DCEC 2838/2017 [2022] HKDC 59 IN THE DISTRICT COURT OF THE HONG KONG SPECIAL ADMINISTRATIVE REGION EMPLOYEES’ COMPENSATION CASE NO. 2838 OF 2017 ________________ IN THE MATTER OF AN APPLICATION BETWEEN: | | CHIU KWAI YUK (趙桂玉) for herself and on behalf of
members of the family of LEE CHI WAI (李志偉), deceased | Applicant | | | and | | | LEE TAK WAH trading as HATCO EXHIBITION PRODUCTION COMPANY
(李德華經營凱高展覽製作公司) | 1st Respondent | | | ASCENT EXHIBITION DESIGN (HONG KONG) LIMITED
(灝瀚展覽設計(香港)有限公司) | 2nd Respondent | | | Employees Compensation Assistance Fund Board | 3rd Respondent |
________________ Coram: His Honour Judge Harold Leong in Court Date of Hearing: 16, 18-19 August 2021 and 20 October 2021 Date of Judgment: 27 January 2022 ___________________ JUDGMENT ___________________
1. This is an Employees’ compensation claim involving the death of an employee, Lee Chi Wai (the “Deceased”) raised by the Applicant on behalf of herself and other family members of the Deceased. [size=1em]Background 2. It is not in disputed that on 9 January 2016, the Deceased was employed for one day by the 1st Respondent as a casual decoration worker to carry out the decoration of one of the booths for the Toy Fair at the Hong Kong Convention and Exhibition Centre (the “Exhibition Centre”). The 1st Respondent was the sub-contractor of the 2nd Respondent. 3. The normal working hours were 9 am to 6 pm but the work actually started at 10 am on that day. As it was not finished by 6 pm, the Deceased and other workers worked overtime. 4. Later, the Deceased went outside for a cigarette break. He then returned and was having a drink of water when he suddenly collapsed. This was around 9:20 pm. Ambulance was called and paramedics upon arrival found the Deceased in an arrested state. Cardiac resuscitation was attempted at the scene and he was then taken to the A&E of Ruttonjee Hospital and after a further hour of attempted cardiac resuscitation, he was certified dead at 10:51pm. 5. Autopsy was performed and the cause of death was found to be cardiac arrest from Acute Myocardial Infarction (“AMI”), more commonly known as a heart attack, due to thrombosis secondary to a plaque rupture in the Left Anterior Descending coronary artery. [size=1em]The issues 6. Under section 5(1) of the Employees’ Compensation Ordinance, the employer’s liability for compensation is stated as: “…if in any employment, personal injury by accident arising out of and in the course of the employment is caused to an employee, his employer shall be liable to pay compensation in accordance with this Ordinance.”
7. Thus the issue here is one of causation (LKK Trans Ltd. V Wong Hoi Chung [2006] 1 HKLRD 980): whether the injury, that is the Acute Myocardial Infarction, was caused by an accident, and whether this accident arose out of and in the course of the employment. [size=1em]Causation in medicine and law 8. It has been said that the medical study of aetiology applies “quite different standards” to causation in law, and causation in law is a matter for the judge and not for the medical experts (Lee Kin-Kai, a patient by his father and next friend, Li Wah v Ocean Tramping Co. Ltd. T/A Ocean Tramping Workshop CACV 64/1989 and CMY v Tam Siu Wing HCPI 809/2006). 9. As the experts in the current case agreed, the medical study of aetiology essentially attempts to identify “risk factors” for a particular disease. This often involves some types of “observation studies”. 10. For example, if medical researchers wish to identify whether a certain habit (say, eating a certain type of preserved meat) is a risk factor for a certain disease (say, cancer of the stomach), a typical study might be that they would identify a group of “eaters” and a group of “non-eaters” who are very much similar in all other variables (e.g. places they live, background, race profile, habits, diet other than eating that type of preserved meat etc.). Thus this is a so-called “controlled” study, meaning that the subjects are controlled, as far as possible, in other variables and only varied by the one condition (eating the type of preserved meat in this case) that the researchers wish to investigate. 11. Depending on the design of the study, both groups might be followed-up for a period of time (say, 10 years in a so-called “cohort” study) at the end of which the researchers will collect data of cases of stomach cancer in both groups. 12. The researchers would put the data into a statistical model to calculate if there was a statistical significance in the difference between occurrence of stomach cancer cases in both group. For example, if the researchers found more cases of stomach cancer in the “eaters” group than the “non-eater” group, and that the difference was calculated to be “statistically significant”, then this study would show that eating this type of preserved meat is a “risk factor” for stomach cancer and the result might then be published in a medical journal. If there was a difference but not significant statistically, then the conclusion would not support that it was a risk factor. 13. Such clinical studies might be repeated many times around the world at various times and sometimes data can be combined into a larger study (so called meta-analysis study) which may give more accurate results than, say, an individual small scale study or even a “case study” report (where one or a few cases were reported). 14. Of course, the result of the study might not show that the non-eaters would never suffer from stomach cancer (there would be a “background occurrence” of stomach cancer), nor that the eaters would likely (on balance of probability, or over 50%) develop stomach cancer. The scenario might be that this was a popular food and the vast majority of the eaters would still not develop stomach cancer. 15. Thus the study might only show that there was an increase in the occurrence by a certain percentage amongst “eaters” over the “background occurrence” amongst non-eaters, and it might well be that the percentage of increase was quite small but yet “statistically significant”. 16. On the other hand, for the issue of causation in law, Sakhrani J stated in the CMY case: “In law, there is a causal link if it is shown on balance of probabilities that the accident was a substantially contributing cause of the injury. A cause is sufficient, it does not need to be the sole cause.”
17. The problem is that the medical study of aetiology essentially is a forward-looking study: if you eat this type of preserved meat, there is an increased chance of stomach cancer. But it does not look at a case retrospectively: if you suffered from stomach cancer, and if you have eaten preserved meat, whether that preserved meat would, on balance of probability, have contributed to your particular case. 18. This is because the study of aetiology may not distinguish whether any one particular case of stomach cancer is “substantively contributed to” by eating the preserved meat or whether it is a “background” occurrence. 19. This fine distinction between medicine and law may not be so important in most cases of traumatic accidents: there is unlikely to be any “background occurrence” of spontaneous ankle fracture so if someone fell from height and then found to suffer from an ankle fracture, there is no question that the fall would have, on balance of probability, “substantially contributed” to the ankle fracture. 20. The problem lies with incidents of non-traumatic accidents which may be insidiously developing over years by multiple risk factors which may or may not be related to employment. [size=1em]“Cocks crowing at sunrise” as an illustration 21. An example discussed during the trial illustrates the problem with applying expert evidence in aetiology to causation in law in such cases: imagine that there is a farm of 100 cocks. In any one hour all through the day, 20 cocks are observed to be crowing. However, in the hour when the sun rises, 30 cocks are observed to be crowing. 22. Thus, in a medical “observation study” / aetiology, sunrise would be deemed a risk factor for crowing. However, this study does not tell us how the sunrise contributed, if at all, to the crowing in each individual case of the 30 crowing cocks. 23. Imagine that we now have the instruction to slaughter the cocks whose crowing is, on balance of probability, contributed to by the sunrise. This study alone could not tell us which of the 30 cocks we have to slaughter: it may well be that out of the 30 cocks that crow, 20 are “background crowers” not affected by the sunrise. 24. Without any further test to show which particular cocks are affected by the sunrise and which are not, we cannot choose. We simply don’t know. [size=1em]Experts’ opinion 25. For the current case, there is no dispute between the experts that this case was one of these non-traumatic accidents which had insidiously developed over years by multiple factors. 26. Dr. David Hu (“Dr. Hu”), the expert for the applicant, gave evidence that there was a list of “risk factors” like genetic disposition (family history and being male), diabetes, high blood pressure, smoking etc. These, over a long period of time, caused the development of atherosclerosis with progressively narrowing of the lumen of the blood vessel in the heart muscle. A plaque formed on the top of this narrowing. The terminal event would be a rupture of the plaque causing bleeding, the resulting clot (thrombosis) had completely obstructed the lumen of the coronary artery (in this case, the Left Anterior Descending Artery very high up near the origin of the artery, which was a particularly dangerous site of obstruction). With the lack of blood supply, the heart went into a cardiac arrhythmia which meant that it could not supply blood to the body. The Deceased lost consciousness and died. 27. Dr. Victor Goh (“Dr. Goh”), the expert for the 3rd respondent, did not dispute this. 28. What the experts disputed was the cause (or “trigger”) of the terminal event: that is, the rupture of the plaque. 29. Both experts have produced a large amount of medical research literature which the court is very grateful of. I shall review some of these. 30. In the article “Mechanisms of Plaque Formation and Rupture”, it is stated that: “Rupture of a thin cap and subsequent thrombosis may be spontaneous, but in some cases, a temporary increase in emotional or physical stress provides the final triggering of the event. Recognised triggers include physical and sexual activity, anger, anxiety, work stress, earthquakes, war and terror attacks, temperature change, infections, and cocaine use. Also simple daily activities or the circadian rhythm of biological pathways may determine the onset of ACS, which are most frequent in the morning.”
31. In another article, “Coronary Plaque Disruption”, it is stated under “Trigger Reduction” that: “…only a small fraction of all myocardial infarctions (about 5%) are related to, or triggered by, vigorous exertion…”
32. As such, these articles suggest that most ruptures were spontaneous (with no identifiable trigger or cause) but in a small fraction of cases, there were identifiable triggers such as vigorous exertion. 33. However, both experts also agreed that there was no medical test or investigation that could verify the trigger or cause of a rupture of the plaque. 34. In other words, using example of cocks crowing at sunrise, the experts confirmed that there was no test to show, of the 30 cocks which crow at the hour of sunrise, which cocks’ crowing are “substantially contributed to” by the sunrise, and which cocks crow anyway irrespective of the sunrise. 35. I would not put it so bald that the absence of a medical test would mean that the applicant could never prove causation in such a case, but bearing in mind that the legal test for causation is “substantially contributed to on balance of probability”, the identification of such a trigger requires support of reasonably convincing medical evidence and not by mere speculation or any form of “extension” or “manipulation” of existing medical knowledge. 36. Scientific researches usually have very well defined and precise criteria, factors and conditions and, unless there are convincing arguments otherwise, the scientific conclusion must only apply to within those precisely defined ambit. 37. For example, if a research is looking at a group of smokers defined as those who smoke 20 cigarettes or more every day, one cannot extrapolate the result to apply to a person who only smokes 1 cigarette a day, and perhaps even suggest that the risk he had should be 1/20 of what was found in the research. The proper answer should be “this is outside the ambit of the research so no conclusion can be drawn”. [size=1em]Dr. Hu’s opinion 38. In his first expert report dated 23 November 2019, Dr. Hu, suggested that “There is no question that his work may contribute to his death” (Trial Bundle page 137). 39. He gave two factors: 1) long working hours (from 9 am to around 9:20 pm) reported in Japan as “Karoshi”, and 2) the occupation being an erratic work schedule. 40. Before we even go into Dr. Hu’s opinion in more details, I have a problem with his statement that “There is no question that his work may contribute…”. 41. It is clear that Dr. Hu was simply raising a possibility: he merely stated that this possibility definitely existed but did not comment on the probability of such a possibility. 42. With such a qualification, I doubt how useful the opinion that follows would be to the court. This is no more useful than saying: “There is no question that you may win the lottery tomorrow if you buy a lottery ticket now.” 43. This is obviously not the test of causation in law. As such, I would think that an expert, if properly instructed, should not be expressing his opinion in this way. 44. Further, Dr. Hu, in his second (joint) expert report stated that “Dr. Hu feels the trigger for plaque rupture and sudden death is a result of work stress and erratic work hours.” 45. Again, I find the wordings of this opinion rather strange. On plain reading, Dr. Hu seems to be expressing a feeling, but the court is not interested in how an expert feels. A feeling might be affected by emotions: sympathy, anger etc. and an opinion formed by such may be biased. The duty of an expert is to present evidence objectively and present his unbiased opinion based on such, and not his personal feelings. [size=1em]Long working hours 46. In any case, with regard to “long working hours” as a factor that may contribute, one of Dr. Hu’s reference (“Overwork: Does it put the heart at risk?”) was a case report of one case of a 31-year-old Japanese reporter who dies after working 159 hours of overtime. The cause of death cause was heart failure (“Karoshi”). The article discussed the condition of “Takotsubo cardiomyopathy” which arose out of “chronic overwork” “stress accumulated over a period of time” “without any time away from work to de-stress”. 47. My observation is that this was a case study report of only one case under extreme overtime work. There was no evidence of such in the current case. More importantly, Dr. Hu agreed that this article was about cardiomyopathy (i.e. disease of the heart muscle) and thus not relevant to the current case of AMI. 48. Dr. Hu also produced an editorial discussing the studies into the relationship between watching sporting events and AMI (“Stress and Myocardial infarction”). 49. But this only suggests a “hypothesis that the emotional intensity of important sporting events and other behaviours associated with spectating such as smoking, binge drinking, and overeating could trigger MI”. 50. In fact, there were conflicting evidence: the article reported that one research paper “found no excess mortality from MI around the important football games” but another “showed admissions from AMI were increased by 25% on the day of and two days after” an important match which was decided by a penalty shoot-out. 51. In my view, the papers quoted were observation studies but not “controlled” only to “emotional stress” because there might be other co-existing risk factors like “smoking, binge drinking, overeating” and also only dealt with quite extreme emotions at very tense sporting moments which is clearly not applicable to the current case. 52. In any case, this remained a “hypothesis” since there were conflicting evidence. I do not think that one can extrapolate the findings to the current case. 53. Another article produced by Dr. Hu (“Mental Stress and sudden cardiac death: asymmetric midbrain activity as a linking mechanism”) is specifically looking at a hypothesis of how mental stress might cause certain brain activities which might induce cardiac arrhythmia and sudden death. This paper again proposes a “hypothesis” and, further, this does not appear to relate to the current case which was death caused by AMI. 54. The most relevant paper produced by Dr. Hu was “Nonlinear associations between working hours and overworked related cerebrovascular and cardiovascular diseases (CCVD)”. There is no question that the current case concerns a type of cardiovascular disease. 55. In this paper, it was stated that: “The most widely adopted quantitative measure used to define whether CCVD are overwork-related is the number of working hours per month.”.
56. The authors discuss the need to consider other possible risk factors associated with long working hours (e.g. smoking, coffee, alcohol, unhealthy diet and lack of exercise etc.) which might cause bias, and thus the need to establish recognition criteria for overwork-related CCVD as an occupational disease. 57. Recognition criteria for overwork-related CCVD was established in 3 countries, Japan, Taiwan and South Korea. According to these criteria: “overtime refers to the hours worked in excess of the standard maximum working hours…in Japan…and Taiwan, the onset of a CCVD can be attributed to overwork, after excluding personal and other workplace risk factors, if an employee (1) work 100 hours or more of overtime during the month prior to the event, or (2) worked an average of 45 hours or more of overtime per month for 2-6 consecutive months prior to the event.”
58. However, in the current case, evidence showed that the Deceased was only employed to work one day for the 1st Respondent and the overtime was from 6 pm to around 9:20 pm when he collapsed, inclusive of a dinner break within that time. In fact, the Deceased was a casual worker and his mother gave evidence that he stayed home about 1/3 of the time. 59. Thus, it would be very unlikely that the Deceased’s work schedule came anywhere near the recognition criteria for “overwork-related CCVD”. 60. It is also of note that the recognition criteria for “overwork-related CCVD” also required “excluding personal risk factors” and of course, as agreed by the experts, smoking was clearly a risk factor. 61. As such, by the recognition criteria as discussed in this paper, the Deceased’s case would not have been diagnosed as a “CCVD attributable to overwork”. [size=1em]Erratic work schedule 62. Dr. Hu suggested that having to “work one day and nothing to do on other days” was an erratic work schedule and “wonders about the psychological impact”. 63. I see no logic in that line of argument: I would have thought that working in a casual manner and having plenty of rest days was the exact opposite of being overworked. Not working is when one de-stress! In fact, none of the research papers produced before the court suggests that being a causal worker having rest days in between work days has any adverse “psychological impact” and is a “risk factor” for cardiovascular disease. 64. Nevertheless, Dr. Hu insisted that this was his definition of “erratic work schedule”. 65. I see another problem with this definition: Dr. Hu was suggesting that having work days and rest days could have a psychological impact that caused the AMI. Logically, he must mean that the alternative, that is, having a normal working schedule (say, a full working week of 5 continuous working days) would not have such a psychological impact. 66. As such, this psychological impact could not have arisen out of work, but out of having some rest days instead of a full working week! Following Dr. Hu’s line of argument, the AMI could not be said to have arisen out of any employment, but out of the Deceased’s own fault as a casual worker in not able to find enough work to fill up a full working week! Such a proposition is, of course, ridiculous. 67. Further, when cross-examined as to how this psychological impact would relate to the employment in question because the Deceased only worked for one day, Dr. Hu said, “then the employer was unlucky to have somebody died in there” and “the thing is he did not die on the day of rest”. 68. I think this raises a question on the impartiality of Dr. Hu. He seemed to be of the view that: if the person died during employment, it was unlucky for the employer who had to pay compensation. 69. This is clearly not the legal position otherwise S5(1) of the ECO would not have used the words accident “arising out of” employment and there would have been no need to prove causation, and only proving that an accident “in the course of” employment would suffice. 70. Back to the example of the cocks crowing at sunrise: Dr. Hu was effectively saying that it was unlucky that the cocks happened to be crowing at sunrise so all 30 of them has to be slaughtered. There is no need to see which cocks’ crowing was caused (or substantially contributed to) by the sunrise. This is clearly wrong. [size=1em]Time pressure and physical stress 71. During his oral evidence, Dr. Hu changed his opinion and claimed it was psychological stress of time pressure and physical stress of climbing up and down a ladder that caused the rupture of the plaque. 72. As far as psychological stress is concerned, there is no evidence to support that the Deceased was psychologically stressed by any time pressure on that day (especially when the Deceased had time for a cigarette break outside the premises just before he collapsed). The applicant’s counsel tried to argue otherwise in closing submissions that taking cigarette break meant that the Deceased must be stressed. I found that argument illogical: if one was so snowed-under in work, he would unlikely to be able to even take a break! 73. Even if there was any psychological stress, there was no evidence supported by medical research that the mere thought of time pressure over a few hours would trigger an AMI. According to the article that Dr. Hu produced, the criteria for psychological stress came from…work 100 hours or more of overtime during the month prior to the event…or worked an average of 45 hours or more of overtime per month for 2-6 consecutive months prior to the event. 74. As far as heavy physical stress is concerned, Dr. Hu’s previous opinion was that there was none. 75. He stated in his first expert report that: “All in all, despite to absence of heavy physical stress, one wonders about the psychological stress.” (Trial Bundle page 137) 76. Even in his second (and joint) expert report dated 14 December 2020), Dr. Hu still maintained that he “feels (that) the trigger for plaque rupture and sudden death is a result of work stress from long and erratic work hours.” (Trial Bundle page 246) 77. Dr. Hu was talking about heavy physical stress as a trigger in his expert report. I cannot see how climbing up and down a few steps on a ladder when installing the decorations on a display booth can be deemed “heavy physical stress”. 78. I am also concerned all the evidence regarding the issues of time pressure and the Deceased’s nature of work were not new. Dr. Hu did not raise these as triggers in his expert report. 79. This may raise some suspicion that, as stated above, Dr. Hu has taken the attitude that: if the accident happened during the employment, the employer was unlucky and must be responsible, so let’s look back and look for a reason. 80. This is the classic fallacy in what is called “confirmation bias” in science. In law, it is called “leading the evidence”. [size=1em]Dr. Goh’s opinion 81. Dr. Goh made a much more detailed factual review of the case. As for triggers for the plaque rupture, he found no apparent emotional or physical stressors from various evidence of witnesses as stated in the Death Investigation Report. 82. Dr. Goh has two propositions. [size=1em]Histologic changes in the heart found at autopsy 83. Dr. Goh is of the view that the autopsy findings of “patchy muscle cell necrosis with mild infiltration of neutrophils” (Autopsy report Trial Bundle page 265) established that the onset of the myocardial infraction as occurring 12-24 hours before the time of death, that is, the trigger for the plaque rupture occurred before the Deceased started working. 84. This opinion was based upon a 2006 article “The pathology of myocardial infarction in the pre- and post-interventional era” (Trial Bundle page 236) and a 1990’s Pathology Textbook “Pathology Basis of Disease”. 85. Dr. Hu argued that this observation of histologic changes after myocardial infraction was based on an old paper based on an animal model (“Experimental Myocardial Infarction in the Rat” published in 1978, Trial Bundle page 261(28) to 261(41)). Further, the Deceased underwent a long course of cardiopulmonary resuscitation and according to the 2019 article “Diagnosis of myocardial infarction at autopsy: AECVP reappraisal in the light of the current clinical classification” (Trial Bundle page 261(1)): “Changes occurring during cardio-pulmonary resuscitation (CPR) and autolysis can mimic the early histologic changes of MI.”
86. I am of the view that we are getting into very academic scientific discussion which may also require input from expert pathologists. In any case, Dr. Goh agreed that the findings of such histologic changes are not deemed to be “diagnostic” regarding the timing of the AMI. [size=1em]Cigarette smoking as a trigger 87. Dr. Goh also proposed that the Deceased’s last cigarette could be a trigger. In the same article quoted above (“Coronary Plaque Disruption”) (Trial Bundle page 261(3)), it was stated that: “The increased risk associated with smoking appears to rapidly reversible by cessation, implicating acute triggering mechanisms (plaque disruption, thrombosis and / or vasoconstriction) rather than chronic atherogenic mechanisms as being primarily responsible for smoking-related disease progression…preliminary autopsy data indicate that smokers have more extracellular lipids in their plaque, which should imply greater vulnerability to rupture.”
88. Dr. Hu disagreed. He asked the rhetorical question: How often do we see a smoking person dies whilst puffing a cigarette? 89. I don’t agree with this line of argument. 90. Firstly, I doubt that we have the data. 91. When an ambulance arrived at the scene of a cardiac arrest, I doubt that the paramedics would be asking the question, “Did anyone see this person smoking when he collapsed?” I also doubt that they would be searching for a cigarette butt at the scene or record this in the ambulance records. Neither would the doctors at A&E, I would imagine, bothered themselves with such information. 92. For the treating medics, how the AMI was triggered would be a purely academic question and would not have altered their management of the patient at all. 93. Secondly, from the article “Mechanism of Plaque Formation and Rupture”, it was stated (Trial Bundle Page 198): “The time relationship between plaque rupture and syndrome onset is not easily assessed because plaque rupture in itself is asymptomatic and the following thrombotic process is highly unpredictable.”
94. Smoking a cigarette may take a few minutes, so even if this has actually triggered the plaque rupture, the progression to AMI and symptoms appearing may not appear immediately within that time period. 95. In any case, I would accept that cigarette smoking may be a risk factor in plaque rupture, but I do not think that we have enough evidence to support that this satisfies the issue of causation in law. [size=1em]Discussion 96. As stated above, the current case illustrates the problem of trying to apply the medical evidence from the study of aetiology to the issue of causation in law. 97. As I have discussed in the case of Yu Kwok Wa v China Telecom Global Limited DCEC 1849/2016, with the advance of medical knowledge, we understand that many of these “non-traumatic accidents” (like AMI in the current case) are really results of a chronic pathological process (coronary artery disease in this case) that have gone on for years cumulating on the one moment: the triggering event or “the straw that finally breaks the camel’s back” (the plaque rupture in this case) which caused the injury. 98. The problem is whether we can really identify this “final straw” or the triggering event when: a) there is no medical investigation test to identify the triggering event (if any), and b) there is an unpredictable period between the triggering event and symptoms appearing.
99. The patient might have done many things over the years prior to the accident that doctors considered to be aetiological risk factors. The patient might have done some or many things that might be considered “triggering events” over any undeterminable period of time prior to the symptoms appearing. 100. However, at best, these aetiological risk factors might only tell us that there was a statistical correlation between them and an increased incidence of the accident (taking the example above: more cocks crowing at sunrise) over a background level of incidence (the cocks that crows at all times of the day irrespective of sunrise or not). The evidence does not tell us whether this particular case is a background incidence or not. 101. This is exactly the problem here: the current medical knowledge is that for the vast majority of cases (95%) of plaque rupture, it would be spontaneous with no identifiable triggering events. 102. As discussed above, there are accidents or diseases where there is medical evidence to support a legal “on balance of probability” test on causation e.g. in traumatic accidents (e.g. broken ankle after a fall) or any of those known “occupational diseases” where the casual link is so strong that the (otherwise rare) disease would not likely happen unless there has been such exposure (e.g. mesothelioma and asbestos exposure). 103. However, in situations when the medical experts could not produce strong enough medical evidence to support the legal issue of causation, they should not be tempted to select one or another of those aetiological risks factors (or “quasi” risk factors) as the “cause” because much of that would have been based on speculation, and perhaps affected by subjective personal feelings. 104. I have quoted above the article of “Nonlinear associations between working hours and overworked related cerebrovascular and cardiovascular diseases (CCVD)”) concerning the recognition criteria for “overwork related CCVD” as an occupational disease. The criteria are being used in at least 3 countries. 105. These criteria also appear to exclude any smokers. One may speculate that this may be a policy reason and / or that the statistical correlation between smoking and CCVD is so much stronger than between overworking and CCVD. 106. It is also telling that these criteria do not involve retrospectively trying to pick one event or another as “a trigger for the terminal event” in order to identify whether the disease was work (or overworked) related or not. 107. I am of the view that such scientific evidence and criteria should provide the best guidance to the court in the present case. 108. As stated above, the Deceased’s case would not have satisfied such criteria so I find, accordingly, that there is not enough evidence to support that the death of the Deceased has arisen out of his employment. [size=1em]Quantum 109. I will assess quantum for the sake of completeness. 110. The only dispute in the average earnings of the Deceased. 111. The applicant was running a business as a co-partner and the tax demand notice issued by the Inland Revenue Department for 2015/16 showed an assessable profit of HK$226,437 of which a sum of HK$125,469 (or HK$10,455.75 per month) was allotted to the Deceased as his personal assessment. 112. The applicant also worked as a casual decoration worker earning a daily rate of HK$650 with overtime allowance. There is no documentary evidence to support what this income was. The mother of the Deceased claimed that she received HK$9,000 per month from the Deceased but her evidence was inconsistent as to number of times and the amount she was paid each time. Other evidence came from the brother of the Deceased regarding his own expenditure (which is not relevant given that the brother was a “sifu” and earned HK$1,000 a day) and perhaps some projected expenditures based on the Deceased’s likely outgoings. 113. Based on these indirect evidence, the applicant claimed that the Deceased likely earned “not less than HK$19,000” per month at the time of the accident. 114. I would accept that the Deceased would have earned some income as a causal worker but I am not convinced that the evidence support that the Deceased earned the amount claimed. 115. Instead, I would estimate the Deceased’s income at the middle figure between HK$10,455.75 and HK$19,000, which comes to HK$14,727.88. 116. As such, the compensation under Section 6(1) should be HK$14,727.88 x 60 = HK$883,672.80 117. The funeral expenses allowed under Section 6(2) should be HK$62,850. 118. As such, should liability be established, the total quantum is HK$(883,672.90 + 62,850 – 200,000 (gratuity sum paid by the 1st and 2nd respondents) = HK$746,522.80 [size=1em]Conclusion 119. I would therefore order that the action be dismissed with costs of the action be to the 1st, 2nd and 3rd respondents to be taxed if not agreed, with certificate for counsel for the 3rd respondent. The applicant’s own costs be taxed in accordance with the Legal Aid Regulations.
| (Harold Leong) | | District Judge |
Miss Julia Lau, instructed by Messrs Hastings & Co., assigned by the Director of Legal Aid Department, for the applicant The 1st respondent appeared in person The 2nd respondent appeared in person Miss Susanna Leong, instructed by Messrs Cheng, Yeung & Co., for the 3rd respondent
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發表於 2022-4-1 14:34:04