement with the distribution of reported cases of dengue in Colombia, Haiti, Honduras, Indonesia, Thailand and Vietnam (Hopp and Foley, 2003). Approximately one-third of the world's population lives in regions where the climate is suitable for dengue transmission (Hales et al., 2002; Rogers et al., 2006b).
The spatial distribution, intensity of transmission, and seasonality of malaria is influenced by climate in sub-Saharan Africa; socio-economic development has had only limited impact on curtailing disease distribution (Hay et al., 2002a; Craig et al., 2004).
Rainfall can be a limiting factor for mosquito populations and there is some evidence of reductions in transmission associated with decadal decreases in rainfall. Interannual malaria variability is climate-related in specific eco-epidemiological zones (Julvez et al., 1992; Ndiaye et al., 2001; Singh and Sharma, 2002; Bouma, 2003; Thomson et al., 2005). A systematic review of studies of the El Niño-Southern Oscillation (ENSO) and malaria concluded that the impact of El Niño on the risk of malaria epidemics is well established in parts of southern Asia and South America (Kovats et al., 2003). Evidence of the predictability of unusually high or low malaria anomalies from both sea-surface temperature (Thomson et al., 2005) and multi-model ensemble seasonal climate forecasts in Botswana (Thomson et al., 2006) supports the practical and routine use of seasonal forecasts for malaria control in southern Africa (DaSilva et al., 2004).
The effects of observed climate change on the geographical distribution of malaria and its transmission intensity in highland regions remains controversial. Analyses of time-series data in some sites in East Africa indicate that malaria incidence has increased in the apparent absence of climate trends (Hay et al., 2002a, b; Shanks et al., 2002). The proposed driving forces behind the malaria resurgence include drug resistance of the malaria parasite and a decrease in vector control activities. However, the validity of this conclusion has been questioned because it may have resulted from inappropriate use of the climatic data (Patz, 2002). Analysis of updated temperature data for these regions has found a significant warming trend since the end of the 1970s, with the magnitude of the change affecting transmission potential (Pascual et al., 2006). In southern Africa, long-term trends for malaria were not significantly associated with climate, although seasonal changes in case numbers were significantly associated with a number of climatic variables (Craig et al., 2004). Drug resistance and HIV infection were associated with long-term malaria trends in the same area (Craig et al., 2004).
A number of further studies have reported associations between interannual variability in temperature and malaria transmission in the African highlands. An analysis of de-trended time-series malaria data in Madagascar indicated that minimum temperature at the start of the transmission season, corresponding to the months when the human-vector contact is greatest, accounts for most of the variability between years
(Bouma, 2003). In highland areas of Kenya, malaria admissions have been associated with rainfall and unusually high maximum temperatures 3-4 months previously (Githeko and Ndegwa, 2001). An analysis of malaria morbidity data for the period from the late 1980s until the early 1990s from 50 sites across Ethiopia found that epidemics were associated with high minimum temperatures in the preceding months (Abeku et al., 2003). An analysis of data from seven highland sites in East Africa reported that short-term climate variability played a more important role than long-term trends in initiating malaria epidemics (Zhou et al., 2004,2005), although the method used to test this hypothesis has been challenged (Hay et al., 2005b).
There is no clear evidence that malaria has been affected by climate change in South America (Benitez et al., 2004) (see Chapter 1) or in continental regions of the Russian Federation (Semenov et al., 2002). The attribution of changes in human diseases to climate change must first take into account the considerable changes in reporting, surveillance, disease control measures, population changes, and other factors such as land-use change (Kovats et al., 2001; Rogers and Randolph, 2006).
Despite the known causal links between climate and malaria transmission dynamics, there is still much uncertainty about the potential impact of climate change on malaria at local and global scales (see also Section 8.4.1) because of the paucity of concurrent detailed historical observations of climate and malaria, the complexity of malaria disease dynamics, and the importance of non-climatic factors, including socio-economic development, immunity and drug resistance, in determining infection and infection outcomes. Given the large populations living in highland areas of East Africa, the limitations of the analyses conducted, and the significant health risks of epidemic malaria, further research is warranted.
Recent investigations of plague foci in North America and Asia with respect to the relationships between climatic variables, human disease cases (Enscore et al., 2002) and animal reservoirs (Stapp et al., 2004; Stenseth, 2006) have suggested that temporal variations in plague risk can be estimated by monitoring key climatic variables.
There is good evidence that diseases transmitted by rodents sometimes increase during heavy rainfall and flooding because of altered patterns of human-pathogen-rodent contact. There have been reports of flood-associated outbreaks of leptospirosis (Weil's diseases) from a wide range of countries in Central and South America and South Asia (Ko et al., 1999; Vanasco et al., 2002; Confalonieri, 2003; Ahern et al., 2005). Risk factors for leptospirosis for peri-urban populations in low-income countries include flooding of open sewers and streets during the rainy season (Sarkar et al., 2002).
Cases of hantavirus pulmonary syndrome (HPS) were first reported in Central America (Panama) in 2000, and a suggested cause was the increase in peri-domestic rodents following increased rainfall and flooding in surrounding areas (Bayard et al., 2000), although this requires further investigation. There are climate-related differences in hantavirus dynamics between northern and central Europe (Vapalahti et al., 2003; Pejoch and Kriz, 2006).
The distribution and emergence of other infectious diseases have been affected by weather and climate variability. ENSO-driven bush fires and drought, as well as land-use and land-cover changes, have caused extensive changes in the habitat of some bat species that are the natural reservoirs for the Nipah virus. The bats were driven to farms to find food (fruits), consequently shedding virus and causing an epidemic in Malaysia and neighbouring countries (Chua et al., 2000).
The distribution of schistosomiasis, a water-related parasitic disease with aquatic snails as intermediate hosts, may be affected by climatic factors. In one area of Brazil, the length of the dry season and human population density were the most important factors limiting schistosomiasis distribution and abundance (Bavia et al., 1999). Over a larger area, there was an inverse association between prevalence rates and the length of the dry period (Bavia et al., 2001). Recent studies in China indicate that the increased incidence of schistosomiasis over the past decade may in part reflect the recent warming trend. The critical 'freeze line' limits the survival of the intermediate host (Oncomelania water snails) and hence limits the transmission of the parasite Schistosoma japonicum. The freeze line has moved northwards, putting an additional 20.7 million people at risk of schistosomiasis (Yang et al., 2005b).
Changes in climate have implications for occupational health and safety. Heat stress due to high temperature and humidity is an occupational hazard that can lead to death or chronic ill-health from the after-effects of heatstroke (Wyndham, 1965; Afanas'eva et al., 1997; Adelakun et al., 1999). Both outdoor and indoor workers are at risk of heatstroke (Leithead and Lind, 1964; Samarasinghe, 2001; Shanks and Papworth, 2001). The occupations most at risk of heatstroke, based on data from the USA, include construction and agriculture/forestry/fishing work (Adelakun et al., 1999; Krake et al., 2003). Acclimatisation in tropical environments does not eliminate the risk, as evidenced by the occurrence of heatstroke in metal workers in Bangladesh (Ahasan et al., 1999) and rickshaw pullers in South Asia (OCHA, 2003). Several of the heatstroke deaths reported in the 2003 and 2006 heatwaves in Paris were associated with occupational exposure (Senat, 2004)
Hot working environments are not just a question of comfort, but a concern for health protection and the ability to perform work tasks. Working in hot environments increases the risk of diminished ability to carry out physical tasks (Kerslake, 1972), diminishes mental task ability (Ramsey, 1995), increases accident risk (Ramsey et al., 1983) and, if prolonged, may lead to heat exhaustion or heatstroke (Hales and Richards, 1987) (see Section 8.5).
Solar ultraviolet radiation (UVR) exposure causes a range of health impacts. Globally, excessive solar UVR exposure has caused the loss of approximately 1.5 million disability-adjusted life years (DALYs) (0.1% of the total global burden of disease) and 60,000 premature deaths in the year 2000. The greatest burdens result from UVR-induced cortical cataracts, cutaneous malignant melanoma, and sunburn (although the latter estimates are highly uncertain due to the paucity of data) (Pruss-Ustun et al., 2006). UVR exposure may weaken the immune response to certain vaccinations, which would reduce their effectiveness. However, there are also important health benefits: exposure to radiation in the ultraviolet B frequency band is required for the production of vitamin D in the body. Lack of sun exposure may lead to osteomalacia (rickets) and other disorders caused by vitamin D deficiencies.
Climate change will alter human exposure to UVR exposure in several ways, although the balance of effects is difficult to predict and will vary depending on location and present exposure to UVR. Greenhouse-induced cooling of the stratosphere is expected to prolong the effect of ozone-depleting gases, which will increase levels of UVR reaching some parts of the Earth's surface (Beggs, 2005; IPCC/TEAP, 2005). Climate change will alter the distribution of clouds which will, in turn, affect UVR levels at the surface. Higher ambient temperatures will influence clothing choices and time spent outdoors, potentially increasing UVR exposure in some regions and decreasing it in others. If immune function is impaired and vaccine efficacy is reduced, the effects of climate-related shifts in infections may be greater than would occur in the absence of high UVR levels (Zwander, 2002; de Gruijl et al., 2003; Holick, 2004; Gallagher and Lee, 2006; Samanek et al., 2006).
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