Foodborne Disease Handbook

Volume III: Plant Toxicants

Y. H. Hui

• Publisher: CRC Press
• Year: 2019
• Print ISBN: 9781315892993
• eBook ISBN: 9781351088992
• Topic: Technology & Engineering
• Subtopic: Food Science
• Index: Technology & Engineering

The Foodborne Disease handbook, Second Edition, Revised and Expanded, could not be appearing at a more auspicious time. Never before has the campaign for food safety been pursued so intensely on so many fronts in virtually every country around the world. This new edition reflects at least one of the many aspects of that intense and multifaceted campaign: namely, that research on food safety has been very productive in the years since the first edition appeared. The Handbook is now presented in four volumes instead of the three of the 1994 edition. Volume 3 of this series of books on food gums and hydrocolloids continues with a pragmatic coverage of three important categories of gum, i.e., the cellulose gums, the plant seed gums, and the pectins. The chemical, physical and functional properties of each of the important food gums in these categories are reviewed and discussed in relation with their utility in food product applications. The four volumes are composed of 86 chapters, a 22% increase over the 67 chapters of the first edition. Much of the information in the first edition has been carried forward to this new edition because that information is still as reliable and pertinent as it was in 1994. This integration of the older data with the latest research findings gives the reader a secure scientific foundation on which to base important decisions affecting the public's health.

II. Selected Plant Toxicants

2
Toxicology of Naturally Occurring Chemicals in Food

Ross C. Beier

U.S. Department of Agriculture, College Station, Texas

Herbert N. Nigg

University of Florida, Lake Alfred, Florida

I. Introduction

A. Milk sickness

B. Phytoalexins

II. Cyanogenic Foods

A. General perspective

B. Cassava (Manihot)

III. Citrus

A. General perspective

B. Limes

IV. Crucifers (Cruciferae, Brassica)

A. Goitrogens

B. Carcinogenicity modulation

V. Fruits and Vegetables (flavonoids)

A. Dietary flavonoids

B. Biological effects of flavonoids

VI. Herbs

A. Asian medicinal herbs

B. Onion and garlic

C. Yarrow

D. Herbal teas

E. Bay leaf

F. Bishop’s weed seed

G. Rosemary and sage

H. Abortifacients

I. Psychoactive substances

VII. Mushrooms

A. Agaricus bisporus

B. Gyromitra esculenta

VIII. Mycotoxins

A. A Global perspective of food safety

B. Food safety and public health hazard

C. Ergot alkaloids in grain foods

D. Ergot alkaloids in cattle

E. Fumonisins

IX. Nightshades (Solanaceae)

A. White potatoes

B. Cholinesterase inhibition

C. Glycoalkaloid content

D. Teratogens

E. Eggplant

F. Green peppers

G. Tomatoes

X. Nitrate-Rich Foods

A. Reduction of nitrate

B. Nitrosation of amines

C. Quantification of N-nitroso compounds

D. Dietary nitrate intake

E. Nitrate levels in plants

XI. Parsleys (Umbelliferae)

A. Biological activities of linear furanocoumarins

B. Celery

C. Parsley

D. Parsnips

E. Figs 112

XII. Oxalate-Rich Foods

A. General perspective

B. Mineral balance

C. Absorption

XIII. Sweet Potatoes (Ipomoea Batatas)

A. Proposed lung toxins

B. Average concentration of the lung toxin ipomeamarone

C. Activation of the lung toxins

D. Sweet potato connection to high rates of asthma

XIV. Tannin-Rich Foods

A. General perspective

B. Effects of tannins

XV. Conclusion

Acknowledgment

References

I. Introduction

The purpose of exploring the potential naturally occurring toxic hazards of food plants is not to suggest an irrational avoidance of these common foods. However, it is important to identify, define, and investigate the natural toxicants in our foods, provide some perspective on these chemicals, and show clearly that their toxicology is unknown in most cases. Many natural toxicants have functions similar to synthetic pesticides or other biohazardous chemicals. Humans apply synthetic pesticides to food and ornamental plants to prevent insect, fungal, and other pest damage. However, plants produce natural toxicants to protect themselves from pathogens and pests. The natural pesticide concentration in our foods may be as much as 10,000 times higher than that of synthetic pesticide residues (1). Because of the protection they provide to plants, these natural chemicals are prime candidates to be bred into plants by plant breeders and producers (2).

The main consideration of the Committee on Food Protection, National Research Council, when reviewing natural toxicants in foods, was “the hope that it may contribute to a more informed, realistic, and sensible attitude on the part of the public toward the food supply” (3). Natural toxic components in foods receive little study today, as was the case in 1966 (4). Most people routinely accept that plants eaten in their “pristine” state not only are absolutely safe for one’s health but are better than plants “manipulated” (e.g., pesticide treated or fertilized with manufactured nutrients) by humans.

Many people believe that if the food is natural, it naturally is good for you; however, consider these cases. The plant family Solanaceae includes species that are highly poisonous and also are used for some common medicinal drugs. For example, Solanum nigrum L. and Atropa belladonna L. are extracted for their bioactive drugs, including atropine, scopolamine, and hyoscyamine. Tobacco also is related to these plants, as are such common food plants as eggplants, garden peppers, tomatoes, and white potatoes. Livestock have died after ingesting potato vines, green potatoes, or tomato vines. Human poisoning episodes and fatalities also have been reported (5, 6, 7, 8, 9 and 10).

There are a number of foods in the human food chain through which exposure to natural toxicants may occur. Some of these are meat, milk, eggs, fish, grains, fruits, herbs, vegetables, and liquids (beer, water, wine, etc.). The first example discussed here of the occurrence of a naturally occurring toxicant appearing in our food chain involves milk. This chapter then discusses notable examples of natural toxins in various food plants and contamination by mycotoxins.

A. Milk Sickness

The disease in humans referred to as milk sickness, was first noted in North Carolina by the time of the American Revolution and today it still remains the classic example of milk poisoning. In animals, the disease is called trembles, which is based on the signs of muscle trembling of poisoned animals. White snakeroot (Eupatorium rugosum Houtt) is the etiological agent responsible for milk sickness in humans and trembles in animals, but over a century went by before the plant was connected with the disease.

Milk sickness in humans was caused by the use of milk or milk products from animals consuming this plant. Trembles in animals was caused by directly ingesting the plant or, in young animals, by utilizing milk from poisoned mothers. A thorough description of the plant, habitat, historical aspects, and isolation of components are presented by Beier and Norman (11). White snakeroot may be found in damp open areas of the woods, shaded areas, along rivers, and in steep canyons. Figure 1 indicates the distribution of white snakeroot throughout the United States (12, 13, 14, 15, 16, 17 and 18).

The first written description of the milk sickness disease was in 1809 by Dr. Thomas Barbee (19). The first published name for the disease, sick stomach, was coined by an anonymous author in 1811. Nancy Hanks Lincoln was among those who died in 1818 during an epidemic at Pigeon Creek, Illinois, of the disease called milk sickness when her son, Abraham Lincoln, was 7 years old (20). Nancy’s great aunt and great uncle, as well as two neighbors, died within a few weeks of each other during the same epidemic.

The disease progresses slowly in humans and is characterized by restlessness with vague pains, vomiting, loss of appetite, constipation, acetone breath, severe acidosis, coma, and death. Recovery from an attack is slow and may never be complete (21).

The literature on white snakeroot is very vast as it has been written about since 1809. Unfortunately, information is so diverse and inconsistent that it is very difficult to follow the true story surrounding white snakeroot poisoning. It is interesting to note that a recent article by Molyneux and James incorrectly gives Drake credit for establishing the causal relationship for the disease (22). In fact, Drake’s outstanding reputation in the scientific community prompted the acceptance of his incorrect theory that poison ivy was the plant responsible for milk sickness, and stopped research into the real cause of the disease (19).

White snakeroot poisoning is still a problem in horses and goats (11). In a single episode during the spring of 1985, 53 angora goats died of white snakeroot poisoning in central Texas, and the total loss at that ranch during the 1985 season was 85 goats (23). It was observed by ranchers and diagnostic laboratory personnel that the goats in the central Texas area that had survived white snakeroot poisoning then apparently would leave the plant alone (J. C. Reagor, persona...

Table of contents

• Cover
• Half Title
• Title Page
• Copyright Page
• Introduction to the Handbook
• Preface
• Table of Contents
• Contributors
• Contents of Other Volumes
• I. Poison Centers
• II. Selected Plant Toxicants
• III. Fungal Toxicants
• Index