Commodity Effective BPL APL AAY

From Families Families Families

Wheat 01- 07- 2002 415 610 200
Rice Common 01- 07- 2002 565 795* 300
Rice Grade-A 01- 07- 2002 565 830 300

(*): Applicable to J&K, Himachal Pradesh, Sikkim, Uttaranchal and NE States.

UNIFORM SPECIFICATION OF ALL VARIETIES OF PADDY (MARKETING SEASON 2009-2010)

Paddy shall be in sound merchantable condition, dry, clean, wholesome of good food value, uniform in colour
and size of grains and free from moulds, weevils, obnoxious smell, Argemone mexicana, Lathyrus sativus
(Khesari) and admixture of deleterious substances.
Paddy will be classified into Grade ‘A’ and Common groups.

Schedule of Specification
Maximum
S.No Refractions
Limits (%)
Foreign matter
1. a) Inorganic 1.0
b) Organic 1.0
Damaged, discoloured, sprouted
2. 4.0
and weevilled grains
Immature, Shrunken and
3. 3.0
shrivelled grains
4. Admixture of lower class 7.0
5. Moisture content 17.0

NOTE:

1. The definitions of the above refractions and method of analysis are to be followed as per BIS “Method of
analysis for foodgrains” IS: 4333 (Part -I):1996, IS: 4333 (Part-II): 2002 and “Terminology for
foodgrains” IS: 2813 -1995, as amended from time to time.
2. The method of sampling is to be followed as per BIS method for sampling of Cereals and Pulses IS:
14818-2000 as amended from time to time.

3. Within the overall limit of 1.0% for organic foreign matter, poisonous seeds shall not exceed 0.5% of
 which Dhatura and Akra seeds (Vicia species) not to exceed 0.025% and 0.2% respectively.

UNIFORM SPECIFICATION FOR GRADE 'A' & COMMON RICE (MARKETING SEASON 2009-2010)

Rice shall be in sound merchantable condition, sweet, dry, clean, wholesome, of good food value, uniform in
colour and size of grains and free from moulds, weevils, obnoxious smell, admixture of unwholesome poisonous
substances, Argemone mexicana and Lathyrus sativus (Khesari) in any form, or colouring agents and all
impurities except to the extent in the schedule below. It shall also conform to PFA Standards:

SCHEDULE OF SPECIFICATION
Maximum Limits
(%)
S.No Refractions
Grade
Common
'A'
Brokens*
1. Raw 25.0 16.0
Parboiled 25.0 16.0
Foreign Matter**
2.
Raw/ Parboiled 0.5 0.5
Damaged # /Slightly
Damaged Grains
3.
Raw 3.0 3.0
Parboiled 4.0 4.0
Discoloured Grains
4. Raw 3.0 3.0
Parboiled 5.0 5.0
Chalky Grains
5.
Raw 5.0 5.0
Red Grains
6.
Raw/Parboiled 3.0 3.0
Admixture of lower class
7.
Raw/ Parboiled 6.0 --
Dehusked Grains
8.
Raw/ Parboiled 12.0 12.0
Moisture content @
9.
Raw/ Parboiled 14.0 14.0

• Including 1% small brokens.

 • Not more than 0.25% by weight shall be mineral matter and not more than0.10% by weight shall be
impurities of animal origin.

• Including pin point damaged grains.@ Rice (both raw and Parboiled) can be procured with moisture
content upto a maximum limit of 15% with value cut. There will be no value cut up to 14%. Between
14% to 15% moisture, value cut will be applicable at the rate of full value.

NOTES APPLICABLE TO THE SPECIFICATION OF GRADE ‘A’ AND COMMON VARIETIES OF

RICE.

1. The definition of the above refractions and method of analysis are to be followed as given in Bureau of
Indian Standard “Method of analysis for Foodgrains” No’s IS: 4333 (Part-I):1996 and IS : 4333 (Part- II): 2002
“ Terminology for Foodgrains” IS: 2813-1995 as amended from time to time. Dehusked grains are rice kernels
whole or broken which have more than ¼th of the surface area of the kernel covered with the bran and
determined as follows:-

ANALYSIS PROCEDURE:- Take 5 grams of rice (sound head rice and brokens) in a petri dish (80X70 mm).
Dip the grains in about 20 ml.of Methylene Blue solution (0.05% by weight in distilled water) and allow to
stand for about one minute. Decant the Methylene Blue solution. Give a swirl wash with about 20-ml.of dilute
hydrochloric acid (5% solution by volume in distilled water). Give a swirl wash with water and pour about 20
ml. of Metanil Yellow solution (0.05% by weight in distilled water) on the blue stained grains and allow to stand
for about one minute. Decant the effluent and wash with fresh water twice. Keep thestained grains under fresh
water and count the dehusked grains. Count the total number of grains in 5 grams of sample under analysis.
Three brokens are counted as one whole grain.

CALCULATIONS:
Percentage of Dehusked grains = N X 100
W
Where N = Number of dehusked grains in 5 grams of sample
W = Total grains in 5 grams of sample.

2. The Method of sampling is to be followed as given in Bureau of Indian Standard “Method of sampling
of Cereals and Pulses” No IS: 14818-2000 as amended from time to time.

3. Brokens less than 1/8th of the size of full kernels will be treated as organic foreign matter. . For
determination of the size of the brokens average length of the principal class of rice should be taken into
account.

4. Inorganic foreign matter shall not exceed 0.25% in any lot, if it is more, the stocks should be cleaned
and brought within the limit. Kernels or pieces of kernels having mud sticking on surface of rice, shall be treated
as Inorganic foreign matter.

In case of rice prepared by pressure parboiling technique, it will be ensured that correct process of parboiling is
adopted i.e. pressure applied, the time for which pressure is pplied, proper gelatinisation, aeration and drying
before milling are adequate so that the colour and cooking time of parboiled rice are good and free from
encrustation of the grains.

UNIFORM SPECIFICATION FOR INDIAN WHEAT OF ALL VARIETIES FOR RABI

MARKETING SEASON 2010 –2011.

Wheat shall:
a. be the dried mature grains of Triticum vulgare, T. compactum, T. sphaerococcum, T. durum, T. aestivum
and T. dicoccum.
b. have natural size, shape, colour and lustre.
c. be sweet, clean, wholesome and free from obnoxious smell, discolouration, admixture of deleterious
substances including toxic weed seeds and all other impurities except to the extent indicated in the
schedule below.
d. be in sound merchantable condition.
e. not have any admixture of Argemone mexicana and Lathyrus sativus (khesari) in any form, colouring
matter and any obnoxious , deleterious and toxic material.

f. Conform to PFA Rules.

Schedule showing the maximum permissible limits of different refractions in Fair Average Quality of Wheat.

Foreign Other food Damaged Slightly Shrivelled &

Matter grains grains damaged Broken grains
% % % grains % %
0.75 2.0 2.0 6.0 7.0

NOTE:

1. Moisture in excess of 12% and upto 14% will be discounted at full value. Stocks containing moisture in
excess of 14% are to be rejected.
2. Within the overall limit specified for foreign matter, the poisonous weed seeds shall not exceed 0.4% of
which Dhatura and Akra (Vicia species) shall not be more than 0.025% and 0.2% by weight respectively.
3. Kernels with glumes will not be treated as unsound grains during physical analysis, the glumes will be
removed and treated as organic foreign matter.
4. Within the overall limit specified for damaged grains, ergot affected grains shall not exceed 0.05 %.
5. In case of stocks having living infestation, a cut at the rate of Rupee One per quintal may be charged as
fumigation charges.
6. For weevilled grains determined by count, following price cuts, in addition to other cuts, if any, will be
imposed.
i. from the beginning of the season till end of August, the rate of cut will be @ Re. 1/- per qtl., for
every 1% or part thereof.
ii. from 1st September till end of October, no cut will be imposed upto 1% while for any excess, the
cut will be @ Re. 1/- per qtl., for every 1% or part thereof.
iii. from 1st November till end of the season no cut will be imposed upto 2% while for any excess,
 the cut will be @ Re. 1/- per qtl., for every 1% or part thereof.

iv. stocks containing weevilled grains in excess of 3% will be rejected.

Method of Analysis

As given in Bureau of Indian Standard No. IS. 4333 (Part I and II) 1967 and as amended from time to time
except for weevilled grains which are to be determined by count method.

DEFINITIONS OF REFRACTIONS:

As contained in BIS Specifications No. 2813-1995.

PRESERVATION:

The Food Corporation of India has an extensive scientific stock preservation system. An on-going programme
sees that both prophylactic and curative treatment is done timely and adequately. Grain in storage is
continuously scientifically graded, preserved by qualified, trained and experienced personnel.

Food-grains are stored in scientifically developed storage structures. Two type of storage have been adopted i.e.
bagged and bulk. In bagged storage food-grains are stored in jute bags in covered godowns as well as in open
under cover and plinth. In bulk storage food-grains are stored in loose form in the mechanical Silos. Storage
under covered and plinth is undertaken as and when there is shortage of covered and bulk storage.

Recently we have started a programme of bulk handling and transportation of food-grains along with bulk
storage with private participation. Two silo complexes of 2 lacs MT capacity each with latest mechanization of
international standard have been constructed at Kaithal in Haryana and Moga in Punjab with facility of bulk
transportation to the ancillary Silos in other Zones by M/s Adani Agri Logistic Ltd. For bulk transportation
special wagons have been constructed and each rake carries approx. 3000 MT at a time from each center.

Scientific preservation of food-grains starts immediately on its arrival in the godowns. Food-grains are stacked
on scientifically developed dunnage material to prevent contact with the ground moisture. Preventive and
curative treatment with the insecticides/fumigants is done periodically till dispatch/issue for consumption. At
present, for preventive treatment FCI is using potent insecticides vis Malathion on fortnightly basis and Delta-
methrin on quarterly basis (once in three months). As and when infestation of storage insects is detected
curative treatment is done with Al. Phosphide immediately. During the year 2009-10 & 20010-11(Upto
June’2010) following quantities of food-grains were imparted preventive and curative treatment with different
insecticides/fumigants:-

Copyright Food Corporation of India, All rights reserved Web Solutions By: DreamTeam

DIRECTORATE OF MARKETING & INSPECTION

DEPARTMENT OF AGRICULTURE & COOPERATION
(i) Particulars of its organizations, functions and duties:-

MANDATE:

The Directorate of Marketing and Inspection (DMI) is an attached Office of the

Ministry of Agriculture. It was set up in the year 1935 to implement the agricultural
marketing policies and programmes of the Central Government. Since its very inception,
the Directorate continues to be responsible for bringing about an integrated development
of marketing of agricultural and allied produce in the country with a view to safeguard
the interests of producer-sellers as well as the consumers. It maintains a close liaison
between the Central and the State Governments in the implementation of agricultural
marketing policies in the country.

ORGANISATIONAL SET UP:

The Directorate is headed by the Agricultural Marketing Adviser to the Govt. of

India (AMA). The Directorate has its Head Office at Faridabad (Haryana), Branch Head
Office at Nagpur (Maharashtra) and 11 Regional Offices at Delhi, Mumbai, Chennai,
Kolkata, Hyderabad, Chandigarh, Jaipur, Lucknow, Bhopal, Kochi and Guwahati and the
Central Agmark Laboratory at Nagpur. Besides, there are 26 Sub-Offices, 16 Regional
Agmark Laboratories (RALs) spread all over the country as per the details given below:-

Sub-Office under Agmark Laboratories

Regional under Regional Office
Regional office
Offices
1. Delhi 1. Dehradun 1.Okhla 2.Ghaziabad
2. Kolkata 1. Patna 1.Kolkata 2.Patna
2.Bhubaneshwar 3.Bhubaneshwar
3.Ranchi
3. Mumbai 1.Nasik Road 2.Ahemdabad 3.Rajkot 1.Mumbai 2.Rajkot
4.Surat 5.Panaji 6.Pune 7.Sangli

4. Bhopal 1.Raipur 1.Bhopal

5. Chennai 1.Bangalore 2.Madurai 3.Hubli 1.Chennai 2.Bangalore
6. Kochi 1.Calicut 2.Thiruvananthapuram 1.Kochi
7. Hyderabad 1. Guntur 2.Vishakhapattanam 1.Guntur
8. Guwahati 1. Shillong 1.Guwahati
9. Lucknow 1.Kanpur 2.Varanasi 1.Kanpur
10. Jaipur Nil 1.Jaipur
11. Chandigarh 1.Jammu 2.Amritsar 3.Abohar 1.Amritsar
4.Shimla

The organizational chart is placed at Annexure-I.

ACTIVITIES:

The activities of the Directorate cover the following areas of agricultural

marketing:

1. Promotion of Standardisation and Grading of agricultural and allied produce

under the Agricultural Produce (Grading & Marking) Act, 1937 as
amended in 1986;
2. Market Research, Surveys and Planning;
3. Agricultural Marketing Reforms
4. Agricultural Marketing Information Network;
5 Promotion of Cold Storage
6. Construction of Rural Godowns
7. Development of Marketing Infrastructure, Grading &
Standardization
8. Training in agricultural marketing;
9. Marketing Extension;

1. STANDARDISATION AND GRADING OF AGRICULTURAL AND

ALLIED PRODUCE (NON-PLAN):

Quality standards for agricultural commodities are framed based on their intrinsic
quality. Food safety factors are being incorporated in the standards to compete in World
trade. Standards are being harmonised with international standards keeping in view the
WTO requirements. Certification of agricultural commodities is carried out for the
benefit of producer/manufacturer and consumer. Certification of adulteration prone
commodities viz. Butter, Ghee, Vegetable Oils, Ground-Spices, Honey, Wheat Atta etc.
is very popular. Blended Edible Vegetable Oils and Fat Spread are compulsorily required
to be certified under Agmark.

The Certification mark under the Agricultural Produce (Grading &

Marking) Act is popularly known as "AGMARK". Grading is carried out in accordance
with the standards notified, following meticulous procedure of sampling, testing,
packaging, marking and sealing as per the instructions issued under the Act and
Rules.

1. 1 FORMULATION OF GRADE STANDARDS:

 Agricultural Produce (Grading & Marking) Act, 1937 empowers the
Central Government to frame grade standards for agricultural produce. The DMI has
formulated Agmark standards for 181 agricultural and allied commodities. Standards
framed under the provisions of the Act are popularly known as AGMARK standards.
The standards are framed in a scientific manner. A sampling plan is first drawn for
collecting adequate number of representative samples of the concerned commodity from
different producing areas and assembling centers over a period of time. These samples
are analyzed in various Regional Agmark Laboratories for various physical and chemical
parameters. On the basis of analytical data generated, grade standards are formulated
keeping in view the standards framed under the provisions of the Prevention of Food
Adulteration Act, 1954.

1.2 GRADING OF AGRICULTURALCOMMODITIES:

The grading activities are directed specifically for the benefit of farmers and
consumers, while they also help the traders in efficient movement of the produce from
the producers to the consumers. Promotion of standardization and grading of agricultural
and allied produce is one of the important activities of the Directorate of Marketing &
Inspection. The Directorate promotes standardization and grading and implements
scheme of certification of agricultural and allied products for orderly marketing under the
provisions of Agricultural Produce (Grading & Marking) Act, 1937 as amended in 1986.
The Certification mark under the Act is popularly known as ‘AGMARK’. Grading is
carried out in accordance with the standards notified, following meticulous procedure of
sampling, testing, packaging, marking and sealing as per the instructions issued under the
provisions of the Act and Rules. It serves as a means of describing the quality of
commodities to be purchased or sold by the buyers or sellers all over the country and
abroad. This establishes a common trade language and avoids the need for physical
checking and handling at many points. The system of grading and certification benefits
both the sellers and buyers in view of the fact that the producer gets price commensurate
with the quality produced by him and consumer gets a quality product. Grading and
certification activities can be broadly classified into -
(i) Grading for Internal Trade
(ii) Grading for Export
(iii) Grading at Producers’ level.

1.2.1 Grading for Internal Trade:

Grading of agricultural commodities for internal trade is voluntary in nature and

is carried out under the provisions of Agricultural Produce (Grading & Marking) Act,
1937. However, as per provision in Prevention of Food Adulteration Rules, 1955
certification of blended edible vegetable oils and fat spread is compulsory under Agmark
for internal trade. The commodities graded under ‘AGMARK’ for internal trade are
classified into two groups; viz. decentralized commodities and centralized commodities.
Decentralised commodities include those items which do not require elaborate testing
facilities. Assessment of their purity and determination of grade is mostly done on the
basis of physical factors or relatively simple tests. Decentralised commodities include
wheat, rice and other cereals, oilseeds, edible nuts, fibre crops, fruit and vegetables etc.
This programme is being implemented through the Marketing Departments of the
concerned State Governments under the guidance of the Directorate of Marketing and
Inspection. Certain powers such as renewal of Certificate of Authorisation, drawl of
check samples, etc. under the provisions of General Grading & Marking Rules, 1988
have also been delegated to Officers of States/ UTs. for grading of decentralized
commodities.

The commodities which require elaborate testing arrangements for assessment of

quality and determination of grade, are classified as centralised commodities. These
include ghee, butter, vegetable oils, oil cakes, powdered spices, honey, wheat Atta,
Besan etc. These require elaborate testing for chemical parameters. The commodities
are tested by the authorized packers in primary grading laboratories for various
prescribed parameters and grades are assigned as per the analytical results. Packers/
manufacturers who can not establish their own laboratories because of cost involved and
recurring expenditure, get themselves attached with State Grading Laboratories (SGLs)/
cooperative/ commercial laboratories.

1.2.2 Grading for Export:

The Export (Quality Control & Inspection) Act, 1963 is administered by the
Ministry of Commerce. The Act empowers the Government to

• Notify commodities which will be subject to quality control and/or inspection

prior to export,
• Establish standards of quality for such notified commodities, and
• Specify the type of quality control and/or inspection to be applied to such
commodities.

In view of economic reforms initiated by the Government of India in early 1990s,

the operation of compulsory quality control and inspection for export commodities had
been simplified. The following steps initiated at the time continued to be operative.

• State Trading Houses, Trading Houses, Export Houses as well as Industrial Units
in Export Processing Zones and 100% Export Oriented Units have been exempted
from the purview of compulsory pre shipment Inspection.
• Units approved by EIAs under the system of In-process Quality Control (IPQC)
have been authorized to issue statutory certificates by themselves.
• Items which were hitherto subjected to compulsory pre shipment inspection have
been exempted from the same, provided the exporter has a firm letter from the
overseas buyer stating that the overseas buyer does not require preshipment
inspection from any official Indian inspection agencies.
 Fish and fishery products, honey, egg products, milk and milk products, black
pepper for USA, Basmati rice for EU have been notified for compulsory preshipment
inspection and certification.

DMI has attended to certification of grapes during this year from different centers
in Maharashtra, Andhra Pradesh and Karnataka.

1.2.3 Grading at Producers’ Level:

For securing adequate return to the producer-sellers, a scheme of Grading at the

Producers’ Level by establishing grading units in Regulated markets and Marketing
Cooperatives was introduced. The main objective of the scheme is to subject the produce
to simple tests, and assign a grade before it is offered for sale. Grading helps the
producer to get price commensurate with the quality of his produce. Cereals, pulses,
oilseeds, spices, fruit and vegetables, fibres, arecanut, coconut and tobacco are some of
the important commodities graded under this programme. The scheme is being
implemented by the States/ UTs.

1.3 NETWORK OF AGMARK LABORATORIES:

Directorate of Marketing & Inspection has set up 16 Regional Agmark

Laboratories (RALs) spread all over the country with Central Agmark Laboratory at
Nagpur as the apex laboratory. These RALs have the mandate to;
(i) analyse research samples of agricultural commodities for framing their
standards and
(ii) analyse check samples drawn under Agmark Certification Programme.

2. MARKETING RESEARCH, SURVEYS AND PLANNING:

Right from its inception, DMI has been undertaking commodity marketing
surveys and in-depth studies of marketing system in respect of various agricultural
commodities in the country. Problem-oriented studies are also undertaken and technical
guidance is rendered to State Governments.

2.1 Market Research and Planning:

At the outset guidelines, questionnaires/ schedules and synopses are prepared and
issued to field offices for collection of data. The field surveys are conducted at the
important centres spread over the entire country. The analysis and interpretation of data is
done by using percentage indices, averages, variance, standard deviation correlation,
regression trends and forecasting tools/ techniques. The report is prepared in an
organized form which includes introduction, methodology, findings, summary,
conclusion and recommendation. Based on these studies/ surveys, a large number of
marketing reports have been published by the Directorate. These reports help planners
and policy makers to formulate various schemes/ programmes from time to time for
development of agricultural marketing system in the country. The important suggestions/
recommendations are also made on the basis of findings of these reports for the benefits
of agriculturists, agri-business dealers and consumers.

2.2 Marketable Surplus and Post-Harvest Losses:

The Directorate is also implementing a scheme for Estimation of Marketable

Surplus and Post-Harvest Losses of Foodgrains. It aims at finding out the quantum of
marketable surplus and post-harvest losses to pin point the causes of losses and to suggest
remedial measures, besides generating data for various user agencies.

2.3 Research Grants:

With a view to attract private and autonomous sector talent, the DMI has provided
Research Grants to eminent scholars, institutions for undertaking research studies to
identify specific problems & constraints in various areas of agricultural marketing and
suggest remedial The financial assistance was provided in the form of grant-in-aid. 33
such projects were sanctioned. Out of them reports on 32 projects have been received
and published.

2.4 Under the Xth Five Year Plan the three schemes i) Market Information Network
ii) Marketable Surplus and Post-harvest Losses of Foodgrains and iii) Research Grants
Scheme have been amalgamated under one scheme namely “Market Research and
Information Network”. Under the new scheme the Directorate has undertaken the
preparation of following commodity profiles:

i) Post harvest profile of Paddy/ Rice

ii) Post harvest profile of Red Gram
iii) Post harvest profile of Bengal Gram
iv) Post harvest profile of Soyabean
v) Post harvest profile of Mustard- Rape seed
vi) Post harvest profile of Wheat
vii) Post harvest profile of Groundnut

Out of these profiles Paddy/ Rice, Bengal Gram, Soyabean, Red Gram and
Mustard- Rape seed have been uploaded on Agmark net portal and are in public domain
can be accessed from www.agmarknet.nic.in.

3. AGRICULTURAL MARKETING REFORMS:

i) Model Act on Agricultural Marketing: This Ministry has formulated a ‘Model

Act’ on agricultural marketing in order to assist the States in removing barriers, whether
legal or policy induced, which introduce inefficiencies and monopoly rents in the
functioning of agricultural markets. The Model Act enables any person, grower or local
authority to establish new markets in any area, removes compulsion on growers to sell
their produce through existing regulated markets, allows establishment of direct purchase
centers and Farmers Markets for direct sale, promote Public Private Partnership in
management and development of markets, establish Special markets for commodities like
Onions, Fruits, Vegetables, Flowers etc.

ii) Contract Farming: In the wake of economic liberalization, the concept of

contract farming in which national or multinational companies enter into contracts for
marketing of agricultural and horticultural produce and also provide technologies and
capital to contract farmers has gained importance.

Model specifications of contract farming agreement and supporting legislation

requiring amendment to the State Acts dealing with agricultural marketing has been
formulated and the same sent to State Governments/ UTs for necessary action.

4. MARKETING RESEARCH AND INFORMATION NETWORK:

4.1 The Marketing Research and Information Network Scheme viz. AGMARKNET
is being implemented by the Department for electronic networking of agricultural
produce wholesale markets in the country for collection and dissemination of price and
market related information. The scheme was launched in the year 2000-01.

4.2 Price related Information: Information on price of agricultural commodities is

collected by Auction Officers in the mandi through the process of auction that takes place
from early in the morning and goes up to lunchtime. The data is usually sent by e-mail
from the mandi in the afternoon indicating the day’s minimum price of the commodity,
the maximum price and the modal price, i.e. the price at which the maximum sales have
taken place. The quantity of arrivals is also reported. E-mail from all the markets are
compiled in the DMI/NIC Headquarter and after verification uploaded on the portal.
Information on the portal is in public domain and can be accessed freely. As on date,
price information in respect of more than 300 commodities and 2000 varieties are
reported on the portal.

4.3 Market related information: In addition to price, several other markets

related information is provided on the portal. These relate to accepted standards of
grades, labeling, sanitary and phyto-sanitary requirements, physical infrastructure of
storage and warehousing, marketing laws, fees payable etc. Efforts are on to prepare a
national atlas of agricultural markets on a GIS Platform that would indicate the
availability of entire marketing infrastructure in the country including storage, cold
storage, markets and related infrastructure. Similarly commodity profiles indicating the
post harvest requirements of important commodities in terms of quality, packing,
standards, etc. are being loaded on to the portal. Commodities already covered include
Rice, Bengal Gram, Red Gram and Mustard/Rapeseed.
7. DEVELOPMENT OF AGRICULTURAL MARKETING
INFRASTRUCTURE, GRADING & STANDARDISATION:

7.1 With a view to attract large private investment in agriculture, a new scheme has
been launched in October 2004 with a Central outlay of Rs.190 crores during Xth Five
Year Plan to develop marketing infrastructure in the country to cater to the post-harvest
requirement of production and marketable surplus of various farm products. A provision
of Rs.70 crore has been made in the budget during 2005-06 for implementation of the
Scheme. This scheme is reform linked and assistance for development of infrastructure
projects will be provided in those States/ Union Territories which permit setting up of
agricultural markets in private and cooperative sectors and allow direct marketing and
contract farming.

7.2 The main objectives of the scheme are to provide additional agricultural
marketing infrastructure to cope up with the large expected marketable surpluses of
agricultural and allied commodities including dairy, poultry, fishery, livestock and minor
forest produce; to promote competitive alternative agricultural marketing infrastructure
by inducement of private and cooperative sector investments; to promote direct
marketing through reduction in intermediaries and handling channels thus enhancing
farmers’ income; and to provide infrastructure facilities for grading, standardization.

7.3 The Rate of subsidy under the scheme is 25% of the capital cost of the project. In
case of North Eastern States, hilly and tribal areas and to entrepreneurs belonging to
Scheduled Caste (SC)/ Scheduled Tribe (ST) and their cooperatives, the rate of subsidy is
33.33%. Maximum amount of subsidy shall be restricted to Rs.50 lakh for each project.
In the case of North Eastern States, hilly and tribal areas and to entrepreneurs belonging
to SC/ ST and their cooperatives, maximum amount of subsidy shall be Rs.60 lakh for
each project. In respect of infrastructure projects of State Agencies, there will be no
upper ceiling on subsidy to be provided under the scheme. The assistance is available to
individuals, Group of farmers/ growers/ consumers, Partnership/Proprietary firms, Non-
Government Organizations, Self Help Groups, Companies, Corporations, Cooperatives,
Cooperative Marketing Federations, Local Bodies, Agricultural Produce Market
Committees & Marketing Boards in the entire country. Subsidy for the projects under the
scheme shall be released through National Bank for Agriculture & Rural Development
for projects financed by the Commercial, Cooperative and Regional Rural Banks,
Agricultural Development Finance Companies, scheduled Primary Cooperative Banks,
North Eastern Development Financial Corporation and other institutions eligible for
refinance from National Bank for Agriculture & Rural Development and through
National Cooperative Development Corporation for projects financed by them or by
Cooperative Banks recognized by the Corporation in accordance with its eligibility
guidelines.
 7.4 Under the scheme the targets for Xth Five year Plan are (i) to develop 1436
number of new marketing infrastructure projects with central assistance of Rs.74.40
crores, (ii) to upgrade/ modernize 49 wholesale markets with central assistance of
Rs.25.30 crores and (iii) to upgrade/ modernize 1454 rural primary markets/ apni mandies
with central assistance of Rs.75.30 crores. The annual targets for the year 2005-06 are (i)
to develop 528 number of new marketing infrastructure projects with central assistance of
Rs.27.37 crores, (ii) to upgrade/ modernize 21 wholesale markets with central assistance
of Rs.10.80 crores, and (iii) to upgrade/ modernize 558 number of rural primary markets/
apni mandies with a central assistance of Rs.28.80 crores. Besides this, modernization/
accreditation of three Agmark laboratories namely Central Agmark Laboratory, Nagpur,
Regional Agmark Laboratories at New Delhi and Mumbai with National Accreditation
Board for Testing & Calibration Laboratories has been proposed to be completed by the
year ending 2005-06, while other six Regional Agmark Laboratories are to be
modernized and accredited during the next year with central allocation of Rs.10 crores.

7.5 Since the scheme is reform linked, it has so far been implemented in those States/
UTs which have introduced reform measures by allowing direct marketing, contract
farming and setting up of markets in private and cooperative sectors. These states are
Madhya Pradesh, Tamil Nadu, Kerala, Manipur, Andaman & Nicobar Islands, Himachal
Pradesh, Punjab, Andhra Pradesh, Sikkim and Nagaland. Sensitization programmes have
been conducted in the States of Madhya Pradesh (dated 22nd Feb, 05), Tamil Nadu (dated
4th March, 05), Kerala (dated 9th March, 05), Manipur (dated 22nd March, 05) and
Andaman & Nicobar Islands (dated 9th April, 05). In addition, Bankers/ Cooperatives
level programmes have also been organized in Kerala on 26th & 27th May, 2005.

Organic acids and their salts

Several organic acids and their salts are common preservation as they have
marked microbiostatic and microbicidal action. Benzoic acid and benzoate are used
for the preservation of vegetables. Sodium benzoate is used in the preservation of
jellies, jams, fruit juice and other acid foods. Salicylic acid and salicylates are used
as preservatives of fruits and vegetable in place of benzoate because the latter is
considered to be deleterious to health of consumer. Scorbic acid is recommended
for foods susceptible to spoilage fungi, e.g., it inhibits mould growth in bread.
Wrapping material for cheese may be treated with it. It is also used in sweet
pickles and for control of lactic fermentations of olives and cucumbers.

Foods prepared by fermentation processes, e.g., milk products, etc. Your

are preserved mainly by lactic, acetic and propionic acids. FlavouringAd Here
extracts of vanilla, lemons are preserved in 50-70% alcohol as it
coagulates cell proteins.

Inorganic acids and their salts

Most common among the inorganic acids and their salts are sodium
chloride, hypochlorites, sulphurous acids and sulphites, sulphur
dioxide, sodium nitrate and sodium nitrite.

(a)Sodium chloride.
Sodium chloride produces high osmotic pressure and, therefore, causes
destruction of many microorganisms by plasmolysis. It causes dehydration of food
as well as microorganisms, releases disinfecting chlorine ion by ionization, reduces
solubility of oxygen in the moisture, sensitizes microbial cells against carbon
dioxide and interferes with the action of proteolytic enzymes. These are the
reasons why this common salt is used widely for preservation either directly or in
brine or curing solutions.

(b) Hypochlorites. The hypochlorous acid an effective germicide provided

Y the organic matter content of the medium is not high. It is oxidative in its
our action. The commonly used forms are sodium and calcium hypochlorites.
Ad Drinking water or water used for washing foods or icing them may be
Here dissolved with hypochlorites.

(c) Sulphurous acids and Sulphites. Sulphurous acid and sulphites are
added to wines as preservatives. Sulphurous acid is used especially in the
preservation of dry fruits. It helps retention of original colour of the preserve
and inhibition of moulds more than either yeasts or bacteria. Potassium
metabisulphite is used in canning.

(d) Sulphur dioxide. Sulphur dioxide has a bleaching effect desired in some
fruits. And also suppresses the growth of yeast moulds. It is used as a gas
to treat drying fruits and is also used in molasses.

(e) Nitrates and Nitrites. Nitrates and nitrites produces an inhibitory effect
on bacterial growth and used usually together in meat and fish preservation
and for retension of red-colour of the meat. Nitrate is changed to nitrous acid
which reacts with myoglobin to give nitric oxide myoglobin. It is the latter
which gives a bright red colour to the meat making it more attractive in
appearance. However, both nitrite and nitrate are poisonous if present in
potable water or food products in more than minimal amounts. This is why
the generous are of these chemicals as preservative in meat and fish
products has been questioned.

Antibiotics
Aureomycin (chlorotetracycline) is the most commonly used antibiotic for the
preservation of animal products under chilling conditions. It is extensively
used for the preservation of poultry, meat, and fish. The antibiotic is applied
to the surface of the fresh meat by dipping it in a solution of the antibiotic or
it may be fed to the animal by mixing it with feed or water for one to several
days before slaughter. Fish are treated by adding the antibiotic in the ice or
water in which they are to be transported.

The indiscriminate use of antibiotics as preservatives, however, should be

prevented or the antibiotics used should be such that is demobilished on
cooking so that the internal flora of man using such food is constantly
exposed to the effect of the antibiotic. It is important because otherwise use
of antibiotics would lead to the development of the antibiotic resistant strains
of microorganisms in the body. Aside from this, some individuals sensitive to
antibiotics becomes exposed constantly to allergy

Osmotic Pressure Treatment

When high osmotic pressure are built in a food by increasing is solute
concentration, microorganisms having osmotic pressure relatively lower are
plasmolysed and eventually die.

Salt is widely used to preserve certain foods. The salting and bringing of fish,
corning of beef, and bringing of green olives are examples of the use of high
salt concentration. With the exception of halophiles, practically no
multiplication of organisms occur in salt concentration of 25%.

Preservation of jellies, jams, maple syrup, and honey is because of high

sugar content. It is not uncommon to find mould growth on the surface of
jelly which has been exposed to air. This may also be due to the
condensation of evaporated water on the surface of the jelly to produce a
layer of less concentrated sugar solution. Osmophilic yeasts occasionally
grow in honey and produce sufficient carbon dioxide to burst the jar.

The food preserved by addition of salts sugars be kept in airtight containers

and stored in cool locations to avoid contamination by high osmotic pressure
tolerating microorganisms such as yeasts and moulds.

Dehydration
Dried foods have been used for centuries, and they are more common throughout the world t
dehydration. Food products containing 10% or less of free moisture are not subjected to spo
effect of dehydration is due mainly to microbistasis. The microorganisms are necessarily kil
critical level.

The critical level is determined by characteristics of the particular organisms and the capacit
the food should be kept in airtight containers so that is not exposed to fluctuations in humidity
microorganism such as moulds and yeasts first, and bacteria later.

Heat
High temperature is one of the most reliable and sagest method of food

(a)Pasteurization
Pasteurization is a process that employes relatively brief exposures to moderately high t
microorganisms. Pasteurization is used specially when the aim is to kill pathogenic organism
high-temperatures.

Since pasteurization does not kill all the microorganisms, it is necessary to store these produc
(HTST) method and low temperature long time (LTLT) method. The minimal heat treatment fo
seconds in the HTST method. Grape wines may be pasteurized for one minute at 81 to 850C a

Spoilage of Cannel Foods

Canned foods may spoil either due to biological or chemical reasons. We would discuss only th

Biological spoilage of canned foods

biological spoilage of canned foods occurs due to the action of various microorganisms. Spore
food spoiling microorganisms because of their heat resistant nature (thermophilic nature). In
through the leakage of the container during cooling and spoil the food. In this way, we can div
(a) Biological spoilage by thermophilic bacteria
Underprocessing of canned foods results in spoilage by thermophilic bacteria, the bacteria tha

(i) Flat sour spoilage. In canned foods, production of acid and no gas is referred to as flat s
spoilage because no gas is produced, i.e., the can remains flat. Thus, the spoilage cannot be d
coagulans and B. stearothermophilus resulting in sour, abnormal odour, sometimes cloudy liq

(ii) Thermophilic anaerobic (TA) spoilage. Clostridium thermosaccharolyticum, Yo

an obligate thermophile, causes spoilage. The can swells and may burst due to
production of CO2 and H2. The food becomes fermented sour, cheesy, and
develops butyric odour.

(iii) Sulfide spoilage. Clostridium nigricans is involved in this spoilage. It produces

H2S gas which is absorbed by the food product. The latter becomes usually
blackened and gives “rotten egg” odour

(iv) Putrefactive anaerobic spoilage. Clostridium sporogenes causes spoilage through put
food. The latter develops

(v) Aerobic sporeformer’s spoilage. Bacillus spp.,the aerobic bacteria, cause

(b) Biological spoilage

Bacillus spp., Clostridium spp., yeasts, and other fungi which are mesophilic(an organism gro
of canned food spoilage. As stated earlier, these organisms enter through the leakage of the c

Clostridium butyricum and C. pasteurianum result in butyric acid type of fermentation in

acidic (tomato juice, fruits, fruit juices, etc.) or medium acidic (corn, peas, spinach, etc.)
food with swelling of the container due to the production of CO2 and H2.

Bacillus subtilis and B. mesenteroides have been reported as spoiling canned sea-foods,
meats, etc. Other mesophilic bacteria which have been reported in cans are Bacillus
polymixa, B.macerans, Streptococcus sp., Pseudomonas, Proteus, etc. Yeasts and moulds
have also been found present in canned foods. Yeasts result in CO 2 production and swelling
of the cans.

Types of Food-Spoilage and Concerned Microorganisms

Spoilage of Noncanned Foods

Food Type of Important Microorganisms Involved

spoilage
Fresh Fruits and Soft rot Rhizopus nigricans, Erwinia carotovera, Pseudononas
vegetables Black mould spp.
 not Aspergillus niger

Gray mould rot Botrytis cinerea

Blue mould rot Penicillium italicum

Pickles Pink yeasts Rhodotorulla

Black pickles Bacillus nigricans

Soft pickles Bacillus spp.

Sugar products, Ropy Yeasts Enterobacter aerogenes, Torula, Saccharomyces

Honey, Syrup Zygosaccharomyces
Moulds
Aspergillus, Penicillium
Pink
Micrococcus roseus
Green
Pseudomonas fluorescens

Concentrated Orange Off flavour Acetobacter, Lactobacillus Leuconostoc

juice
Bread Ropy Bacillus subtilis

Bloody Serratia marcescens

Moulds Aspergillus niger, Penicillium, Rhizopus nigricans

Fresh Meat Putrefaction Alcaligenes, Clostridium, Chromatobacterium,

Proteus vulgaris, Pseudomonas fluorescens
Souring
Chromatobacterium, Lactobacillus, Pseudononas

Cured Meat Mould Aspergillus, Penicillium, Rhizopus, Lactobacillus,

Greening Pediococcus, Streptococcus

Souring Slimy Micrococcus, Pseudomonas, Leuconostoc

Poultry Slimy Alcaligenes, Xanthomonas

 Odour Pseudomonas

Fish Putrefaction Discolouration Alcaligenes, Bacillus, Micrococcus,

Chromobacterium, Flavobacterium, Pseudomonas

Eggs Green rot Pseudomonas Fluorescens

Colourless rot Pseudomonas, Alcaligenes, Chromobacterium,

Coliform bacteria
Fungal rot
Cladosporium, Mucor, Penicillium, Sporotrichum
Black rot
Proteus

f(a) Chemical composition

(i) Foods rich in proteins are degraded by proteolytic
microorganisms. Proteins are degraded into its various components
due to the action of especially gram-negative, spore forming bacteria,
e.g., Proteus, Pseudomonas some cocci, etc.
Protein foods + Proteolytic microbes → Amino acids + Amines +
Ammonia (NH3) + Hydrogen sulfide (H2S)

(ii) Food rich in carbohydrates are degraded by carbohydrate

fermenting microorganisms, particularly yeasts and moulds. Bacteria
like Micrococcus, Leuconostoc, and Streptococcus can also degrade
carbohydrates.
Carbohydrate foods + Carbohydrate fermenting microorganisms →
Acids + Alcohols + Gases

You (iii) Food rich in fats are attacked by relatively few

r Ad Here microorganisms such as moulds and some gram-negative
bacteria. These microorganisms are, therefore, lipolytic
in nature.
Fatty food + Lipolytic microorganisms → Fatty acids +
Glycerol

(b) Acidity
Generally the fruits are acid foods (pH below 4.5) while
nearly all vegetables, fish, meats, and milk-products are
non-acid (pH above 4.5). Since the pH of the acid foods
(fruits) is sufficiently low, they do not allow bacterial
 growth and subsequent spoilage. They are spoiled mainly
by yeasts and moulds. contrary to this, non-acid foods
have sufficiently high pH and are spoiled mainly by
bacteria.

(c) Moisture and osmotic concentration Average 13%

free water is required in food for usual microbial growth.
This is the reason why the foods of high sugar salt
concentrations do not allow most of the microorganisms
to grow. But, specific microbial growths cannot be over-
ruled. 65-70% sugar concentration is required to prevent
mould-growth and 50% to prevent bacterial and yeast
growth

.
Contamination of Plant Food Products

Fruits and Vegetables

Fruits and Vegetables are generally contaminated by
bacteria including species of Bacillus, Enterobacter,
Lactibacillus, Leuconostoc, Pseudomonas, Sarcina,
Staphylococcus, Streptococcus, etc. Various moulds and
yeasts also inhabit the fruits and vegetables.

Fruits and Vegetables get rotten as a result of the microbial

degradation of pectin, the substance responsible for
maintaining the firmness and texture of fruits and
vegetable. Microbes produce pectin esterases and a
polygalacturonases enzymes that hydrolyze pectins
resulting in the formation of soft rots in fruits and
vegetables. 20% of the harvested crops of fruits and
vegetables are lost to spoilage mainly because of the
activities of bacteria and microfungi

Contamination through infection

Fruits and Vegetables are normally susceptible to bacterial, fungal and viral
infections. These infections invade the fruit and vegetable tissue during various
stages of their development and result in the subsequent spoilage.

Contamination through post-harvest handling

 Usually, mechanical handling of fruits and vegetables during post-harvest period
produce “breaks” in them which invite microbial invasion. Sine the pH of the fruits is
relatively acidic (i.e., high in sugar), they are more susceptible to fungi in contrast to
vegetables which are more susceptible to bacteria because of their pH being slightly
higher (5.0 to 7.0; less in sugar).

Cereals Your
Cereals and cereal products contain microorganisms from insects, soil Ad Here
and other sources. Bacillus, Lactobacillus, Micrococcus, Pseudomonas,
etc. are the bacteria which are generally found on freshly harvested
grains. Wheat flours are contaminated mostly by bacteria such as
species of Bacillus, Micrococcus, Sarcina, Serratia, coliforms, etc.
Moulds like Aspergillus, Penicillium, Rhizopus, Neurospora, Endomyces
are also very common

Treatment By Radiations

Gamma rays and high-energy electron beams

Gamma rays and high-energy electron beams have been used
the preservation of fresh perishable, canned, and packaged
foods. They have good penetration and are effective to a depth
of about 15cm in most foods. Food preservation by such
radiation dosage is called ‘cold sterilization’ as it produces only a
few degrees’ rise in temperature of the product.

Ultraviolet rays
Ultraviolet rays are short waves and are used to sterilize the surface of
foods. These rays have been successfully used for the treatment of water
for beverages, aging meats, packaging of sliced bacon, treatment of knives
for slicing bread, for sterilizing utensils, for prevention of spoilage by
organisms on the surface of preserved pickles, cheese and prevention of air
contamination. Cold-storage rooms of meat-processing plants are
sometimes equipped with germicidal lamps which reduce the surface
contamination and permit longer periods of spoilage-free storage.

Radiation pasteurization or sterilization represents a term You

which describes the killing of over 98% but no 100% of the r Ad Here
microorganisms by intermediate dosage of radiation. This
method increases the storage life of some meats, sea-foods,
certain fruits, and vegetables when stored at low temperatures.
Radiation pasteurization provides the possibility of an entirely
new approach to food preservation and could bring about a
radical change in industrial methods of food processing.
However, the effect of radiation on colour, flavour, nutritional
quality of food, odour, texture needs to be more carefully
understood. Similarly, chemical changes in food products
brought about by radiations may cause bad effects on animals
and human beings and need to be more adequately investigated

Microbial ‘Food Poisoning’ Or ‘Food Intoxications;

Bacterial ‘food poisoning’ (Bacterial food intoxications)

There are two major food poisoning or food intoxications caused by bacteria.
These are Botulism and Staphylococoal poisoning.

(a)Botulism
Botulism is caused by the ingestion of food containing the neurotoxin (toxin
that affects the nervous system) produced by Clostridium botulinum, an
anaerobic spore forming bacterium. Sixty to seventy per sent cases of
botulism die. There are 7 types (type A,B,C,D,E,F,G) of these neurotoxins
recognised on the basis of specificity. The neurotoxin of C.botulinum is a
protein. It has been purified and crystallized and is so powerful that only a
dose as low as 0.01 mg is said to be fatal to human beings. The toxin is
absorbed mostly in the small intestine and paralyzes the involuntary
muscles of the body.

Serological Types of Botulism Neurotoxins

Type A: It commonly causes botulism in the western part

of the United States and is more toxic than type B.

Type B: This type occurs more often then type A in most

soils of the world and is less toxic to human beings.

Type C: So far as is known, this type causes botulism of

cattle, fowls, and other animals but not of human beings.
Type D: This type has been reported causing forage
poisoning of cattle in South African countries.

Type E: This type has been obtained chiefly from fish and fish products and
is toxic for human beings.

Type F: This type has been isolated in Denmark and causes human
botoulism

Type G: It has recently been isolated from the soil in Argentina. It does not
concern with human botulism.

Source. The main sources of botulism are canned meat, fish, string beans,
sweet corn, beans, and other low medium acid foods. The foods implicated
are generally those of a type that have undergone some treatment intended
for the preservation of the product such as canning, pickling or smoking, but
one which failed to destroy the spores of this bacterium.

When the intended preservative treatment is inadequate and Your

is followed by storage conditions which permit the germination Ad Here
and growth of the microorganisms, one of the most lethal
toxins known to humanity is produced. The toxin has been
known to persist in foods for long periods, especially when
storage has been at low temperatures. It is unstable at pH
value above 6.8.

Temperature is considered to be the most important factor in

determining whether toxin production will take place and what
the rate of production will be. Various strains of C. Botulinum
types A and b vary in their temperature requirements; a few
strains grow at 10 to 110C. However, the lowest temperature
for germination of spores of the most of the strains is 150C and
maximum of 480C.
Symptoms. Symptoms generally occur within 12 to 36 hours after
consumption of the spoiled food. Early symptoms are digestive disturbances
followed by nausea, vomiting, diarrhoea together with dizziness and
headache. Double vision may occur early and there may be difficulty in
speaking. Mouth may become dry, throat constricted, tongue may get
swollen and coated. Involuntary muscles become paralysed and paralysis
spreads to the respiratory system and to the heart. Death normally results
from respiratory failure.

Your Prevention. Canned food should be properly processed by

Ad Here using approved heat processes. Food that has been cooked but
not well heated should be avoided. Raw foods and frozen foods
thawed and held at room temperature should be avoided.
Gassy and spoiled canned foods should be rejected. Boiling of
suspected food for at least 15 minutes is required.

Treatment. Successful treatment is by the administration of

polyvalent antitoxin in the early stages of infection. Once the
symptoms appear the treatment fails to prove useful.

(b) Staphylococcal-poisoning
This is the most common type of food-poisoning caused due to the food
contaminated with a potent toxin, namely, enterotoxin. This toxin is
produced by certain strains of Staphylococcus aureus. A sudden onset of
illness starts usually within 3 to 6 hours after ingestion of the contaminated
food.

Source. These bacteria are commonly present on the skin, nose and other
parts of human body. People who handle foods carelessly usually transfer
them to the food. Foods most commonly contaminated involve those which
are eaten cold, e.g., cold meat, poultry, salads, bakery products, etc.

Symptoms. As said earlier, the disease starts within 3 to 6 hours after

ingestion of the contaminated food and is manifested by nausea, vomiting,
abdominal pain and diarrhoea within 24 to 48 hours. If the case becomes
severe, dehydration and collapse may follow. However, in usual conditions
death is rare.

Control. The disease can be controlled by preventing the entry of the

bacteria to food. It is important that all susceptible foods are kept under
refrigeration to restrict the growth of the bacteria; and also by the
destruction of the bacteria by heat.

Fungal Food-poisoning (Mycointoxications)

Mycotoxins are chemical substances produced by a variety
of fungi, e.g., aspergilli, penicillin, Rhizopus, Fusarium
spp., and mushrooms. The illness that results from the
ingestion of foods containing fungal toxins is called
‘mycotoxicosis’. Mycologists have come to discover a
number of Mycotoxins which have proved extremely
harmful, sometimes lethal to animals and human beings.
Important ones are as follows

(a)Aflatoxins
Aflatoxins are one of the most potent mycotoxins produced by Aspergillus
flavus and related strains. It has been found that about 60% strains of a.
flavus produce this toxin. This discovery of Aflatoxins is comparatively of
recent origin. In 1960, about 100,000 Turkey poults dies in England within
few months. It was found that the peanut meal such peanut meal was found
toxic and was named ‘aflatoxin’. However, some other fungi, e.g.,
Aspergillus niger, A . oryzae, A. ochraceus, Penicillium citrinum, etc. have
also been reported to produce aflatoxins. So the name aflatoxin is now
generally used for a number of related toxins. Aflatoxins occupy the most
important position among mycotoxins because of their potent carcinogenic
nature and high frequency of occurrence in nature. More specifically,
aflatoxin B1 is one of the most potent aflatoxins. They are responsible for
liver cancer in laboratory animals and even human beings.

(b) Amatoxins and Phallotoxins Your

These two mycotoxins are considered to be produced by the Ad Here
mushroom Amanita phalloides, the so called death cap. This
mushroom is deadly poisonous and almost about 90 to 95%d
deaths of mushroom-eaters in Europe have been due to eating
of this fungus. These two mycotoxins are chemically
cyclopeptides. According to Lincoff and Mitchel (1977) the
most potent amatoxins are α-amanitin and β-amanitin while
the phallodin is the most potent phallotoxin. However, studies
revel the fact that these are the amatoxins which are strongly
poisonous comparatively, and are responsible for producing
hypoglycemia, liver-distrophy and kidney-failure leading to the
death of the victim.

(c) Coprine
This mycotoxin is through to be present in an edible mushroom, namely,
Coprinus atramentanius. This chemical becomes toxic and results in
gastrointestinal upsets and other physical discomforts when the mushroom-
eating is accompanied with alcohol.

(d) Gyromitrin
Gyromitrin (monomethylhydrazine) is deadly poisonous mycotoxin reported
to be present in the fruiting bodies (basidiomata) of saddle fungi (Helvella
spp,) and fales morels (Gyromitra spp.). This toxin is water soluble. It is
through that if the fruiting bodies be parboiled two or three times and the
liquid discarded, the mushrooms become safe to eat.

(e) Ochratoxins
Yo Ochratoxin was first isolated from the filrates as Aspergillus ochraceus
ur Ad
and is now produced by a number of Aspergillus and Penicillium spp.,
Here
with Penicillium viridicatum being the dominating producer. These
mycotoxins represent a group of closely related derivatives of
isocoumarin linked to L-β-phenylalanine, an amino acid, and are
reported mainly in temperate area of North America and Europe.
Ochratoxins occur mainly in grains but have also been reported in
coffee, beans and peanuts, and are toxic to ducklings, chicks and
rates.

(f) Trichothecenes
Trichothecenes are produced by the species of Fusarium, Cephalosporium,
Myrothecium, Trichoderma and Stachybotrys. Out of 30 known
trichothecenes, T-2 toxin, nivalenol and Deoxynivalenol are of common
occurrence, and cause a hyperestrogenic syndrome, haemorrhage and
sometimes abortion in swine.

(g) Zearalenone
This mycotoxin is produced by a number of Fusarium
spp.,e.g.,F.graminearum and F.moniliforme. It occurs predominantly in
maize and is similar to trichothecenes in its effects

Algal food-poisoning (Phycointoxications)

Fish or Shelfish, e.g. Calms, Scallps, Mussles, etc.ingest algae such as
Gymnodynium, Gonyaulax and others. These algae are toxic and result in
fish poisoning in humans. Shelfish harvested on large scales are routinely
assayed to check whether these toxic alga are present in them or not

Food Infections

Bacterial Food Infections

(a) Salmonellosis
This disease is caused through the ingestion of
Salmonella bacteria present in food. A large number of
species and serotypes are involved. An inoculum of
about 600,500 cells is required to become established
and cause illness in the host. These bacteria are gram-
negative, non-spore forming rods and motile by
means of peritrichous flagella. Various species of
Salmonella get ingested with improperly cooked eggs.
Puddings and meat that have been contaminated by
the carries. The carriers may be cats, dogs, chickens,
and others

The disease appears through gastrointestinal infections as a result of the

growth of bacteria in the intestine. Typical symptoms of salmonellosis are
nausea, vomiting, abdominal pain, and diarrhoea. Generally the symptoms
persist for 2 to 4 days. The incubation period ranges between 4 to 36 hours.
Salmonellosis can be prevented by avoiding consumption of contaminated
food, by heat destruction of the bacteria, or by refrigeration to check the
growth of bacteria.

(b) Perfringens poisoning

The disease caused by the strains of Clostridium perfringens (=C.welchii) is
called ‘perfringens poisoning or more technically, Clostridium perfringers-
gastroenteritis’.

This bacterium is a grampositve, anaerobic, non-motile, spore Your

former with an optimum growth temperature of 37-430C. This Ad Here
disease has been caused by the ingestion of prepared meat,
meat products, and poultry. Generally, the meat that has been
cooked and allowed to cool slowly before consumption allows
the growth of these microorganisms. What happens is that the
cooking destroys only the vegetative cells not the spores. The
latter survive the heating applied during cooking and later
germinate into vegetative cells. It could be avoided by adequate
refrigeration of the food.

Symptoms. Symptoms appear in the form of diarrhoea, acute

abdominal pain and , rarely, vomiting when the growth of
microorganisms takes place in the human intestine. Disease
manifestation occurs between 8 to 22 hours after the
contaminated food has been taken.

Prevention. Prevention of the disease includes rapid cooling of cooked

meats and other foods and reheating of the remaining food before further
consumption.

(c) Bacillus cereus gastroenteritis

Bacillus cereus is a gram-positive, aerobic, rod-shaped, spore-forming
bacterium that causes food infections called’ gastroenteritis’. Its spores are
heat resistant and remain viable even after considerable degree of cooling;
they germinate and produce vegetative cells later. It is believed that the
bacterial cells undergo lysis in the intestinal tract and release enterotoxin.

Your Ad (d) Escherichia coli gastroenteritis

Here Escherichia coli bacterium is generally regarded as a part
of the natural flora of the human and animal intestinal
tract. In recent years, however, various serotypes of this
bacterium have been thought responsible for human and
animal diarrhoeal diseases. These bacteria can be
classified into two groups:one group representing
enteropathogenic E. coli and the other representing
enterotoxin producing E.coli.

The enteropathogenic E.coli are pathogenic within the intestinal tract. They
have ability to penetrate epithelial cells of the intestinal mucosa, cause
epithelial necrosis and ulceration resulting in the presence of red blood cells
and large number of neutrophils in the stood during dysentery. This acute
gastroenteritis (dysentery-like syndrome)is generally reported in the new-
born and in infants upto two years of age.

The enterotoxin producing E.coli fail to invade the intestinal mucosa but
release an enterotoxin which causes diarrhoea-like syndrome. The latter
refers to a profuse watery discharge generally from the small intestine. Since
these bacteria do not penetrate and cause epithelial necrosis, red blood cells
and neutrophils are not present in the diarrhoeal stool.

Foods which are highly contaminated or inadequately preserved allow the

growth of such E. coli serotypes. The latter are heat sensitive and can be
destroyed by pasteurization or by proper cooking methods.

(e) Cholera
This disease appearing in this subcontinent is generally called ‘asiatic cholera’
and is caused by Vibrio cholerae had has been the cause of untold sufferings
and death. The symptoms include vomiting and profuse diarrheal (rice-
water) stools which result in mineral deficiency, dehydration and increased
blood acidity of the body tissues leading, finally, to death.

Vibrio cholerae is a gram-positive, uniflagellate bacterium and is transmitted

through contaminated files, water, raw and exposed foods, etc. They find
their way through mouth into the intestines and produces endotoxins which
disintegrate the epithelial cells of the intestines. Death rate is rather high and
course of the disease may be as short as 12 hours after the onset of the first
sysmptoms. The individuals recovering from infections are said to be
effective in controlling the disease. Cholera patients should be kept in
quarantine and all materials contaminated by faeces burnt for checking
infection spread

Non-bacterial Food Infections

(a) Amoebiasis
Entamoeba histolytica is the most important of various protozoa that cause
intestinal diseases. These protozoa are transmitted from person to person
through infected food and water, by direct contact, and by flies. This disease
can be controlled by recognizing the chronic cases from which infective cysts
of the amoeba may be transmitted and by proper sanitation and personal
hygiene

(b) Viral Food Infections

Several viruses are known to be transmitted through food and water and
cause infection in humans and animals. For instance, poliomyelitis is
reported to be a food-borne viral infection carried through milk, Hepatitis
virus is carried through sewage contaminated water and sea-foods causing
‘viral hepatitis’, a common acute systemic infectious disease chiefly affecting
the liver that results in ‘jaundice’.

Bread
Flours and meals for the preparation of bread are usually
made from wheat or rye, occasionally from maize or
barley. They are all high in starch, and the first two
contain a considerable proportion of protein, commonly
designated as ‘gluten’. In addition, there are traces of
sugar and some diastase. Flour is mixed with water to
form a dough. For some type of bread, little sugar is also
added

The series of changes which occur in the flour and other

constituents of the dough before baking into bread is
termed ‘panary fermentation’. An alcoholic fementationa
by yeast is an essential step in the production of bread;
this process is known as the leavening of bread’. A product
of action of microorganisms is involved in the production
of bread

There are three basic types of rising breads:

White or common bread. In this bread preparation the moistened flour is

mixed with yeast, Saccharomyces cerevisiae, and is allowed to stand for
several hours in a warm place. Flour itself contains little free sugar, but
there are sufficient quantities of starch splitting enzymes in it to produce
some sugar during the leavening process. The sugar is rapidly fermented by
the yeast with the production of alcohol and carbon dioxide, the latter
causing the rising of the bread. During the baking process the alcohol is
driven off

Sour bread. This bread is a sour dough, from which a ‘starter’ Your
is saved to inoculate the next batch. The organisms appear to Ad Here
be Escherichia coli and Enterobacter species which produce a
mixed lactic acid fermentation, i.e., accompanying the gas there
is always some lactic acid which tends to make the bread taste
sour

Salt-rising bread. This type of bread is dependent upon the

spontaneous fermentation by (probably) wild yeasts and
common contaminating bacteria, E.coli and Enterobacter types.
In this case, salt is added to the bread which cuts down some of
the extraneous contamination and allows the bread to rise
during fermentation

Common Adulterants/Contaminants
in food and Simple screening tests for their detection

Adulteration in food is normally present in its most crude form, prohibited

substances are either added or partly or wholly substituted. In India normally the
contamination/adulteration in food is done either for financial gain or due to carelessness and lack
in proper hygienic condition of processing, storing, transportation and marketing. This ultimately
results that the consumer is either cheated or often become victim of diseases. Such types of
adulteration are quite common in developing countries or backward countries. However,
adequate precautions taken by the consumer at the time of purchase of such produce can make
him alert to avoid procurement of such food. It is equally important for the consumer to know the
common adulterants and their effect on health.

Injurious Adulterants/Contaminants in Foods and their Health Effects

S.No Adulterant Foods Commonly Diseases or Health

Involved Effects
Adulterants in food
1 Argemone seeds Mustard seeds Epidemic dropsy,
Argemone oil Edible oils and fats Glaucoma,
Cardiac arrest
2 Artificially coloured foreign seeds As a substitute for Injurious to health
cumin seed,
Poppy seed, black
pepper
3 Foreign leaves or exhausted tea Tea Injurious to health, cancer
leaves, saw dust artificially
coloured
4 TCP Oils Paralysis
5 Rancid oil Oils Destroys vitamin A and E
6 Sand, marble chips, stones, filth Food grains, pulses Damage digestive tract
etc.
7 Lathyrus sativus Khesari dal alone or Lathyrism (crippling spastic
Mixed in other pulses paraplegia)
Chemical Contamination
8 Mineral oil (white oil, petroleum Edible oils and fats, Cancer
fractions) Black pepper
9 Lead chromate Turmeric whole and Anemia, abortion,
 powdered, mixed paralysis, brain damage
spices
10 Methanol Alcoholic liquors Blurred vision, blindness,
death
11 Arsenic Fruits such as apples Dizziness, chills, cramps,
sprayed over with lead paralysis, death
arsenate
12 Barium Foods contaminated by Violent peristalisis, arterial
rat poisons (Barium hypertension, muscular
carbonate) twitching, convulsions,
cardiac disturbances
13 Cadmium Fruit juices, soft drinks, ‘Itai-itai (ouch-ouch)
etc. in contact with disease, Increased
cadmium plated salivation, acute gastritis,
vessels or equipment. liver and kidney damage,
Cadmium prostrate cancer
contaminated water
and shell-fish
14 Cobalt Water, liquors Cardiac insufficiency and
mycocardial failure
15 Lead Water, natural and Lead poisoning (foot-drop,
processed food insomnia, anemia,
constipation, mental
retardation, brain damage)

16 Copper Food Vomiting, diarrhoea

17 Tin Food Colic, vomiting
18 Zinc Food Colic, vomiting
19 Mercury Mercury fungicide Brain damage, paralysis,
treated seed grains or death
mercury contaminated
fish

NOTE : Safe limits have been prescribed for above metals in different
food. Continuous use of food contaminated with these metals beyond
safe limits may cause these diseases
Bacterial
contaminati
on
20 Bacillus cereus Cereal products, Food infection (nausea,
custards, puddings, vomiting, abdominal pain,
sauces diarrhoea)
21 Salmonella spp. Meat and meat Salmonellosis (food
products, raw infection usually with fever
vegetables, salads, and chills)
shell-fish, eggs and
egg products, warmed-
up leftovers
22 Shigella sonnei Milk, potato, beans, Shigellosis (bacillary
 poultry, tuna, shrimp, dysentery)
moist mixed foods
23 Staphylococcus aureus Dairy products, baked Increased salivation,
foods especially vomiting, abdominal cramp,
Entero-toxins-A,B,C,D or E custard or cream-filled diarrhoea, severe thirst,
foods, meat and meat cold sweats, prostration
products, low-acid
frozen foods, salads,
cream sauces, etc.
24 Clostridium botulinus toxins Defectively canned low Botulism (double vision,
or medium-acid foods; muscular paralysis, death
A,B,E or F meats, sausages, due to respiratory failure)
smoked vacuum-
packed fish, fermented
food etc.
25 Clostridium.perfringens Milk improperly Nausea, abdominal pains,
processed or canned diarrhoea, gas formation
(Welchii) type A meats, fish and gravy
stocks
26 Diethyl stilbestrol (additive in Meat Sterlites, fibroid tumors etc.
animal feed)
27 3,4 Benzopyrene Skoked food Cancer
28 Excessive solvent residue Solvent extracted oil, Carcinogenic effect
oil cake etc.
29 Non-food grade or contaminated Food Blood clot, angiosarcoma,
packing material cancer etc.
30 Non-permitted colour or Coloured food Mental retardation, cancer
permitted food colour and other toxic effect.
beyond safe limit
31 BHA and BHT beyond safe limit Oils and fats Allergy, liver damage,
increase in serum
chloresterol etc.
32 Monosodium glutamate(flour) Chinese food, meat Brain damage, mental
(beyond safe limit) and meat products retardation in infants
33 Coumarin and dihydro coumarin Flavoured food Blood anticoagulant
34 Food flavours beyond safe limit Flavoured food Chances of liver cancer
35 Brominated vegetable oils Cold drinks Anemia, enlargement of
heart
36 Sulphur dioxide and sulphite In variety of food as Acute irritation of the
beyond safe limit preservative gastro-intestinal tracts etc.
37 Artificial sweetners beyond safe Sweet foods Chances of cancer
limit

Fungal
contaminati
on
38 Aflatoxins Aspergillus flavus- Liver damage and cancer
contaminated foods
such as groundnuts,
cottonseed, etc.
39 Ergot alkaloids from Claviceps Ergot-infested bajra, Ergotism (St.Anthony’s fire-
purpurea Toxic alkaloids, rye meal or bread burning sensation in
 ergotamine, ergotoxin and extremities, itching of skin,
ergometrine groups peripheral gangrene)
40 Toxins from Grains (millet, wheat, Alimentary toxic
oats, rye,etc) aleukia(ATA) (epidemic
Fusarium sporotrichioides panmyelotoxicosis)
41 Toxins from Fusarium Moist grains Urov disease (Kaschin-
sporotrichiella Beck disease)
42 Toxins from Yellow rice Toxic mouldy rice disease

Penicillium inslandicum
Penicillium atricum,
Penicillium citreovirede,
Fusarium, Rhizopus,
Aspergillus
43 Sterigmatocystin from Foodgrains Hepatitis

Aspergillus versicolour
Aspergillus nidulans and bipolaris
44 Ascaris lumbricoides Any raw food or water Ascariasis
contaminated by
human faces
containing eggs of the
parasite
45 Entamoeba histolytica Raw vegetables and Amoebic dysentery
fruits
Viral

46 Virus of infectious Shell-fish, milk, Infectious hepatitis

unheated foods
Hepatitis (virus A) contaminated with
faeces, urine and blood
of infected human
47 Machupo virus Foods contaminated Bolivian haemorrhagic
with rodents urine, fever
such as cereals

Natural
Contaminati
on
48 Flouride Drinking water, sea Excess fluoride causes
foods, tea, etc. fluorosis (mottling of teeth,
skeletal and neurological
disorders)
49 Oxalic acid Spinach, amaranth, Renal calculi, cramps,
etc. failure of blood to clot
50 Gossypol Cottonseed flour and Cancer
cake
51 Cyanogenetic compounds Bitter almonds, apple Gastro-intestinal
seeds, cassava, some disturbances
beans etc.
52 Polycyclic Aromatic Smoked fish, meat, Cancer
 mineral oil-
contaminated water,
Hydrocarbons(PAH) oils, fats and fish,
especially shell-fish
53 Phalloidine (Alkaloid) Toxic mushrooms Mushroom poisoning
(Hypoglycemia,
convulsions, profuse
watery stools, severe
necrosis of liver leading to
hepatic failure and death)
54 Solanine Potatoes Solanine poisoning
(vomiting, abdominal pain,
diarrhoea)
55 Nitrates and Nitrites Drinking water, spinach Methaemoglobinaemia
rhubarb, asparagus, especially in infants, cancer
etc. and meat products and tumours in the liver,
kidney, trachea
oesophagus and lungs.
The liver is the initial site
but afterwards tumours
appear in other organs.
56 Asbestos (may be present in Polished rice, pulses, Absorption in particulate
talc, Kaolin, etc. and in processed foods form by the body may
processed foods) containing anti-caking produce cancer
agents, etc.
57 Pesticide residues (beyond safe All types of food Acute or chronic poisoning
limit) with damage to nerves and
vital organs like liver,
kidney, etc.
58 Antibiotics (beyond safe limit) Meats from antibiotic- Multiple drug resistance
fed animals hardening of arteries, heart
disease

Simple Screening test for Detecting Adulteration in Common Food

S.No Food article Adulteration Test

1 Vegetable oil Castor oil Take 1 ml. of oil in a clean dry test tube. Add 10
ml. Of acidified petroleum ether. Shake
vigorously for 2 minutes. Add 1 drop of
Ammonium Molybdate reagent. The formation
of turbidity indicates presence of Castor oil in
the sample.
Argemone oil Add 5 ml, conc. HNO3 to 5 ml.sample. Shake
carefully. Allow to separate yellow, orange
yellow, crimson colour in the lower acid layer
indicates adulteration.
2 Ghee Mashed Potato Boil 5 ml. Of the sample in a test tube. Cool and
Sweet Potato, etc. a drop of iodine solution. Blue colour indicates
presence of Starch. colour disappears on
 boiling & reappears on cooling.
Vanaspati Take 5 ml. Of the sample in a test tube. Add 5
ml. Of Hydrochloric acid and 0.4 ml of 2%
furfural solution or sugar crystals. Insert the
glass stopper and shake for 2 minutes.
Development of a pink or red colour indicates
presence of Vanaspati in Ghee.
Rancid stuff (old Take one teaspoon of melted sample and 5 ml.
ghee) Of HCl in a stoppered glass tube. Shake
vigorously for 30 seconds. Add 5 ml. Of 0.1% of
ether solution of Phloroglucinol. Restopper &
shake for 30 seconds and allow to stand for 10
minutes. A pink or red colour in the lower(acid
layer) indicates rancidity.
Synthetic Pour 2 gms. Of filtered fat dissolved in ether.
Colouring Matter Divide into 2 portions. Add 1 ml. Of HCl to one
tube. Add 1 ml. Of 10% NaOH to the other
tube. Shake well and allow to stand. Presence
of pink colour in acidic solution or yellow colour
in alkaline solution indicates added colouring
matter.
3 Honey Invert 1. Fiehe’s Test: Add 5 ml. Of solvent ether to
sugar/jaggery 5 ml. Of honey. Shake well and decant the
ether layer in a petri dish. Evaporate
completely by blowing the ether layer. Add 2
to 3 ml. Of resorcinol (1 gm. Of resorcinol
resublimed in 5 ml. Of conc. HCl.)
Appearance of cherry red colour indicates
presence of sugar/jaggery.
2. Aniline Chloride Test : Take 5 ml. Of honey
in a porcelain dish. Add Aniline Chloride
solution (3 ml of Aniline and 7 ml. Of 1:3
HCl) and stir well. Orange red colour
indicates presence of sugar.

4. Pulses/Besan Kesari Add 50 ml. Of dil.HCl to a small quantity of dal

dal(Lathyrus and keep on simmering water for about 15
sativus) minutes. The pink colour, if developed indicates
the presence of Kesari dal.
5 Pulses Metanil Add conc.HCl to a small quantity of dal in a little
Yellow(dye) amount of water. Immediate development of
pink colour indicates the presence of metanil
yellow and similar colour dyes.
Lead Chromate Shake 5 gm. Of pulse with 5 ml. Of water and
add a few drops of HCl. Pink colour indicates
Lead Chromate.
6 Bajra Ergot infested Swollen and black Ergot infested grains will turn
Bajra light in weight and will float also in water
7 Wheat flour Excessive sand & Shake a little quantity of sample with about 10
dirt ml. Of Carbon tetra chloride and allow to stand.
Grit and sandy matter will collect at the bottom.
Excessive bran Sprinkle on water surface. Bran will float on the
surface.
Chalk powder Shake sample with dil.HCl Effervescence
indicates chalk.
8 Common spices Colour Extract the sample with Petroleum ether and
like Turmeric, add 13N H2SO4 to the extract. Appearance of
chilly, curry red colour (which persists even upon adding
powder,etc. little distilled water) indicates the presence of
added colours. However, if the colour
disappears upon adding distilled water the
sample is not adulterated.
9 Black Pepper Papaya Pour the seeds in a beaker containing Carbon
seeds/light tetra-chloride. Black papaya seeds float on the
berries, etc. top while the pure black pepper seeds settle
down.
10 Spices(Ground) Powdered bran Sprinkle on water surface. Powdered bran and
and saw dust sawdust float on the surface.
11 Coriander powder Dung powder Soak in water. Dung will float and can be easily
detected by its foul smell.
Common salt To 5 ml. Of sample add a few drops of silver
nitrate. White precipitate indicates adulteration.
12 Chillies Brick powder grit, Pour the sample in a beaker containing a
sand, dirt, filth, mixture of chloroform and carbon tetrachloride.
etc. Brick powder and grit will settle at the bottom.
13 Badi Elaichi seeds Choti Elaichi Separate out the seeds by physical
seeds examination. The seeds of Badi Elaichi have
nearly plain surface without wrinkles or streaks
while seeds of cardamom have pitted or
wrinkled ends.
14 Turmeric Powder Starch of maize, A microscopic study reveals that only pure
wheat, tapioca, turmeric is yellow coloured, big in size and has
rice an angular structure. While foreign/added
starches are colourless and small in size as
compared to pure turmeric starch.
15 Turmeric Lead Chromate Ash the sample. Dissolve it in 1:7 Sulphuric
acid (H2SO4) and filter. Add 1 or 2 drops of
0.1% dipenylcarbazide. A pink colour indicates
presence of Lead Chromate.
Metanil Yellow Add few drops of conc.Hydrochloric acid (HCl)
to sample. Instant appearance of violet colour,
which disappears on dilution with water,
indicates pure turmeric. If colour persists
Metanil yellow is present.
16 Cumin seeds Grass seeds Rub the cumin seeds on palms. If palms turn
(Black jeera) coloured with black adulteration in indicated.
charcoal dust
17 Asafoetida(Heeng) Soap stone, other Shake a little quantity of powdered sample with
earthy matter water. Soap stone or other earthy matter will
settle at the bottom.
Chalk Shake sample with Carbon tetrachloride (CCl4).
Asafoetida will settle down. Decant the top
layer and add dil.HCl to the residue.
Effervescence shows presence of chalk.
18 Foodgrains Hidden insect Take a filter paper impregnated with Ninhydrin
infestation (1% in alcohol.) Put some grains on it and then
fold the filter paper and crush the grains with
hammer. Spots of bluish purple colour indicate
presence of hidden insects infestation
.

Table 1. Upper limit of grain moisture content for safe storage.

Commodity Moisture content

(% wet basis)
Paddy, rice (raw) 14
Rice (Parboiled) 15
Wheat Kabuligrun, Bengal gram 12
Sorghum, maize, barley, ragi, bajra, pulse, 12.5
turmeric, wheat atta maida besan
Coriander, chillies 10
Groundnut pods 6-7
Mustard seed 5-6

Source Agricultural Engineering Directory 1983

References

Appropriate production practices, careful harvesting,

and proper packaging, storage, and transport all
contribute to good produce quality. This publication
covers postharvest practices suitable for small-scale
operations, and points out the importance of production
and harvesting techniques for improving quality and
storability. Various methods for cooling fresh produce
are discussed, and resources are listed for further information, equipment, and supplies.

Table of Contents

• Introduction

• Production Practices

• Harvest Handling
Some further tips for postharvest handling of lettuce and other leafy greens: package in
breathable or perforated plastic bags; refrigerate at 33º F; carry to market in a portable cooler,
either refrigerated or with ice, and keep in the cooler until ready to display. If displaying
unwrapped heads at a farmers' market, mist occasionally with cold water.

Ethylene

Ethylene, a natural hormone produced by some fruits as they ripen, promotes additional
ripening of produce exposed to it. The old adage that one bad apple spoils the whole bushel is
true. Damaged or diseased apples produce high levels of ethylene and stimulate the other
apples to ripen too quickly. As the fruits ripen, they become more susceptible to diseases.

Ethylene "producers" should not be stored with fruits, vegetables, or flowers that are sensitive
to it. The result could be loss of quality, reduced shelf life, and specific symptoms of injury.
Some examples of ethylene effects include:

• russet spotting of lettuce along the midrib of the leaves;

• loss of green color in snap beans;

• increased toughness in turnips and asparagus spears;

• bitterness in carrots and parsnips;

• yellowing and abscission of leaves in broccoli, cabbage, Chinese cabbage, and

cauliflower;
• accelerated softening of cucumbers, acorn and summer squash;

• softening and development of off-flavor in watermelons;

• browning and discoloration in eggplant pulp and seed;

• discoloration and off-flavor in sweet potatoes;

• sprouting of potatoes;

• increased ripening and softening of mature green tomatoes (8); and

• shattering of raspberries and blackberries. (2)

Ethylene producers include apples, apricots, avocados, ripening bananas, cantaloupes,

honeydew melons, ripe kiwifruit, nectarines, papayas, passionfruit, peaches, pears,
persimmons, plantains, plums, prunes, quinces, and tomatoes. (14) Produce that is sensitive to
ethylene is indicated in Appendix I.

Mixed loads

When different commodities are stored or transported together, it is important to combine only
those products that are compatible with respect to their requirements for temperature, relative
humidity, atmosphere (oxygen and carbon dioxide), protection from odors, and protection from
ethylene. (4)

In regard to cross-transfer of odors, combinations that should be avoided in storage rooms

include: apples or pears with celery, cabbage, carrots, potatoes, or onions; celery with onions
or carrots; and citrus with any of the strongly scented vegetables. Odors from apples and
citrus are readily absorbed by meat, eggs, and dairy products. Pears and apples acquire an
unpleasant, earthy taste and odor when stored with potatoes. It is recommended that onions,
nuts, citrus, and potatoes each be stored separately. (4)

Storage crops

What about the crops that will not be transported and marketed fresh after harvest? Growers
can extend their selling season into the winter months by growing root crops and other
vegetables and fruits suited for long-term storage. The challenge is in keeping quality high by
creating and maintaining the correct storage environment. As Growing for Market editor Lynn
Byczynski notes,

Most storage crops require low temperatures and high humidity, two factors that don't come
together easily. Several others require low humidity and low temperatures. And then there are
a few that fall in between. Root crops such as beets, carrots, turnips, rutabagas, and leeks
store best at 32º F and 90 percent humidity. Potatoes prefer temperatures of 40-60º F and 90
percent humidity. Onions and garlic like it cool—32º—but require less humidity—about 65-75
percent. Winter squash prefer temperatures of 50-60º F, but dry. That's four different types of
storage for vegetables that will hold a month or more: cold and humid; cold and dry; cool and
humid; cool and dry. (10)

The two structural options for storage of these crops are coolers and root cellars. Byczynski
provides an example of a farm using both: "The Seelys have a bank barn, which has the
bottom floor built into a hillside…They have built both coolers and a dry storage room into the
lower floor to provide different combinations of temperature and humidity for the vegetables
they store." Coolers used for root crop storage will require water added to the air and regular
monitoring of the humidity level (see discussion under Preventing moisture loss above.) Some
growers have used concrete basements of houses, closed off from heat and with ventilation to
let in cold winter air, as root cellars. Another idea is to bury a big piece of culvert under a
hillside. (10)

Whatever the method, only "perfect" produce is suitable for long-term storage, so careful
inspection is critical. Any damaged produce is going to spoil and induce spoilage in the rest of
the crop. Byczynski advises growers to "either rub off soil and leave the crops somewhat dirty,
or wash them and let them dry thoroughly before putting them in storage. With onions, garlic,
 winter squash, pumpkins and sweet potatoes, it's important that they be cured thoroughly
before storage" (10).

Back to top

Conclusion

Postharvest handling is the final stage in the process of producing high quality fresh produce.
Being able to maintain a level of freshness from the field to the dinner table presents many
challenges. A grower who can meet these challenges will be able to expand his or her
marketing opportunities and be better able to compete in the marketplace. This document is
intended to serve as an introduction to the topic and a resource pointer; the grower is advised
to seek out more complete information from Extension and other sources.

Back to top

Appendix I

Storage Conditions for Vegetables and Fruits

Temperature % Relative Precooling Storage Ethylene

F humidity Method Life Days sensitive

Apples 30—40 90-95 R,F,H 90-240 Y

Apricots 32 90-95 R,H 7-14 Y

Asparagus 32-35 95-100 H,I 14-21 Y

Avocados 40-55 85-90 14-28 Y

Bananas 56-58 90-95 7-28 Y

Beans, snap 40-45 95 R,F,H 10-14 Y

Beans, lima 37-41 95 7-10

Beets, root 32 98-100 R 90-150

Blackberries 31-32 90-95 R,F 2-3

Blueberries 31-32 90-95 R,F 10-18

Broccoli 32 95-100 I,F,H 10-14 Y

Brussels sprouts 32 95-100 H,V,I 21-35 Y

Cabbage 32 98-100 R,F 90-180 Y

Cantaloupe 36-41 95 H,F 10-14 Y

Carrots, topped 32 98-100 I,R 28-180 Y

Cauliflower 32 90-98 H,V 20-30

Celery 32 98-100 I 14-28 Y

Cherries, sweet 30-31 90-95 H,F 14-21

Corn, sweet 32 95-98 H,I,V 4-6

Cranberries 36-40 90-95 60-120

Cucumbers 50-55 95 F,H 10-14 Y

Eggplant 46-54 90-95 R,F 10-14 Y

Endive 32 90-95 H,I 14-21 Y

Garlic 32-34 65-75 N 90-210

Grapefruit 50-60 85-90 28-42

Grapes 32 85 F 56-180

Kiwifruit 32 95-100 28-84 Y

Leeks 32 95-100 H,I 60-90 Y

Lemons 50-55 85-90 30-180

Lettuce 32 85-90 H,I 14-21 Y

Limes 48-50 85-90 21-35

Mushrooms 32 95 12-17

Nectarines 31-32 95 F,H 14-18 Y

Okra 45-50 90-95 7-14

Onions, bulb 32 65-70 N 30-180

Onions, green 32 95-100 H,I 7-10

Oranges 32-48 85-90 21-56

Peaches 31-32 90-95 F,H 14-28 Y

Pears 32 90-95 F,R,H 60-90 Y

Peas, in pods 32 95-98 F,H,I 7-10 Y

Peppers, bell 40-55 90-95 R,F 12-18 Y

Peppers, hot 45-50 60-70 R,F 14-21 Y

Pineapple 45-55 85-90 14-36

Plums 32 90-95 F,H 14-28 Y

Potatoes, early 50-60 90 R,F 56-140

Potatoes, late 40-50 90 R,F 56-140 Y

Pumpkins 50-60 50-75 N 84-160

Raspberries 32 90-95 R,F 2-3 Y

Rutabagas 32 98-100 R 120-180

Spinach 32 95-100 H,I 10-14 Y

Squash, summer 41-50 95 R,F 7-14 Y

Squash, winter 50-55 50-70 N 84-150

Strawberries 32 90-95 R,F 5-10

Sweet potatoes 55-60 85-90 N 120-210 Y

Tangerines 40 90-95 14-28

Tomatos 62-68 90-95 R,F 7-28 Y

Turnips 32 95 R,H,V,I 120-150

Watermelon 50-60 90 N 14-21

F=forced-air cooling , H=hydrocooling, I=package icing, R=room cooling

V=vacuum cooling, N=no precooling needed

Sources: USDA Agricultural Marketing Service, Kansas State University Cooperative Extension Service

Pest BEETLES in stored grain and grain stores

• Grain Beetles (Oryzaephilus, Cryptolestes, Sitophilus and Ahasverus

species)
• Lesser Grain Borer (Rhyzopertha dominica)
• Clover Weevil (Sitona sp)
• Ground Beetle (Carabidae)
• Mould and fungus beetle (Mycetophagidae, Typhaea, Lathridiidae and
Cryptophagus species)
• Rove Beetle (Staphylinidae)
• Spider Beetle (Ptinus fur)

Pest MOTHS in stored grain and grain stores

• White-Shouldered House Moth (Endrosis sarcitrella)

• Grain Moth (Sitotroga cerealella)
• Brown House Moth (Hofmannophila pseudospretella)
• Mill/flour Moth (Ephestia kuehniella)
Pest MITES in stored grain and grain stores

• Grain Mite (Glycyphagus destructor)

• Predatory Mite (Cheyletus eruditus and Gamasina)
• Flour Mite (Acarus siro)
• Cosmopolitan Food Mite (Lepidoglyphus destructor)

Flour and Grain Mites

The grain or flour mites are one of the most important mites infesting food and feed
products, cereals, dried vegetable materials, cheese, corn and dried fruits. Grain mites
proliferate under high moisture conditions and are often found in conjunction with fungal
growth. Severe infestations result in brownish tinge over the commodity, called "mite
dust" because of the light brown coloring of the mite legs. This "mite dust" gives off a
"minty" odor if the mites are crushed. Grain mites are widely distributed throughout the
temperate regions, but only occur in tropical areas unless a constant influx of new mites
is supplied via contaminated goods.

DESCRIPTION
Flour or grain mites are pale, pearly or grayish white, with legs varying in color from pale
yellow to reddish-brown. Each leg has one claw at the end. As with all mites, they are
smooth, wingless, soft-bodied creatures. The males are from 0.013 to 0.017 inch long,
and the female is from 0.014 to 0.026 inch. The males have enlarged forelegs which bear
a thick spine on the ventral side. These two characters can be used to separate Acarus sp.
from other genera. Juvenile mites are similar in appearance to the adults. The first or
larval stage has only six legs. However, when they molt into the nymphal stage, they
have eight legs like the adults. Mite eggs are oval, smooth, white, and are 0.12 mm long.

LIFE HISTORY
Female grain mites may lay up to 800 eggs, which are deposited on the surface of food
material at the rate of approximately twenty to thirty per day. The eggs may be deposited
singly or scattered at random over the food material. The entire life cycle may take only
nine to eleven days to complete under the optimal conditions of ninety percent humidity
and seventy-seven degrees F. The life cycle is completed in seventeen days at sixty-four
to seventy-one degrees F, and twenty-eight days at fifty to sixty degrees F.

At some time during the juvenile period, grain mites may change into a stage known as
the hypopus. During this unique stage, the body wall hardens and suckers appear on the
underside. These suckers allow the mite to attach to insects and other animals for
dispersal. The eggs and especially the hypopuses appear to be more tolerant of
insecticides than other juveniles or adults; and they may be the primary stage responsible
for resurgences in mite populations after chemical control appeared to have been
successful.

DAMAGE
Grain mites primarily attack the germ. However, they will feed on other parts of the
kernel, as well as mold growing on the grain. These mites are responsible for the spread
of various fungal spores throughout a grain mass and into adjoining bins. When present
in large numbers, the flour or grain mites promote sweating and impart a disagreeable
odor to the grain. Grain mites can cause "grocer's itch" in humans exposed to the mites.
Some persons may be allergic to mites.

CONTROL
Prevention is the best strategy to avoid mite problems in stored grains. Proper bin
sanitation before introduction of new grain minimizes the need for pesticides. Good
sanitation involves the removal of old grain and dust in and around the grain bin. This
includes removal of old grain from corners, floors, and walls and grain that may have
spilled on the exterior of the bin. Any grain remaining when a bin is emptied can harbor
insect infestations which will move into the new grain.

After the bin is cleaned, and all needed repairs have been made, the floor and wall
surfaces both inside and outside the bin should be treated. Take special care to treat all
cracks, crevices, and areas around doorways and other places where insects hide or enter.
Spray the bins about four to six weeks prior to storing grain if the grain is to be stored
longer than six months.
 Before grain is placed in a bin it should be screened to eliminate fine materials and
broken kernels. Grain placed in a clean bin should be checked at two week intervals
during warm months and at one month intervals during cooler months for the presence of
hotspots, moldy areas, and mite activity. If any of these conditions exist, the grain should
be aerated to lower the moisture level and temperature.

At humidities less than fifty-five to sixty percent (commodity at twelve percent moisture
content or less) grain mites can not survive. Grain that is to be stored for longer than six
months may need a protective application of an approved insecticide. Treatments can be
applied as the grain is loaded into the bin through the use of a metering device calibrated
to apply the proper amounts. After the grain is binned and leveled, a surface dressing can
be applied to prevent insects from entering the grain on the surface.

If infestation occurs in spite of these precautions, fumigation of the grain will be

necessary. Because of the higher tolerance of mite eggs to fumigation, the concentration
of gas introduced will need to be fifty percent greater than that for insect control.
Fumigants are highly toxic, and technical knowledge is required for their proper use. A
qualified, licensed pesticide applicator should be contacted to perform the fumigation.

Mites Infesting Stored Foods

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Reference: Ohio State University Extension
Common Name Scientific Name
Grain Mite Acarus siro Linnaeus
Mold Mite Tyrophagus putrescentiae (Schrank)
Cheese Mite Tyrolichus casei Oudemans

Several species of mites infest stored foods and other organic debris such as
grain, flour, cereals, dried fruits and vegetables, pet foods, cheese, dried milk,
ham, sugar, paper, tobacco, molds, bird and animal nests, etc. These mites often
prefer a moist, damp location. Sometimes the surface of infested materials
appears to move due to the enormous numbers of mites (barely visible to the
unaided eye). Heavy infestations of grain mites have a sweet, "minty" odor, best
detected when mites are crushed between the thumb and forefinger, and held to
the nose. Also, a coating or piles of brownish "mite dust" may appear on open
shelving, around the base of flour sacks, on the surface of cheese or in other
foods. Such piles consist of dead and living mites, cast skins and feces.

Prolonged contact with mite infested foods may produce a mild dermatitis known
as "baker's" or "grocer's itch." Other contact may cause bronchial asthma and
dust allergies. Also, if mites are taken internally with infested food, stomach
disorders may result. However, Acarid Mites are responsible for the sharp flavor
of a famous German Cheese, Altenburger "Milkenkase." Anyone ingesting this
cheese (with its thousands of mites) for the first time may have gastrointestinal
disturbances. Mites can survive temperatures near freezing and may become
more prevalent during colder months.

Grain Mite
Identification
The bodies of grain mites are almost colorless, but the mouthparts and legs are
pale yellow to reddish-brown. The adults are about 1/2-mm long, the females
being slightly larger than the males. The body of the male is smoothly rounded at
the hind end; that of the female is more oval with the posterior edges slightly
indented in the middle. The body has a groove across it, dividing it into two
areas. Two pairs of fairly long hairs trail at the end of the body.

The first two pairs of legs are widely separated from the hind two pairs. The front
pair of the male are enlarged, and the femur bears a stout spinelike process on
the underside.

Grain Mite Female (greatly enlarged)

Top or dorsal view, Bottom or ventral view

Life Cycle & Habits

Grain mites commonly occur in dense populations. As many as 10,000 mites in
200-gram samples often have been found in binds of Canadian wheat. In one
study, grain mites comprised 42 percent of the mites taken from 30 farm
granaries in Central Canada. A procession of 50 grain mites has been observed
emerging from the germ of a single wheat kernel. During summer and autumn,
grain mites are commonly attacked by the predatory mite, Cheyletus eruditus
Schrank.

Under highly favorable conditions [a relative humidity (RH) of 87 percent and

temperature of 73 degrees F the life cycle of grain mites may be completed in 9
to 11 days. A female may deposit between 100 and 500 eggs on food over 10 to
12 days. The larval and nymphal stage may be 19 to 20 days with a complete life
cycle of two to five weeks. An RH of 61 percent or lower is detrimental to grain
mites. Grain mite development is extremely sensitive to humidity levels outside
the range of 75 to 85 percent.
The second nymphal form may be replaced by a special stage known as the
"hypopus." This stage is highly resistant to unfavorable conditions, insecticides
and fumigation, and may exist for several months without feeding. The "hypopus"
does not move much under its own power but is transported from place to place
by clinging to small animal forms such as insects or mice. Most hypopi rely on air
currents for distribution. They have been known to survive for at least seven
months in dry flour and can withstand lower temperatures than the active form.
When the hypopi encounters favorable conditions, it sheds its skin and resumes
normal growth and development. The peculiar adaptation through the "hypopus"
stage makes it very difficult to eradicate this mite.

Mold Mite
Identification
Males and females are about 1/2-mm long and have a small translucent body
with almost colorless mouthparts and legs. The body, somewhat slender, bears a
train of hairs which are more numerous and longer than those on the grain mite.
Hairs do not project so stiffly. On the underside of the males, on either side of the
anus, there are two dome-shaped anal suckers. Only trained specialists with
proper magnification can identify mite species and separate males from females.
Specialists at the Vector-borne Disease Unit of the Ohio Department of Health
and/or Acaralogy Unit of The Ohio State University are qualified to make
identification.

Life Cycle & Habits

Under moist conditions and summer temperatures, a generation can be
completed in 8 to 21 days. As the temperature falls, the length of the life cycle
increases greatly. The mold mite will breed readily above 86°F., a temperature
lethal to the grain mite. The mold mite is less tolerant to low temperatures and
cannot develop below 50°F., whereas the grain mite breeds readily well below
this limit. However, in an inactive state, this mite can survive 32°F. At favorable
temperatures and 90 to 100 percent relative humidity, the female will lay an
average of 437 eggs. At a given temperature, larval and nymphal stages require
about equal time for development. Unlike the grain mite, this mite does not
produce a hypopus.

Foods
The mold mite is a pest of many foods, especially those having a high fat or
protein content. Infestations have been found for each of these foods: mixed
feeds; mixed feeds and brewer's yeast; whole wheat flour; soy flour; wheat germ;
cheese; rye bread; white bread; and mixtures of oats, barley and wheat. Other
known foods include cultivated mushrooms, various seeds, fruits, grain and straw
stacks in the field, decaying animal and vegetable matter, herring meal, onion,
bacon, figs, dried milk, cheese, ham, dried bananas, and copra. Their relative
preferences in oilseeds are: peanuts, 14 percent; sunflower seeds, 12 percent;
canola seeds, 10 percent; linseed, 6 percent; palm kernels, 6 percent; poppy
seeds, 4 percent; and cotton seed, 4 percent. They may become pests of
mushroom beds. Apparently, the mold mite has not caused serious damage to
stored products in tropical or subtropical regions. It will attack the bodies of
workers engaged in the copra industry, but it spares their faces.

Cheese Mite
Identification, Life Cycle & Habits
The cheese mite, known to cause dermatitis, is larger than both the grain mite
and the mold mite. It has stout, well-tanned, faintly-wrinkled legs and tanned
mouthparts. Males and females are similar except that females are larger. The
life cycle requires 15 to 18 days at the ideal temperature of 73°F and an RH of 87
percent. No hypopi are formed.

Control Measures
Controlling mites is difficult when moisture and temperature conditions favor their
development.

1. Carefully inspect foods and grains before purchase. Do not carry mite
infested stored foods into the home. Pet foods purchased in bulk and
stored for long periods of time should be checked routinely. Rotate food
materials to remove the older items first.
2. Store foods only in a clean, dry area. Never store foods under damp,
poorly ventilated conditions. If necessary, increase air circulation to reduce
relative humidity and prevent molds and mildews. (Reduce the RH to
below 55 to 60 percent and the moisture content of the media to below 12
percent.) Ventilate and dry areas with a dehumidifier or fan, or simply
open doors of a damp room.
3. If bins or large containers are used for storage, do not dump new
replacement foods (flour, grains, etc.) on older unused foods. Allow the
original contents to become used up or exhausted, if possible. (Unused
materials may become damp and moldy over time.) Avoid prolonged
storage.
4. Place stored foods in containers with tight-fitting lids, ideally screw type.
Stack any flour or packaged foods on pallets to permit air ventilation, and
to prevent possible floor dampness from penetrating sacks or packages.
5. Periodically clean the storage areas, especially cracks, crevices, shelving,
etc. Vacuum and wipe up any spilled foods, eliminating the foci of
infestations by cleaning with attention to horizontal surfaces such as
beams and window ledges.
6. When products become infested with mites, locate the source of
infestation and eliminate it. (Usually it is a forgotten, opened package,
sack, or container unused over a long period of time in a little-disturbed
storage area.)
7. Remove any bird or rodent nests near the storage area. Repair any leaky
water pipes or damp areas nearby where molds can develop. Rodents
 may store seeds, pet food, etc. in wall voids and other locations which
later become mite infested.
8. Suspected mite infested foods can be supercooled (0°F for seven days in
a deep freeze), superheated (140°F for 30 minutes in an oven in shallow
pans), (5 minutes in a microwave), or disposed of in several heavily
wrapped paper bags for garbage disposal. Some bury infested foods deep
in the ground if land and space is available.
9. Remove all remaining food from the storage area. Place uninfested food in
containers with tight-fitting lids. Thoroughly clean and scrub all shelves,
floors, walls, etc. with hot water, strong detergents and allow to completely
dry before using any registered pesticide sprays or before replacing the
stored foods.
10. If a pesticide is needed in the house, apartment, structure or garage, spot-
treat cracks and crevices only to kill hidden mites. Use only legal
pesticides registered for mites in stored food areas such as pyrethrins
containing piperonyl butoxide. Carefully follow all label directions and
safety precautions. (Be sure the pesticide can be legally used in the house
and avoid spray drift onto food, dishes or cooking utensils.) Always read
the label and follow directions and safety precautions.
11. Control of mites in laboratories is often difficult. Laboratory white mice,
rats, hamsters, and guinea pigs sometimes are heavily infested with grain
and other mites. Clean the cages with steam if possible. Remove all
bedding cages and pans, and sterilize cage contents with steam or heat.
12. If the stored food mite infestations cannot be successfully controlled,
contact a reputable pest control operator. (The licensed, professional pest
control operator has the most effective pesticides, equipment and
experience.)
13. For warehouses, storage buildings, food processing plants, mills,
granaries, seed houses, grain elevators, etc., only licensed, certified
pesticide applicators can apply approved fumigants. Bear in mind that
heavier dosages are needed for mite control than are necessary for insect
control. Fumigation eliminates mites present at the time, but does nothing
to correct conditions nor prevent reinfestation

What is Mold?

Molds (and mildew) are fungi. Fungi are neither plant nor animal but, since 1969, have
their own kingdom. The fungi kingdom includes such wonderful organisms as the
delicious edible mushrooms, the makers of the "miracle drug" penicillin and the yeast
that makes our bread rise and our fine wines ferment. Biologically, all fungi have defined
cell walls, lack chlorophyll and reproduce by means of spores. Approximately 100,000
species of fungi have been described and it is estimated that there are at least that many
waiting to be discovered. The vast majority of fungi feed on dead or decaying organic
matter – they are one of the principle agents responsible for the natural recycling of dead
plant and animal life.
.

Determining If You Have Mold

Common household molds have a characteristic "musty" or

"earthy" smell, somewhat like the forest floor deep in the woods.
Growing colonies of mold can also be visually observed in many
cases. Most people are familiar with moldy bread or mold growth
on cheese or other food products that have been kept too long, so
the "green fuzzy" characteristic of most mold growth is familiar.
And those who have lived in Florida have heard the expression
"green shoe syndrome" which refers to the fact that mold is
Spoiled Florida particularly fond
orange. of leather products
left unused for periods of

•
• Return Air Pathways: It is
important that there be sufficient
air flow pathways for the supply
air that is delivered to each room
of a home to return to the air
conditioner's air handler unit (the
box with the blower fan).
Otherwise, the part of the home
Note the pink "splotch" at the bottom-center
containing the main return to the
of this photo. It is the telltale warning sign
air handler unit will be "starved"
that there is a likely mold "bloom" behind
for air, resulting in
the vinyl wall covering.
depressurization of this space with
respect to the outdoors. If this occurs, outdoor air will be drawn through the small
pathways that exist in the exterior building envelope. In hot, humid climates like
Florida's, these air flows can result in the accumulation of moisture within the
gypsum wallboard, especially if it has vinyl wall covering. This, in turn, can result
in the rapid and abundant growth of molds — remember, the cellulose (paper) on
gypsum wallboard makes an excellent, preferred mold food.

If room doors are kept open, there will be sufficient return air pathways.
However, if rooms doors are closed, the rule-of-thumb is that there should be
about 50 square inches of "free" air transfer area for each 100 cfm (cubic feet per
minute) of supply air to the room. In this case, the term "free" means a simple,
clear hole in the wall between the room and the remainder of the home. If, for
appearance and privacy reasons, this hole is to be covered by grilles on each side
of the wall, then the overall return air pathway area needs to be increased by about
40% to account for the air flow resistance of the grilles, or about 70 square inches
per 100 cfm of supply air flow.
• Bathrooms: Most bathrooms, particularly tile in and around showers and tubs is
regularly wet. As a result, most bathrooms grow mold and require regular
cleaning. A weak solution of water and common household bleach can be used to
regularly clean these areas and keep them free of mold. Low-noise bathroom fans
are also recommended to remove excess moisture during periods when it is being
generated by bathing or showering. (See also exhaust fans.)

• Whole-House Ventilation Fans — Opened Windows: Avoid the use of these

fans when it is humid outdoors, especially if you have noticed mold growth in
your home or you are having trouble controlling the relative humidity in your
home. In addition, avoid opening windows for long periods when it is humid
outside (e.g. during nights and evenings) if you are experiencing mold growth
problems in your home.

• Air Conditioner Maintenance: Change your filters regularly and use pleated
filters. Once a year get your air-conditioners professionally serviced. At that time
make sure coils are clean, the condensate drains properly and that the drain pan
has no mold.

• Exterior Water Management: Redirect water away from the home's exterior —
redirect sprinklers so that they don't spray on the walls. Do not landscape with
hills that direct water flow towards the home. Use gutters. Keep down-spouts free
of debris and direct outflow away from the home.

• Small Leaks: Even small water leaks will cause mold problems. Rainwater leaks
from improperly flashed windows, wall and roof penetrations and plumbing leaks
should be promptly repaired. Periodically inspect under sinks and vanities for
signs of water leakage. Use you nose and smell for "musty" or "earthy" odors –
they usually indicate the presence of mold. Fix all water leaks promptly.

• Water Damage: Water damage from flooding or other major water intrusion in
homes should be dried within 24 hours if at all possible. For severe flooding and
severe water damage for more than 48 hours, a trained restoration professional
should be consulted regarding cleanup procedures. Readers are also encouraged to
consult the American Red Cross web site at the bottom of this page for further
information.

• Moisture Condensation: Single-pane, metal windows, which are common in

Florida, generally condense water on the inside in winter. It is good practice to
remove this condensation before it can run off and be absorbed by porous
materials like wood casing or gypsum wallboard. Condensation can also occur on
other surfaces in homes. If condensation is noticed on interior surfaces in summer,
it may indicate a number of problems, including inability to control indoor
humidity; air conditioner supply registers aimed directly at interior surfaces; duct
leakage problems and pressure imbalances; or all of the above. If you notice
indoor surface condensation during summer, you should contact a professional to
help diagnose the cause. However, during early spring when the ground is still
 cool, it is quite possible to experience some condensation on tile floors on slab-
on-grade homes that are open to the outdoors. This should not be a regular
occurrence, but only something that occurs rarely.

• Exhaust Fans: Make sure the clothes dryer vent goes all the way to the outside of
the home, not to the crawlspace or to the inside of the attic or the house. The same
goes for bathroom vent fans. It is also important for the kitchen range hood to
vent to the exterior as well. Recirculating stove and kitchen vents provide no
removal of stovetop moisture and inferior control of cooking related pollutants
compared with venting completely to the outdoors. A major deterrent to the use of
kitchen range hoods is noise. Choose an ultra-quiet, inline ventilation fan for your
range hood. Kitchen and bath exhaust fans should only be used while cooking or
using the bathroom to remove excess moisture generated by these activities.

It is best practice to either have bathroom vent fans interlocked with the light
switch so they do not get left on or have them switched by a manual timer that
will shut them off after a period of time, or control them by humidistat.

• Closets: Fungi like the dark and closets are rarely supplied with conditioned air as
a standard part of air conditioning systems. As a result it is not all that uncommon
to have mold or mildew occur in closets, especially on leather. Leaving the closet
doors open to provide more conditioned air circulation or leaving the closet lights
on with the door closed so as to raise the temperature (which lowers the RH) can
reduce these problems.

• House Plants: Minimize live house plants, especially if you have any trouble
controlling the relative humidity in your home.

Fungal damage in durable foodstuffs with special

reference to storage in the tropics
Contents - Previous - Next

1. What are fungi?

Fungi are micro-organisms generally classified as plants, although there is growing

support for the separation of the fungi and other micro-organisms into an entirely new
kingdom. For this reason Fungi are perhaps best described as plant like micro-organisms
that do not possess chlorophyll.

Fungi may be simple in structure, as are the yeasts which consist of a single cell or chains
of cells that reproduce by "budding" and which generally give rise to rather slimy, pink,
pale brown or cream coloured colonies. Typical moulds on the other hand, are more
complex, multicellular fungi, of variable appearance and colour. Most reproduce by
means of microscopic asexual spores which vary considerably in size and shape and are
formed either on stalks or in special vesicles which grow from, or are embedded in, the
vegetative part of the fungus (mycelium). This consists of many strands (hyphae) which
typically grow together to form a 'mycelial mat'. It is this mycelium that is largely
responsible for the formation of exzymes, fungal toxins, etc. Many fungi also have a
sexual stage in their life cycle. (Note: Except in certain very high moisture content
situations yeasts are relatively unimportant and this supplement refers mainly to the
mould fungi).

Whereas fungi that attack growing plants are fairly restricted in number and are true
pathogens, fungi in stored products are much more numerous and are saprophytic, or only
weakly pathogenic by nature. This also applies to the 'field fungi'. The A/ternaria and
Cladosporium groups are common examples causing a blackening or weathering effect
on unharvested, mature crops of maize, sorghum and other grains. The Fusarium group is
also important at this stage. Once in store the field fungi tend to decline, their place being
taken by such typical storage groups as Aspergillus and Penicillium. These and other
storage moulds often fall within the 'fungi imperfect)', so called because they reproduce
only by asexual means. For descriptive details of the fungi and other micro-organisms
that cause damage in stored produce please see T.S.T.S. OLL.

In common with other living things, when fungi grow they breathe (a process known as
respiration) using oxygen from the air which reacts with the substrate on which they are
growing to produce carbon dioxide, moisture and heat. By-products of the normal growth
process are often of a complex chemical nature and may be beneficial but are sometimes
undesirable.

2. Where do fungi occur?

Fungi are found everywhere. Spores occur in dust and are therefore present in the air we
breathe. All stored commodities are contaminated with fungal spores and these, unlike
insects, cannot be excluded by careful handling and treatment. Even processed foods that
been subjected to high temperatures during their preparation (e.g. oil-seed cake) though
perhaps significantly free of living moulds immediately following processing, are rapidly
recontaminated during packaging and storage. It is, therefore, most important to prevent
fungal spores from germinating and growing into visible colonies.

3. When do fungi grow?

Fungal spores require moisture to germinate and if this is excluded (i.e. if grain is stored
at its safe moisture content or below) moulds generally will not grow. The maximum safe
storage moisture content may be defined as the amount of absorbed water held within a
commodity which is in equilibrium with an atmospheric relative humidity of 70%.
Moisture content is closely bound to temperature. Under certain circumstances,
temperature differences can cause the re-distribution of moisture leading to local mould
growth. Other factors that affect fungal development and the production of spores are
availability of oxygen, light, acidity, and salt/sugar content.
4. Why is it important to prevent fungal growth?

Fungi do a tremendous amount of damage by causing:

1. Direct loss when the grain is too mouldy to eat.

2. Caking in grain and flour, rendering the material difficult to handle.
3. Changes in colour, texture and flavour rendering the produce unacceptable by:

i. fermentation (carbohydrates converted to acids and gas)

ii. putrifaction (protein breakdown), and
iii. rancidity (fats converted to acids).

The latter is especially important in oilseeds (e.g. groundnuts, oil palm kernels) and oily
products (rice-bran, copra etc) where the enzymatic conversion of oil to free fatty acid
results in uneconomic processing or in financial penalties on world markets.

4. Charring or spontaneous combustion if mould growth is unchecked as this

releases heat and grain is a poor conductor of heat. Quite dramatic temperature
rises can occur especially within large bulks or stacks. Normally the temperature
rise Is restricted to a maximum level of about 60°C at which point moulds are
generally inhibited. However, in oilseeds, enzymatic heating can continue even
leading eventually to spontaneous combustion.
5. Reduction in germination capacity of grain.
6. Poisoning in man and animals due to the production of mycotoxins (poisonous
fungal breakdown products) by certain species. Aflatoxin, produced by the
common storage fungus Aspergillus flavus is known, for example, to cause liver
collapse in certain domestic animals.
7. Lung diseases such as asthma and skin allergies if spores are present in the
atmosphere in very high concentrations (e.g. handling mouldy straw or prolonged
exposure when emptying underground pits).
8. Deterioration and weakening of fibres used for packaging or protecting grain (e.g.
jute sacks, tarpaulins). This can lead to spillage or water entry. Container sealing
materials such as stitching and adhesives are also liable to mould attack.
9. Deterioration of store fabrics, especially wood, causing rotting and disintegration.

5. In what practical situations can fungal damage occur?

Fungi can develop if conditions favour their growth at any of the following times:

1. In the field, prior to harvest, when the crop is maturing.

2. After harvest during the drying period.
3. In store. This can occur for two unrelated reasons and it is important to
distinguish between them:

a. due to the premature storage of inadequately dried material, and

 b. due to the re-absorption of water while in store (especially during the wet season),
as follows:

i. exposure to high relative humidity,

ii. through a leaking store roof, cover or container,
iii. water uptake through the floor or walls of a store,
iv. development of temperature gradients in grain leading to condensation.

4. In transit.
5. During processing.

6. Hints on preventing fungal damage

1. Harvest the crop at maturity. Grain harvested prematurely takes longer to dry and
is therefore more susceptible to mould damage. It is also likely to shrivel. The
actively growing crop has a natural resistance to invasion by storage fungi (e.g.
Aspergillus and Penicillium spp.) but this is to some extent lost at maturity or if
the grains are damaged by rodents, insects, etc.
2. Dry the produce as quickly as possible bearing in mind the need for a 'curing'
period in some crops such as groundnuts. Remember that hot sunlight is not
always the best. A method that protects the commodity from rain, dew and damp
soil but allows dry air to pass freely over the produce is ideal. In certain extreme
climates where the air is continuously humid artificial drying may be essential.
3. Avoid physical damage to the produce at all stages of handling. Harvesting and
shelling are two occasions when damage is likely to occur. Broken groundnut
pods, for example, are more easily invaded by moulds than undamaged pods. The
grain skin is also resistant to fungal invasion and should be kept intact if possible.
4. Check the moisture content of the commodity before it is stored. Make sure that it
is quite dry first. if there is any doubt, or if drying has proved to be a problem, do
not store the produce in solid walled containers. 'Pigeon hole' stacking can be
used for bagged produce suspected of being damp as it allows air to circulate
through the stack.
5. Avoid storing warm grain as the heat will be retained and encourage rapid mould
and insect multiplication. Also, if the store structure is cool, condensation may
occur where the warm grain touches the cool surfaces.
6. Ensure that all stores, silos, etc. are in good repair before use.
7. When storing bagged produce, keep it well away from the walls of the store and
use dunnage to raise the sacks away from the floor.
8. Allow newly constructed concrete stores or floors dry out throughly before use. If
possible build a water vapour barrier (e.g. polyethylene sheet, bitumenastic layer)
into the floor and walls during construction.
9. Allow for controlled ventilation around the produce within a store so that air of
high relative humidity can be excluded during the wet season. Ventilate only if
the internal air is moist and the outside air is dry, or if the produce needs cooling.
10. Ideally, produce and store should be maintained at an even temperature.
 11. If produce is thoroughly dry, polyethyelene bags or sheets can be used to exclude
moisture during storage. However, care must be taken to avoid exposure to direct
sunlight or condensation will occur beneath the plastic surface. This is also likely
to occur in a store where the internal temperature fluctuates excessively. To
prevent condensation under these circumstances the top and sides of the stack
should be insulated with a layer (several if possible) of sacks or similar material,
placed outside the plastic sheet.
12. If practical, cover all metal silos to prevent direct sunlight from falling on the
walls. If this is not possible a coat of white paint will help to reflect the heat and
keep the produce cool.
13. Apply adequate pest control measures to prevent insect 'hot spots' from
developing.
14. Do not load or unload grain in the open if it is raining and avoid placing sacks of
produce on wet ground.
15. Ensure that all railway wagons, lorries, small boats and other mobile containers
are adequately covered and in good repair, especially if movement during the
rainy season is likely.
16. It is almost impossible to avoid some fungal damage in traditional underground
pit stores. However, any form of lining which prevents grain from coming into
direct contact with the soil will help. Also, pits should be completely filled; a little
grain in a large pit will usually become very mouldy.

7. The chemical control of storage fungi.

Chemicals for the prevention of mould growth in grain stored for human consumption are
not at present available. The very broad spectrum of moulds found in stored products is
one problem and toxicity to man another. However, propionic and other organic acids
have been successfully used in temperate countries to protect highs moisture content
barley and other grains destined for animal feed. While it may be possible in the future to
use propionic acid in hot climates where drying is a problem, considerable research under
tropical conditions is needed first. Taint and smell are two aspects requiring investigation
if propionic acid is to be applied to grain for human consumption. Furthermore, the
application rate is critical and complete coverage of the grain is necessary before mould
growth commences if adequate control is to be achieved.

8. What should be done with mouldy foodstuffs?

This is a vexed question as no-one wishes to waste food. Indeed, some foods like 'blue'
cheese are purposely infected with fungi. However, since the discovery over the last
decade that a wide range of storage fungi can produce substances that cause disease when
fed to animals there has been considerable speculation as to whether man is at risk
through eating badly stored foodstuffs which have been accidentally contaminated with
fungi. There is strong circumstantial evidence to support such a suggestion, and fungal
invaded grain, pulses and especially oilseeds should therefore be avoided if at all
possible. It is worth noting here that cleaning grain to remove surface fungal growth (this
is, for example, practised in some rural communities with mouldy pit-stored grain), is
unlikely to remove any toxin present within the grain and therefore is not recommended.
Similarly, cooking does not necessarily destroy mould toxins and aflatoxin is a good
example of this. Careful sorting to remove visibly damaged grain is therefore
recommended, and in certain commodities, especially oilseeds such as groundnuts, the
seeds should be cut open and examined for hidden fungal growth within the grain.

The old maxim that mouldy grain can be safely fed to animals therefore no longer
applies. If mouldy grain is used for animal feed it may cause death and at best is likely to
give poor results (e.g. a reduction in expected weight increase). If used it should be
considerably diluted with fungus free material. Extreme care is needed with oilseed cake
in particular, as this is very readily contaminated with aflatoxin, a substance that is toxic
in very small quantities. Appearance is not a good criterion when judging oilseed cake,
for although aflatoxin may have been present in the original seeds, visible mould damage
will not be seen in the finished produce unless re-wetting has occurred.

AFLATOXIN ANALYSIS: OVERVIEW

Aflatoxin is one of the most well-known mycotoxin in tropical and sub-tropical areas.
Crop in these regions or more subject to contamination than those in temperate regions,
since optimal conditions for toxin formation are prevalent in areas with high humidity
and temperature. Toxin-producing fungi can infect growing crops. As a consequence of
insect or other damage, and may produce toxins prior to harvest, or during harvesting and
storage.

The ingestion of food containing aflatoxin may have serious adverse health effects in
man. Aflatoxins are demonstrated liver toxin and liver carcinogens in some animals
including non-human primates. Dose response relationships have been established in
studies on rat and rainbow trout, with 10/tumour incidence estimated to occour at feed
level of AF B1 of 1 µ/kg and 0.1 µ/kg respectively. In some studies, carcinoma of the
colon and kidney have been observed in rats treated with aflatoxin. AF 3(1) causes
chromosomal aberrations and DNA breakage in plant and animal cells after microsomal
activation, gene mulation in several bacterial test systems. In high doses, it may be
teratogenic.

The acute toxicity and carcinogenicity of aflatoxin are greater in male than in female rats;
hormonal involvement may be responsible for this sex-linked difference. Nutritional
status in animals, particularly with respect to lipotropes, proteins, vitamin A, and lipids
(including cyclopropenoid fatty acid) can modify the expression of acute toxicity or
carcinogenicity or both.

Liver cancer is more common in some regions of Africa and Southeast Asia than other
parts of the world when local epidemiological information is considered together with
experimental animal data. It appears that increased exposure to aflatoxins may increase
the risk of primary liver cancer.
In view of the evidence concerning the effects, particularly the carcinogenic effects of
aflatoxin in several animal species, and in view of the association between aflatoxin
exposure levels and human liver cancer, incidence observed in some parts of the world,
exposure to anatoxins should be kept as low as practically achievable. The tolerance
levels for food products established in several countries should be understood as
management tools, intended to facilitate the implementation of aflatoxin control
programmes, and not as exposure limits that necessarily ensure health protection.

Aflatoxins are now recognized to be involed in the aetiology of certain human and animal
diseases. An awareness of the level of contamination of Aflatoxin in natural products can
only be obtained by developing good analytical methodologies for detecting aflatoxin in
foods, mixed feeds and Ingredients, animal tissue, blood, urine and milk.

Aflatoxin detection methods can be divided into three categories

1. rapid presumptive tests to identify samples from agriculture products such as

corn, peanut lots that may contain toxin,
2. rapid screening procedures to determine the presence or absence of toxin,
3. quantitative methods to determine aflatoxin levels.

The presumptive test for aflatoxin in corn in the black light test or Bright Greenish-
Yellow fluorescent test (BOY) based on the fluorescence under ultraviolet light (365
nm.) associated with Aspergillus flavus and A. parasiticus.

Rapid screening tests have included mini column methods that can be done in a
laboratory with minimal facilities, and thin layer chromatography (TLC).

Quantitative methods to determine aflatoxin levels involves extraction, purification of

extract, and measurement of the to

Mold-associated conditions

Molds may excrete liquids or low-volatility gases, but the concentrations are so low that
frequently they cannot be detected even with sensitive analytical sampling techniques.
Sometimes these by-products are detectable by odor, in which case they are referred to as
"ergonomic odors" meaning the odors are detectable, but do not indicate toxicologically
significant exposures.

[edit] Food
Moldy nectarines that were in a refrigerator. The nectarine with black mold is also
affecting the nectarine underneath.

Molds that are most often found on meat and poultry are Alternaria, Aspergillus, Botrytis,
Cladosporium, Fusarium, Geotrichum, Monilia, Manoscus, Mortierella, Mucor,
Neurospora, Oidium, Oosproa, Penicillium, Rhizopus and Thamnidium.[18]

Roughly 25% of the worlds food is contaminated by mycotoxins according to the World
Health Organization.[24] Grains incur considerable losses both in field and storage due to
pathogens and insects. Some of the pathogens and resultant mycotoxins reduce the
nutritional quality of the product. Mycotoxins are toxigenic fungal compounds that can
cause cancer and suppress growth.[25]

Mycotoxins contaminate grains and other food products across the globe and can
significantly impact human health. They can be found growing on grains before harvest
and in storage. When ingested, inhaled, or absorbed through skin, mycotoxins may
reduce appetite and general performance, and cause sickness or death in some cases.[26] [27]
[24]

Mold growing in or on field corn and peanuts are the ones most likely to produce
aflatoxin.[18]

Prevention of mold exposure from food is generally to not buy or to discard food that has
mold growths on it.[18] Also, mold growth in the first place can be prevented by the same
concept of mold growth, assessment, and remediation that prevents air exposure. In
addition, it is especially useful to clean the inside of the refrigerator, and having clean
dishcloths, towels, sponges and mops.[18]

Ruminants are considered to be resistant to the toxic effects of mycotoxins, presumably

due to their superior mycotoxin-degrading microbes.[24] This suggests that since
mycotoxins are difficult to digest by human microbes due to better degradation by rumen
microbes as compared to mono-gastric animals like humans. The carryover of toxins in
animal food may have severe consequences on human health.[28]
[edit] History
In the 1930s, mold was identified as the cause behind the mysterious deaths of farm
animals in Russia and other countries. Stachybotrys chartarum was found growing on
wet grain used for animal feed. The illnesses and deaths also occurred in humans when
starving peasants ate large quantities of rotten food grains and cereals that were heavily
overgrown with the Stachybotrys mold.

In the 1970s, building construction techniques changed in response to the changing

economic realities including the energy crisis. As a result, homes and buildings became
more airtight. Also, cheaper materials such as drywall came into common use. The newer
building materials reduced the drying potential of the structures making moisture
problems more prevalent. This combination of increased moisture and suitable substrates
contributed to increased mold growth inside buildings.

Today, the US Food and Drug Administration and the agriculture industry closely
monitor mold and mycotoxin levels in grains and foodstuffs in order to keep the
contamination of animal feed and human food supplies below specific levels. In 2005
Diamond Pet Foods, a US pet food manufacturer, experienced a significant rise in the
number of corn shipments containing elevated levels of aflatoxin. This mold toxin
eventually made it into the pet food supply, and dozens of dogs and cats died before the
company was forced to recall affected products.

[edit] See also

Fungi portal

• Building biology
• Environmental health
• Occupational asthma
• Environmental engineering
• Ventilation issues in houses
• Occupational safety and health

Prevention and control of mycotoxins in foodgrains in

India
Contents - Previous - Next

R. K. Goyal
Assistant Director (S&R)
Ministry of Food & Civil Supplies
Department of Food
Indian Grain Storage Institute, Hapur 245101, India
1. INTRODUCTION

India is predominantly an agrarian country with nearly three fourths of the people
dependent on agriculture or rural economy. The most outstanding achievement of Indian
agriculture since independence is the phenomenal growth of foodgrains output. During
the last three decades, Indian agriculture has experienced a revolutionary breakthrough in
foodgrain production leading the country from deficit and import arena to the positive
situation of self-sufficiency and buffer stocks. The foodgrain production in the country
increased from 50.8 million tonnes in 1950-51 to 152.37 million tonnes in 1983-84, but
the growth of Indian agriculture still continues to be linlked with the vagaries of nature.
Some of the states in the country have come across the unprecedented draught of the
century for the fourth successive year which has caused tremendous hardship to the
people as also loss of production of foodgrains in those states.

Nearly seventy percent of the total production of foodgrains in India is retained at farm
level where the unscientific and faulty storage conditions enhance the chances of fungal
attack and thereby mycotoxin production. The decomposers of foodgrains i.e. fungi,
bacteria etc. are always present on foodgrains in dormant conditions (usually as spores)
and grow under favourable climatic and other conditions (1). The fungal growth may
cause decrease in germinability, discolouration of grain, heating and mustiness, loss in
weight, biochemical changes and production of toxins. All these changes may occur
before the responsible fungi could be detected on visual examination (2).

The fungi produce a large number of mycotoxins in foodgrains and their products.
Mycotoxins are a group of highly toxic secondary metabolises of the fungi produced
under certain favourable environmental conditions (3). Because of their potent toxic
nature and fairly common occurrence under natural conditions, mycotoxins have attracted
world-wide attention in the recent years. The diseases or physiological abnormalities
resulting due to ingestion of mycotoxins are known as "mycotoxicosis" (4).

2. GENESIS OF THE PROBLEM

Association of mould produced toxins with food commodities has been knowri since
Biblical times but their role in inciting disease syndrome was realised only when it was
discovered that "ergotism" was caused due to consumption of barley and rye infected
with Claviceps purpurea (5). Cardiac beriberi caused by Penicillium citreovirde was
recorded in Japan due to consumption of contaminated rice; Stachybotryotoxicosis of
horses in Soviet Union in 1931; Red Mould Diseases or Black Spot Diseases Caused by
Fusarium sps. in Japan during 1940-50 and Alimentary Toxic Aleukia (ATA) caused by
Fusarium and Cladosponum species in USSR during 1942-47 (6).
The severity of mycotoxin problem was realised during World War II when Russians
eating mouldy overwintered grains sufferred with severe dermal necrosis, leukopenia,
haemorrhages and destruction of bonemarrow._ Fusarium was found to be the causal
organism (7). World-wide scientific recognition of mycotoxin problem was, however,
only in 1960 when it was discovered that the aflatoxins were responsible for the death of
about a lakh turkey poults (Turkey x disease) in England (8). According to Blount, the
"poisonous feed" which caused the havoc and which was the preparation of Brazilian
peanuts, was contaminated with Aspergillus flavus (9).

3. NATURAL OCCURRENCE OF MYCOTOXINS IN INDIA

Cereals constitute the most important food and feed sources which are affected by
various mycotoxic fungi. The problem of natural occurrence of mycotoxins in cereals
aggravated to some extent due to rapidly changing agricultural technology (10). In
general, mycotoxins and particularly aflatoxins seem to pose great problem in the tropics
than in the temperate regions but no part of the world can be considered to be mycotoxin-
free zone due to the movement of various foodstuffs from one part of the globe to the
other (4).

Some of the important commodities which have been found to be naturally contaminated
with one or the other mycotoxins are listed below:

3.1 Maize:

Maize is an excellent substrate for mould growth and mycotoxin production. In India,
systematic survey of maize grains for mycotoxins contamination has been undertaken in
some parts only. However, some reports mainly on aflatoxin contamination in stored
grains have indicated that the problem of aflatoxin contamination is much more serious
than usually visualised (4). In an extensive survey of the important maize growing areas
of Bihar, natural contamination of mycotoxins and particularly of aflatoxin was reported
in the grains of field maize crop (11). Surveys conducted by the Indian Grain Storage
Institute during 1978-79 and 1980-81 indicated contamination of stored maize grain
samples with aflatoxin B1 in the range of 40-510 ppb (12,13).

Under a FAO sponsored Food Contamination Monitoring Project, out of 10 maize

samples collected from Western Uttar Pradesh, 3 samples were found contaminated with
aflatoxin B. in the range of 20-80 ppb (14). Samples of maize collected from traditional
storage structures from various parts of India have shown contamination of aflatoxin B1
in the range of 15680 ppb (15). Fifteen varieties of maize were screened by Bilgrami et al
(16) for aflatoxin production by artificial inoculation of A. parasiticus. Practically ail the
varieties favoured aflatoxin production, but in varying degrees. Maize is a good substrate
for the production of Zearalenone which has been detected frequently in commercial
varieties. Reports of natural occurrence of Zearalenone in standing maize crop are also
available (4).
3.2 Rice:

Rice is also one of the important cereals which favours mycotoxin production. Natural
occurrence of aflatoxin and aflatoxin producing fungi in rice has been reported from
various parts of the world (16). In a survey of paddy harvested from rain affected crop in
Punjab and Haryana, out of 83 samples only 3 ewre found contaminated with aflatoxin B.
in the range of 10-40 ppb (17,18). Rice stored for prolonged periods i.e. 4-8 years has
also been reported to be contaminated with aflatoxin B. in various parts of India (12, 13,
14, 15, 10, 20, 21).

Presence of some other mycotoxins like citrinin, Sterigmatocystin and Ochratoxin has
been detected as natural contaminants of rice in one or the other region of the world.
Only scanty information is available pertaining to these toxins in India (4).

3.3 Wheat:

Wheat does not appear to be a good substrate for aflatoxin elaboration. Survey reveals
that natural contamination of wheat occur but in low profile (30). Out of 223 samples
collected from wheat growing belt of Western U.P. (India), only 9 samples were found
contaminated with aflatoxin B. in the range of 8-40 ppb (4,19,22). In 1985, all the six
flood affected wheat samples collected from Punjab were found contaminated with
aflatoxin B1 in the range of 8-40 ppb (24). There are few other reports of the natural
contamination of aflatoxins in wheat in India (23, 31). Reports of natural occurrence of
Sterigmatocystin in the domestic and imported red & white wheat are also available from
India (32).

3.4 Barley, oats, millets etc.:

Like wheat these small grains also do not favour natural contamination of mycotoxins.
However, some of these grains have been reported suitable substrates for aflatoxin
production. All the four aflatoxins B1, B2, G1, G2 as natural contaminants were isolated
from sorghum grains obtained from ears affected by A. flavus in North India (25). In
Western India sorghum samples were found contaminated with aflatoxin B., the level of
which was significantly correlated with moisture content as well as A. flavus population
(26). A survey in Central U.P. (India) has indicated that sorghum and bajra are also
naturally contaminated with aflatoxin B. during storage (19). It was also noticed that
contamination of aflatoxin degraded quantity-wise with the increase in storage period
during May to September. Perhaps, it was because of the fact that the production of
aflatoxin diecreases with increase in the temperature beyond 25°C. Out of the total
contaminated samples, only 2 samples of sorghum contained 40 ppb, beyond the
prescribed limit of 30 ppb for food in India.

3.5 Pulses & Oilseeds:

A survey under FAO sponsored Food Contamination Monitoring Project in Western

Uttar Pradesh revealed that few samples of pulses including green gram, black gram &
lentil and few samples of cotton seed were found contaminated with aflatoxin B1. The
range being 4-80 ppb in pulses and 35-200 ppb in oilseeds (14). Similarly, ten percent of
stored soybean samples were found contaminated with aflatoxin B. in the range of 4-40
ppb, in a survey in Uttar Pradesh (27).

A survey carried out by the Central Food Technological Research Institute, Mysore and
Regional Research Laboratory Hyderabad revealed that 80 percent of the peanut meal
produced in different states in India was found contaminated with aflatoxin at varying
levels (28).

3.6 Dry fruits & spices:

Aflatoxin has been reported as the main contaminant of coconut and other dry fruits viz.
almond, cashew nut, walnut, raisin, makhana and emblic. In some samples of these dry
fruits, presence of Zearalinone, Citrinin and Ochratoxin has also been reported. Natural
contamination of aflatoxin in various samples of chillies, fennel, cumin, coriander, black
pepper, ginger, cardamom and turmeric and presence of Orchratoxin, Citrinin and
Zearalinone has also been reported in a few samples of spices (33). In a limited survey in
Uttar Pradesh conducted by the Indian Grain Storage Institute, Hapur during 1984-85, it
was revealed that out of 99 dry fruit samples only 19 samples were contaminated with
aflatoxin B1 in the range of trace to 50 ppb (19).

3.7 Milk & Milk Products:

Milk and milk products are consumed by the people of all age groups and are also
important sources of mycotoxin exposure. So far no systematic survey of milk or milk
products has been done in India (33). Some reports indicate that aflatoxin M, upto 8 mg/l
were detected in the milk of buffaloes in Andhra Pradesh (34).

3.8 Cattle & Poultry Feed:

Cereals and oilseeds constitute more than 70 percent fraction of cattle and poultry feed.
Usually, the food which is declared unfit for human consumption finds its way as feed for
animals and poultry birds (33). A number of reports indicated the presence of high
concentrations of aflatoxins as natural contaminants in cattle feed. Presence of
Ochratoxin A and Sterigmatocystin has also been shown in some samples of cattle feed
containing sunflower cake and green gram (35).

4. HIGH RISK AREAS IN INDIA

Being aerobic in nature, mycotoxic fungi require air, moisture, nutrients and suitable
temperature for their growth and metabolism (4). Moisture content of the grain or the
relative humidity surrounding the substrate are the most important factors governing the
growth and aflatoxin production by A. flavus. Climatic conditions in India are most
conducive for mould invasion proliferation and elaboration of mycotoxins. The high risk
areas identified in India are Kerala, Western India, Gangetic plains, north eastern as well
as coastal areas of Andhra Pradesh, Karnataka and Tamil Nadu (16). Unseasonal rains,
flash floods are very common in India which enhance the moisture content of the grain
making them more vulnerable for fungal attack (30).

5. PROBABILITIES OF CONTAMINATION

Warm humid climate provides congenial atmosphere for the growth of fungi and
production of toxins. Aspergillus flavus which is known as storage fungi may infect and
produce aflatoxins in crops in the fields also (30).

Foodgrains are normally harvested at higher moisture content and then dried to bring
down the moisture content up to safe level before storage. Delay in drying to safe
moisture levels increases risks of mould growth and mycotoxin production.

Natural calamities like floods or torrential unseasonal rains during pre, mid or post-
harvest stages may render the crops vulnerable to microbial attack. Annual loss due to
spoilage of high moisture paddy is conservatively estimated to be 10-15% of the total
production of paddy, produced during rainy season in India (22).

Faulty storage conditions may also enhance the chances of microbial attack and
production of mycotoxins. Thus, starting from harvesting of the crop till the food or food
products are consumed by the consumers, there are chances of microbial invasion/fungal
attack at each and every stage/step.

6. R & D CENTRES FOR STUDY OF MYCOTOXINS IN INDIA

Considerable R & D work on mycotoxin contamination is being carried out at the

following centres:

i. National Institute of Nutrition (NIN), Hyderabad.

ii. Central Food Technological Research Institute (CFTRI), Mysore.
iii. Indian Grain Storage Institute (IGSI), Hapur.
iv. Central Drug Research Institute (CDRI), Lucknow.
v. Industrial Toxicology Research Centre (ITRC), Lucknow.
vi. Vallabh Bhai Patel Chest Institute, New Delhi.
vii. Universities/Regional Research Laboratories under the CSIR.
viii. I.C.A.R. and its Centres.
7. REGULATIONS

Eighteen countries all over the world have guidelines or regulations which prescribe
maximum acceptable limits for aflatoxins in food and feeds.

The limits prescribed vary from 0 to 50 ppb in foods and from 0 to 1000 ppb in feeds
(30). The Protein Advisory Group of United Nations has recommended intake maximum
30 ppb aflatoxin in foods rich in protein, where use of contaminated food cannot be
avoided.

In India, the Governmental agencies procure foodgrains confirming to prescribed

specifications thereby minimising the chances of contamination and thus ensure the
supply of good quality foodgrains to the consumers through PDS. At farm level also
quality consciousness is created amongst the farmers through a network of 17 teams of
Save Grain Campaign. These teams educate, motivate and persuade the farmers to adopt
scientific methods of foodgrains storage with a view to minimise the qualitative and
quantitative losses in foodgrains during storage likely to occur due to insects, rats and
moulds. The Quality Control Teams monitor the quality of foodgrains at commercial
level.

8. PREVENTION AND CONTROL OF MYCOTOXINS

Hazards of mycotoxin infected food are now well recognised. Considerable concern has,
therefore, been shown in the recent years towards the control of these toxic metabolises.
Control is attained by preventing the growth of moulds, separation of infected grains,
detoxification and by growing resistant varieties (33).

8.1 Prevention of mould growth:

In stored grain, mould damage may be prevented mainly by three kinds of methods viz.
drying of grain, controlled atmosphere storage and chemical treatment.

8.1.1 Drying of grain: It is an established fact that dry grain stores long, safe from
insects and moulds because the requirements of moisture for their development are not
met. The average Indian farmer perform drying of grain conventionally under direct sun
light (36). The most widely used indigenous practice of grain drying is to spread threshed
grains in thin layers on Kachcha floor with cow-dung in the open sun and stirring it by
human labour till the grains are dried to safe level. Some farmers have also been using
Pucca floors. Sun drying of grains on Kachcha surface was quicker as compared to Pucca
surface, transparent polythene & black polythene. 5.30 percent loss in the moisture
content of maize dried in sun-light could be achieved during 8.5 hours time (36).
Exposure of aflatoxin contaminated groundnut oil to sun light has given very promising
results as it destroyed about 99 percent of the aflatoxins (4). Other methods of grain
drying include mechanical drying, in-bin drying, infrared, microwave or sonic and solar
energy drying. Researches are being conducted to employ these methods also (37).

81.2 Controlled atmosphere storage: The significance of underground storage lies

behind the philosophy of grain cooling and depleting the oxygen content to the desired
level whereby the microbes and insects cannot grow. Air-tight storage also works on the
same phenomenon where the depletion of oxygen by grain respiration manipulates
disinfection by inhibiting aerobic fungi, elimination of mycotoxin production and
conservation of desirable quality factors in the grain. Natural cooling is another effective
method of preserving grain. The low temperature does not allow the microflora to grow
as most of them are thermophillic.

8.1.3 Chemical treatment: Chemical control of fungal deterioration to stored grain is

restricted to the treatment of grain for seed purposes only but not for food and feed.
Experiments conducted by Indian Grain Storage Institute showed that "Grain treat"
(Mixture of propionic acid, acetic acid and benzoic acid) against Aspergillus &
Penicillium sps. did not produce effective results in maize. Seed treatment with Bavistin
and TMTD (Trimethyl thiuram disulphide) at 0.25 per cent concentration gave 100 per
cent protection to wheat grain in one year storage against Aspergillus and Penicillium sps
(37). Certain mild phenolics like perulic acid and O-Vanillin have also been reported to
prevent aflatoxin production on rice, wheat, maize, groundnut and mustard seeds (33).

8.2 Separation of infected grains:

Physical separation of infected grains is an efficient and feasible method of minimising

mycotoxin contamination. This is effected either by manual operation or with the help of
an electronic sorter. Fungal infection of seeds or grain usually imparts characteric colour
or other physical properties.

8.3 Detoxification:

Cooking at atmospheric pressure can destroy about 50 percent of the toxins. Dry roasting
and oil roasting of groundnut reduces aflatoxins to a significant degree. Cooking rice
under 15 Ibs. pressure for 5 minutes gave maximum destruction of aflatoxins (72 percent)
as compared to ordinary cooking or cooking with excess water. Light has also been
employed successfully to destroy aflatoxin in crude groundnut oil. Studies have shown
that visible light is more effective than either ultra-violet or infra-red light (30).

8.4 Growing resistant varieties:

In view of the hazardous effects of mycotoxins, efforts are being made to develop mould
resistant varieties which will be mould free not only in fields as standing crops but during
storage also they will restrict development of moulds.

List of important mycotoxins, producer fungi and principal toxic effects

Mycotoxins Producer fungi Principal toxic effect
Aflatoxins Aspergillus flavus, Potent carcinoge-
A. oryzae, nic, mutagenic,
A. parasiticus teratogenic.
Sterigmatocystin A. versicolor, Carcinogenic
A. nidulans,
A. rugulosus
Ochratoxins A ochraceus, Hepatotoxic,
A. flavus, nephrotoxic
Penicillium
viridicatum
Citrinin P. citrinum, Nephrotoxic
P. viridicatum
Patulin P. patulum, Induces subcutane
P. expansum ous sarcomas
Citreoviridin P. citreoviride Nephrotoxic,
(Yellowed rice producing
toxin) convulsions
Penicillic acid P. pulberulum, Cell necrosis
Penicillium sp.
Rubratoxins P. rubrum, Haemorrhage
P. purpurogenum
Zearalenone (F-2) Fusarium Hyper-estrogenic
graminearum,
F. tricinctum

Trichothecenes F. poae, F. roseum Teratogenic,

(T-2) emetic, cytotoxic
Ergotoxins Claviceps purpurea Abortive;
gangarence
development

EEC Tolerance limits for aflatoxin B.' in animal feed

Sl. No. Commodity Aflatoxin B1 tolerance

not more than (µg/kg)
or ppb.
1. Produce for processing into mixed feed 50
2. Complete feed for cattle, sheep and goats (with the 50
exception of dairy animals, calves and lambs)
3. Complete feed for pigs and poultry (with the exception 20
of infant pigs, chicks, ducklings and turkeys).
4. Animal teed supplements for dairy animals 20
5. Other complete feeds. 10

Aflatoxin Limits in Different Countries

Country Commodity Aflatoxin limit (µkg or ppb.)

1. Belgium Animal feed 40 ***
2. Brazil Ground oilseed cake 50
(export)
3. Canada Nuts and their derived 15 **
products
4. Denmark Groundnuts & Brazil nuts 5-10
5. France Animal feed 700
6. India Groundnut kernel 30
7. Israel All foods 20
8. Italy Groundnuts 50***
9. Japan All foods 10
10. Groundnuts cake for animal 1000
feed mixes
11. Malaysia All foods 0
12. Malavi Groundnuts 5
13. Netherlands Foods & Feeds 5
14. Norway Oilseed cake 600
15. Poland All foods and feeds 5
16. Rhodesin Groundnuts 25
Animal feed 50-400
17. Sweden All foods particularly
Brazil nuts, groundnuts,
groundnut butter 5
Raw-materials for further
processing in Sweden 20
18. U.K. Confectionery, groundnuts, 50
Groundnut flour for
animal feeds 0 - 500 ***
19. U.S.A. Confectionery, groundnuts 20*
All foods & animal feeds 20 - 25

* Aflatoxin B
** Total of aflatoxin B1, B2, C1, C2
*** See Table-3 - EEC limits may apply.

Basic principles of grain drying

Contents - Previous - Next

by Prof. F.W. Bakker-Arkema

INTRODUCTION

Cereal grains and legumes are usually harvested at moisture contents too high for safe
storage. Thus, drying is a necessity. A large amount of water (103.5 kg per tonne of wet
material) has to be removed in drying wet grain from 22 to 13% (w.b.)*. Sufficient
drying air has to be provided to the grain to assure that drying to safe-storage moisture
contents is completed before microbial deterioration of the grain commences. This is the
main objective of all sun and mechanical grain drying systems.

Although much grain in the world is still sun. dried, this review of drying principles will
stress the mechanical drying of the crop in bulk. The paper can be considered a synopsis
of the book "Drying Cereal Grains" by Brooker, Bakker-Arkema and Hall. Each section
represents one Chapter in this text.

Proper understanding of the fundamentals of grain drying requires a basic understanding

of the topics of psychrometrics, grain deterioration, grain moisture equilibrium, air
movement, and drying theory. Each of these topics will be reviewed.

MOIST AIR PROPERTIES

This section is covered in detail in Chapter 2 of Brooker et al. (1974).

The air to be used in grain drying can be considered a mixture of dry air and water vapor.
Psychrometrics refers to the thermodynamic relationships between dry air and water
vapor.

There are three air humidity terms which need to be understood by grain dryer operators:
vapor pressure, relative humidity, and absolute humidity. The water vapor pressure is the
partial pressure exerted by the water vapor molecules in moist air; at saturation it is called
the saturated vapor pressure. The relative humidity is the ratio of the actual water vapor
pressure in the air to the water vapor pressure in saturated air; the relative humidity is
expressed as a decimal or percentage. The absolute humidity is the weight of water vapor
in the air per unit weight of dry air; absolute humidity values of drying air range from
0.005 to 0.1 kg/kg. Each of the three air humidity terms is used frequently in grain drying
calculations.

Three air temperature terms require consideration in dryer design. dry-bulb, wet-bulb,
and dew-point temperature. The dry-bulb temperature is the value registered by an
ordinary thermometer. The wetbulb temperature is the temperature indicated by a
wetwick covered thermometer with air passing over the wick at a speed of at least 5 m/s.
The dewpoint temperature is the temperature at which condensation occurs if moist air is
cooled at constant absolute humidity. The three temperature terms are of significance in
understanding grain drying principles.

Two additional thermodynamic terms of the drying air are required in grain drying
calculations: enthalpy and specific volume. The enthalpy of moist air is the heat content
of the air per unit weight of dry air above a certain reference temperature. The specific
volume of moist air is defined as the volume per unit weight of dry air. Note that both of
these thermodynamic properties are defined in terms of dry air; the same is true for the
absolute humidity.

In Chapter 2 of Brooker et al. (1974), equations are given for calculating each of the eight
thermodynamic properties of moist air defined in the previous paragraphs. Because the
thermodynamic properties of air are so frequently needed in analyzing grain-drying
calculations, charts have been constructed, for various dry-bulb temperature ranges and
atmospheric pressures, of the values calculated from the Brooker psychrometric
equations. These charts are called psychrometric charts.

The vertical axis of the psychrometric chart usually represents the absolute humidity (and
the vapor pressure), the horizontal axis the dry-bulb temperature. Diagonal lines represent
constant enthalpy (and wetbulb) values. The relative humidity lines are curved. The
specific volume lines are drawn obliquely to the horizontal axis. If two of the
thermodynamic values of the air are known, the other properties can be read directly from
the psychrometric chart.

Several processes in grain drying can be followed directly on the psychrometric chart.
These include: heating, humidifying, condensing and drying.
GRAIN QUALITY

This material is covered in more detail in Chapter 3 of Brooker at al. (1974).

The objective of post-harvest drying is to maintain the desired qualities of the grain. It
depends on the enduser of the grain which grain quality factor is most essential. Desirable
properties of the dried grain to be considered by the grain dryer designer might include:
(1) appropriately low and uniform final moisture content, (2) low moldcount of the dried
kernels, (3) low percentage of broken and damaged kernels, (4) high viability (seed), (5)
high head-yield (rice), (6) high bakingquality (wheat), (7) high oil-recovery (soybeans),
(8) high starch-yield (sorghum), (9) high protein-content (wheat), and (10) high test-
weight (maize).

Many countries have official grain standards under which grain is traded; unfortunately,
no international standards have as yet been adopted. Few of the properties listed in the
previous paragraph are contained in the grain standards. In the United States, the
standards for the six grades of paddy includes maximum limits of heat damaged, chalky
and physically damaged kernels, and specified color requirements; moisture content is
not part of the grades. In the Philippines, the five standard grade requirements for paddy
include maximum limits of nine factors, including foreign matter, moisture content, and
cracked kernels. The United States standard for the six grades of maize includes the
factors of moisture content, test weight, broken kernels and foreign material, and
damaged kernels.

The drying-air temperature can have a significant effect on grain-quality although it

should be emphasized that the kernel-temperature rather than the drying-air temperature
should be considered in assessing kerneldamage. In many grain dryers, there is no
significant difference between the air and kernel temperatures (e.g. in in-store dryers), but
in some dryer designs the maximum kernel-temperature is far below the inlet
airtemperature (e.g. in concurrent-flow dryers). The maximum allowable grain-
temperature depends on (1) the use to be made of the grain, (2) the moisture content of
the grain, and (3) the type of grain. For seed grain above 24% (w.b.) moisture content the
safe dryingtemperature is 43°C, and below 24% (w.b.) is 49°C; for milling-wheat above
25% (w.b.) the maximum temperature is 60°C, while at moistures below that level 66°C
drying air can be used. In feedgrain, kerneltemperatures in the 100-120°C range do not
affect the nutritive value of the grain but may increase the susceptibility of the kernels to
breakage.

Research is being conducted to quantify the grainquality deterioration during the drying
process. First order reaction equations have been developed for the decrease during
drying in seed-viability of wheat and the increase in breakage susceptibility of maize. A
somewhat different set of equations has been developed for the dry-matter loss and mold
development during lowtemperature in-store drying.
GRAIN EQUILIBRIUM MOISTURE CONTENT

Chapter 4 in Brooker et al. (1974) should be consulted for additional information on the
topic

The concept of equilibrium moisture content (EMC) is important in grain drying because
the EMC determines the minimum moisture content to which a grain is dried under a
given set of drying conditions. The EMC is defined as the moisture content of a
biological product after it has been exposed to a particular environment for an infinity
long period of time. The EMC of grain is dependent upon the humidity and temperature
of the air, and on the grain-type, grainvariety, grain-maturity, and grain-history.

As an example of the effect of grain-type, consider 16% (w.b.) moisture content wheat
and oats stored at 30°C and 75% relative humidity. Because of the difference in the
equilibrium moisture contents of the two crops at 30°C-75% RH, the wheat will absorb
moisture while the oats will lose water.

EMC values of different grains have been determined over a wide range of temperatures
and relative humidities. These values are available in the literature in table and in graph
form. The graphs are known as EMC isotherms, and are plots at a particular temperature
of the percent moisture content (on the coordinate) versus the percent relative humidity
(on the abscissa).

To facilitate dryer design calculations, equations have been developed for the sigmoid-
shaped EMC isotherms. International agreement appears to have been reached to
recommend the theoretically-based Guggenhein-Anderson-de Boer (GAB) isotherm for
the calculation of the EMC values of all food products including grains. The empirical
isotherm equation developed specifically for grains by Chung-Pfost has been used
extensively in the past for grain dryer design.

EMC data allow calculation of the heat of vaporization of moisture from the grain. This
value is a measure of the energy requirement to dry grain at different moisture contents
and temperatures. Knowledge of the heat of vaporisation of a grain is essential for the
calculation of the fuel consumption of the crop during the drying process.

AIR MOVEMENT

The topic of air movement is discussed in more detail in Chapter 5 in Brooker et al.
(1974).

Drying air fulfills two functions in a mechanical grain drying system: (1) to carry the
necessary energy to the grain to evaporate the moisture, and (2) to carry the evaporated
water out of the grain mass. When air is forced through a bed of grain, resistance to the
flow develops because of friction and turbulence. The resistance, called the pressure
drop, is overcome by providing an excess pressure on the air entrance side of the grain
mass, or by providing a vacuum on the air exit side. The pressure drop through the layer
of grain depends on the rate of airflow, the physical characteristics of the grain kernels,
the bed porosity, the thickness of the layer, the percentage of impurities in the grain, and
the method of filling the dryer.

Pressure drop data for grains and legumes have been determined experimentally over a
wide range of airflow rate. The data is usually plotted on log-log paper in terms of mm of
water column (or Pascal) per meter of bed depth versus airflow rate in m³ per sec per m²
of bed area Equations are available in the literature expressing the pressure drop through
a grain mass in terms of airflow rate, percentage of fines, moisture content, and bed
depth.

In addition to the resistance in the grain, the drying air can encounter resistance in the air-
ducting system of the dryer. The sum of the grain and ducting resistances represents the
system resistance of the dryer.

The air-moving device used in grain drying systems is the fan; it should be able to deliver
the specified volume of air at the correct pressure Two types of fans are in use in grain-
drying installations, the axial-flow and the centrifugal. Axial-flow fans have one or more
impellers (with radial blades) rotating within a cylindrical casing; air flows parallel to the
axis of the fan shaft. Centrifugal fans have an impeller (with blades around its periphery)
rotating within a scroll-shaped casing; the air enters parallel to the impeller shaft and is
fumed 90° before discharge Axial fans are noisier than centrifugal fans, operate at lower
pressures, require less space, and are in general less expensive in delivering a certain air
volume.

The performance of geometrically similar fans is governed by a series of fan laws which
express the effect of speed of rotation of a fan on the volume of air delivered, the pressure
developed and the power required. Proper matching of the pressure drop versus airflow
curve of a fan rotating at a certain speed with that of a drying system results in the
operation of the fan at the desired characteristic pressure and airflow rate of the dryer. If
the match between fan and drying system is correct, the fan will operate close to the
optimum efficiency range of the fan, and near the rated horsepower.

GRAIN DRYING CALCULATIONS

This section parallels Chapter 8 in Brooker et al. (1974).

Drying is a process of simultaneous heat and moisture transfer. A number of biological

products, when drying as single particles under constant external conditions, exhibits a
constant-rate moisture loss during the initial drying period, followed by a falling-rate
drying period. Grains and legumes, however, dry entirely within the falling-rate period.

In order to model the drying of a grain dryer, the drying-rate characteristics of the
individual kernels have to be known in terms of the moisture and temperature changes
occurring at different drying conditions. The drying rate equation fulfills this purpose.

Due to the complexity of the falling-rate graindrying process, engineers prefer to lump
the effects of the different physical drying-transport mechanisms (ie. liquid diffusion,
capillary flow thermal diffusion, vapor diffusion) into a simplified semi-theoretical
diffusion equation with a concentration and temperature dependent diffusion-coefficient.
Values for the effective diffusion-coefficient have been published for most grains
including paddy and maize. A purely empirical dryingrate expression, the so-called "thin-
layer" equation, is frequently used by grain dryer designers; values for the "drying
constant" of cereals and legumes are available in the literature.

Thin-layer (or diffusion) equations describing the drying-rate of individual grains are an
essential part of deep-bed grain-drying models of in-store and continuous-flow dryers.
There are basically two types of drying models, the differential-equation type and the
heat-mass balance type. Each can be divided into nonequilibrium and equilibrium
models. The nonequilibrium/differential-equation grain-drying models are the most
fundamental and general in nature, and give the most accurate predictions of the
dryingrate, the moisture content distribution, and the energy consumption of a particular
dryer-type, regardles of its configuration or grain-type.

Insect pests of stored products

Contents - Previous - Next

Chuwit Sukprakarn

Thailand is one of rice growing countries in the world, the cultivation is about 10 million
hectares and annual production is 19.5 million tons. Rice is grown in all parts of the
country from the Southern border with Malaysia to the Northern border with Laos and
Burma with a distance of about 1,600 kilometres. Most of the rice varieties are irrigated
rice and depended upon rainfall, very few are upland rice. About 20 percents are floating
rice which may grow in water at several metres deep. Rainfall is the most variable
climatic factor affecting rice cultivation. The average annual amounts of rainfall for the
whole country is 1,500 mm (about 60 inches) per year. In the Northeastern Region, only
1,000 mm are common while in the Southern Region the usuall rainfall are about 2,000
mm and may reach up to 2,500 mm.

Besides rice production, Thailand also producing maize, sorghum, mungbean, soybean,
groundnut, cassava etc.
Most of the farmers do not store the grain for a longer period except for replanting. They
generally sell the grain either before harvesting or during threshing for the rent or money
requirement. Nearly all of the grain and other agricultural products therefore are kept in
the mills, godowns or even silos ready to be exported or distributed to the local markets.
For this reason, those who operate storage facilities must know how to protect the grain
from insect infestation. Government organizations as well as the farmers do not
emphasise much research on stored grain insects. Very few research works on stored
grain insects have been undertaken during the recent years, most of the works were
confined on the insect pest attacked in the field rather than the pests of stored grain.

Losses due to insect infestation

The percentage of losses is very difficult to determine and the figures vary from 1 % to as
much as 25%. The official figures however, released by the five ASEAN countries stated
that the member nations lost about 25% of their paddy crop during harvesting and other
post-harvest practices including storage and transportation, and the loss represents 10.5
million tons of paddy whereas FAO reported in 1977, the loss of rice within the
postharvest system for Thailand ranged from 8-14%. In Thailand itself, there is no
official report on losses due to insect infestation. The estimation of losses is based only
upon experiments. For paddy, some investigators reported that the loss in weight for 8
months was at 1.14-3.41% when in farm and more than 5% for commercial storage while
the author reported that grain loss was from 0.05-10.48% for one year storage. The report
recently from the Rice Institute, 20 varieties of paddy seed when stored untreatment for
10 months, the losses varied from 2.06 to 24.30% with an average 4.54%. Other grain
crops eg. maize, sorghum and pulses, these crops have already been infested by the
insects from the fields and also from the poor storage condition. When the grain has no
protection, the insect population will build up rapidly. Therefore, the losses and damages
by insect pests are related to the storage duration. Unfortunately, there is no record on
losses of these crops but it has been observed that the severe damage will occur within a
few months of storage and may reach upto 50% for 6 months storage. This is one of the
reasons why the farmers need not keep the grain in large quantity and longer periods.

Presently, quantity loss is not as important factor as the loss of goodwill in the
international trade. The loss of goodwill between traders and farmers or between
importers and exporters in the international trade could be a serious matter in future
marketing. In the past, some major exporters experienced the embarrassment of some
shipments being declared distressed cargoes. This was due to the presence of some
quantity of insecticide on grain which may cause health hazards to human beings.
Commercial losses can also occur due to the reduction of quality through adulteration or
insect attacks.

The major insect pests can be grouped according to feeding behavior as follows:
Paddy: Rice weevil (Sitophilus oryzae (Linnaeus))
Angoumois grain moth (Sitotroga cerealella (OIivier))
Lesser grain borer (Bhyzopertha dominica (Fabricius))
Siamese grain beetle (Lophocateres pusillus (Klug))
Flat grain beetle (Cryptolestes pusillus (Schonherr))
Rice: Maize weevil (Sitophilus zeamais Motschulsky)
Rice weevil (S. oryzae (Linnaeus))
Red flour beetle (Tribolium castaneum (Herbst))
Rice moth (Corcyra cephalonica Stainton)
Saw-toothed grain beetle (Oryzaephilus surinamensis (Linnaeus))
Flat grain beetle (Cryptolestes pusillus (Schonherr))
Maize & sorghum: Maize weevil (Sitophilus zeamais Motschulsky)
Red flour beetle (Tribolium castaneum (Herbst))
Corn-sap beetle (Carpophilus dimidiatus (Fabricius))
Rice moth (Corcyra cephalonica Stainton)
Tropical warehouse moth (Ephestia cautella (Walker))
Pulses: Cowpea beetle (Callosobruchus maculatus (Fabricius))
Southern cowpea beetle (C. chinensis (Linnaeus))
Tropical warehouse moth (Ephestia cautella (Walker))
Cassava: Coffee bean weevil (Araecurus fasciculatus (Degeer))
Lesser grain borer (Rhyzopertha dominica (Fabricius))
Cigarette beetle (Lasioderrna serricorne (Fabricius))

Biology of Storage Insects

Insects development take place between 17°C and 35°C The optimum temperature for
most storage insects is around 30°C at 75% relative humidity The insects are more
critical in their response to high temperatures. Most insect pests are killed by
temperatures above 40°C. Whereas most stored grain insects are able to withstand
temperatures below freezing for several days but when exposed to 65°C for a few
minutes all the insects are killed.

The number of important storage insects is rather small, being about 30. Most species
have a short life cycle of 4-6 weeks and are universal in their taste.

A number of storage insects lay their eggs in or near produce. After hatching the larvae
into the produce and develop there till after pupal stage. Other pests develop and pupate
on or between the produce.
Adults of storage insects can be long or short living. Bruchids and moths are short living
(up to 3 weeks). They lay most of their eggs during the first week of adulthood. Other
species like Sitophilus and Tribolium can live for 6 to 12 months. Egg deposition takes
place over a prolonged period.

Important parameters in the development and reproduction of storage pests, besides

climate, are the kind and condition of the produce and its moisture content. So at 25°C
and 70% relative humidity the development of Ephestia cautella takes about 30 days on
grains, 43 days on groundnuts and 53 days on cocoa beans. Storage pests can be divided
into primary and secondary pests. Primary pests like Sitophilus or Ephestia species are
able to develop on undamaged produce, while secondary pests will develop only on
produce which was previously damaged by other insects or mechanically. So in stored
produce a certain succession of pests may occur.

In this section only the biology of some major insect pests will be briefly discussed.

1. The rice weevil (Sitophilus oryzae L.)

Order Coleoptera, Family Curculionidae

The weevil is brown to black with two paler reddishbrown patches on each elytra, 2-3
mm long. The female lays about 200 eggs in the grain and the larva feeds and pupates in
the grain. The incubation period lasts 36 days, the larval and pupal period is 20-30 and 3-
7 days respectively. The life cycle is completed in 30-40 days.

2. the red flour beetle (Tribolium castaneum Hbst.)

Order Coleoptera, Family Tenebrionidae

The beetle is 2.3-4.4 mm long, reddish-brown and flat. Eyes large, emaginate; antennae
clavate, 11 segmented. The egg, white, oblong or pear-shaped. A female lays 15-72 eggs
in rice and the incubation period takes 3-7 days. The larva is whitish, worm-like. There
are 6-7 larval instars and the larval period ranges 21-40 days. The pupal period is 3-7
days and the life cycle completed in 26-48 days.

3. The Angoumois grain moth (Sitotroga cerealella Oliv.)

Order Lepidoptera, Family Gelechiidae

A small moth with a wing span of approximately 1/2 inch which can be distinquished by
its pale brown colour and the elongate sharply pointed apices of the hind wings. A female
lays 30-78 white, oblong shaped eggs, singly or in small groups. After hatching the
whitish larva bores into and spends its complete life cycle wishing a single grain,
eventually pupating there. It takes 4-6 days for incubation period and 26-35 days for
larval period. The pupal period takes 3-6 days and the moth can live for 3-7 days.
4. The almond moth (Ephestia cautella W.)

Order Lepidoptera, Family Phycitidae

The moth is greyish or pale grey with two zigzag lines on forewing with a wing span of
about 12-16 mm. A female lays upto 205 eggs in cracks or crevices on grain after which
the female dies soon after. The eggs hatch within 3-6 days. The whitish larvae molt 3
times and complete their life cycle in 27-83 days.

5. The rice moth (Corcyra cephalonica Staint.)

Order Lepidoptera, Family Galleriidae

A medium-sized moth with a wing span of 20-25 mm, the forewings are uniformly pale
brown with the veins slightly darkened. A female lays 44-364 whitish eggs with
incubation of 4-5 days. The larva is white to whitish-grey. The larval period takes 2841
days with 5-7 larval instars. The pupal period is 6-13 days and the moth can survive for
4-6 days.

6. The Cowpea beetle and Southern cowpea beetle (Callosobruchus chinensis L. & C.
maculatus F.)

Order Coleoptera, Family Bruchidae

These two species are resemble in appearance and they occasionally feed on food
together. The size of the Cowpea beetle is little smaller than the Southern Cowpea beetle
(2.0-3.5 mm.: 3.0-4.5 mm). It is small, oval brown beetle with or without black markings
on the elytrae. A female lays more than 10 yellowish eggs (average 50 eggs) on grain
with the incubation period 36 days. The larva feeds and pupates inside the grain then
emerges as adult. The larval and pupal period is 1820 and 3-7 days respectively. The life
cycle completed in 18-33 days and the beetle can survive up to 12 days.

Prevention and control of storage insects

The principal means of prevention is to select a place and method of storing, that suit best
the produce and local conditions. Many products like maize, sorghum, groundnuts etc.
can either be stored as unshelled or as shelled produce.

Unshelled produce such as maize and sorghum can be stored on the cob or in the ear in
rectangular or round cribs constructed from poles, bricks and chickenwire. Because of
good ventilation mould problems are few, but protection against insects and rodents
needs use of pesticides.

Shelled produce can be stored in bags in warehouses or in bulk in silos.

In all cases, strict hygiene is very Important. Warehouses and silos must be cleaned
thoroughly of old infested produce before the new harvest is brought in. Bags should be
stacked on pallets and stand free of walls and celling. Different products should be
stacked separately. Food stores should be swept out every week and the sweepings must
be burned immediately. The storage structures should be closed off to prevent entry by
pests, airtight silos with good thermal insulation offer the best protection.

Admixture the grain or seed with inert substances such as dust or plant parts could
prevent maize and sorghum from insect damage for some period, while in oil seeds and
pulses the admixture the grain with edible oil like palm oil, rice bran oil or peanut oil are
recommended to control the Bruchids.

Temperature Control: Since most stored product insects cannot tolerate extreme
temperature, heating and cooling are logical approaches to insect control. To some extent
it has been a common practice to superheat some comodities for insect control. The
temperatures of 55-60°C maintained for 10 to 12 hours are effective. Actually, these
temperatures kill most insects very quickly but when the grain and materials are involved,
the certain temperature must be kept for several hours to ensure complete penetration.

Low temperature is probably the most important single factor in making long term
storage possible and economical. The insects become inactive and eventually die at a
temperature below 12°C. Freezing quickly kills many insects. Low temperature is also
important in maintaining seed viability.

Moisture Control: Most of the stored grain insects are unable to survive and reproduce
in grain whose moisture content is below 9 per cent. Most favorable grain moistures for
insect development ranges from 12 to 15 per cent. If, by various means, it is possible to
reduce and maintain the moisture below than favorable for reproduction and
development, then we have in effect, controlled the insects.

All agricultural products should be well dried before storage especially for storing in
silos. A high moisture content tends to increase insect and mould development; to
bacterial deterioration, and chemical changes in the produce. When the crop is ripe it still
has a high moisture content. Under dry weather conditions the crop is usually left in the
field to dry, but in the humid tropics artificial drying is often necessary.

Produce should not be stored at moisture contents higher than indicated below.

paddy 15%
rice, maize, wheat, sorghum 13%
millet 16%
cowpeas, beans 15%
groundnuts, cocoa beans 7%
Chemical Control: For the protection of stored produce against the insects the following
groups of pesticides are used:

a) insecticides
b) fumigants

For the protection of store produce, pesticides are often applied shortly before use or
mixed with the produce, which limits the choice of pesticides which can be used and rates
of application. It will be obvious that, for the protection of stored produce, only pesticides
can be used with a rather low mammalian toxicity whose residues easily degrade to
innoxious compounds which can be excreted. Insecticides which are accumulated in the
human body e.g. DDT are of course completely unsuitable for use on stored produce.

Insecticides may be used for spraying wall, floors and ceilings of warehouses or
storerooms in order to kill a residual infestation. The insecticides can also be sprayed
directly on bagged produce. This may prevent or delay reinfestation of insect-free
produce. Insecticides may be mixed with the produce. This can give complete protection
for a long period and may also kill pests which have already infested the produce. The
best way however to disinfect produce, warehouses or storerooms, is by means of
fumigation. The fumigants used penetrate into the grain or compressed products like
tobacco and kill all insects. Some fumigants kill also micro-organisms. After fumigation,
reinfestation must be prevented by insecticides or by storing the produce in an insect
proof silo or container.

Resistance to pesticides is developing fast in storage pests. If this occurs the best way of
protection if probably a combination of fumigation with storage in insect proof containers
or silos.

Insecticides

For the protection of stored products only a few insecticides are in common use.

a) Malathion: This is a safe insecticide which can be admixed to or sprayed on shelled

(threshed) or unshelled (unthreshed) grains. On stored produce only premium grade
malathion must be used. (LD50 = 1400 mg; tolerance 8 ppm for raw cereals (FAO/WHO)
The general recommendation is to mix 100150 9 2% with 100 kg produce.

Malathion dust has some limitations.

1) The product must be dry, (moisture content not higher than 13.5%) otherwise the
malathion breaks down very fast.

2) The formulated malathion dust mostly has a rather short shelf life (not more than 6
months).
Malathion can also be used for spraying walls, floors or the outside of stacks (1000 mg
a.i./m²).

b) Ryrethrins: This is a very safe botanical insecticide but costs are high (LD50 = 1500
mg; tolerance 3 ppm for raw cereals) (FAO/WHO).

Pyrethrins are mostly admixed with a synergist to increase their effectiveness and
stability and to reduce costs. The shelf life of dust formulations is rather short. Rates of
application are:

100 g 0.2% pyrethrins + piperonyl butoxide (1:5) per 90 kg cereals and 100 9 0.1%
pyrethrins + piperonyl butoxide (1:5) per 90 kg beans.

c) Other insecticides

During the past years a number of other insecticides have become available, the use of
which is permitted in several countries.

The most important are the following:

bioresmethrin
bromephos
chlorpyrifos-methyl
fenitrothion
pirimiphos-methyl
tetrachlorvinphos

Rates of application are indicated in the table below.

Grain Bags Warehouses

g.a.i./100 kg g.a.i./m² WP g.a.i./m² WP
dusts
bicresmethrin 0.3
bromophos 0.6.08 1.0-1.25 0.51.0
chlorpyrifos methyl 0.4-.06 — —
fenitrothion 0.8-1.0 0.5 0.5-1.0
pirimiphos-methyl 0.40.6 0.5 0.5
tetrachlorvinphos 1.0-1.5 1.0 2.0 1.0-2.0

Fumigants
A fumigant is a chemical which at the required temperature and pressure can exist in the
gaseous state in sufficient concentration to be lethal to a given pest organism.

Many fumigants are available and several are commonly used throughout the world. Any
confined space which can be made airtight, may be used for fumigations, e.g. silos,
railway, trucks, shipholds, plastic bags, etc. Bagged produce is mostly fumigated under
gasproof sheets.

After fumigation a small amount of unchanged fumigant may remain as a residue.

The following fumigants are commonly in use:

a) Methylbromide. It penetrates easily in large stacks of bagged produce but, without a

special circulation system its use in large silos is limited because of unsatisfactory
distribution of the gas in the grain bulk.

In flat storage, for instance in barges, this does not play a role. Under atmospheric
conditions a fumigation takes 24 hours. Under vacuum conditions only several hours are
needed.

Methylbromide is highly toxic and rather sophisticated equipment such as gas cylinders
piping systems, gas masks and gas detectors are necessary. The fumigation has to be
carried out by trained personnel.

Rates of application under atmospheric pressure are 16-32 g/m³ for 24 hrs depending on
temperature, commodity and the insect or mite species to be controlled.

b) Phosphine. This fumigant is available in the form of tablets (pellets or sachets).

Moisture absorption liberates phosphine which is very toxic to insects. The tablets must
be evenly distributed through the grain by adding them to the grain flow when a bin is
filled.

The tablets can also be inserted in or between bags which then must be covered by air-
tight sheets. Since the development of phosphine starts some hours after application, the
use of phosphine is easy, but gas masks are necessary when aerating large stacks.

Rates of application are 1-1 1/2 tablet per m³ for bagged produce under plastic sheets or
2-5 tablets per ton for grain in silos. A fumigation with phosphine takes 5-7 days, besides
the ease in application phosphine has some other advantages. There is less chance of
affecting the germination capacity than with other fumigants like methylbromide.
However, a preliminary test is always useful. The penetration of phosphine is probably
better than that of methylbromide and costs of fumigation are usually less. Till now
phosphine has not caused residue problems.

c) Liquid fumigants like carbon tetrachloride or mixtures of carbon disulphide, ethylene

dibromide or ethylene dichloride and carbon tetrachloride are easier to handle as they are
less toxic to man. The liquid is poured on the produce or left in trays to evaporate. Such a
fumigation takes several days depending on the temperature and quantity of fumigant
used.

Airtight storages

When grains are stored in an airtight container, the oxygen content in this container will
decrease slowly due to the metabolism of the grains, insects and microorganisms until
there will not be enough oxygen for any insect development. Airtight storage is an
attractive way to protect produce against insects without pesticides, but often the costs of
constructing suitable silos prevent their general use. For airtight storage on a small scale,
oildrums or plastic bags may be used.

The lowest O2 concentration below which insects cannot survive is about 2%. On the
other hand a high CO2 concentration (36%) together with a high O2 concentration (15-
21%) is lethal to storage pests too. The relative humidity has a strong influence on the
effect of the gas concentrations. In general, a low relative humidity increases the
mortality cause by low O2 or high CO2 concentrations. A new development is the use of
CO2 for long-term preservation and fumigation of cereal grains which has been found
more effective and easier to apply than to decrease O2 concentrations.

Table

Sieves

Hand-held sieves

Hand-held sieves are commonly used for assessing the foreign matter content of small
samples of grain. Round-framed sieves with a diameter of 300 to 310 mm are preferred,
although square-framed sieves with sides 300 to 310 mm long may be used. Each set of
sieves should be provided with a bottom pan (receiver), for the collection of material
passing through the screens, and a lid to prevent spillage during the sieving.

Comparability of the results of using hand-held sieves depends primarily on uniformity in

their manufacture and it is essential to use sieves made by a factory whose products are
approved by a standards organisation.

Hand-held sieves should be used in a uniform manner if comparability of results is to be

maintained. Firstly, the sieve should be held level in both hands directly in front of the
body, with the elbows tucked in to the waist. Secondly, using a steady motion, the sieve
should be moved approximately 25 cm to the left and back through the centre position,
smoothly 25 cm to the right and returned to the centre position. This sieving operation
should be repeated exactly 30 times, taking about 30 seconds to do so. No forwards and
backwards or up and down movements are permitted, although a final gentle tap of the
sieve will help to clear it of any material hanging from the perforations before the bottom
pan is removed. When sieves with slotted screens are being used, it is important to ensure
that the long sides of the slots are parallel with the movement of the sieve.

Sack sieves

The foreign matter content of grain is more accurately assessed when the contents of
whole sacks are screened, although this is obviously more time consuming than the hand-
sieving of small samples.

A sack sieve should possess two essential features a hopper for feeding grain gradually
on to the screen and a screen and a screen that moves during the sieving operation. The
slope of a moving screen should ensure that the grain is kept in motion towards the
discharge end. Lateral movement of the screen, as in a rotary type of sieve, is more
efficient in separating out foreign matter than the end-to-end movement of other kinds of
mechanical sieve.

Some standard stove sizes for cereal grains

Locally produced varieties of grain may require sieves to have screens with specifications
significantly different from those indicated in Table 20. Samples of grain should be
checked against standard sieves of different specifications before quantities of sieves are
purchased for grain quality assessment.

Care and maintenance

Sieves of standard quality are precision instruments that should be used and handled with
care, and always kept clean and dry. A proper sieve brush should be used for removing
dust and other material from a sieve after it has been used. Pieces of material stuck in the
perforations should never be pushed through from the top surface of the screen. This can
distort the holes and affect the accuracy of the sieve. Instead, the screen should be tweed
upside down and tapped sharply or the material should be pushed out of blacked
perforations with the finger tip.

Newly manufactured sieves are often coated with a thin film of oil or wax. This must be
removed with warm water and detergent before the sieves are used.

If a sieve is not going to be used for some time, it should be thoroughly cleaned and
coated with oil before storage to prevent possible deterioration. it must be cleaned before
reuse.

Sieves are subject to wear and tear despite due care and attention and they should be
checked periodically for accuracy, by comparing them with standard sieves. This is
normally the responsibility of a national standards organisation or central laboratory in
control of all grain quality matters.

Prevention and control of mycotoxins

Contents - Previous - Next

Maitree Suttajit, Ph.D

INTRODUCTION

Serveral mycotoxins in agricultural products cause health hazards to people and animals
and economical problem. Dangerous mycotoxins are naturally present in foods, feeds and
our environment. They are pathologically classified as hepatotoxins, nephrotoxins,
vomitoxin and neuro-musculotoxin, some of which are potentially carcinogenic and
mutagenic (Table 1). Aflatoxin, for example, is the most potent hepatocarcinogen and
mutagen among mycotoxins. Therefore, the contamination of mycotoxins should be
minimized by designing a series of measures of prevention and control.

STRATEGIES FOR PREVENTION AND CONTROL OF MYCOTOXINS

To design strategies for the reduction or elimination of mycotoxins, knowledge about

their fungal sources are needed. The growth of fungi in crops and agricultural products is
the main cause of toxin formation and related to the concentration of the toxic substances.
Many factors are involved in enhancing the formation of mycotoxins. They are plant
susceptibility to fungi infestation, suitability of fungal substrate, temperate climate,
moisture content and physical damage of seeds due to insects and pests.

Toxin-producing fungi may invade at pre-harvesting period, harvest-time, during post-

harvest handling and in storage. According to the site where fungi infest grains,
toxinogenic fungi can be divided into three groups: (a) field fungi; (b) storage fungi; and
(c) advanced deterioration fungi. The first category includes species of plant pathogenic
fungi, namely, genus Fusarium, e.g. F. moniliforme, F roseus, F. tricinctum and F. nivale.
The "storage fungi" are principally the general Aspergillius and Penicillium, e.g. A.
flavus and A. parasiticus. The "advanced deterioration fungi" normally do not infest
intact grains but easily attack damaged ones and require high moisure content. The
examples of the third group are A. clavatus, A. fumigatus, Chaetomium, Scopulariopsis,
Rhizopus, Mucor, and Absidia.

The prevention of mycotoxins in our environment is a big task. In general, prevention of

the contamination of fungi and their mycotoxins in agricultural commodities can be
divided into these following three levels.

1. Primary prevention
The step of prevention should be initially carried out before the fungal infestation and
mycotoxin contamination. This level of prevention is the most important and effective
plan for reducing fungal growth and mycotoxin production. Several practices have been
recommended to keep the conditions unfavorable for any fungal growth. These include:

• development of fungal resistant varieties of growing plants;

• control field infection by fungi of planting crops;
• making schedule for suitable pre-harvest, harvest and post-harvest;
• lowering moisture content of plant seeds, after post harvesting and during storage;
• Store commodities at low temperature whenever possible;
• Using fungicides and preservatives against fungal growth;
• Control insect infestation in stored bulk grains with approved insecticides.

Table 1: Some mycotoxins, their sources and potential toxicities (1).

Toxins Producing fungi Toxicities

Aflatoxin Aspergillus flavus
Aspergillus parasiticus
Citreoviridin Penicillium viridicatum
Citrinin Penicillium vindicatum
Penicillium citrinum
Cyclochlorotine Penicillium islandicum
Cytochalasin E Aspergillus clavatus
Maltoryzine Aspergillus oryzae
Ochratoxins Aspergillus ochraceus
Patulin Penicilliumc-expansum
Penicillium patulum
PR Toxin Penicillium requeforti
Rubratoxin Penicillium rubrum
Rugulosin Penicillium islandicum
Sterigmatocystin Aspergillus flavus
Aspergillus versicolor
Tremorgens Penicillium and Aspergillus
Trichothecenes Fusarium graminearum Cytotoxicity
Vomitoxin Fusarium graminearum Vomiting
(Deoxynivalenol)
Zearalenone Fusarium
Hepatocarcinogen
and fatty liver
Cardiac beri-beri
Nephrotoxin
Hepatotoxin
Cytotoxicity
Hepatotoxin
Brain & lung hemmorrhage
and carcinogenicity
Liver hemmorrhage and fatty
infiltration
Nephrosis & liver damage
Hepatocarcinogen
Hyper-estrogenic effect

2. Secondary prevention
If the invasion of some fungi begins in commodities at early phase, this level of
prevention will then be required. The existing toxigenic-fungi should be eliminated or its
growth to be stopped to prevent further deterioration and mycotoxin contamination.
Several measures are suggested as follows:

• Stop growth of infested fungi by re-drying the products;

• Removal of contaminated seeds;
• Inactivation or detoxification of mycotoxins contaminated;
• Protect stored products from any conditions which favour continuing fungal
growth.

3. Tertiary prevention

Once the products are heavily infested by toxic fungi, the primary and secondary
preventions would not be then feasible. Any action would not be as effective as the
practices mentioned above, since it will be quite late to completely stop toxic fungi and
reduce their toxin formation. However, some measures should be done to prevent the
transfer of fungi and their health hazardous toxins highly contaminated in products into
our daily foods and environment. For example, peanut oil extracted from poor-graded
peanut seeds always contains very high levels of aflatoxins and the oil-soluble toxin has
to be eliminated by absorption and alkalinization during oilrefining process. Only a few
practices are recommended:

• Complete destruction of the contaminated products;

• Detoxification or destruction of mycotoxins to the minimal level.

Since aflatoxin is the most well-known mycotoxin ever throughly studied and its
prevention and control has been most successfully practiced in various countries,
therefore, this paper will focus on such practices in certain detail for the prevention and
control of aflatoxins mycotoxin contamination. Successful development will bring a great
impact for the increased production of crops and safe and nutritious foods around the
world. A number of researchers have been working on A. flavus-resistant or tolerant
varieties of corn (2-3) and peanut (4-6)

It has been clear that the fungal-resistance of each variety is genotypic. However, the
resistance to invasion of A. flavus has been attributed to several biochemical,
environmental and physical factors. Uncontrollable factors could bring the failure in the
utilization of selected fungal-resistant variety, as shown by laboratory screening, in the
field.

Davis and his co-workers (7) reported the survey and comparison of aflatoxin
contamination in upto 215 corn hybrids grown in Alabama, USA during 1976-81.
Unfortunately, they could not find any hybrid tested resistant to aflatoxin formation. They
were convinced that significant aflatoxin levels generally accompanied stress caused by
high temperature, low rainfall, low moisture-holding capacity of sandy soils and insect
infestation.
A differential pathogenic capacity of various toxigenic strains of A. flavus have been
observed (8). Some strains would require physical damage for their infestation and others
would not. The association of mycotoxin production and physical damage to grain and
drought during grain ripening indicates that Aspergillus spp. are weak pathogens. During
long grain storage, the biochemical activity of grain is much reduced, while invasion of
storage fungi and mycotoxin contamination would increase. More data is needed on the
biochemistry and pathogenesis of toxigenic fungi to understand and evaluate their
genotype.

The germination and viability of maize seeds could be affected by attack of Aspergillus
and Penicillium species and their fungal infestation have been found to be different
among maize genotypes (9-10).

Similarly, genotypes of peanut and biochemical properties of its seed such as tannin
content (11), thin pericarp (12), small amount of cuticular wax (13) and chemical
composition of the pericarps and embryos (14) have been shown to inhibit fungal
invasion by A. flavus and aflatoxin formation.

Recently, antifungal enzymes, chitinase (15) and B-1, 3-glucanase (16), found in a
number of plant seeds, may act as defense against pathogenic fungi, since chitin and
glucan are major polymeric components of many fungal cell walls. Such polysaccharides
in fungal cell wall could be enzymically hydrolysed into smaller products resulting the
damage or killing of fungal mycelia or spores. The role of these enzymes for genotype
evaluation is now being studied. It is foreseen that seeds rich in such antifungal enzymes
likely resist the infestation of fungi. If so, the seeds for breeding would be easily screened
out and used a stock one.

Even there are many technical problems in searching for the "super" plant against
pathogenicity, the development of fungal-resistant plant varieties utilizing genetic
resistance to mycotoxin contamination is still possible and encouraged.

FUNGAL GROWTH INHIBITION

How to prevent growth and invasion of pathogenic fungi in agricultural commodities is

very important in preventing mycotoxin contamination. The inhibition of fungal growth
can be achieved by physical, chemical and biological treatments (17).

• Physical treatment. After the crops have been harvested, drying and proper
storage and suitable transportation of the commodities are of prime importance.
Several flavourable factors contribute to the growth of fungi and aflatoxin
production, namely high moisture content, humid climate, warm temperature
(2540°C), insect infestation and pes damage. Many means and measures to
prevention of fungal contamination have been emphasized and practically done.
 • Drying seeds and commodities to the safe moisture levels (<9% for peanut kernel,
and < 13.5% for corn) (17).
• maintenance of the container or warehouse at low temperature and humidity.
• keep out insects and pests from the storage
• Gamma-irradiation of large-scale commodities (18).
• Chemical treatment with synthetic fungicides
• organic acids: acetic acid (19), propionic acid and butyric acid (20), malonic acid
(21), benzoic acid (22, 23), sorbic acid (24), lactic acid (25), citric acid (25) and
their sodium salts
• sodium chloride (26)
• Benzoic acid derivatives (27): Onitrobenzoate, O-aminobenzoate,
paminobenzoate, benzocain (ethly aminobenzoate), ethyl benzoate, methyl
benzoate and aspirin (O-acetoxy benzoic acid)
• potassium sulfite and potassium fluoride (27)
• dichorvos (28)
• fumigant: ammonia and phosphine (29).
• treatment with natural products from plants or herbs.
• allicin and related substances from garlic and onion extracts (30)
• chitosan or derivative of chitin isolated from crustacean shells (31)
• cinnamon extract: trans-cinnamic acid, trans-cinnamaldehyde, and ferulic acid
(phydroxy-3-methyl cinnamic acid) (32)
• clove oil (32)
• other herbs: thyme, star anise seeds (33), black and white peper (34). plumbago
indica (35).

DECONTAMINATION OF MYCOTOXINS

Contaminated mycotoxins in foods and feeds should be removed, inactivated or

detoxified by physical, chemical and biological means depending on the conditions.
However, the treatment has its own limitations, since the treated products should be
healthsafe from the chemicals used and their essential nutritive value should not be
deteriorated. The following methods are suggested to be applied for effective
decontamination of some mycotoxins.

Physically, fungi-contaminated seeds can be removed by hand picking or photoelectric

detecting machines. The method would consume time and Iabor or expensive.

Organic solvents (chloroform, acetone, hexane and methanol) have been used to extract
aflatoxins for agricultural products, but mainly in vegetable oil refining process (36).

Heating and cooking under pressure can destroy nearly 70% of aflatoxin in rice compared
to under atmospheric pressure only 50% destroyed (37). Dry and oil roastings can reduce
about 50-70% of aflatoxin B1 (38). We could show that only about 10% of total 1242
ppb of aflatoxin B. decreased in naturally contaminated peanut by heating at upto 100°C
(39). Since aflatoxin resists to higher temperature upto 260°C, long-time cooking and
overheating would destruct essential vitamins and amino acids in treated foods.

Ionizing radiation such as gamma-rays can stop growth of food spoilage organisms,
including bacteria, molds and yeasts. It also inactivates pathogenic organisms including
parasitic worms and insect pests. It has been reported that gammairradiation (5-10 M-rad)
caused reduction of aflatoxin (40). The irradiation, however, could not completely
destroy the toxin and its mutagenicity. In our laboratory, only about 30% of total 600 ppb
at aflatoxin B1, either pure toxin or in contaminated peanut, was destroyed by 1 and 5
Mrad or gamma irradiation (23). The treatment combination of gamma irradiation and
ammoniation should be therefore attempted for more aflatoxin decontamination.

Chemical treatment has been used as the most effective means for the removal of
mycotoxins from contaminated commodities. The method should be sure that the
detoxification system is capable of converting the toxin to a nontoxic derivative (s)
without deleterious change in the raw product. Mutagenicity of the treated products
should be assessed. The toxicity may be checked by feeding animals including bouts, egg
embryos, chicken, ducklings and rats. Many common chemicals have been brought to test
the effectiveness in detoxification of aflatoxin. These chemicals include the followings:

• acetic acid (C2H5OH) (41)

• ammonia gas (NH3) or NH4OH (42,49) or ammonium salts, 3-5% (42)
• calcium hydroxide (Ca(OH)2) (43)
• formaldehyde (43, 47)
• hydrogen peroxide (H2O2 (44)
• methylamine (CH3-NH2) (45)
• ozone gas (03) (46)
• phosphoric acid (H3PO4) (47)
• phosphine gas (PH3), very highly toxic!
• sodium bicarbonate (NaHCO3) (48)
• sodium bisulfite (NaHSO3) (49)
• sodium bisulfite (NaOH) (48,49)
• sodium hypochlorite (NaOCI) (50)

The chemical reactions of detoxification of aflatoxin are primary addition of the double
bond of the furan ring and oxidation involving phenol formation and opening of the
lactone ring. In the presence of acid, aflatoxins B. and G. will be converted into their 2-
hydroxy derivatives, aflatoxins B2a respectively.

Other mycotoxins which are like aflatoxin and have a lactone grouping in the molecule
can be similarly destroyed by alkaline condition using ammonia, sodium hydroxide and
sodium bicarbonate. These toxins are patulin, penicillin acid, citreoviridin, citrinin,
cyclochlorotin, ochratoxin A, rubratoxin, trichothecenes and zearalenone.
Clinical SymptomsThere are two groups of toxins that are present in these muhrooms—
the phallotoxins, composed of phallin and phalloidin, and the amanitins, made up of
alpha amanitin and beta amanitin.

The gastro-intestinal symptoms, which appear first and some hours after the mushrooms
are consumed, are produced by the phallotoxins. The amanitins are 10 to 20 times as
toxic as the phallotoxins, and cause the hepatorenal damage that results in the symptoms
appearing later and that in many cases ends in death.

Mycology

Claviceps purpura is the common ergot on rye and wheat. The fungus lives over winter in
the form of sclerotium, a dense mass of fungus cells. Usually the sclerotia are somewhat
larger and also less dense than the seeds of the host plant on which they are borne.

Chemistry

The ergot alkaloids are derivatives of Iysergic acid (ergotamine), isolysergic acid
(ergocristine) or dimethyl ergoline (agoclacine). Pharmacologically, these compounds are
rapid acting, powerful oxytoxics, i.e., they stimulate the smooth muscle of the uterus.
They are also weak vaso-constrictors.

Mycology

The trichothecenes are produced by various species of Fusarium especially Fusarium

graminearum (F. roseum), F. moniliforme, etc.

Chemistry

The trichothecenes are a complex group of sesquiterpenoids containing the trichothecane

nucleus, characterized by an olefinic bond at the 9, 10 position and an epoxy group at the
12, 13 position.

Clinical Symptoms

The Russian descriptions of the disease, dividing the clinical feature into four stages,
indicate that the disease seems to result from toxic injury to the hematopoletic, autonomic
nervous, and endocrine systems.

YELLOWED RICE SYNDROME

History

Epidemics of an acute heart disease broke out in rural Japan a hundred years ago, the
etiology of which was never determined. Uraguchi (1971) analyzed the records of cases
of the disease called acute cardiac beriberi (Shoshinkakke) and concluded that the ailment
was probably a human mycotoxicosis.

Acute cardiac beriberi was associated with the consumption of polished rice and was
initially thought to be an avitaminosis. In 1910, however, the Japanese government took
action to exclude mouldy rice from the markets and the incidence of acute cardiac
beriberi dropped dramatically.

Uraguchi (1971) suggested that acute cardiac beriberi may have resulted from eating
"yellowed rice" Such a foodstuff became pigmented and toxic to rats, and produced
symptoms similar to those observed in humans affected with beriberi.

Penicillium sp.
phialide conidia conidiophore

Mycology

Toxin producing fungi: Penicillium islandicum (Luteoskyrin and cyclochlorotine), P.

citreoviride (citreoviridin), P. rugulosum (Rugutosin) and citrinum (citrinin).

Chemistry

The empirical formula of citreoviridin is C23 H30 O6. It contains one methoxy group and
double bonds.

Clinical Symptoms

The clinical manifestations of acute cardiac beriberi, begin with palpitation, precordial
distress, and tachypnea; fallowed by nausea and vomitting, and difficult breathing.

Within a few days, the patient suffers severe anguish, pain, severe restlessness, or
sometimes violent mania. The right heart is dilated, heart sounds are abnormal, blood
pressure is low, and pulse is rapid, sometimes exceeding 120 beats/min, and the patient
faints.

The dyspnea increases, the skin of the extremities becames cold, dry, and cyanotic, and
the voice becames husky, Finally the pulse becames feeble, the pupils dilated,
consciousness is lost, and respiration fails.

BALKAN NEPHROPATHY

History

In 1957 to 1958, an unusual chronic disease of the kidney occurred endemically in

Yugoslavia, Rumania, and Bulgaria with a prevalence of 3-8 percent, mainly in rural
areas where food is home grown. It was common in 30-50 year- old - females. In
Yugoslavia, 6.5 percent of blood samples contained ochratoxin A at concentrations
between 3 and 5 mg/g serum (Hurt et a/, 1982).

Barnes (1967) suggested that plant toxins or mycotoxins may be an environmental factor
causing this human disease. Krogh et al, (1974) presented preliminary evidence to
associate the human disease with ingestion of ochratoxin A (OTA).

This nephrotoxic compound occurs in feeds and foodstuffs and is considered a major
determinant of porcine nephropathy, a form of kidney damage strikingly similar to that
seen in Balkan nephropathy cases.

Renal porcine nephropathy has been reported regulary from Denmark since 1928. The
law in Denmark requires that all abnormal gross appearance of kidneys must be analysed
for OTA and the toxin concentration exceeds 10 µg/g which corresponds to 50 µg/ml in
the blood, the entire carcass is condemned. Nephropathy has also been reported in
chickens.

Mycology

Toxin-producing fungi: Aspergillus ochraceous and Penicillium viridicatum

Chemistry

Ochratoxin is a dihydroisocoumarin derivative produced by seven species of Penicillium

and six species of Aspergillus including A. ochraceous.

AFLATOXINS

History

Historically, the aflatoxins were discovered as a consequence to the death of 100,000 of

turkey poults ("Turkey X disease"), ducklings and chicks in England in 1960 with a loss
of at least several hundred thousand dollars. The problem was eventually traced to feed
contamination, specifically a shipment of Brazilian peanut meal used as poultry feed
produced by Old Cake Mills, Ltd. in London. This meal, termed Rosetti meal (from the
name of the ship in which it was imported), proved to be both toxic and carcinogenic and
was found to be contaminated with the common fungus, Aspergillus flavus.

The active principles were extracted and isolated from A. flavus cultures by a group in
England and the Netherlands (Van der Zijden. et al, 1962; Nesbitt et al, 1962), chemically
identified by a research group in the U.S. (Asao et al, 1963), and named aflatoxin the "a"
from Aspergillus and the "fla" from flavus.

The aflatoxins are a group of secondary fungal metabolises which have been
epidemiologically implicated as environmental toxin and carcinogens in man. They are
substituted coumarins containing a fused dihydrofurofuran moiety. There are four
primary aflatoxins, named B1, B2, G1 and G2, from their blue and green fluorescence,
respectively, on thin-layer chromatographic plates. As was generally known to be the
case with aflatoxin toxicity and carcinogenicity, a similar potency series, namely AFB1 >
AFB2 > AFG1 > AFG2 > has been established for aflatoxin - induced mutagenic activity
and DNA damage.

Aflatoxin metabolises

AFM1 is a King hydroxylation of AFB1 at the 4 position. This metabolise was first
detected in the milk of cows ingesting AFB1. It has also been detected in the urine of
humans consuming AFB1 contaminated peanut butter. AFM1 could induce typical bile
duct hyperplasia in day - old ducklings characteristic of AFB1.

This hemiacetal AFB2a metabolise is produced by hepatic microsome from AFB1 by

hydration of the 2, 3 vinyl ether double bond resulting in hydroxylation at the 2 position.

It is possible that AFB2a plays an important role in aflatoxin acute toxicity by binding
and inhibiting key enzymes of intermediary metabolism and resulting in liver cell
necrosis.

AFP1 is produced by the O-demethylation of AFB1 and was the major excretory product
in the urine of AFB1 -treated rhesus monkeys, where it was present as glucoronide and
sulfate conjugates. It is formed in vitro by human microsomes. AFP1 was nontoxic to
chicken embryos and nonmutagenic.

AFQ1 is formed from AFB1 by ring hydroxylation of the carbon atom ß to the carbonyl
function of the cyclopentenone ring. It represents one-third to one- half of the metabolises
produced from AFB1 by monkey and human liver microsomes. This methabolite is
nontoxic and only 1-2% is mutagenic as AFB1 in Ames assay.

Reduction of the cyclopentenone carbonyl function of AFB1 to hydroxy group by an

NADPH dependent cytoplasmic enzyme produced AFL. The toxicity of AFL is only 1/18
that of AFB1 in one day - old duckling bile duct hypenplasia assay.

AFLH was formed from AFB1, using both the microsomes and soluble enzyme
preparation from human liver. (Salhab and Hisch, 1975). The compound is a dihydoxyl
derivative of AFB1, with substitutions at a cyclopentenone carbonyl function and the,B
carbon. It was not toxic to the chicken embryo test.

Aflatoxin and Acute Poisoning

1. Taiwan Outbreak
In 1967, there was an outbreak of apparent poisoning of 26 persons in two Taiwan rural
villages (Ling et al, 1967). The victims had consumed moldy rice for up to 3 weeks; they
developed edema of the legs and feet, abdominal pain, vomiting, and palpable livers, but
no fever. The three fatal cases were children between 4 and 8 years. Autopsies were not
done, and the caused of death could not be established. In a retrospective analysis of the
outbreak, a few rice samples from affected households were assayed for aflatoxins. Two
of the samples contained up to 200 ppb aflatoxin B1.

2. Kenya Case

In 1982, an acute hepatitis was reported in Kenya. There were 12 of 20 cases who died
with malaise, abdominal discomfort, with subseguent appearance of dark urine and
jaundice. Local dogs who shared the food were affected, with many deaths. Stored grain
appeared to be the cause of the outbreak. Aflatoxin was detected in two liver samples (39
and 89 ppb). Histologically, there was centrolobuiar necrosis.

3. Uganda Case

Aflatoxin B1 was circumstantially associated with the death of a 15-year-old African boy
in Uganda (Serch - Hanssen, 1970). The youth, his younger brother, and his sister became
ill at the same time; the young sibling survived, but the older boy died 6 days later with
symptoms resembling the victims in the Taiwan outbreak.

An autopsy revealed pulmonary edema, flabby heart. and diffuse necrosis of the liver.
Histology demonstrated centrolobular necrosis with a mild fatty liver, in addition to the
edema and congestion in the lungs.

A sample of the cassava eaten by these children contained 1.7 ppm aflatoxin which
Alpert and Serck Hanssen (1970) suggest may be lethal if such a diet is consumed over a
few weeks. This estimate is based on the acute toxicity of aflatoxin B1 in monkeys.

4. Reye's Syndrome

Reye's syndrome is an acute and often fatal childhood illness which is characterized by
encephalopathy and fatty degeneration of viscera (EFDV). This syndrome was first
described between 1951 and 1962 in Austraria by Reye et al.

Clinically, the main features of this syndrome are vomiting, convulsions and coma.
Hypoglycemia, hypogly, corrhachia and elevated serum transaminases are the most
constant biochemical abnormalities. Fatty degeneration in the liver and kidneys, and
cerebral edema are the major autopsy findings.

Thailand case

As reported by Bourgeois et al (1971), a 3-year-old Thai boy was brought to a Northeast

provincial hospital after a 12-hr illness of fever, vomiting, coma and convulsions. The
child died 6 hours later, and an autopsy revealed marked cerebral with neuronal
degeneration, severe fatty metamorphosis of the liver, kidneys, and heart, and
Iymphocytolysis in the spleen, thymus, and Iymphnodes.

Upon admission of the child to the hospital, a medical team travelled to the boy's home
and obtained a small sample of steamed glutinous rice which had been cooked 2 days
before the onset of the child's illness and reportedly has been the only food the family had
for the past 2 days. The small size of the sample precluded an accurate measurement of
the amount of aflatoxins present but clinical assay indicated the amount was in the parts
per million range. The rice examined also contained toxigenic strains of A. flavus, A.
clavatus, A. ochraceous, and A. niger, (as shown in Table 1, Angsubhakorn et al, 1978).

Table 1: Toxins which may have caused death in a boy with Reye's syndrome in the
village of Baan Kota, Khonkaen Province, Thailand.

Fungi isolated Toxins produced LD50(mg.kg-1) in rat Organs involed

A. clavatus Kotanin — —
Desmethyl Kotanin — —
Cytochalasin E 0.98 Brain-edema
(1 day-Old)
Tryptoquivaline — Tremorgen
Tryptoquivalone — Tremorgen
A. niger Malciformin G. 0.9 (newborn) —
0.87 —
(28 day-old) —
A. ochraceous Ochratoxin A. 22 Renal tubular
necrosis
A. flavus Aflatoxin B1 7.2 (weanling) Hepatic periportal
necrosis

The B. form was found in one or more autopsy specimens from 22 of the 23 Reye's
syndrome cases (Shank et at, 1971) and in several instances, these aflatoxin
concentrations were as high as those seen in specimens from monkeys poisoned with the
aflatoxins (Bourgeois, et al, 1971) (Table 2).

Table 2: Comparison of aflatoxin B1 concentration in autopsy specimens from

Reye's syndromecases and experimetal monkeys poisoned with aflatoxin B1.

Specimen Aflatoxin B1 concentrations (µg/kg

specimen or ml fulid)
Human* Monkey (AFB1 mg.kg-
1)
Brain 1-4 30 (40 5)
Liver 93 163(40.5)
Kidney 1-4 87(40.5)
Bile 8 163(40.5)
Stool 123 —
Stomach content 127 —
Intestinal content 81 —

The trace amounts of aflatoxins in tissue specimens from control cases is thought to
reflect chronic low-level ingestion of the mycotoxin in that area of Thailand.

Introduction

Mycotoxins are toxic metabolises produced by fungi, especially by saprophytic moulds

growing on foodstuffs or animal feeds. They must always have been a hazard to man and
domestic animals, but until the past 30 years their effects have been largely overlooked.
Although poisonous mushrooms are carefully avoided, moulds growing on foods have
generally been considered to cause unaesthetic spoilage, without being dangerous to
health. Between 1960 and 1970 it was established that some fungal metabolises, now
called mycotoxins, were responsible for animal disease and death. In the decade
following 1970 it became clear that mycotoxins have been the cause of human illness and
death as well, and are still causing it.

It is now well established that mycotoxicoses (the diseases caused by mycotoxins) have
been responsible for major epidemics in man and animals at least during recent historic
times. The most important have been ergotism, which killed thousands of people in
Europe in the last thousand years, alimentary toxic aleukia (ATA) which was responsible
for the death of many thousands of people in the USSR in the 1940s;
stachybotryotoxicosis, which killed tens of thousands of horses and cattle in the USSR in
the 1930s; and aflatoxicosis, which killed 100,000 young turkeys in England in 1960 and
has caused death and disease in many other animals, and perhaps man as well. Each of
these diseases is now known to have been caused by growth of specific moulds which
produced one or more potent toxins, usually in one specific kind of commodity or feed.

It is important to distinguish between the effects of bacterial toxins and mycotoxins. The
classic bacterial toxins are proteins, which produce characteristic symptoms in only a few
hours, as the human body recognises them, and produces antibody mediated reactions to
them. Fungal toxins on the other hand, are almost all low molecular weight chemical
compounds which are not detected by antigens, and hence produce no obvious symptoms.
Mycotoxins are insidious poisons.

Mycotoxins can be acutely or chronically toxic, or both, depending on the kind of toxin
and the dose. In animals, acute diseases include liver and kidney damage, attack on the
central nervous system, skin disorders and hormonal effects. Nerve toxins may cause
trembling or even death. Skin disorders may be necrotic lesions or photosensitivity, while
hormonal effects include abortions in cattle, swollen genitals in pigs and a variety of
poorly defined disorders including vomiting in pigs, feed refusal and failure to thrive.
Toxins which act on the liver and kidney are especially difficult to detect and levels much
lower than those producing acute effects are often carcinogenic. When eaten in minute
quantities in the daily diet, they can cause cancers in experimental animals long after the
time of eating. It is probable that humans can be affected the same way.

Acute mycotoxicoses

Table 1 lists a number of mycotoxins, some of the moulds which are known to produce
them, and known or possible acute diseases with which they may be involved. In some
cases, the connection between mycotoxin and disease is fairly well documented. In other,
cause and effect are less certain. The most important disease which may have been due to
mycotoxins, are reviewed briefly below.

Ergotism

Ergotism occurred throughout the past thousand years in central Europe, and has
certainly killed many thousands of people. The fact that it was caused by a fungus has
been known for a long time, since at least 1750. The fungus, Claviceps purpurea, grows
in the ovaries of grains, especially rye, and the resulting sclerotia, called argots, are
difficult to separate from normal grain at milling, and become dispersed in flour made
from the grain.

Ergotism causes constrictions in blood vessels leading to the hands and feet. In extreme
cases death of cells (necrosis), bacterial infections (gangrene) and effects on the mind
(hallucinations) may occur, and in some cases death results. The toxins in argots are now
known to be alkaloids, some of which find use in pharmaceuticals. The last outbreak of
ergotism in Europe occurred in 1954. So far as I am aware, ergotism has not occurred in
Asia, but it has occurred in Ethiopia quite recently (King, 1979).

Alimentary toxic aleukia

ATA caused the deaths of many thousands of people in the USSR, especially in the
Orenburg District around the Caspian Sea, from 1942 to 1948. In some localities,
mortalities were as high as 60% of those afflicted, and 10% of the entire population.
Records show that ATA was also prevalent in earlier years.

ATA is an exceptionally nasty disease, causing fever, bleeding from the skin, nose, throat
and gums, necrosis, and suppression of the immune system. These features are similar to
radiation poisoning, and quite different from those caused by most other mycotoxins, or
bacterial toxins.

During World War II, labour was very scarce in Russia, resulting in delays in harvest,
and also food was very scarce, causing consumption of poor quality grain. Early studies
on ATA were inconclusive. During the 1970s it became clear that ATA was a
mycotoxicosis, and that the toxin responsible for ATA was the trichothecene toxin known
as T-2. It was produced by the growth of Fusarium species, F. sporotrichioides and F.
poae, in grain allowed to remain in the fields unharvested during winter.

Trichothecenes are now regarded as probably the most important mycotoxins, believed to
be responsible for a variety of diseases of both man and domestic animals. Most have
occurred in Europe, the USSR, Japan and the United States (Ueno, 1980). Toxicoses are
usually acute, but Marasas et al. (1979) have suggested that trichothecenes may be
involved in the high incidence of oesophageal cancer in the Republic of Transkei (South
Africa).

Trichothecenes are also at the centre of the "Yellow Rain" controversy which occurred
earlier this decade. According to some sources, trichothecenes were used as a chemical
warfare agent in South East Asia, causing the deaths of thousands of villagers in Laos and
along the ThaiKampuchean border (Watson et al., 1984). The facts in the Yellow rain
controvery have become obscured by politics, but two things are clear: people have died
from chemical poisoning in those areas, and trichothecenes are sufficiently toxic to have
been the cause.

There are no records of ATA in Asia, and it is not clear if trichothecene production is
likely in this region. We are currently carrying out studies aimed at providing information
about this point.

Acute cardiac beriberi

Another human mycotoxicosis of significance, acute cardiac beriberi was a common

disease in Japan, especially in the second half of last century. This disease is
characterised by difficulties with breathing, nausea and vomiting, and after 2 to 3 days,
severe pain and distress. Progressive paralysis may lead to respiratory failure and death.

Beriberi is the general name for vitamin deficiencies resulting from the consumption of
polished rice. Careful work by Uraguchi (1971) showed that acute cardiac beriberi may
not be a vitamin deficiency, but a toxicosis. In 1910 the incidence of acute cardiac
beriberi suddenly decreased in Japan: Uraguchi points out that this coincided with
implementation of a government inspection scheme which dramatically reduced the sale
of mouldy rice. The incidence of true beriberi, resulting from the consumption of
polished rice, was unaffected. It is notable that victims of this acute cardiac beriberi were
often young healthy adults.

Acute cardiac beriberi is caused by citreoviridin, a mycotoxin produced by the

comparatively rare species, Penicillium citreonigrum. Although it no longer occurs in
Japan, there is no proof that acute cardiac beriberi does not still exist in some other part
of Asia.

Onyalai
Onyalai is an acute disease characterised by haemorrhaging lesions in the mouth. It has
been endemic in Africa, especially in Southern Sahara regions for at least 80 years (Rabie
et al., 1975). It is much more common in rural than urban populations, Since many of the
people affected by onaylai subsist on millet, Rabie et al. (1975) suggested the possible
role of a mycotoxin in this disease. Toxigenic isolates of Phoma sorghina were found to
be common in millet consumed by affected populations, and Rabie et al. (1975) were able
to reproduce many of the symptoms of onyalai in rats fed maize and wheat on which P.
sorghina had been grown.

Chronic mycotoxicoses

Some of the toxins discussed in this section (Table 2) may produce acute effects, but they
are more significant because of their ability to cause long term disease. The best known
and most studied of chronic mycotoxicoses are produced by aflatoxins.

Aflatoxins

Aflatoxins were discovered in 1960 following the deaths of 100,000 young turkeys in
England, and high incidences of liver disease in ducklings in Kenya and hatchery reared
trout in the United States, English scientists soon established the cause of all these
problems to be toxins produced by the common moulds Aspergillus flavus and A.
parasiticus. Assay techniques were devised and preliminary toxicological studies carried
out by 1963 (Sargent et al., 1963).

Aflatoxins are named by letters and subscripts. Aflatoxin B1, the most toxic compound,
is usually associated with aflatoxin B2: these compounds are usually formed by both A.
flavus and A. parasiticus. Aflatoxins G1 and G2 are formed only by A. parasiticus (Klich
and Pitt, 1988). Aflatoxins M1 and M2 are formed in milk when aflatoxin B1 and G1 are
ingested in feed.

Aflatoxins have both acute and chronic toxicity in animals, and produce four quite
different effects: acute liver damage, liver cirrhosis, induction of tumours and teratogenic
and other genetic effects.

Acute toxicity of aflatoxins to humans has been encountered only rarely (Shank, 1978).
In 1967, 26 Taiwanese in two farming communities became ill with apparent food
poisoning. Nineteen of those affected were children of whom three died. Rice from
affected households was blackish green and mouldy, and appeared to be of poorer quality
than rice from households which were unaffected. Samples of the mouldy rice contained
about 200 g/kg of aflatoxin B1, which was probably responsible for the outbreak. Post
mortem examinations were not carried out.

In 1974, an outbreak of hepatitis that affected 400 Indian people, of whom 100 died, was
almost certainly due to aflatoxins. The outbteak was traced to corn heavily contaminated
with Aspergillus flavus and containing up to 15 mg/kg aflatoxins. Consumption by some
of the affected adults was estimated to be 2-6 mg in a single day.
It has been suspected for some time that aflatoxin may be a factor in Reye's syndrome, a
common cause of death in South East Asian children. Shank et al. (1971) found
significant levels of aflatoxins (1-4 g/kg) in livers of 23 Thai children who had died of
Reye's syndrome. Children who have died from Reye's syndrome in Czechoslovakia and
in New Zealand have also been found to have had aflatoxins in their livers at autopsy.

Kwashiorkor, a disease of children in Northern Africa and elsewhere in undernourished

populations, which is usually attributed to nutritional deficiencies, may also be related to
aflatoxin intake (Hendrickse et al. 1982). Aflatoxin-induced liver damage may make
these children less able to cope with the high protein diets usually recommended as the
cure for kwashiorkor (Newell, 1983).

Aflatoxins and primary liver cancer

Scarcely two years after the discovery of aflatoxins came the first warnings that they may
cause human liver cancer. This disease has a high incidence in central Africa and South
East Asia. When epidemiological evidence suggested a possible correlation with
mycotoxins in the food supply, field studies were initiated on an international basis.
Epidemiological data were coupled with analyses of those foods that form the staple diets
of stable indigenous populations. Stability in both diet and population is essential in
studies of this kind because of the long induction period (10-20 years) for human liver
cancer.

Ochratoxins

In the early 1970s, observers in Denmark noted a high incidence of nephritis (kidney
inflammation) in pigs at slaughter. A search for possible causes eventually showed the
presence of ochratoxin A, a mycotoxin originally reported from Aspergillus ochraceus.
Analysis of pig feeds showed that 50% of samples contained ochratoxin A at levels up to
27 mg/kg. The mould responsible was reported to be Penicillium viridicatum, but has
more recently been shown to be P. verrucosum (Pitt, 1987). This species occurs
commonly in Danish barley (Frisvad and Viuf, 1985).

The discovery of ochratoxin led to analyses of pork and bacon. It was found that a
significant proportion of ingested ochratoxin lodged unchanged in depot fat. The risk to
humans is difficult to assess, but as pig meats are an important part of the Danish diet and
rural populations usually eat their own uninspected pigs, a risk certainly exists. Death
rates from kidney failure are high in some Danish rural areas and it is resonable to
suppose the cause is ochratoxin.

Penicillium verrocusum has not been reported to occur in Asia. However, Aspergillus
ochraceus and related species which also produce ochratoxin do. The significance of
ochratoxin A in tropical climates has not yet been assessed however.

Conclusions
The potential role of aflatoxins and other mycotoxins in cancer should be sufficient
incentive for further investigations, especially in Asia and other tropical areas where the
occurrence and significance of mycotoxins has not yet been fully assessed.

While it may not be possible to produce a food supply completely free of mycotoxins,
improvements in storage and handling of grains, nuts and other commodities can
minimise mould growth, and so reduce the risk of mycotoxin contamination in food
supplies.

Mycotoxins
J. W. Bennett1* and M. Klich2
Department of Cell and Molecular Biology, Tulane University, New Orleans, Louisiana 70118,1
Agricultural Research Service, Southern Regional Research Center, New Orleans, Louisiana 701242
*
Corresponding author. Mailing address: Department of Cell and Molecular Biology, Tulane University,
New Orleans, LA 70118. Phone: (504) 788-8101. Fax: (504) 788-8765. E-mail: jbennett@tulane.edu .
This article has been cited by other articles in PMC.
ABSTRACT
Mycotoxins are secondary metabolites produced by microfungi that are capable of
causing disease and death in humans and other animals. Because of their pharmacological
activity, some mycotoxins or mycotoxin derivatives have found use as antibiotics, growth
promotants, and other kinds of drugs; still others have been implicated as chemical
warfare agents. This review focuses on the most important ones associated with human
and veterinary diseases, including aflatoxin, citrinin, ergot akaloids, fumonisins,
ochratoxin A, patulin, trichothecenes, and zearalenone.

The term mycotoxin was coined in 1962 in the aftermath of an unusual veterinary crisis
near London, England, during which approximately 100,000 turkey poults died (22, 82).
When this mysterious turkey X disease was linked to a peanut (groundnut) meal
contaminated with secondary metabolites from Aspergillus flavus (aflatoxins), it
sensitized scientists to the possibility that other occult mold metabolites might be deadly.
Soon, the mycotoxin rubric was extended to include a number of previously known
fungal toxins (e.g., the ergot alkaloids), some compounds that had originally been
isolated as antibiotics (e.g., patulin), and a number of new secondary metabolites revealed
in screens targeted at mycotoxin discovery (e.g., ochratoxin A).
The period between 1960 and 1975 has been termed the mycotoxin gold rush (157)
because so many scientists joined the well-funded search for these toxigenic agents.
Depending on the definition used, and recognizing that most fungal toxins occur in by the
 Thus, mycotoxins can be classified as hepatotoxins, nephrotoxins, neurotoxins,
immunotoxins, and so forth. Cell biologists put them into generic groups such as
teratogens, mutagens, carcinogens, and allergens. Organic chemists have attempted to
classify them by their chemical structures (e.g., lactones, coumarins); biochemists
according to their biosynthetic origins (polyketides, amino acid-derived, etc.); physicians
Toxicology and Human Health
Toxicologists tend to concentrate their efforts on hazardous chemicals such as
polyaromatic hydrocarbons, heavy metals, and organic pesticides. Because they have
devoted less effort to natural products, agriculturalists, chemists, microbiologists, and
veterinarians who are often unfamiliar with the basic principles of toxicology have
conducted most of the mycotoxin research. There has been a lot of reinventing of the
wheel and sometimes an imprecise use of toxicology jargon.
For example, mycotoxicoses, like all toxicological syndromes, can be categorized as
acute or chronic. Acute toxicity generally has a rapid onset and an obvious toxic
response, while chronic toxicity is characterized by low-dose exposure over a long time
period, resulting in cancers and other generally irreversible effects (128). Accepting that
it is often difficult to distinguish between acute and chronic effects, many papers on
mycotoxicoses blur this basic dichotomy entirely, and it is not always easy to interpret
the published data on purported health effects. Almost certainly, the main human and
veterinary health burden of mycotoxin exposure is related to chronic exposure (e.g.,
cancer induction, kidney toxicity, immune suppression). However, the best-known
mycotoxin episodes are manifestations of acute effects (e.g., turkey X syndrome, human
ergotism, stachybotryotoxicosis).

o In order to demonstrate that a disease is a mycotoxicosis, it is necessary to

show a dose-response relationship between the mycotoxin and the disease. For human
populations, this correlation requires epidemiological studies. Supportive evidence is
provided when the characteristic symptoms of a suspected human mycotoxicosis are
evoked reproducibly in animal models by exposure to the mycotoxin in question (121).
Human exposure to mycotoxins is further determined by environmental or biological
monitoring. In environmental monitoring, mycotoxins are measured in food, air, or other
samples; in
(238). Milk products can also serve as an indirect source of aflatoxin. When cows
consume aflatoxin-contaminated feeds, they metabolically biotransform aflatoxin B1 into
a hydroxylated form called aflatoxin M1 (267).
Aflatoxin is associated with both toxicity and carcinogenicity in human and animal
populations (70, 186, 193, 232). The diseases caused by aflatoxin consumption are
loosely called aflatoxicosesBecause (279).

A mycotoxin (from Greek μύκης (mykes, mukos) "fungus" and Latin (toxicum)
"poison") is a toxic secondary metabolite produced by organisms of the fungus kingdom,
commonly known as molds.[1][2] The term 'mycotoxin' is usually reserved for the toxic
chemical products produced by fungi that readily colonize crops.[1] Most fungi are aerobic
(use oxygen) and are found almost everywhere in extremely small quantities due to the
minute size of their spores. They consume organic matter wherever humidity and
temperature are sufficient. One mold species may produce many different mycotoxins
and/or the same mycotoxin as another species.[3]

Where conditions are right, fungi proliferate into colonies and mycotoxin levels become
high. The reason for the production of mycotoxins is not yet known; they are neither
necessary for growth nor the development of the fungi.[4] Because mycotoxins weaken the
receiving host, the fungus may use them as a strategy to better the environment for
further fungal proliferation. The production of toxins depends on the surrounding
intrinsic and extrinsic environments and the toxins vary greatly in their severity,
depending on the organism infected and its susceptibility, metabolism, and defense
mechanisms.[5] Some of the health effects found in animals and humans include death,
identifiable diseases or health problems, weakened immune systems without specificity
to a toxin, and as allergens or irritants. Some mycotoxins are harmful to other micro-
organisms such as other fungi or even bacteria; penicillin is one example.[6]

Mycotoxins can appear in the food chain as a result of fungal infection of crops, either by
being eaten directly by humans, or by being used as livestock feed. Mycotoxins greatly
resist decomposition or being broken down in digestion, so they remain in the food chain
in meat and dairy products. Even temperature treatments, such as cooking and freezing,
do not destroy mycotoxins.

Although various wild mushrooms contain an assortment of poisons that are definitely
fungal metabolites causing noteworthy health problems for humans, they are rather
arbitrarily excluded from discussions of mycotoxicology. In such cases the distinction is
based on the size of the producing fungus and human intention.[7] Mycotoxin exposure is
almost always accidental whereas with mushrooms improper identification and ingestion
causing mushroom poisoning is commonly the case. Ingestion of misidentified
mushrooms containing mycotoxins may result in hallucinations. The cyclopeptide-
produced Amanita phalloide is well known for its toxic potential and is responsible for
approximately 90% of all mushroom fatalities.[8] The other primary mycotoxin groups
found in mushrooms include: orellanine, monomethylhydrazine, disulfiram-like,
hallucinogenic indoles, muscarinic, isoxazole, and gastrointestinal (GI)-specific irritants.
[9]
The bulk of this article is about mycotoxins that are found in microfungi other than
poisons from mushrooms or macroscopic fungi.[7]

Many international agencies are trying to achieve universal standardization of regulatory

limits for mycotoxins. Currently, over 100 countries have regulations regarding
mycotoxins in the feed industry, in which 13 mycotoxins or groups of mycotoxins are of
concern.[10] The process of assessing a need for mycotoxin regulation includes a wide
array of in-laboratory testing which includes extracting, clean-up and separation
techniques.[11] Most official regulations and control methods are based on high-
performance liquid techniques (HPLC) through international bodies.[11] It is implied that
any regulations regarding these toxins will be in co-ordinance with any other countries
with which a trade agreement exists. Many of the standards for the method performance
analysis for mycotoxins is set by the European Committee for Standardization(CEN).[11]
Although, one must take note that scientific risk assessment in commonly influenced by
culture and politics which, in turn, will affect trade regulations of mycotoxins.[12] [edit]
Major groups

Aflatoxins are a type of mycotoxin produced by Aspergillus species of fungi, such as A.

flavus and A. parasiticus.[14] The umbrella term aflatoxin refers to four different types of
mycotoxins produced, which are B1, B2, G1, and G2.[15] Aflatoxin B1, the most toxic, is a
potent carcinogen and has been directly correlated to adverse health effects, such as liver
cancer, in many animal species.[14] Aflatoxins are largely associated with commodities
produced in the tropics and subtropics, such as cotton, peanuts, spices, pistachios and
maize.[14][15]

Ochratoxin is a mycotoxin that comes in three secondary metabolite forms, A, B, and C.

All are produced by Penicillium and Aspergillus species. The three forms differ in that
Ochratoxin B (OTB) is a nonchlorinated form of Ochratoxin A (OTA) and that
Ochratoxin C (OTC) is an ethyl ester form Ochatoxin A.[16] Aspergillus ochraceus is
found as a contaminant of a wide range of commodities including beverages such as beer
and wine. Aspergillus carbonarius is the main species found on vine fruit, which releases
its toxin during the juice making process.[17] OTA has been labeled as a carcinogen and a
nephrotoxin, and has been linked to tumors in the human urinary tract, although research
in humans is limited by confounding factors.[16][17]

Citrinin is a toxin that was first isolated from Penicillium citrinum, but has been
identified in over a dozen species of Penicillium and several species of Aspergillus. Some
of these species are used to produce human foodstuffs such as cheese (Penicillium
camemberti), sake, miso, and soy sauce (Aspergillus oryzae). Citrinin is associated with
yellow rice disease in Japan and acts as a nephrotoxin in all animal species tested.
Although it is associated with many human foods (wheat, rice, corn, barley, oats, rye, and
food colored with Monascus pigment) its full significance for human health is unknown.
Citrinin can also act synergistically with Ochratoxin A to depress RNA synthesis in
murine kidneys.[7]

Ergot Alkaloids are compounds produced as a toxic mixture of alkaloids in the sclerotia
of species of Claviceps, which are common pathogens of various grass species. The
ingestion of ergot sclerotia from infected cereals, commonly in the form of bread
produced from contaminated flour, cause ergotism the human disease historically known
as St. Anthony’s Fire. There are two forms of ergotism gangrenous affecting blood
supply to extremities and convulsive which affects the central nervous system. Modern
methods of grain cleaning have significantly reduced ergotism as a human disease,
however it is still an important veterinarian problem. Ergot alkaloids have been used
pharmaceutically.[7]

Patulin is a toxin produced by the P. expansum, Aspergillus, Penicillium, and

Paecilomyces fungal species. P. expansum is especially associated with a range of moldy
fruits and vegetables, in particular rotting apples and figs.[18][19] It is destroyed by the
fermentation process and so is not found in apple beverages, such as cider. Although
patulin has not been shown to be carcinogenic, it has been reported to damage the
immune system in animals.[18] In 2004, the European Community set limits to the
concentrations of patulin in food products. They currently stand at 50 μg/kg in all fruit
juice concentrations, at 25 μg/kg in solid apple products used for direct consumption, and
at 10 μg/kg for children's apple products, including apple juice.[18][19]

Fusarium toxins are produced by over 50 species of Fusarium and have a history of
infecting the grain of developing cereals such as wheat and maize.[20][21] They include a
range of mycotoxins, such as: the fumonisins, which affect the nervous systems of horses
and may cause cancer in rodents; the trichothecenes, which are most strongly associated
with chronic and fatal toxic effects in animals and humans; and zearalenone, which is
not correlated to any fatal toxic effects in animals or humans. Some of the other major
types of Fusarium toxins include: beauvercin and enniatins, butenolide, equisetin, and
fusarins.[22]

[edit] Binding agents and deactivators

In the feed and food industry it has become common practice to add mycotoxin binding
agents such as Montmorillonite or bentonite clay in order to affectively adsorb the
mycotoxins.[23] To reverse the adverse effects of mycotoxins, the following criteria are
used to evaluate the functionality of any binding additive:

• Efficacy of active component verified by scientific data

• A low effective inclusion rate
• Stability over a wide pH range
• High capacity to adsorb high concentrations of mycotoxins
• High affinity to adsorb low concentrations of mycotoxins
• Affirmation of chemical interaction between mycotoxin and adsorbent
• Proven in vivo data with all major mycotoxins
 • Non-toxic, environmentally friendly component

Since not all mycotoxins can be bound to such agents, the latest approach to mycotoxin
control is mycotoxin deactivation. By means of enzymes (esterase, epoxidase), yeast
(Trichosporon mycotoxinvorans) or bacterial strains (Eubacterium BBSH 797),
mycotoxins can be reduced during pre-harvesting contamination. Other removal methods
include physical separation, washing, milling, heat-treatment, radiation, extraction with
solvents, and the use of chemical or biological agents. Irradiation methods have proven to
be effective treatment against mold growth and toxin production.[23]

Food Poisoning Causes

More than 250 known diseases can be transmitted through food. The CDC
estimates unknown or undiscovered agents cause 81% of all food-borne
illnesses and related hospitalizations. Many cases of food poisoning are
not reported because people suffer mild symptoms and recover quickly.
Also, doctors do not test for a cause in every suspected case because it
does not change the treatment or the outcome.

• The known causes of food poisoning can be divided into two

categories: infectious agents and toxic agents.

o Infectious agents include viruses, bacteria, and parasites.

o Toxic agents include poisonous mushrooms, improperly
prepared exotic foods (such as barracuda), or pesticides on fruits
and vegetbles.
• Food usually becomes contaminated from poor sanitation or
preparation. Food handlers who do not wash their hands after using the
bathroom or have infections themselves often cause contamination.
Improperly packaged food stored at the wrong temperature also
promotes contamination.

Food Poisoning Symptoms

Symptoms of food poisoning depend on the type of contaminant and the

amount eaten. The symptoms can develop rapidly, within 30 minutes, or
slowly, worsening over days to weeks. Most of the common contaminants
cause nausea, vomiting, diarrhea, and abdominal cramping. Usually food
poisoning is not serious, and the illness runs its course in 24-48 hours.
• Viruses account for most food poisoning cases where a specific
contaminant is found.

o Noroviruses are a group of viruses that cause a mild illness

(often termed "stomach flu") with nausea, vomiting, diarrhea,
abdominal pain, headache, and low-grade fever. These symptoms
usually resolve in two to three days. It is the most common viral
cause of adult food poisoning and is transmitted from water,
shellfish, and vegetables contaminated by feces, as well as from
person to person. Outbreaks are more common in densely
populated areas such as nursing homes, schools and cruise ships
(hence why the virus is also known as the "Cruise Ship Illness"). The
term norovirus has been approved as the official name for this group
of viruses. Several other names have been used for noroviruses,
including Norwalk-like viruses, caliciviruses (because they belong to
the virus family Caliciviridae), and small round structured viruses.
o Rotavirus: Causes moderate to severe illness with vomiting
followed by watery diarrhea and fever. It is the most common cause
of food poisoning in infants and children and is transmitted from
person to person by fecal contamination of food and shared play
areas.
o Hepatitis A: Causes mild illness with sudden onset of fever,
loss of appetite, and feeling of tiredness followed by jaundice, which
is a yellowing of the eyes and skin. It is transmitted from person to
person by fecal contamination of food.
• Bacteria can cause food poisoning in two different ways. Some
bacteria infect the intestines, causing inflammation and difficulty
absorbing nutrients and water, leading to diarrhea. Other bacteria
produce chemicals in foods (known as toxins) that are poisonous to the
human digestive system. When eaten, these chemicals can lead to
nausea and vomiting, kidney failure, and even death.

o Salmonellae: Salmonellae are bacteria that may cause food

poisoning; the illness itself is often referred to as Salmonella or
Salmonella infection. Salmonellae cause a moderate illness with
nausea, vomiting, crampy diarrhea, and headache, which may come
 back a few weeks later as arthritis (joint pains). In people with
impaired immune systems (such as people with kidney disease or
HIV/AIDS or those receiving chemotherapy for cancer), Salmonellae
can cause a life-threatening illness. The illness is transmitted by
undercooked foods such as eggs, poultry, dairy products, and
seafood.
o Campylobacter: Causes mild illness with fever, watery
diarrhea, headache, and muscle aches. Campylobacter is the most
commonly identified food-borne bacterial infection encountered in
the world. It is transmitted by raw poultry, raw milk, and water
contaminated by animal feces.
o Staphylococcus aureus: Causes moderate to severe
illness with rapid onset of nausea, severe vomiting, dizziness, and
abdominal cramping. These bacteria produce a toxin in foods such
as cream-filled cakes and pies, salads (most at risk are potato,
macaroni, egg, and tuna salads, for example) and dairy products.
Contaminated salads at picnics are common if the food is not chilled
properly.
o Bacillus cereus: Causes mild illness with rapid onset of
vomiting, with or without diarrhea and abdominal cramping. It is
associated with rice (mainly fried rice) and other starchy foods such
as pasta or potatoes. It has been speculated that this bacteria may
also be ued as a potential terrorist weapon.
o Escherichia coli (E coli): Causes moderate to severe
illness that begins as large amounts of watery diarrhea, which then
turns into bloody diarrhea. There are many different types of this
bacteria. The worst strain can cause kidney failure and death (about
3%-5% of all cases). It is transmitted by eating raw or undercooked
hamburger, unpasteurized milk or juices, or contaminated well
water. Outbreaks of food poisoning due to E. coli have also occurred
following ingestion of contaminated produce.
o Shigella (traveler’s diarrhea): Causes moderate to severe
illness with fever, diarrhea containing blood or mucus or both, and
the constant urge to have bowel movements. It is transmitted in
water polluted with human wastes.
 o Clostridium botulinum (botulism): Causes severe illness
affecting the nervous system. Symptoms start as blurred vision. The
person then develops problems talking and overall weakness.
Symptoms then progress to breathing difficulty and the inability to
move arms or legs. Infants and young children are particularly at
risk. It is transmitted in foods such as home-packed canned goods,
honey, sausages, and seafood.

Because botulism can be released in the air, it is considered a

potential biological weapon for terrorists.

o Vibrio cholerae: Causes mild to moderate illness with

crampy diarrhea, headache, nausea, vomiting, and fever with chills.
It strikes mostly in the warmer months of the year and is transmitted
by infected, undercooked, or raw seafood.
• Foodborne illness usually arises from improper handling, preparation, or food
storage. Good hygiene practices before, during, and after food preparation can reduce
the chances of contracting an illness. There is a general consensus in the public health
community that regular hand-washing is one of the most effective defenses against
the spread of foodborne illness. The action of monitoring food to ensure that it will
not cause foodborne illness is known as 'popfood safety'. Foodborne disease can also
be caused by a large variety of toxins that affect the environment. For foodborne
illness caused by chemicals, see Food contaminants.

Foodborne illness can also be caused by pesticides or medicines in food and naturally
toxic substances like poisonous mushrooms or reef fish.

[edit] Bacteria

Bacteria are a common cause of foodborne illness. In the United Kingdom during 2000
the individual bacteria involved were as follows: Campylobacter jejuni 77.3%,
Salmonella 20.9%, Escherichia coli O157:H7 1.4%, and all others less than 0.1%.[3] In
the past, bacterial infections were thought to be more prevalent because few places had
the capability to test for norovirus and no active surveillance was being done for this
particular agent. Symptoms for bacterial infections are delayed because the bacteria need
time to multiply. They are usually not seen until 12–72 hours or more after eating
contaminated food.

Most common bacterial foodborne pathogens are:

 • Campylobacter jejuni which can lead to secondary Guillain–Barré syndrome and
periodontitis[4]
• Clostridium perfringens, the "cafeteria germ"[5]

Salmonella spp. – its S. typhimurium infection is caused by consumption of eggs

or poultry that are not adequately cooked or by other interactive human-animal
pathogens[6][7][8]

Salmonella

• Escherichia coli O157:H7 enterohemorrhagic (EHEC) which causes hemolytic-

uremic syndrome

Other common bacterial foodborne pathogens are:

• Bacillus cereus
• Escherichia coli, other virulence properties, such as enteroinvasive (EIEC),
enteropathogenic (EPEC), enterotoxigenic (ETEC), enteroaggregative (EAEC or
EAgEC)
• Listeria monocytogenes
• Shigella spp.
• Staphylococcus aureus
• Streptococcus
• Vibrio cholerae, including O1 and non-O1
• Vibrio parahaemolyticus
• Vibrio vulnificus
• Yersinia enterocolitica and Yersinia pseudotuberculosis

Less common bacterial agents:

• Brucella spp.
• Corynebacterium ulcerans
• Coxiella burnetii or Q fever
• Plesiomonas shigelloides

[edit] Exotoxins

In addition to disease caused by direct bacterial infection, some foodborne illnesses are
caused by exotoxins which are excreted by the cell as the bacterium grows. Exotoxins
can produce illness even when the microbes that produced them have been killed.
Symptoms typically appear after 1–6 hours depending on the amount of toxin ingested.

• Clostridium botulinum
• Clostridium perfringens
• Staphylococcus aureus
• Bacillus cereus
For example Staphylococcus aureus produces a toxin that causes intense vomiting. The
rare but potentially deadly disease botulism occurs when the anaerobic bacterium
Clostridium botulinum grows in improperly canned low-acid foods and produces botulin,
a powerful paralytic toxin.

Pseudoalteromonas tetraodonis, certain species of Pseudomonas and Vibrio, and some

other bacteria, produce the lethal tetrodotoxin, which is present in the tissues of some
living animal species rather than being a product of decomposition.

[edit] Mycotoxins and alimentary mycotoxicoses

The term alimentary mycotoxicoses refers to the effect of poisoning by Mycotoxins

through food consumption. Mycotoxins sometimes have important effects on human and
animal health. For example, an outbreak which occurred in the UK in 1960 caused the
death of 100,000 turkeys which had consumed aflatoxin-contaminated peanut meal. In
the USSR in World War II, 5000 people died due to Alimentary Toxic Aleukia (ALA).[9]
The common foodborne Mycotoxins include:

• Aflatoxins – originated from Aspergillus parasiticus and Aspergillus flavus. They

are frequently found in tree nuts, peanuts, maize, sorghum and other oilseeds,
including corn and cottonseeds. The pronounced forms of Aflatoxins are those of
B1, B2, G1, and G2, amongst which Aflatoxin B1 predominantly targets the liver,
which will result in necrosis, cirrhosis, and carcinoma.[10][11] In the US, the
acceptable level of total aflatoxins in foods is less than 20 μg/kg, except for
Aflatoxin M1 in milk, which should be less than 0.5 μg/kg.[12] The official
document can be found at FDA's website.[13][14]
• Altertoxins – are those of Alternariol (AOH), Alternariol methyl ether (AME),
Altenuene (ALT), Altertoxin-1 (ATX-1), Tenuazonic acid (TeA) and Radicinin
(RAD), originated from Alternaria spp. Some of the toxins can be present in
sorghum, ragi, wheat and tomatoes.[15][16][17] Some research has shown that the
toxins can be easily cross-contaminated between grain commodities, suggesting
that manufacturing and storage of grain commodities is a critical practice.[18]
• Citrinin
• Citreoviridin
• Cyclopiazonic acid
• Cytochalasins
• Ergot alkaloids / Ergopeptine alkaloids – Ergotamine
• Fumonisins – Crop corn can be easily contaminated by the fungi Fusarium
moniliforme, and its Fumonisin B1 will cause Leukoencephalomalacia (LEM) in
horses, Pulmonary edema syndrome (PES) in pigs, liver cancer in rats and
Esophageal cancer in humans.[19][20] For human and animal health, both the FDA
and the EC have regulated the content levels of toxins in food and animal feed.[21]
[22]

• Fusaric acid
• Fusarochromanone
• Kojic acid
 • Lolitrem alkaloids
• Moniliformin
• 3-Nitropropionic acid
• Nivalenol
• Ochratoxins – In Australia, The Limit of Reporting (LOR) level for Ochratoxin A
(OTA) analyses in 20th Australian Total Diet Survey was 1 µg/kg,[23] whereas the
EC restricts the content of OTA to 5 µg/kg in cereal commodities, 3 µg/kg in
processed products and 10 µg/kg in dried vine fruits.[24]
• Oosporeine
• Patulin – Currently, this toxin has been advisably regulated on fruit products. The
EC and the FDA have limited it to under 50 µg/kg for fruit juice and fruit nectar,
while limits of 25 µg/kg for solid-contained fruit products and 10 µg/kg for baby
foods were specified by the EC.[24][25]
• Phomopsins
• Sporidesmin A
• Sterigmatocystin
• Tremorgenic mycotoxins – Five of them have been reported to be associated with
molds found in fermented meats. These are Fumitremorgen B, Paxilline, Penitrem
A, Verrucosidin, and Verruculogen.[26]
• Trichothecenes – sourced from Cephalosporium, Fusarium, Myrothecium,
Stachybotrys and Trichoderma. The toxins are usually found in molded maize,
wheat, corn, peanuts and rice, or animal feed of hay and straw.[27][28] Four
trichothecenes, T-2 toxin, HT-2 toxin, diacetoxyscirpenol (DAS) and
deoxynivalenol (DON) have been most commonly encountered by humans and
animals. The consequences of oral intake of, or dermal exposure to, the toxins
will result in Alimentary toxic aleukia, neutropenia, aplastic anemia,
thrombocytopenia and/or skin irritation.[29][30][31] In 1993, the FDA issued a
document for the content limits of DON in food and animal feed at an advisory
level.[32] In 2003, US published a patent that is very promising for farmers to
produce a trichothecene-resistant crop.[33]
• Zearalenone
• Zearalenols

[edit] Emerging foodborne pathogens

Many foodborne illnesses remain poorly understood. Approximately sixty percent of

outbreaks are caused by unknown sources.[citation needed]

• Aeromonas hydrophila, Aeromonas caviae, Aeromonas sobria

Proper storage and refrigeration of food help in the prevention of food poisoning

Prevention is mainly the role of the state, through the definition of strict rules of hygiene
and a public services of veterinary surveying of animal products in the food chain, from
farming to the transformation industry and delivery (shops and restaurants). This
regulation includes:
 • traceability: in a final product, it must be possible to know the origin of the
ingredients (originating farm, identification of the harvesting or of the animal) and
where and when it was processed; the origin of the illness can thus be tracked and
solved (and possibly penalized), and the final products can be removed from the
sale if a problem is detected;
• enforcement of hygiene procedures like HACCP and the "cold chain";
• power of control and of law enforcement of veterinarians.

In August 2006, the United States Food and Drug Administration approved Phage
therapy which involves spraying meat with viruses that infect bacteria, and thus
preventing infection. This has raised concerns, because without mandatory labelling
consumers wouldn't be aware that meat and poultry products have been treated with the
spray. [1]

At home, prevention mainly consists of good food safety practices. Many forms of
bacterial poisoning can be prevented even if food is contaminated by cooking it
sufficiently, and either eating it quickly or refrigerating it effectively[citation needed]. Many
toxins, however, are not destroyed by heat treatment.

Mo

o Ascaris lumbricoides
o Eustrongylides sp.
o Trichinella spiralis
o Trichuris trichiura
• Protozoa:
o Acanthamoeba and other free-living amoebae
o Cryptosporidium parvum
o Cyclospora cayetanensis
o Entamoeba histolytica

Giardia lamblia

Giardia lamblia

o Sarcocystis hominis
o Sarcocystis suihominis
o Toxoplasma gondii

Types of Food Spoilage with Causative Organisms

Food Types of spoilage Causative microorganisms

Fresh meat Putrefaction Clostridium, Pseudomonas, Porteus,
Souring Alcaligenes, Chromobacterium.
Chromobacterium,
Lactobacillus,Pseudomonas.
Cured meat Mouldy Penicillium, Aspergillus,Rhizopus.
Souring Pseudomonas, Micrococcus,
Greening Bacillus.
Slimy Lactobacilli Streptococci,Pediococci.

Leuconostoc

Fish Discolouration Pseudomonas

Putrefaction Chromobacterium, Halobacterium,
Micrococcus
Poultry Odour, Slime Pseudomonas, Alcaigenes,
Xanthomonas.
Eggs Green rot Pseudomonas Fluorescens
Colourless rot Pseudomonas, Alcaigenes,
Black rot Chromobacterium, Coliform.
Fungal rot Proteus
Penicillium, Mucor
Fresh fruits Bacterial soft rot Erwinia carotovera, Pseudomonas
and Gray mould rot spp.
vegetables Rhizopus soft rot Botryitis cinerea
Blue mould rot Rhizopus nigrican
Black mould rot Penicillium italicum
Sliminess or Souring Aspergillus niger, Alternaria
Saprophytic bacteria
Pickles,Sauer, Black pickles Bacillus nigricans
kraut Soft pickles Bacillus spp.
Slimy kraut Lactobacillus Plantarum, L.
Pink kraut cucumeris
Rhodotorula(asporogenous yeasts)
Sugar Ropy syrup Aerobacter aerogenes
products, Yeasty Saccharomyces,
Honey, Pink syrup Torula,Zygosaccharomyces
Syrups Green syrup Micrococcus roseus
Mouldy Pseudomonas fluorescens
Aspergillus, Penicillium
Bread Mouldy Rhizopus, Aspergillus
Ropy Penicillium
Red bread Bacillus spp.
Serratia marcesens