The environmental impact of growth-promoting compounds employed by the United States beef cattle industry: history, current knowledge, and future directions.

Alan S. Kolok, Marlo K. Sellin

Research output: Contribution to journalReview article

49 Scopus citations

Abstract

The current state of knowledge regarding the environmental impact of growth-promoting compounds associated with the U.S. beef cattle industry is extensive in some areas but virtually nonexistent in others. The compounds administered to the cattle are quite well understood, as are bovine metabolism and excretion. If the sex and age of the cattle on the feedlot are known, the metabolites excreted by the cattle should be predictable with a great deal of accuracy. The fate, transport, and biological effects of growth-promoting compounds are just beginning to be studied. Most of the research conducted on the fate and transport of growth-promoting compounds has focused on 17beta-E2; however, much of this research was not conducted using feedlot runoff or manure. Studies are needed that focus specifically on manures and runoff from experimental or commercial feedlots. To date, the degree to which growth-promoting compounds are released from feedlots in a bioavailable form remains a point of speculation. The environmental fate and transport of TBA, P, and MGA have not been well studied. Comparisons between the fate and transport of T and 17beta-E2, however, make it clear that compounds with similar structure may behave very differently once released into the environment. Considering that 17beta-E2 is a naturally occurring estrogen and that TBA is a nonaromatizable androgen, it is not surprising that these compounds directly impact the reproductive physiology of fishes. The effects of these two compounds have been well documented, as has been described here; however, the effects of P and MGA exposures have gone largely uninvestigated. This is a serious critical gap in our knowledge base because progestogins play an important role in sex steroid synthesis and reproduction. Clearly, additional research on the consequences of exposures to P and MGA is warranted. The majority of research investigating the effects of 17beta-E2 and TBA metabolites on fish has been conducted in the laboratory and has typically focused on continuous, pharmacological exposures to single compounds. These exposures may not bear much similarity to environmentally relevant exposures, and as such may offer little information regarding biological effects seen in nature. Cattle feedlot runoff is likely to contain a suite of growth-promoting compounds rather than any single compound. Clearly, deciphering the biological effects of exposure to complex mixtures containing androgenic, estrogenic, and progestogenic compounds will remain an important area of study for the next few years. A second complexity associated with the biological runoff from cattle feedlots is the discontinuous nature of the release. It is likely that inadvertent entry of growth-promoting compounds will follow spring snowmelt or rainstorm events. These events will result in intermittent, pulsed exposures to high concentrations of these compounds interspersed by long-term exposures to lower concentrations. The effects of exposure timing and duration should be considered to generate a clearer understanding of the biological consequences of exposures to growth-promoting compounds. To date, a very limited number of studies (only one!) have sought to determine whether fish living in waterways receiving runoff from cattle feedlots are adversely affected by growth-promoting compounds associated with the runoff. Clearly, more field studies need to be conducted before a relationship between cattle feedlot effluent and biological consequences can be elucidated.

Original languageEnglish (US)
Pages (from-to)1-30
Number of pages30
JournalReviews of environmental contamination and toxicology
Volume195
DOIs
StatePublished - 2008

ASJC Scopus subject areas

  • Pollution
  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis

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