This is Section 15.3 of the Arctic Climate Impact Assessment.
Lead Authors: Jim Berner, Christopher Furgal; Contributing Authors: Peter Bjerregaard, Mike Bradley, Tine Curtis, Edward De Fabo, Juhani Hassi, William Keatinge, Siv Kvernmo, Simo Nayha, Hannu Rintamaki, John Warren.
Human health in northern communities is affected via a number of direct and indirect impacts of climate-related changes. “Direct impacts” refers to those health consequences resulting from direct interactions with aspects of the environment that have changed or are changing with local climate (i.e., resulting from direct interactions with physical characteristics of the environment: air, water, ice, land; and for example exposure to thermal extremes).They include such things as difficulties in dealing with heat and cold stress; alleviation of cold stress due to warmer winters; dangers associated with travel and activities on the land resulting from unpredictable weather patterns and ice conditions; and increased incidences of sunburn and rashes as a result of increased sun intensity and exposure to UV-B radiation.
The direct impacts of climate and UV radiation on human health are primarily related to extreme events, temperature, and changes induced by exposure to UV-B radiation. Much of the discussion in this section on the mechanisms involved in these potential impacts involves associations of health events with observed climate change, without assigning causality.Where the effects are understood, the mechanisms are described. However, in many instances, the exact mechanisms are not known, or the relationships between human health and climate variables are multifaceted.
Extreme events (15.3.1)
Some reports indicate that extreme weather events such as droughts, floods, and storms may become more frequent and intense in the future and there is some evidence that this is already occurring. Injury and death are the direct health impacts most often associated with natural disasters. Precipitation regimes are expected to affect the frequency and magnitude of natural processes which can potentially lead to death and injury, such as debris flow, avalanches, and rock falls.
Thunderstorms and high humidity have been associated with short-term increases in hospital admissions for respiratory and cardiovascular diseases. According to Mayer and Avis, there is controversy concerning the incidence and continuation of significant mental health problems, such as post traumatic stress disorders following natural disasters. An increase in the number of mental health disorders has been observed in the United States after natural disasters. Longer periods of extreme weather and storm events could have social impacts on communities that are isolated from regional centers and if major modes of transport are no longer available.The impacts of extreme events on everyday subsistence activities could also affect community and individual well-being.
Indigenous people throughout the Arctic have reported that the weather has become more “unpredictable” and in some cases that extreme or storm events progress more quickly today than in the past. Some northern residents report that this unpredictability limits subsistence activities and travel and increases the risks of people being trapped by weather while outside the community (see Chapter 3).
Yeah, it changes so quick now you find. Much faster than it used to… Last winter when the teacher was caught out it was perfect in the morning, then it went down flat and they couldn’t see a thing. It was like you were traveling and floating in the air, you couldn’t see the ground. Eighteen people were caught out then, and they almost froze, it was bitterly cold. Labrador hunter, as quoted in Furgal et al.
Temperature-related stress (15.3.2)
Warming is projected for some regions of the Arctic (see Chapter 4), and this may result in an increase in the number and magnitude of extreme warm days. Exposure to extreme and prolonged heat is associated with heat cramps, heat exhaustion, and heatstroke. However, because of the low mean temperature in many arctic regions, the likelihood of such events having large impacts on public health for the general population is low. Death rates are higher in winter than in summer and milder winters in some regions could actually reduce the number of deaths during winter months. However, the relationship between increased mortality and winter weather is difficult to interpret and more complex than the association between mortality and morbidity and exposure to high temperatures. For example, many winter deaths are due to respiratory infections such as influenza and it is unclear how influenza transmission would be affected by warmer winter temperatures. Some studies indicate an association between extreme temperature-related events and mortality. For these associated impacts, groups such as the elderly and people affected by cardio-respiratory problems are more vulnerable.
In North America, summer heat waves affect more urban populations than northern people, especially because of the urban heat-island effect.The impact is greater when the high temperatures (>25 ºC) are irregular and occur at the beginning of summer . Indigenous people in some regions of the Arctic are reporting incidences of stress related to temperature extremes not previously experienced. For example, shortness of breath and reduced physical activity (e.g., fishing), and an increase in respiratory discomfort.
Fewer cold days, associated with a general warming trend in some regions during winter, are reported to have the positive effect of allowing people to get out more in winter and so alleviate stress related to extreme cold. However, in Nunavik for example, approximately one to two heat waves occur every 30 years while extreme cold is much more common. In regions where heat waves do not represent a real risk for northern populations, an increase in extreme cold events could have more serious implications. According to Dufour, respiratory problems were responsible for one in seven deaths among the Inuit population of Nunavik. Muir (1991) reported that respiratory problems were the primary reason for visits to the nurse or doctor. Chronic respiratory illnesses are highly prevalent in some northern regions. For example, in Labrador, breathing problems are among the most common long-term medical conditions in adults and children. In these two northern Canadian regions, chronic respiratory illnesses could be amplified by prolonged cold events. Indirect effects of prolonged cold events could also occur as other public health problems are further aggravated. For example, spending a longer period of time in crowded and overheated houses during prolonged cold periods could affect the transmission of viral infections, especially among the elderly, the young, and the physiologically vulnerable (e.g., individuals who are immunosuppressed due to the presence of other diseases or medication). Other factors such as smoking can also modify the incidence of respiratory illnesses.
In the 1970s, scientific research focused for the first time on dramatic rises in mortality every winter, and on smaller rises in unusually hot weather. Heat-related deaths often result from severe dehydration (causing hemoconcentration) resulting from the loss of electrolytes and water in sweat and the inability to regulate body temperature. In northern Sweden, a clear association between atmospheric pressure, changing temperature, and increasing rates of cardiac events was documented. Exposure to low ambient temperatures for long periods brings specific physiological stresses. Cold exposure is part of daily working life in the Arctic. It affects human outdoor activity significantly because the arctic winter is long and cold conditions are severe. Winter, with mean temperatures of less than 0 ºC, lasts for more than seven months in some regions.
The interactions between temperature (in this case cold) and health, and the various health consequences are summarized in Fig. 15.6. Responses to cold may be normal, exaggerated (hyperreactions), or damped (hyporeactions). These result in eventual body cooling and associated impacts. In some instances, hyperreactions may occur which themselves result in disease. Climate models project that cool winter temperatures will persist in many circumpolar regions (see Chapter 4). Cold is likely to remain an environmental cause of illness and death.
Limits of human survival in the thermal environment (188.8.131.52)
Human body heat balance depends on: the thermal environment (air temperature, air velocity, air moisture, and radiative heat gain from sun or artificial sources); the thermal insulation of clothing; and the rate of physical work producing heat via metabolic pathways. For a naked human at rest, the thermoneutral air temperature is 27 ºC. In temperatures above the thermoneutral zone, heat loss is increased by sweating, and in lower temperatures, heat production is increased by muscular work (up to about 1200 W) or by shivering (up to about 500 W). By doing heavy physical work, a naked human can survive at an air temperature of about -5 ºC for several hours. The extreme limits of behavioral temperature regulation depend on available technology, but working at extreme low or high temperatures is possible with special clothing. The removal of body heat by air movement, and its practical application in designing appropriate clothing, is known as the “windchill” effect.
The effects of heat balance are usually classified in terms of five levels: comfort, discomfort, performance degradation, health effects, and tolerance. For an adequately clothed person initial cold problems start to appear at an ambient temperature of 10 ºC when fingers start to cool during light manual work. Even with heavy work, cold problems appear at between -20 and -25 ºC. For optimal manual performance, skin temperature is 32 to 36 ºC. Below a skin temperature of 13 ºC manual performance rapidly deteriorates. Marked changes in ambient temperature can increase or decrease cognitive performance or remain without effect. When effects are seen, cold particularly appears to affect the performance of complex cognitive tasks involving short-term or working memory.
Psychological, whole body, and local physiological acclimatization develops when the thermal environment is changed. Marked acclimatization can be developed within about ten days. In cold, the usual signs of acclimatization are blunted responses of the cardiovascular system (heart rate and blood pressure) and heat production (shivering). Cold-induced vasoconstriction in hands is also attenuated. Heat acclimatization involves increased sweating and earlier onset of sweating.
For healthy active people a 5 to 10 ºC decrease in temperature is not expected to result in serious effects on the maintenance of body heat balance during outdoor work. Humans can compensate for a 10 ºC decrease by wearing additional clothing or by increasing metabolic heat production by 30 to 40 W/min. If the temperature of arctic or subarctic climates increases by 5 to 10 ºC, the climate would still be cool or cold, with cold temperatures still having more impact on human physiology than heat. More serious problems could occur under extreme conditions such as during the coldest winter months in arctic or subarctic climates, if ambient temperatures decrease or the cold season increases markedly in length. There is an upper limit to the thermal insulation of winter clothing. A decrease or increase in ambient temperature, especially if the change is rapid, is a more serious threat for sick and/or elderly people than for healthy individuals capable of a physically active lifestyle.
Cold injuries (184.108.40.206)
Cold-related injuries are immediate pathological consequences of cold exposure. As a consequence of direct or indirect effects of cold, the total injury rate may increase in relation to environmental cold exposure. The rate of slip and fall injuries, for example, increases with decreasing temperature. Increasing rates of slip and fall injuries are seen at temperatures of 0 ºC and below. Low temperature is often a secondary source of injury and may not be reflected at true frequencies in statistical records. Risk of unintentional injury is least at a temperature of about 20 ºC and increases with lower and higher ambient temperatures.
Injuries such as frostbite, hypothermia, and others are linked to body cooling. Cooling injuries occur most often during winter months, especially during the few coldest winter days and are also increased by wind speed. Cooling injuries show a strong relationship with temperature, i.e., the lower the temperature the more injuries occur.The majority of cooling injuries are freezing injuries (e.g., frostbite).
Frostbite generally occurs on the most peripheral parts of the body (head, hands, feet). For the head, frostbite of the ears is almost twice as common as frostbite of the nose and cheek. Several areas of the body may be injured simultaneously. Mild frostbite most commonly occurs in the head region. Frostbite of the feet and hands frequently causes severe tissue damage and requires medical treatment or hospitalization. Young Finnish men reported a 2% annual incidence in frostbite over their lifetimes. Twenty-five percent was blister grade or more severe. In general, the incidence of frostbite varies annually from 0 to 27% among different outdoor occupations. Also, urban people experience more frostbite than rural people for the same thermal environments. Frostbites are comparable to burns in their immediate consequence. The immediate effect of frostbite can be a mild or more severe functional limitation of the injured area, requiring medical attention, and in some cases, hospitalization. The most common latent symptoms of frostbite are local hypersensitivity to cold and pain in the injured area, cold-induced sensations and disturbances in muscular function, and potentially excessive sweating. These latent symptoms may have negative impacts on occupational activities in 13 to 43% of cases. Permanent post-symptoms or invalidity commonly develop as a result of severe frostbite requiring hospitalization. Factors known to cause a predisposition to frostbite include cold-provoked white finger phenomenon, sensitivity to cold, diabetic vascular disease, psychiatric disorders, prior frostbite, older age, and tobacco smoking. Use of certain drugs or alcohol, “cold protective ointment” on the face, and inadequate clothing increase risk of frostbite during cold exposure. Accidents, fatigue, and poor nutrition are also associated with increased frostbite risk.
Cold-related diseases (220.127.116.11)
Cold-related diseases are either caused by cold or are affected by cold exposure. The rate of cooling in different sites of the human body is also modified by individual factors like cardiovascular diseases, diseases of peripheral circulation, respiratory diseases, musculoskeletal diseases, and skin diseases.
The higher incidence of cardiovascular events in colder regions and during winter is well known, and several mechanisms have been suggested based on increased blood pressure, hematological changes, and respiratory infections. Most investigations have used ecological data such as daily temperatures recorded at weather stations and mortality in the general population. Cause-specific mortality is the outcome measure most commonly used. Hospital discharge records, linked with out-of-hospital deaths, provide a powerful tool for detecting even weak effects of temperature.The association of coronary heart disease mortality and temperature is usually U-shaped, mortality being lowest within the range 10 to 20 ºC and higher either side. However, the temperature at which mortality reaches a minimum is lower in colder countries (Fig. 15.7). For example, in Yakutsk, Siberia, temperatures as low as -48 ºC had no effect on coronary mortality rates.
The increase in mortality on the colder side is about 1% per 1 ºC decrease in temperature, but the increase on the warmer side may be very steep. The exact point of the minimum temperature and the magnitude of the effect vary between countries. In Finland, the winter excess mortality from coronary heart disease has leveled off over recent decades. The share of annual mortality from cardiovascular diseases due to cold is estimated at 5 to 20%.
The detailed mechanisms by which cold is related to cardiovascular mortality, either directly or by respiratory infections or indirect effects of winter behaviors such as shoveling snow, have not been clarified. Cold exposure causes an increase in blood pressure and hemoconcentration resulting from fluid shifts, leading to coronary thromboses one to two days after cold exposure. Following the recent decline in influenza mortality, around half the excess winter deaths are now due to coronary thrombosis. These peak about two days after the coldest part of a long period of very cold weather. Around half the remaining winter deaths are due to respiratory disease, and these peak about 12 days after maximum cold days.
Cerebral vascular diseases
The association of temperature and cerebral vascular accidents is similar to that for coronary heart diseases with morbidity and mortality increasing with a decline in temperature. The pattern is often U-shaped, with some increase in numbers at warmer temperatures. The morbidity and mortality of stroke is usually lowest at temperatures of 15 to 20 ºC, however some variations exist. In northeastern Russia stroke mortality only increases at temperatures below 0 ºC.
The gradient of cerebral vascular accidents against temperature is around 1% per 1 ºC decrease in temperature, as for coronary heart diseases. In Japan, the dose– response relationship was similar for intracerebral hemorrhages and cerebral infarctions, whereas in Finland a greater winter excess was observed in the incidence of intracerebral hemorrhage than for other forms of stroke, but no gradient relative to temperature has been reported. A change in temperature of at least a two-day duration is needed for stroke mortality to rise, and the time lag between the temperature change and the maximal increase in mortality is estimated at one to four days.
The long-term trends in the effect of temperature on stroke have not been determined, but the seasonal amplitude of stroke deaths in Finland has diminished since the 1920s.The proportion of stroke-related deaths attributable to the cold season was estimated at 13% in the 1960s, but had diminished to 9% by the 1990s. A British investigation which reported a decline of 57% in the stroke-temperature gradient between 1977 and 1994 also suggested that the effect of environmental temperature on stroke is being modified by other external factors.
Common respiratory cold-related symptoms are watery rhinitis, and as a consequence of constriction of the bronchi, asthma-like symptoms which include wheezing, coughing, and breathing difficulties. Deaths related to respiratory diseases, primarily pneumonia, increase significantly during the winter months. Watery rhinitis is a physiological irritation response to cold air inhalation and is harmless.
The prevalence of breathing problems provoked by exercise and/or cold weather is high among asthmatic subjects (81.6%) and significantly elevated among allergic subjects (45.1%) and people with chronic obstructive pulmonary disease (74.6%). For people with no known respiratory disease, the prevalence is 10.0%.The risk of chronic bronchitis and bronchitic symptoms at the population scale is elevated in outdoor workers in some populations, but is not elevated in regular recreational crosscountry skiers, and the risk of developing asthma is not significantly elevated by regular exercise or work in cold climates. Constriction of the laryngeal area is a momentary reflex in response to cold air and is usually harmless. In very exceptional cases of the disease, known as cold urticaria, this phenomenon may be life-threatening. Air quality and behavioral choices such as smoking are also major influences on the incidence of respiratory diseases.
Peripheral circulatory diseases
The normal responses of the peripheral circulatory system to cold stress can be affected in individuals with vascular diseases. Thermal comfort and physical performance may be decreased and risk of cold injury may be increased. In advanced stages of peripheral arteriolosclerosis, blood vessels are narrowed. Further constriction caused by cold exposure may increase risk of frostbite. A reversible episodic constriction of the blood vessels in fingers and toes is a fairly common pathological response to cold exposure and is known as the Raynaud’s phenomenon. Owing to the constriction of the blood vessels, the blood flow in fingers and toes is markedly reduced at temperatures colder than 10 ºC. Originally, Raynaud’s phenomenon was described as episodic white fingers provoked by cold or other stress factors, together or alone. The population prevalence is 5 to 30% and is related to gender, age, and region of residence. As a clinically significant condition, it has a reported prevalence of 2 to 6%. Cold exposure in a patient with the condition may result in a cluster of different symptoms caused by transient constrictions occurring in the circulation of the heart, lung, kidneys, or brains. The symptoms may vary widely and can include migraine headaches, chest pain, and possible visual effects.
The most familiar and common abnormal skin reaction related to cold exposure is cold urticaria. It is usually a chronic condition and is often provoked by some other physical agent. Symptoms usually occur locally on exposed areas of skin. They sometimes appear during cold exposure but more frequently appear when the skin re-warms after cooling and then disappear again after 20 to 30 minutes. Fifteen percent of the population is subject to symptoms at some stage and the annual average prevalence in Finland is 2 to 4%. Cold urticaria lasts from months to several years. Prevalence of hospitalization for severely affected patients is only around one in 4000. In cold urticaria, skin reaction to cold exposure is characterized by erythema, swelling, wheals, or papules. Other symptoms on cold exposure can be more severe, such as vertigo, headache, nausea, vomiting, tachycardia, dyspnea, flushing, faintness, or rarely, life-threatening anaphylactic shock.
Musculoskeletal diseases and symptoms
There is limited scientific understanding of the relationship between musculoskeletal diseases and cold. Extensor tenosynovitis has been described with windy cold exposure in temperatures from 0 to -25 ºC.The increased incidence of tenosynovitis in female food industry workers was attributed to the low ambient temperature. Local cold exposure in a frozen food factory was associated with a ten times higher incidence of carpal tunnel syndrome than in warm environments. Symptoms of musculoskeletal diseases can vary, and include local or generalized feelings of pain and fatigue of muscles and joints. Low back pain, knee pain, and shoulder pain were significantly more common in cold storage workers than in a thermoneutral environment and were dependent on the duration of the work in the cold environment.
Cold-related immune effects
Cold temperatures and isolation can be immunosuppressive and, in humans who have over-wintered in the Antarctic, suppression of cell-mediated immunity is well documented.The effect of sunlight-induced immunosuppression above (or concomitant with) this temperature/isolation induced immunosuppression remains to be determined.
Changes in the frequency or intensity of natural disasters or extreme weather events can have direct and indirect impacts on human health in the Arctic. In remote locations this is accentuated by a reduced capacity to respond to these events because of the isolated nature of the communities and the often limited health infrastructure present.The variability of such events is likely to increase with future climate changes. Changes in temperature have the potential to influence health in arctic communities in both negative and positive ways. With the low mean annual temperature in many arctic regions, the likelihood of heat events having large health impacts on the general population is low. However, the impacts of these events on individuals with respiratory problems and other conditions can be serious. Fewer colder days associated with winter warming in some regions may actually have several positive health impacts. Impacts of cold temperature are well known and increases in the length or magnitude of extreme cold periods in some regions may have significant negative impacts on the general population, especially for individuals with conditions making them more susceptible to such exposure. Under any climate change scenario, temperature will continue to influence the health of arctic populations both directly and indirectly.
UV-B radiation and arctic human health (15.3.3)
Stratospheric ozone loss has been observed during the winter/spring months over most of the Arctic since the early 1990s. Losses of up to 40% have been recorded in Scandinavia and Siberia, and in Canada, sporadic losses of 10 to 20% or more have been reported. The daily total ozone level in March 1997 at Point Barrow (71.3º N) in Alaska was about 6% below the previous ten-year average, and on 17–18 March 1999, Barrow experienced record low ozone levels for that location in March.
During winter and spring 2001/02, the mean March stratospheric ozone levels show a 5 to 15% loss of ozone compared to the average March value for 1979 to 1986.The 2002/03 winter also had low total ozone values over parts of the Arctic. The decrease was greater than for the previous two winters, but not as great as in the 1990s. During the winter months of 2002/03 (December, January, February, and March) parts of the Arctic, mainly but not limited to Siberia and Scandinavia, had levels up to 45% lower than comparable values for the same area in the early 1980s. Recent data indicate widely diverse ozone losses continuing throughout the year. Figure 15.8 shows the March 2003 anomalies for stratospheric ozone relative to the average March values for 1979 to 1986.
Figure 15.9 shows the large decline in average total ozone values in March over the Arctic (63º–90º N) during the 1990s. McKenzie et al. presented some of the strongest data to date regarding the relationship between ozone loss and increased levels of UV-B radiation. Although their data are for the southern hemisphere the same relationship is highly likely to occur in the Arctic. The data, which reflect ozone levels for the austral summers between 1978/79 and 1998/99 and UV-B radiation levels for the austral summers between 1989/90 and 1998/99 at 45º S (Fig. 15.10), provide strong evidence for increases in UV-B radiation levels in areas where baseline levels were already high, suggesting that man-made perturbations to the ozone layer are occurring as predicted (see also Chapter 5).
UV-B related human health effects include increases in the incidence of skin cancer, potential effects associated with increased suppression of the immune system including weakened resistance to some types of infectious disease, and increased incidence of cataracts as well as changes in Vitamin D3 production in the skin. In the Arctic, increases in UV-B radiation may also interact with other environmental stressors such as chemical pollutants, cold temperature, isolation, and viral illnesses in some populations.The rest of this section describes potential UV-B related health effects.
Ultraviolet-B radiation can initiate a selective down regulation of cell-mediated immunity in mammals, including humans. It is speculated that this may be a natural regulatory mechanism, selected through evolutionary pressure, to prevent autoimmune attack on sunlightdamaged skin. The unusual feature of UV-B-induced immunosuppression is that it redirects cell-mediated immunity to sensitizing antigens from an up or “effector” type response to a down or “suppressor” type response. These antigens can include chemical, viral, and tumor antigens. Significantly, skin pigmentation is not an efficient protection factor against UV-B induced immune suppression. Immunosuppressive effects of UV-B radiation play an important role in UV-B induced skin cancer by preventing the destruction of highly antigenic skin cancers by the immune system.
An in vivo wavelength dependence study by De Fabo and Noonan, for immune suppression of contact hypersensitivity in mice has identified a lightabsorbing substance, residing on skin, as transurocanic acid (UCA). The cis structure of UCA (cis-UCA) formed upon absorption of light by trans- UCA, is known to cause immunosuppression in humans similar to that in mice caused by UV-B radiation. In addition to sunlight modulation of cell-mediated immunity, which may involve susceptibility to certain infectious diseases, cis-UCA may be important for arctic populations for another reason. A recent report indicated that a binding receptor for cis-UCA has been identified as the neurotransmitter 5-hydroxytryptamine, or 5HT (Serotonin). Lack of sunlight is known to play a role in mood disorders, among other factors, in arctic populations. Future studies are needed on the role of UCA in human immunity, as well as on mood disorders linked to sunlight deprivation. Box 15.2 describes the action spectra and biological amplification of UV radiation.
Genetically determined susceptibilities to UV-induced immunosuppression have been shown to exist and appear to be controlled by several interacting Uvs genes involving autosomal and X-linked genes. Such an interaction for UV-immunosuppression had not been described previously and may be unique for this mechanism. A genetically determined high susceptibility to UV-induced immunosuppression may be an important risk factor for UVrelated human diseases not just in arctic populations but in other populations as well.
Skin cancer (18.104.22.168)
Immunosuppressive effects of UV-B radiation play an important role in UV-induced skin cancer by preventing the destruction of highly antigenic skin cancers by the immune system. There are three main types of skin cancer.Two tend not to metastasize and are known as basal and squamous cell carcinoma, and are often referred to collectively as nonmelanoma skin cancer. The third type, which shows a higher mortality, and which can metastasize aggressively, is malignant melanoma of which several subtypes exist. It should be noted however that any potential increase in skin cancer incidence related to reflectance from snow is likely to be mitigated by the projected decrease in snow cover.
There is much experimental evidence of a clear connection between sunlight exposure and non-melanoma skin cancer, and which implicates UV-B radiation as a carcinogen. A relationship between sunlight and malignant melanoma, while less clear, is considered a near certainty. Epidemiological evidence indicates that sporadic or intermittent sunlight exposure can be a very important factor in malignant melanoma development, especially in childhood. But not all sunburn leads to melanoma, as other predisposing factors are needed.The molecular mechanisms underlying the relationship between malignant melanoma and exposure to UV radiation, particularly wavelength specific mechanisms, such as the importance of UV-B radiation, as opposed to UV-A radiation are, at present, unclear. To help clarify these mechanistic pathways, recent developments include, among others, the genetic engineering of a transgenic mouse capable of producing melanoma tumors following UV radiation of neonatal animals. These tumors show a striking similarity to human melanoma. Once the active waveband for melanoma induction is identified, an action spectrum can be constructed. A skin cancer action spectrum has been used to predict increases in nonmelanoma skin cancer by increased UV-B radiation resulting from ozone destruction between 1979 and 1994.
In the Arctic, skin cancer rates are in general low. This is due primarily to the low UV-B radiation levels relative to equatorial regions. Also, skin cancer is rare in arctic indigenous populations consistent with findings elsewhere that skin pigmentation is protective against skin cancer. A recent study, however, involving Danes working in Greenland and cancer risk indicated an elevated risk of melanoma in females. A role for excessive UV radiation exposure in this regard has been suggested.With increasing numbers of non-indigenous people living in the Arctic, the incidence of melanoma and non-melanoma skin cancer must be carefully monitored in both groups. Some indigenous groups in the Arctic are reporting evidence of increased UV-B radiation exposure and are experiencing skin rashes and burns for the first time.
They report a sense that the “sun is hotter”(see also Chapter 3).
The sun burns us easily, it was not very hot in the past. Kuujjuaq, man aged 62 as quoted in Furgal et al.,
The sun was not that hot in the past. Nowadays, it's really hot. My skin burns when I'm out for a while. Sometimes, we stay indoors in a shack. Kuujjuaq, man aged 70 as quoted in Furgal et al.
Non-Hodgkin’s lymphoma (22.214.171.124)
Certain epidemiological evidence suggests a link between non-Hodgkin’s lymphoma and sunlight exposure. This is suggested to be via the immunosuppressive effects of UV-B radiation. A correlation between the occurrence of skin cancer and the occurrence of non-Hodgkin’s lymphoma has also been described. However, in contrast to non-melanoma skin cancer, non-Hodgkin’s lymphoma does not show a latitudinal gradient in the United States, suggesting that UV-B radiation may be a cofactor rather than a primary causative agent of this disease. Danish women working in Greenland are reported to show an excess of lymphatic malignancies, which raises the question of a role for excess UV-B radiation. Autoimmune diseases such as Type-I diabetes and multiple sclerosis may also have an immunosuppressive connection with UV-B radiation. The continued reports regarding correlations between health problems and UV radiation indicate the need for further investigation in relation to ozone loss over the Arctic.
Box 15.2. Action spectra and biological amplification of UV radiation
Photobiological responses are by definition wavelength dependent. However, to compare the biologically-inducing activity of the many spectrally different sources available, from sunlight to sun tanning lamps, it is necessary to consider differences in wavelength efficiency in initiating the biological response, whether it is skin cancer, sunburn, photosynthesis, or immune suppression. In order to make such comparisons, it is necessary to calculate, and then deliver “biologically effective” doses from the optical source. Differences in wavelength efficiency can be accounted for by using an appropriate wavelength-dependence or “action spectrum”. An action spectrum describes the relative efficiency of radiation at different wavelengths to produce a given effect. Health effects experts, for example, rely upon action spectra to provide information regarding which wavelengths in the full spectrum of sunlight or the full spectrum of artificial sunlamps cause sunburn, or DNA damage, or immune suppression. Once experimentally derived, the action spectrum can be multiplied by the spectral output of any given source. In the case of sunburn, the International Commission on Illumination action spectrum for erythema is used to calculate the UV Index, a measure of sun burning effectiveness used worldwide.
Action spectra are also useful in determining increases in biologically effective UV radiation doses due to ozone depletion, known as the “radiation amplification factor” (RAF), and how these increases in UV-B radiation result in “biological amplification” for a given response. For example, to predict changes in skin cancer incidence as a function of stratospheric ozone depletion, two processes are necessary. First, the increase in biologically effective UV-B radiation that results from an ozone loss of 1% must be determined, i.e., the RAF. Second, the ratio of the percentage change in biological effect to the proportional change in biologically effective irradiance – the BAF – needs to be determined.Thus, the total amplification factor for the biological impact is a product of the two: amplification factor = RAF x BAF. More detailed information on ozone depletion, skin cancer, and RAF/BAF determinations is reported by Moan et al., Jones, and Strzhizhovskii.
In addition to providing a weighting function to determine biologically-effective doses, action spectra are useful for helping to identify the initial light-absorbing photoreceptor responsible for triggering a light-driven biological response. Such information can help direct further research on a given photobiological response.
Cataract is a major cause of blindness. In 2002, there were an estimated 180 million people worldwide who were visually disabled. Between 40 and 45 million people are blind. Epidemiological reports and experimental studies indicate that cataract formation is a complicated process with many associated risk factors.The precise mechanism of action is not known although UV-B radiation is very strongly implicated and associations with latitude and climatically different countries have been reported. Furthermore, a recent action spectrum indicated that after correcting for corneal transmittance, the biological sensitivity of the rat lens to UV-B is at least as great at 295 nm as at 300 nm. After correcting for transmittance by the atmosphere, UV-B at 305 nm is suggested to be the most likely wave band to damage the rat lens.
Several types of cataract exist with a varying degree of association with sunlight. Published evidence tends to support the concept that cortical cataract is more likely to be related to UV-B radiation. Another study, however, suggests the opposite when lifetime cumulative UV-B radiation exposure and exposure after teenage years are considered, underscoring the need for further study including detailed wavelength or action spectrum studies on cataract.The importance of dietary factors and cataract also requires further research.
Vitamin D (126.96.36.199)
Vitamin D (calciferol) is a fat-soluble vitamin. It is present in food, but can also be made in human skin after exposure to UV-B radiation from the sun. In general, skin synthesis provides most of the vitamin D to the body (80 to 100%) and with adequate sunlight exposure, dietary vitamin D may be unnecessary.
Many factors can affect vitamin D production such as season, latitude, age, skin color, time spent outdoors, and sun angle. Few foods contain significant amounts of vitamin D that can act as a substitute for sunshine exposure. Fish with a high fat content, such as sardines, salmon, herring, and mackerel are excellent sources of vitamin D. Other important sources are meat, milk, eggs, and fortified foodstuffs. Fortified foodstuffs however, may not be sufficient to preclude the need for sunlight exposure. In one study it was reported that darkskinned, veiled, pregnant women, their infants, and elderly in residential care had the highest vitamin D deficiency of subjects studied.This suggests that vitamin D deficiency may be a bigger risk factor in populations worldwide when other factors reducing exposure to sunlight are considered e.g., arctic populations during long, dark winters. A balance is thus needed between sunshine exposure and risk of excessive sunlight leading to skin cancer or other UV-B related health effects, or insufficient sunlight exposure and hence vitamin D deficiency for diseases such as rickets and certain non-skeletal diseases.
Vitamin D exists in several forms, each with a different activity, and is involved in a large variety of biological functions, including regulatory functions. Briefly, the liver and kidney help convert vitamin D to its active hormone form (calcitriol). For example, in skin vitamin D is produced from UV-B-induced photoconversion of 7-dehydrocholesterol (7-DHC; provitamin D).Vitamin D then undergoes hydroxylation to calcidiol (25-OHD3) in the liver and becomes the major circulating form, and then to calcitriol (vitamin D3 hormone; 1alpha 25-(OH)2D3) in the kidney. 1alpha, 25-(OH)2D3 is carried systemically to distal target organs where it binds to a vast array of nuclear receptors to generate its appropriate biological response.Vitamin D appears, therefore, to be involved in various aspects of fundamental cell regulation.
The major function of vitamin D is to maintain normal blood levels of calcium and phosphorus.Vitamin D aids calcium absorption, helping to form and maintain a strong skeletal structure. Without vitamin D, bones can become thin, brittle, soft, or deformed.Vitamin D prevents rickets in children and osteomalacia in adults, which are skeletal diseases that result in defects that weaken bones. A recent study reports for the first time a link between UV-B radiation exposure and calcitriol synthesis in human skin.
Given the six months of darkness in winter followed in spring/summer by potential excess exposure to UV-B radiation due to ozone depletion, studies in arctic communities on UV-B induction of vitamin D in liver and kidney and vitamin D hormone in skin are of high priority.
Other factors (188.8.131.52)
Many types of pollutant have been identified in arctic biota and the arctic environment, including polyaromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), and heavy metals.There is some evidence of interaction between UV-B radiation and chemical pollutants. For example, aquatic organisms that have ingested UV-B-absorbing PAHs have been shown to exhibit phototoxic effects following exposure to UV-B radiation. A number of persistent organic pollutants, including PCBs, are immunologically damaging even without exposure to UV-B radiation. At present there is little information on the potential for the combined effects of these agents or on immunosuppression from exposure to UV-B radiation alone. In view of such findings and the high levels of persistent organic pollutants in areas of the Arctic, research is required on the combined effects of UV-B radiation, PAHs, and PCBs.
Diet may also be important in UV-B effects in arctic populations. Experimental evidence shows that UVrelated immunosuppression in mice can be increased by increasing dietary histidine and correlates with a modulating increase in trans-urocanic acid. High levels of dietary fat have also been demonstrated to enhance UV-induced immunosuppression in experimental systems and may be a factor in arctic populations as well as high histidine levels in some species of fish and seal.
Activation of viruses by UV radiation is well-documented. Indigenous populations appear predisposed to cancers such as nasopharyngeal and salivary gland cancer.These cancers are thought to be associated with the high viral load in these populations, and genetic factors also appear to be involved. Salivary gland cancer has been linked to UV radiation exposure in several studies on non-arctic populations although a latitude gradient has not been demonstrated. UV-B radiation may be a cofactor. Herpes simplex virus (HSV) is found in all races, cultures, and continents. The virus affects 80 to 90% of the world’s population. Most people have herpes simplex as cold sores or genital herpes. In experimental animal models UV-B radiation was shown to release immune inhibition on HSV expression and lead to HSV manifestation. A similar effect may occur in the human population.Whether enhanced levels of UV-B radiation due to ozone depletion will exacerbate HSV or other viral infections in the arctic population remains to be determined.
The emergence of new infectious diseases and the reemergence of old infectious diseases is also an issue in the Arctic. Given an association between the lowering of resistance to some infectious diseases by UV-B induced immunosuppression in experimental animal systems, plus a lowering of the cellular immune response against hepatitis B vaccination in humans by urocanic acid (section 184.108.40.206), attention to increases in infectious diseases as a consequence of increased exposure to UV-B due to ozone depletion is of high priority.
A lack of detailed information on human health effects due to increased exposure to UV-B radiation in the Arctic precludes an evaluation of risk assessment at present. Skin cancer appears to be a low risk phenomenon in the Arctic particularly in indigenous populations. However, given the long-term likelihood of ozone loss and increased levels of UV-B radiation, it is not clear how long this low risk will be maintained. Indigenous and non-indigenous populations should both be monitored routinely for skin cancers, cataracts, and precursors to such conditions. The effect of UV-B induced immune suppression, alone or in combination with arctic stressors and pollutants, on human or animal populations is also unknown. The implications of increased UV-B exposure on the incidence of viral and infectious diseases in arctic populations need to be addressed. Also, understanding of the interactions between UV-B radiation, pollutants, and traditional diets requires significant effort in the future. Population effects related to UV-B health effects following stratospheric ozone depletion is a major research topic for the Arctic as the stratospheric ozone layer will remain vulnerable for the next decade or so even with full compliance with the Montreal Protocol.
Chapter 15: Human Health
15.2. Socio-cultural conditions, health status, and demography
15.3. Potential impacts of direct mechanisms of climate change on human health
15.4. Potential impacts of indirect mechanisms of climate change on human health
15.5. Environmental change and social, cultural, and mental health
15.6. Developing a community response to climate change and health
15.7. Conclusions and recommendations
- ^Donaldson, G.C.,W.R. Keatinge and S. Nayha, 2003. Changes in summer temperature and heat-related mortality since 1971 in North Carolina, South Finland, and Southeast England. Environmental Research, 91(1):1–7.
- ^data provided by NOAA National Weather Service, 2003. http://www.cpc.ncep.noaa.gov/products/stratosphere/sbuv2to/sbuv2to_anom.html.
- ^1971 and 1972 data are from the BUV instrument on the Nimbus-4 satellite; 1979–1993 data are from the Total Ozone Mapping Spectrometer (TOMS) on Nimbus-7; 1994 data are from the TOMS on Meteor-3; 1996 data are from the SBUV/2 on NOAA-9; 1997 data are from the TOMS on the Earth Probe satellite. (http://www.cmdl.noaa.gov/star/arcticuv2.html)
- ^McKenzie, R., B. Connor and G. Bodeker, 1999. Increased summertime UV radiation in New Zealand in response to ozone loss. Science, 285:1709–1711.
- ^Haines, A. and A.J. McMichael, 1997. Climate change and health: implications for research, monitoring, and policy. British Medical Journal, 315(7112):870–874.
- ^Krupnik, I. and D. Jolly (eds.), 2002.The Earth is Faster Now: Indigenous Observations of Arctic Environmental Change. Arctic Research Consortium of the United States, Fairbanks, Alaska, 384pp.
- ^Koshida, G. and W.Avis, 1998. Étude pan-canadienne sur les impacts et l’adaptation à la variabilité et au changement climatiques.Tome VII: Questions sectorielles.
- ^Kovats, R.S., B. Menne, A.J. McMichael, C. Corvalan and R. Bertollini, 2000. Climate Change and Human Health: Impact and Adaptation. World Health Organization, 48pp.
- ^Mayer, N. and W.Avis (eds.), 1997. Canada Country Study: Climate Impacts and Adaptations, National Cross Cutting Issues,Volume VIII, Cat. No En56-119/7-1997E.
^Fox, S., 2002.These are things that are really happening. In: I. Krupnik and D. Jolly (eds.).The Earth is Faster Now: Indigenous Observations of Arctic Environmental Change, pp. 12–53. Arctic Research Consortium of the United States, Fairbanks, Alaska;
-- Furgal, C., D. Martin and P. Gosselin, 2002. Climate change and health in Nunavik and Labrador: lessons from Inuit knowledge. In: I. Krupnik and D. Jolly (eds.).The Earth is Faster Now: Indigenous Observations of Arctic Environmental Change, pp. 266–300. Arctic Research Consortium of the United States, Fairbanks, Alaska;
-- Krupnik and Jolly, 2002, Op. cit
- ^ Ibid.
- ^Furgal et al., 2002, Op. cit.
^ (Haines and McMichael, 1997;
--Patz, J.A., M.A. McGiihin, S.M. Bernhard, K.L. Ebi, Epstein, P.R.A. Grambsch, D.J. Gubler, P. Rieter, I. Romieu, J.B. Rose, J.M. Samet and J.Trtanj, 2000.The potential health impacts of climate variability and change for the United States: Executive Summary of the report of the health sector of the U.S. national assessment. Environmental Health Perspectives online, http://ehp.niehs.nih.gov/topic/global/patz-full.html.
- ^Patz et al., 2000, Op. cit
- ^ Kovats et al., 2000, Op. cit.
- ^Thouez, J.P.M., B. Singh, P. André and C. Bryant, 1998. Le réchauffement du climat terrestre et les impacts potentiels en géographie des maladies.The Canadian Geographer, 42(1):78–85.
- ^Furgal et al., 2002, Op. cit.
- ^Furgal et al., 2002, Op. cit.
- ^Dufour, R., 1991. La documentation du cancer au Nunavik. DSC du Centre hospitalier de l’Université Laval, 43pp.
- ^Muir, B.L., 1991. L’état de santé des Indiens et des Inuit du Canada Santé et Bien-être social Canada, Santé Canada, Ottawa, 64pp.
- ^LIA, 1997. Environmental Health Study. Final Report. Labrador Inuit Association, Nain, Labrador.
- ^Messner,T.,V. Lundberg and B.Wikstrom, 2003.The Arctic Oscillation and incidence of acute myocardial infarction. Journal of Internal Medicine, 253(6):666–670.
- ^ e.g., Parsons, K.C., 1993. Human Thermal Environments.The Effects of Hot, Moderate and Cold Environments on Human Health, Comfort and Performance.Taylor and Francis.
- ^Quayle, R.G. and Steadman, R.G., 1998.The Steadman windchill: an improvement over present scaling.Weather and Forecasting 13:1187–1193.
- ^Lotens,W.A., 1988. Comparison of predictive models for clothed humans.ASHRAE Transactions, 94:1321–1340.
- ^Palinkas, L.A., 2001. Mental and cognitive performance in the cold. International Journal of Circumpolar Health, 60(3):430–439.
- ^ e.g., Rintamäki, H., 2001. Human cold acclimatization and acclimation. International Journal of Circumpolar Health, 60(3):422–429.
- ^Taylor, M.S., 1992. Cold weather injuries during peacetime military training. Military Medicine, 157(11):602-60-4.
- ^ Ramsey, J.G., C.L. Burford, M.Y. Beshir and R.C. Jensen, 1983. Effects of workplace thermal conditions on safe work behavior. Journal of Safety Research, 14:105–114.
- ^Miller, B.J. and L.R. Chasmar, 1980. Frostbite in Saskatoon: a review of 10 winters. Canadian Journal of Surgery, 23(5):423–426.
- ^Hassi, J and T.M. Mäkinen, 2000. Frostbite: occurrence, risk factors and consequences. International Journal of Circumpolar Health, 59(2):92–98.
- ^Lehmuskallio, E., 1999. Cold protecting ointments and frostbite. A questionnaire study of 830 conscripts in Finland. Acta Dermato-Venereologica, 79(1):67–70.
- ^Keatinge,W.R., 1991. Global warming and health. British Medical Journal, 302:965–966
^Donaldson, G.C.,V.E.Tchernjavskii, S.P. Ermakov, K. Bucher and W.R. Keatinge, 1998a.Winter mortality and cold stress in Yekaterinburg, Russia: interview study. British Medical Journal, 316:514–518.;
-- Näyhä, S., 2002. Cold and the risk cardiovascular diseases. A review. International Journal of Circumpolar Health, 61:373–380.
- ^ Ibid.
- ^Donaldson, G.C. and W.R. Keatinge, 1999. Mortality related to cold weather in elderly people in southeast England, 1979–94. British Medical Journal, 315:1055–1056
- ^Maricq, H.R., P.H. Carpenter, M.C.Weinrich, J.E. Keil, A. Franco, P. Dronet, O.C.M. Poncot and M.V. Maines, 1993. Geographic Variation in the Prevalence of Raynaud’s Phenomenon: Charleston, SC, USA, vs Taentaise, Savoie, France. Journal of Rheumatology, 20:70–76.
- ^Georgitis, J., 1978. Extensor tenosynovitis of the hand from cold exposure. Journal of the Maine Medical Association, 69(4):129–131.
^ Chen, F.Li.T., H. Huang and I. Holmer, 1991. A field study of cold effects among cold store workers in China. Arctic Medical Research, 50(suppl6):99–103.
-- Chiang, H-C.,Y-C. Ko, S-S Chen,T-N.Wu and P-Y. Chang, 1993. Prevalence of shoulder and upper limb disorders among workers in the fish-processing industry. Scandinavian Journal of Work Environment and Health, 19:126–131.
- ^ Chiang H-C., S-S. Chen, H-S.Yu and Y-C. Ko, 1990.The occurrence of carpal tunnel syndrome in frozen food factory employees. Kae Hsiung I Hsueh Tsa Chih, 6(2):73–89.
^Ando, M., 1990. Risk evaluation of stratospheric ozone depletion resulting from chlorofluorocarbons (CFC) on human health. Nippon Eiseigaku Zasshi, 45:947–953. (Abstract in English);
-- Muller, H.K., D.J. Lugg and D.L.Williams, 1988. Cutaneous immune responses in Antarctica. A reflection of immune status? Arctic Medical Research, 47(suppl 1):249–251.;
-- Tingate,T.R., D.J. Lugg, H.K. Muller, R.P. Stowe and D.L. Pierson, 1997. Antarctic isolation: immune and viral studies. Immunology and Cell Biology, 75:275–283.
- ^ NOAA National Weather Service, 2003. http://www.cpc.ncep.noaa.gov/products/stratosphere/sbuv2to/sbuv2to_anom.html
- ^McKenzie, R., B. Connor and G. Bodeker, 1999. Increased summertime UV radiation in New Zealand in response to ozone loss. Science, 285:1709–1711.
- ^Sleijffers, A., J. Garssen and H.Van Loveren, 2002. Ultraviolet radiation, resistance to infectious diseases, and vaccination responses. Methods, 28:111–121.
- ^IASC, 1995. Effects of increased ultraviolet radiation in the Arctic: an interdisciplinary report on the state of knowledge and research needed. 2, 1–56. International Arctic Science Committee, Washington, D.C.
- ^ Ibid.
- ^ De Fabo, E.C. and F.P. Noonan, 1983. Mechanism of immune suppression by ultraviolet irradiation in vivo. I. Evidence for the existence of a unique photoreceptor in skin and its role in photoimmunology. Journal of Experimental Medicine, 158:84–98.
- ^Noonan, F.P. and E.C. De Fabo, 1992. Immunosuppression by ultraviolet B radiation: initiation by urocanic acid. Immunology Today, 13:250–254.
^De Fabo, E.C. and M.L. Kripke, 1979. Dose-response characteristics of immunologic unresponsiveness to UV-induced tumors produced by UV irradiation of mice. Photochemistry and Photobiology, 30:385–390.
-- De Fabo, E. and M. Kripke, 1980.Wavelength dependence and dose-rate independence of UV radiation-induced immunologic unresponsiveness of mice to a UV-induced fibrosarcoma. Photochemistry and Photobiology, 32:183–188.
- ^De Fabo, E.C. and F.P. Noonan, 1983, Op. cit.
- ^ van Strien, G.A. and M.J. Korstanje, 1995.Treatment of contact hypersensitivity with urocanic acid. Archives of Dermatological Research, 287:564–566.
- ^ Sleijffers et al., 2002, Op. cit.
^Nghiem, D.X., J.P.Walterscheid, N. Kazimi and S.E. Ullrich, 2002. Ultraviolet radiation-induced immunosuppression of delayed-type hypersensitivity in mice. Methods, 28(1):25–33.
-- Walterscheid, J.P., D.X. Nghiem and S.E. Ullrich, 2002. Determining the role of cytokines in UV-induced immunomodulation. Methods, 28(1):71–78
- ^Nilssen, O., R. Lipton,T. Brenn, G. Hoyer, E. Boiko and A.Tkatchev, 1997. Sleeping problems at 78 degrees north: the Svalbard Study. Acta Psychiatrica Scandinavica, 95:44–48.
- ^Näyhä, S., E.Vaisanen and J. Hassi, 1994. Season and mental illness in an Arctic area of northern Finland. Acta Psychiatrica Scandinavica, 377:46–49.
^ Nilssen, O.,T. Brenn, G. Hoyer, R. Lipton, J. Boiko and A.Tkatchev, 1999. Self-reported seasonal variation in depression at 78 degree north.The Svalbard Study. International Journal of Circumpolar
- ^Noonan, F.P. and H.A. Hoffman, 1994. Control of UV-B immunosuppression in the mouse by autosomal and sex-linked factors. Immunogenetics, 40:247–256.
- ^ De Fabo and Kripke, 1979, 1980, Op. cit.
^ Fears,T., J. Scotto and M. Schneiderman, 1976. Skin cancer, melanoma, and sunlight. American Journal of Public Health, 66:461–464.;
-- McGovern,V., M. Mihm, C. Bailly, J. Booth,W. Clark, A. Cochran, E. Hardy, J. Hicks, A. Levene, M. Lewis, J. Little and G. Milton, 1973. The classification of malignant melanoma and its histologic reporting. Cancer, 32(6):1446–1457.
^ Armstrong, B.K., A. Kricker and D.R. English, 1997. Sun exposure and skin cancer. Australasian Journal of Dermatology, 38:S1–S6.;
-- Fears et al., 1976, Op. cit.;
-- Parsons, P. and P. Musk, 1982.Toxicity, DNA damage and inhibition of DNA repair synthesis in human melanoma cells by concentrated sunlight. Photochemistry and Photobiology, 36:439–445.
^ Armstrong, B.K. and A. Kricker, 1993. How much melanoma is caused by sun exposure? Melanoma Research, 3(6):395–401.;
-- Berwick, M., 2000. Gene-environment interaction in melanoma. Forum (Genova), 10:191–200.;
-- Bulliard, J.L., 2000. Site-specific risk of cutaneous malignant melanoma and pattern of sun exposure in New Zealand. International Journal of Cancer, 85:627–632.;
-- Fears et al., 1976, Op. cit.;
-- Jemal, A., S.S. Devesa, P. Hartge and M.A.Tucker, 2001. Recent trends in cutaneous melanoma incidence among whites in the United States. Journal of the National Cancer Institute, 93(9):678–683.;
-- Mack,T.M. and B. Floderus, 1991. Malignant melanoma risk by nativity, place of residence at diagnosis, and age at migration. Cancer Causes and Control, 2:401–411.
- ^ Autier, P., J.F. Dore, O. Gefeller, J.P. Cesarini, F. Lejeune, K.F. Koelmel, D. Lienard and U.R. Kleeberg, 1997. Melanoma risk and residence in sunny areas. British Journal of Cancer, 76(11):1521–1524.
- ^ Noonan, F.P., J.A. Recio, H.Takayama, P. Duray and M.R. Anaver, 2001. Neonatal sunburn and melanoma in mice. Nature, 413(6853):271–2.
- ^ Slaper, H., G.J.Velders, J.S. Daniel, F.R. de Gruijl and J.C.Van der Leun, 1996. Estimates of ozone depletion and skin cancer incidence to examine the Vienna Convention achievements. Nature, 384:256–258.
- ^ Nielsen, L.G., M. Frisch and F. Melchers, 1997. Cancer risk in a cohort of Danes working in Greenland. Scandinavian Journal of Social Medicine, 25:44–49.
^ Fox, S., 2002.Op. cit.;
-- Furgal et al., 2002, Op. cit.
- ^ Furgal et al., 2002, Op. cit.
^Langford, I.H., G. Bentham and A.L. McDonald, 1998. Mortality from non-Hodgkin lymphoma and UV exposure in the European Community. Health and Place, 4:355–364.;
-- Zheng and Owens, 2000)
^ Langford et al., 1998, Op. cit.;
-- McKenna, D.B.,V.R. Doherty, K.M. McLaren and J.A. Hunter, 2000. Malignant melanoma and lymphoproliferative malignancy: is there a shared aetiology? British Journal of Dermatology, 143:171–173.;
-- McMichael, A.J. and G.G. Giles, 1996. Have increases in solar ultraviolet exposure contributed to the rise in incidence of non-Hodgkin’s lymphoma? British Journal of Cancer, 73:945–950.;
-- Zheng and Owens, 2000, Op. cit.
- ^ Cliff, S. and P.S. Mortimer, 1999. Skin cancer and non-Hodgkins lymphoproliferative diseases: is sunlight to blame? Clinical and Experimental Dermatology, 24(1):40–41.
- ^Nielsen, L.G., M. Frisch and F. Melchers, 1997, Op. cit.
- ^Staples, J.A., A.L. Ponsonby, L.L. Lim and A.J. McMichael, 2003. Ecologic analysis of some immune-related disorders, including type 1 diabetes, in Australia: latitude, regional ultraviolet radiation, and disease prevalence. Environmental Health Perspectives, 111:518–523.
^ McKenna, D.B., D. Stockton, D.H. Brewster and V.R. Doherty, 2003. Evidence for an association between cutaneous malignant melanoma and lymphoid malignancy: a population-based retrospective cohort study in Scotland. British Journal of Cancer, 88:74–78.;
-- Okada, S., E.Weatherhead, I.N.Targoff, R.Wesley and F.W. Miller, 2003. Global surface ultraviolet radiation intensity may modulate the clinical and immunologic expression of autoimmune muscle disease. Arthritis and Rheumatism, 48:2285–2293.
^Sutherland, B.M. 1995. Action spectroscopy in complex organisms: potentials and pitfalls in predicting the impact of increased environmental UVB. Journal of Photochemistry and Photobiology B 31:29–34;
-- Young, A.R., C.A. Chadwick, G.I. Harrison, O. Nikaido, J. Ramsden and C.S. Potten, 1998.The similarity of action spectra for thymine dimers in human epidermis and erythema suggests that DNA is the chromophore for erythema. Journal of Investigative Dermatology, 111:982–988.
- ^De Fabo and Noonan, 1983, Op. cit
^ McKinlay, A.F. and B.L. Diffey, 1987. A reference action spectrum for ultraviolet induced erythema in human skin. CIE Journal,
- ^ Long, C., 2003. UV Index forecasting practices around the world. Scholarly Publishing and Academic Resources.
- ^Moan, J., A. Dahlback,T. Henriksen and K. Magnus, 1989. Biological amplification factor for sunlight-induced nonmelanoma skin cancer at high latitudes. Cancer Research, 49:5207–5212.
- ^Jones, R.R., 1992. Ozone depletion and its effects on human populations. British Journal of Dermatology, 127:2–6.
- ^Strzhizhovskii (1998).
^ De Fabo, 1980, Op. cit.
-- Noonan and De Fabo, 1993, Op. cit.
- ^ De Fabo and Noonan, 1983, Op. cit.
^Hockwin, O., M. Kojima,Y. Sakamoto, A.Wegener,Y. Bo Shui and K. Sasaki, 1999. UV damage to the eye lens: further results from animal model studies: a review. Journal of Epidemiology, 9:S39-S47.;
-- Katoh, N., F. Jónasson, H. Sasaki, M. Kojima, M. Ono and N. Takahashi, 2001. Cortical lens opacification in Iceland. Risk factor analysis – Reykjavik Eye Study. Acta Ophthalmologica Scandinavica, 79:154–159.;
-- Sasaki, H., F. Jonasson, M. Kojima, N. Katoh, M. Ono, N.Takahashi and K. Sasaki, 2000.The Reykjavik Eye Study – prevalence of lens opacification with reference to identical Japanese studies. Ophthalmologica, 214:412–420.
-- Sasaki, K., H. Sasaki, M. Kojima,Y.B. Shui, O. Hockwin, F. Jonasson, H.M. Cheng, M. Ono, N. Katoh, 1999. Epidemiological studies on UV-related cataract in climatically different countries. Journal of Epidemiology, 9:S33–S38.
-- Taylor, A., P.F. Jacques, L.T. Chylack Jr, S.E. Hankinson, P.M. Khu, G. Rogers, J. Friend,W.Tung, J. K.Wolfe, N. Padhye and W.C. Willett, 2002. Long-term intake of vitamins and carotenoids and odds of early age-related cortical and posterior subcapsular lens opacities. American Journal of Clinical Nutrition, 75:540–549.;
-- Taylor, H., 1989. Ultraviolet radiation and the eye: an epidemiologic study.Transactions of the American Ophthalmological Society, 87:802–853.;
-- West, S., 1999. Ocular ultraviolet B exposure and lens opacities: a review. Journal of Epidemiology, 9:S97–S101.
- ^ Merriam, J.C, L. Stefan, R. Michael, P. Söderberg, J. Dillon, L. Zheng and A. Marcelo, 2000. An action spectrum for UV-B radiation and the rat lens. Investigative Ophthalmology and Visual Science, 41:2642–2647.
^ Hockwin et al., 1999, Op. cit
-- Katoh et al., 2001, Op. cit.;
-- Sasaki H. et al., 2000, Op. cit.;
-- Sasaki K. et al., 1999 Op cit.;
-- West, 1999, Op. cit.
- ^ Hayashi, L.C., S. Hayashi, K.Yamaoka, N.Tamiya, M. Chikuda and E.Yano, 2003. Ultraviolet B exposure and type of lens opacity in ophthalmic patients in Japan. Science of the Total Environment, 302:53–62.
^ Taylor A. et al., 2002. Op. cit.;
-- Valero, M.P., A.E. Fletcher, B.L. De Stavola, J.Vioque and V.C. Alepuz, 2002.Vitamin C is associated with reduced risk of cataract in a Mediterranean population. Journal of Nutrition, 132:1299–1306.;
-- Wegener, A., M. Heinitz and M. Dwinger, 2002. Experimental evidence for interactive effects of chronic UV irradiation and nutritional deficiencies in the lens. Developments in Ophthalmology, 35:113–124.
- ^Glerup, H., K. Mikkelsen, L. Poulsen, E. Hass, S. Overbeck, J.Thomsen, P. Charles and E.F. Eriksen, 2000. Commonly recommended daily intake of vitamin D is not sufficient if sunlight exposure is limited. Journal of Internal Medicine, 247:260–268.
- ^ Holick, M.F., 2001. Sunlight ‘D’ilemma: risk of skin cancer or bone disease and muscle weakness. Lancet, 357:4–6.
- ^Nowson, C.A. and C. Margerison, 2002.Vitamin D intake and vitamin D status of Australians. Medical Journal of Australia, 177:149–152.
^ Fahrleitner, A., H. Dobnig, A. Obernosterer, E. Pilger, G. Leb, K.Weber, S. Kudlacek and B.M. Obermayer-Pietsch, 2002.Vitamin D deficiency and secondary hyperparathyroidism are common complications in patients with peripheral arterial disease. Journal of General Internal Medicine, 17:663–669.;
-- Pasco, J.A., M.J. Henry, G.C. Nicholson, K.M. Sanders and M.A. Kotowicz, 2001.Vitamin D status of women in the Geelong Osteoporosis Study: association with diet and casual exposure to sunlight. Medical Journal of Australia, 175:401–405.
- ^for a comprehensive review of vitamin D see Feldman, D.G.F.H., 2003.Vitamin D. Academic Press
- ^ Lehmann, B.,W. Sauter, P. Knuschke, S. Dressler and M. Meurer, 2003. Demonstration of UV-B-induced synthesis of 1alpha, 25-dihydroxyvitamin D(3) (calcitriol) in human skin by microdialysis. Archives of Dermatological Research, 295:24–28.
- ^ AMAP, 2002. Arctic Pollution 2002: Persistent Organic Pollutants, Heavy Metals, Radioactivity, Human Health, Changing Pathways. Arctic Monitoring and Assessment Programme, Oslo. xii+112pp.
- ^ Huovinen, P., 2000. Ultraviolet radiation in aquatic environments: underwater UV penetration and responses in algae and zooplankton. Jyväskylä Studies in Biological and Environmental Science 86.
- ^ Reilly, S.K. and E.C. De Fabo, 1991. Dietary histidine increases mouse skin urocanic levels and enhances UV-B-induced immune suppression of contact hypersensitivity. Photochemistry and Photobiology, 53:431–438.
- ^ De Fabo et al., 1997, Op. cit.
- ^ Black, H.S., J.I.Thornby, J.E.Wolf, Jr., L.H. Goldberg, J.A. Herd, T. Rosen, S. Bruce, J.A.Tschen, L.W. Scott and S. Jaax, 1995. Evidence that a low-fat diet reduces the occurrence of nonmelanoma skin cancer. International Journal of Cancer, 62:165–169.
- ^ Suzuki,T.,T. Hirano and M. Suyama, 1987. Free imidazole compounds in white and dark muscles of migratory marine fish. Comparative Biochemistry and Physiology B, 87:615–619.
- ^ Hoppner, K., J.M. McLaughlan, B.G. Shah, J.N.Thompson, J. Beare-Rogers, J. Ellestad-Sayed and O. Schaefer, 1978. Nutrient levels of some foods of Eskimos from Arctic Bay, N.W.T., Canada. Journal of the American Dietetic Association, 73(3):257–260.
^ Ando, 1990, Op. cit.;
-- Coetzee,W.F. and E.C. Pollard, 1974. Near-UV effects on the induction of prophage. Radiation Research, 57(2):319–331.;
-- Tingate,T.R., D.J. Lugg, H.K. Muller, R.P. Stowe and D.L. Pierson, 1997. Antarctic isolation: immune and viral studies. Immunology and Cell Biology, 75:275–283.;
-- Zhang, P., M. Nouri, J.L. Brandsma,T. Iftner and B.M. Steinberg, 1999. Induction of E6/E7 expression in cottontail rabbit papillomavirus latency following UV activation.Virology, 263:388–394.;
-- Zmudzka, B.Z., S.A. Miller, M.E. Jacobs and J.Z. Beer, 1996. Medical UV exposures and HIV activation. Photochemistry and Photobiology, 64:246–253.
- ^ Nielsen L. et al., 1997, Op. cit.
- ^Nielsen, N.H., H.H. Storm, L.A. Gaudette and A.P. Lanier, 1996. Cancer in circumpolar Inuit 1969–1988. A summary. Acta Oncologica, 35(5):621–628.
- ^Taylor, J.R., G.J. Schmieder,T. Shimizu, C. Tie and J.W. Streilein, 1994. Interrelationship between ultraviolet light and recurrent herpes simplex infections in man. Journal of Dermatological Science, 8:224–232.
- ^Butler, J.C., A.J. Parkinson, E. Funk, M. Beller, G. Hayes and J.M. Hughes, 1999. Emerging infectious diseases in Alaska and the Arctic: a review and a strategy for the 21st century. Alaska Medicine, 41:35–43.
- ^ Sleijffers, A., J. Garssen and H.Van Loveren, 2002. Ultraviolet radiation, resistance to infectious diseases, and vaccination responses. Methods, 28:111–121.
- ^ Sleijffers, A., A. Kammeyer, F.R. De Gruijl, G.J. Boland, J.Van Hattum, W.A.Van Vloten, H.Van Loveren, M.B.Teunissen and J. Garssen. 2003. Epidermal cis-urocanic acid levels correlate with lower specific cellular immune responses after hepatitis B vaccination of ultraviolet B-exposed humans. Photochemistry and Photobiology, 77: 271–275.
- ^UNEP, 2003. http://www.unep.org/ozone/pdf/Press-Backgrounder.pdf.