Showing posts with label Seminars. Show all posts
Showing posts with label Seminars. Show all posts

TOXIC EFFECT OF HEAVY METALS

TOXIC EFFECT OF HEAVY METALS

BY

ZAINAB FAROK JIBRIL

MARCH, 2018
ABSTRACT
          Heavy metal are generally referred to as those metal which posses a specific density of more 5gkm2 and adversely affect the environment and living organisms. The most commonly found heavy metal in waste water include arsenic, cadmium, chromium e.t.c. which risks for human health and environment and they also enter surrounding by natural means and through human activities. This research was conducted to investigate the toxic effect of heavy metals. Arsenic is none of the most important heavy metals causing disquiet from both ecological and individual health. Lead is a highly toxic metal whose widespread use has caused extensive environmental contamination and health problems in many parts of the word. Mercury adversely affects the marine environment. Cadmium is the deventh toxic heavy metal as per ATSDR ranking. It is a by-product of zinc production which humans or animals may get exposed to at work or in the environment. Once this metal gets absorbed by humans, it will accumulate inside the body through life.       







INTRODUCTION
Metal are substances with high electrical conductivity, malleability and luster, which voluntarily lose their electrons to form cations, metals are found naturally in the earth’s crust and their composition vary among different localities, resulting in spatial variations of surrounding concentrations. The metal distribution in the atmosphere is monitored by the properties of the given metal land various environment factors (Khlifi and Hamza, 2010). The main objective of this review is to provide insight into the sources of heavy metals and their harmful effect on the environment and living organisms. Heavy metals are generally referred density of more than 5gkm3 and adversely affect the environment and living organisms (Jarup, 2003). These metals are quintessential to maintain various biochemical and physiological functions in living organisms when in very low concentrations, however they become noxious when they exceed certain there should concentrations. Although it is acknowledged that heavy metals have many adverse health effects and last for a long period of time, heavy metal exposure contimues and is increasing in manu parts of the world. Heavy metals are significant environmental pollutants and their toxicity is a problem of increasing significance for ecological, involuntary, nutritional and environmental reasons (Jaishankar et al., 2013; Nagajyoti et al., 2010). The most commonly found heavy metals in waste water include arsenic, cadium, chromium, copper, lead, nickel and zink, all of which cause risks for human health and the environment (Lambert et al., 2000). Heavy metals enter the surroundings by natural weathering of the earth’s crush mining, industrial effluents, urban runoff, sewage discharge, insect or disease control agents applied to crops and many others (Moraise et al., 2012). Figure 1 show the global production and consumption of selected toxic metal during 1850-1990 (adapted from Nriagu, 1996).
          The global production and consumption of selected toxic metals during 1850-1990 (adapted from Nriagu, 1996).
          Although these metal have crucial biological functions in plants and animals, sometimes their chemical coordination and oxidation-reduction properties have given them an additional benefit so that they can escape control mechanisms such as homeostasis, transport, compart metallization and binding to required cell constituents. These metals bind with protein sites which are made for them by displacing original metals from their natural binding sites causing malfunctioning of cells and ultimately toxicity. Previous research has found that oxidative deterioration of biological macromolecular is primarily due to binding of heavy metals to the DNA and nuclear protein (flora et al., 2008).
Heavy metals and their toxicity mechanisms
Arsenic
Arsenic is one of the most important heavy metal causing disquiet from both the ecological and individual health stand points [hughes et al 1988]. It has a semimetallic property, is prominently toxic and carcinogenic and is extensively available in the form of oxides or sulfides or as a salt of iron, sodium, calcium, copper, etc. (singh et al., 2007). Asentic is the twentieth most abundant element on earth and its inorganic forms such as arsenite and arsenate compounds are lethdl to the environment and living creatures. Human may encounter arsenic by natural means, industrial sources of from unintended sources. Drinking water may be containes by use of arsenical pesticides, natural miniral deposits or in appropriate disposal of arsenical chemicals. Deliberate consumption of arsenic in case of suicidal attempts or accidental consumption by children may also result in cases of acute poisoning (Manzumder, 2008; saha et al., 1999). Arsenic is a protophydryl group of cells causing mal functioning the sulphydryl group of cells causing mal functioning of cell respiration, enzymes and mitosis (Garden and Quastel, 1948).
Mechanism of arsenie toxicity

In arsenic biotrans formation, harmful in organic arsenic biotra, algae, fungi and humans to give monomethylarsonic acid (MMA) and dimethy larsimi acid (DMA). In this biotransformation process, these inorganic arsenic species (IAS) are converted enzymetically to methy lated arsenicals which are the end metabolites and the biomarker of chronic arsenic exposure.
iAs (V) à iAs (iii) à MMA (V) à DMA (V)
          biomethylation is a detoxification process and end products are methylated inorganic arsenic such as MMA (V) and DMA  (V) is not excreted and remains inside the cell as an intermediate and remains inside the cell as an intermediate product.
Monomethylarsenic acid (MMA iii), an inter mediate product is found to be highly toxic compared to other arsenicals, potentially accountable for arsenic induced carcinogenesis (singh et al., 2007).
LEAD
          Lead is a hihly toxic metal whose widespread use has cause extensive environmental contamination and health problems in many parts of the world. Lead is a bright silvery metal, slightly blush in a dry atmosphere. It begins to tarnish on contact with air, thereby forming a complex mixture of compounds, depending on the given conditions. Figure 2 shows various sources of led pollution in the environment (Sharma and ubey 2005). The sources of lead exposure include mainly industrial processes, food and smoking, drinking water and demostic sources. The sources of lead were gasoline and house paint which has been extended to lead bullets, plumbing pitcher, storage batteries, toys, and faucets (Thurmer et al., 2002). In the US, more than 100 to 200, 000 tons of lead per year is being released  from vehicle exhausts some is taken up by plants, fixation to soil and flow into water bodies, hence human exposure of lead in the general population is either due to food or drinking water (Goyer, 1990). Lead is an extremely toxic heavy metal that disturbs various plant physiological processes and unlike other metals, such as Zinc, copper and manganese, ir does not play any biological functions. A plant with high lead concentration fastens the production of reactive oxygen species (ROS), causing tipid memberance damage that ultimately leads to damage of chlorophyll and photosynthetic processes and suppresses the overall growth of the plant (Najeeb et al., 2014). Some research revealed that lead is capable of inhibiting the growth of tea plant by reducing biomass and debases the tea quality by changing the quality of its components (young sheng et al., 2011). Even at low concentrations, lead treatment was found to cause huge instability in ion uptatke by plants, which in turn leads to significant metabolic changes in photosynthetic capacity and ultimately in a strong inhibition of plant growth (Mostafa et al., 2012).

















Various pollution in the environmental (Adapted from sharama and Dubey, 2015).
Mechanisms of lead toxicity
          Lead metal causes toxicity in living cells by following ionic mechanism and that oxidatioive stress. Many researchers have shown that oxidative stress in living cells is caused by the imbalance between the production of free radicals and the generation of antioxidants to detoxify the reactive intermidiates of to repair the resulting damage. Figure 3 shows the attack of heavy metals on a cell and the balance between ROS production and the subsequent defense presented by antioxidants. Antioxidants as e.g glatathing, present in the cell protect it from free redicals such as H2O2 under the influence of lead, however, of antioxidabts decreases. Since glutathione exists both in reduced (GSH) and oxidized (G S S G) state, the reduced form of glutathione gives Its reducing equivalents (h++e-) from its thiol groups of cystein to ROS in order to make them stable. In the presence of the enzyme glutathrome peroxidase, reduced glutathione readily binds with another molecule of glutathione after donating the election and forms glutathione disulfide (GSSG). The reduced form (GSH) of glutathione accounts for 90% of the total glutathione content and the oxidezed form (GSSG) accounts for 10% under normal additionas. Yet under the condition of oxidative stress, the concentration of GSSG ezcellds the concentration of GSH. Another biomarker for oxidative stress in lipid peroxidation, since the free radicals collects electron from lipid molecules present inside the cell membrane, which eventually cause lipid peroxidation (wadhwa et al., 2012; flora et al., 2012). At very high concentration ROS may cause structural damage to cells, proteins, nucleis acid, membrance and lipids, resulting in a stressed situation at cellular level (Mathew et al., 2011
Figure 3
The attack of heavy metals on a cell and the balance between ROS production and the subsequent defense presented by antioxidants.
The ionic mechanism of lead toxicity occurs mainly due to the ability of lead metal ions to replace other bivalent cations like ca2+, mg2+ fe2+ and monovalent cations Na2+, which ultimately disturbs the biological metabolism of the cell. The ionic mechanism of lead toxicity causes significant changes in various biological processes such as cell adhension, intra and inter-cellular signaling, protein folding, maturation, apoptosis, ionic transportation, enzyme regulation, and release of neurotransmitters. Lead can substitute calcium even in picomolar concentration affecting protein kinase C, which regulates neural excitation and memory storage (flora et al., 2012).
Mercury
The metallic mercury is a naturally occurring metal which is a shiny silver-white, odorless liquid and becomes colorless and odorless gas when heated. Mercury is a very toxic and exceedingly bio accumulative. Its presence adversely affects the marine environment and hence many studies are directed towards the distribution of mercury pollution include anthropogenic activities such as agriculture, municipal waste water discharges, mining, incineration, and discharges of industrial waste water (chen et al. 2012).
Mercury exists mainly in three forms: metallic elements, inorganic salts and organic compounds, each of which possesses different toxicity are present widdly in water resources such as lakes, rivers and oceans where they are taken up by the microorganisms and get transformed into methyl mercury within the microorganism, eventually undergoing bio magnification casing significant disturbance to aquatic lives. Consumption of this contaminated equatic animal is the major route of human exposure to methyl mercury (transande et al., 2005). Mercury is extensively used in thermometers, barometers, pyrometers, hydrometers, mercury are lamps, fluorescent lamps and as a catalyst. It is also being used in pulp and paper industries as a component of batteries and in dental.
Figure 4
          The global usage of mercury for various applications (total in 2005: 3,760 metric tons). Mechanism of mercury toxicity
          Mercury is well known as a hazardous metal and its toxicity is a common cause of acute heavy metal poisoning with cases of 3,596 in 1997 by the American Association, of poison control centers. Methyl mercury is a neurotoxic compound which is responsible for micro tubule destruction, mitochondrial damage, lipid peroxidation and accumulation of neurotoxic molecules such as serotonin, aspartate and glutamate (Patrick 2002). The total amount of mercury emission into the environment has been assessed at 2,200 metric tons annually (ferrara et al., 2000). It is estimated that 8 to 10% of American women have merury levels that would induce neuro logical disorders in any child they gave birth to, according to the both the environment protection agency and national academy of science (haley, 2006). Animal which are exposed to toxic mercury have shown adverse neurological and behavioral changes. Rabbits when exposed to 28.8mg/m3 mercury vapor for 1 to 13 weeks have shown vague pathological changes, marked cellular degeneration and brain necrosis (Ashe et al. , 1953).
          The brain remains the target organ for mercury, yet it can impair any organ and lead to mal functioning of nerves, kidneys and muscles. It can interrupt with intracellular calcium homeo stasis. Mercury binds to freely available thiols as the stability constants are high (Patrick, 2002). Mercury vapors can cause bronchitis, asthma and temporary respiratory problems. Mercury plays a key role in damaging the tertiary and quaternary protein structure and alfers the cellular function by attaching to the selenohydryl and sulfhy dry groups which undergo reaction with methyl mercury and hamper the cellular structure. It also intervenes with the process of transcription and translation resulting in the disappearance of ribosomes and eradication of endoplasmic reticulum and the activity of natural killer cells. The cellular integrity is also affected causing free radical formation. The basis for heavy metal chelation is that even though the mercury sulfhy dryl bond is stable and divided to surrounding sulfhy dryl consisting ligands, it also contributes free sulfhy dryl groups to promote metal mobility within the ligands (bern hoft, 2011).
Cadmium
          Cadmium is the seventh most toxic heavy metal as per ATSDR ranking. It is a byproduct of zinc production which humans or animals may get exposed to at work or in the environment. Once this metal gets absorbed by humans, it will accumulate inside the body throughout life. This metal was first used in World War 1 as a substitute for tin and in paint industries as a pigment. In today’s scenario, it is also being used in rechargeable batteries, for special alloys production and also present in tobacco smoke. About three fourths of cadmium is used in alkaline batteries as an electrode component, the remaining part is used in coatings, pigment and plantings and as a plastic stabilizer. Human may get exposed to this metal primarily by inhalation and ingestion and can suffer from acute and chronic in toxications. Cadmium distributed in the environment will remain in soils and sediment for several decades. Plants gradually take up these metals which get accumulated in them and concentrate along the food chain, reaching ultimately the human body. In the US, more than 500,000 workers get exposed to toxic cadmium each year as per the agency for toxic substance and diss=ease registry (Bernard, 2008, mutlu et l. , 2012). Researchers have shown that in china the total area polluted by cadmium is more than 11,000 hectares and its annual amount of industrial waste of cadmium discharged into the environment is assessed to be more than 680 tons. In japan and china, environment cadmium exposure is comparatively higher than in any other country (Han et al., 2009). Cadmium is predominanthly found in fruit and vegetables due to its high rate of soil-to-plant aransfer (satarug et al., 2011). Cadmium is a highly toxic non essential heavy metal that is well recognized for its adverse influence on the enzymatic systems of cells, oxidative stress and for inducing nutritional deficiency in plants (Irfan et al., 2013)
Mechanism of cadmium toxicity
          The mechanism of cadmium toxicity is not under stood clearly but their effects on cells are known (patrrick, 2003). Cadmium concentration increases 3,000 fold when it binds to cystein- rich protein such as me tallothionein. In the liver, the cystein-matallothionein complex causes hepa to toxicity and then it circulates to the kidney and gets acculated in the renal tissue causing nephro toxicity. Cadmium has the capability to bind with cystein, glutamate, his tidine and aspartate ligands and can lead to the deficiency of iron (castag netto et al., 2002). Cadmium and Zinc have the same oxidation and hence can replace zinc present in metallo thionein, there by inhibiting it from acting as a free radical scavenger within the cell.









Conclusion
          The toxic effects of heavy metals affect the environment and living organisms (jarup, 2003). Heavy metals are significant environmental pollutants and their toxicity is a problems of increasing significant for ecological, evolutionary, nutritional and environment reasons (jaishankar et al., 2013; nagajyti et al., 2010). Most of the commonly heavy metals are found waste water include arsenic cadmium, chromium, copper, lead, nickel and zinc, all of which cause risks for human health and the environment (lambert et al., 2000) various sources at heavy metals include soil erosion, natural weathering of the earth’s crust, mining, industrial effluents, urbanrun off, sewage discharge, insect or disease control agent applied to crops and many others (morals et al., 2012).











Reference
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m.behaviour of mercury in the animal organism
following inhalation. AMA Arch ind Hyg occup med. 1952; 7 (1):19-43 (pubmed)
·        Bernard A. cadmium & its adverse effects on human health. Indian J med Res. 2008; 128 (4): 557- 64 (pubmed)
·        Berhoft. The basis for heavy metal chelation, the bond of sulfhydryl is stable and the division to surrounding sulfhydryl consisting ligands. 2011.
·        Chen leones, Phillips D. mercury pollution include anthropogenic activities. 2012
·        Castagnetto JM, Hennessy SW, Roberts VA, Getzoff ED, tainer JA, pique ME. MDB: the matalloprotien data base and browser at the scripps research institute. Nucleic acids res. 2002; 30 (1):379-382.
·        Ferrere, albretsen J. , albinska D. the total amount of mercury emission into the environment 2000.
·        Flora, shepard N, zisa D, angerio. Picomolar concentration affectinf protein kinase C. 2012
·        Gardon& Quastel. Protoplastic poison affects the sulphy dryl group of cells causing malfunctioning of cells organells 1948.
·        Goyer. Human exposure of lead in the general population due to food or drinking water,1990.
·        Haley. The environmental protection agency and national academy of science 2005.
·        Irfan, alina M, Azrina A, mohd yunus As,. Adverse influence on the enzymatic systems of cells, oxidative stress and for inducing nutritional deficiency in plants 2013.
·        Jaishankar, Abate E, Hussein S, significant environmental pollutants and their toxicity.
·        Jarup. The effect of environment and living organisms 2003.
·        Khlifi & Hamza-chaffa:. The metal distribution in the atmosphere monitored by the properties of the given metal and by various environmental factors. 2010.
·        Nriagu. The global production and cosumption of selected toxic metals during (1850-1990) 1996.
·        Sharma & Dubey. Various sources of lead pollution in the environment, 2005.
·        Trasande, widiak M, ciupa T. consumption of contaminated equatic animal is the major route of human exposure to methyl mercury 2005.
·        Yong sheng, mohd izuan effendi H, mohd zakiuddin S, some research revealed that lead is capable of inhibiting the growth of tea plant by reducing bio-mass and debases the tea quality by changing the quality of its components 2011.





Hardware Form factor


1.0 Introduction
Form factor is an aspect of hardware design which defines and prescribes the size, shape, and other physical specifications of components, particularly in consumer electronics and electronic packaging.( Webopedia and WhatIs.com 2016).  A form factor may represent a broad class of similarly sized components, or it may prescribe a specific standard.
In computers, the form factor is the size, configuration, or physical arrangement of a computing device. The term is commonly used in describing the size and/or arrangement of a device, a computer case or chassis or one of its internal components such as a motherboard or a daughterboard. If you see the term applied to software or programming, it will usually mean the size of the program or the amount of memory required to run the program effectively. When used to refer to the size of a free-standing computer or other device, it's close in meaning to footprint. (Margaret Rouse, 2018)
1.1 Aim
v  The aim of this work is to investigate the Hardware form factor as an aspect of hardware who prescribes the size, shape and other physical specifications of components, particularly in consumer electronic and electronic packages.   
1.2 Objective
v  The objective of this research is to outline the Hardware form factors as a configuration or physical arrangement of a computing device.
 2.0 Review of Related Literature
In computing, the form factor is the specification of a motherboard – the dimensions, power supply type, location of mounting holes, number of ports on the back panel, etc. Specifically, in the IBM PC compatible industry, standard form factors ensure that parts are interchangeable across competing vendors and generations of technology, while in enterprise computing, form factors ensure that server modules fit into existing rack mount systems. Traditionally, the most significant specification is for that of the motherboard, which generally dictates the overall size of the case. Small form factors have been developed and implemented. (Wikipedia, 2018)
Overview of form factors


Comparison of some common motherboard form factors
A PC motherboard is the main circuit board within a typical desktop computer, laptop or server. Its main functions are as follows:
  • To serve as a central backbone to which all other modular parts such as CPU, RAM, and hard drives can be attached as required to create a computer
  • To be interchangeable (in most cases) with different components (in particular CPU and expansion cards) for the purposes of customization and upgrading
  • To distribute power to other circuit boards
  • To electronically co-ordinate and interface the operation of the components
As new generations of components have been developed, the standards of motherboards have changed too. For example, the introduction of AGP and, more recently, PCI Express have influenced motherboard design. However, the standardized size and layout of motherboards have changed much more slowly and are controlled by their own standards. The list of components required on a motherboard changes far more slowly than the components themselves. For example, north bridge microchips have changed many times since their introduction with many manufacturers bringing out their own versions, but in terms of form factor standards, provisions for north bridges have remained fairly static for many years.
Although it is a slower process, form factors do evolve regularly in response to changing demands. IBM's long-standing standard, AT (Advanced Technology), was superseded in 1995 by the current industry standard ATX (Advanced Technology Extended), which still governs the size and design of the motherboard in most modern PCs. The latest update to the ATX standard was released in 2007. A divergent standard by chipset manufacturer VIA called EPIA (also known as ITX, and not to be confused with EPIC) is based upon smaller form factors and its own standards.
Differences between form factors are most apparent in terms of their intended market sector, and involve variations in size, design compromises and typical features. Most modern computers have very similar requirements, so form factor differences tend to be based upon subsets and supersets of these. For example, a desktop computer may require more sockets for maximum flexibility and many optional connectors and other features on board, whereas a computer to be used in a multimedia system may need to be optimized for heat and size, with additional plug-in cards being less common. The smallest motherboards may sacrifice CPU flexibility in favor of a fixed manufacturer's choice. (Wikipedia, 2018)
Notebook computers, for example, are a form factor unto themselves because they all take the same  "clamshell" form, are typically rectangular and open to a keyboard on the flat surface and a screen on the top. Notebooks are also available in a variety of form factors that identify a type of product and market area.
Here are a few different notebook form factors:
An ultrabook is a category of thin and light laptop computers designed to bridge the market gap between tablets and premium notebook PCs. 
A netbook is a small, light, low-power notebook computer that has less processing power than a full-sized laptop but is still suitable for word processing, running a Web browser and connecting wirelessly to the Internet. 
A convertible tablet is a computer that can function as either a standalone touch screen device or as a notebook with a physical keyboard.
In electric motor terminology, a form factor is the amount of rectified current emitted from a direct current (DC) power source and is expressed as a ratio of the root-mean square (rms) value of the current to the average (av) current or Irms/lav. If the form factor differs much from pure non-pulsating DC (a value of 1.0), it indicates the possibility that motor and brush life will be shorter, (Margaret Rouse, 2018)
2.1 Comparisons
Tabular information
Form factor
Originated
Max. size[info 1]
width × depth
Notes
(typical usage, Market adoption, etc.)
IBM 1983
8.5 × 11 in
216 × 279 mm
Obsolete, see Industry Standard Architecture. The IBM Personal Computer XT was the successor to the original IBM PC, its first home computer. As the specifications were open, many clone motherboards were produced and it became a de facto standard.
AT (Advanced Technology)
IBM 1984
12 × 11–13 in
305 × 279–330 mm
Obsolete, see Industry Standard Architecture. Created by IBM for the IBM Personal Computer/AT, an Intel 80286 machine. Also known as Full AT, it was popular during the era of the Intel 80386 microprocessor. Superseded by ATX.
IBM 1985
8.5 × 10–13 in
216 × 254–330 mm
IBM's 1985 successor to the AT motherboard. Functionally equivalent to the AT, it became popular due to its significantly smaller size.
Intel 1995
12 × 9.6 in
305 × 244 mm
Created by Intel in 1995. As of 2017, it is the most popular form factor for commodity motherboards. Typical size is 9.6 × 12 in although some companies extend that to 10 × 12 in.
12 × 10.5 in
305 × 267 mm
Created by the Server System Infrastructure (SSI) forum. Derived from the EEB and ATX specifications. This means that SSI CEB motherboards have the same mounting holes and the same IO connector area as ATX motherboards.
12 × 13 in
305 × 330 mm
Created by the Server System Infrastructure (SSI) forum. Derived from the EEB and ATX specifications. This means that SSI CEB motherboards have the same mounting holes and the same IO connector area as ATX motherboards, but SSI EEB motherboards do not.
16.2 × 13 in
411 × 330 mm
Created by the Server System Infrastructure (SSI) forum. Derived from the EEB and ATX specifications.
1996
9.6 × 9.6 in
244 × 244 mm
A smaller variant of the ATX form factor (about 25% shorter). Compatible with most ATX cases, but has fewer slots than ATX, for a smaller power supply unit. Very popular for desktop and small form factor computers as of 2017.
AOpen 2005
5.9 × 5.9 in
150 × 150 mm
Mini-ATX is considerably smaller than Micro-ATX. Mini-ATX motherboards were designed with MoDT (Mobile on Desktop Technology) which adapt mobile CPUs for lower power requirement, less heat generation and better application capability.
Intel 1999
9.0 × 7.5 in
228.6 × 190.5 mm max.
A subset of microATX developed by Intel in 1999. Allows more flexible motherboard design, component positioning and shape. Can be smaller than regular microATX.
VIA 2001
6.7 × 6.7 in
170 × 170 mm max.
A small, highly integrated form factor, designed for small devices such as thin clients and set-top boxes.
VIA 2003
4.7 × 4.7 in
120 × 120 mm
Targeted at smart digital entertainment devices such as PVRs, set-top boxes, media centers and Car PCs, and thin devices.
VIA 2007
3.9 × 2.8 in
100 × 72 mm max.

VIA 2007
2.953 × 1.772 in
75 × 45 mm

Neo-ITX
VIA 2012
170 × 85 × 35 mm
Used in the VIA Android PC
BTX (Balanced Technology Extended)
Intel 2004
12.8 × 10.5 in
325 × 267 mm max.
A standard proposed by Intel as a successor to ATX in the early 2000s, according to Intel the layout has better cooling. BTX Boards are flipped in comparison to ATX Boards, so a BTX or MicroBTX Board needs a BTX case, while an ATX style board fits in an ATX case. The RAM slots and the PCI slots are parallel to each other.
Processor is placed closest to the fan. May contain a CNR board.
Intel 2004
10.4 × 10.5 in
264 × 267 mm max.

Intel 2004
8.0 × 10.5 in
203 × 267 mm max.

AMD 2007
8.0 × 9.6 in
200 × 244 mm max.

AMD 2007
8.0 × 6.7 in
200 × 170 mm max.

66 × 85 mm
Used in embedded systems and single board computers. Requires a baseboard.
95 × 114 mm
Used in embedded systems and single board computers. Requires a baseboard.
95 × 125 mm
Used in embedded systems and single board computers. Requires a carrier board. Formerly referred to as ETXexpress by Kontron.
COM Express Compact
95 × 95 mm
Used in embedded systems and single board computers. Requires a carrier board. Formerly referred to as microETXexpress by Kontron.
85.6 × 54 mm
A general-purpose "eco-conscious" mass-volume standard based around re-use of legacy PCMCIA. Has two variants: Type I (3.3mm high) and Type II (5.0mm high). Does not require a carrier board if the user-facing end provides power.
55 × 84 mm
Used in embedded systems and single board computers. Requires a carrier board. Formerly referred to as nanoETXexpress by Kontron. Also known as COM Express Ultra and adheres to pin-outs Type 1 or Type 10[1]
58 × 65 mm
Used in embedded systems and single board computers. Requires a carrier board.
Extended ATX (EATX)
Unknown
12 × 13 in
305 × 330 mm
Used in rackmount server systems. Typically used for server-class type motherboards with dual processors and too much circuitry for a standard ATX motherboard. The mounting hole pattern for the upper portion of the board matches ATX.
13.68 × 13 in
347 × 330 mm
Used in rackmount server systems. Typically used for server-class type motherboards with dual processors and too much circuitry for a standard E.ATX motherboard.
9 × 11–13 in
229 × 279–330 mm
Based on a design by Western Digital, it allowed smaller cases than the AT standard, by putting the expansion card slots on a Riser card. Used in slimline retail PCs. LPX was never standardized and generally only used by large OEMs.
8–9 × 10–11 in
203–229 × 254–279 mm
Used in slimline retail PCs.
3.8 × 3.6 in
Used in embedded systems. AT Bus (ISA) architecture adapted to vibration-tolerant header connectors.
3.8 × 3.6 in
Used in embedded systems. PCI Bus architecture adapted to vibration-tolerant header connectors.
3.8 × 3.6 in
Used in embedded systems.
PCI Express architecture adapted to vibration-tolerant header connectors.
3.8 × 3.6 in
Used in embedded systems.
PCI/104-Express without the legacy PCI bus.
Intel 1999
8–9 × 10–13.6 in
203–229 × 254–345 mm
A low-profile design released in 1997. It also incorporated a riser for expansion cards,[2] and never became popular.
UTX
TQ-Components 2001
88 × 108 mm
Used in embedded systems and IPCs. Requires a baseboard.
Intel 1998
14 × 16.75 in
355.6 × 425.4 mm
A large design for servers and high-end workstations featuring multiple CPUs and hard drives.
Unknown
16.48 × 13 in
418 × 330 mm
A proprietary design for servers and high-end workstations featuring multiple CPUs.
EVGA 2008
13.6 × 15 in
345.44 × 381 mm
A large design by EVGA currently featured on two motherboards; the eVGA SR2 and SRX. Intended for use with multiple CPUs. Cases require 9 expansion slots to contain this form-factor.
2005
95 × 114 mm
Used in embedded systems. Requires a baseboard.
1.      For boards which take expansion slots, the length of the expansion card aligns with the depth of the system board. The case may support cards longer than the depth of the main board.
2.2 Maximum number of expansion card slots
ATX case compatible:
Specification
Number
9
7
4
3
2
1



2.3 Visual examples of different form factors





2.4 PC/104 and EBX
PC/104 is an embedded computer standard which defines both a form factor and computer bus. PC/104 is intended for embedded computing environments. Single board computers built to this form factor are often sold by COTS vendors, which benefits users who want a customized rugged system, without months of design and paper work.
The PC/104 form factor was standardized by the PC/104 Consortium in 1992. (Wikipedia, 2018) An IEEE standard corresponding to PC/104 was drafted as IEEE P996.1, but never ratified. (Wikipedia, 2018)
The 5.75 × 8.0 in Embedded Board eXpandable (EBX) specification, which was derived from Ampro's proprietary Little Board form-factor, resulted from a collaboration between Ampro and Motorola Computer Group.
As compared with PC/104 modules, these larger (but still reasonably embeddable) SBCs tend to have everything of a full PC on them, including application oriented interfaces like audio, analog, or digital I/O in many cases. Also it's much easier to fit Pentium CPUs, whereas it's a tight squeeze (or expensive) to do so on a PC/104 SBC. Typically, EBX SBCs contain: the CPU; upgradeable RAM subassemblies (e.g., DIMM); Flash memory for solid state drive; multiple USB, serial, and parallel ports; onboard expansion via a PC/104 module stack; off-board expansion via ISA and/or PCI buses (from the PC/104 connectors); networking interface (typically Ethernet); and video (typically CRT, LCD, and TV).
2.5 Mini PC
Mini PC is a PC small form factor very close in size to an external CD or DVD drive. Mini PCs have proven popular for use as HTPCs.
Examples



.0 Methodology
The method involved internet review based on Search Engines and investigate on Hardware Form Factors
3.1 Evolution and standardization
As electronic hardware has become smaller following Moore's law and related patterns, ever-smaller form factors have become feasible. Specific technological advances, such as PCI Express, have had a significant design impact, though form factors have historically been slower to evolve than individual components. Standardization of form factors is vital for compatibility of hardware from different manufacturers.
Trade-offs
Smaller form factors may offer more efficient use of limited space, greater flexibility in the placement of components within a larger assembly, reduced use of material, and greater ease of transportation and use. However, smaller form factors typically incur greater costs in the design, manufacturing, and maintenance phases of the engineering lifecycle, and do not allow the same expansion options as larger form factors. In particular, the design of smaller form factor computers and network equipment must entail careful consideration of cooling (Wikipedia, 2018). End-user maintenance and repair of small form factor electronic devices such as mobile phones is often not possible, and may be discouraged by warranty voiding clauses; such devices require professional servicing—or simply replacement—when they fail (Wikipedia, 2018).
Examples
Size comparison of various mobile form factors (from smallest to largest: Nintendo DS Lite handheld, Asus Eee PC netbook, and MacBook laptop)
Computer form factors comprise a number of specific industry standards for motherboards, specifying dimensions, power supplies, placement of mounting holes and ports, and other parameters. Other types of form factors for computers include:
Components
Mobile form factors




References
Angel, Jonathan (2010). "Open standard defines tiny expansion modules". LinuxDevices.com. Retrieved 2014-03-18. http://archive.linuxgizmos.com/open-standard-defines-tiny-expansion-modules/
Margaret Rouse, (2018) “Form Factors” https://whatis.techtarget.com/definition/form-factor
Morrison, John (April 4, 2016). "Passive Cooling – An Experiment". SFF Network. Minutiae. Retrieved 13 June 2016.
Motherboards.org (2018) Form Factors Rev 1.3 : NLX" Motherboards.org  http://www.motherboards.org/articles/tech-planations/4_10.html
Prowse, David L. (September 27, 2012). "CompTIA A+ Exam Cram: Mobile Device Hardware and Operating Systems". Pearson IT Certification. Pearson Education. Retrieved 13 June 2016.
Web.archive.org (2008) "PC/104 Embedded Consortium's History". Archived from the original on 2008-02-11. Retrieved 2008-01-29. https://web.archive.org/web/20080211094103/http:/www.pc104.org/history.html

Webopedia (2018) Form factor. Webopedia. Quinstreet Enterprise. Retrieved 13 June 2016. http://www.webopedia.com/TERM/F/form_factor.html 

WhatIs.com (2018) Form factor. WhatIs.com. TechTarget. Retrieved 13 June 2016. http://whatis.techtarget.com/definition/form-facto
Wikipedia (2018) Form Factor Design https://en.wikipedia.org/wiki/Form_factor_%28design%29#cite_note-sff_network-3
Wikipedia (2018) Form Factor Design https://en.wikipedia.org/wiki/Form_factor_%28design%29#cite_note-prowse-4
Wikipedia, (2018) Computer Form Factor Cite Note 4 https://en.wikipedia.org/wiki/Computer_form_factor#cite_note-4


Wikipedia, Computer Form Factor Cite Note 5 (2018) https://en.wikipedia.org/wiki/Computer_form_factor#cite_note-5

Windows for Devices (2018) Atom Module shranks to Nano Size http://www.windowsfordevices.com/c/a/News/Atom-module-shrinks-to-nano-size