46.5 The legal elements of a claim in negligence are that the defendant owed the plaintiff a duty of care; the defendant breached that duty; and the plaintiff suffered damage that was caused by the breach of the duty, and was not too remote from it in law. Where negligence is established, the court may award damages to the plaintiff.
46.6 It has been said that the tort system has, in the past, treated all persons as ‘identical black boxes’ in relation to their risk from exposure to hazardous substances and agents. While there have been some limited exceptions, such as the ‘egg-shell skull’ rule in relation to highly vulnerable plaintiffs (see below), generally there has been no basis for discerning individual risk factors from the risk posed to the general population.
46.7 There are a number of ways in which genetic information and, in particular, genetic test results could potentially be applied by courts in tort actions.
46.8 A defendant in a negligence action might seek to use genetic information to disprove the plaintiff’s allegation that the defendant caused the plaintiff’s injury. For example, where a plaintiff had a genetic predisposition to the same condition that he or she ultimately developed, the defendant could argue that it was the predisposition, rather than the defendant, that caused the injury. Alternatively, a defendant might argue that the predisposition was a contributing cause of the injury in order to minimise his or her own liability. The strength of this argument may depend on the link between the genetic mutation and the occurrence of the disorder (see Chapter 2).
46.9 A plaintiff might seek to rely on genetic tests that show that he or she has a higher susceptibility to a particular chemical agent than an ordinary person in order to establish that exposure to the chemical caused the particular illness or injury, even though other exposed persons remained healthy.
46.10 Alternatively, defendants might argue that they have no duty to protect genetically ‘hyper-susceptible’ persons from harm or injury, in particular where the defendant can show that its product is safe for the ‘normal’ population. However, this argument is inconsistent with an established doctrine of tort law—the ‘eggshell skull’ rule. This rule provides that a defendant is liable for the full damage caused to an unusually susceptible or fragile plaintiff, even if the extent of damage would be less in a ‘normal’ person.
Duty to warn susceptible persons
46.11 A product manufacturer generally has a duty to warn consumers of potential hazards posed by that product. Failure to provide an adequate warning can result in civil liability. With increasing knowledge of susceptibilities to chemicals, pharmaceuticals and other products, it might become necessary to consider to what extent a manufacturer has a duty to warn persons with specific susceptibilities of potential hazards to them.
Assumption of risk
46.12 As more genetic tests become available, defendants could seek to rely on the ‘voluntary assumption of risk’ or ‘contributory negligence’ defence to a tort claim. A defendant might argue that a plaintiff knew, or should have known, that he or she had a genetic susceptibility to a particular agent and therefore should have taken greater precautions to avoid exposure.
46.13 It is unlikely that this argument would be successful in the workplace context because occupational health and safety statutes place a duty on employers to eliminate or minimise workplace hazards. Were it otherwise, employees might be compelled by financial circumstances to accept risks that are considered unacceptable by the general community.
46.14 Chapter 32 discusses the use of genetic monitoring as part of health surveillance of employees exposed to hazardous substances in the workplace. Genetic biomarkers can identify changes in a person’s cells as a result of exposure to toxic substances. These genetic changes could provide a measure of exposure to a substance, or an early diagnostic measure of the development of the disease before the onset of symptoms. Thousands of potential biomarkers have already been identified, most of which had yet to be fully validated scientifically.
46.15 Plaintiffs could potentially rely on biomarkers as evidence of a plaintiff’s exposure to a hazardous agent, and of the harm suffered as a result of exposure. Defendants could rely on the absence of these biomarkers to argue against causation. However, the use of such biomarkers in civil proceedings is likely to be limited until they are fully validated.
Assessment of damages
46.16 Defendants who have been found liable in tort could seek to have the quantum of damages reduced on the basis that the plaintiff has a predisposition to, or is presymptomatic of, a condition that would diminish the plaintiff’s quality of life or lead to a shorter life expectancy. For example, where a defendant is found liable but can establish that the plaintiff would have developed the injury at some point in the future regardless of the defendant’s action, the defendant might seek to have the damages reduced to compensate the plaintiff only for the period for which the defendant’s actions accelerated the development of the injury.
46.17 The defendant might alternatively seek to identify a genetic predisposition, or presymptomatic status, for any disease that could shorten or diminish the quality of the plaintiff’s life. For example, the defendant might seek to rely on genetic tests that reveal the plaintiff is presymptomatic of Huntington’s disease to argue that, because the plaintiff would not be expected to live beyond middle age, the court should reduce the amount of damages accordingly.
 S Berns and G Masel, ‘Negligence’ in G Masel (ed), The Laws of Australia: Torts (1997) Law Book Company Limited, Sydney, vol 33.2, .
 See generally, M Noone, ‘Damages’ in Geoff Masel (ed), The Laws of Australia: Torts (1993) Law Book Company Limited, Sydney, vol 33.10.
 G Marchant, ‘Genetics and Toxic Torts’ (2001) 31 Seton Hall Law Review 949, 953.
 Ibid, 963–964.
 Ibid, 954–956.
 Ibid, 960–963.
 Ibid, 956–957.
 Ibid, 965.
 Ibid, 972.
 Ibid, 976.
 Ibid, 968. The difficulty with this argument is in establishing that a person with a mere predisposition to a multifactorial disease would ultimately have developed the disease.
 Ibid, 969.