Heat Stress and Sudden Infant Death Syndrome Incidence: A United States Population Epidemiologic Study
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Heat Stress and Sudden Infant Death Syndrome Incidence: A United States Population Epidemiologic Study Joshua R. Scheers-Masters, BA*; Mario Schootman, PhD*‡; and Bradley T. Thach, MD* ABSTRACT. Objectives. To determine the role of heat nations without extreme temperature variations, stress in sudden infant death syndrome (SIDS) by exam- such as Great Britain, Tasmania, and New Zea- ining the SIDS rates during periods of extreme environ- land.2–5 Such research has consistently associated in- mental temperatures in a period when most infants were creased SIDS incidence with colder outdoor temper- placed prone for sleep. atures. It has been suggested that some parents may Design. A retrospective study of SIDS rates and mor- tality rates attributable to excessive environmental heat respond to such cold waves by overwrapping infants in relationship to climatologic temperature was per- or excessively increasing room temperatures.3 In formed. Data were collected for each of 454 counties in 4 contrast, a cross-cultural study found comparatively states (Arkansas, Georgia, Kansas, and Missouri) from weak relationships between climatic temperature May 1 to September 30, 1980, and were then summed to and SIDS incidence in communities in the United yield the mortality rates for each 5°F (2.8°C) temperature States.6 Therefore, it is possible that seasonal over- range. wrapping of infants may not be a major cause of Results. 2 analyses revealed significant relation- SIDS in the United States. ships for heat-related mortality rates and both the maxi- Sections of the United States, particularly the Mid- mal daily temperature and mean daily temperature but west, are subject to periodic heat waves, which can demonstrated no such relationships for SIDS rates. No association between SIDS rates and heat-related mortal- lead to severe epidemics of deaths attributable to ity rates was found with Spearman’s ranked correlation, exposure to excessive heat.7 Such conditions present for either the maximal daily temperature or the mean an opportunity to examine the effect of increased daily temperature. environmental temperature on SIDS incidence. We Conclusions. On the basis of our findings of no sig- reasoned that, if thermal stress increases the risk of nificant association between SIDS and either measure of SIDS, then an increase in the number of SIDS deaths temperature during periods of high heat stress-related should be observed when there is an increase in the death rates, it seems unlikely that the heat stress associ- number of heat-related deaths in the general popu- ated with the combination of prone sleep positions and lation. elevated environmental temperatures has a significant role in the development of SIDS. Pediatrics 2004; 113:e586 –e592. URL: http://www.pediatrics.org/cgi/ METHODS content/full/113/6/e586; SIDS, thermal stress, bedding, Population overwrapping, sleep position. This study concentrated on the heat waves of the summer of 1980. In that year, excessive heat from all sources was listed as the underlying cause of death for a total of 1700 deaths across the ABBREVIATIONS. SIDS, sudden infant death syndrome; Tmax, United States,8 which was notably greater than the median of 274 maximal daily temperature; Tavg, average daily temperature. deaths per year from 1979 to 1998 and was the largest number of heat-related deaths during that period.9 To avoid a false-negative finding attributable to seasonal variations in the SIDS rate, the T he thermal stress theory for sudden infant period was restricted to May 1 through September 30, 1980. All death syndrome (SIDS) states that many SIDS deaths attributable to SIDS and exposure to excessive heat result- deaths occur as a result of increased demands ing from weather conditions in each of the counties of the 4 states with the greatest numbers of heat-related deaths, namely, Arkan- on thermoregulatory mechanisms attributable to a sas, Georgia, Kansas, and Missouri, during this period were con- prone sleep position, increased ambient temperature, sidered. and/or a decreased ability to eliminate body heat as a result of excessive clothing covering the infant.1 Data Sources Although the relationship between climatic temper- SIDS mortality data were defined as all records from the Mor- ature and SIDS incidence has been examined care- tality Detail Files, 1979 –1980,10 that fit the aforementioned criteria fully, the studies were performed predominantly in and for which an International Classification of Diseases, 9th revision, code of 798.0 was assigned for the underlying cause of death. Heat-mortality data were defined as all records for which an From the *Edward Mallinckrodt Department of Pediatrics and ‡Department International Classification of Diseases, 9th revision, code of 900.0 of Internal Medicine, Washington University School of Medicine, St Louis, (“death due to excessive heat due to weather conditions”) was Missouri. assigned. Population data for each county were obtained from the Received for publication Sep 25, 2002; accepted Dec 29, 2003. Census of Population and Housing, 1980 (United States): County Pop- Reprint requests to (B.T.T.) Washington University School of Medicine, 660 ulation by Age, Sex, Race, and Spanish Origin,11 with the populations S Euclid, Campus Box 8208, St Louis, MO 63110. E-mail: thach@kids. being defined as the entire population of the county for heat- wustl.edu related deaths and the population ⬍1 year of age for SIDS deaths. PEDIATRICS (ISSN 0031 4005). Copyright © 2004 by the American Acad- Data on the maximal daily temperature (Tmax) and minimal emy of Pediatrics. daily temperature were determined for each county of the 4 states Downloaded from www.aappublications.org/news by guest on August 31, 2021 e586 PEDIATRICS Vol. 113 No. 6 June 2004 http://www.pediatrics.org/cgi/content/full/113/6/e586
studied from the Record of Climatological Observations.12 Tempera- Furthermore, analysis of the relationship between tures for the counties were recorded from a single weather station SIDS rates and heat-related mortality rates with within each county. For counties that were missing data, temper- ature data were calculated as the average of values from 2 weather Spearman’s ranked correlation indicated no associa- stations in 2 bordering counties. If original data were missing for tion for either Tmax (P ⫽ .2080) or Tavg (P ⫽ .8979). all bordering counties, then data for the next closest counties were The 3 infant deaths were diagnosed as being at- used. Average daily temperatures (Tavg) in each location then tributable to environmental heat. The analysis was were calculated as the average of Tmax and the minimal daily temperature. All temperature data were rounded to the nearest repeated after these deaths had been removed from integer. the heat-related category and entered as SIDS deaths. Again, 2 tests demonstrated increases in heat-re- Statistical Analyses lated mortality rates with increasing Tmax values (P For each 5°F temperature range (for example, 60 – 64°F [15.6 – ⬍ .0001) but indicated no such relationship for SIDS 17.8°C]), the population of each county was multiplied by the rates (P ⫽ .605) (Fig 3). Heat-related mortality rates number of days the county experienced that temperature range. increased with Tavg values (P ⬍ .0001), but again These values then were summed for all counties, to yield the total population at risk for each temperature range. The total number of there was no association between SIDS rates and Tavg deaths that occurred in that temperature range then was divided (P ⫽ .945) (Fig 4). In addition, analysis of the recoded by the total population at risk to yield the mortality rate for each data with Spearman’s ranked correlation indicated temperature range. no association for either Tmax (P ⫽ .9572) or Tavg (P ⫽ 2 tests for trend were performed to determine the association .4175). Finally, we considered the possibility that between the SIDS rate and the heat-related death rate for Tavg and Tmax. To determine the association between the SIDS rate and the there could be a threshold for heat stress, increasing heat-related death rate, Spearman’s rank correlation coefficient SIDS risks at higher temperature ranges. Therefore, was used. A P value of ⬍.05 was considered statistically signifi- we analyzed the dichotomized Tavg variable. The rate cant. These analyses were repeated after recoding of any infant for Tavg of ⬍85°F was 3.0 cases per 1 000 000 popu- deaths attributable to exposure to excessive heat as deaths attrib- utable to SIDS. In these cases, the population associated with lation, whereas the rate for ⱖ85°F was 3.4 cases per heat-related deaths was equal to the entire population of the 1 000 000. This difference was not statistically signif- county minus the population ⬍1 year of age. icant (P ⫽ .568). Because of the relatively few cases (111) of SIDS recorded during the study period, we used a simulation to calculate the DISCUSSION empirical power to detect a linear increase in the SIDS rate with increasing temperature. With the available SIDS deaths, the power In this study, we failed to find a relationship be- was calculated to be 0.78 if the SIDS rate at the highest tempera- tween elevated environmental temperatures and the ture was 2.7 times that at the lowest temperature. The power was incidence of SIDS during a period in which deaths 0.70 if the SIDS rate at the highest temperature was 1.8 times that attributable to excessive environmental temperatures at the lowest temperature. If the SIDS rate at the highest temper- ature was 1.5 times that at the lowest temperature, then the power in the general population were increased to epidemic was calculated to be 0.63 (Table 1). levels. Physiologic and epidemiologic research sug- gests increased risks attributable to heat stress RESULTS among prone-sleeping infants, because their ability Between May 1 and September 30, 1980, in the to eliminate heat may be reduced in this position.13,14 states of Arkansas, Georgia, Kansas, and Missouri, a During the period of our study, ⬃72% to 77% of total of 111 SIDS deaths and 402 deaths attributable infants slept prone.15 Therefore, US infants as a to excessive heat resulting from weather conditions group should have been unusually susceptible to were recorded. 2 tests demonstrated increased heat- heat stress. related mortality rates with increasing Tmax values (P The power calculation indicated that the number ⬍ .0001) but indicated no such relationship for SIDS of SIDS deaths studied was sufficient to allow detec- rates (P ⫽ .362) (Fig 1). Also, there was a strong tion of an increase in SIDS rates of 1.8-fold between association between heat-related mortality rates and the highest and lowest temperatures. Smaller in- Tavg values (P ⬍ .0001); however, there was no linear creases would have been undetectable. Increases of association for SIDS rates and Tavg (P ⫽ .713) (Fig 2). this magnitude are relatively small, considering that the differences between summer and winter SIDS rates during the 1980s in New Zealand, for example, TABLE 1. Empirical Power Calculations* were five- to sevenfold.3 Therefore, if the large sea- Increase in SIDS Power sonal variations in SIDS rates observed in the past Rate at Highest were primarily attributable to heat stress, as sug- Versus Lowest Linear Increase Stepwise Increase With Increasing With Increasing gested previously,1,16 then we would expect to have Temperature Temperature Temperature observed changes of this magnitude among heat- stressed infants. Furthermore, the present study in- 6.0 0.89 0.95 3.5 0.83 0.93 dicated that heat-related death rates in the general 2.7 0.78 0.88 population we studied were much higher at the 1.8 0.70 0.73 highest temperature, compared with the lowest. If 1.5 0.63 0.64 SIDS infants are to be considered at high risk for 1.2 0.56 0.60 death attributable to heat stress, then an increase in * For example; the Power is 0.78 if the SIDS rate at the highest death rates of a magnitude comparable to that for temperature is 2.7 times that at the lowest temperature, with a deaths attributable to heat stress in the general pop- linear increase in the SIDS rate with increasing temperature. The power is 0.70 if the SIDS rate at the highest temperature is 1.8 ulation would be expected. The statistical power was times that at the lowest temperature, with a linear increase in the more than adequate to detect such an increase. SIDS rate with increasing temperature. These findings suggest that the heat stress theory Downloaded from www.aappublications.org/news by guest on August 31, 2021 http://www.pediatrics.org/cgi/content/full/113/6/e586 e587
Fig 1. SIDS rates versus heat-related mortality rates for Tmax. Error bars indicate ⫾SEM. It should be noted that, because of the repeated exposure of the populations in this study to the various temperature ranges, resulting in an extremely large population at risk, these daily rates per temperature range have little relationship to annual rates. Fig 2. SIDS rates versus heat-related mortality rates for Tavg. Downloaded from www.aappublications.org/news by guest on August 31, 2021 e588 HEAT STRESS AND SIDS INCIDENCE
Fig 3. SIDS rates versus heat-related mortality rates for Tmax, with infant heat-related deaths recoded as SIDS. Fig 4. SIDS rates versus heat-related mortality rates for Tavg, with infant heat-related deaths recoded as SIDS. for SIDS should be reevaluated. There are confound- theory. Materials that are high in thermal insulation ing factors in interpreting the insulation data, argu- value (as measured in tog units) also contribute to ably the most important findings supporting this death through other mechanisms such as rebreathing Downloaded from www.aappublications.org/news by guest on August 31, 2021 http://www.pediatrics.org/cgi/content/full/113/6/e586 e589
of expired air causing asphyxiation. Studies have tendency for emesis as well as refusal to accept orally found that infant bedding items such as quilts, com- administered fluids when overheated, which make forters, and blankets have a high potential for caus- infants more susceptible to heat stress and related ing rebreathing.17,18 Fleming et al16 found that in- dehydration.27,31 Therefore, for any given thermal fants who died as a result of SIDS were wrapped in exposure, infants may be expected to experience clothing or covered by bedding with a significantly symptoms of heat stress more rapidly than other age greater tog value than were control infants. The groups. increased SIDS risk associated with increased body Second, it might be expected that most parents insulation was highest among prone-sleeping in- would pay particular attention to keeping infants fants. Because prone sleeping and increased insula- cool in hot weather. Evidence suggests that this is not tion can interact to reduce an infant’s ability to elim- the case. A study of heat-stressed infants hospital- inate heat, the investigators attributed the increased ized for treatment found that 68% of the infants’ SIDS risk in the prone position to thermal stress. caretakers were unaware of the need for increased However, those investigators did not include bulky fluid intake by their infants during hot weather and bedding items (such as duvets, quilts, or comforters) had seriously underestimated the seriousness of the covering infants in their multivariate analysis. These infants’ initial symptoms.27 Other studies also indi- items not only are very substantial components of cated a lack of parental perception regarding infant the tog estimate but also place infants at increased heat stress. It has been reported that the practice of risk for rebreathing. In fact, Ponsonby et al19 found leaving sleeping infants in parked cars while parents that the increase in the risk of SIDS resulting from run errands is a frequent cause of heat-related mor- quilt or comforter use was evident only for supine- bidity and death.31–34 It is noteworthy that 24% of sleeping infants, suggesting that heat stress may not mothers admit to this practice, again indicating seri- be the primary mechanism for the increased risk ous underestimation by caretakers of their infants’ associated with these items. ability to cope with increased environmental temper- The thermal stress theory of SIDS originated with atures.32 premortem and postmortem observations of ele- Third, it is unlikely that many infants kept indoors vated body temperature or excessive sweating during the 1980 heat wave received adequate protec- among infants with SIDS.20,21 The observations of tion as a result of access to home air conditioning or overwrapping or elevated room temperature on the fans. A government-sponsored study of the avail- day of death provided additional support for this ability of home air conditioners in the 4 states we theory.16,20,22,23 It is important to note that the ther- studied, spanning 1980 to 1984, indicated that most mal stress theory draws a sharp distinction between households (51%) had inadequate access to air con- SIDS resulting from heat stress and death attribut- ditioners sufficient to reduce the risk of heat stroke.35 able to extreme hyperthermia leading to heat Even more relevant were the findings of a 1980 study stroke.22,24 Therefore, it has been suggested that ther- that found that ⬎80% of the households in the lower mal stress, with or without moderate increases in one-third socioeconomic group did not have air con- body temperature, can result in fatal disruption of ditioning.36 Fans in the home were not found to vital systems among infants predisposed to SIDS.1,25 decrease the risk of heat stroke.37 Therefore, it can be It has been proposed that congenital or acquired inferred that the majority of the infants, including anatomic abnormalities in brainstem centers regu- those at highest risk for SIDS (ie, infants in low- lating respiratory or cardiovascular stability could income households), did not have access to environ- represent the underlying defects that render SIDS ments adequate to eliminate heat stress. infants susceptible to death resulting from heat Fourth, any consideration of the possible relation- stress.26 ship of heat stress to SIDS in the United States must Our reasoning in assuming that a substantial num- also take into account the fact that the population at ber of infants at risk for SIDS experienced significant highest risk for one is also that at highest risk for the heat stress is as follows. First, several factors indicate other. It has been well established in several studies, that young infants can be expected to experience including an analysis of the 1980 heat wave in Mis- more heat stress than older children or adults when souri, that low-income, urban, and African American environmental temperatures increase. The full spec- populations are at highest risk for heat stroke be- trum of heat-related illnesses among infants must be cause of the combination of an urban “heat-island” considered, because more cases of nonlethal environ- effect that increases both indoor and outdoor tem- mental heat-related illnesses (eg, heat prostration peratures, substandard housing, poor ventilation, and water-deficiency heat exhaustion) than actual and decreased access to air conditioning.38–41 When heat stroke occur among infants.27 The actual death infant physiologic factors, the failure of caregivers to rates for infants, compared with the elderly, during perform appropriate interventions, and populations heat waves are less likely to reflect the true incidence at greatest risk for both heat stress and SIDS are of heat stress, because death seems to be less fre- taken into account, it might reasonably be predicted quent among infants diagnosed with heat stroke that, if heat stress per se is a significant cause of SIDS, than in the older population.27 The risk for all heat- SIDS incidence should increase significantly during related illnesses is thought to be increased among summer heat waves, when the number of deaths infants, compared with older children or adults.28–30 attributable to overheating in the general population This is attributed to increased metabolic rate, in- increases. creased surface area/body mass ratio, and increased Heat stress can be defined as a deviation from a Downloaded from www.aappublications.org/news by guest on August 31, 2021 e590 HEAT STRESS AND SIDS INCIDENCE
thermoneutral environment that requires increased Census of Population and Housing, 1980 (United States): County Pop- use of the body’s mechanisms for cooling. In con- ulation by Age, Sex, Race, and Spanish Origin were originally col- lected by the US Department of Commerce, Bureau of the Census. trast, heat stroke, defined as a body temperature of Neither the collectors of the original data nor the Consortium bear ⱖ105°F (ⱖ40.6°C) and altered mental status,42 leads any responsibility for the analyses or interpretations presented to cardiac arrhythmias, seizures, or hypovolemic here. shock, with tachycardia and eventual circulatory col- lapse.43 Depression of central nervous system ther- moregulatory mechanisms is thought to be involved REFERENCES in such deaths.43,44 Because it is difficult to diagnose 1. Harper RM, Kinney HC, Fleming PJ, Thach BT. Sleep influences on heat stroke after death among both infants and homeostatic functions: implications for sudden infant death syndrome. Respir Physiol. 2000;119:123–132 adults, because of the lack of specific pathologic find- 2. Schluter PJ, Ford RP, Brown J, Ryan AP. Weather temperatures and ings, the most important information for the post- sudden infant death syndrome: a regional study over 22 years in New mortem diagnosis comes from body-temperature Zealand. J Epidemiol Community Health. 1998;52:27–33 measurements and death-scene investigations.45–47 3. Mitchell EA, Stewart AW, Cowan SF. Sudden infant death syndrome In this study, there were 3 infant deaths among the and weather temperature. Paediatr Perinat Epidemiol. 1992;6:19 –28 4. Campbell MJ, Rodrigues L, Macfarlane AJ, Murphy MF. Sudden infant 402 deaths attributable to excessive heat exposure. deaths and cold weather: was the rise in infant mortality in 1986 in Two of those deaths occurred on consecutive days in England and Wales due to weather? Paediatr Perinat Epidemiol. 1991;5: Jackson County, Missouri (which includes Kansas 93–100 City). During the summer heat wave, 5 deaths diag- 5. Jones ME, Ponsonby AL, Dwyer T, Gilbert N. The relation between nosed as SIDS occurred in Jackson County, which climactic temperature and sudden infant death syndrome differs among communities: results from an ecologic analysis. Epidemiology. 1994;5: suggests that the medical examiner for that jurisdic- 332–336 tion was accustomed to distinguishing infant deaths 6. Murphy MF, Campbell MJ. Sudden infant death syndrome and envi- attributable to SIDS from heat stroke deaths. Even if ronmental temperature: an analysis using vital statistics. J Epidemiol all 3 heat-related deaths had been attributed to SIDS, Community Health. 1987;41:63–71 the relationship of SIDS incidence to environmental 7. National Oceanic and Atmospheric Administration (United States). Heat Wave: A Major Summer Killer. Washington, DC: United States temperature would have remained insignificant. Department of Commerce; 1985. Available at: www.nws.noaa.gov/ Finally, it must be noted that either genetic or om/brochures/heatwave.pdf acquired abnormalities involving sweat gland func- 8. Centers for Disease Control and Prevention. Heat-related illnesses and tion or the thermoregulatory centers of the brain may deaths: United States, 1994 –1995. MMWR Morb Mortal Wkly Rep. 1995; render individuals vulnerable to heat stress, which 44:465– 468 9. Centers for Disease Control and Prevention. Heat-related deaths: Los can be fatal.48,49 It is also clear that the numbers of Angeles County, California, 1999 –2000, and United States, 1979 –1998. deaths primarily attributable to respiratory or car- MMWR Morb Mortal Wkly Rep. 2001;50:623– 626 diovascular disease increase during periods of envi- 10. United States Department of Health and Human Services, National ronmental heat stress.8,50 This has been attributed to Center for Health Statistics. Mortality Detail Files, 1979 –1980 (computer the fact that accommodation to increased environ- file). Hyattsville, MD: United States Department of Health and Human Services, National Center for Health Statistics; 1985 mental temperatures results in increased demands 11. United States Department of Commerce, Bureau of the Census. Census on the heart and lungs. Accordingly, it would be of Population and Housing, 1980 (United States): County Population by Age, expected that, if infants with SIDS have congenital or Sex, Race, and Spanish Origin (computer file). Washington, DC: United acquired abnormalities of thermoregulation or of re- States Department of Commerce, Bureau of the Census; 1982 spiratory or cardiovascular function, then the num- 12. National Climatic Data Center. Record of climatological observations, October 3, 2001, to January 2, 2002. Available at: http://nndc.noaa.gov/ bers of SIDS deaths would increase during periods of ?subscriptions.shtml dangerously elevated environmental temperatures. 13. Nelson EA, Taylor BJ, Weatherall IL. Sleeping position and infant This did not occur; therefore, it seems unlikely that a bedding may predispose to hyperthermia and the sudden infant death congenital or acquired defect in thermoregulation is syndrome. Lancet. 1989;1:199 –201 an underlying cause of a significant number of infant 14. Ponsonby AL, Dwyer T, Gibbons LE, Cochrane JA, Wang YG. Factors potentiating the risk of sudden infant death syndrome associate with deaths attributed to SIDS. the prone position. N Engl J Med. 1993;329:377–382 The present findings do not exclude the possibility 15. Hoffman HJ, Hillman LS. Epidemiology of the sudden infant death that a combination of factors, including increased syndrome: maternal, neonatal, and postneonatal risk factors. Clin Peri- body insulation or febrile illnesses associated with natol. 1992;19:717–737 the winter months, are causal in certain SIDS cases. 16. Fleming PJ, Gilbert R, Azaz Y, et al. Interaction between bedding and sleeping position in the sudden infant death syndrome: a population More research is needed on potential interactions based case-control study. BMJ. 1990;301:858 – 859 between these factors. However, given that the large 17. Kemp JS, Thach BT. Quantifying the potential of infant bedding to limit majority of infants were placed prone for sleep dur- CO2 dispersal and factors affecting rebreathing in bedding. J Appl ing the period of this study, it seems that heat stress Physiol. 1995;78:740 –745 produced by increased environmental temperatures 18. Carleton JN, Donoghue AM, Porter WK. Mechanical model testing of rebreathing potential in infant bedding materials. Arch Dis Child. 1998; and prone positions alone does not have a substan- 78:323–328 tial causal role in SIDS. 19. Ponsonby AL, Dwyer T, Couper D, Cochrane J. Association between use of a quilt and sudden infant death syndrome: case-control study. ACKNOWLEDGMENTS BMJ. 1998;316:195–196 This research was funded by National Institute of Child Health 20. Stanton AN, Scott DJ, Downham MA. Is overheating a factor in some and Human Development grant HD-10993. unexpected infant deaths? Lancet. 1980;1:1054 –1057 The data used in this study were made available in part by the 21. Beal S, Porter C. Sudden infant death syndrome related to climate. Acta Inter-University Consortium for Political and Social Research. The Paediatr Scand. 1991;80:278 –287 data for the Mortality Detail Files, 1979 –1980, were originally col- 22. Bass M, Kravath RE, Glass L. Death-scene investigation in sudden lected by the National Center for Health Statistics. The data for infant death. N Engl J Med. 1986;315:100 –105 Downloaded from www.aappublications.org/news by guest on August 31, 2021 http://www.pediatrics.org/cgi/content/full/113/6/e586 e591
23. Williams SM, Taylor BJ, Mitchell EA, et al. Sudden infant death 35. Rogot E, Sorlie PD, Backlund E. Air-conditioning and mortality in hot syndrome: insulation from bedding and clothing and its effect modifi- weather. Am J Epidemiol. 1992;136:106 –116 ers. Int J Epidemiol. 1996;25:366 –375 36. Jones TS, Liang AP, Kilbourne EM, Griffin MR. Morbidity and mortality 24. Krous HF, Nadeau JM, Fukumoto RI, Blackbourne BD, Byard RW. associated with the July 1980 heat wave in St. Louis and Kansas City, Environmental hyperthermic infant and early childhood death: circum- MO. JAMA. 1982;247:3327–3331 stances, pathologic changes, and manner of death. Am J Forensic Med 37. Kilbourne EM, Choi K, Jones TS, Thacker SB; Field Investigation Team. Pathol. 2001;22:374 –382 Risk factors for heatstroke. JAMA. 1982;247:3332–3336 25. Fleming PJ, Levine MR, Azaz Y, Wigfield R, Stewart AJ. Interactions 38. Klingenberg E. Heatwave: A Social Autopsy of Disaster in Chicago. Chicago, between thermoregulation and the control of respiration in infants: IL: University of Chicago Press; 2002:81– 84 possible relationship to sudden infant death. Acta Paediatr Suppl. 1993; 39. Smoyer K. Putting risk in its place: methodological considerations for 389:57–59 investigating extreme event health risk. Soc Sci Med. 1998;47:1809 –1824 26. Kinney HC, Filiano JJ, White WF. Medullary serotonergic network 40. Lowery W. The climate of cities. Sci Am. 1967;217(2):15–23 deficiency in the sudden infant death syndrome: review of a 15-year 41. Kalkstein L. Lessons from a very hot summer. Lancet. 1995;346:857– 859 study of a single dataset. J Neuropathol Exp Neurol. 2001;60:228 –247 42. Centers for Disease Control and Prevention. Heat-related deaths: 27. Danks DM, Webb DW, Allen S. Heat illness in infants and young United States, 1993. MMWR Morb Mortal Wkly Rep. 1993;42:558 –560 children. BMJ. 1962;2:287–293 43. Simon HB. Hyperthermia. N Engl J Med. 1993;329:483– 487 28. Kilbourne EM. Heat waves and hot environments. In: Noji EK, ed. The 44. Guyton AC, Hall JE. Textbook of Medical Physiology. 9th ed. Philadelphia, Public Health Consequences of Disasters. New York, NY: Oxford Univer- PA: W.B. Saunders Co; 1996:921 sity Press; 1997:245–269 45. Spitz WU, ed. Spitz and Fisher’s Medicolegal Investigation of Death: Guide- 29. Henschel A, Burton LL, Margolies L, Smith JE. An analysis of the heat lines for the Application of Pathology to Crime Investigation. 3rd ed. Spring- deaths in St. Louis during July, 1966. J Am Public Health. 1969;59: field, IL: Charles C. Thomas; 1993:181 2232–2241 46. Schuliar Y, Savourey G, Besnard Y, Launey JC. Diagnosis of heat stroke 30. Centers for Disease Control and Prevention. Heat-related deaths: Dal- in forensic medicine: contribution of thermophysiology. Forensic Sci Int. las, Wichita and Cooke counties, Texas, and United States. JAMA. 2001;124:205–208 1997;278:462– 463 47. Byard RW, Cohle SD. Sudden Death in Infancy, Childhood, and Adolescence. 31. Wadlington WB, Tucker AL Jr, Fly F, Green HL. Heat stoke in infancy. Cambridge, United Kingdom: Cambridge University Press; 1994:42 Am J Dis Child. 1978;130:1250 –1251 48. Darmstadt GL, Lane A. Ectodermal dysplasias. In: Behrman RE, Klieg- 32. Roberts KB, Roberts EC. The automobile and heat stress. Pediatrics. man RM, Arvin AM, eds. Nelson Textbook of Pediatrics. 15th ed. Phila- 1976;58:101–104 delphia, PA: W. B. Saunders Co; 1996:1837 33. Krous HF, Nadeau JM, Fukumoto RI, Blackbourne BD, Byard RW. 49. Foster KG, Hey EN, O’Connell B. Sweat function in babies with defects Environmental hyperthermic infant and early childhood death. Am J of the central nervous system. Arch Dis Child. 1971;46:444 – 451 Forensic Med Pathol. 2001;22:374 –382 50. McGeehin MA, Mirabelli M. The potential impacts of climate variability 34. King K, Negus K, Vance JC. Heat stress in motor vehicles: a problem in and change on temperature-related morbidity and mortality in the infancy. Pediatrics. 1981;68:579 –582 United States. Environ Health Perspect. 2001;109(suppl 2):185–189 Downloaded from www.aappublications.org/news by guest on August 31, 2021 e592 HEAT STRESS AND SIDS INCIDENCE
Heat Stress and Sudden Infant Death Syndrome Incidence: A United States Population Epidemiologic Study Joshua R. Scheers-Masters, Mario Schootman and Bradley T. Thach Pediatrics 2004;113;e586 DOI: 10.1542/peds.113.6.e586 Updated Information & including high resolution figures, can be found at: Services http://pediatrics.aappublications.org/content/113/6/e586 References This article cites 40 articles, 8 of which you can access for free at: http://pediatrics.aappublications.org/content/113/6/e586#BIBL Subspecialty Collections This article, along with others on similar topics, appears in the following collection(s): Fetus/Newborn Infant http://www.aappublications.org/cgi/collection/fetus:newborn_infant_sub SIDS http://www.aappublications.org/cgi/collection/sids_sub Permissions & Licensing Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: http://www.aappublications.org/site/misc/Permissions.xhtml Reprints Information about ordering reprints can be found online: http://www.aappublications.org/site/misc/reprints.xhtml Downloaded from www.aappublications.org/news by guest on August 31, 2021
Heat Stress and Sudden Infant Death Syndrome Incidence: A United States Population Epidemiologic Study Joshua R. Scheers-Masters, Mario Schootman and Bradley T. Thach Pediatrics 2004;113;e586 DOI: 10.1542/peds.113.6.e586 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://pediatrics.aappublications.org/content/113/6/e586 Pediatrics is the official journal of the American Academy of Pediatrics. A monthly publication, it has been published continuously since 1948. Pediatrics is owned, published, and trademarked by the American Academy of Pediatrics, 345 Park Avenue, Itasca, Illinois, 60143. Copyright © 2004 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 1073-0397. Downloaded from www.aappublications.org/news by guest on August 31, 2021
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