Issues

Volume 165 Issue 11

9 December 1996

Journal Activities The year that was Bronwen Ross (MJA 1996; 165: 592) Editorials Human rights reflections in daily medical practice Richard F Mollica (MJA 1996; 165: 594)Health care reform and quality of care Martin B Van Der Weyden (MJA 1996; 165: 595)Climate, health and medicine in a changing world Erwin K Jackson, Charles S Guest, Alistair J Woodward (MJA 1996; 165: 597) Airwaves Cancer and TV towers: association but not causation Ray A Cartwright (MJA 1996; 165: 599)Cancer incidence and mortality and proximity to TV towers Bruce Hocking, Ian R Gordon, Heather L Grain, Gifford E Hatfield (MJA 1996; 165: 601) Abstract - Article Water Hazards Serious injuries in jet skiers Elizabeth E L Swinburn (MJA 1996; 165: 606)Childhood drowning in New South Wales 1990-1995: a population-based study Daniel T Cass, Frank Ross, Lawrence T Lam (MJA 1996; 165: 610)Outbreak of cryptosporidiosis linked to an indoor swimming pool Jennifer M Lemmon, Jeremy M McAnulty, Jason Bawden-Smith (MJA 1996; 165: 613) Abstract - Article Grave Matters Digging in the desert Christopher D Browne, Maree G Browne (MJA 1996; 165: 617)Revealing secrets of a lost city Estelle Lazer (MJA 1996; 165: 620) Travel Medical travel: an opportunistic disease Yvonne E Cossart (MJA 1996; 165: 624)HUGs: Holidays for undergraduates Judy Harris (MJA 1996; 165: 628) Homeless Hard times for homeless people Helen E Herrman (MJA 1996; 165: 629)Children in homeless families in Melbourne: health status and use of health services Daryl Efron, Jillian R Sewell, Michael Horn, Francoise Jewell (MJA 1996; 165: 630)Asylum seekers: general health status and problems with access to health care Ingrid Sinnerbrink, Derrick M Silove, Vijaya L Manicavasagar, Zachary Steel, Annette Field (MJA 1996; 165: 634) Medicine in Asia Health care delivery system and major health issues in China Kong-Lai Zhang, Min Liu, Dan Li (MJA 1996; 165: 638)Health services in Indonesia Soewarta Kosen, Suriadi Gunawan (MJA 1996; 165: 641) The Research Enterprise The Queensland Institute of Medical Research Lawrie W Powell (MJA 1996; 165: 645)The Garvan Institute of Medical Research John Shine (MJA 1996; 165: 649)Forty years at the pitface in the Walter and Eliza Hall Institute of Medical Research Donald Metcalf (MJA 1996; 165: 652)Australia's fourth Nobel laureate for medicine Antony Basten (MJA 1996; 165: 656) Bites and Stings Worldwide deaths and severe envenomation from jellyfish stings Peter J Fenner, John A Williamson (MJA 1996; 165: 658)Severe envenomation by the taipan (Oxyuranus scutellatus) David A Southern, Victor I Callanan, Geoffrey S Gordon (MJA 1996; 165: 662) food Safety foodborne disease: how to respond? Craig W Hedberg (MJA 1996; 165: 667)foodborne disease: emerging problems and solutions Patricia M Desmarchelier (MJA 1996; 165: 668)foodborne disease: current trends and future surveillance needs in Australia Scott K Crerar, Craig B Dalton, Helen M Longbottom, Edward Kraa (MJA 1996; 165: 672) True Stories An encounter with a Haitian refugee boat Andrew J Galbraith, David C McGiffin (MJA 1996; 165: 678)The caesarean section Douglas N Gow (MJA 1996; 165: 680)

Airwaves

Medical practices 9 December 1996 Free

Cancer and TV towers: association but not causation

Cancer and TV towers: association but not causation A more complete knowledge of the causes of childhood leukaemia is essential before progressing from association to causation MJA 1996; 165: 599 Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". - ©MJA1996 Nothing concentrates public concern more than links -- real or supposed -- between pollution from man-made objects and malignant diseases. This is probably made worse if we do not particularly enjoy the aesthetic appeal of the objects in question, and worse still if we do not understand what the biological effects might be of the pollutants involved. This situation is exemplified by the study by Hocking et al. in this issue of the Journal. They report an excess of leukaemia in people living near the TV towers just north of Sydney, the excesses being mainly in children and in certain time periods. Technically epidemiologists will regard such an observation as an "association" -- that is to say, pretty difficult (if not impossible) to understand in isolation and one which has to be put into context. Is this association in Sydney the product of one of these quirks of distribution? How does one interpret the study of Hocking et al.? Such a question is effectively asking: how can an epidemiological study lead to a causal link being established between radiofrequency irradiation and leukaemia in children? Several informative steps are required. Firstly, is this a new observation? The answer is, nearly but not quite. The authors themselves refer to a rather unsatisfactory study from Honolulu, which might show a non-statistically significant leukaemia excess near radio transmitters. 1 In addition, and potentially more interesting, an extensive study in Britain has shown a nearly twofold excess in leukaemia in residents close to one particular TV transmitter complex -- but only in mixed types of leukaemia in adults and not in children. 2 However, when all the other TV and related radio transmitters in Britain were studied this excess was not confirmed, although a decline in leukaemia incidence with distance from the towers was observed. It should be noted that the adult leukaemias are very different diseases, in terms of causation, from childhood acute leukaemia, 3 as indeed the different types of adult leukaemias are from each other. 4 As these other studies do not unequivocally support the findings of Hocking et al., we are left with two further lines of enquiry. One is to ask whether there are other explanations for the leukaemia excesses in northern Sydney, and the second is to question what is known of the physical properties of this type of non-ionising irradiation and whether there are any abnormal biological effects consequent on exposure of human tissue. There is not a great deal known of the possible harmful biological effects of radiofrequency non-ionising irradiations and nothing which might suggest that they cause malignant diseases. 5 A great deal more is known of the lower energy electromagnetic fields (50-60 Hz), but here, broadly speaking, no studies have yet suggested a likely biological link with a leukaemogenic process. This unsatisfactory state of affairs fuels public and clinical concerns and has led to a small epidemic of studies on childhood leukaemias aimed at investigating (using case-control methods) all known and hypothesised causes of the condition. These studies, in New Zealand, Canada, the United States, the United Kingdom and Germany, are all coming to fruition over the next few years. Not only do they represent the concern of the public, but also the general lack of knowledge of common risk factors for childhood leukaemias. Thus, other possible explanations for the observation of Hocking et al. are limited at the moment. Nevertheless, a good deal of descriptive epidemiology of childhood leukaemias is available, mainly from the United Kingdom. 6 This throws up some remarkable features of the diseases. Leukaemia is not evenly distributed among the childhood population -- it is roughly twice as common in areas that are either geographically isolated from major conurbations or of greater affluence. 7 Furthermore, childhood leukaemias do occasionally form close case aggregations or clusters. 8 Rare diseases will form striking clusters by chance, but in the case of childhood acute lymphoblastic leukaemia more occur than simply by chance. Where and why is not known, but is under investigation. 9 Is this association in Sydney the product of one of these quirks of distribution? Is there a local case excess in an affluent area, or even an unrecognised cluster of leukaemia? The way forward would certainly include a closer look at the Sydney data for evidence of these phenomena. Area cluster statistics should be used, 10 as well as a more rigorous application of point-source statistics, which, for example, look for decline in rates by distance for a putative point hazard. 11 These possible local studies, together with epidemiological studies from elsewhere, might show similar, and thus supporting, results. There is also the possibility of new biological studies supporting a causal link. However, a more complete knowledge of the causes of childhood leukaemia is essential in order to go down the road from association to causation. In that regard we have taken only the first few steps of a very long journey. Ray A Cartwright Professor of Cancer Epidemiology Leukaemia Research Fund, University of Leeds, Leeds, UK Maskarinec G, Cooper J, Swygert L. Investigation of increased incidence in childhood leukaemia near radio towers in Hawaii: preliminary observations. J Environ Pathol Toxicol Oncol 1994; 13: 33-37. Dolk H, Elliott P, Shaddick G, et al. Leukaemia incidence near high power radiotransmitters [abstract]. Epidemiology 1996; 7(Suppl 4): S95. Doll R. The epidemiology of childhood leukaemia. J R Statist Soc Ser A 1989; 152: 341-351. McKinney PA, Alexander FE, Roberts BE, et al. Yorkshire case-control study of leukaemias and lymphomas parallel multivariate analyses of seven disease categories. Leuk Lymphoma 1990; 2: 67-80. National Radiological Protection Board. Electromagnetic fields and the risk of cancer. Report of an Advisory Group on Non-Ionising Radiation. Vol 3, No. l. Chilton, Didcot, Oxfordshire: National Radiological Protection Board, 1992. Draper G, editor. The geographical epidemiology of childhood leukaemia and non-Hodgkin's lymphoma in Great Britain 1966-1983. London: HMSO, 1990. Alexander FE, Ricketts TJ, McKinney PA, Cartwright RA. Community lifestyle characteristics and risk of acute lymphoblastic leukaemia in children. Lancet 1990; 336: 1461-1465. Cartwright RA, Alexander FF, McKinney PA, Ricketts TJ. Leukaemia and lymphoma: an atlas of distribution within areas of England and Wales 1984-1988. London: Leukaemia Research Fund, 1990. Alexander FE, Wray N, Boyle P, et al. Clustering of childhood leukemia: a European study in progress. J Epidemiol Biostat 1996; 1: 13-24. Chen R, Mantel N, Kingberg M. A study of three techniquest of time-space clusters in Hodgkin's disease. Stat Med 1984; 3: 173-184. Bithell JF, Stone RA. On statistical methods for analysing the geographical distribution of cancer cases near nuclear installations. J Epidemiol Commun Health 1989; 43: 79-85. - To top of article - ©MJA 1996 <URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Ray A Cartwright

Medical practices 9 December 1996 Free

Cancer incidence and mortality and proximity to TV towers

Cancer incidence and mortality and proximity to TV towers Bruce Hocking, Ian R Gordon, Heather L Grain and Gifford E Hatfield MJA 1996; 165: 601 For editorial comment, see Cartwright Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discussion - Conclusion - References - Authors' details - ©MJA1996 Abstract Objective: To determine whether there is an increased cancer incidence and mortality in populations exposed to radiofrequency radiations from TV towers. Design: An ecological study comparing cancer incidence and mortality, 1972-1990, in nine municipalities, three of which surround the TV towers and six of which are further away from the towers. (TV radiofrequency radiation decreases with the square of the distance from the source.) Cancer incidence and mortality data were obtained from the then Commonwealth Department of Human Services and Health. Data on frequency, power, and period of broadcasting for the three TV towers were obtained from the Commonwealth Department of Communications and the Arts. The calculated power density of the radiofrequency radiation in the exposed area ranged from 8.0 µW/cm 2 near the towers to 0.2 µW/cm 2 at a radius of 4 km and 0.02 µW/cm 2 at 12 km. Setting: Northern Sydney, where three TV towers have been broadcasting since 1956. Outcome measures: Rate ratios for leukaemia and brain tumour incidence and mortality, comparing the inner with the outer areas. Results: For all ages, the rate ratio for total leukaemia incidence was 1.24 (95% confidence interval [CI], 1.09-1.40). Among children, the rate ratio for leukaemia incidence was 1.58 (95% CI, 1.07-2.34) and for mortality it was 2.32 (95% CI, 1.35-4.01). The rate ratio for childhood lymphatic leukaemia (the most common type) was 1.55 (95% CI, 1.00-2.41) for incidence and 2.74 (95% CI, 1.42-5.27) for mortality. Brain cancer incidence and mortality were not increased. Conclusion: We found an association between increased childhood leukaemia incidence and mortality and proximity to TV towers. MJA 1996; 165: 601-605 Introduction The biological effects of low level electromagnetic fields and any relation to cancer causation are controversial. There have been several epidemiological studies of possible effects of extremely low frequency (50 Hz) fields, 1 but few have looked at radiofrequency radiations (RFR) (i.e., frequencies of 300 kHz to 300 GHz). Goldsmith, 2 in a recent review, concluded that there may be an association between RFRs and cancer; however, a World Health Organization review concluded that there is no clear evidence of detrimental health effects in humans exposed to RFR. 3 An opportunity for studying the effect of RFR presents itself in northern Sydney, New South Wales, where three TV towers are sited in a triangle close to each other (Figure 1). The towers have been used to broadcast three TV services since 1956 and four since 1965. The channel frequencies range from 63 to 215 MHz; the wavelengths (ranging from 5 m to 1 m) are close to body reson ances and hence are maximally absorbed. 3 We compared cancer incidence and cancer mortality for the three municipalities (Lane Cove, Willoughby and North Sydney -- population, 135 000) which immediately surround the TV towers (inner area) with data for six adjacent municipalities (Ryde, Ku-ring-gai, Warringah, Manly, Mosman and Hunters Hill -- population, 450 000) (outer area) (Figure 1), on the basis that the RFR becomes progressively weaker with the square of the distance from the towers across these municipalities. The control municipalities were selected because of the similar distance from the towers to their nearest borders, their resi dents having a similar upper-middleclass socioeconomic status, 4 and their areas being large enough for there to be a decrease in power density. Cancers of interest were leukaemia and brain tumour, especially in childhood, given findings from community studies of extremely low frequency (50 Hz) electro magnetic fields. 1 We had no prior knowledge of, nor had concerns been raised about, clusters of leukaemia cases in the areas close to the towers. Methods Radiofrequency radiation Data for frequency and power of the RFR sources on the towers for the period 1956-1990 were obtained from the Commonwealth Department of Communications and the Arts 5 and are shown in Box 1.1. The TV signals are composed of 100 kW video amplitude modulated (AM) and 10 kW audio frequency modulated (FM) signals, on carrier frequencies which range from 63 to 215 MHz. The combined field strengths at increasing distances were calculated by the method of the United States National Council on Radiation Protection and Measurement 6 (Box 1). There were no TV repeater stations in the inner or outer areas during the survey period. Cancer data The NSW Cancer Registry maintains a comprehensive database allowing distinction between incidence and mortality, and giving residence at the time of report. 4 Data from the registry for 1972 to 1990 are available from HealthWiz 7 and were extracted by municipality, and for sex and age bands 0-14 years, 15-69 years and 70 years and over. The data are available only for the three-digit code categories identified by the International classification of diseases, injuries and causes of death , ninth revision (ICD-9). More refined data are not available for reasons of privacy. Cancer data from before 1972 are not available. Statistical analysis The data were analysed using a Poisson regression model, 8 in which the number of cases or deaths were regarded as Poisson random variables, whose mean is a product of the person-years (i.e., the sum of appropriate mid-year populations) pertaining to the observation and the functions of the explanatory variables. These models give rate ratio estimates for comparisons of interest, adjusted for the other variables. Interactions were examined, and the model tested for goodness-of-fit. We made adjustment for extra-Poisson variation, when necessary, using the "quasi-likelihood" method of McCullagh and Nelder. 9 The explanatory variables fitted in these models were: age in years (0-14, 15-69, 70 and over), sex, calendar period (1972-1978, 1979-1984 and 1985-1990), and area ("inner" [close to the TV towers] and "outer" [more distant]) (Figure 1). For comparisons between the areas of interest and the whole of New South Wales, standardised incidence ratios (SIRs) and standardised mortality ratios (SMRs) were calculated. For these analyses the stratification was by calendar-year (19 separate years), age and sex. Confidence intervals were calculated by the "exact" method. 10 Results Box 2 shows the data structure used in the analysis; the leukaemia cases and person-years in each cell were obtained by summing across the years for that age-group and sex combination. The rate ratios comparing the inner with the outer areas are shown in Boxes 3 and 4. No increase in brain cancer incidence or mortality was found, but there was an increased leukaemia incidence and mortality in the municipalities close to the towers. The rate ratio for childhood leukaemia incidence (Box 4) was 1.58 (95% CI, 1.07-2.34) and for mortality was 2.32 (95% CI, 1.35-4.01). These rates were broadly consistent across the types of leukaemia; for lymphatic leukaemia, the rate ratio was 1.55 for incidence and 2.74 for mortality. Our analysis pooled data from the inner and outer municipalities. To see whether results within each municipality were similar, we performed tests of homogeneity for childhood leukaemia incidence and mortality. No significant heterogeneity was found ( P = 0.10 for incidence and P = 0.13 for mortality). We found no significant overall trends across time for brain cancer or leukaemia incidence, for all ages combined or for children alone. For children, there was a significant overall reduction in leukaemia mortality over time ( P = 0.008), but no significant evidence of a change over time in the differences between the outer and inner areas in brain cancer or leukaemia incidence or mortality, for all ages combined or for children alone. Because a small part of Hunters Hill projects close to the TV towers (Figure 1) and there is a potential confounder there (a factory which used radium until the 1970s in Hunters Hill), the data were analysed excluding Hunters Hill. The incidence rate ratio for childhood leukaemia was 1.56 (95% CI, 1.09-2.22), and for all ages was 1.23 (95% CI, 1.06-1.43). Childhood cancer incidence and mortality (brain cancer and leukaemia) for the inner and outer areas were compared with cancer incidence and mortality data for the whole of New South Wales (Box 5). There was no difference for cancer of the brain. Leukaemia incidence and mortality were significantly increased in the inner area, but incidence and mortality data for the outer area were similar to data for the State as a whole. Discussion This ecological study found an association between residential proximity to TV towers and increased incidence of childhood leukaemia. Study biases Studies of this type are prone to biases. 1. Comparison of the inner and outer areas: Socioeconomic class has been associated with leukaemia, with a positive association with higher socio economic status. However, all muni cipalities considered in the inner and outer areas are ranked in the top two socioeconomic quintiles; further, two out of three of the inner municipalities are in the top quintile, and four out of six of the outer municipalities are in the top quintile. 4 Moreover, for New South Wales as a whole there is no evidence of a socioeconomic gradient for leukaemia. 4 There are small pockets of light industry in the surveyed municipalities, but they are mainly residential. The area closer to the TV towers is subject to much higher traffic density than the outer area, and exhaust fumes contain small traces of benzene, a proven leukaemogen. 11 However, a causal relationship between exhaust fumes and childhood leukaemia has not been established; 11 in occupational studies benzene exposure is related predominantly to acute myeloid leukaemia, 12 but we found an increased incidence/mortality of lymph atic leukaemia in the inner areas. 2. Confounding variables affecting individuals can not be adjusted for. The few recognised causes of leukaemia include ionising radiation, cytotoxic drugs and some uncommon genetic conditions. 13 The only known potential community exposure to ionising radiation in the study area is a factory in Hunters Hill that used radium until the 1970s. There are no high voltage power lines traversing the inner area, but one traverses the outer area and runs along the border between Lane Cove and Ryde in a national park. Individual (household) exposure cannot be determined, and therefore local enhancements and attenuations of RFR , which might influence dose-response calculations, cannot be allowed for. Usually, exposures in flats and houses will be lower than those for free space, such as gardens, parks and schoolyards. 3. Population movement cannot be adjusted for. Thus, miscalculations arise if people move out of, or into, particular areas for selective reasons (e.g., treatment of cancer is offered at Royal North Shore Hospital, which is in the inner area). This would not influence incidence, but could influence mortality data if patients with cancer came to live closer to the hospital for ease of access. However, it appears most childhood leukaemia cases attend children's hospitals not in the study area. A linkage study of cases could resolve this. On the other hand, social mobility would tend to obscure effects that have long latency periods. Duration of residence would need to be determined in a more detailed study. Migration to new towns has been suggested as a confounding factor in childhood leukaemia clusters, 14 with viral spread to susceptible persons, but the areas surveyed in this study are long established. Greaves, 15 using a similar argument, postulated that fewer infectious stimuli in early postnatal life, with later infection at a critical period, may play a major role in precipitating acute lymphoblastic leukaemia. According to this theory, less dense populations mean less exposure to infections early in life and higher rates of leukaemia. However, of the areas surveyed the inner area is the more densely populated (2818 per km 2 , compared with 1378 per km 2 ). 16 Effects of radiofrequency radiation The calculated exposure levels of 8.0 to 0.2 µW/cm 2 in the inner area are very low compared with the Australian Standard 17 public exposure level of 0.2 mW/cm 2 . The mechanism whereby such low energies could cause biological effects is a matter of intense research. A recent report by the Commonwealth Scientific and Industrial Research Organisation (CSIRO) concluded that reliance on thresholds for heat build-up in setting the Australian safety standard may be insufficient. 18 The TV frequencies considered, because of their wavelengths in relation to body heights, are close to body resonance, 3 leading to maximum absorption by both adults (including pregnant women 19 ) and children. However, in considering any biological effects, regard must be given to the modulations (50 Hz to 5 MHz) as much as to the carrier wave. The key video modulation frequencies are pulsed at 50 Hz and 15.6 kHz. Many and conflicting reports have been published about possible biological effects at low energy levels with low frequency amplitude modulations. 3,18,20,21 Stuchly et al. found that 60 Hz low-level fields may act as promoters of cancer. 22 It has been suggested that the biological effects may be on the cell membrane rather than the genetic material, 23 and that low energy signals are detected through non-linear mechanisms, such as stochastic resonance. 24 The disparity between our calculations and the measured power densities could result from various mechanisms, including absorption of the signal and cancellation due to reflections, especially as the minimum of one signal is unlikely to coincide with the minimum of another, even being different for the audio and vision signals of one channel. An extensive measurement program is needed to develop detailed contour maps to better define dose-response relationships. Techniques such as isotonic regression could be used; this enables effects of a point source on a surrounding community to be analysed. 25 The new services since 1980 will have increased the power density due to Tower 1 by four times, most of this being due to ultra high frequency (UHF) TV (526-533 MHz) and FM radio. A number of other services, such as mobile phone and paging services, may have also been established in the surveyed areas. However, these are of much lower power and/or use different carrier frequencies and/or modulations to the TV broadcast services. Radiofrequency radiation and cancer? An association between RFR and childhood leukaemia has not been reported previously. None of the previous studies of RFR has looked at exposure of such a large population (including children) for so long a time to frequencies of maximal body absorption. A study of people working on TV towers did not find evidence of chromosome damage, 26 and among 32 cases of neoplasms of the blood in Telecom Australia employees (retiring for medical reasons or dying) there was no excess in radiocommunication occupations (Hocking, unpublished data). A small study from Honolulu (Hawaii), where broadcast towers are also situated in populated areas, compared census tracts with towers with those without towers and found a non-significant standarised incidence ratio of 1.5 for all types of leukaemia. 27 A preliminary report of a small area study of leukaemia near 20 TV/FM transmission sites in the United Kingdom found a decline in incidence of adult leukaemia with distance, but concluded that "the results give, at most, no more than weak support for an association between residence near transmitters and leukaemia risk". 28 However, that study was restricted to adult leukaemia and incidence, whereas our most significant results were for childhood leukaemia incidence and mortality. The time trend for childhood leukaemia incidence has remained fairly stable, consistent with a constant exposure, and the reduction noted in the childhood leukaemia mortality rate most likely reflects improvements in treatment. If RFR exposure is a relevant (causal) factor, classification of population into inner and outer areas is a proxy for the appropriate exposure variable, which would tend to bias the rate ratios towards the null (i.e., towards no effect) due to non-differential misclassification. This is relevant to the irregular natural boundaries of the municipalities (Figure 1). Analysis by postcode or census collector units would yield more refined data in relation to distance from the towers. Finally, our observation of a more marked association between proximity to TV towers and leukaemia mortality than incidence (Box 4) could be of biological interest if a putative exposure not merely caused the disease but influenced its progression. Conclusion The calculated levels of RFR in the areas with increased childhood leukaemia incidence and mortality are substantially below the current Australian public safety standard. More detailed studies (e.g., relating cases to power density contours) are required to replicate any association and to look for dose-response relationships before any conclusions can be drawn. References Savitz D, Ahlbom A. Epidemiologic evidence of cancer in relation to residential and occupational exposures. In: Carpenter D, Ayrapetyan S, editors. Biological effects of electric and magnetic fields. Chapter II. Vol 2. Sydney: Academic Press, 1994: 233-261. Goldsmith JR. Epidemiologic evidence of radio-frequency (microwave) effects on health in military broadcasting and occupational studies. Int J Occup Med Environ Health 1995; 1: 47-57. World Health Organization. Environmental Health Criteria 137 Electromagnetic fields (300 Hz to 300 GHz). WHO: Geneva, 1993: 164-168, 74-75. Smith D, Taylor R, Coates M. Socioeconomic differentials in cancer incidence and mortality in urban New South Wales 1987-1991. Aust N Z J Public Health 1996; 20: 129-137. Department of Communications and the Arts. Radio and Television Broadcasting Stations. Canberra: AGPS, 1994. National Council on Radiation Protection and Measurement. A practical guide to the determination of human exposure to radiofrequency fields. Bethesda, Md: NCRP, 1993. (NCRP Report No. 119.) HealthWiz. National health database. Commonwealth Department of Human Services and Health. 1991-1996. Canberra: Prometheus Pty Ltd, 1996. Frome EL. The analysis of rates using Poisson regression models. Biometrics 1983; 39: 665-674. McCullagh P, Nelder JA. Generalized linear models. London: Chapman and Hall, 1983: 80-81. Liddell J. Simple exact analysis of the standardised mortality ratio. J Epidemiol Community Health 1984; 38: 85-88. UK Department of the Environment. Expert Panel on Air Quality Standards. Benzene. London: HMSO, 1994. Akasoy M. Benzene carcinogenicity. Boca Raton, Fl: CRC Press, 1988: 119-125. Doll R, Darby S. Childhood leukaemia in the United Kingdom. Radiat Protect Aust 1990; 8(3): 55-61. Childhood leukaemia: an infectious disease? [editorial]. Lancet 1990; 336: 1477-1479. Greaves MF. Etiology of childhood acute lymphoblastic leukemia: a soluble problem? In: Gale RP, Hoelzer D, editors. Acute lymphoblastic leukemia. UCLA Symposium on Molecular and Cellular Biology. New Series Vol 108. New York: Academic Press, 1989. Digital Cadastral Database. Bathurst, NSW: Land Information Centre. Australian Standard AS2772.1. Radiofrequency Radiation Part 1: Maximum Exposure Levels -- 100 kHz to 300 GHz. Sydney: Standards Australia, 1990. Barnett S. Status of research on biological effects and safety of electromagnetic radiation: telecommunications frequencies. Chatswood: Division of Radiophysics CSIRO, 1994. Fleming AHJ, Joyner KH. Estimates of the absorption of radiofrequency radiation by the embryo and foetus during pregnancy. Health Phys 1992; 63: 149-159. Adey R. Effects of weak amplitude modulated microwave fields on calcium efflux from awake cat cerebral cortex. Bioelectromagnetics 1982; 3: 295-307. Adey R. Frequency and power windowing. Proc IEEE (Proceedings of the Institution of Electrical and Electronic Engineers) 1980; 68 (1): 119-125. Stuchly MA, McLean J, Burnett R, et al. Modification of promotion in the mouse skin by exposure to an alternating magnetic field. Cancer Lett 1992; 65: 1-7. Weaver J, Astumian RD. The thermal noise limit for threshold effects of electric and magnetic fields in biological systems. In: Carpenter D, Ayrapetyan S, editors. Biological effects of electric and magnetic fields. Chapter 3, Vol 1. Sydney: Academic Press, 1994: 83-104. Moss F, Wiesenfield K. The benefits of background noise. Sci Am 1995; August: 50-54. Stone RA. Investigations of excess environmental risk around a putative source. Statistical problems and a proposed test. Stat Med 1988; 7: 649-660. Garson MO, McRobert TL, Campbell LJ, et al. A chromosomal study of workers with long-term exposure to RFR. Med J Aust 1991; 155: 289-292. Maskarinec G, Cooper J, Swygert L, et al. Investigation of increased incidence in childhood leukaemia near radio towers in Hawaii: preliminary observations. J Environ Pathol Toxicol Oncol 1994; 13: 33-37. Dolk H, Elliott P, Shaddick P, et al. Leukaemia incidence near high power radio transmitters [abstract]. Epidemiology 1996; 7(Suppl 4): S95.(Received 3 Oct 1995, accepted 25 Sep 1996) Authors' details Bruce Hocking and Associates, 9 Tyrone Street, Melbourne, VIC. Bruce Hocking , FAFOM, FAFPHM, Consultant in Occupational Medicine. Statistical Consulting Centre, University of Melbourne, Melbourne, VIC. Ian R Gordon , PhD, Director. System Innovations in Health, PO Box 125, Melbourne, VIC. Heather L Grain , ADipMRA, GDipDP, Consultant. Broadcast & Radiation Safety Consulting, Melbourne, VIC. Gifford E Hatfield , MSEE, Managing Director. No reprints will be available. Correspondence: Dr B Hocking, 9 Tyrone Street, Camberwell, VIC 3124. To top of article - ©MJA 1996 <URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Bruce Hocking · Ian R Gordon · Heather L Grain · Gifford E Hatfield

Water Hazards

Emergency medicine 9 December 1996 Free

Serious injuries in jet skiers

Serious injuries in jet skiers Elizabeth E L Swinburn Personal motorised watercraft (often referred to as jet skis) are an enjoyable leisure activity on the nation's waterways. However, there have been several serious accidents, and licensing requirements are deficient. Inconsistent reporting of accidents has hindered investigations into the causes. We describe six recent cases and the factors that may have contributed to accidents, and suggest ways to reduce the hazards associated with the sport. MJA 1996; 165: 606 Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Introduction - Discussion - Conclusions - Acknowledgement - References - Author's details - ©MJA1996 Introduction Motorised personal watercraft (MPWC), colloquially referred to as jet skis, are a popular recreational device and are the fastest growing section of the Australian boat market (sales have increased by 10%-15% per year for the last four years). 1 MPWCs are defined by the Waterways Authority (NSW) (formerly, the Maritime Services Board) as a vessel of no more than 3.5 m in length with a fully enclosed hull, which is power driven and designed to be operated by a person standing, sitting astride or kneeling on the craft, but the driver is not sealed inside the vessel. They are distinct from non-motorised personal watercraft (e.g., surf skis, surfboards, canoes and kayaks) and are capable of speeds of up to 72 kt (125 km/h). They are also being trialled as rescue craft by Surf Life Saving Australia Limited. There are many regulations controlling their use which are governed by the Waterways Authority (see Box 1). There are 4300 registered MPWC owners in NSW. 4 During a recent campaign to assess irresponsible use of MPWCs, 1466 MPWCs were stopped and 68 infringement notices were issued. Of these, 55% related to licensing and registration and 21% concerned safety issues. 4 We report six patients who presented to the Royal North Shore Hospital (RNSH) Emergency Department in Sydney over a four-year period (1992-1996) with serious or fatal injuries sustained while riding an MPWC. Four patients were identified by a search of hospital medical records from 1990 to 1995 and another from a search of the trauma database. Another patient was identified after an analysis of Waterways Authority data. The St John Ambulance Service (NSW), Water Police, Surf Life Saving Australia Limited and the Australian Institute of Health and Welfare National Injury Surveillance Unit did not have data on MPWC injuries. Four patients gave permission to publish their case histories, one declined, and the other was unable to be contacted. Case 1 Case 2 Case 3 Case 4 Discussion MPWCs are generally perceived by the public to be a fun (albeit noisy) way to enjoy many of the nation's coastal and inland waterways. There are many hire outlets, especially in holiday areas, and they may advertise that no licence is required. One establishment stated: "If you can sit on a chair when you're drunk, then you can ride a jetski when you're sober." The six patients who presented to our emergency department show that MPWCs can cause accidents that may result in injury or even death. In total, these patients accounted for over 130 hospital-days (18 in the intensive care unit). At time of writing, two patients are still in hospital and there has been one death. Their average age was 31 years, which is similar to that of the 25 cases of MPWC incidents reported to the Waterways Authority (Box 2). Unofficial data collected by the Surfriders Foundation Australia suggest there have been three fatalities in NSW (J Bradley, officer in charge of MPWCs, personal communication). The first report of MPWC injury was in 1989, and involved 13 people injured over the previous three-year period, including two fatalities.5 Three other overseas studies reported injuries to 134 people caused by MPWCs.6-8 None of these studies reported fatalities. The only Australian study pertaining to MPWCs was a case report of a full-thickness vaginal laceration extending to the peritoneal cavity. 9 Although six of the eight drivers involved in serious accidents reported to the Waterways Authority were licensed, it is of concern that the cause of the collision was poor judgement, excess speed or failure to keep a proper lookout in five of these accidents. This suggests that the licensing requirements may be inadequate. Currently, a boat driver's licence is required to operate an MPWC. However, the knowledge pertaining to driving a boat may not be sufficient to drive an MPWC in a safe manner, in the same way that the knowledge and/or skills required to drive a motor vehicle and a motor bike are different and they therefore require separate licences. Of the six cases that presented to our hospital, three riders were licensed and very experienced and two were not licensed. It is not known if the remaining rider was licensed. All that is needed to obtain a boat driver's licence in NSW is to pass a written test set by the Waterways Authority, and the person must be at least 16 years of age. There are no restrictions on MPWC engine capacity; recent models are 1100 cc and weigh over 250 kg without passengers. 10 New licensees can immediately drive any size machine at any speed, whereas (in NSW and some other States) newly licensed motorbike riders are restricted to machines of engine capacity of no greater than 250 cc. Another area of concern is the lack of reporting of MPWC incidents. A requirement of having a boating licence is that when an accident results in death or injury to a person, or damage to property, a written report must be forwarded to the Waterways Authority within 24 hours. 2 Only three of the six cases presenting to our hospital were reported to the Waterways Authority. The United States Coast Guard estimated that only 10% of non-fatal watersports accidents were reported.8 Case 4 was not reported, despite aninvestigation by the NSW Police Service at the time. Anecdotal reports suggest that there is a high incidence of personal injury to MPWC drivers (particularly inexperienced drivers), with bruising to the groin region the most common injury. However, MPWC drivers are often reluctant to report incidents because they fear that this will lead to increased regulation of their sport. All holders of a boat driver's licence are restricted to a blood alcohol level of less than 0.05% (or 5 g/100 mL). Under the Marine (Boating Safety -- Alcohol and Drugs) Act 1991 (NSW), people who present to a hospital after an injury incurred while in charge of a boat or MPWC must have blood taken for blood alcohol testing. Five of the six people who presented to our hospital were not tested for blood alcohol levels (one tested negative). No data are available on whether alcohol was involved in any of the incidents reported to the Waterways Authority. United States data suggest that more than half of boating deaths are associated with alcohol.11 An Australian review of alcohol and accidental drowning reported that, of 29 male victims of moving water-transport accidents, 10 had postmortem blood alcohol concentrations of over 15 g/100 mL.12 The Australasian Jet Sports Boating Association (AJSBA) conducts races in Australia and New Zealand each week and has strict safety regulations. Competitors must wear helmets and many also wear leg protectors and back protectors. Some form of medical coverage is provided at all competitions, and all competitors are covered by insurance. In 10 years of competition there have been no fatalities and no serious injuries. The average age of racers is 30 years. The AJSBA is assisting some States to formulate regulations (M DeBie, General Manager, AJSBA, personal communication). Conclusions The public needs to be educated about the potential dangers involved with riding MPWCs and of the necessity for a boating licence. The Waterways Authority should consider implementing a practical examination for those wishing to drive an MPWC, and possibly also introducing a speed or engine- capacity limit for new licensees. Present deficiencies in the reporting of MPWC accidents need to be addressed. The Waterways Authority accepts reports from anyone involved, not just the licensee. Alerting ambulance and police officers, lifesavers and hospital emergency department staff of the need for reporting incidents would be an effective approach. Emergency department staff also need to be aware that blood must be taken after MPWC accidents to determine blood alcohol concentrations. A simple preaddressed form (similar to the adverse drug reaction report form used by the Australian Drug Evaluation Committee) could be made available to emergency services and hospitals and also to registered MPWC owners and holders of boating licences. A comprehensive reporting system would assist in further research into the incidence, severity and causes of MPWC accidents. Acknowledgement Photos courtesy of the Waterways Authority (NSW). References Lewis D. It's war on the water: a blitz on jetskiers. Sydney Morning Herald 1996 Mar 23; Sect 1: 4. Waterways Authority. NSW safe boating handbook. Sydney: Waterways Authority, May 1995. The Royal Life Saving Society - Australia. Swimming and lifesaving. 3rd ed. Sydney: Mosby Lifeline, 1995. New South Wales Department of Public Works and Services. Media Release. 1996; May 19. Vernberg D, Fine EG, Jagger J. Personal water craft injuries [letter]. JAMA 1989; 261: 1883. Francis RA, Vize R. Personal water craft injuries: experience at a community hospital. Missouri Med 1994; 91: 241-243. Jeffery RS, Caiach S. Waterbike injuries. Br J Sports Med 1991; 25: 232-234. Hamman BL, Miller FB, Fallat ME, Richardson JD. Injuries resulting from motorized personal watercraft. J Pediatr Surg 1993; 28: 920-922. Wein P, Thompson DJ. Vaginal perforation due to jet ski accident. Aust N Z J Obstet Gynaecol 1990; 30: 384-385. Personal watercraft buyers guide. In: King M, editor. Jet Action; 1996 May-June: 54. Bradley J. Growing public menace caused by ineffective control of motorised personal watercraft in the surf. Proceedings of the Local Governments Authority Fourth Annual NSW Coastal Council Conference; 1994 Oct 18-20; Terrigal, NSW. Plueckhahn VD. Alcohol and accidental drowning. Med J Aust 1984; 141: 22-25. (Received 11 June, accepted 30 Sep 1996) Author's details Emergency Department, Royal North Shore Hospital, St Leonards, NSW. Elizabeth E L Swinburn, MB BS. No reprints will be available. Correspondence: Dr E E L Swinburn, Emergency Department, Royal North Shore Hospital, St Leonards, NSW 2065. - To top of article - ©MJA 1996 <URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Environmental health 9 December 1996 Free

Outbreak of cryptosporidiosis linked to an indoor swimming pool

Outbreak of cryptosporidiosis linked to an indoor swimming pool Jennifer M Lemmon, Jeremy M McAnulty and Jason Bawden-Smith MJA 1996; 165: 613 Subsequently cited in Sinclair I, Fairley CK, Hellard ME. Protozoa in drinking water: is legislation the best answer? MJA 1998; 169: 296-297. Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - Authors' details - ©MJA1996 Abstract Objective: To determine the extent and source of a community outbreak of cryptosporidiosis. Design: Questionnaire-based survey and matched case-control study. Setting: Sutherland area in southern Sydney, September 1994 to January 1995. Participants: 70 patients reported by pathology laboratories to have stool specimens positive for cryptosporidia, of whom 43 were surveyed; 35 were compared with age- and neighbourhood-matched controls. Main outcome measures: Demographic characteristics and potential risk factors in the two weeks before onset of illness. Results: Laboratories reported 70 cases of cryptosporidiosis between September 1994 and January 1995. We found no association between illness and foods consumed or contact with people with diarrhoea or sick animals in the two weeks before onset. Seventeen of the case group (49%) reported swimming in a particular indoor swimming pool, compared with only seven controls (20%) (odds ratio, 3.7; P = 0.015). Cryptosporidial oocysts were detected in water from the swimming pool in January 1995. Conclusions: The outbreak of cryptosporidiosis was probably associated with ingestion of water from the indoor swimming pool, presumably contaminated by infected bathers. Recommendations: As it is difficult to eradicate cryptosporidia from swimming pools by either disinfection or filtration, we recommend that:People with recent diarrhoea should avoid public swimming pools; and Non-toilet-trained and faecally incontinent swimmers should be provided with alternative swimming facilities with separate water and filtration systems. To enable appropriate public health responses:Doctors and pathology laboratories should consider cryptosporidiosis in patients with diarrhoea lasting longer than three days; and Laboratory reporting of cryptosporidia to local health departments should be mandatory in all States and Territories. MJA 1996; 165: 613-616 Introduction The protozoan Cryptosporidium parvum was first recognised as a cause of illness in humans in 1976. 1 In the 1980s, cryptosporidia were reported to cause life-threatening, cholera-like illness in the immunosuppressed. 2 Subsequently, cryptosporidia were reported to produce a spontaneously resolving illness in the immunocompetent, characterised by diarrhoea with profuse watery stools lasting days to months, abdominal pain, nausea, vomiting, malaise and low-grade fever. 3 There is no known effective treatment. 4 Cryptosporidia (Figure 1) are common in the environment and are excreted in the faeces of those infected. They can be transmitted through contact with infected cattle, sheep and other animals, 5-7 person-to-person contact, 8 contaminated water supplies 4,9 and swimming. 10-12 Cryptosporidial infection was not a notifiable disease in New South Wales at the time of the study, and many laboratories do not routinely screen stool specimens for crypto sporidia. 3 Thus, we do not know the incidence of this disease in the community, nor the relative importance of different modes of transmission. In January 1995, a general practitioner in the Sydney suburb of Sutherland reported to the Southern Sydney Public Health Unit increases in numbers of patients presenting with watery diarrhoea and of stool specimens positive for cryptosporidia at a local laboratory. We therefore investigated the extent and source of this outbreak of crypto sporidiosis. Figure 1: Cryptosporidium oocysts from a faecal specimen. Modified Ziehl-Neelson stain; original magnification x 1000 (slide courtesy of Dr Stephen A Neville). Methods Methods were similar to those used by McAnulty et al. 10 and included a case survey and investigation of likely sources of the cryptosporidia, by comparison of cases and matched controls and an environmental study. Case survey In January 1995, the five major pathology laboratories serving the Sutherland area (defined as the area bounded by the Pacific Ocean to the east, Georges River to the north and the Royal National Park to the south) were asked to report all stool specimens in which crypto sporidia had been detected since September 1994. Two of the pathology laboratories examined stool specimens microscopically for cryptosporidial oocysts with a modified Ziehl-Neelsen acid-fast stain (modified by decolorising with hydrochloric acid and ethanol and counterstaining with malachite green) if structures suggestive of protozoa were seen on wet-mount examination. 13 The other three laboratories did not screen for cryptosporidia unless requested by the referring medical practitioner. Case patients were defined as people with a stool specimen positive for cryptosporidia between 1 September 1994 and 20 January 1995. Because of the high rate of person-to-person spread, cases were classified as primary (first to report diarrhoea in a household) and secondary (subsequent household cases). All people diagnosed as case patients after 1 December 1994 (and reported before 20 January 1995) and aged over 18 years were interviewed by telephone in January 1995 with a 34-item structured questionnaire. Interview was with parents if the patient was less than 18 years old. The questionnaire asked about the illness and about potential risk factors in the two weeks before onset of illness, including travel outside Sydney; childcare attendance; contact with other people with diarrhoea, or with pets and domestic animals; swimming; and sources of drinking water. The period of two weeks was chosen to include the incubation period for cryptosporidiosis of 1-12 days (average, about seven days). 14,15 People diagnosed before 1 December 1994 were not interviewed in detail because of the potential for poor recall given the time since infection. Case-control study To identify likely sources of infection, we compared potential risk factors of case patients with those of matched control subjects who had had no gastrointestinal symptoms in the previous two weeks, selected from a computerised telephone directory. Each matched control subject lived in the same street as (or within two streets of) the case patient and was matched for age within three years (for case patients younger than eight years), five years (for case patients aged 8-25 years), or 10 years (for case patients older than 25 years). Control subjects were administered a 23-item questionnaire on potential risk factors, referring to the two weeks before Christmas 1994. We chose this period as it was relatively easily identified by subjects and the season was similar or identical to that during the outbreak, so that conditions for swimming (a potential risk factor) were comparable. Differences in characteristics and risk factors between primary and secondary cases were tested for significance with either the c 2 test or, if expected cell size was less than five, with a two-tailed Fisher exact test. Differences between matched pairs of cases and controls were tested for significance with the probability of the maximum likelihood estimate of the odds ratio. 16 Swimming pool investigation We investigated a community swimming pool visited by some case patients (pool A), examining filtration systems and maintenance and chlorination records for the period November 1994 to January 1995. In addition, samples of poolwater and filter backwash water (water passed backwards through the filter to clean it) from this pool were tested for Crypto sporidium oocysts and Giardia cysts. For testing, water was filtered through a polycarbonate membrane (pore size, 2 m m for Cryptosporidium oocysts, or 5 m m for Giardia cysts), which was washed clean; washings were mixed with fluorescent antibody specific for either cryptosporidia or giardia. Particles were sorted by size and fluorescence with a flow cytometer and their identity confirmed by microscopy. 17 Filtration systems used at local government-owned swimming pools in the inner, eastern and southern areas of Sydney were surveyed. Operators were asked over the telephone about the type of filtration system used and whether general-use pools shared their water and filtration systems with pools for infants. Results Case survey We identified 70 cases of cryptospori diosis diagnosed between 1 September 1994 and 20 January 1995. Fortnightly incidence is shown in Figure 2. Characteristics and potential risk factors of the 43 case patients reported between 1 December 1994 and 20 January 1995 are shown in Box 1. (Another five case patients were diagnosed in the week to 20 January but not reported until later and so were not surveyed.) Symptoms included diarrhoea (42 of the 43 patients, 98%), cramping abdominal pain (23, 53%), vomiting (21, 49%), nausea (16, 37%) and fever (16, 37%). None of the people affected reported being immunocompromised; more than half were children aged under 4.5 years. Twenty-eight cases were primary and 15 secondary. The only significant differences between the primary and secondary cases were that secondary-case patients were more likely to be male (80% of secondary cases versus 36% of the primary cases; P < 0.01) and, as expected, were more likely to have had contact with people with diarrhoea (100% of secondary cases versus 25% of primary cases; P < 0.001). Figure 2: Cases of cryptosporidiosis diagnosed by laboratories in the Sutherland area of Sydney, 1 September 1194 - 20 January 1995 (specimen date was unknown for two cases). Case-control study Of the 43 cases reported between 1 December 1994 and 20 January 1995, five were excluded from the case-control study as they lived outside the Sutherland area, and three were excluded as matched controls could not be identified. As primary- and secondary-case patients reported similar potential risk factors, both sets of patients were included in the case-control study. Potential risk factors in the case and control groups are compared in Box 2. There was no association between illness and attendance at childcare, contact with people with diarrhoea, and drinking bottled water or city water. Although more of the case group than the control group reported swimming in the two weeks surveyed, the difference was not significant. However, significantly more in the case group than in the control group reported swimming in pool A. There was no significant association between cryptosporidiosis and swimming in any other pool. Swimming pool investigation Pool A is an indoor heated swimming pool located in a popular community swimming complex that caters for all ages from infants to adults. Average daily attendance between 1 September and 1 December 1994 was 1269 people (range, 1092-1443). The complex includes three outdoor pools (none associated on epidemiological grounds with cryptosporidiosis), as well as the indoor pool. The indoor pool comprises a 25-metre swim area, a teaching and aquarobics area (used by infant and toddler learn-to-swim classes), and a "bubble" area (with air jets, and popular with children). It contains about 1.6 million L of water and has a rapid sand filtration system, separate from the filtration systems for the outdoor pools. Chlorine levels in pool A, documented every three hours between 6 am and 9 pm daily, ranged from 0.55 to 5.0 mg/L. The New South Wales Health Department recommends that chlorine levels for indoor pools be maintained at 1.5 mg/L for those heated to less than 26¡C, and at a minimum of 2.0 mg/L for warmer pools. 18 Pool A was heated to more than 26¡C, and chlorine levels were in the recommended range 28% of the time. Eleven Cryptosporidium oocysts and 57 Giardia cysts were detected in a 55-L sample of the pool water taken in January 1995, but none in a 500-mL sample of filter backwash water. Among the 20 local government-owned pools surveyed, filtration used sand at 19, and fine-grade diatomaceous earth (a porous form of silica, composed of the fossilised shells of a type of alga) was used in the other. At all these pool complexes, general purpose pools and infants' pools shared water and filtration systems. As a result of the investigation, management at pool A erected signs warning patrons of the possibility of pool-water contamination and instructing that people who were not toilet-trained, who were faecally incontinent or who had had diarrhoea in the previous week should not enter the pool. The public was warned through a press release of the possible connection between the pool and cryptosporidiosis. On 20 January 1995, to allay public concern, pool A operators decided to replace the water in the pool and the outbreak subsequently abated. Discussion This is the first report of an outbreak of cryptosporidiosis associated with swimming in Australia. The outbreak, which lasted several months, was also the largest reported point-source outbreak of crypto sporidiosis in Australia. As many laboratories do not routinely screen for cryptosporidia, and as doctors may not order examination of stool specimens and people with diarrhoea may not consult a doctor, 3,9 there were undoubtedly many more cases of cryptosporidiosis than those reported. This outbreak probably began when the water in indoor swimming pool A was contaminated with cryptosporidia from an infected bather. The likelihood of contamination was increased by the pool's use by infants and children too young to be faecally toilet trained (crypto sporidia are present in the faeces of those infected). The infective dose of C. parvum causing illness in humans remains unclear, but recent evidence suggests it is very low (e.g., a dose of 30 oocysts has been reported to cause infection in a healthy volunteer). 19 While chlorine levels in pool A were not optimal, higher levels would have been unlikely to have prevented the outbreak, as cryptosporidial oocysts are extremely resistant to chlorine and can survive many days in chlorinated water. 20 We do not know if protection from ultraviolet light in the indoor pool may have enhanced cryptosporidial survival. While swimming at pool A was strongly associated with crypto sporidiosis, it explained only 49% of cases. No other single pool was significantly associated with illness and, as the epidemic subsided with draining of pool A, others were not tested. However, it is possible that others in the case group were infected at pools other than pool A (although not identified in our survey), or by direct contact with people with the disease, given the small infective dose. The localised nature of the outbreak and the age distribution of those affected (i.e., children or parents) indicated that drinking Sydney water was not a likely source of the outbreak. Detection of cryptosporidial oocysts in water from pool A confirmed the epidemiological findings that C. parvum contaminated the pool. However, the viability of the organisms detected is unknown. Although Giardia cysts were also detected, they are relatively sensitive to chlorine and unlikely to be viable. 20 Furthermore, local laboratories reported no increase in detection of Giardia cysts in stool specimens. Sand filtration systems have been implicated in previous swimming pool-related outbreaks of cryptosporidiosis, 10 and almost all of the local government-operated pools surveyed relied on this type of filtration. An uneven sand surface in this type of filter -ay reduce its efficiency. 11 Alternative filtration systems, such as those with diatomaceous earth, may be more effective in removing oocysts. However, swimming pools with malfunctioning diatomaceous earth filters have also been implicated in outbreaks of crypto sporidiosis. 12 There is not enough information on the comparative effectiveness of different filtration systems to warrant recommending one form of filtration over another at present. Because of the difficulty of eradicating cryptosporidia from swimming pools by either disinfection or filtration, preventing similar outbreaks depends on reducing contamination through the cooperation of swimmers and pool operators. 11 Patrons who have had diarrhoea in the previous week, who are faecally incontinent or not toilet trained should be discouraged from using the pool by signs at the pool entrance and in the change rooms. Similar recommendations have been made for controlling swimming pool-associated crypto sporidiosis in the United States. 10 In addition, new swimming pool complexes should provide separate facilities with their own filtration systems for patrons who are not toilet trained or who are faecally incontinent. People using these facilities should avoid swallowing pool water. Screening swimming pools for crypto sporidia would be of little use at present, as current detection methods do not determine oocyst viability and consequent ability to cause disease. In 1995, a Centers for Disease Control and Prevention workshop concluded that current knowledge about cryptosporidia, and about waterborne cryptosporidiosis in particular, is minimal and does not provide a scientifically sound basis for many essential decisions about the public health risks associated with infection. 21 In Australia, we do not know the incidence of cryptosporidiosis in the community or the extent to which swimming pools contribute to transmission. A first step in obtaining this information is to make cryptosporidiosis a notifiable disease and to encourage doctors and laboratories to consider cryptosporidiosis as a diagnosis in patients with diarrhoea lasting longer than three days. In 1995, South Australia was the only Australian State to require routine reporting of cryptosporidial detection by laboratories and doctors to public health authorities. Since then, Victoria and Queensland have introduced the requirement and New South Wales followed suit on 1 December 1996. Introducing this requirement in all States and Territories would assist in early detection and control of future outbreaks of cryptosporidiosis. Acknowledgements We thank Dr Philip Lye (Sutherland Division of General Practice), Sugermans Pathology (Hurstville), Dr Gary Grohmann (Australian Water Technologies) and the staff of the former Southern Sydney Public Health Unit for their assistance. References Nime FA, Burek JD, Page DL, et al. Acute enterocolitis in a human being infected with the protozoan Crypto sporidium . Gastroenterology 1976; 70: 592-598. Current WL. Cryptosporidiosis parvum : household transmission [editorial]. Ann Intern Med 1994; 120: 518-519. Berkelman RL. Emerging infectious diseases in the United States, 1993. J Infect Dis 1994; 170: 272-277. Gallaher MM, Herndon JL, Nims LJ, et al. Crypto sporidiosis and surface water. Am J Public Health 1989; 79: 39-42. Miron D, Kenes J, Dagan R. Calves as a source of an outbreak of cryptosporidiosis among young children in an agricultural closed community. Pediatr Infect Dis J 1991; 10: 438-441. Casemore DP. Sheep as a source of human cryptosporidiosis. J Infect 1989; 19: 101-104. Reif JS, Wimmer L, Smith JA, Dargatz DA, Cheney JM. Human cryptosporidiosis associated with an epizootic in calves. Am J Public Health 1989; 79: 1528-1530. Newman RD, Zu SX, Wuhib T, et al. Household epidemiology of Cryptosporidium parvum infection in an urban community in northeast Brazil. Ann Intern Med 1994; 120: 500-505. MacKenzie WR, Hoxie NJ, Proctor ME, et al. A massive outbreak in Milwaukee of Cryptosporidium infection transmitted through the public water supply. N Engl J Med 1994; 331: 161-167. McAnulty JM, Fleming DW, Gonzalez AH. A community-wide outbreak of cryptosporidiosis associated with swimming at a wave pool. JAMA 1994; 272: 1597-1600. Joce RE, Bruce J, Kiely D, et al. An outbreak of cryptosporidiosis associated with a swimming pool. Epidemiol Infect 1991; 107: 497-508. Sorvillo FJ, Fujioka K, Nahlen B, et al. Swimming- associated cryptosporidiosis. Am J Public Health 1992; 82: 742-744. Rusnak J, Hadfield TL, Rhodes MM, Gaines JK. Detection of Cryptosporidium oocysts in human fecal specimens by an indirect immunofluorescence assay with monoclonal antibodies. J Clin Microbiol 1989; 27: 1135-1136. Jokiph LJ, Jokiph DMM. Timing of symptoms and oocyst excretion in human cryptosporidiosis. N Engl J Med 1986; 315: 1643-1647. Benenson AS. Control of communicable diseases manual. 16th ed. Washington: American Public Health Association, 1995. Dean AG, Dean JA, Coulombier D. Epi Info Version 6. Atlanta (GA): Centers for Disease Control and Prevention, 1994. Vesey G, Narai J, Ashbolt N, et al. Detection of specific microorganisms in environmental samples using flow cytometry. Methods Cell Biol 1994; 42: Pt B: 489-522. Marsh C. Guidelines for disinfecting public swimming pools and spa pools. Sydney: New South Wales Health Department, 1991. DuPont HL, Chappell CL, Sterling CR, et al. The infectivity of Cryptosporidium parvum in healthy volunteers. N Engl J Med 1995; 332: 13: 885-859. Korich DG, Mead JR, Madore MS, et al. Effects of ozone, chlorine dioxide, chloride and monochloramine on Cryptosporidium parvum oocyst viability. Appl Environ Microbiol 1990; 56: 1423-1428. Centers for Disease Control and Prevention. Assessing the public health threat associated with waterborne cryptosporidiosis: report of a workshop. MMWR Morb Mortal Wkly Rep 1995; 44 (no. RR-6): 15. (Received 17 Apr, accepted 12 Aug 1996) Authors' details Southern (now South Eastern) Sydney Public Health Unit, Sydney, NSW. Jennifer M Lemmon, BNurs, ICC, RGN, Infectious Diseases Consultant; Jeremy M McAnulty, MB BS, MPH, Director; currently, Specialist Medical Adviser, New South Wales Department of Health; Jason Bawden-Smith, MEnvStudies, Environmental Health Officer. No reprints will be available. Correspondence: Ms J M Lemmon, South Eastern Sydney Public Health Unit, PO Box 482, Kogarah, NSW 2217. To top of article - ©MJA 1996 <URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Jennifer M Lemmon · Jeremy M McAnulty · Jason Bawden-Smith

Bites and stings

Emergency medicine 9 December 1996 Free

Worldwide deaths and severe envenomation from jellyfish stings

Worldwide deaths and severe envenomation from jellyfish stingsPeter J Fenner and John A Williamson From our database of fatal and serious human envenomations, we report several cases, look at the distribution of these events, and discuss treatment. MJA 1996; 165: 658 Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Introduction - Distribution of jellyfish and reported envenomations - Sting seasons - Reflections on treatment - Applying vinegar - Removing adherent tentacles - The role of steroid therapy - Chironex fleckeri antivenom - Conclusions - Acknowledgments - References - Authors' details - ©MJA1996 Introduction We have collected worldwide information about jellyfish and their stings since 1990, through personal communication with members of the International Consortium of Jellyfish Stings (ICJS), 1 investigating reports of serious jellyfish stings heard on the "grapevine", and travelling in areas of chirodropid (multitentacled "box" jellyfish) distribution. Annual reports of our data have been published from 1991 to 1993. 2 Our database now records over 1100 individual cases of stings (some severe and fatal), as well as some 1000 monthly reports of jellyfish numbers and stings, from surf life saving clubs in Queensland over the past six years. Our data are only the "tip of the iceberg" and probably an inadequate indication of the extent of the problem worldwide. However, we continue to seek information, now also by internet and e-mail. Our data include information on envenomation by Physalia , the Portu guese man-o'-war or bluebottle. Although not a true jellyfish (actually a siphonophore, or hydroid colony), it stings like one, is popularly regarded as one, and we treat it as one in this article. A brief description of the mechanism of a jellyfish sting is provided in Box 1. While many suspected deaths from envenomation, and the jellyfish species involved, remain inadequately authenticated, documented deaths from jellyfish stings usually involve species of chirodropid, 5,6 described and shown in Box 2. In this article we examine the distribution of serious and fatal jellyfish envenomations (illustrated in the Map), the animals involved and aspects of treatment, and we describe some previously unreported cases (Table). Distribution of jellyfish and reported envenomations Australia In Australia, particularly on the east coast, up to 10 000 stings occur each summer from the bluebottle (Physalia spp.) alone, with others also from the "hair jellyfish" (Cyanea) and "blubber" (Catostylus). More bluebottle stings occur in South Australia and Western Australia, as well as stings from a single-tentacled box jellyfish, the "jimble" (Carybdea rastoni) (personal data) . The chirodropid Chironex fleckeri 3,4,8 is known to be the most lethal jellyfish in the world, 3 and has caused at least 63 recorded deaths in tropical Australian waters off Queensland and the Northern Territory since 1884. 3 Indo-Pacific region The presence of chirodropids has now been confirmed in the tropical Indo-Pa cific ocean from the Maldive Islands 9-12 in the west, eastwards to the Philippines, north to Amani Island, Japan (see below), and south to tropical Australia; this includes Brunei, Sarawak, Sabah (L Marsh, Curator of Marine Invertebrates, West Australian Museum, 1993, personal communication), Papua New Guinea, the Malaysian archipelago, Gulf of Thailand, 8 Java and southern India. 12 Deaths have previously been reported from Penang (Malaysia), the Philippines, Bougainville Island, the Solomon Islands, "North Borneo" (now Sarawak, Brunei, Sabah), and Papua New Guinea (d'Entrecasteaux Islands). 8 Medical officers at the Labuan District Hospital (in Malaysia) have been quoted as saying that there are two to three deaths there each year from jellyfish stings and another one or two victims who survive, but require intensive care and commonly remain unconscious for 12-24 hours. 13 Chirodropid jellyfish are well known in the Philippines, and an estimated annual death rate from jellyfish stings there of 20-40 does not seem excessive (P J F, 1987, personal experience). More recently, Dr Paul Cornelius, of the British Museum of Natural History, has made a similar estimate of fatalities (unpublished observations, April 1994). As a death certificate is not necessary for burial in the Philippines, these estimates cannot be verified. World map showing human fatalities from chirodropid and other jellyfish stings, and presently confirmed and probable chirodropid distribution. The Americas Chirodropids have been described in waters along the eastern coast of the Americas between the Tropics, including the waters around many Caribbean islands. 11,14 Serious stings from these chirodropids have also been reported from beaches in Puerto Rico during the summer months (B Cutress, Associate Investigator, Marine Biology Department, Puerto Rico University, 1992, personal communication). In 1990, a 4-year-old boy at Galveston Island, in the Gulf of Mexico, was stung and died within 20 minutes, despite cardiopulmonary resuscitation. 6 Stinging cells were identified as being from a chirodropid previously described in that region. 14 Three fatal envenomations from Physalia physalis have been reported from Florida and North Carolina, in the United States. 15,16 Serious envenomations have also been reported from both sides of the Atlantic. 17-19 China Apart from Physalia species and chirodropids, the only other jellyfish presently known to cause deaths in humans are large specimens (up to 1 m diameter) of Stomolophus nomurai (Mingliang, Research Assistant, Qingdao Hospital, 1991, personal communication), a jellyfish found in the Yellow Sea between China and South Korea. Reports of eight deaths have now been published, five in detail. 20,21 Victims die with acute pulmonary oedema some 2-24 hours after the initial envenomation. Africa A chirodropid occurs in the tropical oceans of west Africa, 22,23 but we know of no published reports of deaths or serious stings. Although chirodropids have not been reported to occur on the eastern tropical coastline of Africa, they must be expected in these waters. South India and Sri Lanka Serious jellyfish envenomations occur in the Indian region, with peripheral ischaemia reported in at least two victims. 24,25 Although the jellyfish is frequently unidentified, chirodropids, Sanderia and Physalia species occur in this region. Two fatalities were reported recently on the eastern side of the Indian Ocean, on Langkawi Island, a tourist resort in Kedah, a northern state of Malaysia. From the rapid demise of the victims, and appearance of sting marks, they probably died of chirodropid envenomation (Dr Iekhsan Othman, Malaysia, personal communication). 12 Sting seasons In the Southern Hemisphere, chirodropid stings occur mainly in the summer months (December-May), 3 but over a longer season in areas closer to the Equator. In the Northern Territory stings have occurred in every month, with deaths in all months except July. 3,4,8 Chirodropids may occur only in December and January at the southern extreme of their recorded range (just north of Bundaberg, Queensland). 3 In the northern area of Borneo (Northern Hemisphere), stings usually occur in the dry hot season, from March to July, when seas are calm. Reflections on treatment Applying vinegar Two to 10 per cent acetic acid in water was recommended as a first-aid treatment for Chironex fleckeri nematocyst inhibition by Hartwick et al. in 1980. 26 Household vinegar has been a traditional treatment for box jellyfish stings in the Philippines since the turn of the century, although other "traditional" treatments were also used. Fishermen in Kukup also describe stings from cubozoan jellyfish in Malaysia as being treated with vinegar (P J F, personal observation, 1987). We do not know how long this remedy has been used. In two cases recorded on our database ( Table, Cases 3 and 7), victims seemed to stop breathing after vinegar was poured on the envenomed area. Whether this was a cause-related effect is not known; further research is needed. Removing adherent tentacles In another of our cases ( Table, Case 5), removal of the adherent tentacle material was accompanied by impairment of consciousness. Our advice has been for the rescuers to remove the tentacles physically with fingers, if vinegar is unavailable, before applying any compression bandages. 3 While this single report scarcely invalidates such advice, further case studies and research are awaited. The issue of removing adherent tentacle material in any jellyfish (especially serious chirodropid) stinging is complex. Fully extended tentacle material presents most of the nematocysts to the victim's skin, 27 and most will have discharged by the time adherent tentacles on the skin are being dealt with by the first-aiders. However, even partial contraction of tentacle material protects some nematocysts from discharge upon contact, 27 and the response of chirodropid tentacles to sudden entanglement with a human victim seems likely to involve at least some immediate tentacular contraction. Consequently, it seems probable that some nematocysts in adherent tentacle material will remain undischarged, and inappropriate stimulation could result in additional venom being injected into an already seriously envenomed person. If tentacles have not been inactivated with vinegar, 26 it would seem prudent to carefully, but promptly, "pick them off" the patient's skin with minimal handling, and no rubbing, before applying either compression bandages (in the case of serious chirodropid stings) or analgesic cold packs (for use in chirodropid or other cnidarian stings). Applying compression bandages directly over untreated adherent tentacle material cannot be recommended. However, once tentacles have been doused with vinegar for a minimum of 30 seconds, no time should be lost in removing them before applying bandages. 3 One of our cases (Table, Case 3) describes papilloedema after a chirodropid sting. This is the first such observation published, although Heazlewood (personal communication, 1992) reports a case of cerebral oedema in a 4-year-old in Cairns in 1980, after an "irukandji" (the carybdeid Carukia barnesi ) sting. The role of steroid therapy Steroid creams may be useful for mild itching in the immediate healing period after a cubozoan sting, 27 although Burnett 3 now doubts their efficacy. Systemic steroids should be used for severe cases of delayed hypersensitivity, given as prednisone (0.5-1 mg/kg body weight, daily), until the symptoms are fully controlled -- usually just a few days. After such a short course, it is unnecessary to taper the dose. Chironex fleckeri antivenom The exact mechanism of action of Chironex fleckeri venom and antivenom remains incompletely understood, despite several studies. 28,29 The efficacy of Chironex fleckeri antivenom in stings from the Australian chirodropid named Chiropsalmus quadrigatus is also unclear -- as is the exact identification of this species. 3 An early study showed in-vitro neutralisation of the dermatonecrotic, haemolytic and lethal factors of the venom of this Australian species when Chironex antivenom was used. However, although passive immunisation of mice with the antivenom reduced dermato necrosis, it did not protect against the lethal effects of Chiropsalmus quadrigatus venom. 30 Another study, using rabbit antisera prepared against Chironex fleckeri venom, showed no in-vitro cross- protection against the venom of Chiropsalmus quadrigatus . 31 However, the Commonwealth Serum Laboratories (CSL) currently recommends the use of Chironex antivenom for severe envenomation from the Australian " Chiro psalmus quadrigatus ". The possible benefits of Chironex antivenom for severe envenomations by chirodropids worldwide need investigation. Chironex antivenom has been shown to be of little benefit in the "irukandji" syndrome (it neither relieves the pain of envenomation nor reduces any other systemic problem), 32 and is currently not recommended for envenomation from any other (non-chirodropid) jellyfish species. Conclusions Lethal, or potentially lethal, chirodropid jellyfish occur worldwide, around every major land mass in the tropical and some subtropical oceans, and deaths and serious morbidity are more common than previously believed. Physicians practising in these areas, or those advising people who travel to such areas, must be aware of the problem, and advise their patients on awareness, prevention and treatment (summarised in Box 3) of potentially lethal jellyfish envenomation. The toxicology of the venoms needs further study. Acknowledgments We would like to thank Associate Professor Nor Azila and Dr Iekhsan Othman (Malaysia), Loisette Marsh (Australia), Major (Dr) R Hooper (Sabah), Dr T K Chan, Bertha Cutress (Puerto Rico), Drs Y Tomihara, Y Araki and M Kohama (Japan) for assistance with compilation of data. The photograph at the beginning of this section was provided by Surf Life Saving Queensland Inc. References Burnett JW. International consortium of jellyfish stings [letter]. J Wilderness Med 1990: 1; 135-137. Fenner PJ, Williamson JA, Burnett J. Some Australian and international marine envenomation reports; progress summary to October 31 1993. Adelaide: International Consortium for Jellyfish Stings, Department of Hyperbaric Medicine, Royal Adelaide Hospital, 1994. Williamson JA, Fenner PJ, Burnett JW, Rifkin J, editors. Venomous and poisonous marine animals: a medical and biological handbook. Surf Life Saving Australia and University of New South Wales Press Ltd, Sydney, 1996. Currie B, Khanh DM, Alderslade P, et al. Jellyfish envenomation in the Northern Territory of Australia. Toxicon 1992: 30; 501. Fish CJ, Cobb MC. Noxious marine animals of the central and western Pacific Ocean. Res Rep US Fish Ser 1954; 36: 1-45. Bengston K, Nichols MM, Schnadig V, Ellis MS. Sudden death in a child following jellyfish envenomation by Chiropsalmus quadrumanus ; Case report and autopsy findings. JAMA 1991; 266; 10: 1404-1406. Fatal sting in Labuan. Malaysian Straits Times 1992 Jul 22: 1 (Cols 1-2). Cleland JB (Sir), Southcott RV. Injuries to man from marine invertebrates in the Australian region. Special report series no.12. Canberra: NHMRC, 1965. Haeckel E. System der Acraspeden: zweite halfle des System der Medusen . Jena: Gustav Fischer, 1880: 447. Barnes JH. Chironex fleckeri and Chiropsalmus quadrigatus : Morphological distinctions. North Queensland Naturalist 1965; 32: 13-22. Kramp PL. Synopsis of the medusae of the World. J Marine Biol Assoc UK 1961; 40: 304-310. Menon MGK. Scyphomedusae of Krusadai Island. Bull Madras Govt Museum, NS Nat Hist Sect 1936; 1(2): 1-9. Tan NH, Oo SL, Thambyrajah V, Azila N, editors. Advances in venom and toxin research. Proceedings of the Third Asia Pacific Congress on Animal, Plant and Microbial Toxins; 1993 27 Jun-1 Jul; Malaysia. Kuala Lumpur: Malaysian Society on Toxinology, 113-118. Guest WC. The occurrence of the jellyfish Chiro psalmus quadrumanus in Matagorda Bay, Texas. Bull Mar Sci Gulf Carib 1959: 9; 79-83. Burnett JW, Gable WD. A fatal jellyfish envenomation by the Portuguese man-o'-war. Toxicon 1989; 27: 823-824. Stein MR, Marraccini JV, Rothschild NE, Burnett JW. Fatal Portuguese man-o'war ( Physalia physalis ) envenomation. Ann Emerg Med 1989; 18: 312-315. Halstead BW. Poisonous and venomous marine animals of the world. Princeton, NJ; Darwin Press, 1978: 301. Gonzaga RAF. Mordeduras picadas pot animas da forna Portuguesa . Amber-Porto-Portugal. Premio Biol de Medicina Clinics 1984; 165-167. Burnett JW, Fenner PJ, Kokelj F, Williamson JA. Serious Physalia (Portuguese Man-o'-war) stings: implications for scuba divers. J Wilderness Med 1994: 5; 71-76. Mingliang Z. A study on nematocyst dermatitis caused by jellyfish Stomolophus numerai . Acta Acad Med Qingdao 1987; 4: 1. Mingliang Z. The marine stinger. Qingdao: Oceanology University Press, 1992: 51. Kramp PL. The Medusae of the tropical west coast of Africa. Atlantide [report 3]. Copenhagen: University of Copenhagen and British Museum (Natural History), 1955: 288-292. Pages F, Gili JM, Bouillon J. Planktonic cnidarians of the Benguela current. Scientia marina 1992; 56 (suppl): 1-444. Adiga KM. Brachial spasm as a result of a sting. Med J Aust 1984; 140: 180-181. Williamson JA, Burnett JW, Fenner PJ, et al. Acute regional vascular insufficiency after jellyfish envenomation. Med J Aust 1988; 149: 698-701. Hartwick RJ, Callanan V, Williamson JAH. Disarming the box jellyfish: nematocyst inhibition in Chironex fleckeri . Med J Aust 1980; 1: 15-20. Williamson JAH, Le Ray LE, Wolfhart M, Fenner PJ. Acute management of serious envenomation by box-jellyfish ( Chironex fleckeri ). Med J Aust 1984; 141: 851-853. Othman I, Burnett JW. Techniques applicable for the purifying of Chironex fleckeri (box-jellyfish) venom. Toxicon 1990; 28: 821-835. Freeman SE. Actions of Chironex fleckeri toxins on cardiac transmembrane potentials. Toxicon 1974; 12: 395-404. Baxter EH, Marr AGM. Sea wasp ( Chironex fleckeri ) antivenene: neutralising potency against the venom of three other jellyfish species. Toxicon 1974; 12: 223-229. Keen TEB. Comparison of tentacle extracts from Chiropsalmus quadrigatus and Chironex fleckeri. Toxicon 1971; 9: 249-254. Fenner P, Rodgers D, Williamson J. Box jellyfish antivenom and "Irukandji" stings. Med J Aust 1986; 144: 665-666. Authors' details Corner of Palmer and Grendon Streets, North Mackay, QLD. Peter J Fenner, FACTM, FRCGP, General Practitioner and Marine Stinger Officer, Surf Life Saving Queensland Inc. Hyperbaric Medicine Unit, Department of Anaesthesia and Intensive Care, Royal Adelaide Hospital, Adelaide, SA. John A Williamson, FANZCA, FACTM, Director and Associate Professor. No reprints will be available. Correspondence: Dr P J Fenner, PO Box3080, North Mackay, QLD 4740. To top of article - ©MJA 1996 <URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Peter J Fenner · John A Williamson

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Carolyn Quadrio

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Bruce R Tulloh · Marjorie E Goldsworthy

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Treatment decision-making at the end of life: a survey of Australian doctors' attitudes towards patients' wishes and euthanasia

Charles Waddell · Rodger M Clarnette · Michael Smith · Lynn Oldham · Allan Kellehear

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Patterns of alternative medicine use by cancer patients

Stephen D Begbie · Zoltan L Kerestes · David R Bell

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