Andrew William Maxwell v. Keliston Marine (Far East) Ltd (Now in Liquidation) and Another
Read the full judgment text of HCPI 945/2003 on BabelCite. This High Court CFI judgment was delivered on 20 January 2012.
1. In this action, the plaintiff claims damages for loss and damage which he alleges he suffered as a consequence of the asthma that he allegedly developed in the course of working for his employer, the 1 st defendant, in the 2 nd defendant’s tunnel repair works. He had started working in those tunnels in September 2000 and stopped working in February 2001. In this type of claim, it is necessary to ascertain the past health of the plaintiff to determine whether he actually suffers from asthma an
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HCPI 945/2003 IN THE HIGH COURT OF THE HONG KONG SPECIAL ADMINISTRATIVE REGION COURT OF FIRST INSTANCE PERSONAL INJURIES ACTION NO. 945 OF 2003 ------------------------ BETWEEN
------------------------- Before : Hon Bharwaney J in Court Dates of Hearing : 15-18 August 2011, 15 and 22 September 2011 Date of Judgment : 20 January 2012 ----------------------- J U D G M E N T ----------------------- 1.In this action, the plaintiff claims damages for loss and damage which he alleges he suffered as a consequence of the asthma that he allegedly developed in the course of working for his employer, the 1st defendant, in the 2nd defendant’s tunnel repair works. He had started working in those tunnels in September 2000 and stopped working in February 2001. In this type of claim, it is necessary to ascertain the past health of the plaintiff to determine whether he actually suffers from asthma and, if so, when he started suffering from asthma. 2.The plaintiff was born in the United Kingdom on 28 May 1967. He completed his O-Levels and worked for a period of time in the UK before he came to Hong Kong in 1995. He worked in Hong Kong as a foreman in a company called Trident Marine and, in 1997, at the age of 30, he started his own engineering company called Aquatek Engineering Services Limited. This business came to an end in January 2000 because of financial difficulties. Thereafter, the plaintiff was employed by the 1st defendant which was engaged in underwater engineering works. In the course of that employment, the plaintiff carried out welding, sample collection and other underwater engineering work. The plaintiff was qualified to perform wet welding work and, in June 2000, also obtained a Confined Space Worker’s Certificate which enabled him to work in tunnels. Some time that year, the 1st defendant undertook work as a sub-contractor on a project involving repair works in the tunnels of the Strategic Sewage Disposal Scheme, stage 1. The plaintiff was deployed by the 1st defendant to work as a site supervisor during such works. The plaintiff worked in Tunnel C, which was a 4.23-metre diameter tunnel driven through granite rock and lined with concrete. Tunnel C was further sub-divided into two smaller tunnels, C1 and C2, each of 1.35-metre diameter. The length of the tunnels was about 5,300 metres and they ran parallel to each other. The work the plaintiff supervised involved the sealing up of cracks and fissures in the concrete lining of the 1.35-metre diameter tunnels in order to stop water ingress into the tunnels. The material used for sealing up the cracks was TamPUR 150. TamPUR 150 is a single component hydrophilic polyurethane based on toulene diisocyanate (“TDI”) in combination with polyether polyols. It reacts when it comes into contact with water to form a flexible polyurethane seal. 3.The plaintiff initially worked a 10-hour split shift. This was later increased to a 12-hour shift, working on average 6 days/nights per week. The workers were divided into teams of 3 or 4 people working at various locations inside the tunnels where the water leaks were occurring. The plaintiff was responsible for supervising one such team and his duties included training the workers to use the equipment to stop water ingress, maintaining and cleaning the equipment, liaising with site engineers and keeping site progress and attendance records. The TamPUR 150 contained in metal drums was transported to the tunnel work location on a trolley at the start of each shift. In order to stop the water ingress, the workers would first drill holes into the concrete lining of the tunnel, and store packers into these drilled holes. The best description of a packer comes from the evidence of Mr Paolo Nardone, who was employed as the Contracts Manager by Paul Y Construction Company Limited and seconded to work for the 2nd defendant as a project director. He said that the remedial works involved drilling a series of holes (13/16 mm diameter) and inserting a packer (a sort of bicycle wheel valve) into each drilled hole. The holes were drilled on both sides of the cracks from which seepage occurred. The space between the drilled holes was about 150-300 mm. The TamPUR 150 would be injected into these packers using a single piston high-pressure hand pump with an injection nozzle that was pushed into the packer. The force exerted by the hand pump pushed the liquid resin mixture from the metal drum into the packers. From there, the mixture would reach the fissure or crack in the tunnel lining, where it reacted with water to form a flexible seal. Once formed, further water ingress into the tunnel would be stopped. 4.The plaintiff was provided with personal protective equipment when working inside the tunnel that consisted of a paper dust mask, eye goggles, cotton overalls, rubber gloves and rubber Wellington boots. After working for some time in the tunnels, the plaintiff felt unwell and consulted Dr Patrick Au at Quality Healthcare on 7 November 2000. After that consultation, the plaintiff went to a shop in Mongkok and purchased a charcoal particulate filtered mask, at a cost of HK$100, which he used instead of the paper mask. He continued to work in the tunnels until February 2001. 5.It is common ground between the experts engaged on the issue of liability by the parties in this case, Dr Colin Purnell for the plaintiff, and Dr Joseph Kwan for the defendants, that exposure to TDI may lead to sensitisation resulting in conditions such as asthma. Both are experts in the field of occupational safety. The principal route of entry into the body is by inhalation and absorption through the skin. The main risk to health is from inhalation of TDI vapour. It can cause irritation, coughing and difficulty in breathing. At the end of a period of exposure from as little as a few days, the symptoms of irritation are later combined with coughing in the evening after work, accompanied by chest pains, difficulty in breathing and respiratory distress. These later symptoms become worse during the night and disappear in the morning. A sensitised condition can then arise such that asthmatic symptoms are produced on re-exposure to very low TDI concentrations. There have been numerous reports of asthma resulting from exposure to isocyanates, but the level which can induce sensitisation, and asthma, is unknown. The occupational exposure level for TDI is published in the Code of Practice on Control of Air and Purities (Chemical Substances) in the Workplace by the Hong Kong Occupational Safety and Health Branch of the Labour Department. This specifies a limit of 0.005 ppm or 0.036 mg/m3 as the time-weighted average permissible concentration over a 8-hour working day or a 5-day 40-hour working week, and a short-term exposure limit, namely, a 15-minute time-weighted average of airborne concentration of no more than 0.02 ppm or 0.14 mg/m3. The same limits appear in the Health and Safety Executive’s Publication Ex. 40 (UKHSE). These extremely low limits are imposed because of the high hazard to health posed by airborne TDI. 6.Does the plaintiff suffer from the asthma and, if so, when did he become asthmatic? I have reviewed the medical records of the plaintiff. Dr Roland C C Leung, who is a specialist in respiratory medicine and the defendants’ expert in this case, has presented a fair summary of his medical history. The plaintiff has a long-standing history of rhinitis. He had a tonsillectomy and an adenoidectomy in his childhood and sinus drainage in 1989. He has ongoing rhinitis symptoms of nasal congestion and morning sneeze, which sometimes lead to wheezing attacks. His lung function was normal in September 1999 before working in the tunnel. He takes anti-histamines occasionally to control his rhinitis symptoms. There was no history of skin or food allergy, but a family history of rhinitis. There is no family history of asthma. He used to smoke about 10 cigarettes per day for six years until 1996 and has been smoking occasionally since then. About two months after working in the tunnel, he developed a persistent cough. The cough was mainly dry but was particular worse at night and in the early hours of the morning, and had been accompanied by audible wheeze and chest tightness. He consulted Dr Patrick Au at the Quality HealthCare clinic on 7 November 2000. Dr Au diagnosed him as suffering from asthma. Dr Au had noticed the presence of inspiratory and expiratory wheeze on auscultation of the chest (listening to the chest with a stethoscope). He prescribed him with a ventolin inhaler, a bronchodilator. Upon a review by Dr Au one month later on 7 December 2000, his symptoms had improved and his chest was clear, but he was asked to continue with ventolin. Further improvement was noted after another doctor, Dr Clifford Loo, added beclomethasone, an inhaled steroid to reduce airway inflammation, to the ventolin inhaler, on 15 January 2001. Lung function test on 16 January 2001 was normal. Dr Loo referred him to see Dr Ho Hok Fai, a specialist in respiratory medicine, for review and ongoing management of asthma. When seen by Dr Ho on 3 February 2001, the plaintiff complained of occasional wheezing and coughing at night but his chest was clear and lung function test was normal. He was asked to keep a peak flow diary over the subsequent fortnight. This showed a normal peak flow rate of 500-560l/min with no significant variability between morning and evening recordings. On 17 February 2001, Dr Ho increased the dose of inhaled steroid for better asthma control. The plaintiff had resigned from his employment by the 1st defendant on 10 February 2001, and he noticed gradual improvement of asthma symptoms in the following two months. He reduced and came off the steroid inhaler and used ventolin as needed only. Between September 2000 and February 2001, when he was working in the tunnel, he continued to play soccer and other sporting activities regularly and his exercise tolerance had remained largely intact. He had suffered from severe bouts of cough and nocturnal dyspnoea (shortness of breath) even before working in the tunnel and had consulted Dr Loo for these conditions between May 1999 and April 2000. In his assessment of the plaintiff on 11 March 2005, Dr Leung concluded that the plaintiff had clinical features of asthma that consisted of persistent cough with nocturnal worsening, wheezing attacks, chest tightness, and prompt response to bronchodilator therapy. He had no apparent history of asthma prior to working in the tunnel although he did have frequent bouts of cough with dyspnoea, sometimes with concurrent rhinitis symptoms, before September 2000. He concluded that the plaintiff had established asthma. 7.The plaintiff had been examined by his own expert, Dr Joseph Pang, also a specialist in respiratory medicine, who had examined him two years previously on 14 October 2003. Dr Pang had little doubt that the plaintiff suffered from asthma. In their joint report dated 20 February 2011, made after their joint assessment of the plaintiff on 7 December 2010, both experts were of the joint opinion that the plaintiff had established asthma since 2001. I accept that evidence and I find that the plaintiff did not suffer from asthma in the past and only became asthmatic at around the time that he worked in the tunnel project for the 1st defendant. Mr Ashok Sakhrani, who appeared for the defendant, submitted to me that the diagnosis of asthma made by Dr Patrick Au on clinical grounds was not reliable given the fact that the lung function test was consistently normal, that the plaintiff’s complaint of chest tightness was admittedly due to muscular injury and not due to respiratory distress and, above all, that his long-standing history of perennial rhinitis[1] and ongoing rhinitis symptoms, which sometimes led to wheezing attacks, would be confused for asthma. I was referred to Dr Leung’s letter dated 16 August 2011, in which he stated that subjects of allergic rhinitis could manifest symptoms of wheezing. I am not persuaded by these submissions to reject the joint opinion of both experts that the plaintiff had established asthma since 2001. I accept the evidence of Dr Joseph Pang that the fact that his lung function test on 16 January 2001 and his peak flow diary in February 2001 were normal did not detract from this diagnosis as it was perfectly possible to have asthma with normal lung function tests, especially when those tests were conducted after he had started treatment. I also accept his evidence that wheezing is rare in rhinitis and that the whole clinical course of the plaintiff’s illness, after it manifested, was that of asthma and that the role of rhinitis in that illness was, at best, minor. Dr Roland Leung was also of the opinion that the plaintiff had established asthma. He came to this conclusion because the plaintiff had clinical features of asthma that consisted of persistent cough with nocturnal worsening, wheezing attacks, chest tightness and a prompt response to bronchodilator therapy. As I understand Dr Leung’s report, the wheezing that was detected by Dr Patrick Au during his examination of the plaintiff was asthmatic in origin and not caused by rhinitis. Wheezing is an important symptom of asthma whereas the main symptoms of rhinitis are nasal congestion, rhinorrhoea (a runny nose), sneezing, and dripping of secretions from the back of the nose to the throat. Dr Joseph Pang’s evidence is that it is well documented in the medical literature that asthma and rhinitis often co-exist. Indeed Dr Roland Leung said in §3 of his report dated 14 December 2005:
8.I turn to consider the question whether the plaintiff was exposed to TDI and, if so, whether such exposure to TDI caused or materially contributed to the plaintiff developing asthma. 9.There was a substantial amount of evidence adduced about the quality of air in the tunnels, whether or not the 2nd defendant properly monitored the level of dust, gas and radon inside the tunnel, whether the extractor fans worked properly, whether they were properly maintained, including whether or not the flexiducts of the air extraction system were properly maintained. One of the photographs produced before me showed a significant gap in the flexiduct at the connecting point. There was also a lot of evidence adduced of inspections carried out by the Labour Department personnel to ensure compliance with safety regulations. All this evidence is peripheral to the central issue that I must address, namely, whether or not the plaintiff was exposed to TDI, whether any such exposure caused or materially contributed to him developing asthma and, if so, whether or not the defendants were negligent and/or in breach of statutory duty for permitting such exposure to occur. 10.As regards the latter, it was alleged that, in breach of Regulation 12(3) and 12(4)(a) of the Occupational Safety and Health Regulations, the defendants, being persons responsible for the workplace, failed to ensure, as far as reasonably practicable, that the air within the workplace was kept free of impurities, and failed to take all reasonably practicable steps to protect employees employed at the workplace from inhaling impurities and to prevent accumulation of the impurities at the workplace. Regulation 12(6) of the Regulations defines impurities as including, but not being limited to, fumes, dust and disease-causing bacteria. Although not specifically addressed in the submissions before me, I have little difficulty in concluding that TDI vapour was an impurity within the meaning of this Regulation. 11.No point was taken that there was any difference in the duty of care owed to the plaintiff by the 1st and 2nd defendants in negligence or that there was any difference in the duties imposed on them under statute. Neither was the point taken that the defendants were not aware of the hazards posed by the use of substances containing TDI. Clearly, the greater the hazard posed by any dangerous substance, the higher must be the standard of care that has to be adopted in the handling of that dangerous substance in order to reduce, or to eliminate, as the case may require, the risk of their employees being harmfully exposed to such dangerous substances. 12.I now turn to consider the main defence raised by the defendants, namely, that they had discharged their duty of care and their statutory duty in this case, by adopting a closed system of delivering the TamPUR 150 resin that eliminated the risk of exposure to TDI vapour. 13.I accept the evidence of Mr Paolo Nardone, the Project Director of the 2nd defendant who confirmed that the plaintiff’s job was to supervise the drilling of holes into the concrete wall of the tunnel, the insertion of packers and grouting injections of TamPUR 150 into cracks by means of manually operated hand pumps. The plaintiff was employed to supervise these works, and not to undertake them himself. He explained that at the other end of the hose from the hand-held suction pump was a small nozzle which went into the crack of the tunnel wall to be filled. It is common ground that the nozzle would be pressed against the packer that had been inserted into pre-drilled openings on the tunnel wall. Mr Nardone stated that “there was, therefore, very little (if any) exposure of the chemical to the air”. I understand him to say by that that the risk of exposure of TDI to the air was very little. I also accept the evidence of Mr Nardone that the Korfman fans on the Kwun Tong side of the tunnel operated to push air into the tunnels and that, after travelling for an hour in the tunnels, that air would exit from the Tseung Kwan O side of the tunnels. He had himself witnessed the use of TamPUR 150 in Tunnel C. On the occasion that he went inside one of the tunnels, the humidity was about 98% and the temperature was well over 30 degrees. He saw TamPUR 150 resin being injected into the cracks. When the resin was seen coming out of the crack, that was the signal for the worker to stop pumping. He did not see any resin leak out of the injection hose because there was a tight-fit between the injecting nozzle and the packer. Mr Nardone also gave evidence that it took milli-seconds for the resin to react with the water to form the seal. I shall deal with this aspect of his evidence when I deal with the expert’s evidence on this point. 14.The plaintiff’s evidence was that there would be minor leakage from the nozzle, very fine leakage, when the injection hose was pulled out. He described the leakage as resembling a fine spider’s web, which was not reacting to any water and which would get airborne. When the injection hose was removed, the non-return valve stayed inside the packer and the resin within the packer remained in its original state because there was no water in the packer with which it could react. There would, however, be a minor leakage from every packer, in the form of spider webs, which reacted with the moisture in the atmosphere. The bottom left-hand corner of photograph 25 showed a packer with a stem protruding out from its base. Similar stems can be seen at the base of the packers shown on photographs 27 and 28, being the minor leakage from the non-return valves of the packers. The photographs on p 34-35 of Bundle 8, namely photograph Nos. 25, 26, 27 and 28, showed the packers covered with foam which had already reacted with water. Before it reached that stage, it would have been in a liquid syrupy form. Photograph 23 on p 23 showed a worker injecting a resin into a packer. The packers on the left side of that photograph had already been injected with resin and were whitish in colour because of the leakage of resin, whereas the ones on the right were packers which have not yet been injected and did not show any signs of resin leakage. The minor leakage from the packers eventually formed into a shape of a stem as shown in these photographs. 15.The plaintiff gave evidence that TamPUR 150 resin could also be seen coming out of the cracks before it started to foam. The photographs also showed water coming through the tunnel wall in droplets. These streams of water carried resin into the tunnel. The reaction took minutes, not seconds, but before the reaction took place, the resin had already come through the cracks. 16.The critical question that arises from this evidence is whether it took seconds or minutes for the hazardous resin, containing TDI, to turn into a safe polyurethane seal. 17.Dr Joseph Kwan, the Occupational and Environmental Health and Safety Consultant engaged by the defendants, produced a report dated 22 August 2006 and gave evidence before me. It was his evidence that a very comprehensive and appropriate safety management programme was in place which met international best practice. The work process involving the application of TamPUR 150 was essentially a “closed” system which would serve to deliver the TamPUR 150 directly from the drum to the pump and the hose into the cracks and the fissures. This operation, if conducted properly, would not result in any contact of the concerned worker to this material. Furthermore, TamPUR 150 would react rapidly upon exposure to water to form an elastomeric seal. Once exposed to water and moisture, the TDI would be rapidly consumed to form the polyurethane polymer. Once formed, the polymer would no longer possess the toxic properties of TDI. The reaction started within seconds of contact between TamPUR 150 and water. The fast occurring reaction quickly consumed the TDI and changed it into a non-toxic polymeric foam. 18.Dr Kwan also relied on the absence of any complaints from 46 men working in tunnel C every day for a period of 6 months, and the absence of complaints of skin irritation from the plaintiff, to support his conclusion that there was an effective closed system in place in the tunnels. 19.Dr Kwan was of the opinion that any resin that escaped from the closed system would react very quickly in the very humid areas inside the tunnel. The higher the humidity and the higher the temperature, the faster the reaction and the shorter would be the gelling time. He was not aware of any study to show how much TDI was left in the resin at any stage during the reaction. All safety personnel would say that TDI was hazardous, but toxicity is only one element of the risk assessment. If the operation was handled appropriately, one could handle very dangerous matters in a very safe manner. It was his opinion that the closed system adopted in the present case was a good example of good practice. 20.The more water there was, the more it would facilitate the reaction. When he was referred to photographs showing drips and showers of water, and when he was asked what the level of exposure to TDI was in the particular scenario depicted in those photographs, he answered, very fairly, that without being there, he could not really say what the actual situation was but, from the documents he examined, and based on the method described and the copious amount of water, he would imagine that it would be minimal. Dr Kwan conceded that the dust masks provided to the employees were not designed for use against TDI. If the photographs dripping water was dripping TDI resin instead, then he would prescribe the personal protective equipment (“PPE”) mentioned in Dr Purnell’s report, but he did not see from these photographs that there was major exposure to TDI to the extent that he would prescribe the PPE mentioned. Dr Kwan also conceded that it is possible for the resin to drip down, with the dripping water, if there was a channel behind the concrete connecting the packer with the crack from where the water was dripping. However, as the resin was then in contact with water, the reaction would have started. However, PPE might be warranted if there was a massive quantity of TDI in the cracks and not enough water to react with it, which was not the case here. 21.Dr Kwan did not offer any comment on the substances that could be seen protruding from the packers in the photograph Nos. 25 to 28, and he did not offer any opinion evidence to contradict the evidence of the plaintiff that this material was the reacted resin which had leaked during the injection process. 22.I asked Dr Kwan this specific question :
and he answered, again very fairly, that he would not know as he was not there. As he saw it, if you had a person with some symptoms and toxic materials were present, in order to connect the two, you had to document the exposure. He did not see a clear-cut connection from the evidence. If the plaintiff had been spray painting with just a paper mask for protection, then he would say that it was highly likely that his asthma was from the exposure to TDI, but not with the closed system that was described on the documents in this case. 23.Dr Purnell was called by the plaintiff to give evidence. He is an Occupational Hygienist, Safety Practitioner, and an Environmental Auditor. Notwithstanding an aggressive cross-examination, he maintained the opinions contained in his two expert reports. He referred to the risk assessment in respect of the tunnel repairs and grouting works prepared by the 2nd defendant as part of the project safety plan. The hazards listed included oxygen deficiency and toxic gas. However, the risk assessment did not specifically mention the hazards associated with the use of TamPUR in the tunnel repair works and a requirement to wear respiratory protection during the lining repair work was not stated under the PPE column for this work activity. In his opinion, in the absence of appropriate respiratory protection, inhalation of vapours from TamPUR 150 was likely to have occurred during the process of dispensing the TamPUR 150, injecting the TamPUR 150 resin into cracks and fissures, and cleaning the pump and injection hoses and nozzles. In his opinion, the paper mask provided was inadequate because the paper mask was designed to prevent inhalation of dust and would not provide any protection from inhalation of TDI vapour, which would pass straight through the paper and be inhaled. In his opinion, a filtering mask provided with a charcoal cartridge and a particulate filter with an assigned protection factor of at least 20 should have been provided. I find that the particulate filter mask subsequently acquired by the plaintiff from Mongkok for HK$100 was unlikely to have satisfied this high standard of protection. 24.In his supplemental report, Dr Purnell said that the TDI content of TamPUR 150, being an average of 5.81%, was quite high and amounted to about 1.4 kg of TDI in a 25-kg drum of TamPUR 150. He also noted that the risk assessment statement prepared by the 2nd defendant as part of the project safety plan, which did not specifically mention the hazards associated with the use of TamPUR in the tunnel repair works, was dated 29 May 2001, so it might not have actually been prepared or actioned in 2000. He referred to Dr Kwan’s opinion that the operation, if properly conducted, would not result in any contact of the concerned worker to TamPUR 150 resin, implying that the operation could be carried out without any risk of the resin escaping. The evidence, however, suggested to Dr Purnell that that was not the case in practice. The resin injection operation could not be described as a closed system if resin could be released from a crack or fissure when the worker attempting to seal water ingress. In his view, the egress of resin was unavoidable despite the fact that TamPUR 150 resin reacted rapidly with water. He supported his opinion by reference to the photographs and the evidence of the plaintiff that leakage of syrupy resin occurred at the non-return valve of the packers. 25.Dr Purnell was asked about the test results on TamPUR 150 appearing on p 141 of Bundle 4. His evidence was that the table was unclear; for example, when it stated that tests were done at 25 degrees, it was not specifically stated whether that was a reference to the temperature of TamPUR 150 or to the ambient temperature. The table showed the cream time, which was the length of time that passed before the foaming reaction started. He said that one should not read too much into the data as the cream time changed inconsistently with the ratio of water and resin and also changed inconsistently with the temperature. However, what clearly emerged was that cream time was shorter than the rise time (when foam was being produced) for any temperature shown by the table. The rise time was important in forming a rigid structure. Overall, the table showed that it took over a minute to complete the rise time in whatever temperature the test was conducted. I accept the evidence contained in this table and the opinion of Dr Purnell that it took minutes, not seconds, to form a sealant. The table showed that, with a ratio of 1 part water and 1 part TamPUR 150 resin, at a temperature of 30ºC, the cream time, i.e. the length of time before foaming reaction started, was 25 seconds, and the rise time, i.e. the length of time to complete the foaming reaction, was 90 seconds. Notwithstanding possibly higher temperatures, and most definitely a much higher humidity inside the tunnels, I have little difficulty in concluding that it would have taken at least a minute or so for the reaction to be completed and for the non-toxic sealant to be formed, rather than the milliseconds suggested by Mr Nardone, whose evidence in this connection I do not accept. Whilst I accept Dr Kwan’s opinion that the creaming and rise time was shorter with larger quantities of water and high heat and humidity, I conclude that, even so, such shorter time was not a matter of seconds. 26.It was, I think, common ground between the two experts that TDI was consumed in the reaction process so that, at some point in time, and at the very latest, at the time when the polymer had been fully formed, there was no toxic TDI left. I accept the evidence of Dr Kwan that there was no study to show how much TDI was left in the resin at any stage during the reaction. Dr Purnell also conceded that he would not know what level of TDI was consumed in the reacting resin that was pushed out through the cracks and how much TDI remained in that reacting resin before the reaction was finally completed. However, this evidence must be viewed in the context of the other evidence, which I also accept, that TamPUR 150 had a very high percentage of TDI, being almost 6%, and that its toxicity was higher than, for example, the isocyanates in car paints which usually had about 0.5% TDI. When the TamPUR 150 resin mixed with water, it heated up and vaporised, creating a foamy gel. Although the reaction might have started where the resin was injected through the packers at the face of the tunnel, as the creaming time and foaming time took more than a minute, the reaction was still continuing when the reacting resin was exposed through the cracks of the tunnel face. If there was a lot of water coming out of the cracks, it would carry resin out of the cracks sooner, leaving the resin less time to complete the foaming process. I accept the opinion of Dr Purnell that TamPUR 150 was not designed to seal cracks with so much amount of water flowing out of them. In respect of some of these larger cracks, the workers had to use three, 25-kg, drums to gain any ability to seal the leak. The resin would form a spray if it burst out from a crack and a small percentage of that spray would become vapour which could be inhaled. If it did not burst out from the crack, the resin would dribble out onto the floor of the tunnel and continue its reaction, in this exposed state, until it solidified on the floor of the tunnel. 27.I accept the evidence of Mr Nardone that air was being extracted from the tunnels at the Tseung Kwan O end and that the source of fresh air into the tunnel was the Kwun Tong end, where the plaintiff’s team was working. It follows that I do not accept the evidence of Dr Purnell insofar as he suggested that the opposite was the case.To be fair to Dr Purnell, he agreed that photograph No. 3 on p 23 of Bundle 8 showed the vertical duct for ingress of fresh air. I accept the defence case that this photograph was a photograph taken from the Kwun Tong end. Accordingly, the dust and polluted air inside the tunnel and the TDI vapour leaking into the tunnel was being pushed towards the Tseung Kwan O end, at the acceptable linear air flow rate of about 1.5 metres per second. 28.A second aspect of Dr Purnell’s evidence which I found difficult to accept was his opinion that the foaming resin could create sufficient pressure to cause the concrete lining to fracture and to seep through such fractures. I can readily accept that the reacting resin would be forced out of the incompletely sealed cracks, but I find it difficult to accept that the pressure created by the foaming resin would be sufficient to cause the concrete lining to fracture. Apart from these two aspects of Dr Purnell’s evidence, I accept his evidence in preference to the evidence of Dr Kwan in so far as such evidence conflicted with the evidence of Dr Purnell. 29.Mr. Sakhrani made cogent submissions to me that :
30.I have little hesitation in concluding that the plaintiff’s evidence that the TamPUR 150 would get everywhere, including his hair and clothes, when they were pumping in the TamPUR 150 in the overhead position, was a gross exaggeration. I am satisfied, from the evidence that the plaintiff gave during the course of his cross-examination, that the stains on his overalls, as can be seen from the photographs in Bundle 8, were largely on the thighs, the ends of the sleeves and in the buttock region, and were caused by those parts of the overalls coming into contact with excavation dust and debris, and were not caused by contact with TamPUR 150 resin. 31.However, I accept the evidence of the plaintiff that there was leakage of uncured resin from the packers and from the cracks in the tunnel wall. Even if the reaction had started before the resin became exposed, the process of reacting with water continued after the resin was exposed. This continuing reaction with water caused the resin to heat up, to become vaporised, and to turn into a foamy substance and, as it was doing so, it gave off toxic TDI vapour which could be inhaled by the plaintiff. Although there is no evidence of the rate of consumption of TDI in the course of the reaction, I infer, from the high concentration of TDI in the resin (an average of 5.81%) and its toxic qualities (as demonstrated by the ultra low levels of tolerable exposure) that toxic TDI vapour was present in the confined tunnels in quantities in excess of the tolerable levels, notwithstanding that the quantity of leaked uncured resin was minor, that the reaction time was shorter, and that there were large quantities of water present in the hot and humid tunnels, and notwithstanding the proper handling of the hand pumps by the workers and the acceptable linear air flow rate of about 1.5 metres per second. 32.I am not prepared to conclude, based on the evidence I have heard, that exposure to TDI caused the plaintiff to develop asthma. However, I am prepared to infer, on a balance of probabilities, from the totality of the evidence I have heard and received, that the plaintiff was exposed to TDI vapour during the period of time when he was working in the tunnels, and that such exposure materially contributed to him developing asthma in that it acted in conjunction with the other triggers present in the tunnel environment, namely, the dusty, polluted, hot and humid conditions under which they worked for long periods of time, where the air was full of pollutants and other irritants. I draw such an inference from the temporal coincidence between the development of asthma and the presence of TDI vapour in the tunnels. I find that the plaintiff was exposed to TDI vapour in the tunnels and that the exposure to TDI vapour materially contributed to the onset of asthma, in the sense that its causative potency was neither de minimis nor insignificant. I make this finding after having had regard to the hazardous nature of this substance, and its well known and well documented propensity for causing individuals exposed to it, even in extremely low concentrations or for short periods of time, to develop asthma. 33.I do not shy away from drawing this inference just because other workers in the tunnel were not affected by exposure to TDI. I accept that the plaintiff was particularly vulnerable, given his chronic rhinitis, to develop asthma. This vulnerability supports the inference I have drawn that his exposure to TDI vapour materially contributed to him developing asthma in that it acted in conjunction with the other triggers present in the tunnel environment. A tortfeasor must take his victim as he finds him. The defendants cannot claim that the damage suffered by the plaintiff was not reasonably foreseeable even if they did not know that he was vulnerable to developing asthma. 34.This is not a case like Wilsher v. Essex AHA [1998] AC 1074 where there were distinct and competing causes, and where each possible cause might have caused the injury complained of independently, operating in a different way from the other competing causes. This is a case of possible cumulative causes, as was Bonnington Castings Ltd. v. Wardlaw [1956] AC 613 where the claimant contracted pneumoconiosis from inhaling air containing silica dust in his workplace. The main source of the dust came from an innocent source for which the employers were not in breach of duty. However, some of the dust (“the guilty dust”) came from equipment which the employer had failed to maintain. There was no evidence of the proportion of innocent and guilty dust inhaled by the claimant and such evidence as there was indicated that the greater proportion of the silica dust came from the innocent source. This evidence, and absence of evidence, notwithstanding, the House of Lords drew the inference that the guilty dust materially contributed to the disease. As a scientist, Dr Kwan needed a clear-cut connection, from the evidence, between exposure to TDI and the onset of asthma. In a case of possible cumulative causes, the court does not require proof that exposure to the TDI actually caused the onset of asthma. The court may infer, as I have done, from the toxic properties of TDI and from the finding that the plaintiff was exposed to TDI vapour, that such exposure materially contributed to the damage complained of, namely, the onset of asthma. 35.I find that the system of work in the tunnels gave rise to a foreseeable risk of exposure to toxic levels of TDI vapour and that the defendants were in breach of their duty in negligence to the plaintiff in failing to provide him with a filtering mask provided with a charcoal cartridge and a particulate filter with an assigned protection factor of at least 20. No evidence was adduced before me to suggest that the cost of such equipment was excessive or prohibitive. 36.I also find that the defendants are liable to the plaintiff for breach of the statutory duties contained in Regulations 12(3) and 12(4)(a) of the Occupational Safety and Health Regulations, in that the defendants, being persons responsible for the workplace, failed to ensure, as far as reasonably practicable, that the air within the tunnels was kept free of impurities, namely, toxic TDI vapour, and failed to take all reasonably practicable steps to protect employees employed in the tunnels from inhaling toxic TDI vapour, and to prevent accumulation of the toxic TDI vapour in the tunnels. 37.For the reasons expressed above, and notwithstanding his usual eloquence, I do not accept any of the submissions of Mr Sakhrani that I have set out above. I find liability established. As the defendants did not raise any plea of contributory negligence in its pleadings, it cannot now do so at this late stage at trial. If anything, a proper risk assessment on the use of TamPUR 150 ought to have resulted in the implementation of screening procedures to screen out vulnerable individuals like the plaintiff. Quantum 38.The plaintiff was 33 years old at the time that he contracted asthma whilst working in the tunnel repair project. He will be 45 years old on 28 March this year. I have already referred to his prior medical history when dealing with the issue of liability. In his report dated 1 November 2003, Dr Pang noted that the plaintiff continued to have symptoms intermittently since April 2001 up to the time of his examination in October 2003. These consisted of occasional chest tightness before bed, and wheezing and sneezing in the morning, although he could sleep through the night. Respiratory tract infections, inhalation of fumes, cigarettes smoke and even laughing could provoke wheezing. He also noticed a decrease in his exercise tolerance, and he became short of breath easily on walking and swimming. A game of soccer in the summer of 2002 and a sports dive in February 2003 made him feel so short of breath that he gave up sports altogether. He used ventolin up to 2 – 4 times a day and anti-histamines intermittently for rhinitis. Dr Pang was of the view that the plaintiff had received appropriate therapy for his asthma but that he did not continue with beclomethasone for reasons that were unclear to Dr Pang. Dr Pang was of the opinion that inhaled beclomethasone should be restarted and would assist recovery and further improvement could be expected. The treatment of his rhinitis would also improve his sense of well being and his respiratory symptoms. Dr Pang was of the view that the plaintiff’s asthma was mild at the time of his examination and that he fell in the category of Class 1 respiratory impairment with no impairment of the whole person. He did not need any sick leave and, with proper treatment and compliance with medication, his prognosis was good. Appropriate period of sick leave, as a result of his occupational asthma would be one month, bearing in mind the strenuous nature of his job. 39.The defendants’ specialist, Dr Leung, examined the plaintiff on 11 March 2005. Dr Leung was also of the view that the plaintiff had bronchial asthma of mild degree with no impairment of the whole person. The two experts jointly assessed the plaintiff on 7 December 2010 and, in their joint report dated 22 February 2011, they noted that the plaintiff continued to suffer the same symptoms of chest tightness in the morning, tickling sensation in the throat causing cough, and wheeze at night. He had not been on any regular maintenance therapy for asthma until one month prior to this assessment when he was referred to Dr Jane Chan, a specialist in respiratory medicine, for asthma management. She put him on regular inhalation of a budesonide-formoterol combination and a daily dose of an oral tablet. His asthma symptoms had improved significantly since then, and he only needed to use the ventolin inhaler up to 3 times a day. The plaintiff also had chronic rhino-conjunctivits with symptoms of nasal congestion, runny nose, sneezing and itchy, watery eyes. These were well controlled by the daily use of a nasal spray and an anti-histamine tablet. He had quit smoking temporarily in February 2008 but had gone back to smoking 2 to 10 cigarettes per day. He admitted that asthma was not a major obstacle to employment for him. A lung function test performed at the time of their examination was normal. 40.The experts commented that the plaintiff had established asthma since 2001, but that it was well controlled. The poor asthma control was largely due to the plaintiff’s failure to use preventive treatment with inhaled steroid, as recommended by the experts in their previous medical reports. This had led to limitation of physical activities, which, in turn, resulted in feelings of low esteem and reduced quality of life. The normal lung function indicated no major structural damage to the airways at the time of the assessment. In a further letter dated 9 June 2001, the experts expressed their joint opinion that the plaintiff was receiving proper treatment for asthma and that no further treatment was recommended. From the examination of the plaintiff and the records of Dr Jane Chan, it was apparent that the plaintiff’s mild asthma was readily controllable by drugs. However, he had to take these regularly which he had not done in the past. He did not require any other treatments. There was no restriction on the activities of patients with mild asthma when they were well controlled. Such activities include heavy exertion and work in challenging environments. Normal lung function test results were a very important indication of well-controlled asthma. His lung function tests were completely normal when tested on 16 October 2003. Further tests on 29 November 2010 were only very mildly abnormal, and they were completely normal when repeated on 7 December 2010 and 24 January 2011. The treating doctor, Dr Jane Chan, considered that his asthma was mild on 29 November 2010, and well controlled from 24 January 2011 up to the last time she saw him on 14 March 2011. 41.The plaintiff does not seek damages for PSLA simply for his mild asthma, which is well controlled by medication. He also seeks damages for anxiety neurosis, and loss of prospects of developing a career as a commercial diver. He alleges that both was caused by the asthma he suffered. 42.In their joint report dated 22 February 2011, Drs Pang and Leung stated that, in 2002, the plaintiff went to see Dr Tatia Lee for a neuro-psychological assessment which revealed normal frontal function and average intellectual ability. Between January and July of 2004, he took regular medications prescribed by Dr Sylvia Chen, a psychiatrist, presumably for anxiety neurosis. An MRI scan of the brain was suggested, but this was not performed until May 2009 when Dr Tsang Ki Lun, a neurologist, recommended it again. The MRI scan showed dilation of the ventricular systems suggested of normal pressure hydrocephalus (excess of fluid). A lumbar puncture was performed in September 2009 and, since then, he had recurrent headache for which he was treated by another neurologist, Dr Brian Choa, up to the present time. Dr Choa also referred him to see Dr Calais Chan, a clinical psychologist, for stress management. The plaintiff did not find that helpful. His physical activities had been limited by breathing difficulties such that he could no longer play soccer and swim. This lack in confidence in sporting activities that he used to enjoy has been very frustrating for him. He had difficulty falling asleep and would wake up at least once on most nights but not typically because of wheeze or chest tightness. Even so, he would take 1 to 2 puffs of ventolin inhaler. He admitted that this was mainly related to stress. He suffered from frequent anxiety attacks with symptoms of palpitation, sweatiness in the palms, and hyperventilation; these were particularly worsened when speaking in public. He had also developed a phobia to heights. He had been unemployed since 2004, except for casual short-term jobs lasting for a few days. His wife provided financial support for the family that included a six-year old son and a two-month old daughter. Both experts agreed that the plaintiff had significant anxiety symptoms that had definite effects on his physical as well as his social activities. They recommended continued treatment by neurologists and/or psychiatrists. 43.They were also of the opinion that he was medically unfit to resume employment as a commercial diver at present because of chronic asthma, albeit of a mild degree of severity. However, his mild asthma could be readily controlled by regular treatment and, if this was achieved, his respiratory disease should not prove to be a barrier to such employment. However, they were not in a position to comment on his future employability from the anxiety neurosis point of view. In response to the question put to them, namely, when they believed the plaintiff would be fit to resume employment as a commercial diver, they replied, in their joint letter of 9 June 2011, that they could not answer that question with complete confidence as they were not involved in his medical care. However, they pointed out that his recent lung function tests were normal and that his treating doctor, Dr Jane Chan, was of the view that his mild asthma was well controlled from January 2011 up to the last time she saw him in March 2011. 44.It is recorded in the notes of his treating doctor, Dr Clifford Loo, that the plaintiff came to consult him on 24 April 2003 when he had started a new job and was suffering from work related anxiety with symptoms such as blushing, sweating, dry mouth and insomnia. He was given a trial of valium and propranolol to help him cope with his anxiety. Upon his return on 26 June 2003, the plaintiff claimed to have good response to that medication but that work was still stressful for him. He was given a repeat prescription. The plaintiff again complained of persistent stress from work, giving him insomnia when he returned to see Dr Loo on 21 October 2003. Although he wanted a long-term medication, he was prescribed with valium for one month. On 5 January 2004, the plaintiff had suffered another stressful time at work and was referred to see Dr Sylvia Chan for his persistent anxiety neurosis. Dr Loo saw him again in respect of his anxiety neurosis on 2 June 2005 and he was given a brief course of anxiolytic drug. 45.In a note dated 25 October 2010, Dr Calais Chan, the clinical psychologist, stated that the plaintiff had been referred to him for psychological treatment by Dr Brian Choa. He had attended a total of 3 clinical sessions since 11 August 2010, 1 September 2010 and 20 September 2010. During the clinical sessions, the plaintiff presented a range of anxiety and stress symptoms including increase palpitation, sweating, trembling hands, and blushing face on periodic basis. He also reported acute attacks of anxiety, especially when driving across bridges, taking lifts or escalators as well as ascending heights. He had told Dr Chan that he did not have any previous history of anxiety disorders or psychiatric illness prior to a work-related accident involving chemical intoxication some years ago in 2001. Since then, he had been having chronic worries and anxiety about his health status, work disabilities, financial matters as well as ongoing personal litigation. The plaintiff was diagnosed by Dr Chan as suffering from a chronic case of adjustment disorder with anxiety, primarily caused by the alleged work-related accident in result of his disabilities in 2001. 46.Whilst the report of Dr Calais Chan, as a treating doctor, is admissible before me, I am not satisfied, on the strength of that report alone, and absent other expert evidence on point, that the anxiety neurosis, which the plaintiff undoubtedly suffers from, was caused or contributed to by the plaintiff developing asthma when he worked in the tunnel repair works for the defendants. The plaintiff was covered by his wife’s medical insurance programme and which enabled him to consult Dr Clifford Loo frequently. Indeed, as can be seen from Dr Loo’s note of 13 August 2010, the plaintiff visited him on 27 occasions from January 1998 to March 2010 for a variety of ailments including cough and stomach upsets, ankle pain and hip pain, and flu. He consulted Dr Loo for the very first time for anxiety on 25 April 2003 when he complained to him that he suffered from work-related anxiety as a result of starting a new job. I do not accept the plaintiff’s assertion, which he made during his cross-examination, that he had been suffering from anxiety for a long period of time and which had been exacerbated by reason of work-related stress. He visited Dr Loo for an upset stomach on 26 June 2002, and again on 28 January 2003. If he had been suffering from anxiety at that time, or before then, I have no doubt that he would have consulted Dr Loo and sought treatment for such anxiety. After he left the 1st defendant’s employment, the plaintiff worked for Bostwick Bo-Shan. The plaintiff did not allege in his evidence that he had suffered from work-related anxiety whilst he was working there. His complaint of work-related anxiety was made when he commenced working with a firm called Kaba, which he did some time after leaving Bostwick Bo-Shan. Dr Calais Chan’s opinion, that his adjustment disorder with anxiety was primarily caused by the alleged work-related accident involving exposure to hazardous chemicals and resulting disabilities in 2001, was based solely on the plaintiff’s assertion and was not supported by Dr Loo’s medical notes. For the reasons I have stated above, I do not accept that his anxiety neurosis was either caused or contributed to by the onset of asthma during his work on the tunnel repair project. 47.The plaintiff’s continuing anxiety neurosis clearly prevents him from pursuing a career as a commercial diver. In addition, as was clearly brought up in the course of his cross-examination, the plaintiff accepted that, at the time that he had sent an email, in December 2000, to the Underwater Centre, in Tasmania, making enquiries about enrolling in their HSE course which would enable him to pursue a career as a full-time commercial diver, his physical, mental and emotional health was not such as would have prevented him from developing that career. His reasonably good health was consistent with the improvement in his condition following treatment from Dr Patrick Au and Dr Clifford Loo. The plaintiff also acknowledged that, in fact, he did not have the financial ability at that time to pursue the HSE course in Tasmania. It would have cost HK$100,000, for the course, as well as additional expenditure for living and travelling expenses. The successful completion of that course might have enabled him to pursue saturation diving. However, it was clear from the evidence that there was no saturation diving work available in the shallow seas of Hong Kong. I do accept the plaintiff’s evidence that he had performed diving work in the past, which is detailed in §§43 and 44 of his supplementary witness statement dated 25 May 2011. However, I also find that his inability to continue such diving work was the result of his anxiety neurosis. Does the mild but well controlled asthma that he suffers from create a handicap for him in the labour market of commercial divers, assuming that his anxiety neurosis is cured? I give an affirmative answer to that question, notwithstanding that I accept the joint opinion of the experts in this case that he could resume commercial diving once his mild asthma was well controlled by medication. There is no suggestion, however, that his anxiety neurosis can be cured in the foreseeable future to the extent that it would no longer prevent him from taking up commercial diving work. Faced with this reality, I can only conclude that the greater part of the loss of earning capacity as a commercial diving is caused by the anxiety neurosis, with only a minor contribution from the mild asthma that he suffers from, but which can be well controlled if he is more disciplined in taking appropriate medication. 48.On the basis of the above findings, I go on to assess damages for PSLA and damages for loss of earning capacity. The plaintiff has not been able to establish to my satisfaction that he has suffered actual loss of earnings as a result of developing asthma during the tunnel repair works. The plaintiff joined Bostwick Bo-Shan on 1 March 2001, almost immediately after he left the 1st defendant’s employment, and remained working there until 26 November 2002, earning about HK$20,000 per month. On 14 April 2003, he joined Kaba where he remained until 31 October 2004, earning HK$32,000 a month, and leaving only because the work was no longer available. His earnings at Bostwick Bo-Shan were similar to his earnings for performing diving work for the 1st defendant before September 2000, and his earnings at Kaba were similar to his earnings for the tunnel repair works that he performed for the 1st defendant from September 2000 up to the time he ceased that work in February 2001. I am not satisfied, on this evidence, that the plaintiff suffered from any actual loss of earnings as a result of the onset of mild asthma in November 2000. I accept the opinion of Dr Leung that he is medically fit to work in a variety of jobs where he would be protected from excessive exposure to irritants. 49.The plaintiff claims damages for PSLA on the basis that the plaintiff’s injury falls within the serious injury category. The defendants submit that the award for PSLA should not to exceed HK$75,000. There are no authorities on point but Mr Sakhrani was able to refer to the UK Judicial Studies Board Guidelines in respect of asthma. The following extract is taken from the 10th Edition (December 2010) of those guidelines :
50.I am of the view that the present case falls within category (c) as set out above. I am not bound by these guidelines but, in the absence of authorities on point, I find them to be a helpful reference point to me in the task of assessing the award for PSLA in this case. His unrelated anxiety neurosis has contributed substantially to the plaintiff giving up strenuous sports. On the other hand, the fact that he suffers from chronic rhinitis must mean that his asthma, albeit mild and well controlled, would aggravate his suffering were he to have an asthmatic attack when he was also suffering from rhinitis. Further, although his current impairment of the whole person from his asthma was nil, I cannot ignore the possibility of it getting worse in older age. All things considered, I assess damages for PSLA in the sum of HK$250,000 in the present case. 51.I assess damages for loss of earning capacity caused by the plaintiff’s asthmatic condition in the sum of HK$150,000. Notwithstanding that the loss of earning capacity as a commercial diving caused by his mild and well controlled asthma is minor, and that his total loss of earning capacity in this field of work is substantially caused by his unrelated anxiety neurosis, I feel justified in making an award in this amount given the impediment posed by his asthma, which can be induced by strenuous exercise, to him developing his career in the lucrative field of commercial diving. 52.This is not an appropriate case to award damages for loss of congenial employment. 53.I award, in full, the amount claimed for pre-trial expenses incurred in respect of medical expenses, medication and inhalers and travelling expenses in the sum of HK$72,850. 54.Interest is claimed on this amount at half the usual rate, i.e. at 4% per annum, for 11 years. This action was commenced in 2003 and ought to have been tried much earlier. I am only prepared to award interest on this sum at 4% per annum for a period of 8 years from November 2000. For the same reason, I award interest at 2 % per annum on damages for PSLA from the date of service of the writ to the end of October 2008, and not to the date of judgment. 55.The plaintiff also claims future expenses for medical consultation, medication and travel in the sum of HK$5,000 per annum. I am prepared to award this claim in full. Given his current age of 45 years, I apply a multiplier of 17 to this amount to produce a total award of HK$85,000 under this head of claim. 56.I direct the parties to exchange written submissions on costs within 14 days from the date of this Judgment. The submissions should be concise, setting out in draft form the order of costs sought, together with brief submissions in support of such proposed order.
Mr Victor Tulsi Gidwani, instructed by Messrs Burke & Co., for the Plaintiff Mr Ashok Sakhrani, instructed by Messrs Szwina Pang, Edward Li & Co., for 1stDefendant and Messrs Deacons, for 2ndDefendant [1] Perennial allergic rhinitis is to be distinguished from seasonal allergic rhinitis, also known as hay fever. The latter is triggered by seasonal allergens such as pollens. The former may occur year-round and be triggered by indoor allergens. | |||||||||||||||||||||||||||||
Cases cited in this judgment
Further hearings and rulings under HCPI 945/2003