Liability for Prenatal Harm in the Workplace: the Need for Reform

JurisdictionUnited States,Federal
CitationVol. 17 No. 02
Publication year1993


Liability for Prenatal Harm in the Workplace: The Need for Reform(fn*)

Steven S. Paskal(fn**)

I. Introduction

Fifteen percent of all recognized pregnancies result in spontaneous abortion(fn1) and seven percent of liveborn infants are afflicted with birth defects.(fn2) Although there are innumerable workplace stressors that are known or suspected to cause such injuries, there have been very few prenatal injury lawsuits brought against employers to date.(fn3) In the last fifteen years, however, considerable attention has been focused on the issue,(fn4) and the frequency of such lawsuits can be expected to increase.

This Article describes the causes of action available under current Washington law when a workplace hazard contributes to an adverse reproductive outcome such as miscarriage, birth defects, transplacental carcinogenesis, or other prenatal injury.(fn5) Part II delineates the wide variety of workplace conditions that may lead to an adverse reproductive outcome, ranging from emotional stress, cigarette smoke, and fall hazards to more traditional teratogen exposures such as lead. Part III describes the types of reproductive harm that can form the basis of a lawsuit in Washington. Part rV notes the theories of liability and the potential defendants, including employers, co-employees, consultants, manufacturers, and others contributing to such an outcome. Part IV also offers a prediction that the number of lawsuits alleging such injury are likely to increase dramatically. Part V discusses defenses available to an employer. Part VI identifies the goals that should be served under any proposed solution. Finally, Part VII argues for a legislative approach towards an equitable balancing of childrens' health interests against womens' employment opportunities and employers' concerns about massive tort liability.

II. Prenatal Harm in the Workplace

Most people's conception of prenatal injury revolves around images of children born with missing or shortened limbs because of their mothers' exposure to teratogenic chemicals. These extreme examples, however, are but a small part of a wide spectrum of prenatal injuries attributable to an even wider assortment of occupational conditions. For an attorney or legislator to comprehend the true magnitude of the potential liability faced by today's employer one must look at the larger picture. This is best accomplished by tracking human reproduction and pointing out the stages where an occupational insult can cause disruption and injury. For the sake of simplicity, this Article will discuss only fertilization and development leading to a single child.(fn6)

A. Preconception Congenital Injury

Conception begins when one gamete from each parent join.(fn7) The male contributes spermatozoa containing half of the genetic material that will direct the development of the child.(fn8) Spermatozoa originate from a normally inexhaustible pool of progenitor cells in the testes.(fn9) These progenitor cells number in the many millions and routinely divide and subdivide to produce new spermatozoa for fertilization.(fn10) The average ejaculation contains 200 to 300 million spermatozoa of which only one will fertilize the female's ovum.(fn11) Throughout his life, the male's sperm cells, at various stages of maturation, are vulnerable to chemical or physical disturbances that may alter their genetic material in such a way that fertilization will not be successful or will lead to a defect in the child.(fn12)

Many chemicals as well as ionizing radiation have been shown to cause aberrations in spermatozoa.(fn13) While no "marker"(fn14) genetic disorders have been isolated for specific exposures, epidemiological studies have correlated several occupations with above average incidences of certain birth defects(fn15) as well as with higher rates of miscarriage among the spouses of exposed males.(fn16) Paternally-mediated prenatal harm has also been alleged in civil suits.(fn17)

The female contributes one of a finite number of ova, each of which, like the spermatozoon, contains half of the genetic material of the new child.(fn18) The female's supply of ova is fixed from conception and declines with age.(fn19) By the age of sixteen or so, when a woman can be expected to enter the work force, the number of oogonia (Greek for parents of eggs) number less than 400.(fn20) These "parent" cells are frozen in a stage of cell division.(fn21) Every ovarian cycle (approximately twenty-eight days) about twenty oogonia proceed through the last stages of division, but only one reaches the mature stage of an ovum.(fn22) The same types of chromosomal damage that affect the spermatozoa can similarly impact the ova before they are fertilized and with similar consequences.(fn23)

B. Miscarriage

At ovulation, the surviving, dominant ovum is released from its housing, the follicle, and proceeds through the oviduct, where it may be fertilized by the entry of one spermatozoon.(fn24) Once the ovum is fertilized, it becomes a "zygote" and proceeds to divide and grow.(fn25) Given proper genetic guidance, adequate nutrients, and correct hormonal stimuli from the mother's endocrine system, the zygote will implant in the endometrial lining of the uterus and begin to grow.(fn26) While custom varies somewhat, the general rule is that the developing child is termed a zygote through the third week of pregnancy, an embryo during weeks three through eight, and a fetus thereafter until birth.(fn27) The point at which the fetus becomes viable is generally presumed to be at twenty weeks and 500 grams (1.1 lbs.).(fn28)

If the genetic material of the spermatozoon or the ovum has been interfered with by chemicals or radiation in a manner that has significantly diminished its integrity, the conceptus will not successfully implant and flourish in the endometrium of the mother.(fn29) In human populations, the types and severity of parental exposures (or other factors) that can prevent the successful implantation of fertilized ova is open to speculation. This is because embryos that do not implant and survive for a week or so are neither detected nor counted in epidemiologic studies as a miscarriage.(fn30)

While genetic harm that prevents successful implantation may be hard to measure, such harm can also lead to later miscarriages that are more easily documented and epidemiologi-cally correlated with many workplace factors.(fn31) Even exposures as widespread as to video display terminals are suspected of causing increased miscarriage rates.(fn32) Of note is the histologic finding that a large percentage of spontaneous abortions show chromosomal abnormalities that are incompatible with life.(fn33) Accordingly, lawsuits alleging miscarriage and early death because of maternal exposures are beginning to make their way through the courts.(fn34)

C. Disruption of Organogenesis

During the first twelve weeks, the embryo undergoes organogenesis, literally the birth of its organs.(fn35) This process is a very precise, genetically programmed sequence of accelerated cell division and differentiation that results in the conversion of a single amorphous cell mass into a rudimentary anthropomorphic organism with all the proper parts.(fn36) The only organ systems that are not completely formed by the twelfth week are the central nervous system and genitalia, which continue to grow and develop until even after birth.(fn37) If this process is interfered with, the result can be undesirable gross congenital malformations that have been labeled terata (literally, monsters).(fn38)

During organogenesis, timing is everything. Chemical or physical teratogens (radiation, therapeutic drugs, industrial pollutants) may have completely different effects depending on the day incurred.(fn39) Dramatic manifestations of this phenomenon can be elicited in animal studies.(fn40) For example, when pregnant rats are given excessive doses of vitamin A on day eight of gestation, skeletal malformations result, while if given on day twelve, the same dose results in cleft palate formation.(fn41) Technically, teratogenesis is limited to this stage of development.(fn42)

The most dramatic human experience with teratogens has been associated with pharmaceuticals, of which thalidomide is the most notorious. Thalidomide is a mild sedative that was harmless to pregnant women except between days thirty-five and fifty of pregnancy.(fn43) Unfortunately, approximately 10,000 European women, unaware of the risks, took thalidomide during that thirty-five to fifty day period and gave birth to children with phocomelia.(fn44) Pharmaceuticals have also been the most litigated of human teratogens, including Thalidomide,(fn45) Bendectin,(fn46) Dilantin,(fn47) and spermicidal jellies.(fn48)

Several nonpharmaceuticals have also been implicated as teratogens based on animal studies or epidemiological data.(fn49) Interestingly, the only litigation involving workplace exposure to a teratogen involved one of the best known, rubella, and was the first such case reported in the United States.(fn50) As more attention is focused on the teratogenic potential of workplace exposures, it can be expected that litigation involving nonpharmaceutical-based teratogenesis will increase.

Chemical or biological agents are not the only way to affect teratogenesis. In fact, one...

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