Target Organ Toxicity in Marine and Freshwater

Teleosts Volume 2 Systems 1st Edition William Benson

- Downloadable PDF 2025

https://ebookfinal.com/download/target-organ-toxicity-in-marine-and-
freshwater-teleosts-volume-2-systems-1st-edition-william-benson/

Visit ebookfinal.com today to download the complete set of

ebooks or textbooks
Here are some recommended products that we believe you will be
interested in. You can click the link to download.

Phytoplankton Productivity Carbon Assimilation in Marine

and Freshwater Ecology 1st Edition Colin Reynolds

https://ebookfinal.com/download/phytoplankton-productivity-carbon-
assimilation-in-marine-and-freshwater-ecology-1st-edition-colin-
reynolds/

Target Discovery and Validation Reviews and Protocols

Volume 2 Emerging Molecular Targets and Treatment Options
1st Edition Mouldy Sioud
https://ebookfinal.com/download/target-discovery-and-validation-
reviews-and-protocols-volume-2-emerging-molecular-targets-and-
treatment-options-1st-edition-mouldy-sioud/

New Trends in Marine and Freshwater Toxins Food and Safety

Concerns Food and Safety Concerns 1st Edition Ana G.
Cabado
https://ebookfinal.com/download/new-trends-in-marine-and-freshwater-
toxins-food-and-safety-concerns-food-and-safety-concerns-1st-edition-
ana-g-cabado/

The Staunton Shakespeare Volume 2 1st Edition William

Shakespeare

https://ebookfinal.com/download/the-staunton-shakespeare-volume-2-1st-
edition-william-shakespeare/
Real time Systems Scheduling Volume 2 1st Edition Maryline
Chetto

https://ebookfinal.com/download/real-time-systems-scheduling-
volume-2-1st-edition-maryline-chetto/

Handbook of Dynamical Systems Volume 2 1st Edition B.

Fiedler

https://ebookfinal.com/download/handbook-of-dynamical-systems-
volume-2-1st-edition-b-fiedler/

Formal Languages Automata and Numeration Systems Volume 2

1st Edition Michel Rigo

https://ebookfinal.com/download/formal-languages-automata-and-
numeration-systems-volume-2-1st-edition-michel-rigo/

Advances in Marine Biology Volume 71 First Edition Curry

https://ebookfinal.com/download/advances-in-marine-biology-
volume-71-first-edition-curry/

Advances in Marine Biology Volume 70 First Edition Curry

https://ebookfinal.com/download/advances-in-marine-biology-
volume-70-first-edition-curry/
Target Organ Toxicity in Marine and Freshwater
Teleosts Volume 2 Systems 1st Edition William Benson
Digital Instant Download
Author(s): William Benson
ISBN(s): 0415248396
Edition: 1
File Details: PDF, 2.92 MB
Year: 2001
Language: english
Target Organ Toxicity in Marine and
Freshwater Teleosts
 New Perspectives: Toxicology and the Environment

Target Organ Toxicity in

Marine and Freshwater
Teleosts
Volume 2—Systems
Edited by

Daniel Schlenk
Department of Environmental Sciences University of
California Riverside, California USA
William H.Benson
Gulf Ecology Division, National Health and
Environmental Effects Research Laboratory US
Environmental Protection Agency Gulf Breeze, Florida
USA

London and New York

 First published 2001
by Taylor & Francis
11 New Fetter Lane, London EC4P 4EE
Simultaneously published in the USA and Canada
by Taylor & Francis
29 West 35th Street, New York, NY 10001
Taylor & Francis is an imprint of the Taylor & Francis Group
This edition published in the Taylor & Francis e-Library, 2005.
“To purchase your own copy of this or any of Taylor & Francis or Routledge’s collection of
thousands of eBooks please go to www.eBookstore.tandf.co.uk.”
© 2001 Daniel Schlenk and William H.Benson
All rights reserved. No part of this book may be reprinted or reproduced or utilised in any form or
by any electronic, mechanical, or other means, now known or hereafter invented, including
photocopying and recording, or in any information storage or retrieval system, without permission
in writing from the publishers.
British Library Cataloguing in Publication Data
A catalogue record for this book is available from the British Library
Library of Congress Cataloging in Publication Data

ISBN 0-203-36141-5 Master e-book ISBN

ISBN 0-203-37397-9 (Adobe eReader Format)

ISBN 0-415-24839-6 (Print Edition)
 Contents

List of contributors vii

Foreword viii
Copyright acknowledgments ix

1 General mechanisms of toxicity 1

DANIEL SCHLENK
Introduction 1
Disposition of xenobiotics 1
Chemical reactions of reactive intermediates/ultimate toxicants 7
Exceeding capacity of cellular defense mechanisms 10
Specific cellular targets 12
Targets involving repair and cellular regeneration 19
Summary 23
2 Toxic responses of the nervous system 27
RUSSELL L.CARR AND JANICE E.CHAMBERS
Introduction 27
Nervous system physiology 28
Chlorinated hydrocarbon insecticides 41
Pyrethroids 48
Anticholinesterase insecticides 54
Metals 63
Organics 66
Natural toxins 67
Conclusions 74
 v

3 Fish immunotoxicology: understanding mechanisms of action 97

CHARLES D.RICE
Introduction 97
Innate, non-specific, and first-line defenses 103
Antigen processing and presentation for specific responses 109
Fish as models in biomedical research 114
Historical approaches to immunotoxicology 115
Mechanisms of action of some immunotoxicants 116
Autoimmunity and hypersensitivity: a frontier in fish immunotoxicology 119
The neuroendocrine-immune connection 122
Summary 127
4 Neurobehavioral toxicity in fish 141
EDWARD E.LITTLE AND SANDRA K.BREWER
Introduction 141
Neural basis of behavioral toxicity 144
Toxicant impacts on higher behavioral function 162
Ecologic relevance of behavior as a predictor of contaminant effects in the natural 164
environment
Conclusions 166
5 Toxic responses of the reproductive system 177
LISA D.ARCAND-HOY AND WILLIAM H.BENSON
Introduction 177
Hypothalamus-pituitary-gonadal axis 178
Gonadal development 182
Oocyte growth and maturation 186
Modes of nutrition 188
Targets for chemical toxicity 189
Egg-level effects 191
Alteration in egg yolk nutrients 191
Assessment of reproductive effects 195
Assessment of reproductive function 195
vi

Reproductive toxicity guidelines 196

Conclusions 199

Index 205
 Contributors

Lisa D.Arcand-Hoy is at Blasland, Bouck & Lee, Inc., Syracuse, NY, USA
William H.Benson is at the Gulf Ecology Division, National Health and
Environmental Effects Research Laboratory, US Environmental Protection Agency, Gulf
Breeze, FL, USA
Sandra K.Brewer is at the Department of Biological Sciences, University of
Missouri, Columbia, MO, USA
Russell L.Carr is at the Center for Environmental Health Sciences, Mississippi State
University, MS, USA
Janice E.Chambers is at the Center for Environmental Health Sciences, Mississippi
State University, MS, USA
Edward E.Little is at the US Geologic Survey, Columbia Environmental Research
Center, Columbia, MO, USA
Charles D.Rice is at the Department of Environmental Toxicology, Clemson
University, Pendleton, SC, USA
Daniel Schlenk is at the Department of Environmental Sciences, University of
California, Riverside, CA, USA
 Foreword

The field of aquatic toxicology is increasing in importance because it is now commonly

accepted that humans cannot continue to discharge their wastes and byproducts into
streams, rivers, and oceans without having impacts on those ecosystems. As a result,
efforts are focusing on reducing wastestreams from both point and non-point sources, as
well as reducing the impacts of historic discharges through remediation and cleanup. This
has led to considerable contention around the question “How clean is clean enough?” To
answer this question aquatic toxicologists have conducted extensive research and written
many books, looking at the effects of toxicants both at comparatively simple levels of
biological organization (e.g. the biomarker approach) and less commonly at highly
complex levels of organization (population and community impacts).
The challenge has been to link these two approaches. It is comparatively easy to determine
the effects and mechanisms by which chemical contaminants affect cellular function,
largely through laboratory investigations. Field investigations can demonstrate causal
relationships between certain classes of contaminants and effects on individual organisms,
but it is extremely rare for effects of chemical contaminants to be specifically discernible at
the population or community level, especially in open marine and estuarine ecosystems.
Increasingly, we are realizing that fitness of individual organisms may need to be the level
of biological function which we need to protect in aquatic ecosystems, much as we
currently do for human health. This requires assessing organ function, and it is surprising
that there are not good reference texts for assessing organ system function in fish species
exposed to chemical contaminants. This second volume addresses that void and will be a
valuable reference to the practicing aquatic toxicologist.
Tracy K.Collier
Northwest Fisheries Science Center
 Copyright acknowledgments

The authors and publishers would like to thank the following for granting permission to
reproduce material in this work.
W.B.Saunders Co., Philadelphia, for permission to reproduce Figure 3.1, originally
published as Figure 3.1 in Tizard, I.R. 1996. Veterinary Immunology—An Introduction.
W.B.Saunders Co., Philadelphia, for permission to reproduce Figure 3.2, originally
published as Figure 11.1 in Stoskopf 1996. Fish Medicine.
W.H.Freeman and Co., New York, for permission to reproduce Figure 3.6, originally
published as Figure 10.8 in Kuby, J. 1994. Immunology, 2nd edn.
The Company of Biologists Ltd, Cambridge, UK, for permission to reproduce
Figure 5.2, originally published as Figure 1 in Satoh, N. and Egami, N. 1972. Sex
differentiation of germ cells in the teleost, Oryzias latipes, during normal embryonic
development. Journal of Embryology and Experimental Morphology 28(2):385–395.
x
 1
General mechanisms of toxicity
Daniel Schlenk

Introduction
The overall purpose of this book is to provide a reference describing specific toxicities in
various organs of teleost fish. It is important to note that any given agent may have
multiple targets, and that the concentration of the agent to which the fish is exposed can
also have dramatic effects on the target(s) for the xenobiotic in question. As many of the
mechanisms eliciting tissue damage at a particular target are shared, this introductory
chapter is intended to focus upon general cellular mechanisms of toxicity. Most of the
mechanisms that are to be discussed have been identified primarily in mammalian systems
(see Gregus and Klaassen, 1996) with limited studies performed in teleosts.
Consequently, the purpose of this chapter is to discuss potential mechanisms of cellular
toxicity that have been elucidated primarily from mammalian studies and to identify
information gaps or mechanisms that have yet to be explored in fish.

Disposition of xenobiotics
As demonstrated in Figure 1.1, xenobiotic disposition as well as interaction with a target
involves several processes, including absorption, distribution, biotransformation, and
elimination. Involvement of these processes depends not only upon the physiochemical
parameters of the xenobiotic but also upon the location and molecular constitution of the
target (i.e. receptor/protein, lipid, DNA, etc.). There are primarily three mechanisms by
which a toxicant gains access to a cellular target: direct interaction with the target;
interaction with the target following absorption; and interaction with the target following
absorption and biotransformation.

Direct interaction with target

Because fish are in direct contact with the aqueous environment, exposure occurs over the
entire body surface. Many of the mechanisms involved in direct target interactions involve
disruption of plasma membranes or direct inhibition or destruction of specific receptors
located in the plasma membrane. Putative targets may include: (1) the dermal surface of
the fish which is susceptible to non-receptor-mediated plasma membrane disruption by
2 DANIEL SCHLENK

Figure 1.1 Dispositional processes of xenobiotic fate.

caustic agents (i.e. acids/bases), leading to a variety of lesions such as loss of sensory
tubricles or ulcerations of the epidermis and/or erosion of fins; (2) extracellular receptors
involved in osmoregulation and/or gas exchange found primarily in the gill (i.e. Na+, K+-
ATPases, H+ transporters, Cl• channels)—numerous agents, including organic
surfactants or metals, may have significant interactions with these targets; (3) extracellular
receptors involved in nutrient uptake or nitrogenous waste excretion (ammonia) in the gut
or gill respectively; (4) epithelial tissue of gut or eye which may undergo general
ulceration following interaction with caustic agents and/or metal oxides (gut).

Interaction with target following absorption

Absorption of xenobiotics may occur either passively or actively. Passive mechanisms of
absorption are controlled by a number of factors, including size, lipophilicity and/or
polarity of the compound as it moves down a concentration gradient, and the thickness of
the plasma membrane. Active processes of xenobiotic absorption usually involve the
substitution, or ‘hijacking’ by a structurally similar xenobiotic, with an endogenous ligand
for a specific receptor/transporter. Such receptor-mediated processes may or may not
require energy.
Intracellular damage may occur to the tissue which directly absorbs the xenobiotic
following passage through the plasma membrane. Such intracellular damage is common in
the gill. Alternatively, the compound may be transported or distributed to other organs,
where it may cause more significant damage. For example, the absorption of a
cholinesterase-inhibiting pesticide may not cause significant damage at the site of
absorption (i.e. gill) but will affect the central nervous system following transport to the
appropriate target(s) (neuron or neuromuscular junction). Transport and distribution of a
particular agent to a target is typically implemented by the circulatory system of the
organism and is influenced by several factors:
 GENERAL MECHANISMS OF TOXICITY 3

Binding and subsequent sequestration of the agent at the site of absorption

One of the best examples of this phenomenon is the binding of organic and inorganic
agents by melanin in the skin of fish (Van Leeuwen et al., 1986). The binding to melanin
efficiently sequesters the compound in the skin, preventing its distribution to other
organs.

Binding of the agent in the circulatory system by plasma proteins (i.e. albumin
and lipoproteins)
Several studies with therapeutic agents used in fish culture have indicated that plasma
protein binding significantly alters bioavailability and distribution in certain species such as
catfish and trout (Plakas et al., 1992; Jarboe et al., 1993). Metals are also primarily bound
to blood proteins (Roesijadi and Robinson, 1994). The specific form of plasma protein
may also be critical as some tissues have albumin-specific receptors and may preferentially
accumulate albumin-bound xenobiotics (Heath, 1995).

Specialized barriers
As in mammals, blood-brain barriers have been identified in several species of fish through
dye uptake studies and histologically (Castejon, 1983; Lane, 1991). In addition, evidence
for a blood-testes barrier has also been observed. Consequently, distribution to these
particular tissues would be diminished unless the xenobiotic is highly lipophilic or can
mimic endogenous ligands taken up by active transport mechanisms within those
particular systems.

Storage sites
In contrast to intracellular sequestration at the site of absorption, organic lipophilic agents
may be transported to specific storage sites that are abundant in lipid, such as fat bodies.
Alternatively, certain metals have the propensity to accumulate in bone. Although lipid
content in fish has been shown to have considerable impact on the accumulation of organic
agents, the role of bone metabolism has not been extensively examined.

Blood flow to and from potential target systems

Because most gut-absorbed material is transported via the portal venous system to the liver,
this tissue is generally considered to be the primary target for gut-absorbed chemicals.
Chemicals that are absorbed through the gill or skin would have a different primary
circulatory route from dietary chemicals. Blood transport from the gill would suggest that
the brain or, possibly, the kidney (depending on the species) may receive a more
significant blood flow and thus may be more susceptible targets.
4 DANIEL SCHLENK

Elimination away from the target

As mentioned above, cells possess numerous membrane transporters that are not only
important for cellular absorption but also involved in cellular excretion of absorbed
compounds. P-Glycoprotein homologs, also known as the multixenobiotic resistance
mechanism (MXR), are often found in cells undergoing neoplastic transformation (Juliano
and Ling, 1976). The MXR non-specifically exports a host of organic and inorganic
toxicants out of cells following absorption. The MXR has been observed in tumors and in
damaged tissues from several fish species (Kleinow et al., 1996; Kohler et al., 1998;
Cooper et al., 1999). Additional mechanisms to enhance elimination from the animal
through the urine or feces involve various biotransformation processes discussed below.

Interaction with target following biotransformation

Bioactivation versus detoxification

Most organic xenobiotics are absorbed in fish and other organisms as relatively non-polar
lipophilic chemicals. In an attempt to enhance the elimination of chemicals of this nature,
the cell utilizes a series of enzymes to modify radically the structures to polar, water-
soluble compounds. The enzymatic process of altering organic chemical structure
(biotransformation) consists of two phases. Phase I biotransformation reactions typically
involve the insertion of a polar atom (i.e. oxygen) or fragmentation of the molecule,
leading to access of polar atoms (i.e. hydrolysis). Such radical alterations of structure
often lead to the formation of reactive intermediates, necessitating a second phase of
biotransformation which conjugates the intermediates to endogenous macromolecules
which are in large cellular supply (i.e. glucose, water, peptides). If certain phase II
processes are compromised or overwhelmed, the reactive intermediates may adversely
affect proteins, lipids or nucleic acids which serve critical cellular functions, resulting in
toxicity. Although uncommon, reactive intermediates may also be formed through phase
II pathways. For example, in mammals, glutathione conjugates of halogenated aliphatic
hydrocarbons may eventually be hydrolyzed to thiols or methyl thioether metabolites
which may rearrange to electrophilic episulfonium species or become oxygenated by
phase I monooxygenases to electrophilic sulfoxides respectively. Certain glucuronides
may even become hydrolyzed by bacteria after reaching the gut, allowing the aglycone to
be reabsorbed; a process known as enterohepatic circulation. Although phase I
bioactivation has been observed in fish, bioactivation through phase II processes has yet to
observed.

Ultimate toxicants and reactive intermediates

Biotransformation of non-polar lipophilic compounds to polar hydrophilic products
typically involves radical structural modification which may result in the formation of
reactive intermediates or ultimate toxicants. Although there are some exceptions, most
 GENERAL MECHANISMS OF TOXICITY 5

reactive intermediates exist as either electron-deficient molecules (electrophiles) or

unstable molecular fragments (free radicals).

ELECTROPHILES
Electron-deficient molecules often result from phase I biotransformation reactions
(Table 1.1). Oxidation reactions catalyzed by cytochrome P450 or other enzymes can lead
to the formation of numerous electrophilic metabolites including, but not limited to,
epoxides, ketones, arene oxides, quinones, quinoneimines, or acyl halides. Heterolytic
bond cleavage can also lead to the formation of positively charged electrophiles. For
example, cleavage of the sulfoester conjugate of aromatic amines leads to the formation of
the highly reactive aryl nitrenium ion. The oxidation of AsO43• to AsO32• /(As3+) and
elemental mercury to Hg2+ are examples of inorganic electrophiles. Electron-rich
moieties found in amino acids and nucleic acids such as thiols and amines are generally
thought to be the molecular targets for these intermediates.

FREE RADICALS
Containing one or more unpaired electrons in its outer orbital, free radicals are typically
formed by accepting or losing single electrons during, respectively, reduction or oxidation
reactions. Toxicants capable of accepting single electrons from reduction reactions can
elicit toxicity by forming free radicals. The reduced toxicant typically transfers the extra
electron to molecular oxygen, leading to the formation of a superoxide anion radical and
the oxidized toxicant which can receive an additional electron. This process of the
acceptance and donation of electrons and regeneration of the parent compound is known
as ‘redox cycling’ (Figure 1.2) and can lead to the formation of a large number of
superoxide anion molecules from a single molecule of toxicant.
Single electron reduction reactions may also lead to homolytic bond fission in certain
xenobiotics, especially halogenated aliphatic hydrocarbons such as carbon tetrachloride.
Such reactions lead to a dehalogenation of carbon tetrachloride to the trichloromethyl
radical (Figure 1.3). Interaction of this reactive intermediate with molecular oxygen leads
to the formation of another highly reactive metabolite known as the trichloromethylperoxy
radical, which may abstract protons from lipids causing lipid peroxidation (see below).
Additional one-electron processes that lead to the formation of free radicals are described
by the Haber-Weiss and Fenton reactions (Figure 1.4). Transition metals such as iron and
copper act as electron donors to various peroxides (which may be the dismutated
products of superoxide anion), leading to the formation of the most reactive reduced
oxygen species, the hydroxyl radical.
In addition to electron-accepting xenobiotics, nucleophilic toxicants (chemicals
containing electron-donating atoms—aromatic amines, hydrazines, phenols, thiols) may
form superoxide anion radicals through peroxidase-catalyzed transfer of one electron from
the xenobiotic to molecular oxygen. Aromatic compounds having two ortho or para
phenolic groups may undergo two sequential one-electron oxidations, ultimately leading
to the formation of quinones. Depending upon the physicochemical properties of the
 6 DANIEL SCHLENK

Figure 1.2 Potential pathways for oxidative stress (see Di Giulio et al., 1995).
 GENERAL MECHANISMS OF TOXICITY 7

Figure 1.3 One-electron reduction of halogenated methanes.

Figure 1.4 Haber-Weiss and Fenton reactions.

specific toxicant, quinones not only may act as redox cyclers generating superoxide but
also are classic electrophiles (see above) and undergo attack by nucleophilic molecules
found in cellular proteins and nucleic acids.

Chemical reactions of reactive intermediates/ ultimate

toxicants

General cellular targets

Electron-deficient molecules formed through cellular biotransformation processes are
prone to attack by nucleophilic molecules within any given cell, leading to the potential
formation of toxicant-biomolecule adducts. Consequently, biomolecules having large
electron densities, such as thiols and basic amine moieties, would be susceptible targets of
electrophiles. As free radicals may donate or abstract electrons from targets, molecules
containing atoms that are inclined toward electron acceptance or loss would be prime
targets for free radical attack. Many biomolecules possess these general features, and it is
likely that more than one type of reaction may occur with the cellular target. Discussion of
general cellular targets will be limited to protein, lipid and nucleic acids.

Protein
As proteins contain numerous atoms that are excellent reducing agents (i.e. thiols),
oxidation of protein thiols to disulfides or sulfenic acids is a common outcome following
8 DANIEL SCHLENK

interactions with free radicals. Hydrogen abstraction of thiols by neutral free radicals may
also form thiyl radicals, eventually leading to similar disulfides and sulfenic acid products.
Hydroxyl radicals may also remove protons from methylene groups of amino acids,
leading to the formation of carbonyls which tend to bind amines of proteins or DNA
covalently, thus causing cross-linking. In addition, thiols are also excellent nucleophiles
and provide potential sites for covalent binding of electrophilic toxicants. Non-covalent
binding through hydrogen and ionic bonds may also occur with proteins having
appropriate tertiary structure (i.e. helices) such as membrane receptors or enzymes.
Covalent or non-covalent binding could significantly inhibit the catalytic activity of an
enzyme or signal transduction pathway initiated by a receptor. For example, the
mimicking of calcium by lead or 17β;-estradiol by nonylphenols can have significant
functional effects for their receptors or enzymes. Many enzymes and receptors require
cofactors such as metals or organic moieties such as porphyrins or folic acid. If cofactors
are modified (i.e. electron transfer to iron in hemoglobin) then protein function may be
severely altered (i.e. methemoglobinemia); also, if the affected protein is critical for cell
maintenance, it is likely that cell viability may be ultimately compromised.

Lipid
Possibly the most common reaction that occurs between toxicants and lipids is that of
lipid peroxidation. The primary targets are unsaturated lipids found throughout cellular
membranes. Bis-vinylic methylene protons are highly susceptible to abstraction by free
radicals (Figure 1.5). Abstraction of either of these protons by free radicals such as
hydroxyl radical leads to the formation of conjugated dienes, which may undergo Fenton
chemistry and form lipid peroxyl radicals, and lipid hydroperoxides. These intermediates
not only serve as endogenous toxicants but also result in significantly altered membrane
integrity and function. As most cellular organelles as well as the plasma membrane is
largely lipid in constitution, altered integrity could result in loss of osmotic gradients,
leading to cell death if unrepaired.

Nucleic acids
Like thiol-containing proteins, nucleic acids are electron-rich molecules that can
covalently bind electrophilic toxicants. In contrast to thiols, which tend to bind covalently
soft electrophiles (i.e. quinones), purine-associated oxygens and nitrogens are more likely
to attack hard electrophiles (i.e. alkyl carbonium ions). Covalent binding of DNA by
various electrophiles disrupts replicative and transcriptional activities of polymerases,
and, if unrepaired, may lead to genomic mutation. Because DNA exists as a double helix
through significant hydrogen bonding, non-covalent intercalation by planar toxicants may
also lead to mutation. DNA is also susceptible to attack by free radicals as hydroxyl
radicals tend to bind the C-8 position of guanine and abstraction of protons on the pentose
sugar of DNA by free radicals may lead to hydrolytic strand breaks. Alteration of the
genome through any of these mechanisms may lead to modified protein function which
Figure 1.5 Initiation of lipid peroxidation.
GENERAL MECHANISMS OF TOXICITY 9
Another Random Scribd Document
with Unrelated Content
of Abel Butler. SMITH BUTLER m. Tluiuklul Houghton Dec. 20, 1780,
who died Dec. 27, 1783, aged 27. SIMEON BUTLER married Nabby
Rice June 10, 1789. LUTHER B UTLER married Han nah Wil son of
Putney, Aug. 25, 1790. TEMPLE FAMILY. MOSES TEMPLE was the
ancestor of the Temples who settled in Dummerston before 1770.
According to the usual difference in time from generation to
generation, he was born 1665. His son, Richard, was the father of
JOSEPH TEMPLE, SETST., who was born about 1718. Joseph Sen.
was a native of Massachusetts and a cooper by trade. He married
Mary, sister of Samuel Laughton ; — children : Joseph, b. in
Worcester, Mass., Dec. 23, 1734 ; Parmenasm. Anna, dau. of John
Laughton Jr. about 1777 ; Amos, unmarried; Samuel m. widow Wing
; Daniel, unmarried ; Joanna
 DUMMEESTON. 91 married 1st. John Citiwford, 2d. Aarou
Wilder Dec. 26, 1784; Phebe "died of nervous headache." Joseph
Sen., Joseph Jr. and John Crawford were among the membei's of the
Congregational church when first organized in 1779. Joseph Sen. set
out seven small elms near his son's house, now occupied by Alonzo
Bradley. Only one of these trees is left standing. It measures I'S feet
around, is nearly 100 feet in height and estimated to contain 8 cords
of wood. It stands in the roadside a few rods north ol' the houhe,
and a statelier looking tree, the passer-by will seldom find. It is also
related of Mr. Temple that on one occasion, when he was returning
on horse-back from a visit to Worcester, a violent storm of wind
arose. While passing through the wo
 32 VERMONT HISTORICAL MAGAZINE. The father of these
children was in the skirmish at Westminster, Mar. 13, 1775. He was
knocked clown and, for a time, supposed to be -lead. His skull was
fractured on the left side of the forehead, and the scar remained
during life. He had a pewter basin, which he carried, with a blanket,
in his knapsack. It was hit by one or two bullets which did not
penetrate, but left depressions. The marks were so plainly to be
seen that the basin was kept, as a relic, in the family many years. At
last a tin peddler secured the trophy for old pewter, but not by fair
means. He took advantage of Joseph Temple's (3d) good nature,
crushed the basin with his hands, spoiling it for a relic, and then paid
the price which Mr. Ten"ple asked for the spoiled dish. Joseph Jr.,
deeded the farm to his son, Joseph. Mar. 16, 1802, who m., Dec. 29,
1803, Amy, dau. of William Perry of Putney, a sea captain. Their
children were : Amos, b. Sept. 9, 1804, ra. Marilla Bennett. Amy, b.
Jan. 24, 1807, m. Alfred Bennett, Nov. 12, 1829 ; Sally, b. 1809,
married Calvin Bradley Nov. 12, 1829 ; Emeline, b. Dec. 12, 1814 ;
Zilpha, b. Mar. 19, 1819, m. Willa d Dodge, Sept. 5, 1837. When Mr.
Temple and wife became aged, he deeded the farm, Apr. 9, 1859, to
Alfred Bennett and continued to live with him on the old homestead.
Mr. Bennett had four children : two died young. Harriet, his
daughter, m. Alonzo Bradley ; Joseph F., his son, m. Augusta Bradley,
and his father, Alfred, deeded the farm to him Jan. 8, 1872. He died
May 23, 1872, aged 69. Joseph F. Bennett died Oct. 15, 1875,
leaving a widow and one daughter. The three Joseph Temples and
their wives died on the old homestead. Joseph Jr., died Mar. 23,
1832, aged 88 ; Lois, his wife, d. June 23, 1829, aged 88 ; Joseph
(3d) died Mar. 16, 1870, aged 89 ; Amy, his wife, d. Aug. 31, 18G1,
aged nearly 82. COL. WILLIAM SARGEANT and Rachel, his wife,
were residents alalso in this town as far back as Revolutionary times.
Their children were : Sarah, b. July 10, 1780; William Todd, Sept. 1,
1782 ; Mary, Sept. 23, 1784; James, Avig. 28, 1786; Jonathan, July
10, 1788 ; Benjamin, Dec. 21, 1790; George, Dec 12, 1792; Charles,
Oct. 9, 1794; and Lucretia, Mar. 28, 1797. JA&ON DUNX'AN,
Assistant judge of the county court 4 years and town clerk 29 years,
d. Dec, 15, 1839, aged 90. Sarah Gates, his wife, died Sept. 13,
1842, aged 86 yrs. Their children were Joseph, born Aug. 24, 1776,
m. Miranda Taylor d. in Chester, 1863, aged 87 ; Jonas, b. Aug. 15,
1778, d. Mar. 13, 1813 ; Jason, b. Sept. 18. 1780, d. in Newfane ;
Silas, b. Mar. 12, 1783, d. Feb. 15, 1784; Priscilla, b. Feb. 15, 1785 ;
Samuel, b. Feb. 15, 1788 ; Alvan, b. Nov, 19, 1791, d. in Leicester,
Mass.. Aug. 2, 1813 ; Tyler, b. Aug. 8, 1794 ; Sarah, b.Mar. 19,1797.
Jason Duncan was the first schoolteacher in town. Wheu a young
man, he taught a small school in a dwellinghouse on the river road
in the eastern part of the town. [It is, also stated on page 36, that
Charles Davenport taught the first school ] Samuel Duncan was a
distant relative of Dr. Abel and first cousin to Judge Duncan. Samuel
lived and died on the place where Clark Rice once lived. No buildings
are now standing
The text on this page is estimated to be only 1.00%
accurate

n 1^ C^^'l;^ M ^ C/
 DUMMERSTON. 93 in the place He had a family of 1 1
children. Samuel, his son, died on the same place where his father
had lived. The earliest record we have of the Duncan family is that
of JOHN DUNCAN and Sarah Button, who were born in
Massachusetts, probably, about 1690. Their children were : Sarah,
who m. Uriah Parmeter of Sudbury, Mass. ; John m. Sarah Rogers
ofBillerica; Samuel ra. 1st. Mehitable Barton of Sutton, 2d. Hannah
Livingston ; Daniel m. Sarah Rice of Conway ; Simeon m. Bridget
Richardson of Bil lerica ; Abigail m. Samuel Stone, of Ireland.
BiUerica was first settled about the year 1653, and among the
names of the first principal settlers are John Rogers and Thomas
Richardsou, probably, ancestors of the wives of John and Sim. eon
Duncan. '■'During the French and Indian war, Aug. 5, 1695, the
Indians made an attack on the inhabitants of this place. In the
northerly part of the town, on the east of Concord river, lived several
families, who, though withoat garrisons and in time of war, felt no
apprehensions of danger. Their remot?ness from the frontiers might
have contributed to their apparent security. The Indians came
suddenly upon them in the day time. They entered the house of
John Rogers while he was sleeping, and discharged an arrow at him,
which entered his neck and pierced the jugular vein. Awakened by
this sudden attack, he started up, seized the arrow, which he forcibly
withdrew, and expired will the instrument of death in his hand. A
woman being in the chamber, threw herself out of the window, and,
though severely Avounded, made her escape coaeaHng herself
among the flags. A young woman was scalped and left for dead but
survived the painful operation, and lived many years afterwards. A
son and daughter of Mr. Rogers were made prisoners. Thomas
Rogers and his son were kiUed." The children of Daniel and Sarah
(Rice) Duncan were : Sally m. James Jackscn of Petersham. Mass ;
John m. Rebecca Meacham of New Salem ; Daniel m. Zurvilla Rice of
"Worcester, Mass. Lovina m. John Rice of Petersham ; Abel m. Lydia
Mills of Petersham, about 1770; children : Abel Jr., b. in Petersham,
Feb. 22, 1772; Nathan m. Betsey Winn of Chester ; Rufus m. Lucy
Kimbol of Chester ; Anna m. Amos Heald of Chester ; Lucy m. Jason
Duncan Jr. of Dummerston ; Charles m. Patty Carter of Weathersfield
; Johnm. Caroline Hastings of Charlestown, N. H. ; Arad ; George ;
Lydia m. Daniel Church of Chester. JOSEPH DUNCAN ESQ., was town
clerk 37 years. He represented the towm in 1828, '29, '36, '37. He
lived on the paternal farm many years and was much respected as a
citizen of the town. He was a consistent member of the
Congregational church and a leader of the choir in singing for a long
time. His father. Judge Duncan, had b-ien leader of the choir after
the church was organized in 1779. Joseph Duncan mai-ried Miranda
Taylor, who died in Chester. Children b. in Dummerston : Miranda, b.
July 7, 1797 ; Joseph, b. Dec. 14, 1798, m. 1st. Maria Blake, 2d.
Loretta S. Pratt, Dee. 2, 1820 ; Silas, b. 1801, d. 1803 ; Orsamus, b.
May 2, 1804 ; Sophia, born Mar. 23, 1810, m. Linus Williams Aug. 5,
1834 ; Samuel, G., b. Sept. 27, 1812, m. ; Hoyt, Eliza A., b. Jan. 20,
1815, m. Edwin Bemis.
 94 VERMONT HISTORICAL MAGAZINE. DR. ABEL DUNCAN
married Lydia Miller dau. of Hosea and Lydia (West) Miller, born in
Dummerston Nov. 8, 1778 ; married Aug. 28, 1805 ;— Children :
Charles Morris, born July 1, 1808, married Lucinda P^stabrook of
Brattleboro, dau. of John Estabrook and Lucinda Stockwell, his wife,
Aug. 1833. Fanny Maria, b. June 22, 1810, m. Joel Knight Jr. Jan. 1,
1829 ; Lydia Eveline, b. Aug. 1, 1313, m. Marshall Newton, Apr. 4,
1833. Mrs. Duncan died in 1869, aged 90. The spotted fever, a
violent epidemic, raged in town in the winter of 1812-13, and many
died. Dr. Abel Duncan was very active and successful, but at length
was attacked with the fever, himself, and died Mar. 5, 1813, aged 42
years. Dr. C. M. Duncan was a son of Dr. Abel Duncan and was in
practice for a time. He removed to Sherburne, Mass. Simeon
Duncan, Avho married Bi'idget Richardsoa, was the father of Judge
Jason Duncan, who died in Dummerston, Dec. 15, 1839, aged 90
years. Jason Duncan and Dr. Abel Duncan's father were cousins. The
Judge married Sarah Gates about 1774. DR. SEWELL WALKER, an
early physician of Dummerston, was the seventh son of Jonas and
Sarah (Davis) Walker, born March 10, 1796. He m. 1st. Lucretia,
daughter of Marshall Miller. Children : Lucretia, b. Aug. 6, 1825,
married Pliny F. Walker ; Esther, b. Mar. 26, 1828, m. Lorenzo D.
Thayer ; Alexander C, b. Sept. 26, 1829, m. and lives in Farley, Iowa.
Dr. Walker, m. 2d. Catharine Bemis, Oct. 21, 1838. The children of
Jonas aud Polly (Miller) Walker were Laura, b. Nov. 28. 1814, m.
Mason Bennett ; Levi M. b. May 25, 1816, m. 1st. Mrs. A'daline
Winslow, 2d., Pi'iscilla Sampson ; Jonas b. 1818, d. 1826 ; George W.
b. Sept. 25, 1822, m. Susan Dutton ; Emily, b. May 30, 1726, m.
James Brown : Eliza, b. Sept. 1, 1827, m. S. J. Smith ; Jane b. Aug.
4, 1831, m. Anthony Huntley; Caroline, b. Aug. 7, 1819, died 1820.
The children of Daniel and Mary (StockwellJ) Walker were : Dana,
born Apr. 30, 1809, m. . Joel, b. Sept. 9, 1810, m. ; Sally, b. 1812, d.
1834: Edson, b. Oct. 27, 1813, m. ; Harriet N.. b. Apr. 24, 1815, m.
1st. Wm. Bennett, 2d. Marcus Perry ; Relief, b. Sept. 15, 1817, m.
Granville French ; Mary, b. Dec. 14. 1819, m. ' Eaton of New Salem,
Mass. Daniel 2d. b. 1822, d. 1854 ; Samuel N., b. Apr. 1824, married
Julia A. Miller ; Pliny F., b. Jane 4. 1826, m. Lucretia Walker. The
children of Reuben and Lydia (Miller) Walker were : Lucretia, b. Sept.
26, 1822, m. Samuel Martin ; Chester H., b. Jan. 5, 1824, m. Sarah
Martin ; Julia and Jane, Feb. 23, 1828 ; Jane d. young, Julia m.
Charles E. Taft. Horatio N.,b. Jan. 17, 1830, m. Carrie French ;
Marshall, b. Dec. 12, 1831, m. Nellie Fairbanks ; Sarali R., b. Jan. 31,
1839, m. Dr. Clark. Phineas. the eldest brother of Dr.
 DUMMERSTON. 95 Sewall Walkei". married, probably, Anna
Newton, who had a daughter, Deborah Newton, b. May 2, 1808.
Their chikben were : Louisa, born Dec. 17, 1810; Lyman P., b. June
19, 1812; Elvira, b. Apr. 11, 1814. Dr. Walker prosecuted his
professional studies with Doctor Alexander Campbell, then of Putney
and received the degr e of M. D. from the Academy of Medicine at
Castleion, Dec. 2, 1823. He was elected a member of the Medi cal
Society of Middlebury, Vt.June 19, 1822, at a meeting of the Society
held at Middlebury at that time. He had previously been elected a
member of the Dartmouth Medical Society at Hanover, Nov. 2, 1820.
He was elected a member of the Vermont Second Medical Society
established in the County of Windham, June 14, 1824. He
commenced the practice of medicine in his native town where the
whole of his professional life was spent. He was twice married. His
second wife survived him several years. He lived with his first wife,
Lucretia Miller, 13 years. She was the mother of three cJiildren, now
living. The death of Dr. Walker was a severe public loss, having
fulfilled the duties of his profes sion for about 40 years. He attended
faithfully upon the sick ones committed to his care, never neglecting
his patients, and his success was equal to his fidelity. The disease
which terminated his life was an attack of the lungs. He died Apr. 14,
1868, aged 66 years. Mary, second daughter of Doctor Sewall Walker
(overlooked in the foregoing record) b. Apr. 1824, m. first Loyal
Smith, 2d. Benj. F. Willard. For Portrait see frontisplate . DR.
THOMAS AMSDEN was a resident in 1778. (Of whom we have no
further particulars.) DR. ISAAC N. KNAPP was a cotemporary of Dr.
Walker, both were physicians in 1831, and both had a long and
extensive practice. Doctor Knapp died Aug. 23, 1856, aged 67. DR.
THOMAS BAKER, \^The candid Doctor, '\ Came to this town from
Oxford, Mass., 1783. It is said, on one occasion in his practice, he
was called to see a sick person in the evening but being in a
condition not to deal out medicine, intelligently, at the time, as
members of the family noticed, his prescription was not used. Very
early, next morning, the Doctor came in haste and asked excitedly
about the patient and the medicine. After learning that the medicine
had not been given as he ordered, he said, after looking at it, "You
did "vvell not to give it to the Avoman, for if you had it would have
killed her dead as the devil." "The fact is," said he, "people wait till
they are almost dead, then send for drunken Dr. Baker." JONAS
WALKER died Feb." 13, 1817, aged 67 ; Sarah, his wife, d. 1831,
aged 76. Their children were iPhineas, b. Oct. 11, 1779 ; Jonas, b.
June 25, 1781 ; Daniel, b. July 11, 1783; Lyman, b. June 25, 1785 ;
William, b. May 22, 1787; Sally, b. March 15, 1790; John, b. Jan. 29,
1793; Sewall, b. March 10, 1796, and Reuben, b. Mar. 29, 1798.
CLARK FAMILY. THOMAS CLARK, a resident of this town in 1760,
came from Worcester, Mass. That portion of Worcester, in which he
lived, together with parts of Sutton, Leicester, and Oxford, was
incorporated a town by the name of Ward in 1778, and was so
named in honor of Artemas Ward, the first Major-Gener 
 96 VERMONT HISTORICAL MAGAZINE. al in the
Revolutionary war, who died at Shrewsbury, Oct. 28, 1700. It
received the name of Auburn, in 1837. Mr. Clark married Catherine
Ward, about 1772 ; children : Thaddeus, b. May 13, 1775, d. Sept.
17, 1777 ; Thomas, b. July 20, 1767, m. Mrs. Martha (Tenney) Bond,
Dec. 27, 1818; Thaddeus, b. Mar. 2, 1779, married Catherine Ryan of
Putney, died — ; Jonas, b. July 29, 1781, m. Betsey Florida, Jan. 16,
1803 ; Amasa, u. Oct. 23, 1783, m. 1st. Arathusa Whitcomb. 2d.
Mrs. Phebe (Boyden) Bemis ; Gardner, b. Nov. 28, 1785, d. July 12,
1825; Catherine, b. May 8, 1788, m. Ezra Florida, Nov. 26, 1811 ;
Polly, b. Aug. 24, 1790, m. 1st. John Robertson, Mar. 28, 1814, 2d.
Samuel Knight, 1844 ; John, b. Mar. 12, 1795, m. Sarah Stockwell,
June 10, 1810, died,—. Thomas and Catherine Clark lived to be quite
aged. He died Jan. 26, 1837, aged 91 ; she died May 3, 1834, aged
84. Children of Thomas and Martha Clark : Martha, b. Oct. 30, 1819,
m. William E. Ryther of Bernardston, Mass. Mary, b. July 25, 1823,
m. 1st George Hildreth, 2d, Alonzo Button ; Thomas, b. Apr. 19,
1825, m. Julia A. Adams of Marlboro ; Eli, b. May 4, 1828, m.
Cornelia Hubbard of Royalston, Massachusetts. Thomas died Nov.
24, 1765, aged 88 ; Martha, his wife, died, 1840, aged 55. Jonas
and Betsey Clark had a daughter, Catherine, who m. Orrin Heath of
Corinth, also, a son, John. Jonas d. Dec. 22, 1866, aged 85. Children
of Amasa and Arathusa Clark: Catherine F., b. Oct. 3, 1814, n). John
Woodbury ; Caroline A., m. Alvin D. French. She died and he
married, 2d. Mrs. Phebe (Boyden) Bemis, and had one son, Charles
A., who married Ellen Farr of Chesterfield, N. H. Amasa died Nov. 30,
1856, aged 83. Catherine, who married Ezra Florida, died Sept. 27,
1827. Mary (Polly), her sister, died Jan. 2, 1883, aged 92. When her
first husband, Mr. Robertson, died and his property was settled she
offered to take, as her share, a piece of land worth $1500, but the
heirs preferred to give her $100 a year instead so long as she lived.
The amt. paid to her by the heirs was $4300. John married Sarah
Stockwell, Mar. 31, 1818; their children: John S. m. Louisa, an
adopted daughter of Thaddeus Clark. George AV. married Mary Ann
Boyden, Sept. 2, 1644; Laura m. Dr. A. F. Tuttle of Clinton, Mich ;
Charles F. ; Jane m. Enoch G. Cook ; Fletcher M. James Clark
married Betsey Duncan, Oct. 14, 1800. Nathaniel and Lydia Clark
were the parents of Warren, b. 1809, and Ferdinand, b. 1810. Moses
Clark married Lucy Cook, June 10, 1810. Arba Clark m. 1st. Laura
Knight, Jan. 18, 1820 ; had one son, Osman ; married 2d. Catherine
Black July 26, 1835. JOHN FRENCH, who tended the first grist-mill
built in town, at Slab Hollow, was born July 2, 1735 ; Mary Wilcox,
his wife, June 22, 1740, m. Dec. 10, 1759. Children: John, b. Oct.
10, 1760, d. Mar. 17,
 DUMMERSTON. 9? 1847, aged 87; Sarah, born Mar. 28
1762; Rachel, b. Mar, 28, 1764. m. Abel Haven ; Mmbod, b. Nov. 26,
1767 ; Abel, b. Mar. 3, 1769 ; Mary, born Nov. 24, 1770Reuben, b.
July 11, 1772; Jemima, h. June 24, 1774; Silence, born June 13,
1776; Joel, b. Dec. 10, 1773, died 1779 ; Joel 2d., b. Mar. 31, 1780; i
Rebecca, b. June, 1783; Solomon,! h. Apr. 9, 178o« Sarah married
Ichiibod Onion, and when she died, he married Jemima for his
second wife. Their children had the name. Onion changed to
Deming. MARSHALL MILLEU married widow Abigail Boyden, Nov. 17,
1778. Their childrpn were : Abigail, b. July 30, 1779, died Oct. 13,
1801 ; Marshall, b. Oct. 21, 1780, m. 1st. Betsey Campbell, she died
Apr. 26, 1813, aged 26 years, 2d. Sophia Charlotte Porter, daughter
^f Hon, Samuel Porter July 9, 1815, who died July i2, 1860, aged 79
years 9 mos. Luther, b. Mar, 7, 1782. m. Lurane Knapp, died Apr. 2,
1832 ; Thomas, b. Apr. 21, 1783, married Harriet Moore, May 9,
1810, died Mar. 25, 1865, iE 82; Ebenezer, b. May 10, 1785, married
Ama Farr ; Dana, born Aug, 5, 1786, m. Sally Keyes ; Polly, born
Dec. 13, 1787, married Jonas Walker Dec. 2, 1813, who died April
16, 1873, Aged 91 years. His wife died Feb. 26, 1847. William, b,
July 3, 1789, married Esther Knight, Sept. — 1814, who d. Apr. 14,
1862, aged 66 ; he died Feb. 18, 1877, aged 87 years ; Royal, born
Feb, 15, 1891, m. Betsey Cook Nov. 13, 1813 ; Lydia, b. June 5,
1793, m. Chester Haven Sept. 21, 1814, after his death, m. Reuben
Walker, who was 13 killed by being thrown from a wagon, Apr. 21,
1860 ; Levi, b. Feb. 3, 1797 ; Lucretia, b. Sept. 13, 1798, m. Doctor
SewaU Walker. She died May 22, 1838, Marshall MiUer died June 10,
1807, aged 53. His death was caused by jimiping from a window in
the fifth story of a house which was then on fire. Abigail, his wife,
died Jan. 26, 1829, aged 73 years, RICE FAMILY. EPHRAiM RICE
married J oanua . He came from Petersham, Mass., where all his
children were born, to Dummerston, and was a resident of the town
in 1779. Children ; Ezekiel, b. Mar. 27, 1761, m. Judiali WiUard May
23, 1782 ; Elijah, b. Oct. 14, 1.64, m. Anna Miller, dau. of Capt.
Vespasian Miller. Wilder, b. Sept. a. 1766; Caty, b. Oct. 27, 1768;
Molly, born Mar. U, 1771, m. Jacob Hadley, Nov. 27, 1788 ; Joanna,
b. June 17, 1775. [See sketch of Ephraim Rice, from "Hall's History."]
Abraham Rice married Lucy Nourse Feb. 17, 1785, and were
residents of the town at that time. Had one child, Joshua, b. Aug.
23, 1785. Deacon Amos Rice died May 31, 1807. Martha — , his
wife, died Apr. 10, 1808,, One, Amos Rice m. Susan Davenport, Feb.
22, 1816. John Rice, also from Petersham, m. Levinah [Lovina] .
Children : Sarah, b. June 29, 1767 ; John, 1769, died, infant. David,
b. Dec. 29, 1770 : John Jr., 1774, d. 1777 ; Joel, b. 1776, d. 1777 ;
Samuel, b. Sept. 24, 1778 ; Polly, born in Dummerston. Aug. 9, 1782
; Lydia, b. June 13, 1789. Gardner Rice married Lydia . Children :
Dolly, born June 9, 1809 ; Amos, 1792; Lydia, 1794; Patty,
 98 VERMONT HISTORICAL MAGAZINE. 1796 ; Nabby, 1798
; Roxanna, 1800 ; Simeon, 2802; Gardner Jr., 1804; Nelson, 1806 ;
Phylinda, 1808 ; Ezekiel, 1810 ; Francis, 1812, Clark Rice, son of
Elijah, once owned the large farm, "Rice place," in the south part of
the town. ELIJAH AND ANNA (mILLEr) RICE. Elijah was born Oct.
14, 1764 ; Anna Miller, born July 22, 1766. They were married Nov.
29, 1787. Children : Arathusa, b. Oct. 12, 1788; Abigail, b. Oct. 17,
1790, m. Jacob Ha.Uey a Methodist minister ; Abel. b. Aug. 27,
1792, m. Polly Hadley and removed West ; Elias, b. Dec. 12, 1794,
died young ; Clark, b. July 8, 1797; Lovina and Lewis, [twins], b.
Jan. 17, 1800, and Lovina m. Ephraim Hadley ; William M. b. June 5,
1802, married Dolly Whitney ; Almira, b. Mar. 9, 1807, m. Lewis
Holton ; Daniel, b. July 28, 1809, m. Maria Munn. Elijah Rice and
wife were Congregationalists, and were very constant in their
attendan
The text on this page is estimated to be only 27.00%
accurate

ELIJAH RICE.
ANNA MILLER RICE.
CLARK RICE.
 DUMMERSTON. 99 children were : Fauny. born March 31,
1813 ; Isaac, b. Nov. 15, 1784; Charles, b. July 25, 1786 ; Dolly, b,
Apr. 6, 1788 ; George Anson, b. Dec. €, 1789 ; William, b. Dec. 10,
1791 ; Joel, b. Nov. 21, 1793; Nathan, b. Aug. 13, 1795; Asa, b.
June 12, 1797 ; Catherine, b. July 24, 1799 ; Maria, b. Sept. 18,
1807: Major William died Apr. 16, 1802, iiged 40. His wife died July
7, 1823, aged 62 years. An incident remembered in the town :
MAJOR WILLIAM MILLEK and Hannah, his wife, lived in the eastern
part of the town on the Connecticut river road, and owned good
lands. They were the parents of eleven children. Mrs. Miller was
always kind to the poor and ever willing to relieve the wants of the
suifering. About the year 1786, there was in this section an alarming
scarcity of grain for family food. The Millers parted with all they that
they could to the needy, and the last bushel of wheat, except a
baking of flour for their own family was ground and eaten before the
new grain had been cut. The destitution was much greater on the
newly cleared and rougher hill-land of Halifax. Joseph Worden came
one night, at a late hour, from that town, and stopped at Miller's.
Mrs, Miller rose from her bed, baked the last flour she had by the
fire, and gave him a part of the loaf for his supper. Hm said that he
had never tasted anything so good in his life, for he was weak and
weary, and had tasted no bread for several days. The next day the
men went into the wheat-field, picked off the ripest ears, thi-
eshedout a bushel or more, and had it gi-ound. Mrs. Miller was
sifting some flour for baking, when Mr. Worden, her brother, came to
her, the tears standing iu his eyes, ''Sister," said he, "wont you put
the bran into my bag ?" This proof of his family's want so affected
her that she gave him more than half of all the flour she had, and
the happy man started for home, knowing that he could now relieve
the necessities of his family." JOHN BENNETT one of the early
settlers in town, was from Shrewsbury, Mass. He bought a farm in
Dummerston, of Parmenas Templci in 1783. He married Lucretia
Rice, of Lancaster, 1778, who died in this town Jan. 26, 1811, JE 51.
His death is not recorded. He was a son of Josiah Bennett Jr., who
married Abigail Graves, of vSudbury, Aug. 13. 1751. Children :
Elizabeth, born Feb. 10, 1753, m., it is supposed, Luther Rice," of
Lancaster, 1 780 ; John, b. June 23, 1755 ; D->rcas, b. Apr. 1758,
m. Oliver Hale of Marlboro in 1778 ; Josiah Sen. m. Hannah Ross, of
Lancaster, Nov. 27, 1728, and was admitted to the church, 1731 ,
and died before 1751. Children : Josiah Jr., born Dec. 18, 1730.
Miriam, Dec. 23, 1732, m. Ebenezer Cutter Jr., of Grafton, Nov. 28,
1764; Asa, b. Apr. 26, 1735, m. Sibyl Barnes, of Marlboro, June 1784
; Experience, b. Mar. 26, 1739 ; Jonas, b. Mar. 11, 1741, died young
; Lydia, b. Oct. 9, 1747 ; Jonas, born Feb. 11, 1749, m. Mary
Williams, July 10, 1773. Jonathan, a brother of Josiah Sen. had a
son, David, born Oct. 21, 1749, who died before 1779, as in that
vear
 100 VERMONT HISTORICAL MAGAZINT^. his widow, Persis
[Cutting] Bennett, m. Philip Branscom. Deacon David Bennett of
Dummerston, died June 9, 1848, M 87. Rev, Jonas Bennett, his son,
m. Adaline, dan. of Edward Miller. Josiah and Jonathan were
stfpposed to be the sons of Samuel Bennett, probably from
Lancaster, born, 1690, died Dec. 5, 1762, aged 72. The children of
John and Lucretia Bennett, of this town, were Judah, b. 1778;
Nancy, b. 1780; Lucy, born 1781 ; John D., born in Dumraerston.
1784; Dorcas, born, 1787, married Ezekiel L. Chapman ; Henry L.,
Allyn O., Franklin W., Almyra. 1801. He married 2d, Polly Codding,
Oct. 25, 1812. Children: Lockhart W and Melinda. NORCROSS
FAMILY. THOMAS NORCROSS, a LondoD merchant, born about 1550,
is of the first generation of the Norcross family so far as the name
has been traced. Jeremiah of the second gen. b. about 1595, came
to America in 1638, and settled in Watertown, Mass. Richard of the
3d. gen. was born in 1621 ; resided in Watertown, died in 1709.
Richard of the 4tn. gen., born 1660; resided in "Western, Mass., died
1745 ; Joseph of the 5th gen., b. 1701 ; resided in Weston and
Princeton, Mass., died 1789. SAMUEL of the 6th gen., born 1745 ;
resided in Marlboro, and was the first Norcross, who settled in this
state. He died 1812. His wife was Rachel Harvey, who died 1811. He
was a soldier in the Revolutionary war, and belonged to an artillery
company at a fort in Boston Harbor at the time the British evacuated
Boston in 1775. He had eleven children: Candace, b. Dec. 5, 1776,
died 1778 ; Samuel, born Jan 9, 1769, died young ; Nahum, born
May 9, 1771, d. Jan. 26, 1851; Eber, b. May 23 1 772 ; resided in
No. Easton, N. J., died 1861, aged 89. Rachel, b. Sept. 13, 1774, d.
1836 ; Benaiah, b. Dec. 20, 1776 ; resided in Chesterfield, N. H., d.
1860, aged 85; Zebrina, b. Apr. 18, 1779, res. in Chesterfield, N. H.,
Darius, b. Oct. 9, 1781, res. Lockport, N. J., died 1838; Lu(iy, born
Aug. 2, 1784 ; Shepard, b. Mar. 9, 1788, res. in No. Easton, N. J . ;
Annis, born Oct. 7, 1790, NAHUM came to Dummerston ; married
Zeruiah Roel, Jan. 17, 1796. She was born Sept. 7, 1778, died Apr. 8,
1840. Their children were: Betsey, born Nov. 24, 1797, married
Aaron Grimes ; Luke, born July 15, 1799, died in infancy ; Luke 2d.,
born June 9, 1801 ; married Louisa French ; Mary, b. Oct. 9, 1803,
m. William Woodard ; Moses, born May 29, 1806 ; Sarah, born Dec.
7, 1808, married Anson Woodard ; Charlotte, born Nov. 24, 1809, m.
first Ebenezer Wis wall, 2d, Warren Stearns ; Orison, born Nov. 22,
1812, married Sophia Howe, Nov. 1833 ; Blucher, born May 15,
1815, m. Betsey, dau. of Lyman Huntley. None of the children of
Nahum Norcross are now living. Orison d. Aug. 21, 1873, and
Sophia, his wife, died July 19, 1871. Luke died June 22, 1876, and
Louisa, his wife, d. Nov. 17, 1881. Blucher, the youngest, d. in 1880.
 DUMMERSTON. 101 PIERCE FAMILY. William and Patty
Pierce were the parents of Josiah, Sally, Moses and Henry. Henry
married Philadelphia Thomas ; children : Sophia, b. about 1792, m.
Isaac Libby of Boston, Mass ; Sa'ly m. Harlow Williams of Milford,
Mass. Joseph, b. 1797, died young ; Martha, b. 1800, m. Doton
Smith, Middleboro, Mass. ; Joseph (2d.), m. Melinda — ; Betsey, b.
1804, m. Allen Knight, of Brattleboro ; John m. Althea Springer.
Maine ; Polly married Luther Thayer, Apr. 19, 1837, died 1859 ; Lucy
m. Benjamin Newton of Shrewsbury, Mass. ; George ; Lydia married
Amasa McFarland of Hopkinton, Mass. ; Phila married Josephus
Cutler of HoUiston, JOSIAH PIERCE came from Upton, Mass., to
Dummerston, in 1793. Upton was not an original grant, but was
Taken from the town ships of Mendon, Sutton, and Hopkin ton, a
locality from which several of the early settlers removed to this town.
The children of Josiah and Sarah Pierce were : William, b. in Upton,
Mar. 12, 1792 ; Jacob ; HoUis, born May 7, 1796 ; Anson, in 1798 ;
Hannah, b. Dec. 18, 1803 ; Joel, b. Jan. 22, 1806 ; Susanna, born
Jan. 19, 1809. William was drowned in West river Apr. 11, 1825,
while crossing it in a skiff about a mile north of the old bridge-place.
Henry and Moses Pierce were brothers of Josiah and came from
Hopkinton. Their sister, Sally, was the wife of Philip Bemis. Moses
Pierce m. Patty Barnes ; children : Asa, Eli, Ruhama, and Ira. ISAAC
REED became a resident of this town about the time of his marriage
to Abigail Mcwain, Sept. 2,1790. Their ch. were : Lucy, b. July 27,
1791, died 1823 ; Sally married Ephraim Brown, Aug. 1814; David
m. Betsey Fairbanks, 1824 ; Leavitt, his twin brother, m, 1st. Emeline
Hubbard, May 27, 1830, 2d. Clarissa F. Miller ; Isaac, m. Catherine B.
Alexander, Dec. 3, 1829 ; Eliza, m. Joseph Miller, March 3, 1841. The
children of Ephraim and Sally Brown were Charles, b. Feb. 12, 1813 ;
Nancy, b. Nov. 30, 1815 ; James, m. Emily Walker. Children of David
and Betsey Reed : Adin Thayer, b. Dec. 28, 1826 ; Lucy M. born Apr.
23. 1828 ; Fanny E. b. Dec. 8, 1829 ; George F., born Oct. 2, 1831 ;
Louisa P., born Feb. 28, 1836 ; Mary C, born Feb. 26, 1838 : David
Henry, b. Oct. 3, 1840. Isaac Jr., had James A., Maria, Charlotte, and
Ellen, of whom James only is living. Leavitt had Romanzo and Eliza
Welcome to our website – the ideal destination for book lovers and
knowledge seekers. With a mission to inspire endlessly, we offer a
vast collection of books, ranging from classic literary works to
specialized publications, self-development books, and children's
literature. Each book is a new journey of discovery, expanding
knowledge and enriching the soul of the reade

Our website is not just a platform for buying books, but a bridge
connecting readers to the timeless values of culture and wisdom. With
an elegant, user-friendly interface and an intelligent search system,
we are committed to providing a quick and convenient shopping
experience. Additionally, our special promotions and home delivery
services ensure that you save time and fully enjoy the joy of reading.

Let us accompany you on the journey of exploring knowledge and

personal growth!

ebookfinal.com