Background Children are particularly vulnerable to the effects of extreme temperatures.
Objective To examine the relationship between extreme temperatures and paediatric emergency department admissions (EDAs) in Brisbane, Australia, during 2003–2009.
Methods A quasi-Poisson generalised linear model combined with a distributed lag non-linear model was used to examine the relationships between extreme temperatures and age-, gender- and cause-specific paediatric EDAs, while controlling for air pollution, relative humidity, day of the week, influenza epidemics, public holiday, season and long-term trends. The model residuals were checked to identify whether there was an added effect due to heat waves or cold spells.
Results There were 131 249 EDAs among children during the study period. Both high (RR=1.27; 95% CI 1.12 to 1.44) and low (RR=1.81; 95% CI 1.66 to 1.97) temperatures were significantly associated with an increase in paediatric EDAs in Brisbane. Male children were more vulnerable to temperature effects. Children aged 0–4 years were more vulnerable to heat effects and children aged 10–14 years were more sensitive to both hot and cold effects. High temperatures had a significant impact on several paediatric diseases, including intestinal infectious diseases, respiratory diseases, endocrine, nutritional and metabolic diseases, nervous system diseases and chronic lower respiratory diseases. Low temperatures were significantly associated with intestinal infectious diseases, respiratory diseases and endocrine, nutritional and metabolic diseases. An added effect of heat waves on childhood chronic lower respiratory diseases was seen, but no added effect of cold spells was found.
Conclusions As climate change continues, children are at particular risk of a variety of diseases which might be triggered by extremely high temperatures. This study suggests that preventing the effects of extreme temperature on children with respiratory diseases might reduce the number of EDAs.
- Child Health
- Communicable Diseases
- Environmental Health
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Climate change has been recognised as the biggest global threat to health in the 21st century.1 The average global surface temperature has increased, and the frequency and intensity of extreme weather events have also risen,2 ,3 posing a huge threat to human health and well-being. In particular, the adverse effects of extreme temperatures on morbidity have become a great public health concern.4
Previous studies of the impact of temperature on morbidity have focused mainly on adults, particularly the elderly.5 ,6 Children are particularly vulnerable to environmental hazards,7–11 but limited studies have examined the relationship between temperature and morbidity among children.12 In previous studies, temperature was considered as a continuous risk factor, and the exposure–response relationship between temperature and specific paediatric morbidity was assessed. However, to date, no study has quantified the effects of extreme temperatures on a wide range of health outcomes among children.
Some public health publications have emphasised that persistent extreme temperatures may increase the incidence of paediatric diseases. Heat waves (or cold spells) were more likely to be considered as a distinct event in the literature, and the excess morbidity due to heat waves (or cold spells) was calculated by comparing heat wave (or cold spell) days with non-heat-wave (or non-cold-spell) days.13–16 Some researchers have argued that the effects of heat waves and cold spells on human health might be due to the main effect of daily temperature fluctuations, and also the added effect of persistent extreme temperatures.17–19 To the best of our knowledge, no study has separately quantified the effects of daily temperatures and added the effects of persistent extreme temperatures on paediatric morbidity.
This study examined three key questions: (i) what is the relationship between extreme temperatures and paediatric emergency department admissions (EDAs) in Brisbane, Australia? (ii) is there any added effect due to heat waves and cold spells? (iii) which subgroups of children are more sensitive to extreme temperatures?
Brisbane is the capital of Queensland, located on the east coast of Australia (27° 30′ S, 153° 00′ E). It has a subtropical climate, and generally experiences mild winters and hot summers, and thus the heat–health relationship in Brisbane needs particular research attention.20–22 Children aged 0–14 years account for 20% of the residential population in Brisbane.23 EDA data for the period 1 January 2003 to 31 December 2009 were obtained from Queensland Health. Before the data were collected, ethical approval was obtained from the human research ethics committee of Queensland University of Technology. Because the data were de-identified and aggregated, written consent was not needed. Data on EDAs were classified according to the International Classification of Disease, 10th version. The main paediatric diseases in Brisbane during 2003–2009 were analysed, including all-cause diseases, intestinal infectious diseases (A00–A09), endocrine, nutritional and metabolic diseases (E00–E90), nervous system diseases (G00–G99), respiratory diseases (J00–J99), acute upper respiratory infections (J00–J06), chronic lower respiratory diseases (J40–J47) (most of which were EDAs for childhood asthma), digestive system diseases (K00–K93) and genitourinary system diseases (N00–N99).
Daily data on maximum and minimum temperatures and relative humidity in Brisbane for the same period were retrieved from the Australian Bureau of Meteorology. Daily data on average particulate matter ≤10 µm (PM10) (µg/m3) and 8 h maximum ozone (O3) (ppb) were obtained from the Queensland Department of Environmental and Resources Management. The data were collected from two monitor stations in Brisbane, and then averaged.
Definitions of heat wave and cold spell
To date, owing to variations in population characteristics and adaptation,21 ,24–26 there are no standard definitions for heat waves and cold spells. In this study, we combined intensity and duration of extreme temperatures to define both heat waves and cold spells: (1) intensity: the 4th (13.5°C) and 5th (13.8°C) centiles of daily mean temperature as the cold threshold, and the 95th (26.5°C) and 96th (26.7°C) centiles of the daily mean temperature as the hot threshold; (2) duration: a minimum of 2–4 consecutive days with temperatures below the cold threshold or above the hot threshold.
Stage I: estimation of the main temperature effects on paediatric EDAs
To quantify the main effect of temperature on paediatric EDAs, we used a quasi-Poisson generalised linear regression model combined with a distributed lag non-linear model (DLNM). Many studies have reported a lagged effect of temperature on morbidity.27 ,28 Further, the temperature–morbidity relationship has been found to be non-linear.29 Thus, we used the DLNM to examine both non-linear and lagged effects of temperature simultaneously.30 Previous studies have reported that there is no ‘best’ temperature indicator,31 ,32 and daily mean temperature was used in this study. A ‘natural cubic spline–natural cubic spline’ DLNM was used to examine the temperature effect using four degrees of freedom (df) and 4 df for the temperature and lag dimensions, respectively. Previous research has shown that the cold effects on morbidity last for more than 7 days, while heat effects are relatively acute.4 We found that there was a negligible effect of temperature on paediatric EDAs for lags above 21 days, and we therefore used a maximum lag of 21 days to examine the effect of temperature.
Several different covariates were included in the model. PM10, O3 and relative humidity were controlled for as potential confounders using a natural cubic spline with 4 df. Maximum lags of 21 days were also used for PM10, O3 and relative humidity. Seasonal and long-term trends were controlled for using a natural cubic spline with 8 df per year of data. Influenza epidemics and public holidays were also controlled for in the model. For the choice of df for all non-linear functions, we used a Poisson model and checked the Akaike information criterion and residuals. After the best df was chosen, we changed the Poisson model to a quasi-Poisson model. Day of week was controlled for as a categorical variable.
When all the other parameters had been confirmed, we checked the temperature–EDAs plot and chose the reference temperature by visual inspection. We evaluated the relative risk of paediatric EDAs associated with high temperature (≥26.5°C, 95th centile of mean temperature) relative to the reference temperature (24.0°C). Similarly, we evaluated the relative risk of paediatric EDAs associated with low temperature (≤13.8°C, 5th centile of mean temperature) relative to the reference temperature (24.0°C).
Stage II: examining the added effects of heat waves and cold spells
Previous studies have reported that sustained periods of heat and cold produce an added effect on mortality which is independent of main temperature effects.18 ,19 ,33 We analysed the residuals of the stage I model to examine the possible added effects of heat waves and cold spells—that is, we took the residuals of the model in stage I and then performed the analysis for heat waves and cold spells. We assumed a maximum lag of 21 days for the delayed effects of heat waves and cold spells. EDAs for childhood asthma on extreme temperature days were compared with non-extreme temperature days.
Effect estimates were obtained for both male and female children, different age groups (0–4, 5–9 and 10–14 years) and different EDA categories. To perform sensitivity analyses, we varied the df (8–15 per year) for time to control for both seasonal and long-term trend. We also varied the df (5–7) for temperature and humidity for the DLNM. All data analysis was conducted using the R statistical environment (V.2.12.2) with the ‘dlnm’ package used to fit the regression model.34
In total, there were 131 249 EDAs among children in the whole study period. Table 1 shows the summary statistics for mean temperature, relative humidity, air pollutants and total, cause-specific, age-specific and gender-specific paediatric EDAs. The average mean temperature was 20.6°C (range 9.0–34.2), and the average relative humidity was 57.3% (5.0%–98.0%). The average values of O3 and PM10 were 22.3 ppb (5.0–60.0) and 16.0 µg/m3 (4.4–355.2), respectively. The daily number of EDAs was greater among children aged 0–4 years (mean 33.5, SD 11.2) than those aged 5–9 years (mean 9.3, SD 4.0) and 10–14 years (mean 8.7, SD 3.9). The daily number of EDAs was greater among male children (mean 28.9, SD 9.6) than female children (mean 22.5, SD 7.9).
Figure 1A presents the decomposed distribution of paediatric EDAs, showing a strong seasonal trend. The daily distributions of PM10, O3 and relative humidity are presented in figure 1B–D. Figure 2 shows the cumulative effects of temperature on total, age- and gender-specific paediatric EDAs, and demonstrates that paediatric EDAs increased during both high and low temperatures. Hot and cold effects were much greater among male children than female children. For age-specific paediatric EDAs, it can be seen that children aged 0–4 years were vulnerable to heat effects, and those aged 10–14 years were sensitive to both hot and cold effects.
Figure 3 shows the effects of high temperature (95th centile (26.5°C) and low temperature (5th centile (13.8°C) relative to the threshold temperature (24.0°C)) on total paediatric EDAs according to the lags. Both hot and cold effects persisted, and cold effects were relatively more acute.
Table 2 shows the cumulative effects of both high (26.5°C) and low (13.8°C) temperatures on total and cause-specific paediatric morbidity at lags of 0–1, 0–13 and 0–21 days. High temperatures were statistically significantly associated with the following paediatric diseases: intestinal infectious diseases, respiratory diseases, endocrine, nutritional and metabolic diseases, nervous system diseases and chronic lower respiratory diseases. Low temperatures were significantly associated with intestinal infectious diseases, respiratory diseases and endocrine, nutritional and metabolic diseases.
Table 3 shows the daily excess EDAs for total and cause-specific paediatric EDAs on heat wave (or cold spell) days as opposed to non-heat wave (or non-cold spell) days. The number of heat waves and cold spells is shown in table 4. Using heat wave definitions of a minimum of 2 days’ temperature sustained over the 95th or 96th centile, we found there was no significant increase in total and cause-specific EDAs in heat waves. However, using heat wave definitions of a minimum of 3 days’ temperature sustained over the 95th or 96th centile, we found there were significant increases in EDAs for chronic lower respiratory diseases in heat waves. There was no significant increase in paediatric EDAs during cold spells.
To conduct a sensitivity analysis, we changed the df (8–15 per year) for time to control for season. We also varied the df (5–7) for temperature and relative humidity, and found that the effects of high (26.5°C) and low (13.8°C) temperatures decreased slightly when the df for time, temperature or relative humidity was increased, but were still significant.
This study yielded several notable findings. Both high and low temperatures had significant impacts on paediatric EDAs. Male children were more vulnerable to temperature effects. Children aged 0–4 years were more vulnerable to heat effects and children aged 10–14 years were more sensitive to both hot and cold effects. Both hot and cold effects persisted. Effects of high temperature were found on several paediatric diseases, including intestinal infectious diseases, respiratory diseases, endocrine, nutritional and metabolic diseases, nervous system diseases and chronic lower respiratory diseases. Low temperature significantly affected paediatric intestinal infectious diseases, respiratory diseases and endocrine, nutritional and metabolic diseases. No significant added effects due to heat waves or cold spells were seen, with the exception of an added effect of heat waves on paediatric chronic lower respiratory diseases.
This study suggests that male children may be more vulnerable to extreme temperatures than female children, a finding that is supported by previous research.35 ,36 The primary reasons for the observed gender difference in vulnerability to extreme temperatures may include variations in anthropometry, body composition (eg, sexual dimorphism) and social behaviour (eg, daily activity). During cold exposure, female children have a reduced thermal gradient for metabolic heat removal, and lower cardiovascular and metabolic responses than male children.37 However, some researchers found that the risk of death increases in female children during heat waves and is greater than in male children.38 Basu39 argued that differences in the effect of temperature on male and female subjects varied among different locations and populations, indicating that the differences in vulnerability to extreme temperatures in the male children and female children of our study might also be due to socioeconomic characteristics and adaptive capacity of children in Brisbane.
Another finding of our study is that children aged 0–4 or 10–14 years are more vulnerable to extreme temperatures than children aged 5–9 years. Children 0–4 years of age have been found to be vulnerable to hot and cold,14 ,40–42 especially to persistent hot episodes.14 ,16 ,43 Children aged 10–14 years may play outdoors more often than younger children, which may increase their exposures to extreme temperatures. In young female children, menarche usually occurs between the age of 10 and 14,17 and the increase in ovarian hormones among female children at this stage might influence their thermoregulation function,44 resulting in their vulnerability to extreme temperatures.
As the temperature changes, the automatic thermoregulation of humans responds to maintain thermal comfort so that mental and physical activities can be pursued without detriment to health. Temperatures exceeding these limits increase the risk of diseases. The lag structure of temperature effects on paediatric EDAs found in this study is not consistent with that found for the wider population. In this study, the effects of high temperature lasted for a couple of weeks, a figure that is not comparable with previous studies that reported shorter lag effects,28 ,45 indicating that high temperature may have a longer-lasting effect on children than on adults. We found that the cold effects on total paediatric EDAs lasted for 1–2 weeks, which is consistent with the lag duration of cold effects on other health outcomes, such as general practice consultations.46 Although some of the findings are similar to those for other climates, the threshold temperatures for increases in morbidity and mortality vary with regions.
In this study, we found associations for some commonly reported diseases in children, such as intestinal infectious diseases47–50 and respiratory diseases,15 ,28 and also for other conditions that have received less attention. These include endocrine, nutritional and metabolic diseases and nervous system diseases, indicating that parents and caregivers need to pay more attention to children during high and low temperatures.
Admissions for respiratory disease were found to increase in both high and low temperatures in this study. The effect of low temperatures on respiratory diseases may be due partially to cross-infection from indoor crowding.51 ,52 Low temperatures assist survival of bacteria in water droplets.53 Furthermore, low temperatures may increase the incidence of paediatric influenza, and consequently, increase paediatric respiratory diseases.54 Results from the adult population suggest that in cold temperatures respiratory tract infections may occur through either inhalation of cold air (eg, the temperature of the respiratory surface becomes optimal for virus transmission and replication), cooling of the body surface or through cold stress, which causes pathophysiological responses that may contribute to increased susceptibility to these infections. Cold stress might also alter the immune system and affect the susceptibility to respiratory tract infections.55 ,56 The reasons for the effect of high temperatures on respiratory diseases are unknown. Interestingly, we found that childhood chronic lower respiratory disease was vulnerable to high temperatures, indicating that EDAs for this disease in Brisbane might increase in the future as climate change continues and the global surface average temperature increases.
The results show that both high and low temperatures had large effects on endocrine diseases. These results correspond to those of a study conducted by Pudpong and Hajat57 in Thailand, which demonstrated an increase of diabetic outpatient visits during high temperatures in the total population. Semenza et al58 found that diabetic admissions increased during heat waves in Chicago. It was reported that the autonomic control and endothelial function of people with diabetes is sensitive to extreme temperatures, which may explain the biological mechanism.59 We also found that low temperatures had an adverse effect on endocrine diseases, indicating that EDAs for childhood endocrine diseases may increase during cold days.
We found that admissions for nervous system disease increased during hot days, possibly owing to the negative effects of some psychotropic drugs,60 ,61 decreased self-care capacity60 and physiological vulnerability.61 High temperatures may trigger the potential symptoms of people with existing nervous system disorders.
We found that there were no added effects due to heat waves or cold spells except for paediatric chronic lower respiratory diseases. Thus the increase of paediatric EDAs during persistent extreme temperatures for Brisbane was mainly due to daily high or low temperatures, but not due to the effects caused by persistent periods of high or low temperatures. Persistent high temperatures were associated with 9–11 EDAs a day for paediatric chronic lower respiratory diseases, depending on the severity of heat waves. This indicates that parents and caregivers should take more protective measures during extreme temperatures and persistent hot days to prevent their children from chronic lower respiratory diseases attacks. Chronic lower respiratory disease was one of the leading causes of death globally in 2010,62 ,63 and the findings of this study show that the more intense, frequent and long heat waves in the future will probably increase the burden caused by this disease. Two reasons may explain the absence of an added effect during cold spells. First, children may wear more clothes after experiencing a cold day. Second, Brisbane has a subtropical climate and rarely has really cold days for more than a few days, reducing the likelihood of a cold spell occurring.
Potential intervention strategies need to be developed for children's particular vulnerability to both low and high temperatures. The ideal way of handling extreme temperatures is through primary prevention —for example, health education.64 A heat early warning system can be of great use, especially for those parents whose children have a history of chronic lower respiratory diseases.
Strengths and limitations
This study has three major strengths. First, to the best of our knowledge, this is the first study which specifically examines the effect of extreme temperatures on a wide range of diseases in children in the Southern Hemisphere. Even though children are regarded as a population subgroup vulnerable to temperature extremes, little empirical research has been conducted to date. Second, advanced statistical methods were used to quantify the lagged and cumulative effects of extreme temperatures on paediatric EDAs. Finally, vulnerabilities to extreme temperatures among groups of different age and gender were assessed and compared.
Three limitations of this study should also be acknowledged. First, we focused on only one city, which means that our findings should only be generalised to other regions and climates with caution. However, our findings may stimulate further research in other populations. Second, infants were not specifically analysed as a subgroup because of lack of data, even though they are particularly vulnerable to temperature effects. Further studies should focus more on the impact of extreme temperatures on morbidity in infants. Finally, there may be some exposure misclassification bias because we used aggregated data on temperature and air pollution rather than individual exposure data.
Our findings demonstrate significant effects of high and low temperatures on a variety of paediatric diseases. The added effects of persistent extreme temperatures on most paediatric EDAs appeared to be negligible when compared with the main effects, but paediatric chronic lower respiratory disease was very sensitive to both extreme temperatures and heat waves. In addition, male children, children aged 0–4 years, and children aged 10–14 years were at particular risk. These findings indicate that parents and caregivers need to be aware of the adverse health effects of extreme temperatures and employ appropriate protective measures (eg, adjustment of exposure, clothing and hydration).
What is already known on this subject
Extreme temperatures have impacts on paediatric intestinal infectious diseases and respiratory diseases.
Children aged 0–4 years are particularly vulnerable to extreme temperatures.
What this study adds
Our results show that male children are more vulnerable to temperature effects. Children aged 0–4 years are more vulnerable to heat effects and children aged 10–14 years are more sensitive to both hot and cold effects.
Hot temperature effects were seen on several paediatric diseases, including intestinal infectious diseases, respiratory diseases, endocrine, nutritional and metabolic diseases, nervous system diseases and chronic lower respiratory diseases, while low temperature significantly affected paediatric intestinal infectious diseases, respiratory diseases and endocrine, nutritional and metabolic diseases.
There was an added effect of heat waves on paediatric chronic lower respiratory diseases.
We would like to thank Dr Cunrui Huang for his valuable comments on the early draft, and we greatly appreciate Dr Adrian Barnett's insightful comments on the manuscript revision.
Contributors ZX and ST designed this study. ZX analysed the data and wrote the first draft. ST, WH, HS, LRT, XY and JW contributed to the manuscript revision.
Funding ST was funded by a National Health and Medical Research Council research fellowship (No 553043).
Competing interests None.
Ethics approval Human research ethics committee of Queensland University of Technology.
Provenance and peer review Not commissioned; externally peer reviewed.
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