Incremental Harm as a Basis of Product Liability - John C. Wunsch, P.C.
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Incremental Harm as a Basis of Product Liability

Product liability law imposes liability against manufacturers of “unreasonably” dangerous products. The danger inherent within a product can range from the manifest to the latent, from the direct to the indirect.

Primary Risks. These are the obvious risks a product poses to a user. You can fall off a motorcycle, you can sustain a cut to the finger from an electric saw. Courts typically do not require a product manufacturer to warn of “obvious” risks. The trouble with that rule is what constitutes “obviousness.” Is it a risk that’s visually apparent? Or does it include discoverable risks?

Secondary Risks. These are the less obvious risks that can be perceived during use. A construction company purchases a pressure-activated nail gun. The risk to the user being injured by a projected nail versus the risk to another on the worksite being so injured. To someone who accidentally brushes up against a pressure-activated product while on a worksite, the risk is both unexpected and non-obvious.

Tertiary Risks. These are hidden risks––the kind manufacturers are expected to seek out and discover. A manufacturer of a powder used on the face fails to warn of long-term inhalation risks. Primary risks can become tertiary risks. Drugs have side effects, but they also have adverse interactions with other drugs. Drug manufacturers are required to warn not only of obvious hazards, but of harmful interactions with other drugs as well. The failure to warn of such risks is actionable since the consumer should have the choice not the manufacturer of deciding what risks they’re willing to accept.

In the setting of a pandemic of obesity and related chronic diseases, the American Heart Association recently released a scientific statement recommending reductions in added-sugar intake to no more than 100 to 150 kcal/d for most Americans.  The statement identified sugar-sweetened beverages (SSBs) as the primary source of added sugars in the American diet. Although it has long been suspected that SSBs contribute at least in part to the obesity epidemic, only in recent years have large epidemiological studies been able to substantiate the relationship between SSB consumption and long-term weight gain, T2DM, and cardiovascular risk. It is thought that SSBs contribute to weight gain because of their high added-sugar content, low satiety, and potential incomplete compensation for total energy, leading to increased energy intake. In addition, because of their high amounts of rapidly absorbable carbohydrates such as various forms of sugar and high-fructose corn syrup (HFCS) and the large quantities consumed, SSBs may increase T2DM and cardiovascular risk independently of obesity as a contributor to a high dietary glycemic load (GL), leading to inflammation, insulin resistance, and impaired β-cell function. Fructose from any sugar or HFCS may also increase blood pressure and promote the accumulation of visceral adiposity, dyslipidemia, and ectopic fat deposition because of increased hepatic de novo lipogenesis.[1]

Food is an example of a product where a primary risk can become a tertiary risk. Those who drink soft drinks throughout the day may not know the full extent of what’s happening to their bodies, unaware of the terms “inflammation,” “insulin resistance,” and “impaired β -cell function.”

A large proportion of people with obesity or NAFLD [nonalcoholic fatty liver disease] have insulin resistance, and most people with insulin resistance have increased liver fat concentration. Fabbrini et al demonstrated that insulin resistance and other metabolic perturbations in obesity correlate better with liver fat than with visceral adipose tissue. In contrast to observations in healthy individuals, participants with insulin resistance and NAFLD have been found to have elevated rates of DNL [de novo lipogenesis] in both the fasting and postprandial states (26% of VLDL-TG)[ very low-density lipoprotein triglycerides]. Moreover, analysis of liver biopsy specimens collected from participants with NAFLD and chronically elevated DNL revealed that 26% of their liver fat was produced de novo, supporting the hypothesis that hepatic DNL may be an important contributor not only to postprandial lipids secreted by the liver but also to liver fat accumulation.[2] 

In certain well-defined instances, the law should recognize a new category of product liability based on injuries and death arising out of a product having caused “incremental harm”––serious bodily injury or death as a result of multiple small accumulations over a period of many years––each exposure in itself relatively harmless, but over extended periods causing serious harm. Courts have been reluctant to accept this type of case, but there are good reasons why liability should attach.

The time horizon is irrelevant. It’s irrelevant from the standpoint of the injured consumer whether their injury occurs instantaneously or over an extended period of time. Were one to simply collapse the time frame, as if replayed in accelerated motion, the harm inflicted would be obvious and unmistakable.

There’s no practical difference. There’s no practical difference between an IV drip that causes harm to a patient over 6 minutes as opposed to 6 months––or even 6 years. The fact that harm occurred in small increments should not excuse those responsible.

Small harms are insidious. The most serious harms we take intentional steps to avoid. Insidious harms are those where we’ve been lulled into believing that “this must be safe or they would not have permitted this to be sold.” We do not take steps to avoid these harms since we’ve been assured the risks are negligible, harmless. When we later find out we’ve been deceived, the law of product liability should be large enough to recognize “incremental harm” as a basis of liability.

[1] Vasanti S. Malik, Barry M. Popkin, George A. Bray, Jean-Pierre Després, Frank B. Hu, Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk, Circulation, March 22, 2010, http://circ.ahajournals.org/content/121/11/1356.full

[2] Jean-Marc Schwarz, Michael Clearfield, Kathleen Mulligan, Conversion of Sugar to Fat: Is Hepatic de Novo Lipogenesis Leading to Metabolic Syndrome and Associated Chronic Diseases?, The Journal of the American Osteopathic Association, August 2017, Vol. 117, 520-527,

http://jaoa.org/article.aspx?articleid=2646761

 

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